S-VV
Member
- Joined
- Jul 23, 2018
- Messages
- 599
It's right there in the study, look it upWho paid for the studies?
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It's right there in the study, look it upWho paid for the studies?
To be fair aspirin being good for weight loss was something "Everyone" knew - I'd seen it on muscle/body building forums, paleo...it was only here I ever saw a post that "Actually, it made me gain weight"
I think Trenbolone Replacement Therapy + Nandrolone 250mg for “joint support” + “physiological” 400mg test + hGH for “anti aging” may have something to do with it.It seems intuitive to me that given how far ahead of the curve bro-science tends to be sometimes that bodybuilders and pwoerlifters of all people would notice if suddenly their mitochondria weren't functioning as well as they could be even if it was something like "oh i'm feeling weaker suddenly is anyone else experiencing this?" which i've literally NEVER seen despite being a part of some of those communities.
I don't know how well mitochondria damage translates to real strength losses especially in the short term but I've noticed HUGE differences in strength and recovery since starting on aspirin in the .5 gram range despite my body weight going down somewhat and lean mass staying relatively constant
It seems intuitive to me that given how far ahead of the curve bro-science tends to be sometimes that bodybuilders and pwoerlifters of all people would notice if suddenly their mitochondria weren't functioning as well as they could be even if it was something like "oh i'm feeling weaker suddenly is anyone else experiencing this?" which i've literally NEVER seen despite being a part of some of those communities.
I don't know how well mitochondria damage translates to real strength losses especially in the short term but I've noticed HUGE differences in strength and recovery since starting on aspirin in the .5 gram range despite my body weight going down somewhat and lean mass staying relatively constant
I think Trenbolone Replacement Therapy + Nandrolone 250mg for “joint support” + “physiological” 400mg test + hGH for “anti aging” may have something to do with it.
Not to be rude but your options are to lift on hrt by doing nothing to counteract the inundation of xenoestrogens and PUFA everywhere from childhood or to lift on trt. There is no such thing as a natty or physiologically pristine lifter in either the andeogenic or estrogenic direction unless you grew up and still live in the amazon or something but even uncontacted tribes have some level of micro plastic poisoning. I dont take about androgens but I sympathize with those who do. Anyways none of that is related to aspirin unless you're implying that literally everyone who comments on it is on tren
Can you elaborate, pls? What kind of disease is this and how many children get it?Children that get Reyes disease after taking aspirin are not so lucky.
Thanks"In the 1980s, there was a big publicity campaign warning parents that giving aspirin to a child with the flu could cause the potentially deadly Reye syndrome. Aspirin sales declined sharply, as sales of acetaminophen (Tylenol, etc.) increased tremendously. But in Australia, a study of Reye syndrome cases found that six times as many of them had been using acetaminophen as had used aspirin. (Orlowski, et al., 1987) "
Aspirin, brain, and cancer
Every more time I get the conclusion that Peat's idea are to the people die more soon .
Lol.Every more time I get the conclusion that Peat's idea are to the people die more soon .
Thank youWith regards to aspirin and beta-oxidation, that study used to scare me too, but now I realize how unimportant it is. Here are some quotes:
"β-Oxidation in control and RS fibroblasts was similarly affected by increasing concentrations of hydroxyhippurate and gentisate, inhibition reaching 30% by 6 mM and 50% by 12 mM. However, salicylate affected palmitate oxidation differentially in fibroblasts from controls and RS patients. RS patients cells were more inhibited at low concentrations of salicylate (Fig. 2). Inhibition began at 0.5 mM and was 18% (P<0.05, paired t-test) at 1 mM."
"Salicylate at 5 mM inhibited control rates by 11% (P<0.01, paired t-test) while RS cell rates were inhibited by 29% (P<0.01, paired t-test). At higher concentrations of salicylate the effect on rates of palmitate oxidation in RS and control cells converged, causing 45% and 43% inhibition, respectively, at 15 mM."
"But in control cells, 0.5 to 1 mM salicylate significantly enhanced (Fig. 2) the rate of β-oxidation."
And then if you look at the pictures, you how just how weak this effect is for both aspirin and it's metabolites.
Remember, 1mM is a 2g-3g dose, 4g-5g over an entire day. And in normal control cells, you don't start seeing any real noticeable inhibition of anything up until about 3mM. And even then, for controls it's only like 5% by 3mM in everything tested, and even for RS cells it's still only 18% by 1mM.
In fact, looking at controls, beta-oxidation of palmitate is actually enhanced at 1mM-2mM.
And of course also, a dose of aspirin is going to be split amongst all of it's metabolites. So taking a 3g dose of aspirin to get 1.25mM blood levels means that the dose is going to be split amongst metabolites. Each metabolite might only have levels of .3mM.
Real, actual problems in beta-oxidation don't actually start until 5mM or so, and even then they're still not that strong. It only starts getting really intense at 10mM and upwards, in control cells.
5mM would be something like 10g-15g and 20g over the course of a day. You'd have other problems to worry about besides beta-oxidation at doses like that.
Of course, everyone's cells are going to be different, many people have unknown mutations, or combinations of genes that result in overall low activity and flux of a metabolic pathway. Beta-oxidation is going to wildly differ amongst people and even in the same person depending on their diet and environment. But I'm confident that as long as aspirin doses are kept under 1g (2g a day), the effect on fat burning/beta-oxidation would be very very small. And if doses are kept to under 1000mg-500mg per day, then effects would be miniscule. As in, virtually undetectable.
Excellent post.With regards to aspirin and beta-oxidation, that study used to scare me too, but now I realize how unimportant it is. Here are some quotes:
"β-Oxidation in control and RS fibroblasts was similarly affected by increasing concentrations of hydroxyhippurate and gentisate, inhibition reaching 30% by 6 mM and 50% by 12 mM. However, salicylate affected palmitate oxidation differentially in fibroblasts from controls and RS patients. RS patients cells were more inhibited at low concentrations of salicylate (Fig. 2). Inhibition began at 0.5 mM and was 18% (P<0.05, paired t-test) at 1 mM."
"Salicylate at 5 mM inhibited control rates by 11% (P<0.01, paired t-test) while RS cell rates were inhibited by 29% (P<0.01, paired t-test). At higher concentrations of salicylate the effect on rates of palmitate oxidation in RS and control cells converged, causing 45% and 43% inhibition, respectively, at 15 mM."
"But in control cells, 0.5 to 1 mM salicylate significantly enhanced (Fig. 2) the rate of β-oxidation."
And then if you look at the pictures, you how just how weak this effect is for both aspirin and it's metabolites.
Remember, 1mM is a 2g-3g dose, 4g-5g over an entire day. And in normal control cells, you don't start seeing any real noticeable inhibition of anything up until about 3mM. And even then, for controls it's only like 5% by 3mM in everything tested, and even for RS cells it's still only 18% by 1mM.
In fact, looking at controls, beta-oxidation of palmitate is actually enhanced at 1mM-2mM.
And of course also, a dose of aspirin is going to be split amongst all of it's metabolites. So taking a 3g dose of aspirin to get 1.25mM blood levels means that the dose is going to be split amongst metabolites. Each metabolite might only have levels of .3mM.
Real, actual problems in beta-oxidation don't actually start until 5mM or so, and even then they're still not that strong. It only starts getting really intense at 10mM and upwards, in control cells.
5mM would be something like 10g-15g and 20g over the course of a day. You'd have other problems to worry about besides beta-oxidation at doses like that.
Of course, everyone's cells are going to be different, many people have unknown mutations, or combinations of genes that result in overall low activity and flux of a metabolic pathway. Beta-oxidation is going to wildly differ amongst people and even in the same person depending on their diet and environment. But I'm confident that as long as aspirin doses are kept under 1g (2g a day), the effect on fat burning/beta-oxidation would be very very small. And if doses are kept to under 1000mg-500mg per day, then effects would be miniscule. As in, virtually undetectable.
@BigYellowLemon That part may be false but what about the tinnitus? Aspirin gave me permanent tinnitus, it's been weeks and nothing changed. It's literally ototoxic.