um interestingly I've had my finger on the puls of these drugs since their Origins my PhD lab my dissertation lab was one of the first funded labs in the US to study the incretins these gut hormones because it was at a medical school where they were pioneering some of the earliest versions of What uh of the gastric bypass procedures and that was leading as the guts were being replumbed um you know moved around that was leading to profound differences in gp1 it didn't even have a name yet if I can recall at the time we just knew there was a bunch of hormones coming from the gut that were massively changed post gastric bypass so I have sorry to interrupting so for those that are listening 99% of people w't know this so gp1 is actual natural we we do produce it anyway yeah gp1 is a hormone made from the intestines what what's been funny for me as a professor who teaches a graduate level Endocrinology course is that on the very first day of class I show my students the prototypical end endine organs the thyroid gland the adrenal glands the gonads the testes and the ovaries these famous endocrine glands and then I show them the brain it makes hormones the heart makes hormones muscles make hormones the bone makes hor bones make hormones and yes even the intestines and among these dozens of hormones is glp1 and mind you some others that are being exploit not exploited are being leveraged with regards to various medications when the glp1 receptor agonists so so a drug now that is injected that essentially takes the glp1 signal and dials it up tremendously to a super physiological level in its earliest stages and I will touch on this in my talk today I was quite an advocate of them because it was a relatively low dose and the only real effect was that it would inhibit glucagon and as glucagon was inhibited being insulin's opposite whereas insulin wants to reduce blood glucose glucagon wants to increase blood glucose with the inhibition of glucagon came a very quick and often substantial reduction in blood glucose thereby resolving people's type 2 diabetes quite well and at the time it was just noticed as a somewhat Charming side effect that the people tended to eat a little less well that has now been fully exploited I'll use the word then that now quite liberally by dialing up this dose by four or five times and now it's a different name of a drug it's literally the same molecule just at a different concentration with its own patent and now its own name and now the main effect is this essential I'm going to be a little dramatic which doesn't suit my job as a scientist well but it does leave an impression on people essentially is a paralysis of the intestines that's the main mechanism of action where people will say I take these drugs and the food noise goes away yeah it's because food is now staying in your stomach for over 24 hours when slows gastric empting yes you can do quite nicely with fiber yeah that's right yeah so there are that's part of what I end my talk with today which is basically painting this picture that glp1 is undoubtedly a metabolic Advantage we want glp1 protein will increase it fats various fats will increase not all kinds certain carbohydrates will but so too does fiber fiber directly stimulates the L cells of the small intestine which are the cells that make gp1 so there are a lot of ways for people to take advantage of gp1 whose main effect is to promote a sense of satiety by slowing the intestines down if the intestinal movement slows down a little it'll help you feel Fuller longer the problem with these glp1 agonists these drugs is it slows them down too much where you have actual cases where people experience permanent paralysis of the intestines and are left to get nutrition through infusion for the rest of their life and have a colostomy bag or some other way of defecating that doesn't involve the use of their intestines because they're dead essentially e