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Vitamin D deficiency in older adults
Low vitamin D levels can impact cognitive functioning in older adults.1 As vitamin D levels decrease, cognitive impairment increases.
Vitamin D deficiency can occur because few foods contain this nutrient2 and patients have limited exposure to sunlight—vitamin D is produced when sunlight strikes the skin.2 In addition to rickets, low levels of vitamin D have been linked to slower information processing in middle age and older men, cognitive decline, mood disorders, and altered brain development and function resulting in neurodegenerative diseases and other medical disorders.3
One study suggested that one-half of adults age >60 do not get sufficient vitamin D, with an even higher rate among women with Alzheimer’s disease.4 Patients in dementia units typically are not tested for vitamin D levels. These patients rarely leave the unit, which leaves them deprived of the vitamin D provided by sunlight. Even patients exposed to sunlight may receive minimal vitamin D because they use sunscreen.
The following protocol can help patients who may benefit from vitamin D supplementation and increased sun exposure.
Obtain and assess vitamin D levels. Evaluate your patient’s level in the context of physical or cognitive symptoms and other lab values:
- deficient: <12 ng/mL
- inadequate: 12 to 20 ng/mL
- adequate: ≥20 ng/mL.2
Order dietary assessment to identify foods that may increase vitamin D levels. The best sources are fish—salmon, tuna, and mackerel—fish oils, beef, liver, cheese, and egg yolks.2 Several food products, including milk and orange juice, are fortified with vitamin D.
Suggest a daily vitamin D supplement ranging from 400 IU/d to 1,000 IU/d. The Institute of Medicine suggests 600 IU/d for patients age 60 to 70 and 800 IU/d for those age ≥71. For vitamin D deficient patients, recommend >1,000 IU/d.1
Recommend 15 minutes per day in the sun without sunscreen from spring to autumn; late summer to fall is ideal because vitamin D’s half-life is 30 days. Midday is the best time to produce vitamin D.5
Recheck the patient’s Mini-Mental State Examination score every 4 months. Vitamin D supplementation is correlated with cognitive functioning.6
Disclosure
Dr. LaFerney reports no financial, relationship with any company whose, products are mentioned in this article, or with manufacturers of competing, products.
1. Mayo Clinic. Vitamin D. http://www.mayoclinic.com/health/vitamin-d/NS_patient-vitamind/DSECTION=dosing. Updated October 1 2011. Accessed September 26, 2012.
2. National Institutes of Health. Office of Dietary Supplements. Dietary supplement fact sheet: vitamin D. http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional. Accessed September 26, 2012.
3. Lee DM, Tajar A, Ulubaev A, et al. Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men. J Neurol Neurosurg Psychiatry. 2009;80(7):722-729.
4. Wilkins CH, Sheline YI, Roe CM, et al. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006;14(12):1032-1040.
5. Webb AR, Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status. Photochem Photobiol. 2006;82(6):1697-1703.
6. Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007;460(2):202-205.
Low vitamin D levels can impact cognitive functioning in older adults.1 As vitamin D levels decrease, cognitive impairment increases.
Vitamin D deficiency can occur because few foods contain this nutrient2 and patients have limited exposure to sunlight—vitamin D is produced when sunlight strikes the skin.2 In addition to rickets, low levels of vitamin D have been linked to slower information processing in middle age and older men, cognitive decline, mood disorders, and altered brain development and function resulting in neurodegenerative diseases and other medical disorders.3
One study suggested that one-half of adults age >60 do not get sufficient vitamin D, with an even higher rate among women with Alzheimer’s disease.4 Patients in dementia units typically are not tested for vitamin D levels. These patients rarely leave the unit, which leaves them deprived of the vitamin D provided by sunlight. Even patients exposed to sunlight may receive minimal vitamin D because they use sunscreen.
The following protocol can help patients who may benefit from vitamin D supplementation and increased sun exposure.
Obtain and assess vitamin D levels. Evaluate your patient’s level in the context of physical or cognitive symptoms and other lab values:
- deficient: <12 ng/mL
- inadequate: 12 to 20 ng/mL
- adequate: ≥20 ng/mL.2
Order dietary assessment to identify foods that may increase vitamin D levels. The best sources are fish—salmon, tuna, and mackerel—fish oils, beef, liver, cheese, and egg yolks.2 Several food products, including milk and orange juice, are fortified with vitamin D.
Suggest a daily vitamin D supplement ranging from 400 IU/d to 1,000 IU/d. The Institute of Medicine suggests 600 IU/d for patients age 60 to 70 and 800 IU/d for those age ≥71. For vitamin D deficient patients, recommend >1,000 IU/d.1
Recommend 15 minutes per day in the sun without sunscreen from spring to autumn; late summer to fall is ideal because vitamin D’s half-life is 30 days. Midday is the best time to produce vitamin D.5
Recheck the patient’s Mini-Mental State Examination score every 4 months. Vitamin D supplementation is correlated with cognitive functioning.6
Disclosure
Dr. LaFerney reports no financial, relationship with any company whose, products are mentioned in this article, or with manufacturers of competing, products.
Low vitamin D levels can impact cognitive functioning in older adults.1 As vitamin D levels decrease, cognitive impairment increases.
Vitamin D deficiency can occur because few foods contain this nutrient2 and patients have limited exposure to sunlight—vitamin D is produced when sunlight strikes the skin.2 In addition to rickets, low levels of vitamin D have been linked to slower information processing in middle age and older men, cognitive decline, mood disorders, and altered brain development and function resulting in neurodegenerative diseases and other medical disorders.3
One study suggested that one-half of adults age >60 do not get sufficient vitamin D, with an even higher rate among women with Alzheimer’s disease.4 Patients in dementia units typically are not tested for vitamin D levels. These patients rarely leave the unit, which leaves them deprived of the vitamin D provided by sunlight. Even patients exposed to sunlight may receive minimal vitamin D because they use sunscreen.
The following protocol can help patients who may benefit from vitamin D supplementation and increased sun exposure.
Obtain and assess vitamin D levels. Evaluate your patient’s level in the context of physical or cognitive symptoms and other lab values:
- deficient: <12 ng/mL
- inadequate: 12 to 20 ng/mL
- adequate: ≥20 ng/mL.2
Order dietary assessment to identify foods that may increase vitamin D levels. The best sources are fish—salmon, tuna, and mackerel—fish oils, beef, liver, cheese, and egg yolks.2 Several food products, including milk and orange juice, are fortified with vitamin D.
Suggest a daily vitamin D supplement ranging from 400 IU/d to 1,000 IU/d. The Institute of Medicine suggests 600 IU/d for patients age 60 to 70 and 800 IU/d for those age ≥71. For vitamin D deficient patients, recommend >1,000 IU/d.1
Recommend 15 minutes per day in the sun without sunscreen from spring to autumn; late summer to fall is ideal because vitamin D’s half-life is 30 days. Midday is the best time to produce vitamin D.5
Recheck the patient’s Mini-Mental State Examination score every 4 months. Vitamin D supplementation is correlated with cognitive functioning.6
Disclosure
Dr. LaFerney reports no financial, relationship with any company whose, products are mentioned in this article, or with manufacturers of competing, products.
1. Mayo Clinic. Vitamin D. http://www.mayoclinic.com/health/vitamin-d/NS_patient-vitamind/DSECTION=dosing. Updated October 1 2011. Accessed September 26, 2012.
2. National Institutes of Health. Office of Dietary Supplements. Dietary supplement fact sheet: vitamin D. http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional. Accessed September 26, 2012.
3. Lee DM, Tajar A, Ulubaev A, et al. Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men. J Neurol Neurosurg Psychiatry. 2009;80(7):722-729.
4. Wilkins CH, Sheline YI, Roe CM, et al. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006;14(12):1032-1040.
5. Webb AR, Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status. Photochem Photobiol. 2006;82(6):1697-1703.
6. Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007;460(2):202-205.
1. Mayo Clinic. Vitamin D. http://www.mayoclinic.com/health/vitamin-d/NS_patient-vitamind/DSECTION=dosing. Updated October 1 2011. Accessed September 26, 2012.
2. National Institutes of Health. Office of Dietary Supplements. Dietary supplement fact sheet: vitamin D. http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional. Accessed September 26, 2012.
3. Lee DM, Tajar A, Ulubaev A, et al. Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men. J Neurol Neurosurg Psychiatry. 2009;80(7):722-729.
4. Wilkins CH, Sheline YI, Roe CM, et al. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006;14(12):1032-1040.
5. Webb AR, Engelsen O. Calculated ultraviolet exposure levels for a healthy vitamin D status. Photochem Photobiol. 2006;82(6):1697-1703.
6. Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007;460(2):202-205.
A psychiatric approach to vasovagal syncope
Discuss this article at www.facebook.com/CurrentPsychiatry
Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.1 Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.
Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.2
I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.
Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.
Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,2 a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.3 In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.4 In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.5
CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.6 Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.
Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.7
Disclosure
Dr. LaFerney reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Leftheriotis D, Michopoulos I, Flevari P, et al. Minor psychiatric disorders and syncope: the role of psychopathology in the expression of vasovagal reflex. Psychother Psychosom. 2008;77(6):372-376.
2. White CM, Tsikouris JP. A review of pathophysiology and therapy of patients with vasovagal syncope. Pharmacotherapy. 2000;20(2):158-165.
3. Stone KJ, Viera AJ, Parman CL. Off-label applications for SSRIs. Am Fam Physician. 2003;68(3):498-504.
4. Baris Kaya E, Abali G, Aytemir K, et al. Preliminary observations on the effect of amitriptyline treatment in preventing syncope recurrence in patients with vasovagel syncope. Ann Noninvasive Electrocardiol. 2007;12(2):153-157.
5. James JJ, Wilson AR, Evans AJ, et al. The use of a short-acting benzodiazepine to reduce the risk of syncopal episodes during upright stereotactic breast biopsy. Clin Radiol. 2005;60(3):394-396.
6. Newton JL, Kenny RA, Baker CR. Cognitive behavioural therapy as a potential treatment for vasovagal/neurocardiogenic syncope—a pilot study. Europace. 2003;5(3):299-301.
7. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation. 2002;106(13):1684-1689.
Discuss this article at www.facebook.com/CurrentPsychiatry
Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.1 Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.
Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.2
I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.
Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.
Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,2 a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.3 In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.4 In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.5
CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.6 Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.
Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.7
Disclosure
Dr. LaFerney reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Discuss this article at www.facebook.com/CurrentPsychiatry
Vasovagal syncope—also called neurocardiogenic syncope—is a brief loss of consciousness caused by a sudden drop in heart rate and blood pressure usually diagnosed and treated by a cardiologist. Psychiatrists rarely are consulted in such cases, but evidence suggests these patients often have comorbid psychiatric disorders.1 Psychiatrists can aid cardiologists in treating patients troubled by recurring episodes of vasovagal syncope.
Similar to panic disorder, vasovagal syncope can occur following a trigger or without any warning. After an initial event, vasovagal syncope episodes may never occur again, may occur occasionally, or may be frequent. Cardiologists use Holter monitoring, echocardiography, laboratory testing, stress testing, tilt table monitoring, and other methods to rule out cardiac causes of syncope. For patients whom a cardiac or neurologic cause cannot be determined, there is no recommended treatment, although beta blockers commonly are used.2
I suggest a protocol that includes psychiatric evaluation, pharmacotherapy, cognitive-behavioral therapy (CBT), and patient education.
Psychiatric evaluation. Because psychiatric disorders often accompany vasovagal syncope, patients should undergo a thorough psychiatric evaluation, and any comorbid psychiatric disorders should be addressed according to current treatment guidelines.
Pharmacotherapy. Because serotonin (5-HT) may play a key role in blood pressure regulation and vasovagal syncope,2 a selective serotonin reuptake inhibitor (SSRI) may be an option. Evidence suggests paroxetine and sertraline may help prevent vasovagal syncope, and other SSRIs may share this benefit.3 In 1 nonrandomized trial of 74 patients with a history of vasovagal syncope, amitriptyline prevented recurrent episodes.4 In a small trial, sublingual lorazepam, 2 to 4 mg, prevented vasovagal attacks in patients undergoing a procedure that previously triggered syncope.5
CBT can help patients identify and modify thoughts that trigger syncope. In a small case series, CBT led to significant reductions in syncopal episodes.6 Educate patients about environmental triggers of vasovagal events they can avoid, such as dehydration, hot rooms, long periods of standing, and emotional events. Patients who have known triggers that usually cannot be avoided, such as the sight of blood and other conditioned responses, may be helped by behavioral therapies such as systematic desensitization. Patients with known body triggers may be able to take prophylactic medication—for example, patients who are known to faint when nauseous may be able to take prochlorperazine to prevent a syncopal episode.
Patient education. Patients who experience presyncopal symptoms such as lightheadedness, visual dimming, nausea, and weakness should be instructed to lie down on the floor with their legs up at the first sign of an impending episode. If sitting, they can put their head between their knees. Progressive relaxation should be avoided. Patients might be able to block an episode by crossing their legs and tensing their muscles.7
Disclosure
Dr. LaFerney reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Leftheriotis D, Michopoulos I, Flevari P, et al. Minor psychiatric disorders and syncope: the role of psychopathology in the expression of vasovagal reflex. Psychother Psychosom. 2008;77(6):372-376.
2. White CM, Tsikouris JP. A review of pathophysiology and therapy of patients with vasovagal syncope. Pharmacotherapy. 2000;20(2):158-165.
3. Stone KJ, Viera AJ, Parman CL. Off-label applications for SSRIs. Am Fam Physician. 2003;68(3):498-504.
4. Baris Kaya E, Abali G, Aytemir K, et al. Preliminary observations on the effect of amitriptyline treatment in preventing syncope recurrence in patients with vasovagel syncope. Ann Noninvasive Electrocardiol. 2007;12(2):153-157.
5. James JJ, Wilson AR, Evans AJ, et al. The use of a short-acting benzodiazepine to reduce the risk of syncopal episodes during upright stereotactic breast biopsy. Clin Radiol. 2005;60(3):394-396.
6. Newton JL, Kenny RA, Baker CR. Cognitive behavioural therapy as a potential treatment for vasovagal/neurocardiogenic syncope—a pilot study. Europace. 2003;5(3):299-301.
7. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation. 2002;106(13):1684-1689.
1. Leftheriotis D, Michopoulos I, Flevari P, et al. Minor psychiatric disorders and syncope: the role of psychopathology in the expression of vasovagal reflex. Psychother Psychosom. 2008;77(6):372-376.
2. White CM, Tsikouris JP. A review of pathophysiology and therapy of patients with vasovagal syncope. Pharmacotherapy. 2000;20(2):158-165.
3. Stone KJ, Viera AJ, Parman CL. Off-label applications for SSRIs. Am Fam Physician. 2003;68(3):498-504.
4. Baris Kaya E, Abali G, Aytemir K, et al. Preliminary observations on the effect of amitriptyline treatment in preventing syncope recurrence in patients with vasovagel syncope. Ann Noninvasive Electrocardiol. 2007;12(2):153-157.
5. James JJ, Wilson AR, Evans AJ, et al. The use of a short-acting benzodiazepine to reduce the risk of syncopal episodes during upright stereotactic breast biopsy. Clin Radiol. 2005;60(3):394-396.
6. Newton JL, Kenny RA, Baker CR. Cognitive behavioural therapy as a potential treatment for vasovagal/neurocardiogenic syncope—a pilot study. Europace. 2003;5(3):299-301.
7. Krediet CT, van Dijk N, Linzer M, et al. Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation. 2002;106(13):1684-1689.