When the Caregiver Needs Care: the Plight of Vulnerable Caregivers

2002 Mar;92(3):409-13.

When the caregiver needs care: the plight of vulnerable caregivers.

Navaie-Waliser M1, Feldman PH, Gould DA, Levine C, Kuerbis AN, Donelan K

Abstract

Objectives

This study examined the characteristics, activities, and challenges of high-risk informal caregivers.

Methods

Telephone interviews were conducted with a nationally representative cross-section of 1002 informal caregivers. Vulnerable caregivers with poor health or a serious health condition were compared with nonvulnerable caregivers.

Results

Thirty-six percent of caregivers were vulnerable. Compared with nonvulnerable caregivers, vulnerable caregivers were more likely to have difficulty providing care, to provide higher-intensity care, to report that their physical health had suffered since becoming a caregiver, to be aged 65 years or older, to be married, and to have less than 12 years of education.

Conclusions

Reliance on informal caregivers without considering the caregiver‘s ability to provide care can create a stressful and potentially unsafe environment for the caregiver and the care recipient.

Citation

 

Does Cognitive Training Prevent Cognitive Decline?

2017 Dec 19. doi: 10.7326/M17-1531. [Epub ahead of print]

Does Cognitive Training Prevent Cognitive Decline?: A Systematic Review.

Butler M1, McCreedy E1, Nelson VA1, Desai P1, Ratner E1, Fink HA1, Hemmy LS1, McCarten JR1, Barclay TR1, Brasure M1, Davila H1, Kane RL1.

Abstract

Background

Structured activities to stimulate brain function-that is, cognitive training exercises-are promoted to slow or prevent cognitive decline, including dementia, but their effectiveness is highly debated.

Purpose

To summarize evidence on the effects of cognitive training on cognitive performance and incident dementia outcomes for adults with normal cognition or mild cognitive impairment (MCI).

Data Sources

Ovid MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and PsycINFO through July 2017, supplemented by hand-searches.

Study Selection

Trials (published in English) lasting at least 6 months that compared cognitive training with usual care, waitlist, information, or attention controls in adults without dementia.

Data Extraction

Single-reviewer extraction of study characteristics confirmed by a second reviewer; dual-reviewer risk-of-bias assessment; consensus determination of strength of evidence. Only studies with low or medium risk of bias were analyzed.

Data Synthesis

Of 11 trials with low or medium risk of bias, 6 enrolled healthy adults with normal cognition and 5 enrolled adults with MCI. Trainings for healthy older adults were mostly computer based; those for adults with MCI were mostly held in group sessions. The MCI trials used attention controls more often than trials with healthy populations. For healthy older adults, training improved cognitive performance in the domain trained but not in other domains (moderate-strength evidence). Results for populations with MCI suggested no effect of training on performance (low-strength and insufficient evidence). Evidence for prevention of cognitive decline or dementia was insufficient. Adverse events were not reported.

Limitation

Heterogeneous interventions and outcome measures; outcomes that mostly assessed test performance rather than global function or dementia diagnosis; potential publication bias.

Conclusion

In older adults with normal cognition, training improves cognitive performance in the domain trained. Evidence regarding prevention or delay of cognitive decline or dementia is insufficient.

Primary Funding Source

Agency for Healthcare Research and Quality.

Citation

http://annals.org/aim/article-abstract/2666420/does-cognitive-training-prevent-cognitive-decline-systematic-review

Copyright © 2017 American College of Physicians. All Rights Reserved.

 

Body Mass Index and Risk of Dementia

2017 Nov 21. pii: S1552-5260(17)33811-6. doi: 10.1016/j.jalz.2017.09.016. [Epub ahead of print]

Body mass index and risk of dementia: Analysis of individual-level data from 1.3 million individuals.

Kivimäki M1, Luukkonen R2, Batty GD3, Ferrie JE4, Pentti J5, Nyberg ST5, Shipley MJ6, Alfredsson L7, Fransson EI8, Goldberg M9, Knutsson A10, Koskenvuo M2, Kuosma E2, Nordin M11, Suominen SB12, Theorell T13, Vuoksimaa E14, Westerholm P15, Westerlund H13, Zins M9, Kivipelto M16, Vahtera J17, Kaprio J14, Singh-Manoux A18, Jokela M19

Abstract

INTRODUCTION:

Higher midlife body mass index (BMI) is suggested to increase the risk of dementia, but weight loss during the preclinical dementia phase may mask such effects.

METHODS:

We examined this hypothesis in 1,349,857 dementia-free participants from 39 cohort studies. BMI was assessed at baseline. Dementia was ascertained at follow-up using linkage to electronic health records (N = 6894). We assumed BMI is little affected by preclinical dementia when assessed decades before dementia onset and much affected when assessed nearer diagnosis.

RESULTS:

Hazard ratios per 5-kg/m2 increase in BMI for dementia were 0.71 (95% confidence interval = 0.66-0.77), 0.94 (0.89-0.99), and 1.16 (1.05-1.27) when BMI was assessed 10 years, 10-20 years, and >20 years before dementia diagnosis.

CONCLUSIONS:

The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short.

Citation

 

 

Caregiving as a Risk Factor for Mortality: the Caregiver Health Effects Study

1999 Dec 15;282(23):2215-9.

Caregiving as a risk factor for mortality: the Caregiver Health Effects Study.

Schulz R1, Beach SR.

Abstract

Context

There is strong consensus that caring for an elderly individual with disability is burdensome and stressful to many family members and contributes to psychiatric morbidity. Researchers have also suggested that the combination of loss, prolonged distress, the physical demands of caregiving, and biological vulnerabilities of older caregivers may compromise their physiological functioning and increase their risk for physical health problems, leading to increased mortality.

OBJECTIVE:

To examine the relationship between caregiving demands among older spousal caregivers and 4-year all-cause mortality, controlling for sociodemographic factors, prevalent clinical disease, and subclinical disease at baseline.

Design

Prospective population-based cohort study, from 1993 through 1998 with an average of 4.5 years of follow-up.

Setting

Four US communities.

Participants

A total of 392 caregivers and 427 noncaregivers aged 66 to 96 years who were living with their spouses.

Main Outcome Measure

Four-year mortality, based on level of caregiving: (1) spouse not disabled; (2) spouse disabled and not helping; (3) spouse disabled and helping with no strain reported; or(4) spouse disabled and helping with mental or emotional strain reported.

Results

After 4 years of follow-up, 103 participants (12.6%) died. After adjusting for sociodemographic factors, prevalent disease, and subclinical cardiovascular disease, participants who were providing care and experiencing caregiver strain had mortality risks that were 63% higher than noncaregiving controls (relative risk [RR], 1.63; 95% confidence interval [CI], 1.00-2.65). Participants who were providing care but not experiencing strain (RR, 1.08; 95 % CI, 0.61-1.90) and those with a disabled spouse who were not providing care (RR, 1.37; 95% CI, 0.73-2.58) did not have elevated adjusted mortality rates relative to the noncaregiving controls.

Conclusions

Our study suggests that being a caregiver who is experiencing mental or emotional strain is an independent risk factor for mortality among elderly spousal caregivers. Caregivers who report strain associated with caregiving are more likely to die than noncaregiving controls.

Citation

https://www.ncbi.nlm.nih.gov/pubmed/10605972

 

American Academy of Neurology Guideline Update: Mild Cognitive Impairment

2017 Dec 27. pii: 10.1212/WNL.0000000000004826. doi: 10.1212/WNL.0000000000004826. [Epub ahead of print]

Practice guideline update summary: Mild cognitive impairment: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology.

Petersen RC1, Lopez O1, Armstrong MJ1, Getchius TSD1, Ganguli M1, Gloss D1, Gronseth GS1, Marson D1, Pringsheim T1, Day GS1, Sager M1, Stevens J1, Rae-Grant A1.

Abstract

Objective

To update the 2001 American Academy of Neurology (AAN) guideline on mild cognitive impairment (MCI).

Methods

The guideline panel systematically reviewed MCI prevalence, prognosis, and treatment articles according to AAN evidence classification criteria, and based recommendations on evidence and modified Delphi consensus.

Results

MCI prevalence was 6.7% for ages 60-64, 8.4% for 65-69, 10.1% for 70-74, 14.8% for 75-79, and 25.2% for 80-84. Cumulative dementia incidence was 14.9% in individuals with MCI older than age 65 years followed for 2 years. No high-quality evidence exists to support pharmacologic treatments for MCI. In patients with MCI, exercise training (6 months) is likely to improve cognitive measures and cognitive training may improve cognitive measures.

Major Recommendations

Clinicians should assess for MCI with validated tools in appropriate scenarios (Level B). Clinicians should evaluate patients with MCI for modifiable risk factors, assess for functional impairment, and assess for and treat behavioral/neuropsychiatric symptoms (Level B). Clinicians should monitor cognitive status of patients with MCI over time (Level B).

Cognitively impairing medications should be discontinued where possible and behavioral symptoms treated (Level B). Clinicians may choose not to offer cholinesterase inhibitors (Level B); if offering, they must first discuss lack of evidence (Level A).

Clinicians should recommend regular exercise (Level B). Clinicians may recommend cognitive training (Level C).

Clinicians should discuss diagnosis, prognosis, long-term planning, and the lack of effective medicine options (Level B), and may discuss biomarker research with patients with MCI and families (Level C).

Citation

http://n.neurology.org/content/early/2017/12/27/WNL.0000000000004826

Copyright © 2017 American Academy of Neurology.

 

Pharmacologic Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1529. [Epub ahead of print]

Pharmacologic Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia: A Systematic Review.

Fink HA1, Jutkowitz E1, McCarten JR1, Hemmy LS1, Butler M1, Davila H1, Ratner E1, Calvert C1, Barclay TR1, Brasure M1, Nelson VA1, Kane RL1.

Abstract

Background

Optimal treatment to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia is uncertain.

Purpose

To summarize current evidence on the efficacy and harms of pharmacologic interventions to prevent or delay cognitive decline, MCI, or dementia in adults with normal cognition or MCI.

Data Sources

Several electronic databases from January 2009 to July 2017, bibliographies, and expert recommendations.

Study Selection

English-language trials of at least 6 months’ duration enrolling adults without dementia and comparing pharmacologic interventions with placebo, usual care, or active control on cognitive outcomes.

Data Extraction

Two reviewers independently rated risk of bias and strength of evidence; 1 extracted data, and a second checked accuracy.

Data Synthesis

Fifty-one unique trials were rated as having low to moderate risk of bias (including 3 that studied dementia medications, 16 antihypertensives, 4 diabetes medications, 2 nonsteroidal anti-inflammatory drugs [NSAIDs] or aspirin, 17 hormones, and 7 lipid-lowering agents).

In persons with normal cognition, estrogen and estrogen-progestin increased risk for dementia or a combined outcome of MCI or dementia (1 trial, low strength of evidence); high-dose raloxifene decreased risk for MCI but not for dementia (1 trial, low strength of evidence); and antihypertensives (4 trials), NSAIDs (1 trial), and statins (1 trial) did not alter dementia risk (low to insufficient strength of evidence).

In persons with MCI, cholinesterase inhibitors did not reduce dementia risk (1 trial, low strength of evidence).

In persons with normal cognition and those with MCI, these pharmacologic treatments neither improved nor slowed decline in cognitive test performance (low to insufficient strength of evidence).

Adverse events were inconsistently reported but were increased for estrogen (stroke), estrogen-progestin (stroke, coronary heart disease, invasive breast cancer, and pulmonary embolism), and raloxifene (venous thromboembolism).

Limitation

High attrition, short follow-up, inconsistent cognitive outcomes, and possible selective reporting and publication.

Conclusion

Evidence does not support use of the studied pharmacologic treatments for cognitive protection in persons with normal cognition or MCI.

Primary Funding Source

Agency for Healthcare Research and Quality.

Citation

http://annals.org/aim/article-abstract/2666418/pharmacologic-interventions-prevent-cognitive-decline-mild-cognitive-impairment-clinical-alzheimer

Copyright © 2017 American College of Physicians. All Rights Reserved.

Physical Activity Interventions in Preventing Cognitive Decline and Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1528. [Epub ahead of print]

Physical Activity Interventions in Preventing Cognitive Decline and Alzheimer-Type Dementia: A Systematic Review.

Brasure M1, Desai P1, Davila H1, Nelson VA1, Calvert C1, Jutkowitz E1, Butler M1, Fink HA1, Ratner E1, Hemmy LS1, McCarten JR1, Barclay TR1, Kane RL1.

Abstract

Background

The prevalence of cognitive impairment and dementia is expected to increase dramatically as the population ages, creating burdens on families and health care systems.

Purpose

To assess the effectiveness of physical activity interventions in slowing cognitive decline and delaying the onset of cognitive impairment and dementia in adults without diagnosed cognitive impairments.

Data Sources

Several electronic databases from January 2009 to July 2017 and bibliographies of systematic reviews.

Study Selection

Trials published in English that lasted 6 months or longer, enrolled adults without clinically diagnosed cognitive impairments, and compared cognitive and dementia outcomes between physical activity interventions and inactive controls.

Data Extraction

Extraction by 1 reviewer and confirmed by a second; dual-reviewer assessment of risk of bias; consensus determination of strength of evidence.

Data Synthesis

Of 32 eligible trials, 16 with low to moderate risk of bias compared a physical activity intervention with an inactive control. Most trials had 6-month follow-up; a few had 1- or 2-year follow-up. Evidence was insufficient to draw conclusions about the effectiveness of aerobic training, resistance training, or tai chi for improving cognition. Low-strength evidence showed that multicomponent physical activity interventions had no effect on cognitive function. Low-strength evidence showed that a multidomain intervention comprising physical activity, diet, and cognitive training improved several cognitive outcomes. Evidence regarding effects on dementia prevention was insufficient for all physical activity interventions.

Limitation

Heterogeneous interventions and cognitive test measures, small and underpowered studies, and inability to assess the clinical significance of cognitive test outcomes.

Conclusion

Evidence that short-term, single-component physical activity interventions promote cognitive function and prevent cognitive decline or dementia in older adults is largely insufficient. A multidomain intervention showed a delay in cognitive decline (low-strength evidence).

Citation

http://annals.org/aim/article-abstract/2666417/physical-activity-interventions-preventing-cognitive-decline-alzheimer-type-dementia-systematic

Copyright © 2017 American College of Physicians. All Rights Reserved.

 

Over-the-Counter Supplement Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia

2017 Dec 19. doi: 10.7326/M17-1530. [Epub ahead of print]

Over-the-Counter Supplement Interventions to Prevent Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer-Type Dementia: A Systematic Review.

Butler M1, Nelson VA1, Davila H1, Ratner E1, Fink HA1, Hemmy LS1, McCarten JR1, Barclay TR1, Brasure M1, Kane RL1.

Abstract

Background

Optimal interventions to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia are uncertain.

Purpose

To summarize the evidence on efficacy and harms of over-the-counter (OTC) supplements to prevent or delay cognitive decline, MCI, or clinical Alzheimer-type dementia in adults with normal cognition or MCI but no dementia diagnosis.

Data Sources

Multiple electronic databases from 2009 to July 2017 and bibliographies of systematic reviews.

Study Selection

English-language trials of at least 6 months’ duration that enrolled adults without dementia and compared cognitive outcomes with an OTC supplement versus placebo or active controls.

Data Extraction

Extraction performed by a single reviewer and confirmed by a second reviewer; dual-reviewer assessment of risk of bias; consensus determination of strength of evidence.

Data Synthesis

Thirty-eight trials with low to medium risk of bias compared ω-3 fatty acids, soy, ginkgo biloba, B vitamins, vitamin D plus calcium, vitamin C or β-carotene, multi-ingredient supplements, or other OTC interventions with placebo or other supplements. Few studies examined effects on clinical Alzheimer-type dementia or MCI, and those that did suggested no benefit. Daily folic acid plus vitamin B12 was associated with improvements in performance on some objectively measured memory tests that were statistically significant but of questionable clinical significance. Moderate-strength evidence showed that vitamin E had no benefit on cognition. Evidence about effects of ω-3 fatty acids, soy, ginkgo biloba, folic acid alone or with other B vitamins, β-carotene, vitamin C, vitamin D plus calcium, and multivitamins or multi-ingredient supplements was either insufficient or low-strength, suggesting that these supplements did not reduce risk for cognitive decline. Adverse events were rarely reported.

Limitation

Studies had high attrition and short follow-up and used a highly variable set of cognitive outcome measures.

Conclusion

Evidence is insufficient to recommend any OTC supplement for cognitive protection in adults with normal cognition or MCI.

Primary Funding Source

Agency for Healthcare Research and Quality.

Citation

http://annals.org/aim/article-abstract/2666419/over-counter-supplement-interventions-prevent-cognitive-decline-mild-cognitive-impairment

Copyright © 2017 American College of Physicians. All Rights Reserved.