Have addressed this before, but there is a battle going on right now between Big Pharma, which is happy to promote and sell these drugs because they make a lot of money, and medical practitioners, including doctors, nurses, PAs, dieticians, etc. that are focusing more on the root cause of the problem-ultra processed food. A loud proponent of the latter is the book Good Energy by Casey and Calley Means. Big Pharma has the upper hand right now, because we know that it is easier for most people to take a drug than it is to make lifestyle and diet changes, particularly when ultra processed food is highly palatable and not satiating, driving those who cannot control the urge to eat to eat more, causing obesity.
There are two ways of addressing this (1) Eat a diet consisting of whole foods high in protein and exercise; (2) Medicine that helps you restrict your calories. Many people are too busy to exercise regularly, but they could find lots of ways to get some extra movement in by taking stairs instead of elevators, parking further from the store, etc., but I digress.
The dolt in this thread has mocked people and thinks this is funny that obese people lack willpower. They don't. There is something different in their gut-brain interaction.
Interesting article in Scientific American on this, linked below, with some quotes- and this one nails the problem for obese people:
When GLP-1 released from the gut latches on to the vagus nerve, the nerve sends signals up the brain stem to the nucleus tractus solitarius (NTS), a bundle of sensory neurons deep in the brain. The NTS is “the first place that [receives] all incoming satiety signaling from the gut,” Hayes says. “It’s like a processing hub for energy-balance control.”
Because of its short lifespan, it’s unlikely that natural GLP-1 produced in the intestines reaches high enough concentrations in the brain to affect satiety. But the NTS doesn’t just relay incoming satiety signals from the gut—it also produces GLP-1 itself. Although the details of the mechanism are not yet fully understood, researchers have found that the primary source of GLP-1 in the brain is preproglucagon (PPG) neurons in the NTS. When activated, they act like an emergency brake at the end of the meal, flooding the brain with GLP-1 to send the message to stop eating. This effectively shuts down areas in the brain involved in feeding response, homeostatic controls, energy balance and decision-making about food—as well as the liking and wanting of food and impulsive behaviors associated with eating. For people with obesity, these neurons and hormonal activity might be a clue—one that the new drugs are bringing to light.
Compared with the naturally occurring hormone, the drugs have a stronger structure that better withstands degradation and allows them to be bioactive for hours—the newest formulas can last up to a week. This gives them the potential to act on the brain and stimulate those receptors for longer periods, Mojsov says"
So, while I may have come out strongly against such drugs in past posts, for some, they may need a GLP-1 boost that their bodies cannot naturally produce. For the pharma bros, they should celebrate and not mock these people. It seems to be some sort of chemical imbalance that impacts signalling between the gut and brain.
This is similar to other brain behaviors that react to pharmaceuticals:
"Like Hall,
some people using GLP-1 receptor agonists report not only a decreased desire for food but reduced cravings for alcohol, nicotine, drugs, online shopping, nail picking—the list goes on. These effects are driving a spate of research into possible overlapping circuitry linking compulsive behaviors, appetite and satiety."
The tide has turned, and Big Pharma is in the driver seat. The question is, what will the long term impacts and side effects be of such drugs?
As I noted above, most people can't find the time or desire to exercise regularly. In the research article linked below, and many other research articles, namely by George A. Brooks, PhD at Cal Berkeley have shown that high intensity exercise increase GLP-1 (and lactate in the blood), which inhibits appetite. Incidentally, I have observed that even while fasting, after a long and intense mountain bike ride exceeding 90% max heart rate for a good portion of the ride, I am not hungry.
From the linked article: "High-intensity exercise
inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY)."
So, people can make a choice, exercise hard/eat less, or take a drug. It's easier to take the drug. I would not judge those who choose the latter. The more I have read have convinced me that some people need some extra help to suppress their desire to eat too much.
Blockbuster weight-loss drugs are revealing how appetite, pleasure and addiction work in the brain
www.scientificamerican.com
High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given ...
www.ncbi.nlm.nih.gov