For each person’s height, a range of healthy weights has been defined. Dividing an adult’s weight in kilograms by the square of height in meters gives a number called the Body Mass Index (BMI). It’s not a perfect standard, but it’s often used to identify the lines that separate healthy weight from overweight, and overweight from obese. Getting to a healthy weight and staying there is very important for good health. Too much body weight often means too much fat tissue, and fat tissue can have dangerous effects on health. Overweight or obesity, too, increase the risk for many medical diseases. In the United States, more than a third of adults are obese. The medical cost each year for an obese adult is estimated to be $1,429 higher than for someone of normal weight.1 Some scientists point with alarm to the increase in obesity. They warn that this is going to raise the rate of Alzheimer’s disease development in our population, which is already increasing due to higher numbers of people who are older or overweight.2
Weight and its Connection to Alzheimer’s
I’m not sure that being overweight, in and by itself, is always the problem when we’re talking about Alzheimer’s disease. It seems possible that obesity, for at least some people, is a sign of unhealthy dietary habits that have their own bad effects on health. We’re bombarded by advertisements for foods that give us lots of empty calories and are unhealthy for us. They provide an easy, quick, but not very effective way of squelching hunger.
Overeating, of course, is not the only reason for obesity. People who are obese, too, can have medical diseases that increase their weight or interfere with a healthier lifestyle. Severe arthritis, for example, can make physical exercise more difficult and increase both inactivity and weight. In addition, some overweight-related illnesses independently increase the risk for Alzheimer’s. With increased weight, a person is more likely to develop diabetes or high blood pressure and we know that these diseases increase the risk for Alzheimer’s disease. There may be some people, as well, whose increased weight is a sign of cognitive difficulty rather than an effect. Weight increase, for example, could be a sign of apathy, decreased physical activity, and poorer self-care at the beginning of a cognitive decline.
Insulin and the Brain
Excess weight itself, though, has its own special dangers concerning the brain. Most of the attention about this has focused on the important pancreatic hormone, insulin. Increased weight is linked with resistance to the metabolic effects of insulin. This is true even in people who are not obese or diabetic. When the body becomes resistant to insulin, the pancreas responds by churning out more of the hormone until the organ fails, resulting in type 2 diabetes.
Extra insulin in the bloodstream actually interferes with the brain’s energy supply by lowering the amount of fuel (glucose) that gets into the brain. Insulin, we are also learning, has important direct effects on the brain that are reduced with resistance.
Insulin itself crosses through the brain’s protective security system (the “blood brain barrier”) and attaches to special receptor molecules on brain cells. These receptors are located in synapses in brain areas that need to work properly in order to make memories. Synapses are structures that permit a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron.
Among other actions, insulin influences the process that helps to preserve long-term memories.3 Finally, insulin has effects on the brain’s energy metabolism, and has a regulatory effect on how the brain gets rid of toxic amyloid, and other important brain functions.
Considering all these ways that insulin protects and assists the brain, some researchers have tried to treat Alzheimer’s disease by spraying insulin high up inside the nose. From the nasal cavity, insulin is easily absorbed into the brain and has been shown to boost mental activity. Investigations of the potential treatment role for intranasal insulin are ongoing but this treatment is not yet in clinical use for the treatment of AD except in research studies.
Weight Loss and Alzheimer’s
The link between obesity and cognitive decline has been well established for mid-life, but later on there is a different connection between weight and Alzheimer’s. In later life, the onset of Alzheimer’s disease is often linked with loss of weight.4 This can be a huge concern for caregivers, and there may be many contributing reasons for this weight loss. Decreased motivation and self-care, changes in appetite and awareness of the body’s needs, less attention to mealtimes and preparation, greater social isolation, and altered metabolism may all contribute to this problem. There may even be genetic factors. A connection has been reported, for example, between increased weight loss in Alzheimer’s disease and the presence of a specific APOE gene.5
What practical advice should we take away from talking about weight and Alzheimer’s disease? The most important idea, I think, is that the risk factors we can change have to be addressed in mid-life or even earlier in order to benefit us later on. Proper exercise and a healthy diet are easily accessible tools that can help us reduce the risk not only for Alzheimer’s disease but for many other medical problems as well. Stated in a more positive way, a healthy lifestyle which includes weight management can increase the likelihood of optimal aging, prolonged independence, and a greater quality of life.
- Alzheimer’s Disease Toolkit (Helpful Information to Understand and Manage Alzheimer's Disease)
- Expert Information on Alzheimer's Disease (Articles)
- Decreasing Your Risk of Alzheimer’s (Article)
- Alzheimer's Prevention: Nutrition & Lifestyle (Fact Sheet)
Suggested Additional Readings:
1. http://www.cdc.gov/obesity/data/adult.html - accessed 10/31/15.
2. Nepal B, Brown LJ, and Anstey KJ. Rising midlife obesity will worsen future prevalence of dementia. PLOS ONE September 2014;9:1-5.
3. Cholerton B, Baker LD, Craft S. Insulin, cognition, and dementia. European Journal of Pharmacology 2013;719:170-9.
4. Tolppanen AM, Ngandu T, Kareholt I, et al. Midlife and late-life body mass index and late-life dementia: results from a prospective population-based cohort. J Alzheimers Dis 2014;38:201-9.
5. Backman K, Joas E, Waern M, et al. 37 years of body mass index and dementia: Effect modification by the APOE genotype: Observations from the prospective population study of women in Gothenburg, Sweden. J Alzheimers Dis 2015 Sep 15, PMID: 26402098.
This content was last updated on: October 2, 2018
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