Perfect Transformation

My latest on Medscape makes the case that no, diet and and exercise are not better than medications for obesity. As in literally not better. Idealistically maybe there's room for argument (though I don't think so tbh), but the data on drugs' superiority is unequivocal (registration on the website is free, it's not a paywall)

https://www.medscape.com/viewarticle/no-diet-and-exercise-are-not-better-than-drugs-obesity-2024a1000mgl?fbclid=IwY2xjawKFpNFleHRuA2FlbQIxMQABHuWYmHFUhuZRi92O9it_W4KPUKrAE4YbYrgvou7LC-zEdAHDAgHbsFUgJ_NK_aem_t24f-INZOa8I4vo6AV67og

No, Diet and Exercise Are Not Better Than Drugs for Obesity There’s no debate that diet and exercise aren’t more effective for people with obesity than antiobesity medications, contends Yoni Freedhoff, MD.

HHVB® GLP-1 Slimming & Health Boost Drops help control blood sugar by boosting insulin secretion and inhibiting glucagon release, stabilizing blood sugar levels. GLP-1 also delays gastric emptying and increases satiety, reducing food intake and promoting weight loss. Weight loss improves insulin sensitivity, lowers blood sugar, and reduces diabetes complications, making HHVB® an effective tool in diabetes management.

Wrote up some very brief thoughts on how weight loss may increase the risk of su***de and self-harm in lieu of the report that the EU is investigating if there is an association between GLP1 use (the new generation of antiobesity medications) and same. This association already seen post bariatric surgery and frankly it would not surprise me if we end up seeing this with effective antiobesity medications too. While there are a number of plausible mechanisms, I'd venture unmet expectations the primary pathway

https://yonifreedhoffmd.substack.com/p/brief-thoughts-on-suicidal-ideation?r=lpiej&utm_campaign=post&utm_medium=web&fbclid=IwY2xjawKFpUpleHRuA2FlbQIxMQABHjE5-06N99TKUce7jtxLgaW9WNnhIr3wke_oqIq76gzilPrjFtfdV5-OtdC3_aem_jQMtS304eLD0yujNPT9thw&triedRedirect=true

Brief Thoughts On Suicidal Ideation Post Weight Loss With Surgery Or Ozempic Is it a consequence of unmet expectations?

Storage and Breakdown of Fat
Fats in food consumed by the body are broken down during digestion into fatty acids and glycerol, which enter the bloodstream and are transported throughout the body. Excess fatty acids are synthesized into triglycerides in the liver and fat cells and then stored. When we consume too many calories, the body stores this excess fat as adipose tissue for use during times of high energy demand.
Storage: When we eat, fat is broken down in the intestines, and fatty acids and glycerol enter the bloodstream. They are transported through the bloodstream to adipose tissue, where they are converted into triglycerides and stored in fat cells. This process is regulated by hormones such as insulin, which prompts fat cells to combine fatty acids and glycerol to form triglycerides and store them.
Catabolism: Fat stores are mobilized when the body needs energy (e.g., during exercise or hunger). Hormones such as adrenaline and noradrenaline activate lipolytic enzymes in fat cells that begin to break down stored triglycerides into fatty acids.
Release and Transport of Fatty Acids
Broken-down fatty acids are transported through the bloodstream to the liver, muscles, and other tissues that use fatty acids as an energy source. Fatty acids can be transported where they are needed for energy via fatty acid-binding proteins (FABP) and plasma proteins such as albumin.
Muscles: During exercise, muscle cells have a high energy demand, especially during aerobic exercise, and fat becomes an important energy source. Fatty acids enter the muscle cell and are broken down into carbon dioxide and water through the process of "beta-oxidation" in the mitochondria, which also releases ATP (cellular energy).
Liver: Fatty acids also enter the liver, where liver cells convert them through fatty acid oxidation into ketone bodies, which serve as an energy source for the brain and other tissues, especially during long periods of fasting or on a low-carbohydrate diet like the ketogenic diet.
β-Oxidation (Process of Fatty Acid Oxidation)
In the cells, fatty acids enter the mitochondria and undergo β-oxidation, which is the primary catabolic process for fatty acids. Each oxidation process removes two carbon atoms to create an acetyl-coenzyme A (acetyl-CoA). These acetyl-coenzyme A molecules enter the tricarboxylic acid cycle (also known as the Krebs cycle) and ultimately pass through the respiratory chain to produce ATP. This process is the central step in the energy-providing process for fats.
Production and Use of Ketone Bodies
When the body is exposed to prolonged fasting or low carbohydrate intake, the liver converts fatty acids into ketone bodies. Ketone bodies (including acetoacetic acid, beta-hydroxybutyric acid, and acetone) are a highly efficient energy source, especially for the brain. Normally, the brain relies primarily on glucose, but during periods of starvation, it uses ketone bodies as an alternative energy source.
Regulation of Fat Metabolism
Fat metabolism is regulated by a variety of hormones and enzymes. Here are some key regulators:
Insulin: Insulin is the main storage hormone in fat metabolism. When blood sugar levels are high, insulin secretion increases, promoting fat storage. Insulin inhibits lipolysis and helps store energy as fat.
Epinephrine and Norepinephrine: These hormones are released in response to stress, exercise, or hunger and promote the breakdown of fat, releasing fatty acids into the bloodstream.
Growth Hormone: This hormone is important during childhood growth; it also helps with the breakdown of fat and promotes the release of fatty acids.
Testosterone and Estrogen: S*x hormones also affect fat distribution and metabolism. For example, testosterone contributes to fat burning, while estrogen can promote fat storage in certain areas, such as the thighs and buttocks.