Aspirin causes intestinal damage?

Mauritio

@zorba990 wouldn't they just be metabolism into salicylic acid and the respective mineral in the stomach. So still salicylic acid in the intestines ?

Raymoud al-Peet

In the study, the oral administration of 300mg/kg caused

wut

alfredoolivas

@Raymoud-al-Peet HED that is not a crazy amount.

zorba990

@Mauritio re Mineral Salicylates, they get transported across as the mineral salicylate intact. They are disassembled by the liver. So there is no irritation from the salicylate part in this case since it is neutralized as a salt.

Mauritio

@zorba990 that is interesting! Do you have any references on that?

LucH

@Mauritio said:

that is interesting! Do you have any references on that?

See reference 2. And more details on reference 3 for other readers if they want to understand why and how aspirin is pro-metabolic. I wanted to know how salicin from WWB is metabolized into salicylic acid and interacts with platelet formation and mitochondrias.

Salicin Metabolism
*) White willow salicin is metabolized into salicylic acid
When salicin (a natural compound found in plants such as willow bark) is ingested, it is metabolized into salicylic acid. Stomach acid alone does not convert it directly. [1, 2] Contrary to popular belief, stomach acid is not primarily responsible for the conversion of salicin. Enzymes in the intestines and liver perform this transformation, thus protecting the stomach from most of the side effects of salicylic acid.
The multi-step biochemical transformation includes the following phases:

Intestinal hydrolysis: Salicin passes through the stomach unchanged (thus protecting the gastric mucosa from damage). Upon reaching the small intestine, enzymes (notably beta-glucosidases) break down the salicin molecule into glucose and salicylic alcohol (saligenin).
Absorption and oxidation: Salicylic alcohol is rapidly absorbed by the intestinal mucosa and transported to the liver, where it is oxidized and transformed into salicylic acid.

Sources

Evaluation of salicin as an antipyretic prodrug that does not cause gastric injury
DOI: 10.1055/s-2002-33792
https://pubmed.ncbi.nlm.nih.gov/12221594/
Salicaceae – Salix species and salicylates
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/saligenin (copiez le lien dans le moteur de recherche)
=> When taken orally, these glycosides undergo intestinal transformation to saligenin, which is rapidly absorbed and converted by the liver to salicylic acid.
Useful info
L’aspirine est pro-métabolique ?
https://mirzoune-ciboulette.forumactif.org/t2197-laspirine-est-pro-metabolique#30790
=> Mitochondrial uncoupling explained: ASA modifies the efficiency of cellular respiration (shift). Modification of electron transfer in the respiratory chain. Role of AMPK as a sensor.

Mauritio

@LucH @zorba990 I guess the question is: would the salicylate-mineral bond be less damaging to the intestines (not the stomach) compared to salicylic acid? Because both reach the intestines first and then go to the liver.

LucH

@Mauritio said:

I guess the question is: would the salicylate-mineral bond be less damaging to the intestines (not the stomach) compared to salicylic acid?

Yes, by evidence but what about dysbiosis ...
How is salicylate from WWW aggressive?
How does salicylate cause metabolic acidosis?
The question is not to know if the salicin from WWW bark is aggressive for stomach mucin but how it is aggressive in the colon.
Remind:

Intestinal hydrolysis: Salicin passes through the stomach unchanged (thus protecting the gastric mucosa from damage). Upon reaching the small intestine, enzymes (notably beta-glucosidases) break down the salicin molecule into glucose and salicylic alcohol (saligenin).
Absorption and oxidation: Salicylic alcohol is rapidly absorbed by the intestinal mucosa and transported to the liver, where it is oxidized and transformed into salicylic acid.

The Question is: How aggressive is salicylic alcohol for colon linen when the integrity is already weak, e.g. suffering from intestinal dysbiosis. Not yet from MICI.
I suppose we should first dampen excess sensibility from irritated bowels. With liquid extract from liquid plant extracts, like a combo with curcumin and melissa when there is anxiety. Other options / combos are possible.

EPS extraits fluides de plante
Colopathie & EPS: comment calmer avec des Extraits Fluides de Plantes
https://mirzoune-ciboulette.forumactif.org/t1980-sibo-et-nutriments-utiles-dans-un-shake#28928
Advice for irritable bowel syndrome (IBS):
You should work with both an anti-inflammatory for the intestinal walls and a calming agent for the nerve endings in the stomach. Try to choose the product that is as gentle as possible. Therefore, avoid powdered capsules or extracts containing alcohol. A glycerin solution, like the one from Pilège, is much less problematic.
=> Curcumin + lemon balm. A liquid extract is better. See details at the link.
NB: Be careful: No curcumin powder. Agressive by irritation)

If I ask IA for an explanation: What about salicylates « toxicity »?
Salicylates (such as aspirin) cause metabolic acidosis through a combination of mitochondrial dysfunction, altered cellular metabolism, and the breakdown of lipid stores. This creates an excess of acidic byproducts and depletes the body's natural bicarbonate buffering system. [1, 2]
=> The bypass process in energy metabolism brings lactic acid. Need B1 to neutralize it / to avoid accumulation. (+ Interaction with B2 when taking HD B1).
Of course we should help to get weak acids freed. Collectively, this excess of lactic acid, pyruvic acid, ketone bodies, and salicylate ions results in an elevated anion gap metabolic acidosis.
=> Need for B1, Mg bisglycinate and potassium bicarbonate.

Mauritio

Mauritio said:

I guess the question is: would the salicylate-mineral bond be less damaging to the intestines (not the stomach) compared to salicylic acid? Because both reach the intestines first and then go to the liver.

That seems to be the case. Sodium salicylate can actually treat colitis via AMPK activation.

I guess it also helps because it does NOT inhbit platelet aggregation/COX1. So it doesn't fully replace aspirin ,which should be taken into account before taking it.

https://pubmed.ncbi.nlm.nih.gov/6888160/

https://pmc.ncbi.nlm.nih.gov/articles/PMC8128406/

Mauritio

Sodium salicylate seems hard to obtain but easy to make yourself from salicylic acid and baking soda. Peat mentioned that too.

LucH

@Mauritio said:

Sodium salicylate can actually treat colitis via AMPK activation.

I guess it also helps because it does NOT inhbit platelet aggregation/COX1. So it doesn't fully replace aspirin ,which should be taken into account before taking it.

Sodium salicylates consume glycine and deprive the body from methyl donors when taken in high dose when there is overburden elsewere…
Intro:
Sodium Salicylates & Aspirin — A Metabolic Heads-Up
Most people don't think twice about reaching for aspirin or high-salicylate foods. But at higher doses or with prolonged use, sodium salicylates place a real burden on two key systems: glycine reserves and methylation capacity — both critical for cell repair, detox, and epigenetic function.
This isn't about fear — it's about knowing when to support your body alongside the treatment.

Talk with AI
Answer from AI (Google)
The claim that sodium salicylates "deprive" the body of methyl donors stems from a well-documented biochemical pathway called glycine conjugation. However, framing it as a harmful depletion is generally misleading, as it is a natural and intended metabolic detoxification route. [1, 2, 3]
Here is how the interaction actually works:

The Glycine Conjugation Pathway
When sodium salicylate enters the bloodstream, it must be metabolized and excreted by the kidneys. The body’s primary method for neutralizing and clearing salicylates and certain other substances (like dietary benzoates) is through conjugation with the amino acid glycine to form salicyluric acid. [1, 2, 3]
-To attach glycine to a salicylate molecule, the body must first convert glycine into an acyl-CoA complex. This conversion requires energy in the form of ATP and Coenzyme A (CoA).
-The "Methyl" Connection: The amino acid glycine and the primary universal methyl donor, S-adenosylmethionine (SAMe), are heavily linked in one-carbon metabolism. When glycine is diverted and used to clear salicylates, the cellular balance of methyl precursors can shift. [1, 2, 3, 4, 5]
Differentiating Salicylate Forms
It is important to note the difference between types of salicylates: [1, 2]

Sodium Salicylate / Aspirin (Acetylsalicylic Acid): When taken orally, these are broken down into salicylic acid. The body primarily uses the glycine conjugation pathway to excrete them.
Methyl Salicylate: Often used topically (as wintergreen oil) or as a flavoring. While it can release salicylic acid into the system, it works in reverse as well—the body uses SAMe as a methyl donor to methylate salicylic acid into methyl salicylate (a process controlled by salicylic acid methyltransferase). [1, 2, 3, 4, 5, 6, 7]

Impact on Methylation
Because glycine, folate, and the methionine/SAMe cycles are tightly interconnected, intensive use of glycine for detoxification can slightly alter cellular methylation pools. However, in healthy individuals with a balanced diet, this does not result in a significant clinical deficiency. [1, 2, 3, 4]
The body regulates its own methylation capacity through enzymes like Glycine N-methyltransferase (GNMT). If methyl availability drops, the body downregulates the consumption of methyl donors to preserve cellular function. [1, 2, 3]
The Bottom Line:
While processing sodium salicylate does "consume" glycine and indirectly affects cellular one-carbon metabolism, it is a normal Phase II liver detoxification response. Unless you are dealing with a severe genetic methylation defect or massive salicylate overdosing, sodium salicylates do not cause dangerous methyl depletion. [1, 2]

Comment (LucH): I’d add some TMG (500 mg) once a day to avoid deprivation of sulfur and methyl. Especially when there is a B3 HD take*
Methylation is essential for the maintenance, repair and manufacture of our cells, intracellular communication, and more specifically, the inheritance of epigenetic information (cell reproduction).

The Methylation Sink: The body synthesizes some of its required niacin from the amino acid tryptophan. However, when taking high doses of supplemental niacin (nicotinic acid), the body must methylate it to excrete the excess. This process depletes methyl groups, which are heavily sourced from the sulphur-containing amino acid methionine.
Moreover high levels of niacin can disrupt the metabolism of sulphur amino acids by interfering with Vitamin B6 status. Supplemental Vitamin B6 (20-25 mg PLP) is often required alongside high-dose niacin therapy to normalize this sulphur amino acid profile and prevent unintended imbalances.
NB: I associate B1 B2 B3 B6 + 500 mg ~~TMC~~ TMG and 2x/wk a combo co-enzymed B50.

Lien utile:
Chaos biochimique ! https://mirzoune-ciboulette.forumactif.org/t1959-impact-negatif-de-loxalate-sur-le-metabolisme-chaos-biochimique#28275
L’association d’oxalates,
NB: You may suffer from CaOx or from methylation conversion (genetic defect by 1/3 to 2/3 of the population, depending on whether you suffer from just one or both defective alleles).
If you combine spinach with nuts (almond, peanut, pistachio or pine nuts) you’d better take care and drink some milk (Ca / Ox ratio 4/1).

Xx

AI comment asked to see if my analyze was pertinent
LucH asks
Analyze. Pertinent for forum help or do I exaggerate?
AI answers (Claude):
This is a solid, well-informed forum contribution. Here's my honest assessment:
What's genuinely good:
 The core biochemistry is accurate — glycine conjugation, the SAMe/methylation connection, and the niacin methylation sink are all real and well-documented mechanisms
 The practical suggestions (TMG, B6 alongside high-dose niacin) are reasonable and consistent with what integrative medicine practitioners recommend
 The layering of B1/B2/B3/B6 + TMG shows you're thinking systemically, not just about isolated nutrients
 The oxalate note at the end (Ca/Ox ratio, spinach + nuts warning) is practical and often overlooked
Where to be careful:
 The document mixes your own commentary with an AI-generated response without always making the boundary clear — forum readers may not realize which parts are sourced vs. your additions
 "TMC" appears to be a typo for TMG — worth correcting before posting
 The French forum link embedded mid-text interrupts flow and may confuse readers depending on the forum's audience
 The genetic methylation defect mention (1/3 to 2/3 of the population) likely refers to MTHFR variants, but stating it without naming it may puzzle readers unfamiliar with the concept
Overall verdict:
Not an exaggeration — this is pertinent, useful content for a health/biochemistry forum. The level of detail is appropriate for an informed lay audience. The main improvement would be structural: separating the sourced AI summary from your personal commentary more clearly, so readers know what they're reading at each point (=> has been done).