Does Aspirin Inhibit Mitochondrial Respiration?

Astolfo

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Wonder how common are those ototoxic side effects caused from aspirin intake.
 

snacks

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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"

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
 

S-VV

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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.
 

Peater

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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'm one of those freaks that hasn't noticed anything either way even at 600 - 900mg a day. Apart from extra hair shedding but I'm not worried by that. Plenty more where it came from :D
 

Astolfo

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Im taking 500 mg x 2 a day. What’s the minimum therapeutic and maximum safe dosage?
 

snacks

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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
 

S-VV

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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

You misunderstand. I did not say that steroids are bad, in fact, I quite like them (except tren, that sh*t will give you homicidal urges)

What I said is that a very big segment of bodybuilders, especially the more experimental ones, are very enhanced: androgens, hgh, high dose T3, carbergoline and other D-agonists, aromatase inhibitors, SARMS, PED5 inhibitors, hCG etc...

These things can compensate for a lot of dysfunction (confirmed by my personal experimentation), that say, high dose aspirin may induce. Children that get Reyes disease after taking aspirin are not so lucky.
 
J

jb116

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"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
 

Vinny

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"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
Thanks
 

Curiousman

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Every more time I get the conclusion that Peat's idea are to the people die more soon .
 
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Can't you just read the study?

First of all, the concentrations used in the study are very high. 1mM concentrations in a human would require you to eat 2g-3g as an initial dose, and that would only last 8 hours max, you'd have to keep redosing. To sustain those levels all day you'd need a total daily dose of like 4g-5g aspirin. Some people do do those doses, but the majority do not. Those are the doses someone with cancer would take, not someone on this forum.

Secondly, that doesn't really matter anyways, as this study isn't about showing that aspirin is toxic to normal cells. This study is about proving that aspirin can potentiate the damage and cell death caused by the "mitochondrial permeability transition". It's about proving aspirin activates it and potentiates it's effects.

Note that in this study, they used high concentrations of aspirin on stressed hepatocytes (liver cells) that had been purposefully infected with a virus that makes them sensitive to TNF. And secondly, they used a cancer cell line, which you want aspirin to kill.

"To render normally unresponsive hepatocytes sensitive to TNF-α, we blocked NF-κB with an IκB-superrepressor expressing adenovirus (Ad5IκB)."

"Although 1 mM salicylate by itself caused virtually no loss of cell viability, salicylate potentiated cell killing induced by 1 μM Br-A23187 from 12.7, 25.0, and 53.0% at 30, 60, and 90 min, respectively, to 15.9, 55.3, and 79.2% (Fig. 1)."


"In the current study, 1 mM salicylate caused very little cell killing assessed by propidium iodide fluorometry in IκB superrepressor expressing hepatocytes and in [stressed but normal] hepatocytes not treated with adenovirus (Fig. 3; some data not shown). At a 30-fold lower concentration than used previously, TNF-α (1 ng/ml) caused only modest apoptotic cell death 3.3, 8.8, and 35.5% after 8, 12, and 24 h, respectively (Fig. 3). By contrast, when cells were exposed to TNF-α plus salicylate, cell killing doubled or more to 22.9, 32.1, and 70.1%, respectively, after 12, 16, and 24 h (Fig. 3). After longer times, virtually all cells lost viability (data not shown). CsA nearly completely prevented this salicylate-enhanced apoptosis after low-dose TNF-α (Fig. 3)."

In the normal hepatocytes, they used a virus to block NF-kB, which is one of the most important proteins in the body. It's activated during stress and turns in a shitton of anti-stress genes that allows cells to cope with stressors and a new environment. And they used a virus to turn it off. NF-kB is what stuff like sulforphane and curcumin activate. Aspirin only kills cells when that protein is turned off, plus the cell is stressed both toxic chemicals or hormones.

Aspirin also causes cell death im the cancer cell line. That doesn't really need much explaining.

"Aspirin and other NSAIDS appear to be chemopreventive against colon, lung, and breast cancer, possibly by promoting apoptosis of transformed cells (Shiff and Rigas, 1997)."

And none of this has to do with "destroying mitochondria".
 
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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.
 

Vinny

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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.
Thank you
 
J

jb116

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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.
Excellent post.
Reminds me of the aspirin smear campaign during the Kansas flu aka "spanish flu." They used doses upwards of 30g so they could say aspirin is hazardous for your health.
 

Astolfo

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@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.
 
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@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.

Yeah the tinnitus is probably (definitely) real. Don't really have anything to say about that besides it can cause it in certain people. I imagine only in high doses though. What dosages were you taking?
 
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