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Glucose and lipid levels in early adulthood found to be associated with Alzheimer’s disease

Researchers from Boston University School of Medicine found that low HDL, high LDL, and high glucose levels at midlife are all associated with an increased risk of Alzheimer’s disease later in life. (Picture: A comparison of a health brain (left) compared to a Alzheimer’s diseased brain (right)).

A Boston University research team has found that neglecting cholesterol and glucose levels early in adulthood may increase your risk of Alzheimer’s disease (AD) later in life. Lower HDL (high-density lipoproteins) and high triglyceride levels detected in blood as early as age 35 are linked to a greater prevalence of Alzheimer’s disease several decades later, according to the researchers. They also discovered that high blood glucose levels assessed between the ages of 51 and 60 are linked to an increased risk of Alzheimer’s disease in the future.

Author Lindsay A. Farrer, PhD, said in a news release, “While our findings confirm other studies that linked cholesterol and glucose levels measured in blood with future risk of Alzheimer’s disease, we have shown for the first time that these associations extend much earlier in life than previously thought.”

The experts suggest that while high LDL has been repeatedly linked to an increased risk of Alzheimer’s disease, the link between HDL and AD has been inconclusive, possibly because most research investigating these relationships were performed using a sample of people aged 55 and up at the time of the study.

The data for this investigation came from individuals in the Framingham Heart Study, who were evaluated at four-year intervals spanning the majority of their adult lives. At each assessment and across three age ranges during adulthood, correlations of AD with several known risk factors for diabetes and heart disease (including triglyceride levels, cholesterol, blood glucose levels, blood pressure, smoking, and BMI) were assessed.

The study’s results showed that lower HDL (good cholesterol) levels are associated with an increased risk of Alzheimer’s disease in early adulthood (35-50 years) and midlife (51-60 years), along with high blood glucose levels during midlife.

First author Xiaoling Zhang, MD, PhD, stated in the press release, “These findings show for the first time that cardiovascular risk factors, including HDL which has not been consistently reported as a strong risk factor for AD, contribute to future risk of AD starting as early as age 35.”

In conclusion, Dr. Farrer summarized the findings, adding that, “Intervention targeting cholesterol and glucose management starting in early adulthood can help maximize cognitive health in later life.”


The study was published in Alzheimer’s & Dementia on March 23rd, 2022.

Abstract. Introduction. It is unknown whether vascular and metabolic diseases assessed in early adulthood are associated with Alzheimer’s disease (AD) later in life. Methods. Association of AD with lipid fractions, glucose, blood pressure, body mass index (BMI), and smoking obtained prospectively from 4932 Framingham Heart Study (FHS) participants across nine quadrennial examinations was evaluated using Cox proportional hazard and Kaplan-Meier models. Age-, sex-, and education-adjusted models were tested for each factor measured at each exam and within three adult age groups (early = 35-50, middle = 51-60, and late = 61-70). Results. A 15 mg/dL increase in high density lipoprotein (HDL) cholesterol was associated with decreased AD risk during early (15.4%, P = 0.041) and middle (17.9%, P = 0.014) adulthood. A 15 mg/dL increase in glucose measured during middle adulthood was associated with 14.5% increased AD risk (P = 0.00029). These findings remained significant after adjusting for treatment. Discussion. Our findings suggest that careful management of cholesterol and glucose beginning in early adulthood can lower AD risk.

Zhang, X, Tong, T, Chang, A, et al. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimer’s Dement. 2022; 1- 13. https://doi.org/10.1002/alz.12641

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