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The act of losing weight necessitates reduction of the mass of triglyceride stored in fat cells, so this sounds like a "duh", but whether it accelerates it through activating beneficial pathways is another matter. (E.g., how similar is a GLP-1 agonist to say diet alone or diet+exercise?)

There are many GLP-1 agonists approved now. Some are approved for type-2 diabetes as one trade name, and may also be approved under another trade name at a higher dosage. For example, Lixisenatide came off-patent for diabetes in 2020 but it doesn't have an obesity formulation in the US. The various GLP-1 agonists have slightly different risk profiles of causing pancreatitis and/or thyroid cancers.

I don't know though maybe the freezing method (cryolipolysis) could potentially be useful for some people, but it's probably still too soon to characterize its long-term risks and other benefits.

Also, CagriSema (cagrilintide (long-acting amylin analogue) & semaglutide) is promising for obesity.




I think cryolipolysis can only reduce subcutaneous fat, not visceral fat.


There's really no good mechanical way to preferentially kill adipose visceral cells to prevent them from storing excess energy in the first place. It's mostly a cosmetic procedure to reduce subcutaneous adipose population with fewer risks than mechanical surgery, but I bet it has very slight benefits but not enough to equal clinical management of obesity.

Maybe in the future there will be a temporary immunotherapy target to get the immune system to attack adipose cells but then terminate/unlearn before it gets too carried away.


>Maybe in the future there will be a temporary immunotherapy target to get the immune system to attack adipose cells but then terminate/unlearn before it gets too carried away.

Unlearning is usually not a thing for our immune system. I don't think this would even be the most promising target. Imagine being able to reverse autoimmune disorders.


> Imagine being able to reverse autoimmune disorders

That would be awesome. Perhaps if it were possible dump the state of memory B cells (I'm wondering if flow cytometry can do this), classify and inventory immunoglobulins, filter them out via perfusion, and custom program naive B cells and add them back to the body. Memory T cell types seem way messier but some should be tunable with epigenetic levers. We will eventually learn how to hack the adaptive immune system, but it's going to take a lot of research time and effort to produce to a specific autoimmune therapy for a specific clinical problem likely customized to a single individual.




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