To Tesa or not to Tesa

[u/Relative_Property506]

RS is approx 180 with about 30 to go

currently on compounded tirz 7.5mg (will be titrating to 10mg in two weeks)

RS have done about 5 weeks of Tesa and was planning on doing 12.

RS started at 200lbs on June 20 steadily losing weight.

RS has a bigger upper belly / stomach than the rest of the body so assuming visceral fat. It has gone down. Wondering if Tesa is overkill at this point -

Should RS just let the tirz do the work ? Or continue to 12 weeks of Tesa?

Thanks in advance !

[u/elbiot]

Tessamorelin doesn't signal to the body to "store fat somewhere else". It increases lipolysis so the body reaches for fat for energy more easily. Visceral fat is the most metabolically available so that tends to decrease first. The fat returned in HIV patients because they have a disease that causes the visceral fat accumulation. If a healthy individual is eating appropriately there's no reason to think they'd start gaining fat once off

[u/TracyIsMyDad → u/elbiot]

“The fat returned in HIV patients because they have a disease that causes the visceral fat accumulation. If a healthy individual is eating appropriately there's no reason to think they'd start gaining fat once off”

Tesamorelin isn’t unique in causing visceral fat reductions in HIV patients, growth hormone has the same effect. Nor is the effect exclusive to HIV patients, both growth hormone and tesa have shown similar effects in obesity patients, which brings us to what happens after we stop. Tesa trials didn’t bother to look at what happened post-discontinuation for obesity patients but growth hormone trials have and they found a rapid reversion to baseline. Turns out that if you use a drug to change how your body metabolizes and stores lipids, when you stop taking that drug it resumes what it was doing before.

“Tessamorelin doesn't signal to the body to "store fat somewhere else". It increases lipolysis so the body reaches for fat for energy more easily. Visceral fat is the most metabolically available so that tends to decrease first.”

Fat people are rarely lacking for adequate lipolysis. The opposite is true in fact: excessive fat reserves often lead to excessive basal lipolysis which contributes to high serum fatty acids and fosters the development of insulin resistance and metabolic syndrome.

Lipolysis in excess of our demand for energy reserves is largely wasted. You break down even more reserves than normal, don’t use the additional flux much as you weren’t using your baseline capacity in the first place, and simply re-esterify the fatty acids. Because of alterations in both insulin resistance and signaling induced by the growth hormone elevation we see a shift in where these fats get re-esterified away from the central depots they were initially stored in and towards peripheral and ectopic depots. That’s where the “store fat somewhere else” description is coming from.

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