Aspirin can prevent the depletion of PUFA

Daniil

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"All UGTs tested, except 1A4, 2B15, and 2B17, catalyzed salicylic acid phenolic and acyl glucuronidation. Ratios of salicylic acid phenolic to acyl glucuronide formation varied more than 12-fold from 0.5 for UGT1A6 to 6.1 for UGT1A1. These results suggest that all UGTs except 1A4, 2B15, and 2B17 might be involved in the glucuronidation of salicylic acid in vivo."

I came across this study by chance and found that glucuronic acid is involved in the deactivation of aspirin metabolites. Glucuronic acid can also safely remove PUFA from the body, and @haidut previously mentioned that this is a safe way to deplete PUFA. Now I can try to explain a number of paradoxical side effects that people can observe from taking aspirin. Such as hair loss. I think that glucuronic acid is used to deactivate the aspirin metabolites instead of deplete the pufa, what can lead to the accumulation of pufa and side effects.
 
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haidut

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"All UGTs tested, except 1A4, 2B15, and 2B17, catalyzed salicylic acid phenolic and acyl glucuronidation. Ratios of salicylic acid phenolic to acyl glucuronide formation varied more than 12-fold from 0.5 for UGT1A6 to 6.1 for UGT1A1. These results suggest that all UGTs except 1A4, 2B15, and 2B17 might be involved in the glucuronidation of salicylic acid in vivo."

I came across this study by chance and found that glucuronic acid is involved in the deactivation of aspirin metabolites. Glucuronic acid can also safely remove PUFA from the body, and @haidut previously mentioned that this is a safe way to deplete PUFA. Now I can explain a number of paradoxical side effects that people can observe from taking aspirin. Such as hair loss. I think that glucuronic acid is used to deactivate the aspirin metabolites instead of deplete the pufa, what leads to the accumulation of pufa and side effects.

Where did you see in the study any indication that aspirin affects the depletion/excretion of PUFA? I also don't see any discussion in the study that aspirin affects/inhibits the glucuronidation process. So, care to explain how exactly the study supports the title of your post or your claims of aspirin's "patadoxical" side effects?
 
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Daniil

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Where did you see in the study any indication that aspirin affects the depletion/excretion of PUFA? I also don't see any discussion in the study that aspirin affects/inhibits the glucuronidation process. So, care to explain how exactly the study supports the title of your post or your claims of aspirin's "patadoxical" side effects?
Obviously, in the presence of aspirin, you will have less glucuronic acid to glucuronize PUFA and other toxins, as aspirin will expend it.
However, many other drugs also consume glucuronic acid(for example, paracetamol) or inhibit the process of glucuronidation(for example, amitriptyline). So aspirin is not something special.
 

JKX

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Obviously, in the presence of aspirin, you will have less glucuronic acid to glucuronize PUFA and other toxins, as aspirin will expend it.
However, many other drugs also consume glucuronic acid(for example, paracetamol) or inhibit the process of glucuronidation(for example, amitriptyline). So aspirin is not something special.
Why would less be made available when its something your body would produce in response to a toxin? Higher toxic load, more glucoronic acid. Your body is clever and always responds to a problem in the exact manner it requires to. You dont provide a reason or mechanism for your conclusions? And I believe the opposite is true.

Disagree with you, Aspirin is something special:



Anything that improves liver function will improve removal of toxins.
 
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Daniil

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Why would less be made available when its something your body would produce in response to a toxin? Higher toxic load, more glucoronic acid. Your body is clever and always responds to a problem in the exact manner it requires to. You dont provide a reason or mechanism for your conclusions? And I believe the opposite is true.

Disagree with you, Aspirin is something special:



Anything that improves liver function will improve removal of toxins.
The body may be smart, but the speed of the enzyme systems is limited. I also think there may be a million reasons that can prevent the body from producing more glucuronic acid. Or do you have anything about aspirin stimulating the synthesis of glucuronic acid? I didn't find it.

The fact that aspirin helps the liver in a certain context is not surprising. Aspirin affects a large number of factors in addition to glucuronic acid. I didn't say it was always bad or anything like that. But I am interested in the issue of pufa depletion.
 
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Daniil

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I should have written in the headline: "Aspirin and other drugs.."
 

LA

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basically - I live on protein, whole milk, no starch, extra dark chocolate, coffee, aspirin, distilled water poured through charcoal filters, powdered Vit C, B-complex supplements, and other odd experiments
These things are how I was "Peating" before I found the Peat forum AFTER I found his articles (on two sites now) way back in 2001. His articles are I why I kept taking the aspirin even after health "professionals" tried to talk me out of it. Yes I know that Dr. Peat does not recommend Ascorbic Acid and I have read what he has written on it. Everyone is different
 
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TheBeard

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basically - I live on protein, whole milk, no starch, extra dark chocolate, coffee, aspirin, distilled water poured through charcoal filters, powdered Vit C, B-complex supplements, and other odd experiments
These things are how I was "Peating" before I found the Peat forum AFTER I found his articles (on two sites now) way back in 2001. His articles are I why I kept taking the aspirin even after health "professionals" tried to talk me out of it. Yes I know that Dr. Peat does not recommend Ascorbic Acid and I have read what he has written on it. Everyone is different

How are your blood markers for kidney function after all those years on Aspirin ?
 

LA

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TheBeard

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Where did you see in the study any indication that aspirin affects the depletion/excretion of PUFA? I also don't see any discussion in the study that aspirin affects/inhibits the glucuronidation process. So, care to explain how exactly the study supports the title of your post or your claims of aspirin's "patadoxical" side effects?

Well, aspirin drives metabolism towards glucose-burning instead of fat-burning.

So if fat are never burnt, how are you getting rid of PUFA ?
 

Dr. B

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Well, aspirin drives metabolism towards glucose-burning instead of fat-burning.

So if fat are never burnt, how are you getting rid of PUFA ?
the fat burning system is there for a reason, if it wasn't, just going for a quick sprint or weightlifting or any other stressful exercise would instantly lead to us burnin up sugar stores and then converting muscles, tissues, organs to sugar.
i think aspirin/niacinamide, if you're using them, require you to use them alongside a massive amount of sugar. otherwise, their inhibition on fat burning, could encourage them to actually have a catabolic effect? as if you use them, you are forcing the body to burn sugar, and if youre not eating enough sugar, the body will break down its tissues/muscles to supply the sugar. i think aspirin stimulates AMPK which is the opposite of mTOR. berberine is another supplement which activates AMPK much stronger than aspirin. its used by bodybuilders and overweight people to cut weight.
if you take the aspirin/niacinamide but don't provide that excess sugar, they will just have a catabolic effect and turn tissues into sugar. it seems like in either case they will reduce fat loss or even cause fat gain if they are forcing sugar burning.
 

yerrag

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Well, aspirin drives metabolism towards glucose-burning instead of fat-burning.

So if fat are never burnt, how are you getting rid of PUFA ?

I think that while young and strong, deal with the PUFA burning to get rid of the PUFA, and get some help with vitamin E supplementation.

Four years of being on a PUFA-free nutrition lifestyle while burning off PUFA stores will rid your body of lot of PUFA, enough to make one metabolize sugar very efficiently.

If we hold on to the PUFA stores, it will come back to bite us in old age, when we are less able to handle it.
 

Hans

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Well, aspirin drives metabolism towards glucose-burning instead of fat-burning.

So if fat are never burnt, how are you getting rid of PUFA ?
When are fat never burning? If you're going to say when you take aspirin or niacinamide, then please show a show where free fatty acids drop to zero for even 1 hour.

Point is, we're always burning fat even when we use meldonium. They routine give people with diabetes 3-4g sodium salicylate and their ffas drop slowly over time.
In studies where they give large doses of niacinamide, ffas hardly move.
 

Dr. B

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When are fat never burning? If you're going to say when you take aspirin or niacinamide, then please show a show where free fatty acids drop to zero for even 1 hour.

Point is, we're always burning fat even when we use meldonium. They routine give people with diabetes 3-4g sodium salicylate and their ffas drop slowly over time.
In studies where they give large doses of niacinamide, ffas hardly move.
interesting, i thought it was mostly anecdotal, some claim niacinamide/aspirin caused fat gain didnt Haidut also have a post from 3-5 years ago he said he stopped using niacinamide due to it causing fat gain. but it could be simply due to eating more
 

CLASH

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interesting, i thought it was mostly anecdotal, some claim niacinamide/aspirin caused fat gain didnt Haidut also have a post from 3-5 years ago he said he stopped using niacinamide due to it causing fat gain. but it could be simply due to eating more
Excess nicotinamide can deplete methyl groups and lead to insulin resistance. This seems a more plausible reason to the fat gain, than lowering fat oxidation.

As Hans pointed out there is never a point where there is no fat oxidation. Fat oxidation exists on a spectrum.
 

Dr. B

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Excess nicotinamide can deplete methyl groups and lead to insulin resistance. This seems a more plausible reason to the fat gain, than lowering fat oxidation.

As Hans pointed out there is never a point where there is no fat oxidation. Fat oxidation exists on a spectrum.
ah i forgot
just using 100mg daily of 70mg niacinamide/30mg niacin caused hypothyroid symptoms in me... i couldnt test it out for long term with betaine but there seems to be less impact when i used it alongside 500mg betaine TMG.
btw, creatine should spare methyl groups right as it should spare methionine/choline which normally would be used to create the creatine?
what about weight gain from aspirin?
also with these two substances, wouldnt they require massive doses of carbs? if you dont supply the massive carbs, cortisol will increase to metabolize tissues for sugar. if you do supply the carbs, youll have the carbs but could gain weight due to high caloric intake? cuz technically if you lower FFA/encourage sugar burning that would increase demand for sugars and if youre not eating them the body will convert tissues to sugars.
 

yerrag

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Excess nicotinamide can deplete methyl groups and lead to insulin resistance. This seems a more plausible reason to the fat gain, than lowering fat oxidation.

As Hans pointed out there is never a point where there is no fat oxidation. Fat oxidation exists on a spectrum.
Good points.

There are two camps then, as I see it, w/r to dealing with PUFA stores in the body on the way to getting rid of them as much as possible.

Both agree on going cold turkey on PUFA in order to keep from accumulating more, or trying as much since we can't avoid it totally. With the goal of eventually having low enough PUFA FFAs in the blood that does not interfere significantly with sugar metabolism and low oxidative stress from the prevention of lipid peroxidation.

Option X involves taking aspirin and niacinamide for the purpose of inhibiting lipolysis and fatty acid oxidation.

Option Y involves none of that.

Option X gives instant results as far as improving sugar metabolism while Option Y requires waiting 4 years.

Option Y allows one to get rid of PUFA stores in a big way (significant doesn't have that impact) after 4 years of slowly using it up daily while with Option X more PUFA stores remain.

During the 4 years, Option X minimizes lipid peroxidaton while Option Y doesn't. Though after 4 years, the situation changes as with Option Y, there is a lot of PUFA stores reduction, and Option Y begins to have less PUFA fatty acids in the blood from having less PUFA stores, as. compared to Option X.

During the 4 years, Option X can already eat plenty of white sugar and drink regular Coke (assuming the only reason he has blood sugar problems is because of PUFA blocking sugar absorption and metabolism) while Option Y has to manage his poor sugar metabolism by eating complex carbohydrates that include fiber to keep his blood sugar from swinging high and low, keeping his blood sugar stable.

After 4 years though, Option X still has to go with aspirin and niacinamide to manage his high PUFA stores, while Option Y is not needing such crutches anymore.

Instant gratification vs. working to earn a 4 yr. diploma in good sugar metabolism is a choice.

Note; Vitamin E intake during the 4 years is highly suggested for Option Y.
 

yerrag

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I also should ask:

Who is more likely to backslide and indulge in PUFA escapades; Option X or Option Y.

I think Option X, because his mindset is that he has two amulets, aspirin and niacinamide, that give him special powers.
 

MrGilbert

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Option X or Option Y.
What about Option Z: fat free diet?
 

yerrag

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What about Option Z: fat free diet?
You can try to convince me by explaining the pros and cons.
 

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