Can't say I went full-vegan, but I did adopt a much healthier diet. But, like, I'd expect to eke out at least a little benefit from that. Regardless, I'll have time to try again in the future.
Hi Bombadier,
It is great that you are eating healthier and feeling better. Good health is always positive. There are some aspects of the vegan diet that I did not fully appreciate when I first wrote the
original post. I knew that eating vegan made me feel better, but I didn't always connect it with the my understanding of how the POIS Cascade stack worked. I think now I can explain a little better why going full-vegan is important.
Part of the goal in the POIS Cascade Stack is to replace arachidonic acid (AA) with other omega fatty acids that do not produce
inflammatory prostaglandins like PGE
2. The reason for eating a vegan diet is that plants do not produce arachidonic acid (AA).
Eicosanoids are a group of mostly inflammatory molecules (like prostaglandin PGE
2 and Leukotriene LTB
4) produced from the arachidonic acid cascade when AA is
oxidized by C
OX or L
OX enzymes. In the study
Ref1, they show that omega-3 fatty acids like EPA can only reduce inflammatory prostaglandins from the AA cascade when dietary AA consumption from food is eliminated. They tested 4 groups of animals, (1)the control group (OA) with a normal healthy diet, (2)a group fed a high-AA/low-EPA diet (AA), (3)a group fed a low-AA/high-EPA diet (EPA), (4)a group fed an equal amount of AA and EPA (AA+EPA). The total eicosanoids produced from the AA cascade are summed (pooled) in the below chart.
This (AA+EPA) result shows that it does not matter how healthy a diet seems to be. If the amount of AA in the diet is significant, then omega-3 supplementation has very little effect on reducing AA and its effects in the body. Other studies testing AA+DHA show similar results. This is because cell walls in the body have a preference to store AA over omega-3s. I'm still not sure how CLA works, but it seems to modify the body's composition of other omega fatty acids (shifting the type of fat that the body stores).
A more detailed look at the data shows that a low-AA/high-EPA diet (EPA) not only reduces inflammatory molecules (PGE
2, PGF
2a, LTB
4, LTE
4), but it also boost the relatively anti-inflammatory molecule LTE
5.
"Dietary AA is almost exclusively associated with animal products." (
Ref1)
The omega-6 arachidonic acid is only produced naturally in animal fat. The below table shows some of the foods with the highest AA content.
This means that removing AA from your diet will probably mean removing all sources of animal fat from your diet (vegan diet). If you are not on a low-AA diet, I don't see any advantage to taking omega-3 supplements.
Only when you are on a low-AA (vegan) diet should you expect benefits from the omega-3s in the POIS Cascade stack. It is important to note that most inflammatory molecules (i.e. cytokines, histamine, etc...) rely upon the arachidonic acid cascade to cause inflammation. If the AA cascade is blocked, molecules like histamine and IL-8 cannot produce inflammation or inflammatory diseases. Vegan diets are typically low in vitamin D3, vitamin B12 and creatine. But a vegan diet supplemented with vitamin D3, B12 and a methyl-donor (betaine TMG) should
in-principle reduce inflammation throughout the body and produce better health.
My medical test show that my recent markers for inflammation are low (9. platelet counts, 9. sedimentation rate, 10. cholesterol, 12. homocysteine, 13. tryptase). Also, I rarely get
DOMS from exercise any more. Maybe that means something or maybe it doesn't. In any case, I'm sorry for the confusion on my part. I did not always understand how important this type of diet was to my results. But I hope this clarifies the significance of the vegan diet in this stack.
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For those that cannot eat vegan, an alternative way of reducing prostaglandins and inflammation is to take COX and NF-kappaB inhibitors. For example, taking one (only one) of the follow COX inhibitors:
--Aspirin (500mg, 90 minutes pre-activity)
--Indomethacin (50mg, 2 hours pre-activity, with food, 4.5-hour half-life)
--Naproxen (500mg, 3 hours pre-activity, with food, 8-hour half-life)
and some of the following NF-kappaB inhibitors:
--vitamin D3 (2000-4000 IU daily, sublingual)
--caffeine (65-100mg, 90 minutes pre-activity)
--Tylenol/Paracetamol/acetaminophen (250-500mg, 95 - 115 minutes pre-activity)
--selenium/selenomethione (100-200 mcg daily, dosage depends on the amount of selenium from diet)
Flavonoids like luteolin, quercetin and curcumin can also downregulate NF-kB and inhibit COX, but only when they are consumed daily over time through food, teas and/or supplements (see
post1,
post2).
All COX inhibitors have vasoconstriction properties since most protaglandins (like PGE
2) are vasodilators. Caffeine and paracetamol are also vasoconstrictors (see
Betaherpesvirinae stack and About Vasoconstrictors notes). Naproxen has an 8-hour half-life and can help reduce nocturnal emission (NE) induced POIS when taken before bed-time. However, naproxen has more side-effects than aspirin or indomethacin when taken daily over several months. Some anti-histamine medications such as Benadryl (diphenhydramine) and Claritin (loratadine) are associated with long-term memory loss and cognitive decline (see
post). Zyrtec/Xyzal (cetirizine/levocetirizine) and Allegra (fexofenadine) are not associated with cognitive decline.
Consult with your physician or medical care professional before taking pharmaceutical drugs. Make sure these do not interact with your current medications.Ref1: "
Antithetic relationship of dietary arachidonic acid and eicosapentaenoic acid on eicosanoid production in vivo" (1994)