Does Aspirin Affect Fat Loss?
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@sphagnum I think people overcomplicate this way too much. If you're fat, there is literally nothing that will even get close to the benefits you will get from becoming lean. Aspirin can help you get there by reducing inflammation along the way, but what really matters is that you get lean if you're fat.
Caffeine + aspirin can work synergistically to oppose inflammation and help the liver clear the fat influx caused by being in a deficit.
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@Peatful I am familiar with the Randall Cycle and was going to mention it in the OP but didn't want to pigeon hole replies in case there were answers outside of that.
I know the Randall Cycle never fully shuts down the fat or carb burning in either direction, but I also don't know how far aspirin swings things in favor of carb burning.
Does aspirin simply 'normalize' a metabolically compromised person's RC back to carb burning, or does it push it to a point where fat burning is minimized and fat retention is still an issue?
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@jamezb46
I agree that lean is the way to go, but achieving fat loss requires that fat be metabolized for energy when in said deficit. I don't know if aspirin may cause a great slowing of this by keeping the switch turned to carb burning.I'm also not sure how much of a deficit is safe without causing issues with thyroid and stress hormones, but that's a whole story I suppose.
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Just realized the title says Fact Loss.
Wtf… -
@sphagnum said in Does Asprin Affect Fact Loss?:
I don't know if aspirin may cause a great slowing of this by keeping the switch turned to carb burning.
I won't take this "possibility" into account.
Impact of HD aspirin on platelet aggregation curve
https://mirzoune-ciboulette.forumactif.org/t2143-english-corner-impact-of-hd-aspirin-on-platelet-aggregation-curve#30423
My definition of “uncoupling energy metabolism”:
Uncoupling energy metabolism involves separating the ATP production process from the mitochondrial respiratory chain. This mechanism allows energy to be dissipated as heat (thermogenesis), thereby regulating cellular metabolism, free radical production, and potentially protecting against oxidative damage.
ATP = molecular energy source.Useful inof:
*) Aspirin's Role in Mitochondrial Oxygen Consumption and Fever
"Probably because of aspirin’s anti-fever effect, the medical culture tends to think of it as anti-thermogenic, despite its known stimulation of mitochondrial oxygen consumption. Like thyroid hormone, aspirin prevents stress-induced loss of sodium, which is an important part of our temperature and energy regulating system."
November 2020 - Ray Peat's Newsletter.
*) Aspirin and Inflammation: The Lesser-Known Pro-Oxidant Effect
"The fact that the inflammation-promoting enzymes, aromatase, cyclooxygenase, and nitric oxide synthase, which are inhibited by an oxidizing environment are also inhibited by aspirin, would strongly suggest that aspirin and salicylic acid are functioning as pro-oxidants."
July 2016 - Ray Peat's Newsletter.
*) Aspirin's Increased Vitamin K Requirement
"Aspirin makes you need more vitamin K, even when you aren’t using much. People who use aspirin for arthritis or cancer often take several grams a day."
Email Response by Ray Peat.
*) Impact of HD aspirin on platelet aggregation curve
https://mirzoune-ciboulette.forumactif.org/t2143-english-corner-impact-of-hd-aspirin-on-platelet-aggregation-curve#30423
NB: Life of platelet is affected until new ones are made if energy and material is available to make new ones. 10-12 days delay. Even with low amount (81 mg ASA).
Excerpt:
Summary
• Aspirin irreversibly inhibits platelet aggregation for the platelet’s lifespan (~10 days).
• Higher doses don’t add to inhibition but can alter COX-2 and redox signaling.
• Chronic, uninterrupted use leads to adaptive resistance.
• In a preventive or metabolic context, a reasonable rhythmic pattern might be:
5–10 days on => 10–14 days off, to reset platelets and avoid adaptation.
• Antioxidant sufficiency (vit E, C) and nutrient cofactors (D3, K2, Ca, B3) are key to maintaining balance. -
To lose fat you need to reduce mTOR activation, e.g. the body's growth signal. Else it will always reserve some of the calories you eat to build even more fat reserves and it becomes a endless cycle of e.g. not losing weight.
Reducing mTOR is primarily achieved through AMPK.
The three main ways to increase AMPK are:
- Intermittent Fasting
- Exercise (particularly HIIT, you need to be out of breath afterwards, weightlifting doesn't increase AMPK unless you go very high volume, neither does walking or light exercise)
- Exogenous AMPK like Berberine
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@sphagnum I think fact depletion is what they do on the low toxin forum
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Probably does coz it’s an anti microbial and and anything that reduces bacteria will reduce enodotoxin which contributes to weight gain.
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@16characterstwas why would reduce endotoxin increase weight gain?
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@risingfire sorry that wasn’t clear.. it is more like the opposite of what i was trying to say. let’s try again:
Endotoxin measure correlates positively with being overweight and that relation seems to be causative.
Seeing so, anything that reduces bacteria (a producer of endotoxin) would reduce endotoxin. -
Fat loss has absolutely nothing to do with metabolic efficiency. When the body has enough nutrients it will spend some of that nutrients on building new fat cells. This can only be stopped by inhibiting mTOR activation, usually through APMK, which naturally happens during fasting and during heavy exercise. The threshold is high, passively burning more energy will not suddenly spike APMK.
