Sleep Medicine

Children who suffer from persistent bad dreams may be at increased risk for cognitive impairment or Parkinson’s disease (PD) later in life, new research shows.

Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.

It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.

However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.

“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.

He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.

The study was published online February 26 in The Lancet journal eClinicalMedicine.

Statistically significant

The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.

At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).

Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).

By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.

After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.

Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).

The associations remained when incident cognitive impairment and incident PD were analyzed separately.

Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).

The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).

Mechanism unclear

“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.

“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.

It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.

“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.

Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.

Clinical implications?

There are established treatments for childhood nightmares, including nonpharmacologic approaches.

“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.

But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?

“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.

The study received no external funding. Dr. Otaiku reports no relevant disclosures.

A version of this article first appeared on Medscape.com.

Children who suffer from persistent bad dreams may be at increased risk for cognitive impairment or Parkinson’s disease (PD) later in life, new research shows.

Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.

It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.

However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.

“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.

He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.

The study was published online February 26 in The Lancet journal eClinicalMedicine.

Statistically significant

The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.

At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).

Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).

By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.

After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.

Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).

The associations remained when incident cognitive impairment and incident PD were analyzed separately.

Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).

The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).

Mechanism unclear

“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.

“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.

It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.

“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.

Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.

Clinical implications?

There are established treatments for childhood nightmares, including nonpharmacologic approaches.

“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.

But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?

“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.

The study received no external funding. Dr. Otaiku reports no relevant disclosures.

A version of this article first appeared on Medscape.com.

Children who suffer from persistent bad dreams may be at increased risk for cognitive impairment or Parkinson’s disease (PD) later in life, new research shows.

Compared with children who never had distressing dreams between ages 7 and 11 years, those who had persistent distressing dreams were 76% more likely to develop cognitive impairment and roughly seven times more likely to develop PD by age 50 years.

It’s been shown previously that sleep problems in adulthood, including distressing dreams, can precede the onset of neurodegenerative diseases such as Alzheimer’s disease (AD) or PD by several years, and in some cases decades, study investigator Abidemi Otaiku, BMBS, University of Birmingham (England), told this news organization.

However, no studies have investigated whether distressing dreams during childhood might also be associated with increased risk for cognitive decline or PD.

“As such, these findings provide evidence for the first time that certain sleep problems in childhood (having regular distressing dreams) could be an early indicator of increased dementia and PD risk,” Dr. Otaiku said.

He noted that the findings build on previous studies which showed that regular nightmares in childhood could be an early indicator for psychiatric problems in adolescence, such as borderline personality disorder, attention-deficit/hyperactivity disorder, and psychosis.

The study was published online February 26 in The Lancet journal eClinicalMedicine.

Statistically significant

The prospective, longitudinal analysis used data from the 1958 British Birth Cohort Study, a prospective birth cohort which included all people born in Britain during a single week in 1958.

At age 7 years (in 1965) and 11 years (in 1969), mothers were asked to report whether their child experienced “bad dreams or night terrors” in the past 3 months, and cognitive impairment and PD were determined at age 50 (2008).

Among a total of 6,991 children (51% girls), 78.2% never had distressing dreams, 17.9% had transient distressing dreams (either at ages 7 or 11 years), and 3.8% had persistent distressing dreams (at both ages 7 and 11 years).

By age 50, 262 participants had developed cognitive impairment, and five had been diagnosed with PD.

After adjusting for all covariates, having more regular distressing dreams during childhood was “linearly and statistically significantly” associated with higher risk of developing cognitive impairment or PD by age 50 years (P = .037). This was the case in both boys and girls.

Compared with children who never had bad dreams, peers who had persistent distressing dreams (at ages 7 and 11 years) had an 85% increased risk for cognitive impairment or PD by age 50 (adjusted odds ratio, 1.85; 95% confidence interval, 1.10-3.11; P = .019).

The associations remained when incident cognitive impairment and incident PD were analyzed separately.

Compared with children who never had distressing dreams, children who had persistent distressing dreams were 76% more likely to develop cognitive impairment by age 50 years (aOR, 1.76; 95% CI, 1.03-2.99; P = .037), and were about seven times more likely to be diagnosed with PD by age 50 years (aOR, 7.35; 95% CI, 1.03-52.73; P = .047).

The linear association was statistically significant for PD (P = .050) and had a trend toward statistical significance for cognitive impairment (P = .074).

Mechanism unclear

“Early-life nightmares might be causally associated with cognitive impairment and PD, noncausally associated with cognitive impairment and PD, or both. At this stage it remains unclear which of the three options is correct. Therefore, further research on mechanisms is needed,” Dr. Otaiku told this news organization.

“One plausible noncausal explanation is that there are shared genetic factors which predispose individuals to having frequent nightmares in childhood, and to developing neurodegenerative diseases such as AD or PD in adulthood,” he added.

It’s also plausible that having regular nightmares throughout childhood could be a causal risk factor for cognitive impairment and PD by causing chronic sleep disruption, he noted.

“Chronic sleep disruption due to nightmares might lead to impaired glymphatic clearance during sleep – and thus greater accumulation of pathological proteins in the brain, such as amyloid-beta and alpha-synuclein,” Dr. Otaiku said.

Disrupted sleep throughout childhood might also impair normal brain development, which could make children’s brains less resilient to neuropathologic damage, he said.

Clinical implications?

There are established treatments for childhood nightmares, including nonpharmacologic approaches.

“For children who have regular nightmares that lead to impaired daytime functioning, it may well be a good idea for them to see a sleep physician to discuss whether treatment may be needed,” Dr. Otaiku said.

But should doctors treat children with persistent nightmares for the purpose of preventing neurodegenerative diseases in adulthood or psychiatric problems in adolescence?

“It’s an interesting possibility. However, more research is needed to confirm these epidemiological associations and to determine whether or not nightmares are a causal risk factor for these conditions,” Dr. Otaiku concluded.

The study received no external funding. Dr. Otaiku reports no relevant disclosures.

A version of this article first appeared on Medscape.com.

Nutritional deficiencies are one of the many causes of or contributors to symptoms in patients with psychiatric disorders. In this article, we discuss the prevalence of iron deficiency and its link to poor mental health, and how proper treatment may improve psychiatric symptoms. We also offer suggestions for how and when to test for and treat iron deficiency in psychiatric patients.

A common condition

Iron deficiency is the most common mineral deficiency in the world. According to the World Health Organization (WHO), approximately 25% of the global population is anemic and nearly one-half of those cases are the result of iron deficiency.¹ While the WHO has published guidelines defining iron deficiency as it relates to ferritin levels (<15 ug/L in adults and <12 ug/L in children), this estimate might be low.^2,3 Mei et al² found that hemoglobin and soluble transferrin receptors can be used to determine iron-deficient erythropoiesis, which indicates a physiological definition of iron deficiency. According to a study of children and nonpregnant women by Mei et al,² children with ferritin levels <20 ug/L and women with ferritin levels <25 ug/L should be considered iron-deficient. If replicated, this study suggests the prevalence of iron deficiency is higher than currently estimated.² Overall, an estimated 1.2 billion people worldwide have iron-deficiency anemia.⁴ Additionally, patients can be iron deficient without being anemic, a condition thought to be at least twice as common.⁴

Essential for brain function

Research shows the importance of iron to proper brain function.⁵ Iron deficiency in pregnant women is associated with significant neuropsychological impairments in neonates. Rodent studies have demonstrated the importance of iron and the effects of iron deficiency on the hippocampus, corpus striatum, and production of monoamines.⁵ Specifically, iron is a necessary cofactor in the enzymes tryptophan hydroxylase and tyrosine hydroxylase, which produce serotonin, dopamine, and norepinephrine. In rodent studies, monoamine deficits secondary to iron deficiency persist into adulthood even with iron supplementation, which highlights the importance of preventing iron deficiency during pregnancy and early life.⁵ While most research has focused on the impact of iron deficiency in infancy and early childhood, iron deficiency has an ongoing impact into adulthood, even if treated.⁶

Iron deficiency and psychiatric symptoms

Current research suggests an association between iron deficiency or low ferritin levels and psychiatric disorders, specifically depression, anxiety, and schizophrenia. In a web survey of 11,876 adults, Hidese et al⁷ found an association between a self-reported history of iron deficiency anemia and a self-reported history of depression. Another study of 528 municipal employees found an association between low serum ferritin concentrations and a high prevalence of depressive symptoms among men; no statistically significant association was detected in women.⁸ In an analysis of the Taiwan National Health Insurance Database from 2000 to 2012, Lee et al⁹ found a statistically significant increased risk of anxiety disorders, depression, sleep disorders, and psychotic disorders in patients with iron deficiency anemia after controlling for multiple confounders. Xu et al¹⁰ used quantitative susceptibility mapping to assess the iron status in certain regions of the brain of 30 patients with first-episode psychosis. They found lower levels of iron in the bilateral substantia nigra, left red nucleus, and left thalamus compared to healthy controls.¹⁰ Kim et al¹¹ found an association between iron deficiency and more severe negative symptoms in 121 patients with first-episode psychosis, which supports the hypothesis that iron deficiency may alter dopamine transmission in the brain.

Iron deficiency has been associated with psychopathology across the lifespan. In a population-based study in Taiwan, Chen et al¹² found an association between iron deficiency anemia and psychiatric disorders in children and adolescents, including mood disorders, autism spectrum disorder, attention-deficit/hyperactivity disorder, and developmental disorders. At the other end of the age spectrum, in a survey of 1,875 older adults in England, Stewart et al¹³ found an association between low ferritin levels (<45 ng/mL) and depressive symptoms after adjusting for demographic factors and overall health status.

In addition to specific psychiatric disorders and symptoms, iron deficiency is often associated with nonspecific symptoms such as fatigue.¹⁴ Fatigue is a symptom of numerous psychiatric disorders and is included in the DSM diagnostic criteria for major depressive disorder and generalized anxiety disorder.¹⁵

Iron supplementation might improve psychiatric symptoms

Some evidence suggests that using iron supplementation to treat iron deficiency can improve psychiatric symptoms. In a 2013 systematic literature review of 10 studies, Greig et al¹⁶ found a link between low iron status and poor cognition, poor mental health scores, and fatigue among women of childbearing age. In this review, 7 studies demonstrated improvement in cognition and 3 demonstrated improvement in mental health with iron supplementation.¹⁶ In a 2021 prospective study, 19 children and adolescents age 6 to 15 who had serum ferritin levels <30 ng/mL were treated with oral iron supplementation for 12 weeks.¹⁷ Participants showed significant improvements in sleep quality, depressive symptoms, and general mood as assessed via the Pittsburgh Sleep Quality Index, Center for Epidemiologic Studies Depression Scale, and Profile of Mood States (POMS) questionnaires, respectively.¹⁷ A randomized controlled trial of 219 female soldiers who were given iron supplementation or placebo for 8 weeks during basic combat training found that compared to placebo, iron supplementation led to improvements in mood as measured by the POMS questionnaire.¹⁸ Lastly, in a 2016 observational study of 412 adult psychiatric patients, Kassir¹⁹ found most patients (81%) had iron deficiency, defined as a transferrin saturation coefficient <30% or serum ferritin <100 ng/mL. Although these cutoffs are not considered standard and thus may have overrepresented the percentage of patients considered iron-deficient, more than one-half of patients considered iron-deficient in this study experienced a reduction or elimination of psychiatric symptoms following treatment with iron supplementation and/or psychotropic medications.¹⁹

Continue to: Individuals with iron deficiency...

Individuals with iron deficiency without anemia also may see improvement in psychiatric symptoms with iron treatment. In a 2018 systematic review, Houston et al²⁰ evaluated iron supplementation in 1,170 adults who were iron-deficient but not anemic. They found that in these patients, fatigue significantly improved but physical capacity did not.²⁰ Additionally, 2 other studies found iron treatment improved fatigue in nonanemic women.^21,22 In a 2016 systematic review, Pratt et al²³ concluded, “There is emerging evidence that … nonanemic iron deficiency … is a disease in its own right, deserving of further research in the development of strategies for detection and treatment.” Al-Naseem et al²⁴ suggested severity distinguishes iron deficiency with and without anemia.

Your role in assessing and treating iron deficiency

Testing for and treating iron deficiency generally is not a part of routine psychiatric practice. This might be due to apathy given the pervasiveness of iron deficiency, a belief that iron deficiency should be managed by primary care physicians, or a lack of familiarity with how to treat it and the benefits of such treatment for psychiatric patients. However, assessing for and treating iron deficiency in psychiatric patients is important, especially for individuals who are highly susceptible to inadequate iron levels. People at risk for iron deficiency include pregnant women, infants, young children, women with heavy menstrual bleeding, frequent blood donors, patients with cancer, individuals who have gastrointestinal (GI) surgeries or disorders, and those with heart failure.²⁵

Assessment. Iron status can be assessed through an iron studies panel. Because a patient can have iron deficiency without anemia, a complete blood count (CBC) alone does not suffice.²⁶ The iron panel includes serum iron, serum ferritin, serum transferrin or total iron-binding capacity (TIBC), and calculated transferrin saturation (TSAT), which is the ratio of serum iron to TIBC.

Iron deficiency is diagnosed if ferritin is <30 ng/mL, regardless of the hemoglobin concentration or underlying condition, and confirmed by a low TSAT.²⁶ In most guidelines, the cutoff value for TSAT for iron deficiency is <20%. Because the TSAT can be influenced by iron supplements or iron-rich foods, wait several hours to obtain blood after a patient takes an oral iron supplement or eats iron-rich foods. If desired, clinicians can use either ferritin or TSAT alone to diagnose iron deficiency. However, because ferritin can be falsely normal in inflammatory conditions such as obesity and infection, a TSAT may be needed to confirm iron deficiency if there is a high clinical suspicion despite a normal ferritin level.²⁶

Treatment. If iron deficiency is confirmed, instruct your patient to follow up with their primary care physician or the appropriate specialist to evaluate for any underlying etiologies.

Continue to: Iron deficiency should be treated...

Iron deficiency should be treated with supplementation because diet alone is insufficient for replenishing iron stores. Iron replacement can be oral or IV. Oral replacement is effective, safe, inexpensive, easy to obtain, and easy to administer.²⁷ Oral replacement is recommended for adults whose anemia is not severe or who do not have a comorbid condition such as pregnancy, inflammatory bowel conditions, gastric surgery, or chronic kidney disease. When anemia is severe or a patient has one of these comorbid conditions, IV is the preferred method of replacement.²⁷ In these cases, defer treatment to the patient’s primary care physician or specialist. 

There are no clear recommendations on the amount of iron per dose to prescribe.²⁷ The maximum amount of oral iron that can be absorbed is approximately 25 mg/d of elemental iron. A 325 mg ferrous sulfate tablet contains 65 mg of elemental iron, of which approximately 25 mg is absorbed and utilized.²⁷

Emerging evidence suggests that excessive iron dosing may reduce iron absorption and increase adverse effects. In a study of 54 nonanemic young women with iron deficiency who were given iron supplementation, Moretti et al²⁸ found that a large oral dose of iron taken in the morning increased hepcidin, which decreased the absorption of iron taken later for up to 48 hours. They found that 40 to 80 mg of elemental iron given on alternate days may maximize the fractional iron absorbed, increase dosage efficacy, reduce GI exposure to unabsorbed iron, and improve patients’ ability to tolerate iron supplementation.²⁸

Adverse effects from iron supplements occur in up to 70% of patients.²⁷ These can include metallic taste, nausea, vomiting, flatulence, diarrhea, epigastric pain, constipation, and dark stools.²⁷ Using a liquid form may help reduce adverse effects because it can be more easily titrated.²⁷ Tell patients to avoid enteric-coated or sustained-release iron capsules because these are poorly absorbed. Be cautious when prescribing iron supplementation to older adults because these patients tend to have more adverse effects, especially constipation, as well as reduced absorption, and may ultimately need IV treatment. Iron should not be taken with food, calcium supplements, antacids, coffee, tea, or milk.²⁷

The amount of iron present, cost, and adverse effects vary by supplement. The Table^27,29-33 provides more information on available forms of iron. Many forms of iron supplementation are available over-the-counter, and most are equally effective.²⁷ Advise patients to use iron products that have been tested by an independent company, such as ConsumerLab.com. Such companies evaluate products to see if they contain the amount of iron listed on the product’s label; for contamination with lead, cadmium, or arsenic; and for the product’s ability to break apart for absorption.³⁴

Six to 8 weeks of treatment with oral iron supplementation may be necessary before anemia is fully resolved, and it may take up to 6 months for iron stores to be repleted.²⁷ If a patient cannot tolerate an iron supplement, reducing the dose or taking it with meals may help prevent adverse effects, but also will reduce absorption. Auerbach²⁷ recommends assessing tolerability and rechecking the patient’s CBC 2 weeks after starting oral iron replacement, while also checking hemoglobin and the reticulocyte count to see if the patient is responding to treatment. An analysis of 5 studies found that a hemoglobin measurement on Day 14 that shows an increase ≥1.0 g/dL from baseline predicts longer-term and sustained treatment response to continued oral therapy.³⁵ There is no clear consensus for target ferritin levels, but we suggest aiming for a ferritin level >100 ug/L based on recommendations for the treatment of restless legs syndrome.³⁶ We recommend ongoing monitoring every 4 to 6 weeks.

Bottom Line

Iron deficiency is common and can cause or contribute to psychiatric symptoms and disorders. Consider screening patients for iron deficiency and treating it with oral supplementation in individuals without any comorbidities, or referring them to their primary care physician or specialist.

Related Resources

• Berthou C, Iliou JP, Barba D. Iron, neuro-bioavailability and depression. EJHaem. 2021;3(1):263-275.

Nutritional deficiencies are one of the many causes of or contributors to symptoms in patients with psychiatric disorders. In this article, we discuss the prevalence of iron deficiency and its link to poor mental health, and how proper treatment may improve psychiatric symptoms. We also offer suggestions for how and when to test for and treat iron deficiency in psychiatric patients.

A common condition

Iron deficiency is the most common mineral deficiency in the world. According to the World Health Organization (WHO), approximately 25% of the global population is anemic and nearly one-half of those cases are the result of iron deficiency.¹ While the WHO has published guidelines defining iron deficiency as it relates to ferritin levels (<15 ug/L in adults and <12 ug/L in children), this estimate might be low.^2,3 Mei et al² found that hemoglobin and soluble transferrin receptors can be used to determine iron-deficient erythropoiesis, which indicates a physiological definition of iron deficiency. According to a study of children and nonpregnant women by Mei et al,² children with ferritin levels <20 ug/L and women with ferritin levels <25 ug/L should be considered iron-deficient. If replicated, this study suggests the prevalence of iron deficiency is higher than currently estimated.² Overall, an estimated 1.2 billion people worldwide have iron-deficiency anemia.⁴ Additionally, patients can be iron deficient without being anemic, a condition thought to be at least twice as common.⁴

Essential for brain function

Research shows the importance of iron to proper brain function.⁵ Iron deficiency in pregnant women is associated with significant neuropsychological impairments in neonates. Rodent studies have demonstrated the importance of iron and the effects of iron deficiency on the hippocampus, corpus striatum, and production of monoamines.⁵ Specifically, iron is a necessary cofactor in the enzymes tryptophan hydroxylase and tyrosine hydroxylase, which produce serotonin, dopamine, and norepinephrine. In rodent studies, monoamine deficits secondary to iron deficiency persist into adulthood even with iron supplementation, which highlights the importance of preventing iron deficiency during pregnancy and early life.⁵ While most research has focused on the impact of iron deficiency in infancy and early childhood, iron deficiency has an ongoing impact into adulthood, even if treated.⁶

Iron deficiency and psychiatric symptoms

Current research suggests an association between iron deficiency or low ferritin levels and psychiatric disorders, specifically depression, anxiety, and schizophrenia. In a web survey of 11,876 adults, Hidese et al⁷ found an association between a self-reported history of iron deficiency anemia and a self-reported history of depression. Another study of 528 municipal employees found an association between low serum ferritin concentrations and a high prevalence of depressive symptoms among men; no statistically significant association was detected in women.⁸ In an analysis of the Taiwan National Health Insurance Database from 2000 to 2012, Lee et al⁹ found a statistically significant increased risk of anxiety disorders, depression, sleep disorders, and psychotic disorders in patients with iron deficiency anemia after controlling for multiple confounders. Xu et al¹⁰ used quantitative susceptibility mapping to assess the iron status in certain regions of the brain of 30 patients with first-episode psychosis. They found lower levels of iron in the bilateral substantia nigra, left red nucleus, and left thalamus compared to healthy controls.¹⁰ Kim et al¹¹ found an association between iron deficiency and more severe negative symptoms in 121 patients with first-episode psychosis, which supports the hypothesis that iron deficiency may alter dopamine transmission in the brain.

Iron deficiency has been associated with psychopathology across the lifespan. In a population-based study in Taiwan, Chen et al¹² found an association between iron deficiency anemia and psychiatric disorders in children and adolescents, including mood disorders, autism spectrum disorder, attention-deficit/hyperactivity disorder, and developmental disorders. At the other end of the age spectrum, in a survey of 1,875 older adults in England, Stewart et al¹³ found an association between low ferritin levels (<45 ng/mL) and depressive symptoms after adjusting for demographic factors and overall health status.

In addition to specific psychiatric disorders and symptoms, iron deficiency is often associated with nonspecific symptoms such as fatigue.¹⁴ Fatigue is a symptom of numerous psychiatric disorders and is included in the DSM diagnostic criteria for major depressive disorder and generalized anxiety disorder.¹⁵

Iron supplementation might improve psychiatric symptoms

Some evidence suggests that using iron supplementation to treat iron deficiency can improve psychiatric symptoms. In a 2013 systematic literature review of 10 studies, Greig et al¹⁶ found a link between low iron status and poor cognition, poor mental health scores, and fatigue among women of childbearing age. In this review, 7 studies demonstrated improvement in cognition and 3 demonstrated improvement in mental health with iron supplementation.¹⁶ In a 2021 prospective study, 19 children and adolescents age 6 to 15 who had serum ferritin levels <30 ng/mL were treated with oral iron supplementation for 12 weeks.¹⁷ Participants showed significant improvements in sleep quality, depressive symptoms, and general mood as assessed via the Pittsburgh Sleep Quality Index, Center for Epidemiologic Studies Depression Scale, and Profile of Mood States (POMS) questionnaires, respectively.¹⁷ A randomized controlled trial of 219 female soldiers who were given iron supplementation or placebo for 8 weeks during basic combat training found that compared to placebo, iron supplementation led to improvements in mood as measured by the POMS questionnaire.¹⁸ Lastly, in a 2016 observational study of 412 adult psychiatric patients, Kassir¹⁹ found most patients (81%) had iron deficiency, defined as a transferrin saturation coefficient <30% or serum ferritin <100 ng/mL. Although these cutoffs are not considered standard and thus may have overrepresented the percentage of patients considered iron-deficient, more than one-half of patients considered iron-deficient in this study experienced a reduction or elimination of psychiatric symptoms following treatment with iron supplementation and/or psychotropic medications.¹⁹

Continue to: Individuals with iron deficiency...

Individuals with iron deficiency without anemia also may see improvement in psychiatric symptoms with iron treatment. In a 2018 systematic review, Houston et al²⁰ evaluated iron supplementation in 1,170 adults who were iron-deficient but not anemic. They found that in these patients, fatigue significantly improved but physical capacity did not.²⁰ Additionally, 2 other studies found iron treatment improved fatigue in nonanemic women.^21,22 In a 2016 systematic review, Pratt et al²³ concluded, “There is emerging evidence that … nonanemic iron deficiency … is a disease in its own right, deserving of further research in the development of strategies for detection and treatment.” Al-Naseem et al²⁴ suggested severity distinguishes iron deficiency with and without anemia.

Your role in assessing and treating iron deficiency

Testing for and treating iron deficiency generally is not a part of routine psychiatric practice. This might be due to apathy given the pervasiveness of iron deficiency, a belief that iron deficiency should be managed by primary care physicians, or a lack of familiarity with how to treat it and the benefits of such treatment for psychiatric patients. However, assessing for and treating iron deficiency in psychiatric patients is important, especially for individuals who are highly susceptible to inadequate iron levels. People at risk for iron deficiency include pregnant women, infants, young children, women with heavy menstrual bleeding, frequent blood donors, patients with cancer, individuals who have gastrointestinal (GI) surgeries or disorders, and those with heart failure.²⁵

Assessment. Iron status can be assessed through an iron studies panel. Because a patient can have iron deficiency without anemia, a complete blood count (CBC) alone does not suffice.²⁶ The iron panel includes serum iron, serum ferritin, serum transferrin or total iron-binding capacity (TIBC), and calculated transferrin saturation (TSAT), which is the ratio of serum iron to TIBC.

Iron deficiency is diagnosed if ferritin is <30 ng/mL, regardless of the hemoglobin concentration or underlying condition, and confirmed by a low TSAT.²⁶ In most guidelines, the cutoff value for TSAT for iron deficiency is <20%. Because the TSAT can be influenced by iron supplements or iron-rich foods, wait several hours to obtain blood after a patient takes an oral iron supplement or eats iron-rich foods. If desired, clinicians can use either ferritin or TSAT alone to diagnose iron deficiency. However, because ferritin can be falsely normal in inflammatory conditions such as obesity and infection, a TSAT may be needed to confirm iron deficiency if there is a high clinical suspicion despite a normal ferritin level.²⁶

Treatment. If iron deficiency is confirmed, instruct your patient to follow up with their primary care physician or the appropriate specialist to evaluate for any underlying etiologies.

Continue to: Iron deficiency should be treated...

Iron deficiency should be treated with supplementation because diet alone is insufficient for replenishing iron stores. Iron replacement can be oral or IV. Oral replacement is effective, safe, inexpensive, easy to obtain, and easy to administer.²⁷ Oral replacement is recommended for adults whose anemia is not severe or who do not have a comorbid condition such as pregnancy, inflammatory bowel conditions, gastric surgery, or chronic kidney disease. When anemia is severe or a patient has one of these comorbid conditions, IV is the preferred method of replacement.²⁷ In these cases, defer treatment to the patient’s primary care physician or specialist. 

There are no clear recommendations on the amount of iron per dose to prescribe.²⁷ The maximum amount of oral iron that can be absorbed is approximately 25 mg/d of elemental iron. A 325 mg ferrous sulfate tablet contains 65 mg of elemental iron, of which approximately 25 mg is absorbed and utilized.²⁷

Emerging evidence suggests that excessive iron dosing may reduce iron absorption and increase adverse effects. In a study of 54 nonanemic young women with iron deficiency who were given iron supplementation, Moretti et al²⁸ found that a large oral dose of iron taken in the morning increased hepcidin, which decreased the absorption of iron taken later for up to 48 hours. They found that 40 to 80 mg of elemental iron given on alternate days may maximize the fractional iron absorbed, increase dosage efficacy, reduce GI exposure to unabsorbed iron, and improve patients’ ability to tolerate iron supplementation.²⁸

Adverse effects from iron supplements occur in up to 70% of patients.²⁷ These can include metallic taste, nausea, vomiting, flatulence, diarrhea, epigastric pain, constipation, and dark stools.²⁷ Using a liquid form may help reduce adverse effects because it can be more easily titrated.²⁷ Tell patients to avoid enteric-coated or sustained-release iron capsules because these are poorly absorbed. Be cautious when prescribing iron supplementation to older adults because these patients tend to have more adverse effects, especially constipation, as well as reduced absorption, and may ultimately need IV treatment. Iron should not be taken with food, calcium supplements, antacids, coffee, tea, or milk.²⁷

The amount of iron present, cost, and adverse effects vary by supplement. The Table^27,29-33 provides more information on available forms of iron. Many forms of iron supplementation are available over-the-counter, and most are equally effective.²⁷ Advise patients to use iron products that have been tested by an independent company, such as ConsumerLab.com. Such companies evaluate products to see if they contain the amount of iron listed on the product’s label; for contamination with lead, cadmium, or arsenic; and for the product’s ability to break apart for absorption.³⁴

Six to 8 weeks of treatment with oral iron supplementation may be necessary before anemia is fully resolved, and it may take up to 6 months for iron stores to be repleted.²⁷ If a patient cannot tolerate an iron supplement, reducing the dose or taking it with meals may help prevent adverse effects, but also will reduce absorption. Auerbach²⁷ recommends assessing tolerability and rechecking the patient’s CBC 2 weeks after starting oral iron replacement, while also checking hemoglobin and the reticulocyte count to see if the patient is responding to treatment. An analysis of 5 studies found that a hemoglobin measurement on Day 14 that shows an increase ≥1.0 g/dL from baseline predicts longer-term and sustained treatment response to continued oral therapy.³⁵ There is no clear consensus for target ferritin levels, but we suggest aiming for a ferritin level >100 ug/L based on recommendations for the treatment of restless legs syndrome.³⁶ We recommend ongoing monitoring every 4 to 6 weeks.

Bottom Line

Iron deficiency is common and can cause or contribute to psychiatric symptoms and disorders. Consider screening patients for iron deficiency and treating it with oral supplementation in individuals without any comorbidities, or referring them to their primary care physician or specialist.

Related Resources

• Berthou C, Iliou JP, Barba D. Iron, neuro-bioavailability and depression. EJHaem. 2021;3(1):263-275.

Nutritional deficiencies are one of the many causes of or contributors to symptoms in patients with psychiatric disorders. In this article, we discuss the prevalence of iron deficiency and its link to poor mental health, and how proper treatment may improve psychiatric symptoms. We also offer suggestions for how and when to test for and treat iron deficiency in psychiatric patients.

A common condition

Iron deficiency is the most common mineral deficiency in the world. According to the World Health Organization (WHO), approximately 25% of the global population is anemic and nearly one-half of those cases are the result of iron deficiency.¹ While the WHO has published guidelines defining iron deficiency as it relates to ferritin levels (<15 ug/L in adults and <12 ug/L in children), this estimate might be low.^2,3 Mei et al² found that hemoglobin and soluble transferrin receptors can be used to determine iron-deficient erythropoiesis, which indicates a physiological definition of iron deficiency. According to a study of children and nonpregnant women by Mei et al,² children with ferritin levels <20 ug/L and women with ferritin levels <25 ug/L should be considered iron-deficient. If replicated, this study suggests the prevalence of iron deficiency is higher than currently estimated.² Overall, an estimated 1.2 billion people worldwide have iron-deficiency anemia.⁴ Additionally, patients can be iron deficient without being anemic, a condition thought to be at least twice as common.⁴

Essential for brain function

Research shows the importance of iron to proper brain function.⁵ Iron deficiency in pregnant women is associated with significant neuropsychological impairments in neonates. Rodent studies have demonstrated the importance of iron and the effects of iron deficiency on the hippocampus, corpus striatum, and production of monoamines.⁵ Specifically, iron is a necessary cofactor in the enzymes tryptophan hydroxylase and tyrosine hydroxylase, which produce serotonin, dopamine, and norepinephrine. In rodent studies, monoamine deficits secondary to iron deficiency persist into adulthood even with iron supplementation, which highlights the importance of preventing iron deficiency during pregnancy and early life.⁵ While most research has focused on the impact of iron deficiency in infancy and early childhood, iron deficiency has an ongoing impact into adulthood, even if treated.⁶

Iron deficiency and psychiatric symptoms

Current research suggests an association between iron deficiency or low ferritin levels and psychiatric disorders, specifically depression, anxiety, and schizophrenia. In a web survey of 11,876 adults, Hidese et al⁷ found an association between a self-reported history of iron deficiency anemia and a self-reported history of depression. Another study of 528 municipal employees found an association between low serum ferritin concentrations and a high prevalence of depressive symptoms among men; no statistically significant association was detected in women.⁸ In an analysis of the Taiwan National Health Insurance Database from 2000 to 2012, Lee et al⁹ found a statistically significant increased risk of anxiety disorders, depression, sleep disorders, and psychotic disorders in patients with iron deficiency anemia after controlling for multiple confounders. Xu et al¹⁰ used quantitative susceptibility mapping to assess the iron status in certain regions of the brain of 30 patients with first-episode psychosis. They found lower levels of iron in the bilateral substantia nigra, left red nucleus, and left thalamus compared to healthy controls.¹⁰ Kim et al¹¹ found an association between iron deficiency and more severe negative symptoms in 121 patients with first-episode psychosis, which supports the hypothesis that iron deficiency may alter dopamine transmission in the brain.

Iron deficiency has been associated with psychopathology across the lifespan. In a population-based study in Taiwan, Chen et al¹² found an association between iron deficiency anemia and psychiatric disorders in children and adolescents, including mood disorders, autism spectrum disorder, attention-deficit/hyperactivity disorder, and developmental disorders. At the other end of the age spectrum, in a survey of 1,875 older adults in England, Stewart et al¹³ found an association between low ferritin levels (<45 ng/mL) and depressive symptoms after adjusting for demographic factors and overall health status.

In addition to specific psychiatric disorders and symptoms, iron deficiency is often associated with nonspecific symptoms such as fatigue.¹⁴ Fatigue is a symptom of numerous psychiatric disorders and is included in the DSM diagnostic criteria for major depressive disorder and generalized anxiety disorder.¹⁵

Iron supplementation might improve psychiatric symptoms

Some evidence suggests that using iron supplementation to treat iron deficiency can improve psychiatric symptoms. In a 2013 systematic literature review of 10 studies, Greig et al¹⁶ found a link between low iron status and poor cognition, poor mental health scores, and fatigue among women of childbearing age. In this review, 7 studies demonstrated improvement in cognition and 3 demonstrated improvement in mental health with iron supplementation.¹⁶ In a 2021 prospective study, 19 children and adolescents age 6 to 15 who had serum ferritin levels <30 ng/mL were treated with oral iron supplementation for 12 weeks.¹⁷ Participants showed significant improvements in sleep quality, depressive symptoms, and general mood as assessed via the Pittsburgh Sleep Quality Index, Center for Epidemiologic Studies Depression Scale, and Profile of Mood States (POMS) questionnaires, respectively.¹⁷ A randomized controlled trial of 219 female soldiers who were given iron supplementation or placebo for 8 weeks during basic combat training found that compared to placebo, iron supplementation led to improvements in mood as measured by the POMS questionnaire.¹⁸ Lastly, in a 2016 observational study of 412 adult psychiatric patients, Kassir¹⁹ found most patients (81%) had iron deficiency, defined as a transferrin saturation coefficient <30% or serum ferritin <100 ng/mL. Although these cutoffs are not considered standard and thus may have overrepresented the percentage of patients considered iron-deficient, more than one-half of patients considered iron-deficient in this study experienced a reduction or elimination of psychiatric symptoms following treatment with iron supplementation and/or psychotropic medications.¹⁹

Continue to: Individuals with iron deficiency...

Individuals with iron deficiency without anemia also may see improvement in psychiatric symptoms with iron treatment. In a 2018 systematic review, Houston et al²⁰ evaluated iron supplementation in 1,170 adults who were iron-deficient but not anemic. They found that in these patients, fatigue significantly improved but physical capacity did not.²⁰ Additionally, 2 other studies found iron treatment improved fatigue in nonanemic women.^21,22 In a 2016 systematic review, Pratt et al²³ concluded, “There is emerging evidence that … nonanemic iron deficiency … is a disease in its own right, deserving of further research in the development of strategies for detection and treatment.” Al-Naseem et al²⁴ suggested severity distinguishes iron deficiency with and without anemia.

Your role in assessing and treating iron deficiency

Testing for and treating iron deficiency generally is not a part of routine psychiatric practice. This might be due to apathy given the pervasiveness of iron deficiency, a belief that iron deficiency should be managed by primary care physicians, or a lack of familiarity with how to treat it and the benefits of such treatment for psychiatric patients. However, assessing for and treating iron deficiency in psychiatric patients is important, especially for individuals who are highly susceptible to inadequate iron levels. People at risk for iron deficiency include pregnant women, infants, young children, women with heavy menstrual bleeding, frequent blood donors, patients with cancer, individuals who have gastrointestinal (GI) surgeries or disorders, and those with heart failure.²⁵

Assessment. Iron status can be assessed through an iron studies panel. Because a patient can have iron deficiency without anemia, a complete blood count (CBC) alone does not suffice.²⁶ The iron panel includes serum iron, serum ferritin, serum transferrin or total iron-binding capacity (TIBC), and calculated transferrin saturation (TSAT), which is the ratio of serum iron to TIBC.

Iron deficiency is diagnosed if ferritin is <30 ng/mL, regardless of the hemoglobin concentration or underlying condition, and confirmed by a low TSAT.²⁶ In most guidelines, the cutoff value for TSAT for iron deficiency is <20%. Because the TSAT can be influenced by iron supplements or iron-rich foods, wait several hours to obtain blood after a patient takes an oral iron supplement or eats iron-rich foods. If desired, clinicians can use either ferritin or TSAT alone to diagnose iron deficiency. However, because ferritin can be falsely normal in inflammatory conditions such as obesity and infection, a TSAT may be needed to confirm iron deficiency if there is a high clinical suspicion despite a normal ferritin level.²⁶

Treatment. If iron deficiency is confirmed, instruct your patient to follow up with their primary care physician or the appropriate specialist to evaluate for any underlying etiologies.

Continue to: Iron deficiency should be treated...

Iron deficiency should be treated with supplementation because diet alone is insufficient for replenishing iron stores. Iron replacement can be oral or IV. Oral replacement is effective, safe, inexpensive, easy to obtain, and easy to administer.²⁷ Oral replacement is recommended for adults whose anemia is not severe or who do not have a comorbid condition such as pregnancy, inflammatory bowel conditions, gastric surgery, or chronic kidney disease. When anemia is severe or a patient has one of these comorbid conditions, IV is the preferred method of replacement.²⁷ In these cases, defer treatment to the patient’s primary care physician or specialist. 

There are no clear recommendations on the amount of iron per dose to prescribe.²⁷ The maximum amount of oral iron that can be absorbed is approximately 25 mg/d of elemental iron. A 325 mg ferrous sulfate tablet contains 65 mg of elemental iron, of which approximately 25 mg is absorbed and utilized.²⁷

Emerging evidence suggests that excessive iron dosing may reduce iron absorption and increase adverse effects. In a study of 54 nonanemic young women with iron deficiency who were given iron supplementation, Moretti et al²⁸ found that a large oral dose of iron taken in the morning increased hepcidin, which decreased the absorption of iron taken later for up to 48 hours. They found that 40 to 80 mg of elemental iron given on alternate days may maximize the fractional iron absorbed, increase dosage efficacy, reduce GI exposure to unabsorbed iron, and improve patients’ ability to tolerate iron supplementation.²⁸

Adverse effects from iron supplements occur in up to 70% of patients.²⁷ These can include metallic taste, nausea, vomiting, flatulence, diarrhea, epigastric pain, constipation, and dark stools.²⁷ Using a liquid form may help reduce adverse effects because it can be more easily titrated.²⁷ Tell patients to avoid enteric-coated or sustained-release iron capsules because these are poorly absorbed. Be cautious when prescribing iron supplementation to older adults because these patients tend to have more adverse effects, especially constipation, as well as reduced absorption, and may ultimately need IV treatment. Iron should not be taken with food, calcium supplements, antacids, coffee, tea, or milk.²⁷

The amount of iron present, cost, and adverse effects vary by supplement. The Table^27,29-33 provides more information on available forms of iron. Many forms of iron supplementation are available over-the-counter, and most are equally effective.²⁷ Advise patients to use iron products that have been tested by an independent company, such as ConsumerLab.com. Such companies evaluate products to see if they contain the amount of iron listed on the product’s label; for contamination with lead, cadmium, or arsenic; and for the product’s ability to break apart for absorption.³⁴

Six to 8 weeks of treatment with oral iron supplementation may be necessary before anemia is fully resolved, and it may take up to 6 months for iron stores to be repleted.²⁷ If a patient cannot tolerate an iron supplement, reducing the dose or taking it with meals may help prevent adverse effects, but also will reduce absorption. Auerbach²⁷ recommends assessing tolerability and rechecking the patient’s CBC 2 weeks after starting oral iron replacement, while also checking hemoglobin and the reticulocyte count to see if the patient is responding to treatment. An analysis of 5 studies found that a hemoglobin measurement on Day 14 that shows an increase ≥1.0 g/dL from baseline predicts longer-term and sustained treatment response to continued oral therapy.³⁵ There is no clear consensus for target ferritin levels, but we suggest aiming for a ferritin level >100 ug/L based on recommendations for the treatment of restless legs syndrome.³⁶ We recommend ongoing monitoring every 4 to 6 weeks.

Bottom Line

Iron deficiency is common and can cause or contribute to psychiatric symptoms and disorders. Consider screening patients for iron deficiency and treating it with oral supplementation in individuals without any comorbidities, or referring them to their primary care physician or specialist.

Related Resources

• Berthou C, Iliou JP, Barba D. Iron, neuro-bioavailability and depression. EJHaem. 2021;3(1):263-275.

Insomnia – difficulty falling or staying asleep – was associated with a 69% greater risk of having a myocardial infarction than among adults without insomnia, according to new research.

Those who slept 5 or fewer hours per night had the highest risk for MI, and those with both diabetes and insomnia had double the risk for MI, compared with patients without these comorbidities.

amenic181/Getty Images

The findings are from a meta-analysis of studies in more than 1 million patients, almost all without prior MI who were, on average, in their early 50s and followed for 9 years.

Yomna E. Dean, a medical student at Alexandria (Egypt) University, reported these results in a press briefing, and the study was simultaneously published in Clinical Cardiology. It will be presented at the upcoming at the annual scientific sessions of the American College of Cardiology.

“Insomnia and ]at least] 5 hours of sleep are highly associated with increased incidence of MI, an association comparable to that of other MI risk factors and as such, it should be considered as a risk factor for MI and to be incorporated into MI prevention guidelines,” the researchers concluded.

“We believe that [insomnia] should be screened and patients should be educated about the importance of sleep because nowadays insomnia is no longer a disease – sleep deprivation could also be a life choice,” Ms, Dean told a press conference prior to the meeting.

“Clinicians must educate the patients about the importance of sleep in maintaining a healthy heart and encourage proper sleep hygiene,” Ms. Dean reiterated in an email. “And if a patient still has insomnia, other methods should be considered such as cognitive-behavior[al] therapy for insomnia [CBT-I].”
 

Adds to growing evidence

This study does not allow any conclusion about whether treating insomnia will reduce heart attack risk, Jennifer L. Martin, PhD, president of the American Academy of Sleep Medicine, noted in a comment. Nor does it report the diversity of study participants, since insomnia is also a health equity issue, she noted, and insomnia symptoms and comorbidities were self-reported.

However, this analysis “adds to the growing evidence that poor quality or insufficient sleep is associated with poor health,” said Dr. Martin, professor of medicine at the University of California, Los Angeles, who was not involved with this research.

The study reinforces the recommendation from the American Heart Association, which includes “Get Healthy Sleep” as one of “Life’s Essential 8” for heart health, Dr. Martin noted.

“Particularly in primary care where disease prevention and health promotion are important, clinicians should be asking all patients about their sleep – just like they ask about diet and exercise – as a key aspect of maintaining heart health,” she said.

Advice about basic sleep hygiene advice is a first step, she noted.

When improved sleep hygiene is not enough to address chronic insomnia, the AASM’s clinical practice guidelines and the guidelines of the Department of Veterans Affairs/Department of Defense, recommend first-line treatment with CBT-I, typically offered by a sleep specialist or mental health clinician.

Similarly, the American College of Physicians suggests that sleeping pills should be reserved for short-term use in patients who may not benefit sufficiently from CBT-I.
 

Sleeping too little, too much, equally harmful

“Studies have found that insomnia and subsequent sleep deprivation puts the body under stress,” Ms. Dean said. “This triggers cortisol release which could accelerate atherosclerosis,” and increase risk of MI.

For this analysis, the researchers identified nine observational studies, published from 1998 to 2019, with data on incident MI in adults who had insomnia.

The diagnosis of insomnia was based on ICD diagnostic codes or on the DSM‐5, which defines insomnia as the presence of any of the following three symptoms: difficulty initiating sleep, difficulty maintaining sleep, or early morning awakening with inability to return to sleep. Patients with sleep apnea were excluded.

The studies were in populations in China, Germany, Norway, Taiwan, United Kingdom, and United States, in 1.1 million adults aged 18 and older. The patients had a mean age of 52 years and 13% had insomnia.

During follow-up, 2,406 of 153,881 patients with insomnia, and 12,398 of 1,030,375 patients without insomnia had an MI.

In the pooled analysis, patients with insomnia had a significantly increased risk of MI (relative risk, 1.69; P < .00001), after adjusting for age, gender, diabetes, hypertension, high cholesterol, and smoking.

Sleeping 5 hours or less was associated with a greater risk for MI than sleeping 6 hours, or 7-8 hours, but sleeping 9 hours or more was just as harmful.

Patients who had difficulty initiating and maintaining sleep – two symptoms of insomnia – had a 13% increased risk for MI compared with other patients (RR, 1.13; P = .003).

However, patients who had nonrestorative sleep and daytime dysfunction despite adequate sleep – which is common – did not have an increased risk of MI, compared with other patients (RR, 1.06; P = .46).

Women with insomnia had a 2.24-fold greater risk for MI than other women, whereas men with insomnia had a 2.03-fold greater risk for MI than other men.

Patients with insomnia had a greater risk for MI than those without insomnia in subgroups based on patients’ age (< 65 and > 65), follow up duration (≤ 5 years and > 5 years), and comorbidities (diabetes, hypertension, and hyperlipidemia).

The authors reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Insomnia – difficulty falling or staying asleep – was associated with a 69% greater risk of having a myocardial infarction than among adults without insomnia, according to new research.

Those who slept 5 or fewer hours per night had the highest risk for MI, and those with both diabetes and insomnia had double the risk for MI, compared with patients without these comorbidities.

amenic181/Getty Images

The findings are from a meta-analysis of studies in more than 1 million patients, almost all without prior MI who were, on average, in their early 50s and followed for 9 years.

Yomna E. Dean, a medical student at Alexandria (Egypt) University, reported these results in a press briefing, and the study was simultaneously published in Clinical Cardiology. It will be presented at the upcoming at the annual scientific sessions of the American College of Cardiology.

“Insomnia and ]at least] 5 hours of sleep are highly associated with increased incidence of MI, an association comparable to that of other MI risk factors and as such, it should be considered as a risk factor for MI and to be incorporated into MI prevention guidelines,” the researchers concluded.

“We believe that [insomnia] should be screened and patients should be educated about the importance of sleep because nowadays insomnia is no longer a disease – sleep deprivation could also be a life choice,” Ms, Dean told a press conference prior to the meeting.

“Clinicians must educate the patients about the importance of sleep in maintaining a healthy heart and encourage proper sleep hygiene,” Ms. Dean reiterated in an email. “And if a patient still has insomnia, other methods should be considered such as cognitive-behavior[al] therapy for insomnia [CBT-I].”
 

Adds to growing evidence

This study does not allow any conclusion about whether treating insomnia will reduce heart attack risk, Jennifer L. Martin, PhD, president of the American Academy of Sleep Medicine, noted in a comment. Nor does it report the diversity of study participants, since insomnia is also a health equity issue, she noted, and insomnia symptoms and comorbidities were self-reported.

However, this analysis “adds to the growing evidence that poor quality or insufficient sleep is associated with poor health,” said Dr. Martin, professor of medicine at the University of California, Los Angeles, who was not involved with this research.

The study reinforces the recommendation from the American Heart Association, which includes “Get Healthy Sleep” as one of “Life’s Essential 8” for heart health, Dr. Martin noted.

“Particularly in primary care where disease prevention and health promotion are important, clinicians should be asking all patients about their sleep – just like they ask about diet and exercise – as a key aspect of maintaining heart health,” she said.

Advice about basic sleep hygiene advice is a first step, she noted.

When improved sleep hygiene is not enough to address chronic insomnia, the AASM’s clinical practice guidelines and the guidelines of the Department of Veterans Affairs/Department of Defense, recommend first-line treatment with CBT-I, typically offered by a sleep specialist or mental health clinician.

Similarly, the American College of Physicians suggests that sleeping pills should be reserved for short-term use in patients who may not benefit sufficiently from CBT-I.
 

Sleeping too little, too much, equally harmful

“Studies have found that insomnia and subsequent sleep deprivation puts the body under stress,” Ms. Dean said. “This triggers cortisol release which could accelerate atherosclerosis,” and increase risk of MI.

For this analysis, the researchers identified nine observational studies, published from 1998 to 2019, with data on incident MI in adults who had insomnia.

The diagnosis of insomnia was based on ICD diagnostic codes or on the DSM‐5, which defines insomnia as the presence of any of the following three symptoms: difficulty initiating sleep, difficulty maintaining sleep, or early morning awakening with inability to return to sleep. Patients with sleep apnea were excluded.

The studies were in populations in China, Germany, Norway, Taiwan, United Kingdom, and United States, in 1.1 million adults aged 18 and older. The patients had a mean age of 52 years and 13% had insomnia.

During follow-up, 2,406 of 153,881 patients with insomnia, and 12,398 of 1,030,375 patients without insomnia had an MI.

In the pooled analysis, patients with insomnia had a significantly increased risk of MI (relative risk, 1.69; P < .00001), after adjusting for age, gender, diabetes, hypertension, high cholesterol, and smoking.

Sleeping 5 hours or less was associated with a greater risk for MI than sleeping 6 hours, or 7-8 hours, but sleeping 9 hours or more was just as harmful.

Patients who had difficulty initiating and maintaining sleep – two symptoms of insomnia – had a 13% increased risk for MI compared with other patients (RR, 1.13; P = .003).

However, patients who had nonrestorative sleep and daytime dysfunction despite adequate sleep – which is common – did not have an increased risk of MI, compared with other patients (RR, 1.06; P = .46).

Women with insomnia had a 2.24-fold greater risk for MI than other women, whereas men with insomnia had a 2.03-fold greater risk for MI than other men.

Patients with insomnia had a greater risk for MI than those without insomnia in subgroups based on patients’ age (< 65 and > 65), follow up duration (≤ 5 years and > 5 years), and comorbidities (diabetes, hypertension, and hyperlipidemia).

The authors reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Insomnia – difficulty falling or staying asleep – was associated with a 69% greater risk of having a myocardial infarction than among adults without insomnia, according to new research.

Those who slept 5 or fewer hours per night had the highest risk for MI, and those with both diabetes and insomnia had double the risk for MI, compared with patients without these comorbidities.

amenic181/Getty Images

The findings are from a meta-analysis of studies in more than 1 million patients, almost all without prior MI who were, on average, in their early 50s and followed for 9 years.

Yomna E. Dean, a medical student at Alexandria (Egypt) University, reported these results in a press briefing, and the study was simultaneously published in Clinical Cardiology. It will be presented at the upcoming at the annual scientific sessions of the American College of Cardiology.

“Insomnia and ]at least] 5 hours of sleep are highly associated with increased incidence of MI, an association comparable to that of other MI risk factors and as such, it should be considered as a risk factor for MI and to be incorporated into MI prevention guidelines,” the researchers concluded.

“We believe that [insomnia] should be screened and patients should be educated about the importance of sleep because nowadays insomnia is no longer a disease – sleep deprivation could also be a life choice,” Ms, Dean told a press conference prior to the meeting.

“Clinicians must educate the patients about the importance of sleep in maintaining a healthy heart and encourage proper sleep hygiene,” Ms. Dean reiterated in an email. “And if a patient still has insomnia, other methods should be considered such as cognitive-behavior[al] therapy for insomnia [CBT-I].”
 

Adds to growing evidence

This study does not allow any conclusion about whether treating insomnia will reduce heart attack risk, Jennifer L. Martin, PhD, president of the American Academy of Sleep Medicine, noted in a comment. Nor does it report the diversity of study participants, since insomnia is also a health equity issue, she noted, and insomnia symptoms and comorbidities were self-reported.

However, this analysis “adds to the growing evidence that poor quality or insufficient sleep is associated with poor health,” said Dr. Martin, professor of medicine at the University of California, Los Angeles, who was not involved with this research.

The study reinforces the recommendation from the American Heart Association, which includes “Get Healthy Sleep” as one of “Life’s Essential 8” for heart health, Dr. Martin noted.

“Particularly in primary care where disease prevention and health promotion are important, clinicians should be asking all patients about their sleep – just like they ask about diet and exercise – as a key aspect of maintaining heart health,” she said.

Advice about basic sleep hygiene advice is a first step, she noted.

When improved sleep hygiene is not enough to address chronic insomnia, the AASM’s clinical practice guidelines and the guidelines of the Department of Veterans Affairs/Department of Defense, recommend first-line treatment with CBT-I, typically offered by a sleep specialist or mental health clinician.

Similarly, the American College of Physicians suggests that sleeping pills should be reserved for short-term use in patients who may not benefit sufficiently from CBT-I.
 

Sleeping too little, too much, equally harmful

“Studies have found that insomnia and subsequent sleep deprivation puts the body under stress,” Ms. Dean said. “This triggers cortisol release which could accelerate atherosclerosis,” and increase risk of MI.

For this analysis, the researchers identified nine observational studies, published from 1998 to 2019, with data on incident MI in adults who had insomnia.

The diagnosis of insomnia was based on ICD diagnostic codes or on the DSM‐5, which defines insomnia as the presence of any of the following three symptoms: difficulty initiating sleep, difficulty maintaining sleep, or early morning awakening with inability to return to sleep. Patients with sleep apnea were excluded.

The studies were in populations in China, Germany, Norway, Taiwan, United Kingdom, and United States, in 1.1 million adults aged 18 and older. The patients had a mean age of 52 years and 13% had insomnia.

During follow-up, 2,406 of 153,881 patients with insomnia, and 12,398 of 1,030,375 patients without insomnia had an MI.

In the pooled analysis, patients with insomnia had a significantly increased risk of MI (relative risk, 1.69; P < .00001), after adjusting for age, gender, diabetes, hypertension, high cholesterol, and smoking.

Sleeping 5 hours or less was associated with a greater risk for MI than sleeping 6 hours, or 7-8 hours, but sleeping 9 hours or more was just as harmful.

Patients who had difficulty initiating and maintaining sleep – two symptoms of insomnia – had a 13% increased risk for MI compared with other patients (RR, 1.13; P = .003).

However, patients who had nonrestorative sleep and daytime dysfunction despite adequate sleep – which is common – did not have an increased risk of MI, compared with other patients (RR, 1.06; P = .46).

Women with insomnia had a 2.24-fold greater risk for MI than other women, whereas men with insomnia had a 2.03-fold greater risk for MI than other men.

Patients with insomnia had a greater risk for MI than those without insomnia in subgroups based on patients’ age (< 65 and > 65), follow up duration (≤ 5 years and > 5 years), and comorbidities (diabetes, hypertension, and hyperlipidemia).

The authors reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

FRANCE – Conducted every 5 years since 2005, the Cancer Survey documents the knowledge, perceptions, and way of life of the French people in relation to cancer. The French National Cancer Institute (InCA), in partnership with Public Health France (SPF), has published the results of its 2021 survey. The researchers analyzed responses to telephone interviews of a representative sample of almost 5,000 individuals aged 15-85 years.

This study shows how thinking has changed over time and how difficult it is to alter preconceived notions.
 

Is cancer hereditary?

The report shows that 67.7% of respondents believe that cancer is a hereditary disease. Respondents were asked to explain their answer. “Data show that medical practices for cancer treatment substantiate this belief [that cancer is hereditary],” wrote the authors of the report.

“Indeed, health care professionals almost systematically ask questions about family history of breast cancer and, when a family member has been diagnosed with cancer, medical monitoring of other family members is often sought out, thus reinforcing the belief that cancer is hereditary,” they said.

Furthermore, there seems to be confusion regarding the role of genes in the development of cancer. A person can inherit cancer-predisposing genes, not cancer itself. The authors highlighted their concern that this confusion may “lead people to think that prevention measures are unnecessary because cancer is inherited.”
 

Misconceptions about smoking

About 41% of smokers think that the length of time one has been smoking is the biggest determining factor for developing cancer; 58.1% think the number of cigarettes smoked per day has a bigger impact.

Experts at InCA and SPF put the debate to rest, stating that prolonged exposure to carcinogenic substances is far more toxic. As for the danger threshold concerning the number of cigarettes smoked per day, respondents believed this to be 9.2 cigarettes per day, on average. They believed that the danger threshold for the number of years as an active smoker is 13.4, on average.

“The [survey] respondents clearly understand that smoking carries a risk, but many smokers think that light smoking or smoking for a short period of time doesn’t carry any risks.” Yet it is understood that even occasional tobacco consumption increases mortality.

This was not the only misconception regarding smoking and its relationship with cancer. About 34% of survey respondents agreed with the following statement: “Smoking doesn’t cause cancer unless you’re a heavy smoker and have smoked for a long time.” Furthermore, 43.3% agreed with the statement, “Pollution is more likely to cause cancer than smoking,” 54.6% think that “exercising cleans your lungs of tobacco,” and 61.6% think that “a smoker can prevent developing cancer caused by smoking if they know to quit on time.”
 

Overweight and obesity

Although diet and excess weight represent the third and fourth biggest avoidable cancer risk factors, after smoking and alcohol, only 30% of survey respondents knew of this link.

“Among the causes of cancer known and cited by respondents without prompting, excessive weight and obesity were mentioned only 100 times out of 12,558 responses,” highlighted the authors of the report. The explanation put forward by the authors is that discourse about diet has been more focused on diet as a protective health factor, especially in preventing cardiovascular diseases. “The link between cancer and diet is less prominent in the public space,” they noted.
 

Breastfeeding and cancer

About 63% of survey respondents, which for the first time included both women and men, believe that breastfeeding does not affect mothers’ risk of breast cancer, but this is a misconception. And almost 1 in 3 respondents said that breastfeeding provides health benefits for the mother.

Artificial UV rays

Exposure to UV rays, whether of natural or artificial origin, is a major risk factor for skin cancer. However, 1 in 5 people (20.9%) think that a session in a tanning bed is less harmful than sun exposure.

Daily stress

Regarding psychological factors linked to cancer, the authors noted that risk factors not supported by scientific evidence were, ironically, cited more often by respondents than proven risk factors. There is a real knowledge gap between scientific data and the beliefs of the French people. For example, “working at night” is largely not seen as a risk factor, but data show that it presents a clear risk. However, “not being able to express one’s feelings,” “having been weakened by traumatic experiences,” and “being exposed to the stress of modern life” are seen as risk factors of cancer, without any scientific evidence.

Cigarettes and e-cigarettes

About 53% of respondents agreed that “e-cigarettes are just as harmful or more harmful than traditional cigarettes.” Nicotine and the flavors in e-cigarettes are largely perceived as “very” or “extremely” harmful to the health of a person. However, the authors note that “no published study on nicotine substitutes has shown harmful effects on the health of a person, let alone determined it a risk factor for cancer. The nicotine doses in e-cigarettes are similar to traditional nicotine substitutes, and no cytotoxic effect of nicotine in its inhaled form has been found.” There seems to be confusion between dependence and risk of cancer.

Alcohol consumption

Eight of 10 respondents believe that “some people can drink a lot of alcohol all their life without ever getting cancer,” which goes against the scientific literature. The authors of the report state that the negative effects of alcohol on health seem poorly understood. Although alcohol is the second biggest cause of cancer, only a third of survey respondents cited it without having been prompted as one of the main causes of cancer. And 23.5% even think that “in terms of decreasing your risk of cancer, it’s better to drink a little wine than to drink no wine at all.”

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

FRANCE – Conducted every 5 years since 2005, the Cancer Survey documents the knowledge, perceptions, and way of life of the French people in relation to cancer. The French National Cancer Institute (InCA), in partnership with Public Health France (SPF), has published the results of its 2021 survey. The researchers analyzed responses to telephone interviews of a representative sample of almost 5,000 individuals aged 15-85 years.

This study shows how thinking has changed over time and how difficult it is to alter preconceived notions.
 

Is cancer hereditary?

The report shows that 67.7% of respondents believe that cancer is a hereditary disease. Respondents were asked to explain their answer. “Data show that medical practices for cancer treatment substantiate this belief [that cancer is hereditary],” wrote the authors of the report.

“Indeed, health care professionals almost systematically ask questions about family history of breast cancer and, when a family member has been diagnosed with cancer, medical monitoring of other family members is often sought out, thus reinforcing the belief that cancer is hereditary,” they said.

Furthermore, there seems to be confusion regarding the role of genes in the development of cancer. A person can inherit cancer-predisposing genes, not cancer itself. The authors highlighted their concern that this confusion may “lead people to think that prevention measures are unnecessary because cancer is inherited.”
 

Misconceptions about smoking

About 41% of smokers think that the length of time one has been smoking is the biggest determining factor for developing cancer; 58.1% think the number of cigarettes smoked per day has a bigger impact.

Experts at InCA and SPF put the debate to rest, stating that prolonged exposure to carcinogenic substances is far more toxic. As for the danger threshold concerning the number of cigarettes smoked per day, respondents believed this to be 9.2 cigarettes per day, on average. They believed that the danger threshold for the number of years as an active smoker is 13.4, on average.

“The [survey] respondents clearly understand that smoking carries a risk, but many smokers think that light smoking or smoking for a short period of time doesn’t carry any risks.” Yet it is understood that even occasional tobacco consumption increases mortality.

This was not the only misconception regarding smoking and its relationship with cancer. About 34% of survey respondents agreed with the following statement: “Smoking doesn’t cause cancer unless you’re a heavy smoker and have smoked for a long time.” Furthermore, 43.3% agreed with the statement, “Pollution is more likely to cause cancer than smoking,” 54.6% think that “exercising cleans your lungs of tobacco,” and 61.6% think that “a smoker can prevent developing cancer caused by smoking if they know to quit on time.”
 

Overweight and obesity

Although diet and excess weight represent the third and fourth biggest avoidable cancer risk factors, after smoking and alcohol, only 30% of survey respondents knew of this link.

“Among the causes of cancer known and cited by respondents without prompting, excessive weight and obesity were mentioned only 100 times out of 12,558 responses,” highlighted the authors of the report. The explanation put forward by the authors is that discourse about diet has been more focused on diet as a protective health factor, especially in preventing cardiovascular diseases. “The link between cancer and diet is less prominent in the public space,” they noted.
 

Breastfeeding and cancer

About 63% of survey respondents, which for the first time included both women and men, believe that breastfeeding does not affect mothers’ risk of breast cancer, but this is a misconception. And almost 1 in 3 respondents said that breastfeeding provides health benefits for the mother.

Artificial UV rays

Exposure to UV rays, whether of natural or artificial origin, is a major risk factor for skin cancer. However, 1 in 5 people (20.9%) think that a session in a tanning bed is less harmful than sun exposure.

Daily stress

Regarding psychological factors linked to cancer, the authors noted that risk factors not supported by scientific evidence were, ironically, cited more often by respondents than proven risk factors. There is a real knowledge gap between scientific data and the beliefs of the French people. For example, “working at night” is largely not seen as a risk factor, but data show that it presents a clear risk. However, “not being able to express one’s feelings,” “having been weakened by traumatic experiences,” and “being exposed to the stress of modern life” are seen as risk factors of cancer, without any scientific evidence.

Cigarettes and e-cigarettes

About 53% of respondents agreed that “e-cigarettes are just as harmful or more harmful than traditional cigarettes.” Nicotine and the flavors in e-cigarettes are largely perceived as “very” or “extremely” harmful to the health of a person. However, the authors note that “no published study on nicotine substitutes has shown harmful effects on the health of a person, let alone determined it a risk factor for cancer. The nicotine doses in e-cigarettes are similar to traditional nicotine substitutes, and no cytotoxic effect of nicotine in its inhaled form has been found.” There seems to be confusion between dependence and risk of cancer.

Alcohol consumption

Eight of 10 respondents believe that “some people can drink a lot of alcohol all their life without ever getting cancer,” which goes against the scientific literature. The authors of the report state that the negative effects of alcohol on health seem poorly understood. Although alcohol is the second biggest cause of cancer, only a third of survey respondents cited it without having been prompted as one of the main causes of cancer. And 23.5% even think that “in terms of decreasing your risk of cancer, it’s better to drink a little wine than to drink no wine at all.”

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

FRANCE – Conducted every 5 years since 2005, the Cancer Survey documents the knowledge, perceptions, and way of life of the French people in relation to cancer. The French National Cancer Institute (InCA), in partnership with Public Health France (SPF), has published the results of its 2021 survey. The researchers analyzed responses to telephone interviews of a representative sample of almost 5,000 individuals aged 15-85 years.

This study shows how thinking has changed over time and how difficult it is to alter preconceived notions.
 

Is cancer hereditary?

The report shows that 67.7% of respondents believe that cancer is a hereditary disease. Respondents were asked to explain their answer. “Data show that medical practices for cancer treatment substantiate this belief [that cancer is hereditary],” wrote the authors of the report.

“Indeed, health care professionals almost systematically ask questions about family history of breast cancer and, when a family member has been diagnosed with cancer, medical monitoring of other family members is often sought out, thus reinforcing the belief that cancer is hereditary,” they said.

Furthermore, there seems to be confusion regarding the role of genes in the development of cancer. A person can inherit cancer-predisposing genes, not cancer itself. The authors highlighted their concern that this confusion may “lead people to think that prevention measures are unnecessary because cancer is inherited.”
 

Misconceptions about smoking

About 41% of smokers think that the length of time one has been smoking is the biggest determining factor for developing cancer; 58.1% think the number of cigarettes smoked per day has a bigger impact.

Experts at InCA and SPF put the debate to rest, stating that prolonged exposure to carcinogenic substances is far more toxic. As for the danger threshold concerning the number of cigarettes smoked per day, respondents believed this to be 9.2 cigarettes per day, on average. They believed that the danger threshold for the number of years as an active smoker is 13.4, on average.

“The [survey] respondents clearly understand that smoking carries a risk, but many smokers think that light smoking or smoking for a short period of time doesn’t carry any risks.” Yet it is understood that even occasional tobacco consumption increases mortality.

This was not the only misconception regarding smoking and its relationship with cancer. About 34% of survey respondents agreed with the following statement: “Smoking doesn’t cause cancer unless you’re a heavy smoker and have smoked for a long time.” Furthermore, 43.3% agreed with the statement, “Pollution is more likely to cause cancer than smoking,” 54.6% think that “exercising cleans your lungs of tobacco,” and 61.6% think that “a smoker can prevent developing cancer caused by smoking if they know to quit on time.”
 

Overweight and obesity

Although diet and excess weight represent the third and fourth biggest avoidable cancer risk factors, after smoking and alcohol, only 30% of survey respondents knew of this link.

“Among the causes of cancer known and cited by respondents without prompting, excessive weight and obesity were mentioned only 100 times out of 12,558 responses,” highlighted the authors of the report. The explanation put forward by the authors is that discourse about diet has been more focused on diet as a protective health factor, especially in preventing cardiovascular diseases. “The link between cancer and diet is less prominent in the public space,” they noted.
 

Breastfeeding and cancer

About 63% of survey respondents, which for the first time included both women and men, believe that breastfeeding does not affect mothers’ risk of breast cancer, but this is a misconception. And almost 1 in 3 respondents said that breastfeeding provides health benefits for the mother.

Artificial UV rays

Exposure to UV rays, whether of natural or artificial origin, is a major risk factor for skin cancer. However, 1 in 5 people (20.9%) think that a session in a tanning bed is less harmful than sun exposure.

Daily stress

Regarding psychological factors linked to cancer, the authors noted that risk factors not supported by scientific evidence were, ironically, cited more often by respondents than proven risk factors. There is a real knowledge gap between scientific data and the beliefs of the French people. For example, “working at night” is largely not seen as a risk factor, but data show that it presents a clear risk. However, “not being able to express one’s feelings,” “having been weakened by traumatic experiences,” and “being exposed to the stress of modern life” are seen as risk factors of cancer, without any scientific evidence.

Cigarettes and e-cigarettes

About 53% of respondents agreed that “e-cigarettes are just as harmful or more harmful than traditional cigarettes.” Nicotine and the flavors in e-cigarettes are largely perceived as “very” or “extremely” harmful to the health of a person. However, the authors note that “no published study on nicotine substitutes has shown harmful effects on the health of a person, let alone determined it a risk factor for cancer. The nicotine doses in e-cigarettes are similar to traditional nicotine substitutes, and no cytotoxic effect of nicotine in its inhaled form has been found.” There seems to be confusion between dependence and risk of cancer.

Alcohol consumption

Eight of 10 respondents believe that “some people can drink a lot of alcohol all their life without ever getting cancer,” which goes against the scientific literature. The authors of the report state that the negative effects of alcohol on health seem poorly understood. Although alcohol is the second biggest cause of cancer, only a third of survey respondents cited it without having been prompted as one of the main causes of cancer. And 23.5% even think that “in terms of decreasing your risk of cancer, it’s better to drink a little wine than to drink no wine at all.”

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

Irregular sleep – such as inconsistent sleep duration or sleep timing – may increase the risk of developing atherosclerosis among adults older than age 45, a new report suggests.

In particular, variation in sleep duration of more than 2 hours per night in the same week was tied to higher rates of atherosclerosis.

“Poor sleep is linked with several cardiovascular conditions, including heart disease, hypertension, and type 2 diabetes,” lead author Kelsie M. Full, PhD, MPH, assistant professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., said in an interview.

“Overall, we found that participants who slept varying amounts of hours throughout the week (meaning that one night they slept less, one night they slept more) were more likely to have atherosclerosis than participants who slept about the same amount of time each night,” she said.

The study was published online in the Journal of the American Heart Association.
 

Analyzing associations

Dr. Full and colleagues examined data from 2032 participants in the Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study, which included adults aged between 45 and 84 years in six U.S. communities who completed 7-day wrist actigraphy assessment and kept a sleep diary between 2010 and 2013.

For subclinical markers of cardiovascular disease, participants underwent assessments of coronary artery calcium, carotid plaque presence, carotid intima-media thickness, and ankle-brachial index.

The research team assessed sleep duration, or the total number of minutes of sleep in a night, and sleep timing regularity, which was determined on the basis of the time someone initially fell asleep each night. They adjusted for cardiovascular disease risk factors and sleep characteristics, such as obstructive sleep apnea, sleep duration, and sleep fragmentation.

The average age of the participants was 68.6 years, and 53.6% were women. About 37.9% identified as White, 27.6% as Black or African American, 23.4% as Hispanic American, and 11.1% as Chinese American.

During the 7-day period, about 38% of participants experienced a change in sleep duration of more than 90 minutes, and 18% experienced a sleep duration change of more than 120 minutes. Those who had irregular sleep were more likely to be non-White, current smokers, have lower average annual incomes, have work shift schedules or did not work, and have a higher average body mass index.

For the study, sleep duration irregularity was defined as a standard deviation of more than 120 minutes. Those participants who had a greater degree of sleep irregularity were more likely to have high coronary artery calcium burden than those whose sleep duration was more more regular, defined as an SD of 60 minutes or less (> 300; prevalence ratio, 1.33; 95% confidence interval, 1.03-1.71), as well as abnormal ankle-brachial index (< 0.9, prevalence ratio, 1.75;95% CI, 1.03-2.95).

Further, those with irregular sleep timing (SD > 90 minutes) were more likely to have a high coronary artery calcium burden (prevalence ratio, 1.39; 95% CI, 1.07-1.82) in comparison with those with more regular sleep timing (SD < 30 minutes).

“The biggest surprise to me was that 30% of the participants in the study had total sleep times that varied by more than 90 minutes over the course of the week,” Dr. Full said. “This is consistent with prior studies that suggest that a large proportion of the general public have irregular sleep patterns, not just shift workers.”
 

Investigating next steps

In additional analyses, Dr. Full and colleagues found that sleep duration regularity continued to be associated with high coronary artery calcium burden and abnormal ankle-brachial index when accounting for severe obstructive sleep apnea, average nightly sleep duration, and average sleep fragmentation.

Notably, when sleep duration was added, all participants with more irregular sleep durations (SD > 60 minutes) were more likely to have a high coronary artery calcium burden, compared with those with regular sleep durations (SD < 60 minutes). The results remained when participants who reported shift work, including night shift work, were excluded.

Additional studies are needed to understand the mechanisms, the study authors wrote. Night-to-night variability in sleep duration and sleep timing can cause desynchronization in the sleep-wake timing and circadian disruption.

“A key issue highlighted in this study is that sleep irregularity itself, independent of how much sleep people were getting, was related to heart health. Sleep is a naturally recurring phenomenon, and maintaining regularity helps provide stability and predictability to the body,” Michael Grandner, PhD, associate professor of psychiatry and director of the sleep and health research program at the University of Arizona, Tucson, said in an interview.

Dr. Grandner, who wasn’t involved with this study, has researched sleep irregularity and associations with cardiovascular disease, diabetes, obesity, and many other adverse outcomes.

“When people have very irregular sleep schedules, it may make it harder for the body to optimally make good use of the sleep it is getting, since it such a moving target,” he said. “The unique angle here is the ability to focus on regularity of sleep.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Center for Advancing Translational Sciences of the National Institutes of Health. One author received grants and consulting fees from pharmaceutical companies unrelated to the research. The other authors and Dr. Grandner disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Irregular sleep – such as inconsistent sleep duration or sleep timing – may increase the risk of developing atherosclerosis among adults older than age 45, a new report suggests.

In particular, variation in sleep duration of more than 2 hours per night in the same week was tied to higher rates of atherosclerosis.

“Poor sleep is linked with several cardiovascular conditions, including heart disease, hypertension, and type 2 diabetes,” lead author Kelsie M. Full, PhD, MPH, assistant professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., said in an interview.

“Overall, we found that participants who slept varying amounts of hours throughout the week (meaning that one night they slept less, one night they slept more) were more likely to have atherosclerosis than participants who slept about the same amount of time each night,” she said.

The study was published online in the Journal of the American Heart Association.
 

Analyzing associations

Dr. Full and colleagues examined data from 2032 participants in the Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study, which included adults aged between 45 and 84 years in six U.S. communities who completed 7-day wrist actigraphy assessment and kept a sleep diary between 2010 and 2013.

For subclinical markers of cardiovascular disease, participants underwent assessments of coronary artery calcium, carotid plaque presence, carotid intima-media thickness, and ankle-brachial index.

The research team assessed sleep duration, or the total number of minutes of sleep in a night, and sleep timing regularity, which was determined on the basis of the time someone initially fell asleep each night. They adjusted for cardiovascular disease risk factors and sleep characteristics, such as obstructive sleep apnea, sleep duration, and sleep fragmentation.

The average age of the participants was 68.6 years, and 53.6% were women. About 37.9% identified as White, 27.6% as Black or African American, 23.4% as Hispanic American, and 11.1% as Chinese American.

During the 7-day period, about 38% of participants experienced a change in sleep duration of more than 90 minutes, and 18% experienced a sleep duration change of more than 120 minutes. Those who had irregular sleep were more likely to be non-White, current smokers, have lower average annual incomes, have work shift schedules or did not work, and have a higher average body mass index.

For the study, sleep duration irregularity was defined as a standard deviation of more than 120 minutes. Those participants who had a greater degree of sleep irregularity were more likely to have high coronary artery calcium burden than those whose sleep duration was more more regular, defined as an SD of 60 minutes or less (> 300; prevalence ratio, 1.33; 95% confidence interval, 1.03-1.71), as well as abnormal ankle-brachial index (< 0.9, prevalence ratio, 1.75;95% CI, 1.03-2.95).

Further, those with irregular sleep timing (SD > 90 minutes) were more likely to have a high coronary artery calcium burden (prevalence ratio, 1.39; 95% CI, 1.07-1.82) in comparison with those with more regular sleep timing (SD < 30 minutes).

“The biggest surprise to me was that 30% of the participants in the study had total sleep times that varied by more than 90 minutes over the course of the week,” Dr. Full said. “This is consistent with prior studies that suggest that a large proportion of the general public have irregular sleep patterns, not just shift workers.”
 

Investigating next steps

In additional analyses, Dr. Full and colleagues found that sleep duration regularity continued to be associated with high coronary artery calcium burden and abnormal ankle-brachial index when accounting for severe obstructive sleep apnea, average nightly sleep duration, and average sleep fragmentation.

Notably, when sleep duration was added, all participants with more irregular sleep durations (SD > 60 minutes) were more likely to have a high coronary artery calcium burden, compared with those with regular sleep durations (SD < 60 minutes). The results remained when participants who reported shift work, including night shift work, were excluded.

Additional studies are needed to understand the mechanisms, the study authors wrote. Night-to-night variability in sleep duration and sleep timing can cause desynchronization in the sleep-wake timing and circadian disruption.

“A key issue highlighted in this study is that sleep irregularity itself, independent of how much sleep people were getting, was related to heart health. Sleep is a naturally recurring phenomenon, and maintaining regularity helps provide stability and predictability to the body,” Michael Grandner, PhD, associate professor of psychiatry and director of the sleep and health research program at the University of Arizona, Tucson, said in an interview.

Dr. Grandner, who wasn’t involved with this study, has researched sleep irregularity and associations with cardiovascular disease, diabetes, obesity, and many other adverse outcomes.

“When people have very irregular sleep schedules, it may make it harder for the body to optimally make good use of the sleep it is getting, since it such a moving target,” he said. “The unique angle here is the ability to focus on regularity of sleep.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Center for Advancing Translational Sciences of the National Institutes of Health. One author received grants and consulting fees from pharmaceutical companies unrelated to the research. The other authors and Dr. Grandner disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Irregular sleep – such as inconsistent sleep duration or sleep timing – may increase the risk of developing atherosclerosis among adults older than age 45, a new report suggests.

In particular, variation in sleep duration of more than 2 hours per night in the same week was tied to higher rates of atherosclerosis.

“Poor sleep is linked with several cardiovascular conditions, including heart disease, hypertension, and type 2 diabetes,” lead author Kelsie M. Full, PhD, MPH, assistant professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., said in an interview.

“Overall, we found that participants who slept varying amounts of hours throughout the week (meaning that one night they slept less, one night they slept more) were more likely to have atherosclerosis than participants who slept about the same amount of time each night,” she said.

The study was published online in the Journal of the American Heart Association.
 

Analyzing associations

Dr. Full and colleagues examined data from 2032 participants in the Multi-Ethnic Study of Atherosclerosis Sleep Ancillary Study, which included adults aged between 45 and 84 years in six U.S. communities who completed 7-day wrist actigraphy assessment and kept a sleep diary between 2010 and 2013.

For subclinical markers of cardiovascular disease, participants underwent assessments of coronary artery calcium, carotid plaque presence, carotid intima-media thickness, and ankle-brachial index.

The research team assessed sleep duration, or the total number of minutes of sleep in a night, and sleep timing regularity, which was determined on the basis of the time someone initially fell asleep each night. They adjusted for cardiovascular disease risk factors and sleep characteristics, such as obstructive sleep apnea, sleep duration, and sleep fragmentation.

The average age of the participants was 68.6 years, and 53.6% were women. About 37.9% identified as White, 27.6% as Black or African American, 23.4% as Hispanic American, and 11.1% as Chinese American.

During the 7-day period, about 38% of participants experienced a change in sleep duration of more than 90 minutes, and 18% experienced a sleep duration change of more than 120 minutes. Those who had irregular sleep were more likely to be non-White, current smokers, have lower average annual incomes, have work shift schedules or did not work, and have a higher average body mass index.

For the study, sleep duration irregularity was defined as a standard deviation of more than 120 minutes. Those participants who had a greater degree of sleep irregularity were more likely to have high coronary artery calcium burden than those whose sleep duration was more more regular, defined as an SD of 60 minutes or less (> 300; prevalence ratio, 1.33; 95% confidence interval, 1.03-1.71), as well as abnormal ankle-brachial index (< 0.9, prevalence ratio, 1.75;95% CI, 1.03-2.95).

Further, those with irregular sleep timing (SD > 90 minutes) were more likely to have a high coronary artery calcium burden (prevalence ratio, 1.39; 95% CI, 1.07-1.82) in comparison with those with more regular sleep timing (SD < 30 minutes).

“The biggest surprise to me was that 30% of the participants in the study had total sleep times that varied by more than 90 minutes over the course of the week,” Dr. Full said. “This is consistent with prior studies that suggest that a large proportion of the general public have irregular sleep patterns, not just shift workers.”
 

Investigating next steps

In additional analyses, Dr. Full and colleagues found that sleep duration regularity continued to be associated with high coronary artery calcium burden and abnormal ankle-brachial index when accounting for severe obstructive sleep apnea, average nightly sleep duration, and average sleep fragmentation.

Notably, when sleep duration was added, all participants with more irregular sleep durations (SD > 60 minutes) were more likely to have a high coronary artery calcium burden, compared with those with regular sleep durations (SD < 60 minutes). The results remained when participants who reported shift work, including night shift work, were excluded.

Additional studies are needed to understand the mechanisms, the study authors wrote. Night-to-night variability in sleep duration and sleep timing can cause desynchronization in the sleep-wake timing and circadian disruption.

“A key issue highlighted in this study is that sleep irregularity itself, independent of how much sleep people were getting, was related to heart health. Sleep is a naturally recurring phenomenon, and maintaining regularity helps provide stability and predictability to the body,” Michael Grandner, PhD, associate professor of psychiatry and director of the sleep and health research program at the University of Arizona, Tucson, said in an interview.

Dr. Grandner, who wasn’t involved with this study, has researched sleep irregularity and associations with cardiovascular disease, diabetes, obesity, and many other adverse outcomes.

“When people have very irregular sleep schedules, it may make it harder for the body to optimally make good use of the sleep it is getting, since it such a moving target,” he said. “The unique angle here is the ability to focus on regularity of sleep.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Center for Advancing Translational Sciences of the National Institutes of Health. One author received grants and consulting fees from pharmaceutical companies unrelated to the research. The other authors and Dr. Grandner disclosed no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Sleep disturbances are consistently high throughout the course of psychosis, with later stages associated with distinctive brain wave activity during sleep, a new review and meta-analysis shows.

For example, compared with their healthy peers, participants in a chronic psychosis stage had reduced density, amplitude, and duration of spindles – or bursts of brainwave activity during sleep identified by electroencephalography.

“The results suggest sleep could be an important target [and] an area of research and clinical intervention that could make a difference” in the lives of patients at risk for psychosis, study investigator Fabio Ferrarelli, MD, PhD, associate professor of psychiatry and director of the Sleep and Schizophrenia Program, University of Pittsburgh School of Medicine, told this news organization.

University of Pittsburgh

‘Window of opportunity’

Researchers separate psychosis into stages. During the “clinically high-risk for psychosis” (CHR-P) stage, patients have milder symptoms but do not have a diagnosable psychotic disorder. Those in the early psychosis (EP) stage have had a first episode of psychosis. When they reach a cut-off, often at 5 years, they are considered to have chronic psychosis (CP).

Previous studies have shown that altered sleep often precedes a psychotic episode in early psychosis, and disrupted sleep contributes to predicting transition to psychosis in youth at risk for the condition. Individuals with CP commonly report sleep disturbances, such as insomnia.

Following a literature search, the investigators for this current meta-analysis selected 21 studies assessing sleep disturbance prevalence in 5,135 patients. They also selected 39 studies measuring sleep alterations subjectively (for example, sleep quality) and/or objectively (for example, sleep architecture and sleep oscillation) in 1,575 patients and 977 healthy controls.

The included studies measured the prevalence of sleep disturbances and/or sleep characteristics at different psychosis stages using polysomnography, EEG, actigraphy, or self-reports.

The pooled prevalence of sleep disturbances was 50% across clinical stages (95% confidence interval, 40%-61%). The prevalence was 54% in CHR-P, 68% in EP, and 44% in CP.

The prevalence of insomnia as the primary sleep disturbance was 34% of pooled cases, 48% of the EP group, and 27% of the CP group.

“What’s interesting is the rate of sleep disturbances is relatively stable across stages,” said Dr. Ferrarelli. “This is important because you have a window of opportunity to do some early intervention in people who are at risk that can prevent things from getting worse.”

He suggests clinicians screen for insomnia in early-course patients and perhaps recommend cognitive behavioral therapy (CBT) for insomnia. As well, they should promote sleep hygiene measures for at-risk patients, including such things as avoiding caffeine, alcohol, and screen time before bedtime and adopting a regular sleep pattern.

“These are people at risk, which means they have a 20%-30% chance of eventually developing a psychotic disorder,” said Dr. Ferrarelli. “Maybe disrupted sleep is one of the factors that can make a difference.”
 

Altered sleep architecture

To compare sleep quality between clinical and control groups, studies used total scores on the Pittsburgh Sleep Quality Index (PSQI), where a score over 5 indicates a sleep problem.

There was a significant standardized mean difference in pooled cases versus controls (SMD, 1.0; 95% CI, 0.7-1.3; P < .001). Each clinical group showed poorer sleep quality, compared with controls.

When assessing sleep architecture abnormalities, stage-specific case-control comparisons showed these were driven by EP and CP stages.

Altered sleep characteristics in both these stages included increased sleep onset latency, increased wake after sleep onset, and reduced sleep efficiency.

Compared with controls, CP was the only clinical group with more arousals. Patients with CP also had more arousals than the CHR-P group, and the number of arousals was significantly affected by medication.

The findings indicate the effects of antipsychotic medications on sleep should be closely monitored, especially in CP, the investigators write.

They add that clinicians should consider medication adjustments, such as decreased doses or switches to another compound.
 

‘Robust’ spindle results

As for spindle parameters, pooled cases showed significantly decreased spindle density (SMD, –1.06), spindle amplitude (SMD, –1.08), and spindle duration (SMD, −1.21), compared with controls. Stage-specific comparisons revealed these deficits were present in both EP and CP relative to controls.

Dr. Ferrarelli noted the results for spindle abnormalities were among “the most robust” and show that these abnormalities “tend to get worse over the course of the illness.”

The spindle data are “a lot more informative” than that provided by other sleep parameters “in the sense they can yield what could be wrong, where it could be, and potentially what you can do about it,” said Dr. Ferrarelli.

“This might be an objective measure that could be used to identify individuals who have a psychosis disorder, monitor progression of illness, and for prognostic reasons,” he added.

He noted that spindles may also represent a promising target for treatment interventions and added that non-invasive transcranial magnetic stimulation has shown promise in restoring sleep oscillations, including spindles.

Another way to evoke target-brain activity may be through auditory tones – with a patient listening to a particular sound through headphones while asleep, Dr. Ferrarelli said.
 

Reaffirms previous data

Commenting on the study, Jeffrey A. Lieberman, MD, professor and chair in psychiatry at Columbia University, New York, and a past president of the American Psychiatric Association, noted that the review “just reaffirms what has been reported by individual studies for decades.”

That so many at-risk study subjects had a sleep abnormality is not surprising, said Dr. Lieberman, who was not involved with the current research.

“How many individuals in late adolescence or early adulthood have sleep problems?” he asked. “I would venture to say it’s probably a lot. So the question is: How distinctive is this from what occurs in people who don’t develop the illness?”

The aim of sleep research in the area of schizophrenia has long been to disentangle the effects of medication and environmental factors from the disease and to be able to treat patients to normalize their sleep, said Dr. Lieberman.

“But it’s not clear from these results how one would do that,” he added.

The authors “don’t fundamentally tell us anything about the underlying cause of the illness or the pathophysiology, and they don’t really offer any kind of clear direction for clinical intervention,” he said.

The study was supported by the National Institute of Mental Health. Dr. Ferrarelli reported grants from the National Institute of Mental Health during the conduct of the study. Dr. Lieberman has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Sleep disturbances are consistently high throughout the course of psychosis, with later stages associated with distinctive brain wave activity during sleep, a new review and meta-analysis shows.

For example, compared with their healthy peers, participants in a chronic psychosis stage had reduced density, amplitude, and duration of spindles – or bursts of brainwave activity during sleep identified by electroencephalography.

“The results suggest sleep could be an important target [and] an area of research and clinical intervention that could make a difference” in the lives of patients at risk for psychosis, study investigator Fabio Ferrarelli, MD, PhD, associate professor of psychiatry and director of the Sleep and Schizophrenia Program, University of Pittsburgh School of Medicine, told this news organization.

University of Pittsburgh

‘Window of opportunity’

Researchers separate psychosis into stages. During the “clinically high-risk for psychosis” (CHR-P) stage, patients have milder symptoms but do not have a diagnosable psychotic disorder. Those in the early psychosis (EP) stage have had a first episode of psychosis. When they reach a cut-off, often at 5 years, they are considered to have chronic psychosis (CP).

Previous studies have shown that altered sleep often precedes a psychotic episode in early psychosis, and disrupted sleep contributes to predicting transition to psychosis in youth at risk for the condition. Individuals with CP commonly report sleep disturbances, such as insomnia.

Following a literature search, the investigators for this current meta-analysis selected 21 studies assessing sleep disturbance prevalence in 5,135 patients. They also selected 39 studies measuring sleep alterations subjectively (for example, sleep quality) and/or objectively (for example, sleep architecture and sleep oscillation) in 1,575 patients and 977 healthy controls.

The included studies measured the prevalence of sleep disturbances and/or sleep characteristics at different psychosis stages using polysomnography, EEG, actigraphy, or self-reports.

The pooled prevalence of sleep disturbances was 50% across clinical stages (95% confidence interval, 40%-61%). The prevalence was 54% in CHR-P, 68% in EP, and 44% in CP.

The prevalence of insomnia as the primary sleep disturbance was 34% of pooled cases, 48% of the EP group, and 27% of the CP group.

“What’s interesting is the rate of sleep disturbances is relatively stable across stages,” said Dr. Ferrarelli. “This is important because you have a window of opportunity to do some early intervention in people who are at risk that can prevent things from getting worse.”

He suggests clinicians screen for insomnia in early-course patients and perhaps recommend cognitive behavioral therapy (CBT) for insomnia. As well, they should promote sleep hygiene measures for at-risk patients, including such things as avoiding caffeine, alcohol, and screen time before bedtime and adopting a regular sleep pattern.

“These are people at risk, which means they have a 20%-30% chance of eventually developing a psychotic disorder,” said Dr. Ferrarelli. “Maybe disrupted sleep is one of the factors that can make a difference.”
 

Altered sleep architecture

To compare sleep quality between clinical and control groups, studies used total scores on the Pittsburgh Sleep Quality Index (PSQI), where a score over 5 indicates a sleep problem.

There was a significant standardized mean difference in pooled cases versus controls (SMD, 1.0; 95% CI, 0.7-1.3; P < .001). Each clinical group showed poorer sleep quality, compared with controls.

When assessing sleep architecture abnormalities, stage-specific case-control comparisons showed these were driven by EP and CP stages.

Altered sleep characteristics in both these stages included increased sleep onset latency, increased wake after sleep onset, and reduced sleep efficiency.

Compared with controls, CP was the only clinical group with more arousals. Patients with CP also had more arousals than the CHR-P group, and the number of arousals was significantly affected by medication.

The findings indicate the effects of antipsychotic medications on sleep should be closely monitored, especially in CP, the investigators write.

They add that clinicians should consider medication adjustments, such as decreased doses or switches to another compound.
 

‘Robust’ spindle results

As for spindle parameters, pooled cases showed significantly decreased spindle density (SMD, –1.06), spindle amplitude (SMD, –1.08), and spindle duration (SMD, −1.21), compared with controls. Stage-specific comparisons revealed these deficits were present in both EP and CP relative to controls.

Dr. Ferrarelli noted the results for spindle abnormalities were among “the most robust” and show that these abnormalities “tend to get worse over the course of the illness.”

The spindle data are “a lot more informative” than that provided by other sleep parameters “in the sense they can yield what could be wrong, where it could be, and potentially what you can do about it,” said Dr. Ferrarelli.

“This might be an objective measure that could be used to identify individuals who have a psychosis disorder, monitor progression of illness, and for prognostic reasons,” he added.

He noted that spindles may also represent a promising target for treatment interventions and added that non-invasive transcranial magnetic stimulation has shown promise in restoring sleep oscillations, including spindles.

Another way to evoke target-brain activity may be through auditory tones – with a patient listening to a particular sound through headphones while asleep, Dr. Ferrarelli said.
 

Reaffirms previous data

Commenting on the study, Jeffrey A. Lieberman, MD, professor and chair in psychiatry at Columbia University, New York, and a past president of the American Psychiatric Association, noted that the review “just reaffirms what has been reported by individual studies for decades.”

That so many at-risk study subjects had a sleep abnormality is not surprising, said Dr. Lieberman, who was not involved with the current research.

“How many individuals in late adolescence or early adulthood have sleep problems?” he asked. “I would venture to say it’s probably a lot. So the question is: How distinctive is this from what occurs in people who don’t develop the illness?”

The aim of sleep research in the area of schizophrenia has long been to disentangle the effects of medication and environmental factors from the disease and to be able to treat patients to normalize their sleep, said Dr. Lieberman.

“But it’s not clear from these results how one would do that,” he added.

The authors “don’t fundamentally tell us anything about the underlying cause of the illness or the pathophysiology, and they don’t really offer any kind of clear direction for clinical intervention,” he said.

The study was supported by the National Institute of Mental Health. Dr. Ferrarelli reported grants from the National Institute of Mental Health during the conduct of the study. Dr. Lieberman has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Sleep disturbances are consistently high throughout the course of psychosis, with later stages associated with distinctive brain wave activity during sleep, a new review and meta-analysis shows.

For example, compared with their healthy peers, participants in a chronic psychosis stage had reduced density, amplitude, and duration of spindles – or bursts of brainwave activity during sleep identified by electroencephalography.

“The results suggest sleep could be an important target [and] an area of research and clinical intervention that could make a difference” in the lives of patients at risk for psychosis, study investigator Fabio Ferrarelli, MD, PhD, associate professor of psychiatry and director of the Sleep and Schizophrenia Program, University of Pittsburgh School of Medicine, told this news organization.

University of Pittsburgh

‘Window of opportunity’

Researchers separate psychosis into stages. During the “clinically high-risk for psychosis” (CHR-P) stage, patients have milder symptoms but do not have a diagnosable psychotic disorder. Those in the early psychosis (EP) stage have had a first episode of psychosis. When they reach a cut-off, often at 5 years, they are considered to have chronic psychosis (CP).

Previous studies have shown that altered sleep often precedes a psychotic episode in early psychosis, and disrupted sleep contributes to predicting transition to psychosis in youth at risk for the condition. Individuals with CP commonly report sleep disturbances, such as insomnia.

Following a literature search, the investigators for this current meta-analysis selected 21 studies assessing sleep disturbance prevalence in 5,135 patients. They also selected 39 studies measuring sleep alterations subjectively (for example, sleep quality) and/or objectively (for example, sleep architecture and sleep oscillation) in 1,575 patients and 977 healthy controls.

The included studies measured the prevalence of sleep disturbances and/or sleep characteristics at different psychosis stages using polysomnography, EEG, actigraphy, or self-reports.

The pooled prevalence of sleep disturbances was 50% across clinical stages (95% confidence interval, 40%-61%). The prevalence was 54% in CHR-P, 68% in EP, and 44% in CP.

The prevalence of insomnia as the primary sleep disturbance was 34% of pooled cases, 48% of the EP group, and 27% of the CP group.

“What’s interesting is the rate of sleep disturbances is relatively stable across stages,” said Dr. Ferrarelli. “This is important because you have a window of opportunity to do some early intervention in people who are at risk that can prevent things from getting worse.”

He suggests clinicians screen for insomnia in early-course patients and perhaps recommend cognitive behavioral therapy (CBT) for insomnia. As well, they should promote sleep hygiene measures for at-risk patients, including such things as avoiding caffeine, alcohol, and screen time before bedtime and adopting a regular sleep pattern.

“These are people at risk, which means they have a 20%-30% chance of eventually developing a psychotic disorder,” said Dr. Ferrarelli. “Maybe disrupted sleep is one of the factors that can make a difference.”
 

Altered sleep architecture

To compare sleep quality between clinical and control groups, studies used total scores on the Pittsburgh Sleep Quality Index (PSQI), where a score over 5 indicates a sleep problem.

There was a significant standardized mean difference in pooled cases versus controls (SMD, 1.0; 95% CI, 0.7-1.3; P < .001). Each clinical group showed poorer sleep quality, compared with controls.

When assessing sleep architecture abnormalities, stage-specific case-control comparisons showed these were driven by EP and CP stages.

Altered sleep characteristics in both these stages included increased sleep onset latency, increased wake after sleep onset, and reduced sleep efficiency.

Compared with controls, CP was the only clinical group with more arousals. Patients with CP also had more arousals than the CHR-P group, and the number of arousals was significantly affected by medication.

The findings indicate the effects of antipsychotic medications on sleep should be closely monitored, especially in CP, the investigators write.

They add that clinicians should consider medication adjustments, such as decreased doses or switches to another compound.
 

‘Robust’ spindle results

As for spindle parameters, pooled cases showed significantly decreased spindle density (SMD, –1.06), spindle amplitude (SMD, –1.08), and spindle duration (SMD, −1.21), compared with controls. Stage-specific comparisons revealed these deficits were present in both EP and CP relative to controls.

Dr. Ferrarelli noted the results for spindle abnormalities were among “the most robust” and show that these abnormalities “tend to get worse over the course of the illness.”

The spindle data are “a lot more informative” than that provided by other sleep parameters “in the sense they can yield what could be wrong, where it could be, and potentially what you can do about it,” said Dr. Ferrarelli.

“This might be an objective measure that could be used to identify individuals who have a psychosis disorder, monitor progression of illness, and for prognostic reasons,” he added.

He noted that spindles may also represent a promising target for treatment interventions and added that non-invasive transcranial magnetic stimulation has shown promise in restoring sleep oscillations, including spindles.

Another way to evoke target-brain activity may be through auditory tones – with a patient listening to a particular sound through headphones while asleep, Dr. Ferrarelli said.
 

Reaffirms previous data

Commenting on the study, Jeffrey A. Lieberman, MD, professor and chair in psychiatry at Columbia University, New York, and a past president of the American Psychiatric Association, noted that the review “just reaffirms what has been reported by individual studies for decades.”

That so many at-risk study subjects had a sleep abnormality is not surprising, said Dr. Lieberman, who was not involved with the current research.

“How many individuals in late adolescence or early adulthood have sleep problems?” he asked. “I would venture to say it’s probably a lot. So the question is: How distinctive is this from what occurs in people who don’t develop the illness?”

The aim of sleep research in the area of schizophrenia has long been to disentangle the effects of medication and environmental factors from the disease and to be able to treat patients to normalize their sleep, said Dr. Lieberman.

“But it’s not clear from these results how one would do that,” he added.

The authors “don’t fundamentally tell us anything about the underlying cause of the illness or the pathophysiology, and they don’t really offer any kind of clear direction for clinical intervention,” he said.

The study was supported by the National Institute of Mental Health. Dr. Ferrarelli reported grants from the National Institute of Mental Health during the conduct of the study. Dr. Lieberman has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Too little sleep or poor sleep quality during the teen years can significantly increase the risk for multiple sclerosis (MS) during adulthood, new research suggests.

In a large case-control study, individuals who slept less than 7 hours a night on average during adolescence were 40% more likely to develop MS later on. The risk was even higher for those who rated their sleep quality as bad.

On the other hand, MS was significantly less common among individuals who slept longer as teens – indicating a possible protective benefit.

While sleep duration has been associated with mortality or disease risk for other conditions, sleep quality usually has little to no effect on risk, lead investigator Torbjörn Åkerstedt, PhD, sleep researcher and professor of psychology, department of neuroscience, Karolinska Institutet, Stockholm, told this news organization.

“I hadn’t really expected that, but those results were quite strong, even stronger than sleep duration,” Dr. Åkerstedt said.

“We don’t really know why this is happening in young age, but the most suitable explanation is that the brain in still developing quite a bit, and you’re interfering with it,” he added.

The findings were published online in the Journal of Neurology, Neurosurgery and Psychiatry.
 

Strong association

Other studies have tied sleep deprivation to increased risk for serious illness, but the link between sleep and MS risk isn’t as well studied.

Previous research by Dr. Åkerstedt showed that the risk for MS was higher among individuals who took part in shift work before the age of 20. However, the impact of sleep duration or quality among teens was unknown.

The current Swedish population-based case-control study included 2,075 patients with MS and 3,164 without the disorder. All participants were asked to recall how many hours on average they slept per night between the ages of 15 and 19 years and to rate their sleep quality during that time.

Results showed that individuals who slept fewer than 7 hours a night during their teen years were 40% more likely to have MS as adults (odds ratio [OR], 1.4; 95% confidence interval [CI], 1.1-1.7).

Poor sleep quality increased MS risk even more (OR, 1.5; 95% CI, 1.3-1.9).

The association remained strong even after adjustment for additional sleep on weekends and breaks and excluding shift workers.
 

Long sleep ‘apparently good’

The researchers also conducted several sensitivity studies to rule out confounders that might bias the association, such as excluding participants who reported currently experiencing less sleep or poor sleep.

“You would expect that people who are suffering from sleep problems today would be the people who reported sleep problems during their youth,” but that didn’t happen, Dr. Åkerstedt noted.

The investigators also entered data on sleep duration and sleep quality at the same time, thinking the data would cancel each other out. However, the association remained the same.

“Quite often you see that sleep duration would eliminate the effect of sleep complaints in the prediction of disease, but here both remain significant when they are entered at the same time,” Dr. Åkerstedt said. “You get the feeling that this might mean they act together to produce results,” he added.

“One other thing that surprised me is that long sleep was apparently good,” said Dr. Åkerstedt.

The investigators have conducted several studies on sleep duration and mortality. In recent research, they found that both short sleep and long sleep predicted mortality – “and often, long sleep is a stronger predictor than short sleep,” he said.
 

Underestimated problem?

Commenting on the findings, Kathleen Zackowski, PhD, associate vice president of research for the National Multiple Sclerosis Society in Baltimore, noted that participants were asked to rate their own sleep quality during adolescence, a subjective report that may mean sleep quality has an even larger association with MS risk.

“That they found a result with sleep quality says to me that there probably is a bigger problem, because I don’t know if people over- or underestimate their sleep quality,” said Dr. Zackowski, who was not involved with the research.

“If we could get to that sleep quality question a little more objectively, I bet that we’d find there’s a lot more to the story,” she said.

That’s a story the researchers would like to explore, Dr. Åkerstedt reported. Designing a prospective study that more closely tracks sleeping habits during adolescence and follows individuals through adulthood could provide valuable information about how sleep quality and duration affect immune system development and MS risk, he said.

Dr. Zackowski said clinicians know that MS is not caused just by a genetic abnormality and that other environmental lifestyle factors seem to play a part.

“If we find out that sleep is one of those lifestyle factors, this is very changeable,” she added.

The study was funded by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, AFA Insurance, the European Aviation Safety Authority, the Tercentenary Fund of the Bank of Sweden, the Margaretha af Ugglas Foundation, the Swedish Foundation for MS Research, and NEURO Sweden. Dr. Åkerstadt has been supported by Tercentenary Fund of Bank of Sweden, AFA Insurance, and the European Aviation Safety Authority. Dr. Zackowski reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Insomnia disorder is common throughout the lifespan, affecting up to 22% of the population.¹ Insomnia has a negative effect on patients’ quality of life and is associated with reported worse health-related quality of life, greater overall work impairment, and higher utilization of health care resources compared to patients without insomnia.²

Fortunately, many validated diagnostic tools are available to support physicians in the care of affected patients. In addition, many pharmacologic and nonpharmacologic treatment options exist. This review endeavors to help you refine the care you provide to patients across the lifespan by reviewing the evidence-based strategies for the diagnosis and treatment of insomnia in children, adolescents, and adults.

Defining insomnia

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) defines insomnia disorder as a predominant complaint of dissatisfaction with sleep quantity or quality, associated with 1 or more of the following³:

1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)

2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)

3. Early-morning awakening with inability to return to sleep.

Sleep difficulty must be present for at least 3 months and must occur at least 3 nights per week to be classified as persistent insomnia.³ If symptoms last fewer than 3 months, insomnia is considered acute, which has a different DSM-5 code ("other specified insomnia disorder").³ Primary insomnia is its own diagnosis that cannot be defined by other sleep-wake ­cycle disorders, mental health conditions, or medical diagnoses that cause sleep disturbances, nor is it attributable to the physiologic effects of a substance (eg, substance use disorders, medication effects).³

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.

The International Classification of Sleep Disorders, 3rd edition (ICSD-3) notably consolidates all insomnia diagnoses (ie, “primary” and “comorbid”) under a single diagnosis (“chronic insomnia disorder”), which is a distinction from the DSM-5 diagnosis in terms of classification.⁴ Diagnosis of insomnia requires the presence of 3 criteria: (1) persistence of sleep difficulty, (2) adequate opportunity for sleep, and (3) associated daytime dysfunction.⁵

How insomnia affects specific patient populations

Children and adolescents. Appropriate screening, diagnosis, and interventions for insomnia in children and adolescents are associated with better health outcomes, including improved attention, behavior, learning, memory, emotional regulation, quality of life, and mental and physical health.⁶ In one study of insomnia in the pediatric population (N = 1038), 41% of parents reported symptoms of sleep disturbances in their children.⁷ Pediatric insomnia can lead to impaired attention, poor academic performance, and behavioral disturbances.⁷ In addition, there is a high prevalence of sleep disturbances in children with neurodevelopmental disorders.⁸

Insomnia is the most prevalent sleep disorder in adolescents but frequently goes unrecognized, and therefore is underdiagnosed and undertreated.⁹ Insomnia in adolescents is associated with depression and suicidality.^9-12 Growing evidence also links it to anorexia nervosa,¹³ substance use disorders,¹⁴ and impaired neurocognitive function.¹⁵

Continue to: Pregnant women

Pregnant women. Sleep disorders in pregnancy are common and influenced by multiple factors. A meta-analysis found that 57% to 74% of women in various trimesters of pregnancy reported subthreshold symptoms of insomnia¹⁶; however, changes in sleep duration and sleep quality during pregnancy may be related to hormonal, physiologic, metabolic, psychological, and posture mechanisms.^17,18

Sleep quality also worsens as pregnancy progresses.¹⁶ Insomnia coupled with poor sleep quality has been shown to increase the risk for postpartum depression, premature delivery, prolonged labor, and cesarean delivery, as well as preeclampsia, gestational hypertension, stillbirth, and large-for-­gestational-age infants.^19,20

Older adults. Insomnia is a common complaint in the geriatric population and is associated with significant morbidity, as well as higher rates of depression and suicidality.²¹ Circadian rhythms change and sleep cycles advance as people age, leading to a decrease in total sleep time, earlier sleep onset, earlier awakenings,and increased frequency of waking after sleep onset.^21,22 Advanced age, polypharmacy, and high medical comorbidity increase insomnia prevalence.²³

Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.²¹ Sleep loss also has been linked to increased rates of hypertension, coronary ­ar­tery disease, myocardial infarction, and possibly stroke.^21,22 Poor sleep has been associated with increased rates of cortical atrophy in community-dwelling older adults.²¹ Daytime drowsiness increases fall risk.²² Older adults with self-reported decreased physical function also had increased rates of insomnia and increased rates of daytime sleepiness.²²

Making the diagnosis: What to ask, tools to use

Clinical evaluation is most helpful for diagnosing insomnia.²⁴ A complete work-up includes physical examination, review of medications and supplements, evaluation of a 2-week sleep diary (kept by the patient, parent, or caregiver), and assessment using a validated sleep-quality rating scale.²⁴ Be sure to obtain a complete health history, including medical events, substance use, and psychiatric history.²⁴

Continue to: Inquire about sleep initiation...

Inquire about sleep initiation, sleep maintenance, and early awakening, as well as behavioral and environmental factors that may contribute to sleep concerns.^10,18 Consider medical sleep disorders that have overlapping symptoms with insomnia, including obstructive sleep apnea (OSA), restless leg syndrome (RLS), or circadian rhythm sleep-wake disorders. If there are co-occurring chronic medical problems, reassess insomnia symptoms after the other medical diagnoses are controlled.

TABLE 1^25-29 includes a list of validated screening tools for insomnia and where they can be accessed. Recommended screening tools for children and adolescents include daytime sleepiness questionnaires, comprehensive sleep instruments, and self-assessments.^25,30 Although several studies of insomnia in pregnancy have used tools listed in TABLE 1,^25-29 only the Insomnia Severity Index has been validated for use with this population.^26,27 Diagnosis of insomnia in older adults requires a comprehensive sleep history collected from the patient, partners, or caregivers.²¹

Measuring sleep performance

Several aspects of insomnia (defined in ­TABLE 2^31-33) are targeted as outcome measures when treating patients. Sleep-onset latency, total sleep time, and wake-after-sleep onset are all formally measured by polysomnography.^31-33 Use polysomnography when you suspect OSA, narcolepsy, idiopathic hypersomnia, periodic limb movement disorder, RLS, REM behavior disorder (characterized by the loss of normal muscle atonia and dream enactment behavior that is violent in nature³⁴), or parasomnias. Home polysomnography testing is appropriate for adult patients who meet criteria for OSA and have uncomplicated insomnia.³⁵ Self-reporting (use of sleep logs) and actigraphy (measurement by wearable monitoring devices) may be more accessible methods for gathering sleep data from patients. Use of wearable consumer sleep technology such as heart rate monitors with corresponding smartphone applications (eg, Fitbit, Jawbone Up devices, and the Whoop device) are increasing as a means of monitoring sleep as well as delivering insomnia interventions.³⁶

Actigraphy has been shown to produce significantly distinct results from self-­reporting when measuring total sleep time, sleep-onset latency, wake-after-sleep onset, and sleep efficiency in adult and pediatric patients with insomnia.³⁷ Actigraphy yields distinct estimates of sleep patterns when compared to sleep logs, which suggests that while both measures are often correlated, actigraphy has utility in assessing sleep continuity in conjunction with sleep logs in terms of diagnostic and posttreatment ­assessment.³⁷

Continue to: Treatment options

Treatment options: Start with the nonpharmacologic

Both nonpharmacologic and pharmacologic interventions are available for the treatment of insomnia. Starting with nonpharmacologic options is preferred.

Nonpharmacologic interventions

Sleep hygiene. Poor sleep hygiene can contribute to insomnia but does not cause it.³¹ Healthy sleep habits include keeping the sleep environment quiet, free of interruptions, and at an adequate temperature; adhering to a regular sleep schedule; avoiding naps; going to bed when drowsy; getting out of bed if not asleep within 15 to 20 minutes and returning when drowsy; exercising regularly; and avoiding caffeine, nicotine, alcohol, and other substances that interfere with sleep.²⁴ Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.³⁸

Sleep hygiene education is often insufficient on its own.³¹ But it has been shown to benefit older adults with insomnia.^19,32

Sleep hygiene during pregnancy emphasizes drinking fluids only in the daytime to avoid awakening to urinate at night, avoiding specific foods to decrease heartburn, napping only in the early part of the day, and sleeping on either the left or the right side of the body with knees and hips bent and a pillow under pressure points in the second and third trimesters.^18,39

Pediatric insomnia. Sleep hygiene is an important first-line treatment for pediatric insomnia, especially among children with attention-deficit/hyperactivity disorder.⁴⁰

Continue to: CBT-I

Cognitive behavioral therapy for insomnia (CBT-I). US and European guidelines recommend CBT-I—a multicomponent, nonpharmacologic, insomnia-focused psychotherapy—as a first-line treatment for short- and long-term insomnia^32,41,42 across a wide range of patient demographics.^17,43-47 CBT-I is a multiweek intensive treatment that combines sleep hygiene practices with cognitive therapy and behavioral interventions, including stimulus control, sleep restriction, and relaxation training.^32,48 CBT-I monotherapy has been shown to have greater efficacy than sleep hygiene education for patients with insomnia, especially for those with medical or psychiatric comorbidities.⁴⁹ It also has been shown to be effective when delivered in person or even digitally.^50-52 For example, CBT-I Coach is a mobile application for people who are already engaged in CBT-I with a health care provider; it provides a structured program to alleviate symptoms.⁵³

Although CBT-I methods are appropriate for adolescents and school-aged children, evaluations of the efficacy of the individual components (stimulus control, arousal reduction, cognitive therapy, improved sleep hygiene practices, and sleep restriction) are needed to understand what methods are most effective in this population.⁹

Cognitive and/or behavioral Interventions. Cognitive therapy (to change negative thoughts about sleep) and behavioral interventions (eg, changes to sleep routines, sleep restriction, moving the child’s bedtime to match the time of falling asleep [bedtime fading],⁴¹ stimulus control)^9,43,54-56 may be used independently. Separate meta-analyses support the use of cognitive and behavioral interventions for adolescent insomnia,^9,43 school-aged children with insomnia and sleep difficulties,^43,49 and adolescents with sleep difficulties and daytime fatigue.⁴¹ The trials for children and adolescents followed the same recommendations for treatment as CBT-I but often used fewer components of the treatment, resulting in focused cognitive or behavioral interventions.

Cognitive behavioral therapy for insomnia is a first-line treatment for short- and long-term insomnia across a wide range of patients.

One controlled evaluation showed support for separate cognitive and behavioral techniques for insomnia in children.⁵⁴ A meta-analysis (6 studies; N = 529) found that total sleep time, as measured with actigraphy, improved among school-aged children and adolescents with insomnia after treatment with 4 or more types of cognitive or behavioral therapy sessions.⁴³ Sleep-onset latency, measured by actigraphy and sleep diaries, decreased in the intervention group.⁴³

A controlled evaluation of CBT for behavioral insomnia in school-aged children (N = 42) randomized participants to CBT (n = 21) or waitlist control (n = 21).⁵⁴ The 6 CBT sessions combined behavioral sleep medicine techniques (ie, sleep restriction) with anxiety treatment techniques (eg, cognitive restructuring).⁵⁴ Those in the intervention group showed statistically significant improvement in sleep latency, wake-after-sleep onset, and sleep efficiency (all P ≤ .003), compared with controls.⁵⁴ Total sleep time was unaffected by the intervention. A notable change was the number of patients who still had an insomnia diagnosis postintervention. Among children in the CBT group, 14.3% met diagnostic criteria vs 95% of children in the control group.⁵⁴ Similarly, at the 1-month ­follow-up, 9.5% of CBT group members still had insomnia, compared with 86.7% of the control group participants.⁵⁴

Continue to: Multiple randomized and nonranomized studies...

Multiple randomized and nonrandomized studies have found that infants also respond to behavioral interventions, such as establishing regular daytime and sleep routines, reducing environmental noises or distractions, and allowing for self-soothing at bedtime.⁵⁵ A controlled trial (N = 279) of newborns and their mothers evaluated sleep interventions that included guidance on bedtime sleep routines, starting the routine 30 to 45 minutes before bedtime, choosing age-appropriate calming bedtime activities, not using feeding as the last step before bedtime, and offering the child choices with their routine.⁵⁶ The intervention group ­demonstrated longer sleep duration (624.6 ± 67.6 minutes vs 602.9 ± 76.1 minutes; P = .01) at 40 weeks postintervention compared with the control group.⁵⁶

The clinically significant outcomes of this study are related to the guidance offered to parents to help infants achieve longer sleep. More intervention-group infants were allowed to self-soothe to sleep without being held or fed, had earlier bedtimes, and fell asleep ≤ 15 minutes after being put into bed than their counterparts in the control group.⁵⁶

Exercise. As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective. One study of patients older than 60 years (N = 43) showed that a 16-week moderate exercise regimen slightly improved total sleep time by an average of 42 minutes (P = .05), sleep-onset latency improved an average of 11.5 minutes (P = .007), and global sleep quality improved by 3.4 points as measured by the Pittsburgh Sleep Quality Index (PSQI; P ≤ .01).⁵⁷ No significant improvements occurred in sleep efficiency. Exercise is one of several nonpharmacologic alternatives for treating insomnia in pregnancy.⁵⁸

As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective.

A lack of uniformity in patient populations, intervention protocols, and outcome measures confounded results of 2 systematic reviews that included comparisons of yoga or tai chi as standalone alternatives to CBT-I for insomnia treatment.^58,59 Other interventions, such as mindfulness or relaxation training, have been studied as insomnia interventions, but no conclusive evidence about their efficacy exists.^45,59

Pharmacologic interventions

Pharmacologic treatment should not be the sole intervention for the treatment of insomnia but should be used in combination with nonpharmacologic interventions.³² Of note, only low-quality evidence exists for any pharmacologic interventions for insomnia.³² The decision to prescribe medications should rely on the predominant sleep complaint, with sleep maintenance and sleep-onset latency as the guiding factors.³² Medications used for insomnia treatment (TABLE 3^32,60,61)are classified according to these and other sleep outcomes described in TABLE 1.^25-29 Prescribe them at the lowest dose and for the shortest amount of time possible.^32,62 Avoid medications listed in TABLE 4^{32,36,59,60,62-69} because data showing clinically significant improvements in insomnia are lacking, and analysis for potential harms is inadequate.³²

Continue to: Melatonin is not recommended

Melatonin is not recommended for treating insomnia in adults, pregnant patients, older adults, or most children because its effects are clinically insignificant,³² residual sedation has been reported,⁶⁰ and no analysis of harms has been undertaken.³² Despite this, melatonin is frequently utilized for insomnia, and patients take over-the-counter melatonin for a myriad of sleep complaints. Melatonin is indicated in the treatment of insomnia in children with neurodevelopmental disorders. (See discussion in "Prescribing for children.")

Hypnotics are medications licensed for short-term sleep promotion in adults and can induce tolerance and dependence.³² Nonbenzodiazepine-receptor agonists at clinical doses do not appear to suppress REM sleep, although there are reports of increases in latency to REM sleep.⁷⁰

Antidepressants. Although treatment of insomnia with antidepressants is widespread, evidence of their efficacy is unclear.^32,62 The tolerability and safety of antidepressants for insomnia also are uncertain due to limited reporting of adverse events.³²

The use of sedating antidepressants may be driven by concern over the longer-term use of hypnotics and the limited availability of psychological treatments including CBT-I.³² Sedating antidepressants are indicated for comorbid or secondary insomnia (attributable to mental health conditions, medical conditions, other sleep disorders, or substance use or misuse); however, there are few clinical trials studying them for primary insomnia treatment.⁶² Antidepressants—­tricyclic antidepressants included—can reduce the amount of REM sleep and increase REM sleep-onset latency.^71,72

Antihistamines and antipsychotics. Although antihistamines (eg, hydroxyzine, diphenhydramine) and antipsychotics frequently are prescribed off-label for primary insomnia, there is a lack of evidence to support either type of medication for this purpose.^36,62,73 H1-antihistamines such as hydroxyzine increase REM-onset latency and reduce the duration of REM sleep.⁷³ Depending on the specific medication, second-­generation antipsychotics such as olanzapine and quetiapine have mixed effects on REM sleep parameters.⁶⁵

Continue to: Prescribing for children

Prescribing for children. There is no FDA-approved medication for the treatment of insomnia in children.⁵² However, melatonin has shown promising results for treating insomnia in children with neurodevelopmental disorders. A systematic review (13 trials­; N = 682) with meta-analysis (9 studies; n = 541) showed that melatonin significantly improved total sleep time compared with placebo (mean difference [MD] = 48.26 minutes; 95% CI, 36.78-59.73).⁸ In 11 studies (n = 581), sleep-onset latency improved significantly with melatonin use.⁸ No difference was noted in the frequency of wake-after-sleep onset.⁸ No medication-related adverse events were reported. Heterogeneity (I² = 31%) and inconsistency among included studies shed doubt on the findings; therefore, further research is needed.⁸

Prescribing in pregnancy. Prescribing medications to treat insomnia in pregnancy is complex and controversial. No consistency exists among guidelines and recommendations for treating insomnia in the pregnant population. Pharmacotherapy for insomnia is frequently prescribed off-label in pregnant patients. Examples include benzodiazepine-receptor agonists, antidepressants, and gamma-aminobutyric acid–reuptake inhibitors.⁴⁵

Pharmacotherapy in pregnancy is a unique challenge, wherein clinicians consider not only the potential drug toxicity to the fetus but also the potential changes in the pregnant patient’s pharmacokinetics that influence appropriate medication doses.^39,74 Worth noting: Zolpidem has been associated with preterm birth, cesarean birth, and low-birth-weight infants.^45,74 The lack of clinical trials of pharmacotherapy in pregnant patients results in a limited understanding of medication effects on long-term health and safety outcomes in this population.^39,74

There is no FDA-approved medication for the treatment of insomnia in children.

A review of 3 studies with small sample sizes found that when antidepressants or antihistamines were taken during pregnancy, neither had significant adverse effects on mother or child.⁶⁸ Weigh the risks of medications with the risk for disease burden and apply a shared decision-making approach with the patient, including providing an accurate assessment of risks and safety information regarding medication use.³⁹ Online resources such as ReproTox (www.reprotox.org) and MotherToBaby (https://mothertobaby.org) are available to support clinicians treating pregnant and lactating patients.³⁹

Prescribing for older adults. Treatment of insomnia in older adults requires a multifactorial approach.²² For all older adults, start interventions with nonpharmacologic treatments for insomnia followed by treatment of any underlying medical and psychiatric disorders that affect sleep.²¹ If medications are required, start with the lowest dose and titrate upward slowly. Use sedating low-dose antidepressants for insomnia only when the older patient has comorbid depression.⁶⁰ Although nonbenzodiazepine-receptor agonists have improved safety profiles compared with benzodiazepines, their use for older adults should be limited because of adverse effects that include dementia, serious injury, and falls with fractures.⁶⁰

Keep these points in mind

Prescribing medications to treat insomnia in pregnancy is complex and controversial.

Poor sleep has many detrimental health effects and can significantly affect quality of life for patients across the lifespan. Use nonpharmacologic interventions—such as sleep hygiene education, CBT-I, and cognitive/behavioral therapies—as first-line treatments. When utilizing pharmacotherapy for insomnia, consider the patient’s distressing symptoms of insomnia as guideposts for prescribing. Use pharmacologic treatments intermittently, short term, and in conjunction with nonpharmacologic options.

CORRESPONDENCE
Angela L. Colistra, PhD, LPC, CAADC, CCS, 707 Hamilton Street, 8th floor, LVHN Department of Family Medicine, Allentown, PA 18101; [email protected]

Insomnia disorder is common throughout the lifespan, affecting up to 22% of the population.¹ Insomnia has a negative effect on patients’ quality of life and is associated with reported worse health-related quality of life, greater overall work impairment, and higher utilization of health care resources compared to patients without insomnia.²

Fortunately, many validated diagnostic tools are available to support physicians in the care of affected patients. In addition, many pharmacologic and nonpharmacologic treatment options exist. This review endeavors to help you refine the care you provide to patients across the lifespan by reviewing the evidence-based strategies for the diagnosis and treatment of insomnia in children, adolescents, and adults.

Defining insomnia

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) defines insomnia disorder as a predominant complaint of dissatisfaction with sleep quantity or quality, associated with 1 or more of the following³:

1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)

2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)

3. Early-morning awakening with inability to return to sleep.

Sleep difficulty must be present for at least 3 months and must occur at least 3 nights per week to be classified as persistent insomnia.³ If symptoms last fewer than 3 months, insomnia is considered acute, which has a different DSM-5 code ("other specified insomnia disorder").³ Primary insomnia is its own diagnosis that cannot be defined by other sleep-wake ­cycle disorders, mental health conditions, or medical diagnoses that cause sleep disturbances, nor is it attributable to the physiologic effects of a substance (eg, substance use disorders, medication effects).³

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.

The International Classification of Sleep Disorders, 3rd edition (ICSD-3) notably consolidates all insomnia diagnoses (ie, “primary” and “comorbid”) under a single diagnosis (“chronic insomnia disorder”), which is a distinction from the DSM-5 diagnosis in terms of classification.⁴ Diagnosis of insomnia requires the presence of 3 criteria: (1) persistence of sleep difficulty, (2) adequate opportunity for sleep, and (3) associated daytime dysfunction.⁵

How insomnia affects specific patient populations

Children and adolescents. Appropriate screening, diagnosis, and interventions for insomnia in children and adolescents are associated with better health outcomes, including improved attention, behavior, learning, memory, emotional regulation, quality of life, and mental and physical health.⁶ In one study of insomnia in the pediatric population (N = 1038), 41% of parents reported symptoms of sleep disturbances in their children.⁷ Pediatric insomnia can lead to impaired attention, poor academic performance, and behavioral disturbances.⁷ In addition, there is a high prevalence of sleep disturbances in children with neurodevelopmental disorders.⁸

Insomnia is the most prevalent sleep disorder in adolescents but frequently goes unrecognized, and therefore is underdiagnosed and undertreated.⁹ Insomnia in adolescents is associated with depression and suicidality.^9-12 Growing evidence also links it to anorexia nervosa,¹³ substance use disorders,¹⁴ and impaired neurocognitive function.¹⁵

Continue to: Pregnant women

Pregnant women. Sleep disorders in pregnancy are common and influenced by multiple factors. A meta-analysis found that 57% to 74% of women in various trimesters of pregnancy reported subthreshold symptoms of insomnia¹⁶; however, changes in sleep duration and sleep quality during pregnancy may be related to hormonal, physiologic, metabolic, psychological, and posture mechanisms.^17,18

Sleep quality also worsens as pregnancy progresses.¹⁶ Insomnia coupled with poor sleep quality has been shown to increase the risk for postpartum depression, premature delivery, prolonged labor, and cesarean delivery, as well as preeclampsia, gestational hypertension, stillbirth, and large-for-­gestational-age infants.^19,20

Older adults. Insomnia is a common complaint in the geriatric population and is associated with significant morbidity, as well as higher rates of depression and suicidality.²¹ Circadian rhythms change and sleep cycles advance as people age, leading to a decrease in total sleep time, earlier sleep onset, earlier awakenings,and increased frequency of waking after sleep onset.^21,22 Advanced age, polypharmacy, and high medical comorbidity increase insomnia prevalence.²³

Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.²¹ Sleep loss also has been linked to increased rates of hypertension, coronary ­ar­tery disease, myocardial infarction, and possibly stroke.^21,22 Poor sleep has been associated with increased rates of cortical atrophy in community-dwelling older adults.²¹ Daytime drowsiness increases fall risk.²² Older adults with self-reported decreased physical function also had increased rates of insomnia and increased rates of daytime sleepiness.²²

Making the diagnosis: What to ask, tools to use

Clinical evaluation is most helpful for diagnosing insomnia.²⁴ A complete work-up includes physical examination, review of medications and supplements, evaluation of a 2-week sleep diary (kept by the patient, parent, or caregiver), and assessment using a validated sleep-quality rating scale.²⁴ Be sure to obtain a complete health history, including medical events, substance use, and psychiatric history.²⁴

Continue to: Inquire about sleep initiation...

Inquire about sleep initiation, sleep maintenance, and early awakening, as well as behavioral and environmental factors that may contribute to sleep concerns.^10,18 Consider medical sleep disorders that have overlapping symptoms with insomnia, including obstructive sleep apnea (OSA), restless leg syndrome (RLS), or circadian rhythm sleep-wake disorders. If there are co-occurring chronic medical problems, reassess insomnia symptoms after the other medical diagnoses are controlled.

TABLE 1^25-29 includes a list of validated screening tools for insomnia and where they can be accessed. Recommended screening tools for children and adolescents include daytime sleepiness questionnaires, comprehensive sleep instruments, and self-assessments.^25,30 Although several studies of insomnia in pregnancy have used tools listed in TABLE 1,^25-29 only the Insomnia Severity Index has been validated for use with this population.^26,27 Diagnosis of insomnia in older adults requires a comprehensive sleep history collected from the patient, partners, or caregivers.²¹

Measuring sleep performance

Several aspects of insomnia (defined in ­TABLE 2^31-33) are targeted as outcome measures when treating patients. Sleep-onset latency, total sleep time, and wake-after-sleep onset are all formally measured by polysomnography.^31-33 Use polysomnography when you suspect OSA, narcolepsy, idiopathic hypersomnia, periodic limb movement disorder, RLS, REM behavior disorder (characterized by the loss of normal muscle atonia and dream enactment behavior that is violent in nature³⁴), or parasomnias. Home polysomnography testing is appropriate for adult patients who meet criteria for OSA and have uncomplicated insomnia.³⁵ Self-reporting (use of sleep logs) and actigraphy (measurement by wearable monitoring devices) may be more accessible methods for gathering sleep data from patients. Use of wearable consumer sleep technology such as heart rate monitors with corresponding smartphone applications (eg, Fitbit, Jawbone Up devices, and the Whoop device) are increasing as a means of monitoring sleep as well as delivering insomnia interventions.³⁶

Actigraphy has been shown to produce significantly distinct results from self-­reporting when measuring total sleep time, sleep-onset latency, wake-after-sleep onset, and sleep efficiency in adult and pediatric patients with insomnia.³⁷ Actigraphy yields distinct estimates of sleep patterns when compared to sleep logs, which suggests that while both measures are often correlated, actigraphy has utility in assessing sleep continuity in conjunction with sleep logs in terms of diagnostic and posttreatment ­assessment.³⁷

Continue to: Treatment options

Treatment options: Start with the nonpharmacologic

Both nonpharmacologic and pharmacologic interventions are available for the treatment of insomnia. Starting with nonpharmacologic options is preferred.

Nonpharmacologic interventions

Sleep hygiene. Poor sleep hygiene can contribute to insomnia but does not cause it.³¹ Healthy sleep habits include keeping the sleep environment quiet, free of interruptions, and at an adequate temperature; adhering to a regular sleep schedule; avoiding naps; going to bed when drowsy; getting out of bed if not asleep within 15 to 20 minutes and returning when drowsy; exercising regularly; and avoiding caffeine, nicotine, alcohol, and other substances that interfere with sleep.²⁴ Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.³⁸

Sleep hygiene education is often insufficient on its own.³¹ But it has been shown to benefit older adults with insomnia.^19,32

Sleep hygiene during pregnancy emphasizes drinking fluids only in the daytime to avoid awakening to urinate at night, avoiding specific foods to decrease heartburn, napping only in the early part of the day, and sleeping on either the left or the right side of the body with knees and hips bent and a pillow under pressure points in the second and third trimesters.^18,39

Pediatric insomnia. Sleep hygiene is an important first-line treatment for pediatric insomnia, especially among children with attention-deficit/hyperactivity disorder.⁴⁰

Continue to: CBT-I

Cognitive behavioral therapy for insomnia (CBT-I). US and European guidelines recommend CBT-I—a multicomponent, nonpharmacologic, insomnia-focused psychotherapy—as a first-line treatment for short- and long-term insomnia^32,41,42 across a wide range of patient demographics.^17,43-47 CBT-I is a multiweek intensive treatment that combines sleep hygiene practices with cognitive therapy and behavioral interventions, including stimulus control, sleep restriction, and relaxation training.^32,48 CBT-I monotherapy has been shown to have greater efficacy than sleep hygiene education for patients with insomnia, especially for those with medical or psychiatric comorbidities.⁴⁹ It also has been shown to be effective when delivered in person or even digitally.^50-52 For example, CBT-I Coach is a mobile application for people who are already engaged in CBT-I with a health care provider; it provides a structured program to alleviate symptoms.⁵³

Although CBT-I methods are appropriate for adolescents and school-aged children, evaluations of the efficacy of the individual components (stimulus control, arousal reduction, cognitive therapy, improved sleep hygiene practices, and sleep restriction) are needed to understand what methods are most effective in this population.⁹

Cognitive and/or behavioral Interventions. Cognitive therapy (to change negative thoughts about sleep) and behavioral interventions (eg, changes to sleep routines, sleep restriction, moving the child’s bedtime to match the time of falling asleep [bedtime fading],⁴¹ stimulus control)^9,43,54-56 may be used independently. Separate meta-analyses support the use of cognitive and behavioral interventions for adolescent insomnia,^9,43 school-aged children with insomnia and sleep difficulties,^43,49 and adolescents with sleep difficulties and daytime fatigue.⁴¹ The trials for children and adolescents followed the same recommendations for treatment as CBT-I but often used fewer components of the treatment, resulting in focused cognitive or behavioral interventions.

Cognitive behavioral therapy for insomnia is a first-line treatment for short- and long-term insomnia across a wide range of patients.

One controlled evaluation showed support for separate cognitive and behavioral techniques for insomnia in children.⁵⁴ A meta-analysis (6 studies; N = 529) found that total sleep time, as measured with actigraphy, improved among school-aged children and adolescents with insomnia after treatment with 4 or more types of cognitive or behavioral therapy sessions.⁴³ Sleep-onset latency, measured by actigraphy and sleep diaries, decreased in the intervention group.⁴³

A controlled evaluation of CBT for behavioral insomnia in school-aged children (N = 42) randomized participants to CBT (n = 21) or waitlist control (n = 21).⁵⁴ The 6 CBT sessions combined behavioral sleep medicine techniques (ie, sleep restriction) with anxiety treatment techniques (eg, cognitive restructuring).⁵⁴ Those in the intervention group showed statistically significant improvement in sleep latency, wake-after-sleep onset, and sleep efficiency (all P ≤ .003), compared with controls.⁵⁴ Total sleep time was unaffected by the intervention. A notable change was the number of patients who still had an insomnia diagnosis postintervention. Among children in the CBT group, 14.3% met diagnostic criteria vs 95% of children in the control group.⁵⁴ Similarly, at the 1-month ­follow-up, 9.5% of CBT group members still had insomnia, compared with 86.7% of the control group participants.⁵⁴

Continue to: Multiple randomized and nonranomized studies...

Multiple randomized and nonrandomized studies have found that infants also respond to behavioral interventions, such as establishing regular daytime and sleep routines, reducing environmental noises or distractions, and allowing for self-soothing at bedtime.⁵⁵ A controlled trial (N = 279) of newborns and their mothers evaluated sleep interventions that included guidance on bedtime sleep routines, starting the routine 30 to 45 minutes before bedtime, choosing age-appropriate calming bedtime activities, not using feeding as the last step before bedtime, and offering the child choices with their routine.⁵⁶ The intervention group ­demonstrated longer sleep duration (624.6 ± 67.6 minutes vs 602.9 ± 76.1 minutes; P = .01) at 40 weeks postintervention compared with the control group.⁵⁶

The clinically significant outcomes of this study are related to the guidance offered to parents to help infants achieve longer sleep. More intervention-group infants were allowed to self-soothe to sleep without being held or fed, had earlier bedtimes, and fell asleep ≤ 15 minutes after being put into bed than their counterparts in the control group.⁵⁶

Exercise. As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective. One study of patients older than 60 years (N = 43) showed that a 16-week moderate exercise regimen slightly improved total sleep time by an average of 42 minutes (P = .05), sleep-onset latency improved an average of 11.5 minutes (P = .007), and global sleep quality improved by 3.4 points as measured by the Pittsburgh Sleep Quality Index (PSQI; P ≤ .01).⁵⁷ No significant improvements occurred in sleep efficiency. Exercise is one of several nonpharmacologic alternatives for treating insomnia in pregnancy.⁵⁸

As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective.

A lack of uniformity in patient populations, intervention protocols, and outcome measures confounded results of 2 systematic reviews that included comparisons of yoga or tai chi as standalone alternatives to CBT-I for insomnia treatment.^58,59 Other interventions, such as mindfulness or relaxation training, have been studied as insomnia interventions, but no conclusive evidence about their efficacy exists.^45,59

Pharmacologic interventions

Pharmacologic treatment should not be the sole intervention for the treatment of insomnia but should be used in combination with nonpharmacologic interventions.³² Of note, only low-quality evidence exists for any pharmacologic interventions for insomnia.³² The decision to prescribe medications should rely on the predominant sleep complaint, with sleep maintenance and sleep-onset latency as the guiding factors.³² Medications used for insomnia treatment (TABLE 3^32,60,61)are classified according to these and other sleep outcomes described in TABLE 1.^25-29 Prescribe them at the lowest dose and for the shortest amount of time possible.^32,62 Avoid medications listed in TABLE 4^{32,36,59,60,62-69} because data showing clinically significant improvements in insomnia are lacking, and analysis for potential harms is inadequate.³²

Continue to: Melatonin is not recommended

Melatonin is not recommended for treating insomnia in adults, pregnant patients, older adults, or most children because its effects are clinically insignificant,³² residual sedation has been reported,⁶⁰ and no analysis of harms has been undertaken.³² Despite this, melatonin is frequently utilized for insomnia, and patients take over-the-counter melatonin for a myriad of sleep complaints. Melatonin is indicated in the treatment of insomnia in children with neurodevelopmental disorders. (See discussion in "Prescribing for children.")

Hypnotics are medications licensed for short-term sleep promotion in adults and can induce tolerance and dependence.³² Nonbenzodiazepine-receptor agonists at clinical doses do not appear to suppress REM sleep, although there are reports of increases in latency to REM sleep.⁷⁰

Antidepressants. Although treatment of insomnia with antidepressants is widespread, evidence of their efficacy is unclear.^32,62 The tolerability and safety of antidepressants for insomnia also are uncertain due to limited reporting of adverse events.³²

The use of sedating antidepressants may be driven by concern over the longer-term use of hypnotics and the limited availability of psychological treatments including CBT-I.³² Sedating antidepressants are indicated for comorbid or secondary insomnia (attributable to mental health conditions, medical conditions, other sleep disorders, or substance use or misuse); however, there are few clinical trials studying them for primary insomnia treatment.⁶² Antidepressants—­tricyclic antidepressants included—can reduce the amount of REM sleep and increase REM sleep-onset latency.^71,72

Antihistamines and antipsychotics. Although antihistamines (eg, hydroxyzine, diphenhydramine) and antipsychotics frequently are prescribed off-label for primary insomnia, there is a lack of evidence to support either type of medication for this purpose.^36,62,73 H1-antihistamines such as hydroxyzine increase REM-onset latency and reduce the duration of REM sleep.⁷³ Depending on the specific medication, second-­generation antipsychotics such as olanzapine and quetiapine have mixed effects on REM sleep parameters.⁶⁵

Continue to: Prescribing for children

Prescribing for children. There is no FDA-approved medication for the treatment of insomnia in children.⁵² However, melatonin has shown promising results for treating insomnia in children with neurodevelopmental disorders. A systematic review (13 trials­; N = 682) with meta-analysis (9 studies; n = 541) showed that melatonin significantly improved total sleep time compared with placebo (mean difference [MD] = 48.26 minutes; 95% CI, 36.78-59.73).⁸ In 11 studies (n = 581), sleep-onset latency improved significantly with melatonin use.⁸ No difference was noted in the frequency of wake-after-sleep onset.⁸ No medication-related adverse events were reported. Heterogeneity (I² = 31%) and inconsistency among included studies shed doubt on the findings; therefore, further research is needed.⁸

Prescribing in pregnancy. Prescribing medications to treat insomnia in pregnancy is complex and controversial. No consistency exists among guidelines and recommendations for treating insomnia in the pregnant population. Pharmacotherapy for insomnia is frequently prescribed off-label in pregnant patients. Examples include benzodiazepine-receptor agonists, antidepressants, and gamma-aminobutyric acid–reuptake inhibitors.⁴⁵

Pharmacotherapy in pregnancy is a unique challenge, wherein clinicians consider not only the potential drug toxicity to the fetus but also the potential changes in the pregnant patient’s pharmacokinetics that influence appropriate medication doses.^39,74 Worth noting: Zolpidem has been associated with preterm birth, cesarean birth, and low-birth-weight infants.^45,74 The lack of clinical trials of pharmacotherapy in pregnant patients results in a limited understanding of medication effects on long-term health and safety outcomes in this population.^39,74

There is no FDA-approved medication for the treatment of insomnia in children.

A review of 3 studies with small sample sizes found that when antidepressants or antihistamines were taken during pregnancy, neither had significant adverse effects on mother or child.⁶⁸ Weigh the risks of medications with the risk for disease burden and apply a shared decision-making approach with the patient, including providing an accurate assessment of risks and safety information regarding medication use.³⁹ Online resources such as ReproTox (www.reprotox.org) and MotherToBaby (https://mothertobaby.org) are available to support clinicians treating pregnant and lactating patients.³⁹

Prescribing for older adults. Treatment of insomnia in older adults requires a multifactorial approach.²² For all older adults, start interventions with nonpharmacologic treatments for insomnia followed by treatment of any underlying medical and psychiatric disorders that affect sleep.²¹ If medications are required, start with the lowest dose and titrate upward slowly. Use sedating low-dose antidepressants for insomnia only when the older patient has comorbid depression.⁶⁰ Although nonbenzodiazepine-receptor agonists have improved safety profiles compared with benzodiazepines, their use for older adults should be limited because of adverse effects that include dementia, serious injury, and falls with fractures.⁶⁰

Keep these points in mind

Prescribing medications to treat insomnia in pregnancy is complex and controversial.

Poor sleep has many detrimental health effects and can significantly affect quality of life for patients across the lifespan. Use nonpharmacologic interventions—such as sleep hygiene education, CBT-I, and cognitive/behavioral therapies—as first-line treatments. When utilizing pharmacotherapy for insomnia, consider the patient’s distressing symptoms of insomnia as guideposts for prescribing. Use pharmacologic treatments intermittently, short term, and in conjunction with nonpharmacologic options.

CORRESPONDENCE
Angela L. Colistra, PhD, LPC, CAADC, CCS, 707 Hamilton Street, 8th floor, LVHN Department of Family Medicine, Allentown, PA 18101; [email protected]

Insomnia disorder is common throughout the lifespan, affecting up to 22% of the population.¹ Insomnia has a negative effect on patients’ quality of life and is associated with reported worse health-related quality of life, greater overall work impairment, and higher utilization of health care resources compared to patients without insomnia.²

Fortunately, many validated diagnostic tools are available to support physicians in the care of affected patients. In addition, many pharmacologic and nonpharmacologic treatment options exist. This review endeavors to help you refine the care you provide to patients across the lifespan by reviewing the evidence-based strategies for the diagnosis and treatment of insomnia in children, adolescents, and adults.

Defining insomnia

The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) defines insomnia disorder as a predominant complaint of dissatisfaction with sleep quantity or quality, associated with 1 or more of the following³:

1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)

2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)

3. Early-morning awakening with inability to return to sleep.

Sleep difficulty must be present for at least 3 months and must occur at least 3 nights per week to be classified as persistent insomnia.³ If symptoms last fewer than 3 months, insomnia is considered acute, which has a different DSM-5 code ("other specified insomnia disorder").³ Primary insomnia is its own diagnosis that cannot be defined by other sleep-wake ­cycle disorders, mental health conditions, or medical diagnoses that cause sleep disturbances, nor is it attributable to the physiologic effects of a substance (eg, substance use disorders, medication effects).³

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.

The International Classification of Sleep Disorders, 3rd edition (ICSD-3) notably consolidates all insomnia diagnoses (ie, “primary” and “comorbid”) under a single diagnosis (“chronic insomnia disorder”), which is a distinction from the DSM-5 diagnosis in terms of classification.⁴ Diagnosis of insomnia requires the presence of 3 criteria: (1) persistence of sleep difficulty, (2) adequate opportunity for sleep, and (3) associated daytime dysfunction.⁵

How insomnia affects specific patient populations

Children and adolescents. Appropriate screening, diagnosis, and interventions for insomnia in children and adolescents are associated with better health outcomes, including improved attention, behavior, learning, memory, emotional regulation, quality of life, and mental and physical health.⁶ In one study of insomnia in the pediatric population (N = 1038), 41% of parents reported symptoms of sleep disturbances in their children.⁷ Pediatric insomnia can lead to impaired attention, poor academic performance, and behavioral disturbances.⁷ In addition, there is a high prevalence of sleep disturbances in children with neurodevelopmental disorders.⁸

Insomnia is the most prevalent sleep disorder in adolescents but frequently goes unrecognized, and therefore is underdiagnosed and undertreated.⁹ Insomnia in adolescents is associated with depression and suicidality.^9-12 Growing evidence also links it to anorexia nervosa,¹³ substance use disorders,¹⁴ and impaired neurocognitive function.¹⁵

Continue to: Pregnant women

Pregnant women. Sleep disorders in pregnancy are common and influenced by multiple factors. A meta-analysis found that 57% to 74% of women in various trimesters of pregnancy reported subthreshold symptoms of insomnia¹⁶; however, changes in sleep duration and sleep quality during pregnancy may be related to hormonal, physiologic, metabolic, psychological, and posture mechanisms.^17,18

Sleep quality also worsens as pregnancy progresses.¹⁶ Insomnia coupled with poor sleep quality has been shown to increase the risk for postpartum depression, premature delivery, prolonged labor, and cesarean delivery, as well as preeclampsia, gestational hypertension, stillbirth, and large-for-­gestational-age infants.^19,20

Older adults. Insomnia is a common complaint in the geriatric population and is associated with significant morbidity, as well as higher rates of depression and suicidality.²¹ Circadian rhythms change and sleep cycles advance as people age, leading to a decrease in total sleep time, earlier sleep onset, earlier awakenings,and increased frequency of waking after sleep onset.^21,22 Advanced age, polypharmacy, and high medical comorbidity increase insomnia prevalence.²³

Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.

Studies have shown that older adults who sleep fewer than 5 hours per night have an increased risk for diabetes and metabolic syndrome.²¹ Sleep loss also has been linked to increased rates of hypertension, coronary ­ar­tery disease, myocardial infarction, and possibly stroke.^21,22 Poor sleep has been associated with increased rates of cortical atrophy in community-dwelling older adults.²¹ Daytime drowsiness increases fall risk.²² Older adults with self-reported decreased physical function also had increased rates of insomnia and increased rates of daytime sleepiness.²²

Making the diagnosis: What to ask, tools to use

Clinical evaluation is most helpful for diagnosing insomnia.²⁴ A complete work-up includes physical examination, review of medications and supplements, evaluation of a 2-week sleep diary (kept by the patient, parent, or caregiver), and assessment using a validated sleep-quality rating scale.²⁴ Be sure to obtain a complete health history, including medical events, substance use, and psychiatric history.²⁴

Continue to: Inquire about sleep initiation...

Inquire about sleep initiation, sleep maintenance, and early awakening, as well as behavioral and environmental factors that may contribute to sleep concerns.^10,18 Consider medical sleep disorders that have overlapping symptoms with insomnia, including obstructive sleep apnea (OSA), restless leg syndrome (RLS), or circadian rhythm sleep-wake disorders. If there are co-occurring chronic medical problems, reassess insomnia symptoms after the other medical diagnoses are controlled.

TABLE 1^25-29 includes a list of validated screening tools for insomnia and where they can be accessed. Recommended screening tools for children and adolescents include daytime sleepiness questionnaires, comprehensive sleep instruments, and self-assessments.^25,30 Although several studies of insomnia in pregnancy have used tools listed in TABLE 1,^25-29 only the Insomnia Severity Index has been validated for use with this population.^26,27 Diagnosis of insomnia in older adults requires a comprehensive sleep history collected from the patient, partners, or caregivers.²¹

Measuring sleep performance

Several aspects of insomnia (defined in ­TABLE 2^31-33) are targeted as outcome measures when treating patients. Sleep-onset latency, total sleep time, and wake-after-sleep onset are all formally measured by polysomnography.^31-33 Use polysomnography when you suspect OSA, narcolepsy, idiopathic hypersomnia, periodic limb movement disorder, RLS, REM behavior disorder (characterized by the loss of normal muscle atonia and dream enactment behavior that is violent in nature³⁴), or parasomnias. Home polysomnography testing is appropriate for adult patients who meet criteria for OSA and have uncomplicated insomnia.³⁵ Self-reporting (use of sleep logs) and actigraphy (measurement by wearable monitoring devices) may be more accessible methods for gathering sleep data from patients. Use of wearable consumer sleep technology such as heart rate monitors with corresponding smartphone applications (eg, Fitbit, Jawbone Up devices, and the Whoop device) are increasing as a means of monitoring sleep as well as delivering insomnia interventions.³⁶

Actigraphy has been shown to produce significantly distinct results from self-­reporting when measuring total sleep time, sleep-onset latency, wake-after-sleep onset, and sleep efficiency in adult and pediatric patients with insomnia.³⁷ Actigraphy yields distinct estimates of sleep patterns when compared to sleep logs, which suggests that while both measures are often correlated, actigraphy has utility in assessing sleep continuity in conjunction with sleep logs in terms of diagnostic and posttreatment ­assessment.³⁷

Continue to: Treatment options

Treatment options: Start with the nonpharmacologic

Both nonpharmacologic and pharmacologic interventions are available for the treatment of insomnia. Starting with nonpharmacologic options is preferred.

Nonpharmacologic interventions

Sleep hygiene. Poor sleep hygiene can contribute to insomnia but does not cause it.³¹ Healthy sleep habits include keeping the sleep environment quiet, free of interruptions, and at an adequate temperature; adhering to a regular sleep schedule; avoiding naps; going to bed when drowsy; getting out of bed if not asleep within 15 to 20 minutes and returning when drowsy; exercising regularly; and avoiding caffeine, nicotine, alcohol, and other substances that interfere with sleep.²⁴ Technology use prior to bedtime is prevalent and associated with sleep and circadian rhythm disturbances.³⁸

Sleep hygiene education is often insufficient on its own.³¹ But it has been shown to benefit older adults with insomnia.^19,32

Sleep hygiene during pregnancy emphasizes drinking fluids only in the daytime to avoid awakening to urinate at night, avoiding specific foods to decrease heartburn, napping only in the early part of the day, and sleeping on either the left or the right side of the body with knees and hips bent and a pillow under pressure points in the second and third trimesters.^18,39

Pediatric insomnia. Sleep hygiene is an important first-line treatment for pediatric insomnia, especially among children with attention-deficit/hyperactivity disorder.⁴⁰

Continue to: CBT-I

Cognitive behavioral therapy for insomnia (CBT-I). US and European guidelines recommend CBT-I—a multicomponent, nonpharmacologic, insomnia-focused psychotherapy—as a first-line treatment for short- and long-term insomnia^32,41,42 across a wide range of patient demographics.^17,43-47 CBT-I is a multiweek intensive treatment that combines sleep hygiene practices with cognitive therapy and behavioral interventions, including stimulus control, sleep restriction, and relaxation training.^32,48 CBT-I monotherapy has been shown to have greater efficacy than sleep hygiene education for patients with insomnia, especially for those with medical or psychiatric comorbidities.⁴⁹ It also has been shown to be effective when delivered in person or even digitally.^50-52 For example, CBT-I Coach is a mobile application for people who are already engaged in CBT-I with a health care provider; it provides a structured program to alleviate symptoms.⁵³

Although CBT-I methods are appropriate for adolescents and school-aged children, evaluations of the efficacy of the individual components (stimulus control, arousal reduction, cognitive therapy, improved sleep hygiene practices, and sleep restriction) are needed to understand what methods are most effective in this population.⁹

Cognitive and/or behavioral Interventions. Cognitive therapy (to change negative thoughts about sleep) and behavioral interventions (eg, changes to sleep routines, sleep restriction, moving the child’s bedtime to match the time of falling asleep [bedtime fading],⁴¹ stimulus control)^9,43,54-56 may be used independently. Separate meta-analyses support the use of cognitive and behavioral interventions for adolescent insomnia,^9,43 school-aged children with insomnia and sleep difficulties,^43,49 and adolescents with sleep difficulties and daytime fatigue.⁴¹ The trials for children and adolescents followed the same recommendations for treatment as CBT-I but often used fewer components of the treatment, resulting in focused cognitive or behavioral interventions.

Cognitive behavioral therapy for insomnia is a first-line treatment for short- and long-term insomnia across a wide range of patients.

One controlled evaluation showed support for separate cognitive and behavioral techniques for insomnia in children.⁵⁴ A meta-analysis (6 studies; N = 529) found that total sleep time, as measured with actigraphy, improved among school-aged children and adolescents with insomnia after treatment with 4 or more types of cognitive or behavioral therapy sessions.⁴³ Sleep-onset latency, measured by actigraphy and sleep diaries, decreased in the intervention group.⁴³

A controlled evaluation of CBT for behavioral insomnia in school-aged children (N = 42) randomized participants to CBT (n = 21) or waitlist control (n = 21).⁵⁴ The 6 CBT sessions combined behavioral sleep medicine techniques (ie, sleep restriction) with anxiety treatment techniques (eg, cognitive restructuring).⁵⁴ Those in the intervention group showed statistically significant improvement in sleep latency, wake-after-sleep onset, and sleep efficiency (all P ≤ .003), compared with controls.⁵⁴ Total sleep time was unaffected by the intervention. A notable change was the number of patients who still had an insomnia diagnosis postintervention. Among children in the CBT group, 14.3% met diagnostic criteria vs 95% of children in the control group.⁵⁴ Similarly, at the 1-month ­follow-up, 9.5% of CBT group members still had insomnia, compared with 86.7% of the control group participants.⁵⁴

Continue to: Multiple randomized and nonranomized studies...

Multiple randomized and nonrandomized studies have found that infants also respond to behavioral interventions, such as establishing regular daytime and sleep routines, reducing environmental noises or distractions, and allowing for self-soothing at bedtime.⁵⁵ A controlled trial (N = 279) of newborns and their mothers evaluated sleep interventions that included guidance on bedtime sleep routines, starting the routine 30 to 45 minutes before bedtime, choosing age-appropriate calming bedtime activities, not using feeding as the last step before bedtime, and offering the child choices with their routine.⁵⁶ The intervention group ­demonstrated longer sleep duration (624.6 ± 67.6 minutes vs 602.9 ± 76.1 minutes; P = .01) at 40 weeks postintervention compared with the control group.⁵⁶

The clinically significant outcomes of this study are related to the guidance offered to parents to help infants achieve longer sleep. More intervention-group infants were allowed to self-soothe to sleep without being held or fed, had earlier bedtimes, and fell asleep ≤ 15 minutes after being put into bed than their counterparts in the control group.⁵⁶

Exercise. As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective. One study of patients older than 60 years (N = 43) showed that a 16-week moderate exercise regimen slightly improved total sleep time by an average of 42 minutes (P = .05), sleep-onset latency improved an average of 11.5 minutes (P = .007), and global sleep quality improved by 3.4 points as measured by the Pittsburgh Sleep Quality Index (PSQI; P ≤ .01).⁵⁷ No significant improvements occurred in sleep efficiency. Exercise is one of several nonpharmacologic alternatives for treating insomnia in pregnancy.⁵⁸

As a sole intervention, exercise for insomnia is readily available and low cost, but it is not universally effective.

A lack of uniformity in patient populations, intervention protocols, and outcome measures confounded results of 2 systematic reviews that included comparisons of yoga or tai chi as standalone alternatives to CBT-I for insomnia treatment.^58,59 Other interventions, such as mindfulness or relaxation training, have been studied as insomnia interventions, but no conclusive evidence about their efficacy exists.^45,59

Pharmacologic interventions

Pharmacologic treatment should not be the sole intervention for the treatment of insomnia but should be used in combination with nonpharmacologic interventions.³² Of note, only low-quality evidence exists for any pharmacologic interventions for insomnia.³² The decision to prescribe medications should rely on the predominant sleep complaint, with sleep maintenance and sleep-onset latency as the guiding factors.³² Medications used for insomnia treatment (TABLE 3^32,60,61)are classified according to these and other sleep outcomes described in TABLE 1.^25-29 Prescribe them at the lowest dose and for the shortest amount of time possible.^32,62 Avoid medications listed in TABLE 4^{32,36,59,60,62-69} because data showing clinically significant improvements in insomnia are lacking, and analysis for potential harms is inadequate.³²

Continue to: Melatonin is not recommended

Melatonin is not recommended for treating insomnia in adults, pregnant patients, older adults, or most children because its effects are clinically insignificant,³² residual sedation has been reported,⁶⁰ and no analysis of harms has been undertaken.³² Despite this, melatonin is frequently utilized for insomnia, and patients take over-the-counter melatonin for a myriad of sleep complaints. Melatonin is indicated in the treatment of insomnia in children with neurodevelopmental disorders. (See discussion in "Prescribing for children.")

Hypnotics are medications licensed for short-term sleep promotion in adults and can induce tolerance and dependence.³² Nonbenzodiazepine-receptor agonists at clinical doses do not appear to suppress REM sleep, although there are reports of increases in latency to REM sleep.⁷⁰

Antidepressants. Although treatment of insomnia with antidepressants is widespread, evidence of their efficacy is unclear.^32,62 The tolerability and safety of antidepressants for insomnia also are uncertain due to limited reporting of adverse events.³²

The use of sedating antidepressants may be driven by concern over the longer-term use of hypnotics and the limited availability of psychological treatments including CBT-I.³² Sedating antidepressants are indicated for comorbid or secondary insomnia (attributable to mental health conditions, medical conditions, other sleep disorders, or substance use or misuse); however, there are few clinical trials studying them for primary insomnia treatment.⁶² Antidepressants—­tricyclic antidepressants included—can reduce the amount of REM sleep and increase REM sleep-onset latency.^71,72

Antihistamines and antipsychotics. Although antihistamines (eg, hydroxyzine, diphenhydramine) and antipsychotics frequently are prescribed off-label for primary insomnia, there is a lack of evidence to support either type of medication for this purpose.^36,62,73 H1-antihistamines such as hydroxyzine increase REM-onset latency and reduce the duration of REM sleep.⁷³ Depending on the specific medication, second-­generation antipsychotics such as olanzapine and quetiapine have mixed effects on REM sleep parameters.⁶⁵

Continue to: Prescribing for children

Prescribing for children. There is no FDA-approved medication for the treatment of insomnia in children.⁵² However, melatonin has shown promising results for treating insomnia in children with neurodevelopmental disorders. A systematic review (13 trials­; N = 682) with meta-analysis (9 studies; n = 541) showed that melatonin significantly improved total sleep time compared with placebo (mean difference [MD] = 48.26 minutes; 95% CI, 36.78-59.73).⁸ In 11 studies (n = 581), sleep-onset latency improved significantly with melatonin use.⁸ No difference was noted in the frequency of wake-after-sleep onset.⁸ No medication-related adverse events were reported. Heterogeneity (I² = 31%) and inconsistency among included studies shed doubt on the findings; therefore, further research is needed.⁸

Prescribing in pregnancy. Prescribing medications to treat insomnia in pregnancy is complex and controversial. No consistency exists among guidelines and recommendations for treating insomnia in the pregnant population. Pharmacotherapy for insomnia is frequently prescribed off-label in pregnant patients. Examples include benzodiazepine-receptor agonists, antidepressants, and gamma-aminobutyric acid–reuptake inhibitors.⁴⁵

Pharmacotherapy in pregnancy is a unique challenge, wherein clinicians consider not only the potential drug toxicity to the fetus but also the potential changes in the pregnant patient’s pharmacokinetics that influence appropriate medication doses.^39,74 Worth noting: Zolpidem has been associated with preterm birth, cesarean birth, and low-birth-weight infants.^45,74 The lack of clinical trials of pharmacotherapy in pregnant patients results in a limited understanding of medication effects on long-term health and safety outcomes in this population.^39,74

There is no FDA-approved medication for the treatment of insomnia in children.

A review of 3 studies with small sample sizes found that when antidepressants or antihistamines were taken during pregnancy, neither had significant adverse effects on mother or child.⁶⁸ Weigh the risks of medications with the risk for disease burden and apply a shared decision-making approach with the patient, including providing an accurate assessment of risks and safety information regarding medication use.³⁹ Online resources such as ReproTox (www.reprotox.org) and MotherToBaby (https://mothertobaby.org) are available to support clinicians treating pregnant and lactating patients.³⁹

Prescribing for older adults. Treatment of insomnia in older adults requires a multifactorial approach.²² For all older adults, start interventions with nonpharmacologic treatments for insomnia followed by treatment of any underlying medical and psychiatric disorders that affect sleep.²¹ If medications are required, start with the lowest dose and titrate upward slowly. Use sedating low-dose antidepressants for insomnia only when the older patient has comorbid depression.⁶⁰ Although nonbenzodiazepine-receptor agonists have improved safety profiles compared with benzodiazepines, their use for older adults should be limited because of adverse effects that include dementia, serious injury, and falls with fractures.⁶⁰

Keep these points in mind

Prescribing medications to treat insomnia in pregnancy is complex and controversial.

Poor sleep has many detrimental health effects and can significantly affect quality of life for patients across the lifespan. Use nonpharmacologic interventions—such as sleep hygiene education, CBT-I, and cognitive/behavioral therapies—as first-line treatments. When utilizing pharmacotherapy for insomnia, consider the patient’s distressing symptoms of insomnia as guideposts for prescribing. Use pharmacologic treatments intermittently, short term, and in conjunction with nonpharmacologic options.

CORRESPONDENCE
Angela L. Colistra, PhD, LPC, CAADC, CCS, 707 Hamilton Street, 8th floor, LVHN Department of Family Medicine, Allentown, PA 18101; [email protected]

Everybody wants a younger heart

As more people live well past 90, scientists have been taking a closer look at how they’ve been doing it. Mostly it boiled down to genetics. You either had it or you didn’t. Well, a recent study suggests that doesn’t have to be true anymore, at least for the heart.

Scientists from the United Kingdom and Italy found an antiaging gene in some centenarians that has shown possible antiaging effects in mice and in human heart cells. A single administration of the mutant antiaging gene, they found, stopped heart function decay in middle-aged mice and even reversed the biological clock by the human equivalent of 10 years in elderly mice.

©ktsimage/thinkstockphotos.com

When the researchers applied the antiaging gene to samples of human heart cells from elderly people with heart problems, the cells “resumed functioning properly, proving to be more efficient in building new blood vessels,” they said in a written statement. It all kind of sounds like something out of Dr. Frankenstein’s lab.
 

I want to believe … in better sleep

The “X-Files” theme song plays. Mulder and Scully are sitting in a diner, breakfast laid out around them. The diner is quiet, with only a few people inside.

Mulder: I’m telling you, Scully, there’s something spooky going on here.

Scully: You mean other than the fact that this town in Georgia looks suspiciously like Vancouver?

Mulder: Not one person we spoke to yesterday has gotten a full night’s sleep since the UFO sighting last month. I’m telling you, they’re here, they’re experimenting.

Scully: Do you really want me to do this to you again?

Mulder: Do what again?

Scully: There’s nothing going on here that can’t be explained by the current research. Why, in January 2023 a study was published revealing a link between poor sleep and belief in paranormal phenomena like UFOS, demons, or ghosts. Which probably explains why you’re on your third cup of coffee for the morning.

Mulder: Scully, you’ve literally been abducted by aliens. Do we have to play this game every time?

Scully: Look, it’s simple. In a sample of nearly 9,000 people, nearly two-thirds of those who reported experiencing sleep paralysis or exploding head syndrome reported believing in UFOs and aliens walking amongst humanity, despite making up just 3% of the overall sample.

Alexandra Gorn/Unsplash

Furthermore, about 60% of those reporting sleep paralysis also reported believing near-death experiences prove the soul lingers on after death, and those with stronger insomnia symptoms were more likely to believe in the devil.

Mulder: Aha!

Scully: Aha what?

Mulder: You’re a devout Christian. You believe in the devil and the soul.

Scully: Yes, but I don’t let it interfere with a good night’s sleep, Mulder. These people saw something strange, convinced themselves it was a UFO, and now they can’t sleep. It’s a vicious cycle. The study authors even said that people experiencing strange nighttime phenomena could interpret this as evidence of aliens or other paranormal beings, thus making them even more susceptible to further sleep disruption and deepening beliefs. Look who I’m talking to.

Mulder: Always with the facts, eh?

Scully: I am a doctor, after all. And if you want more research into how paranormal belief and poor sleep quality are linked, I’d be happy to dig out the literature, because the truth is out there, Mulder.

Mulder: I hate you sometimes.

It’s ChatGPT’s world. We’re just living in it

Have you heard about ChatGPT? The artificial intelligence chatbot was just launched in November and it’s already more important to the Internet than either Vladimir Putin or “Rick and Morty.”

What’s that? You’re wondering why you should care? Well, excuuuuuse us, but we thought you might want to know that ChatGPT is in the process of taking over the world. Let’s take a quick look at what it’s been up to.

“ChatGPT bot passes law school exam”

“ChatGPT passes MBA exam given by a Wharton professor”

“A freelance writer says ChatGPT wrote a $600 article in just 30 seconds”

And here’s one that might be of interest to those of the health care persuasion: “ChatGPT can pass part of the U.S. Medical Licensing Exam.” See? It’s coming for you, too.

The artificial intelligence known as ChatGPT “performed at >50% accuracy across [the three USMLE] examinations, exceeding 60% in most analyses,” a group of researchers wrote on the preprint server medRxiv, noting that 60% is usually the pass threshold for humans taking the exam in any given year.

Mohamed Hassan/PxHere

Everybody wants a younger heart

As more people live well past 90, scientists have been taking a closer look at how they’ve been doing it. Mostly it boiled down to genetics. You either had it or you didn’t. Well, a recent study suggests that doesn’t have to be true anymore, at least for the heart.

Scientists from the United Kingdom and Italy found an antiaging gene in some centenarians that has shown possible antiaging effects in mice and in human heart cells. A single administration of the mutant antiaging gene, they found, stopped heart function decay in middle-aged mice and even reversed the biological clock by the human equivalent of 10 years in elderly mice.

©ktsimage/thinkstockphotos.com

When the researchers applied the antiaging gene to samples of human heart cells from elderly people with heart problems, the cells “resumed functioning properly, proving to be more efficient in building new blood vessels,” they said in a written statement. It all kind of sounds like something out of Dr. Frankenstein’s lab.
 

I want to believe … in better sleep

The “X-Files” theme song plays. Mulder and Scully are sitting in a diner, breakfast laid out around them. The diner is quiet, with only a few people inside.

Mulder: I’m telling you, Scully, there’s something spooky going on here.

Scully: You mean other than the fact that this town in Georgia looks suspiciously like Vancouver?

Mulder: Not one person we spoke to yesterday has gotten a full night’s sleep since the UFO sighting last month. I’m telling you, they’re here, they’re experimenting.

Scully: Do you really want me to do this to you again?

Mulder: Do what again?

Scully: There’s nothing going on here that can’t be explained by the current research. Why, in January 2023 a study was published revealing a link between poor sleep and belief in paranormal phenomena like UFOS, demons, or ghosts. Which probably explains why you’re on your third cup of coffee for the morning.

Mulder: Scully, you’ve literally been abducted by aliens. Do we have to play this game every time?

Scully: Look, it’s simple. In a sample of nearly 9,000 people, nearly two-thirds of those who reported experiencing sleep paralysis or exploding head syndrome reported believing in UFOs and aliens walking amongst humanity, despite making up just 3% of the overall sample.

Alexandra Gorn/Unsplash

Furthermore, about 60% of those reporting sleep paralysis also reported believing near-death experiences prove the soul lingers on after death, and those with stronger insomnia symptoms were more likely to believe in the devil.

Mulder: Aha!

Scully: Aha what?

Mulder: You’re a devout Christian. You believe in the devil and the soul.

Scully: Yes, but I don’t let it interfere with a good night’s sleep, Mulder. These people saw something strange, convinced themselves it was a UFO, and now they can’t sleep. It’s a vicious cycle. The study authors even said that people experiencing strange nighttime phenomena could interpret this as evidence of aliens or other paranormal beings, thus making them even more susceptible to further sleep disruption and deepening beliefs. Look who I’m talking to.

Mulder: Always with the facts, eh?

Scully: I am a doctor, after all. And if you want more research into how paranormal belief and poor sleep quality are linked, I’d be happy to dig out the literature, because the truth is out there, Mulder.

Mulder: I hate you sometimes.

It’s ChatGPT’s world. We’re just living in it

Have you heard about ChatGPT? The artificial intelligence chatbot was just launched in November and it’s already more important to the Internet than either Vladimir Putin or “Rick and Morty.”

What’s that? You’re wondering why you should care? Well, excuuuuuse us, but we thought you might want to know that ChatGPT is in the process of taking over the world. Let’s take a quick look at what it’s been up to.

“ChatGPT bot passes law school exam”

“ChatGPT passes MBA exam given by a Wharton professor”

“A freelance writer says ChatGPT wrote a $600 article in just 30 seconds”

And here’s one that might be of interest to those of the health care persuasion: “ChatGPT can pass part of the U.S. Medical Licensing Exam.” See? It’s coming for you, too.

The artificial intelligence known as ChatGPT “performed at >50% accuracy across [the three USMLE] examinations, exceeding 60% in most analyses,” a group of researchers wrote on the preprint server medRxiv, noting that 60% is usually the pass threshold for humans taking the exam in any given year.

Mohamed Hassan/PxHere

Everybody wants a younger heart

As more people live well past 90, scientists have been taking a closer look at how they’ve been doing it. Mostly it boiled down to genetics. You either had it or you didn’t. Well, a recent study suggests that doesn’t have to be true anymore, at least for the heart.

Scientists from the United Kingdom and Italy found an antiaging gene in some centenarians that has shown possible antiaging effects in mice and in human heart cells. A single administration of the mutant antiaging gene, they found, stopped heart function decay in middle-aged mice and even reversed the biological clock by the human equivalent of 10 years in elderly mice.

©ktsimage/thinkstockphotos.com

When the researchers applied the antiaging gene to samples of human heart cells from elderly people with heart problems, the cells “resumed functioning properly, proving to be more efficient in building new blood vessels,” they said in a written statement. It all kind of sounds like something out of Dr. Frankenstein’s lab.
 

I want to believe … in better sleep

The “X-Files” theme song plays. Mulder and Scully are sitting in a diner, breakfast laid out around them. The diner is quiet, with only a few people inside.

Mulder: I’m telling you, Scully, there’s something spooky going on here.

Scully: You mean other than the fact that this town in Georgia looks suspiciously like Vancouver?

Mulder: Not one person we spoke to yesterday has gotten a full night’s sleep since the UFO sighting last month. I’m telling you, they’re here, they’re experimenting.

Scully: Do you really want me to do this to you again?

Mulder: Do what again?

Scully: There’s nothing going on here that can’t be explained by the current research. Why, in January 2023 a study was published revealing a link between poor sleep and belief in paranormal phenomena like UFOS, demons, or ghosts. Which probably explains why you’re on your third cup of coffee for the morning.

Mulder: Scully, you’ve literally been abducted by aliens. Do we have to play this game every time?

Scully: Look, it’s simple. In a sample of nearly 9,000 people, nearly two-thirds of those who reported experiencing sleep paralysis or exploding head syndrome reported believing in UFOs and aliens walking amongst humanity, despite making up just 3% of the overall sample.

Alexandra Gorn/Unsplash

Furthermore, about 60% of those reporting sleep paralysis also reported believing near-death experiences prove the soul lingers on after death, and those with stronger insomnia symptoms were more likely to believe in the devil.

Mulder: Aha!

Scully: Aha what?

Mulder: You’re a devout Christian. You believe in the devil and the soul.

Scully: Yes, but I don’t let it interfere with a good night’s sleep, Mulder. These people saw something strange, convinced themselves it was a UFO, and now they can’t sleep. It’s a vicious cycle. The study authors even said that people experiencing strange nighttime phenomena could interpret this as evidence of aliens or other paranormal beings, thus making them even more susceptible to further sleep disruption and deepening beliefs. Look who I’m talking to.

Mulder: Always with the facts, eh?

Scully: I am a doctor, after all. And if you want more research into how paranormal belief and poor sleep quality are linked, I’d be happy to dig out the literature, because the truth is out there, Mulder.

Mulder: I hate you sometimes.

It’s ChatGPT’s world. We’re just living in it

Have you heard about ChatGPT? The artificial intelligence chatbot was just launched in November and it’s already more important to the Internet than either Vladimir Putin or “Rick and Morty.”

What’s that? You’re wondering why you should care? Well, excuuuuuse us, but we thought you might want to know that ChatGPT is in the process of taking over the world. Let’s take a quick look at what it’s been up to.

“ChatGPT bot passes law school exam”

“ChatGPT passes MBA exam given by a Wharton professor”

“A freelance writer says ChatGPT wrote a $600 article in just 30 seconds”

And here’s one that might be of interest to those of the health care persuasion: “ChatGPT can pass part of the U.S. Medical Licensing Exam.” See? It’s coming for you, too.

The artificial intelligence known as ChatGPT “performed at >50% accuracy across [the three USMLE] examinations, exceeding 60% in most analyses,” a group of researchers wrote on the preprint server medRxiv, noting that 60% is usually the pass threshold for humans taking the exam in any given year.

Mohamed Hassan/PxHere

The risk of health harms from alcohol is low for people who consume two standard drinks or fewer per week, but it’s higher with greater consumption, according to new guidance from the Canadian Centre on Substance Use and Addiction.

“Drinking less is better,” says the guidance, which replaces Canada’s 2011 Low-Risk Drinking Guidelines (LRDGs).

Developed in consultation with an executive committee from federal, provincial, and territorial governments; national organizations; three scientific expert panels; and an internal evidence review working group, the guidance presents the following findings:

• Consuming no drinks per week has benefits, such as better health and better sleep, and it’s the only safe option during pregnancy.
• Consuming one or two standard drinks weekly will likely not have alcohol-related consequences.
• Three to six drinks raise the risk of developing breast, colon, and other cancers.
• Seven or more increase the risk of heart disease or stroke.
• Each additional drink “radically increases” the risk of these health consequences.

“Alcohol is more harmful than was previously thought and is a key component of the health of your patients,” Adam Sherk, PhD, a scientist at the Canadian Institute for Substance Use Research at the University of Victoria (B.C.), and a member of the scientific expert panel that contributed to the guidance, said in an interview. “Display and discuss the new guidance with your patients with the main message that drinking less is better.”

Peter Butt, MD, a clinical associate professor at the University of Saskatchewan, Saskatoon, and cochair of the guidance project, said in an interview: “The World Health Organization has identified over 200 ICD-coded conditions associated with alcohol use. This creates many opportunities to inquire into quantity and frequency of alcohol use, relate it to the patient’s health and well-being, and provide advice on reduction.”

“Canada’s Guidance on Alcohol and Health: Final Report” and a related infographic were published online Jan. 17.
 

Continuum of risk

The impetus for the new guidance came from the fact that “our 2011 LRDGs were no longer current, and there was emerging evidence that people drinking within those levels were coming to harm,” said Dr. Butt.

That evidence indicates that alcohol causes at least seven types of cancer, mostly of the breast or colon; is a risk factor for most types of heart disease; and is a main cause of liver disease. Evidence also indicates that avoiding drinking to the point of intoxication will reduce people’s risk of perpetrating alcohol-related violence.

Responding to the need to accurately quantify the risk, the guidance defines a “standard” drink as 12 oz of beer, cooler, or cider (5% alcohol); 5 oz of wine (12% alcohol); and 1.5 oz of spirits such as whiskey, vodka, or gin (40% alcohol).

Using different mortality risk thresholds, the project’s experts developed the following continuum of risk:

• Low for individuals who consume two standard drinks or fewer per week
• Moderate for those who consume from three to six standard drinks per week
• Increasingly high for those who consume seven standard drinks or more per week

The guidance makes the following observations:

• Consuming more than two standard drinks per drinking occasion is associated with an increased risk of harms to self and others, including injuries and violence.
• When pregnant or trying to get pregnant, no amount of alcohol is safe.
• When breastfeeding, not drinking is safest.
• Above the upper limit of the moderate risk zone, health risks increase more steeply for females than males.
• Far more injuries, violence, and deaths result from men’s alcohol use, especially for per occasion drinking, than from women’s alcohol use.
• Young people should delay alcohol use for as long as possible.
• Individuals should not start to use alcohol or increase their alcohol use for health benefits.
• Any reduction in alcohol use is beneficial.

Other national guidelines

“Countries that haven’t updated their alcohol use guidelines recently should do so, as the evidence regarding alcohol and health has advanced considerably in the past 10 years,” said Dr. Sherk. He acknowledged that “any time health guidance changes substantially, it’s reasonable to expect a period of readjustment.”

“Some will be resistant,” Dr. Butt agreed. “Some professionals will need more education than others on the health effects of alcohol. Some patients will also be more invested in drinking than others. The harm-reduction, risk-zone approach should assist in the process of engaging patients and helping them reduce over time.

“Just as we benefited from the updates done in the United Kingdom, France, and especially Australia, so also researchers elsewhere will critique our work and our approach and make their own decisions on how best to communicate with their public,” Dr. Butt said. He noted that Canada’s contributions regarding the association between alcohol and violence, as well as their sex/gender approach to the evidence, “may influence the next country’s review.”

Commenting on whether the United States should consider changing its guidance, Timothy Brennan, MD, MPH, chief of clinical services for the Addiction Institute of Mount Sinai Health System in New York, said in an interview, “A lot of people will be surprised at the recommended limits on alcohol. Most think that they can have one or two glasses of alcohol per day and not have any increased risk to their health. I think the Canadians deserve credit for putting themselves out there.”

Dr. Brennan said there will “certainly be pushback by the drinking lobby, which is very strong both in the U.S. and in Canada.” In fact, the national trade group Beer Canada was recently quoted as stating that it still supports the 2011 guidelines and that the updating process lacked full transparency and expert technical peer review.

Nevertheless, Dr. Brennan said, “it’s overwhelmingly clear that alcohol affects a ton of different parts of our body, so limiting the amount of alcohol we take in is always going to be a good thing. The Canadian graphic is great because it color-codes the risk. I recommend that clinicians put it up in their offices and begin quantifying the units of alcohol that are going into a patient’s body each day.”

A version of this article originally appeared on Medscape.com.

The risk of health harms from alcohol is low for people who consume two standard drinks or fewer per week, but it’s higher with greater consumption, according to new guidance from the Canadian Centre on Substance Use and Addiction.

“Drinking less is better,” says the guidance, which replaces Canada’s 2011 Low-Risk Drinking Guidelines (LRDGs).

Developed in consultation with an executive committee from federal, provincial, and territorial governments; national organizations; three scientific expert panels; and an internal evidence review working group, the guidance presents the following findings:

• Consuming no drinks per week has benefits, such as better health and better sleep, and it’s the only safe option during pregnancy.
• Consuming one or two standard drinks weekly will likely not have alcohol-related consequences.
• Three to six drinks raise the risk of developing breast, colon, and other cancers.
• Seven or more increase the risk of heart disease or stroke.
• Each additional drink “radically increases” the risk of these health consequences.

“Alcohol is more harmful than was previously thought and is a key component of the health of your patients,” Adam Sherk, PhD, a scientist at the Canadian Institute for Substance Use Research at the University of Victoria (B.C.), and a member of the scientific expert panel that contributed to the guidance, said in an interview. “Display and discuss the new guidance with your patients with the main message that drinking less is better.”

Peter Butt, MD, a clinical associate professor at the University of Saskatchewan, Saskatoon, and cochair of the guidance project, said in an interview: “The World Health Organization has identified over 200 ICD-coded conditions associated with alcohol use. This creates many opportunities to inquire into quantity and frequency of alcohol use, relate it to the patient’s health and well-being, and provide advice on reduction.”

“Canada’s Guidance on Alcohol and Health: Final Report” and a related infographic were published online Jan. 17.
 

Continuum of risk

The impetus for the new guidance came from the fact that “our 2011 LRDGs were no longer current, and there was emerging evidence that people drinking within those levels were coming to harm,” said Dr. Butt.

That evidence indicates that alcohol causes at least seven types of cancer, mostly of the breast or colon; is a risk factor for most types of heart disease; and is a main cause of liver disease. Evidence also indicates that avoiding drinking to the point of intoxication will reduce people’s risk of perpetrating alcohol-related violence.

Responding to the need to accurately quantify the risk, the guidance defines a “standard” drink as 12 oz of beer, cooler, or cider (5% alcohol); 5 oz of wine (12% alcohol); and 1.5 oz of spirits such as whiskey, vodka, or gin (40% alcohol).

Using different mortality risk thresholds, the project’s experts developed the following continuum of risk:

• Low for individuals who consume two standard drinks or fewer per week
• Moderate for those who consume from three to six standard drinks per week
• Increasingly high for those who consume seven standard drinks or more per week

The guidance makes the following observations:

• Consuming more than two standard drinks per drinking occasion is associated with an increased risk of harms to self and others, including injuries and violence.
• When pregnant or trying to get pregnant, no amount of alcohol is safe.
• When breastfeeding, not drinking is safest.
• Above the upper limit of the moderate risk zone, health risks increase more steeply for females than males.
• Far more injuries, violence, and deaths result from men’s alcohol use, especially for per occasion drinking, than from women’s alcohol use.
• Young people should delay alcohol use for as long as possible.
• Individuals should not start to use alcohol or increase their alcohol use for health benefits.
• Any reduction in alcohol use is beneficial.

Other national guidelines

“Countries that haven’t updated their alcohol use guidelines recently should do so, as the evidence regarding alcohol and health has advanced considerably in the past 10 years,” said Dr. Sherk. He acknowledged that “any time health guidance changes substantially, it’s reasonable to expect a period of readjustment.”

“Some will be resistant,” Dr. Butt agreed. “Some professionals will need more education than others on the health effects of alcohol. Some patients will also be more invested in drinking than others. The harm-reduction, risk-zone approach should assist in the process of engaging patients and helping them reduce over time.

“Just as we benefited from the updates done in the United Kingdom, France, and especially Australia, so also researchers elsewhere will critique our work and our approach and make their own decisions on how best to communicate with their public,” Dr. Butt said. He noted that Canada’s contributions regarding the association between alcohol and violence, as well as their sex/gender approach to the evidence, “may influence the next country’s review.”

Commenting on whether the United States should consider changing its guidance, Timothy Brennan, MD, MPH, chief of clinical services for the Addiction Institute of Mount Sinai Health System in New York, said in an interview, “A lot of people will be surprised at the recommended limits on alcohol. Most think that they can have one or two glasses of alcohol per day and not have any increased risk to their health. I think the Canadians deserve credit for putting themselves out there.”

Dr. Brennan said there will “certainly be pushback by the drinking lobby, which is very strong both in the U.S. and in Canada.” In fact, the national trade group Beer Canada was recently quoted as stating that it still supports the 2011 guidelines and that the updating process lacked full transparency and expert technical peer review.

Nevertheless, Dr. Brennan said, “it’s overwhelmingly clear that alcohol affects a ton of different parts of our body, so limiting the amount of alcohol we take in is always going to be a good thing. The Canadian graphic is great because it color-codes the risk. I recommend that clinicians put it up in their offices and begin quantifying the units of alcohol that are going into a patient’s body each day.”

A version of this article originally appeared on Medscape.com.

The risk of health harms from alcohol is low for people who consume two standard drinks or fewer per week, but it’s higher with greater consumption, according to new guidance from the Canadian Centre on Substance Use and Addiction.

“Drinking less is better,” says the guidance, which replaces Canada’s 2011 Low-Risk Drinking Guidelines (LRDGs).

Developed in consultation with an executive committee from federal, provincial, and territorial governments; national organizations; three scientific expert panels; and an internal evidence review working group, the guidance presents the following findings:

• Consuming no drinks per week has benefits, such as better health and better sleep, and it’s the only safe option during pregnancy.
• Consuming one or two standard drinks weekly will likely not have alcohol-related consequences.
• Three to six drinks raise the risk of developing breast, colon, and other cancers.
• Seven or more increase the risk of heart disease or stroke.
• Each additional drink “radically increases” the risk of these health consequences.

“Alcohol is more harmful than was previously thought and is a key component of the health of your patients,” Adam Sherk, PhD, a scientist at the Canadian Institute for Substance Use Research at the University of Victoria (B.C.), and a member of the scientific expert panel that contributed to the guidance, said in an interview. “Display and discuss the new guidance with your patients with the main message that drinking less is better.”

Peter Butt, MD, a clinical associate professor at the University of Saskatchewan, Saskatoon, and cochair of the guidance project, said in an interview: “The World Health Organization has identified over 200 ICD-coded conditions associated with alcohol use. This creates many opportunities to inquire into quantity and frequency of alcohol use, relate it to the patient’s health and well-being, and provide advice on reduction.”

“Canada’s Guidance on Alcohol and Health: Final Report” and a related infographic were published online Jan. 17.
 

Continuum of risk

The impetus for the new guidance came from the fact that “our 2011 LRDGs were no longer current, and there was emerging evidence that people drinking within those levels were coming to harm,” said Dr. Butt.

That evidence indicates that alcohol causes at least seven types of cancer, mostly of the breast or colon; is a risk factor for most types of heart disease; and is a main cause of liver disease. Evidence also indicates that avoiding drinking to the point of intoxication will reduce people’s risk of perpetrating alcohol-related violence.

Responding to the need to accurately quantify the risk, the guidance defines a “standard” drink as 12 oz of beer, cooler, or cider (5% alcohol); 5 oz of wine (12% alcohol); and 1.5 oz of spirits such as whiskey, vodka, or gin (40% alcohol).

Using different mortality risk thresholds, the project’s experts developed the following continuum of risk:

• Low for individuals who consume two standard drinks or fewer per week
• Moderate for those who consume from three to six standard drinks per week
• Increasingly high for those who consume seven standard drinks or more per week

The guidance makes the following observations:

• Consuming more than two standard drinks per drinking occasion is associated with an increased risk of harms to self and others, including injuries and violence.
• When pregnant or trying to get pregnant, no amount of alcohol is safe.
• When breastfeeding, not drinking is safest.
• Above the upper limit of the moderate risk zone, health risks increase more steeply for females than males.
• Far more injuries, violence, and deaths result from men’s alcohol use, especially for per occasion drinking, than from women’s alcohol use.
• Young people should delay alcohol use for as long as possible.
• Individuals should not start to use alcohol or increase their alcohol use for health benefits.
• Any reduction in alcohol use is beneficial.

Other national guidelines

“Countries that haven’t updated their alcohol use guidelines recently should do so, as the evidence regarding alcohol and health has advanced considerably in the past 10 years,” said Dr. Sherk. He acknowledged that “any time health guidance changes substantially, it’s reasonable to expect a period of readjustment.”

“Some will be resistant,” Dr. Butt agreed. “Some professionals will need more education than others on the health effects of alcohol. Some patients will also be more invested in drinking than others. The harm-reduction, risk-zone approach should assist in the process of engaging patients and helping them reduce over time.

“Just as we benefited from the updates done in the United Kingdom, France, and especially Australia, so also researchers elsewhere will critique our work and our approach and make their own decisions on how best to communicate with their public,” Dr. Butt said. He noted that Canada’s contributions regarding the association between alcohol and violence, as well as their sex/gender approach to the evidence, “may influence the next country’s review.”

Commenting on whether the United States should consider changing its guidance, Timothy Brennan, MD, MPH, chief of clinical services for the Addiction Institute of Mount Sinai Health System in New York, said in an interview, “A lot of people will be surprised at the recommended limits on alcohol. Most think that they can have one or two glasses of alcohol per day and not have any increased risk to their health. I think the Canadians deserve credit for putting themselves out there.”

Dr. Brennan said there will “certainly be pushback by the drinking lobby, which is very strong both in the U.S. and in Canada.” In fact, the national trade group Beer Canada was recently quoted as stating that it still supports the 2011 guidelines and that the updating process lacked full transparency and expert technical peer review.

Nevertheless, Dr. Brennan said, “it’s overwhelmingly clear that alcohol affects a ton of different parts of our body, so limiting the amount of alcohol we take in is always going to be a good thing. The Canadian graphic is great because it color-codes the risk. I recommend that clinicians put it up in their offices and begin quantifying the units of alcohol that are going into a patient’s body each day.”

A version of this article originally appeared on Medscape.com.