The Risks Associated with Metformin and Ozempic

The following article should be of interest to many Iranian Americans who take these two drugs.

Ozempic and Metformin are among the most widely-prescribed drugs for controlling blood glucose and appetite (weight gain). Although their precise mechanisms of actions are still being investigated and seem to be somewhat different, these drugs both seem to alter glucose metabolism by stimulating the release of glucagon-like peptide 1 (GLP-1). What is GLP-1?

Glucagon-like peptide (GLP-1) is a hormone that stimulates insulin secretion from the pancreas and curbing our appetite. So by promoting this insulin-like hormone, these drugs basically biohack (fool) an insulin-resistant brain, which would normally override or ignore insulin signaling. But what is insulin and why does our body/brain become insulin-resistant?

Insulin signals the level of blood sugar to the brain and is one of the three main biochemical signals (besides Leptin and Ghrelin) or hormones that act as energy-management (metabolic) signaling and appetite control messengers between the body and the brain. The brain, as our master energy regulator will take all these signals, as well as the body’s other metabolic needs and energy deficits, into account and will issue an executive order to the body to eat or resist/ignore food. A reason people keep eating despite having enough glucose in their blood, is that an overstressed or overanxious brain overrides the hunger/appetite feedback loop and decides to make up for the energy it loses in times of stress, particularly with foods high in sugar, fat (like ice cream) and salt (chips or fries). As our body’s most energy-hungry organ, the brain craves fat and sugar as energy-dense foods during “fake” or “stress” hunger. Salty food is also desired as it causes high blood pressure and flow to the brain in times of stress. Over time, the brain’s resistance to insulin signaling by the body, leads to “insulin-resistance,” also called Type II diabetes.

Our body balances the anabolic action of insulin (anabolic means it helps building tissue or create energy by clearing glucose from the blood) by releasing Glucagon, a hormone that puts the body into the catabolic mode, which means glucagon stimulates breaking down fat, glycogen, bones and even some bones and muscles to release more glucose into the blood). The Glucagon-like peptide (GLP-1), stimulated by both Metformin and Ozempic, is a protein that tips this balance in favor of insulin and against glucagon. In other words, both of these drugs try to fool an insulin-resisting brain into releasing more insulin.

The Problems and Risks

There are some major problems with biohacking the brain-body satiety and appetite feedback loops. The reported bone and muscle losses associated with Ozempic use perhaps occur because over time, the brain will notice the artificial spikes in GLP-1 and Insulin-to- Glucagon ratio, so it becomes GLP-1 resistant (as well as insulin-resistant), secretes more Glucagon, and revert to the catabolic mode, breaking down bones and muscles. This can be amplified by imbalances in the gut microbiome and excessive visceral fat.

With metformin, gastrointestinal side effects are common, occurring in up to 75% of those who take the drug. Metformin’s physiologic actions through insulin sensitization, inhibition of oxidative phosphorylation in mitochondria, and enhanced glucose uptake from the blood into the intestine, lead to increased lactate production and several notable risks, including gastrointestinal symptoms (nausea, vomiting, and diarrhea), increased lactate production, reduced lactate clearance, and the potential to induce lactic acidosis (metformin-associated lactic acidosis, or MALA). The resultant metabolic acidosis can be severe and lead to a shock state, impaired myocardial contractility, decreased function of catecholamines, and subsequent multiorgan dysfunction. Patients often present with vague signs and symptoms. They may initially complain of gastrointestinal side effects such as nausea, vomiting, abdominal pain, and/or diarrhea, which are commonly seen with metformin use and toxicity. The patient may also complain of dyspnea (sleep issues), dizziness, lightheadedness, fatigue, or general malaise in the setting of acidosis. In fact, the Metformin’s earlier predecessor, Phenformin, was withdrawn from the market in the late 1970s after it was discovered to be associated with lactic acidosis.

Approximately 90% of the absorbed metformin is excreted unchanged, renally suggesting little to no drug metabolism. Since most of the drug is renally excreted, acute or chronic renal failure can contribute to accumulation and toxicity.

You can read the full article HERE.

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