Filip left a comment asking about aspirin, this was another one of those comments turned into post type deals.
So speaking of aspirin. There are some dots to connect here, and definitely some different trains of thought that you can ride, but have a look at the following articles and follow the paper trail.
Paterson, J. R., Baxter, G., Dreyer, J. S., Halket, J. M., Flynn, R., & Lawrence, J. R. (2008). Salicylic acid sans aspirin in animals and man: persistence in fasting and biosynthesis from benzoic acid. Journal of Agricultural and Food Chemistry, 56(24), 11648–52. doi:10.1021/jf800974z
“To examine the possibility of a gastrointestinal bacterial source for SA, two small groups of germ-free mice were assayed for SA. The pooled serum from six mice treated with neomycin, 100 mg/kg/day, for 4 days before sacrifice had a slightly higher concentration of SA in serum (0.309 μmol/L) than the pooled serum sample from six untreated animals (0.268 μmol/L). Another germ-free animal model studied was the Sprague−Dawley rat delivered by caesarean section, reared in a sterile environment, and fed sterilized food. A group of eight such germ-free animals had a pooled serum SA level of 0.166 μmol/L, approximately 2.5 times greater than the pooled serum salicylic acid level of 0.069 μmol/L from a group of control animals. The net effect of minimizing or eliminating a contribution from colonic bacteria in these animal models was therefore enhancement of serum SA levels in the host animal.”
“Results of SA levels in a large variety of animals showed that those species regarded as primarily carnivorous had levels comparable to those measured in herbivores. Some bacteria, notably mycobacterial, yersinia, and pseudomonas species, synthesize SA to enhance iron chelation, so there was a possibility that gut, particularly colonic, bacteria might be the source of SA not readily explicable by lack of dietary exposure. However, preliminary study of two germ-free animal models reported here showed the net effect of minimizing or eliminating a contribution from colonic bacteria was, in fact, an increase in serum SA levels.”
A review of the literature by Heiby cites an interesting experiment on rat that perhaps shed some light on the risk of stomach bleeding. Aspirin was far more toxic to rats fed a high carbohydrate diet than it was to rats fed a high protein diet. A deficiency of magnesium increased this toxicity, especially in pregnant animals. Gastric ulceration in non-pregnant rats was very severe on the high carbohydrate diet (14, p. 255). On the basis of these animal studies, it is interesting to speculate that the apparent increase over the last half-century in the risk of stomach bleeding due to aspirin use may be the result of the large increase in dietary carbohydrate during the same period.
I originally came across that here. But as it is written there, there are differences in the in-text citations and I was not able to track down a paper to verify that observation.
And Peter mentions this (there is also a bit on coconut oil in the following paragraph if you follow the link, for the few that asked about that):
Anyone reading Chris or Emma’s blogs will realise that aspirin, and possibly other related salycilates from plants, cause the pancreas the secrete extra insulin. Avoid. Gluten and wheat germ agglutinin (both from wheat, barley and rye) are (or contain) insulin mimetics, avoid. Casein stimulates insulin secretion, avoid. Pharmaceutical NSAID probably do the same as salycilates, avoid if possible.
O.k. Now for some of my thoughts.
As for daily use, I don’t know. In general, I like things that uncouple the mitochondria. However, to speculate, there is a difference between an energy substrate that uncouples mitochondria and a compound that uncouples mitochondria. I think that the latter can deplete ATP to an extent that is undesirable (which would be dose dependent)., but I can also think of some situations where that type of uncoupling would confer some desired effects. In my endotoxin and fructose post I talked about depleted ATP impacting tight-junction (occluding junctions or zonulae occludentes) integrity. Which makes this interesting. Whereas some saturated fat (e.g. palmitic acid) which also uncouples the mitochondria maintains tight-junction integrity.
Speculating some more, a lot of people get nosebleeds from aspirin use. When you get a nose bleed, you notice it, blood dripping out of your nose, that to me is like a rupture. You don’t notice one or two blood cells on your upper lip, you notice a good amount of blood coming out. That is a tremendous failure in the integrity of the tight-junctions in capillaries. Now imagine consuming some fructose (which is depleting ATP too and probably weakening tight-junctions). It is hardening your arteries and when they are nice and calcified, lets say you take some aspirin and one of your calcified capillaries “fractures”, but see now your blood is thin and blood comes spouting out. Sounds quite like an aneurysm.
Because fructose isn’t going to calcify your vascular system overnight, I’m sure little microscopic breaks happen here and there in the tight-junctions which get clotted. Imagine a wooden handrail that thousands of people have run their hands across, some parts keep their shine, other parts chip off and loose their luster. It’s a handrail with character. Or have you ever filled a balloon up and over time you notice certain parts of it are thin and thick as the air diffuses out? Between the clotting and inflammation, I’d say damaged parts of the vascular system might swell much like the thick and thin sections of a balloon under uneven pressure caused by variations in thinness and thickness of vascular/capillary walls. Have you ever untied a worn out balloon that has been sitting in the sun and tried to blow it back up again? It’s never quite the same, and I would imagine the brittleness from the deteriorated rubber would be an interesting way to think about the pathophysiology of a nose bleed or aneurysm. It just fractures at a weak point and pops if you blow it up big enough e.g. a sudden increase in heart rate.
O.k. now this brings me back to aspirin. Sometimes when I’m writing with an old fashioned pencil the tip breaks off in a way where you can kind of fit it back into the pencil and continue writing with it. That of course is not very versatile because you almost always have to write with less pressure and kind of turn the angle of the pencil where the lead broke to keep the bit of lead in. If you have some clots just waiting to break off it would make sense to lower the viscosity of your blood so as not to disturb them. I would say aspirin would be pretty useful for that.
Anyway, I think aspirin might be useful to solve some acute symptoms. And hey, maybe a low-dose aspirin is legit. But don’t forget about the first paper. Like I said, there are a few different trains of thought to ride. Preventing an “aspirin deficiency” would be a better bet. At least that is what I think.