New Diabetic Drugs and Cancer: 5 Reasons for Concern



I have been very vocal in my opposition to the new class of diabetic drugs that affect the GLP-1 pathway derived from the gila monster.

But something never even occurred to me until I read an editorial attached to this article.  Something jaw dropping that I’m shocked I didn’t think about before.

Why on Earth would the gila monster, a very venomous reptile (although luckily also incredibly slow) produce a non-toxic substance in its saliva that positively affects its own gastrointestinal tract and the way it handles glucose?

Sounds like such a reasonable question once it’s been asked.  Here’s the answer.

The gila monster only eats several times per year.  In between meals, it’s entire GI tract shrinks from non-use and atrophies much like a deflated balloon.  But when it finally catches something slower than itself, the GI system of the gila monster has to go from zero to 60 in a very short period of time.  This is where the hormone GLP-1 comes in.

GLP-1 rapidly expands the GI tract of the gila monster, causing a rapid cell division of all the cells involved.  And then someone decided that this might be a good drug to treat diabetes.

They must’ve been smoking something considered illegal in most US states without a prescription to give a hormone that forces cells to rapidly divide to the point of danger.

This is likely why there is a growing strong undercurrent of researchers expressing grave concern over this entire class of drugs.  This particular study should feed their arguments further.  Researchers looked at the pancreas of diabetics (who had passed away and given their organs up for donation) and compared how it looked at under a microscope in those who had been on incretin therapy for his or her diabetes.  Here’s what they found:

  1. Those on incretin therapy had an approximately 40% increase in the mass of his or her pancreas.
  2. This increase came from both increased number of cells as well as precancerous cells (increased pancreatic intraepithelial neoplasia),
  3. The pancreata in those treated with incretin therapy had evidence of α-cell hyperplasia and glucagon-expressing microadenomas.
  4. β-Cell mass (the cells that produce insulin) was increased almost 600% in those taking incretins.
  5. Interestingly, despite this massive increase in beta cell numbers, diabetes persisted.

Overall, there were very clear concerns with precancerous and cancerous growth among the cells of the pancreas in these patients treated with incretin therapy.  For me, the most shocking aspect is the massive increase in the number of cells producing insulin, and yet this still wasn’t the answer for these patients.

In other words, despite doing (and, arguably, overdoing) what the class of drug is supposed to do, it still did nothing to fix the problem of the diabetes.

Guess that leaves lifestyle changes.

James Bogash

For more than a decade, Dr. Bogash has stayed current with the medical literature as it relates to physiology, disease prevention and disease management. He uses his knowledge to educate patients, the community and cyberspace on the best way to avoid and / or manage chronic diseases using lifestyle and targeted supplementation.







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Category: Diabetes (Type 2)
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