Obesity, or having excess body fat, is a known risk factor for dementia. But new research indicates the risk level depends on where the fat is stored on the body, and that it may be time to swap out the scale for a tape measure.
Obesity during middle age, generally 40 to 60 years old, has consistently been associated with a higher risk of dementia later in life. However, reports of whether excess fat is helpful or harmful for the cognitive function of adults over age 65 have varied. The conflicting results can be explained by the way obesity has been measured in prior studies [1], according to new evidence from a recent population study examining the relationship between obesity and cognitive function in more than 5000 people over age 60. This study suggests that dementia risk is most associated with central obesity, or having excess belly fat.
The body mass index (BMI) is the most commonly used measure of overall obesity, or overall level of body fat. It is based on the relationship between height and weight. BMI is calculated according to the formula: BMI = weight (in pounds) ÷ height (in inches squared) × 703. A BMI between 18.5-25 is considered healthy, while greater than 25 is overweight, and greater than 30 is considered obese [2]. For a 6-foot-tall man, a weight of 170 lbs. would result in a healthy BMI of 23, whereas at a weight of 270 lbs. and corresponding BMI of 37, the man would be defined as obese.
However, since the BMI does not directly measure fat, it is possible for someone with lots of muscle mass to be incorrectly classified as obese. Furthermore, due to changes in body composition during aging, the BMI is not a reliable measure of obesity in the elderly [3]. The recent population study found that BMI was not necessarily associated with cognitive function in older adults [1], whereas a measure of central obesity, the waist-to-hip ratio (WHR), was linked to cognitive decline. This measure of central obesity has also been related to a higher risk of developing late-onset Alzheimer's disease and was found to be superior to BMI in predicting cardiovascular outcomes in the elderly [4].
WHR is calculated by dividing the distance around the smallest part of the waist by the distance around the largest part of the hips. Women with a WHR greater than 0.85 and men with a WHR greater than 0.90 are considered to have central obesity [5]. Importantly, it is possible to have central obesity without overall obesity. For example, a 5-foot 5 woman weighing 140 lbs. would have a healthy BMI of 23, but if most of her fat was in the belly region then she could still be centrally obese [5].
People who have a high BMI and central obesity are at the greatest risk for dementia (3.5 times increased risk). But, people with a healthy BMI who are centrally obese still have an estimated two times higher risk for developing dementia than people without excess belly fat [6]. Otherwise healthy middle-aged adults with central obesity were found to have smaller brain volumes, indicating possible brain shrinkage [7], which may be related to their increased risk for dementia later in life.
Belly fat, also known as visceral fat, can harm the brain because it produces hormones and chemicals that promote inflammation and insulin resistance [8]. Consequently, excess belly fat can also increase the risk for developing diabetes, and has been shown to be a strong predictor of cognitive decline in older people with diabetes [9].
These results are consistent with a general connection between central obesity and dementia risk throughout life, and support the importance of maintaining a healthy diet and physical activity regimen. Therefore, to help lessen dementia risk, remember to keep track of changes in width and not just overall weight.
Betsy Mills, PhD, is a member of the ADDF's Aging and Alzheimer's Prevention program. She critically evaluates the scientific evidence regarding prospective therapies to promote brain health and/or prevent Alzheimer's disease, and contributes to CognitiveVitality.org. Dr. Mills came to the ADDF from the University of Michigan, where she served as the grant writing manager for a clinical laboratory specializing in neuroautoimmune diseases. She also completed a Postdoctoral fellowship at the University of Michigan, where she worked to uncover genes that could promote retina regeneration. She earned her doctorate in neuroscience at Johns Hopkins University School of Medicine, where she studied the role of glial cells in the optic nerve, and their contribution to neurodegeneration in glaucoma. She obtained her bachelor's degree in biology from the College of the Holy Cross. Dr. Mills has a strong passion for community outreach, and has served as program presenter with the Michigan Great Lakes Chapter of the Alzheimer's Association to promote dementia awareness.
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