For some years I have been intrigued by the idea that Alzheimer’s disease might be a special type of diabetes (sometimes called Type 3 Diabetes). You can read the evidence for this hypothesis here.
A recent study published in the journal Alzheimer’s and Dementia reports the observation that sugary drink consumption may be linked to Alzheimer’s disease. Here is the abstract:
Excess sugar consumption has been linked with Alzheimer’s disease (AD) pathology in animal models.
We examined the cross-sectional association of sugary beverage consumption with neuropsychological (N = 4276) and magnetic resonance imaging (N = 3846) markers of preclinical Alzheimer’s disease and vascular brain injury (VBI) in the community-based Framingham Heart Study. Intake of sugary beverages was estimated using a food frequency questionnaire.
Relative to consuming less than one sugary beverage per day, higher intake of sugary beverages was associated with lower total brain volume (1–2/day, β ± standard error [SE] = −0.55 ± 0.14 mean percent difference, P = .0002; >2/day, β ± SE = −0.68 ± 0.18, P < .0001), and poorer performance on tests of episodic memory (all P < .01). Daily fruit juice intake was associated with lower total brain volume, hippocampal volume, and poorer episodic memory (all P < .05). Sugary beverage intake was not associated with VBI in a consistent manner across outcomes.
Higher intake of sugary beverages was associated cross-sectionally with markers of preclinical AD.
This result would be consistent with the Type 3 Diabetes hypothesis. But note that the study is correlational and based on self-report. Sugary beverage consumption might be a proxy for some other variable.
Dr. Greger has the details:
So argues this important piece in Scientific American (sorry, it’s behind a paywall). So far drugs that target Alzheimer’s have been disappointing. Our best evidence suggests that lifestyle interventions (exercise, improvements in diet, and cognitive engagement) really do help.
From The Journal of Alzheimer’s Disease, “Midlife Physical Activity and Cognition Later in Life: A Prospective Twin Study.” Here is the abstract:
Background: Physical activity has been associated with a reduced risk of cognitive decline but the nature of this association remains obscure. Objective: To study associations between midlife physical activity and cognition in old age for a prospective cohort of Finnish twins. Methods: Physical activity in the Finnish Twin Cohort was assessed using questionnaire responses collected in 1975 and 1981. After a mean follow-up of 25.1 years, the subjects’ (n = 3050; mean age 74.2; range 66–97) cognition was evaluated with a validated telephone interview. Both participation in vigorous physical activity, and the volume of physical activity, divided into quintiles, were used as predictors of cognitive impairment. Metrics collected by TELE were used to categorize participants as: cognitively impaired, suffering mild cognitive impairment, or cognitively healthy. Results: Participation in vigorous physical activity compared to non-participation for both 1975 and 1981 was associated with a lower risk of cognitive impairment in individual-based analyses (fully adjusted OR 0.50, 95% CI 0.35–0.73). Pairwise analyses yielded similar but statistically non-significant associations. In terms of the volume of physical activity, the most active quintile of individuals (OR 0.69, 95% CI 0.46–1.04) had a reduced risk of cognitive decline compared with the most sedentary quintile in the fully adjusted model although no clear dose-response was found. Conclusion: Vigorous midlife physical activity was associated with less cognitive impairment but without a clear dose-response association between the volume of physical activity and cognition.
Don’t get your hopes up yet. The findings reflect animal research, but here is the story from ScienceDaily:
Using LED lights flickering at a specific frequency, researchers have shown that they can significantly reduce the beta amyloid plaques seen in Alzheimer’s disease in the visual cortex of mice. This treatment appears to work by stimulating brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.
A very surprising finding reported in The New York Times:
Despite fears that rates were going to explode as the population grows older and fatter, and has more, a large nationally representative survey has found the reverse. Dementia is actually on the wane. And when people do get dementia, they get it at older and older ages.
You can read the original study here. The key points:
Question Has the prevalence of dementia among older adults in the United States changed between 2000 and 2012?
Findings In this observational cohort study of more than 21 000 US adults 65 years or older from the nationally representative Health and Retirement Study, dementia prevalence declined significantly, from 11.6% in 2000 to 8.8% in 2012.
Meaning Population brain health seemed to improve between 2000 and 2012; increasing educational attainment and better control of cardiovascular risk factors may have contributed to the improvement, but the full set of social, behavioral, and medical factors contributing to the improvement is still uncertain.
What are the causes of this good news?:
Increases in the level of education among the later-born cohort accounted for some of the decreased dementia risk, and there was some evidence that improvements in treatments for cardiovascular risk factors (eg, diabetes) may also have played a role. However, the full set of social, behavioral, and medical factors contributing to the decline in dementia prevalence is still uncertain.
A paper published in the journal Hypertension, here is the abstract:
Background—Age-related dementia, most commonly caused by Alzheimer disease or cerebrovascular factors (vascular dementia), is a major public health threat. Chronic arterial hypertension is a well-established risk factor for both types of dementia, but the link between hypertension and its treatment and cognition remains poorly understood. In this scientific statement, a multidisciplinary team of experts examines the impact of hypertension on cognition to assess the state of the knowledge, to identify gaps, and to provide future directions.
Methods—Authors with relevant expertise were selected to contribute to this statement in accordance with the American Heart Association conflict-of-interest management policy. Panel members were assigned topics relevant to their areas of expertise, reviewed the literature, and summarized the available data.
Results—Hypertension disrupts the structure and function of cerebral blood vessels, leads to ischemic damage of white matter regions critical for cognitive function, and may promote Alzheimer pathology. There is strong evidence of a deleterious influence of midlife hypertension on late-life cognitive function, but the cognitive impact of late-life hypertension is less clear. Observational studies demonstrated a cumulative effect of hypertension on cerebrovascular damage, but evidence from clinical trials that antihypertensive treatment improves cognition is not conclusive.
Conclusions—After carefully reviewing the literature, the group concluded that there were insufficient data to make evidence-based recommendations. However, judicious treatment of hypertension, taking into account goals of care and individual characteristics (eg, age and comorbidities), seems justified to safeguard vascular health and, as a consequence, brain health.