Is Alzheimer's Type 3 Diabetes?

A study published recently by Proceedings of the National Academy of Sciences reports that insulin drugs used to keep diabetes under control may also shield nerve cells from harmful neuro-toxic proteins called called amyloid beta-derived diffusible ligands (ADDLs).

This has created hope that bolstering insulin signaling can protect neurons from harm, and thereby help slow the onset of dementia in diabetic persons as they age. Indeed, disturbances in glucose metabolism have been reported in so-called “Alzheimer’s Disease” (AD) for decades, with the theory being that the brains of diabetics either lack sufficient glucose to function properly, or that excess sugar in the bloodstream of a diabetic does vascular damage that affects blood flow to neurons and increases the formation of neuro-proteins. A study in the American Psychological Association’s January issue of Neuropsychology confirmed that even people who keep diabetes in check are more likely than those without the condition to experience mental decline over time. Another study in the January issue of Diabetes involving thousands of Swedish twins reported that developing diabetes before age 65 corresponds to a 125% increased risk for Alzheimer’s.

There is thus a scientific basis for the connection between one’s glucose metabolism and the onset of dementia. However, there is a deeper message to be found than that which has cropped up in the media (1) that insulin drugs are the answer to AD, and (2) that AD can thusly be considered Diabetes Part 3.

Let’s take on the latter claim first. As we have argued in The Myth of Alzheimer’s, the severe brain aging that we call “AD” is caused by multiple factors, amongst which are: inflammation, vascular damage, oxidative stress, the formation of abnormal proteins, and other age-related processes such as altered glucose metabolism. Thus, impaired sugar metabolism certainly might contribute to these processes but is not the single cause in itself, and the AD-as-Diabetes-Part-3 claim is misleading.

As for the second claim, the real message should not be that late-stage insulin drug treatments are thenswer to dementia, but rather that making lifestyle changes across the life course (particularly in the form of diet and exercise) to help avoid the Western cluster of chronic diseases (obesity, vascular problems, hypertension, diabetes, high cholesterol, etc) will ultimately contribute to healthier metabolism and be beneficial for the brain.

In other words, we shouldn’t be thinking exclusively in terms of treating the symptoms, but rather in terms of addressing a wider range of more fundamental processes.