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Depression and type 2 diabetes mellitus can separately increase the risk for dementia, but that risk is even greater when both conditions are present. Further, the increased risk was greatest in younger patients, increasing almost fivefold among those under 65 years, compared with those with neither depression nor diabetes, researchers said in a study published April 15.
In the largest study to date that examined dementia risk in those with comorbid depression and diabetes, Dr. Wayne Katon of the University of Washington, Seattle, and his colleagues found an enhancement of risk for dementia in those with both conditions. The finding is worrisome, because diabetes is occurring at ever-younger ages, and people are living longer than ever.
Knowing from previous studies that depression increases the risk of all-cause dementia and taking into account that depression is associated with increased risk for diabetes, Dr. Katon and his colleagues examined both separate and summed all-cause dementia risks for depression and diabetes They said their study was the first to assess the excess risk of these two diagnoses over that of the general population (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0082]).
Drawing on large and comprehensive Danish national health registries, the population-based cohort study included a total of 2,454,532 adults who were at least 50 years old and without dementia at enrollment. Of these, 477,133 (19.4%) had depression; 223,174 (9.1%) had diabetes; 95,691 (3.9%) had both. Patient group allocations, as well as incident dementia diagnoses, were determined by tracking physician-assigned diagnosis codes and by interrogating a prescription registry. Statistical analysis adjusted for the effect of other comorbidities, as well as for potentially confounding demographic variations.
During the 7 years of the follow-up period, the hazard ratio for developing dementia among those with comorbid depression and diabetes was 2.17 (95% confidence interval, 2.10-2.24); for those with depression alone, 1.20 (95% CI, 1.17-1.23), and for those with diabetes alone, 1.83 (95% CI, 1.80-1.87). For those younger than age 65 years, the hazard ratio for dementia with both DM and depression was 4.84 (95% CI, 4.21-5.55).
The study’s strengths included the large sample size and the very small attrition rate inherent in the robust Danish database. However, the population’s homogeneity limits generalizability. Additionally, only those who sought treatment for depression or diabetes were included, creating a selection bias toward more severe disease.
Though the study’s overall findings are clear, the causality is not. However, Dr. Katon and his coauthors observed, “Although underlying causal mechanisms are unclear, one explanation could be that depression and [diabetes] have many shared risk factors for dementia,” including obesity, inflammation, and vascular disease.
A globally aging population coupled with increased prevalence of chronic disease earlier in life in the developed world presents a demographic and health challenge: How do we help people live well, longer into old age?
The burgeoning field of geroscience seeks to unlock biological and environmental clues that will help us live well as we continue to live longer. With a goal of pushing back the onset of age-related morbidities, especially dementia, cross-disciplinary geroscience research seeks to pinpoint biomarkers of aging. These may include inflammatory markers, direct examination of telomere length, and other measures of oxidative stress.
 |
Dr. Charles F. Reynolds III |
Mediators of age-related morbidity include genetic, dietary, and pharmacologic manipulation, as well as exercise, with its powerful pleiotropic effects. All are important and must be coupled with minimizing such behavioral health risks as smoking, insufficient sleep, inactivity, and social isolation if quality of life is to be maintained into old age. Cross-disciplinary research funded by the MacArthur Foundation Research Network on an Aging Society shows the powerful impact of a healthy lifestyle.
Some health interventions are critical: More aggressive depression treatment, for example, may help delay dementia. Treatment of depression helps both by improving cognition and by facilitating better overall health; for example, patients with diabetes have improved glycemic control when depression is treated. Targeted and evidence-based interventions for depression can preserve cognitive function, reduce disability, and improve adherence to other medical and lifestyle interventions for chronic disease.
Dr. Charles F. Reynolds III is the University of Pittsburgh Medical Center Endowed Professor in Geriatric Psychiatry, and director of the Aging Institute at the university and of the John A. Hartford Center of Excellence in Geriatric Psychiatry. These points are summarized from his editorial accompanying Dr. Katon’s article, published online in JAMA Psychiatry on April 15. (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0174]). His disclosures include pharmaceutical support from Bristol-Myers Squibb, Forest, Pfizer, and Eli Lilly.
A globally aging population coupled with increased prevalence of chronic disease earlier in life in the developed world presents a demographic and health challenge: How do we help people live well, longer into old age?
The burgeoning field of geroscience seeks to unlock biological and environmental clues that will help us live well as we continue to live longer. With a goal of pushing back the onset of age-related morbidities, especially dementia, cross-disciplinary geroscience research seeks to pinpoint biomarkers of aging. These may include inflammatory markers, direct examination of telomere length, and other measures of oxidative stress.
|
Dr. Charles F. Reynolds III |
Mediators of age-related morbidity include genetic, dietary, and pharmacologic manipulation, as well as exercise, with its powerful pleiotropic effects. All are important and must be coupled with minimizing such behavioral health risks as smoking, insufficient sleep, inactivity, and social isolation if quality of life is to be maintained into old age. Cross-disciplinary research funded by the MacArthur Foundation Research Network on an Aging Society shows the powerful impact of a healthy lifestyle.
Some health interventions are critical: More aggressive depression treatment, for example, may help delay dementia. Treatment of depression helps both by improving cognition and by facilitating better overall health; for example, patients with diabetes have improved glycemic control when depression is treated. Targeted and evidence-based interventions for depression can preserve cognitive function, reduce disability, and improve adherence to other medical and lifestyle interventions for chronic disease.
Dr. Charles F. Reynolds III is the University of Pittsburgh Medical Center Endowed Professor in Geriatric Psychiatry, and director of the Aging Institute at the university and of the John A. Hartford Center of Excellence in Geriatric Psychiatry. These points are summarized from his editorial accompanying Dr. Katon’s article, published online in JAMA Psychiatry on April 15. (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0174]). His disclosures include pharmaceutical support from Bristol-Myers Squibb, Forest, Pfizer, and Eli Lilly.
A globally aging population coupled with increased prevalence of chronic disease earlier in life in the developed world presents a demographic and health challenge: How do we help people live well, longer into old age?
The burgeoning field of geroscience seeks to unlock biological and environmental clues that will help us live well as we continue to live longer. With a goal of pushing back the onset of age-related morbidities, especially dementia, cross-disciplinary geroscience research seeks to pinpoint biomarkers of aging. These may include inflammatory markers, direct examination of telomere length, and other measures of oxidative stress.
|
Dr. Charles F. Reynolds III |
Mediators of age-related morbidity include genetic, dietary, and pharmacologic manipulation, as well as exercise, with its powerful pleiotropic effects. All are important and must be coupled with minimizing such behavioral health risks as smoking, insufficient sleep, inactivity, and social isolation if quality of life is to be maintained into old age. Cross-disciplinary research funded by the MacArthur Foundation Research Network on an Aging Society shows the powerful impact of a healthy lifestyle.
Some health interventions are critical: More aggressive depression treatment, for example, may help delay dementia. Treatment of depression helps both by improving cognition and by facilitating better overall health; for example, patients with diabetes have improved glycemic control when depression is treated. Targeted and evidence-based interventions for depression can preserve cognitive function, reduce disability, and improve adherence to other medical and lifestyle interventions for chronic disease.
Dr. Charles F. Reynolds III is the University of Pittsburgh Medical Center Endowed Professor in Geriatric Psychiatry, and director of the Aging Institute at the university and of the John A. Hartford Center of Excellence in Geriatric Psychiatry. These points are summarized from his editorial accompanying Dr. Katon’s article, published online in JAMA Psychiatry on April 15. (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0174]). His disclosures include pharmaceutical support from Bristol-Myers Squibb, Forest, Pfizer, and Eli Lilly.
Depression and type 2 diabetes mellitus can separately increase the risk for dementia, but that risk is even greater when both conditions are present. Further, the increased risk was greatest in younger patients, increasing almost fivefold among those under 65 years, compared with those with neither depression nor diabetes, researchers said in a study published April 15.
In the largest study to date that examined dementia risk in those with comorbid depression and diabetes, Dr. Wayne Katon of the University of Washington, Seattle, and his colleagues found an enhancement of risk for dementia in those with both conditions. The finding is worrisome, because diabetes is occurring at ever-younger ages, and people are living longer than ever.
Knowing from previous studies that depression increases the risk of all-cause dementia and taking into account that depression is associated with increased risk for diabetes, Dr. Katon and his colleagues examined both separate and summed all-cause dementia risks for depression and diabetes They said their study was the first to assess the excess risk of these two diagnoses over that of the general population (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0082]).
Drawing on large and comprehensive Danish national health registries, the population-based cohort study included a total of 2,454,532 adults who were at least 50 years old and without dementia at enrollment. Of these, 477,133 (19.4%) had depression; 223,174 (9.1%) had diabetes; 95,691 (3.9%) had both. Patient group allocations, as well as incident dementia diagnoses, were determined by tracking physician-assigned diagnosis codes and by interrogating a prescription registry. Statistical analysis adjusted for the effect of other comorbidities, as well as for potentially confounding demographic variations.
During the 7 years of the follow-up period, the hazard ratio for developing dementia among those with comorbid depression and diabetes was 2.17 (95% confidence interval, 2.10-2.24); for those with depression alone, 1.20 (95% CI, 1.17-1.23), and for those with diabetes alone, 1.83 (95% CI, 1.80-1.87). For those younger than age 65 years, the hazard ratio for dementia with both DM and depression was 4.84 (95% CI, 4.21-5.55).
The study’s strengths included the large sample size and the very small attrition rate inherent in the robust Danish database. However, the population’s homogeneity limits generalizability. Additionally, only those who sought treatment for depression or diabetes were included, creating a selection bias toward more severe disease.
Though the study’s overall findings are clear, the causality is not. However, Dr. Katon and his coauthors observed, “Although underlying causal mechanisms are unclear, one explanation could be that depression and [diabetes] have many shared risk factors for dementia,” including obesity, inflammation, and vascular disease.
Depression and type 2 diabetes mellitus can separately increase the risk for dementia, but that risk is even greater when both conditions are present. Further, the increased risk was greatest in younger patients, increasing almost fivefold among those under 65 years, compared with those with neither depression nor diabetes, researchers said in a study published April 15.
In the largest study to date that examined dementia risk in those with comorbid depression and diabetes, Dr. Wayne Katon of the University of Washington, Seattle, and his colleagues found an enhancement of risk for dementia in those with both conditions. The finding is worrisome, because diabetes is occurring at ever-younger ages, and people are living longer than ever.
Knowing from previous studies that depression increases the risk of all-cause dementia and taking into account that depression is associated with increased risk for diabetes, Dr. Katon and his colleagues examined both separate and summed all-cause dementia risks for depression and diabetes They said their study was the first to assess the excess risk of these two diagnoses over that of the general population (JAMA Psychiatry 2015 April 15 [doi:10.1001/jamapsychiatry.2015.0082]).
Drawing on large and comprehensive Danish national health registries, the population-based cohort study included a total of 2,454,532 adults who were at least 50 years old and without dementia at enrollment. Of these, 477,133 (19.4%) had depression; 223,174 (9.1%) had diabetes; 95,691 (3.9%) had both. Patient group allocations, as well as incident dementia diagnoses, were determined by tracking physician-assigned diagnosis codes and by interrogating a prescription registry. Statistical analysis adjusted for the effect of other comorbidities, as well as for potentially confounding demographic variations.
During the 7 years of the follow-up period, the hazard ratio for developing dementia among those with comorbid depression and diabetes was 2.17 (95% confidence interval, 2.10-2.24); for those with depression alone, 1.20 (95% CI, 1.17-1.23), and for those with diabetes alone, 1.83 (95% CI, 1.80-1.87). For those younger than age 65 years, the hazard ratio for dementia with both DM and depression was 4.84 (95% CI, 4.21-5.55).
The study’s strengths included the large sample size and the very small attrition rate inherent in the robust Danish database. However, the population’s homogeneity limits generalizability. Additionally, only those who sought treatment for depression or diabetes were included, creating a selection bias toward more severe disease.
Though the study’s overall findings are clear, the causality is not. However, Dr. Katon and his coauthors observed, “Although underlying causal mechanisms are unclear, one explanation could be that depression and [diabetes] have many shared risk factors for dementia,” including obesity, inflammation, and vascular disease.
FROM JAMA PSYCHIATRY
Key clinical point: Comorbid depression and type 2 diabetes mellitus increased dementia risk by more than the summed separate risks.
Major finding: The excess risk for dementia in comorbid depression and diabetes was more than twice that for those with neither diagnosis and greater than the individual summed risks; the effect was greatest for those under age 65 years, with a hazard ratio of 4.84.
Data source: Population-based cohort study of approximately 2.5 million Danish adults, with data drawn from centralized Danish national patient registers between 2007 and 2013.
Disclosures: The study was funded by the National Institutes of Health and by an unrestricted grant from the Lundbeck Foundation. The authors reported no conflicts of interest.
