Science

...clinical trials and those discovered in "phase IV" safety monitoring of approved drugs, to compare the relative risks with the risks of not taking a drug.

I have a familial risk of type 2 diabetes, along with a familial history of obesity, the latter having manifested itself relatively late in life, having previously been managed by the famous invective of "diet and exercise." As I age, and as my professional responsibilities have multiplied, my creaky bones and demands on my time have basically precluded, diet and exercise.

My grandfather, who had access to neither commonly available medications like metformin, or for that matter, semaglutide, lost his legs shortly before dying from diabetes.

My wife, who doesn't like me injecting myself - or asking her to inject me - with semaglutide every Sunday, made sure I heard about the blindness thing. On the other hand, I decided to take semaglutide after hearing a scientific lecture on GLP-1 peptides on the topic at a scientific meeting.

I have a genetic susceptibility to Barrett's esophagus, which is why my father and my uncle, both heavy smokers (which I am not) got esophageal cancer before lung cancer. Mechanistically, esophageal cancer is initiated by nitrosamines, which have been identified as impurities in certain formulations of metformin. Knowing this, I still take metformin.

There are millions of people who take GLP-1 drugs, and given their modes of action - they are glucagon isosteres as opposed to insulin isosteres, but clearly are interactive peptide hormones - it's not entirely surprising that a subset face risks of this type, circulatory effects, expressed in the eyes, since insulin a generated from proinsulin where the cleaved peptide is responsible for preventing the venous responses that lead to limb atrophy, and ultimately amputation, as in my grandfather's case. It is therefore not entirely surprising that agonist effects of what is, basically, a peptide, balance in such a way as antagonist effects to produce a side effect.

The real question is, however, is how many of the people who take GLP-1 drugs, numbering now in the tens of millions, would have died from complications of obesity and diabetes, without the drug, compared with the number of persons who have had vision effects.

All questions of this type, whether in medicine or in energy science, need to be examined on a risk benefit basis. I can't think of any drug that is risk free. Hell, there aren't many foods that are risk free. A risk associated with not taking the drug may be worse (death) than the risk of blindness, which is apparently very low given the number of instances of reported blindness and the size of the populations using the drugs.