Does Diabetes Cause Alzheimer’s Disease?
That’s the question researchers in Sweden are pondering after the findings of a recent study indicate that individuals diagnosed with mid-life diabetes are 1.5 times more likely to develop Alzheimer’s disease later in life.
Lead researcher Elina Rönnemaa, MD, of the Uppsala University, Uppsala, Sweden, and her colleagues followed a group of 2,269 Swedish men for 32 years to track any connection between insulin problems at age 50 and dementia later. She found 102 men had developed Alzheimer’s disease, 57 had developed vascular dementia, and 235 more had other forms of dementia and cognitive impairment.
It was the men who were found to have low levels of insulin secretion, signaling diabetes, at age 50 who were one and on-half times more likely to be diagnosed later with Alzheimer’s disease. Other risk factors were considered – blood pressure, body mass index, cholesterol, and education – but it was the low insulin secretion that proved to have the most significant impact on the development of Alzheimer’s disease.
Healthy insulin levels are important to normal brain function and Rönnemaa suspects it’s the damage to blood vessels caused by impaired insulin output that may generate the onset of Alzheimer’s disease.
Researchers also weighed the importance of a particular gene, APOE4, which increases the risk for developing Alzheimer’s disease. In study participants who had diabetes, or low insulin levels, but who did not also have the APOE4 gene, the risk of Alzheimer’s disease was the strongest.
Rönnemaa’s study received grants from Uppsala University Hospital and the Swedish Research Council. Neurology, the journal published by the American Academy of Neurology includes the full details of the study in its April 9 online issue.
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This is on PubMed.
Zandi PP, Anthony JC, Khachaturian AS, et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. Arch Neurol. 2004 Jan; 61(1): 82-8
BACKGROUND: Antioxidants may protect the aging brain against oxidative damage associated with pathological changes of Alzheimer disease (AD).
OBJECTIVE: To examine the relationship between antioxidant supplement use and risk of AD. DESIGN: Cross-sectional and prospective study of dementia. Elderly (65 years or older) county residents were assessed in 1995 to 1997 for prevalent dementia and AD, and again in 1998 to 2000 for incident illness. Supplement use was ascertained at the first contact.
SETTING: Cache County, Utah. PARTICIPANTS: Among 4740 respondents (93%) with data sufficient to determine cognitive status at the initial assessment, we identified 200 prevalent cases of AD. Among 3227 survivors at risk, we identified 104 incident AD cases at follow-up. MAIN OUTCOME MEASURE: Diagnosis of AD by means of multistage assessment procedures.
RESULTS: Analyses of prevalent and incident AD yielded similar results. Use of vitamin E and C (ascorbic acid) supplements in combination was associated with reduced AD prevalence (adjusted odds ratio, 0.22; 95% confidence interval, 0.05-0.60) and incidence (adjusted hazard ratio, 0.36; 95% confidence interval, 0.09-0.99). A trend toward lower AD risk was also evident in users of vitamin E and multivitamins containing vitamin C, but we saw no evidence of a protective effect with use of vitamin E or vitamin C supplements alone, with multivitamins alone, or with vitamin B-complex supplements.
CONCLUSIONS: Use of vitamin E and vitamin C supplements in combination is associated with reduced prevalence and incidence of AD. Antioxidant supplements merit further study as agents for the primary prevention of AD.