The link between dementia and high blood sugar could hardly be more clear.

The effect is so pronounced, Alzheimer’s has been dubbed type 3 diabetes. Even when your glucose – blood sugar – is well within what doctors call the “normal” range, it impairs brain function and memory.

So keeping your blood sugar under control should be a top priority, not only to avoid diabetes and all the complications that come with it, but to maintain brain health as well.

With this in mind, British and Chinese scientists recently decided to test an experimental treatment designed to keep blood sugar under control. They wanted to see if it would benefit Alzheimer’s patients, too.

This is what they found.

Designed for Diabetes: The Triple Receptor Agonist

For the study, researchers used old mice with genetic mutations that provoke a form of hereditary Alzheimer’s seen in humans.

The mice were injected daily with three hormones, GLP-1, GIP and glucagon. The first two stimulate a reduction in blood glucose by increasing insulin production. GLP-1 also reduces appetite. Glucagon improves liver function and the rate at which calories are burned.

The drug is called a triple receptor agonist. It has already shown promising results in reducing blood sugar, body fat and weight in diabetes studies.

The three hormones also act as brain growth factors. These are impaired in patients with Alzheimer’s.

Protects the Brain in Multiple Ways

At the end of two months the researchers found:

  • a significant improvement in learning and memory – the treated mice performed much better in a maze test compared to those not given the drug
  • a slowdown in the rate of neuron (brain cell) loss
  • increased levels of a critical brain growth hormone called BDNF that helps create new brain cells and protects existing ones
  • reduced quantities of a signaling molecule that promotes death of neurons and increased levels of another that prevents nerve cells from dying
  • enhanced numbers of a protein that helps maintain communication between neurons
  • reduction in the total volume of beta amyloid – the protein linked to Alzheimer’s
  • less inflammation in the brain
  • lower amounts of damaging oxidative stress

By reducing the cell-damaging effect of excess glucose, boosting brain-protecting insulin, and acting on different biological pathways that affect dementia, the researchers believe the drug “holds clear promise” as a new treatment for Alzheimer’s.

The lead researcher, Professor Christian Holscher, said, “These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that were originally developed to treat Type 2 diabetes but have shown consistent protective effects in several studies.

“Here we show that a novel triple receptor drug shows promise as a potential treatment for Alzheimer’s…”

Lifestyle Changes Prevent Diabetes

The study was well received by the scientific community, but John Hardy, professor of neuroscience at University College London, reminds us that animal models are often a poor predictor of human experience.

He said that “several other drugs have shown positive results in mice models of Alzheimer’s and then failed in human trials.”

He believed the results were “at best the first step in demonstrating that a drug might work in man.”

While scientists are focused on drug development, the real lesson we should draw from the diabetes-Alzheimer’s connection is the need for lifestyle changes. The best way to avoid both diseases is healthy eating habits, weight loss and exercise.

Low calorie weight loss diets have been shown to reverse even longstanding diabetes, and low carbohydrate diets also help keep blood sugar balanced. Just half an hour of moderate physical activity five days a week can reduce diabetes risk by up to 40%.

There are also a number of nutrients proven to help control blood sugar such as the mineral chromium and the spice, cinnamon.

With so much we can do for ourselves to keep blood sugar in check, there’s really little need to rely on drugs.


  1. https://www.ncbi.nlm.nih.gov/pubmed/29050859
  2. https://www.eurekalert.org/pub_releases/2017-12/lu-dd122017.php