Hi
Nas, vitamin B1 is in the POIS Cascade. Please see the "
The POIS Cascade stack: With food, twice daily (fat soluble):" section of the
original post for details. I also discuss B1 in the explanation of the POIS Cascade Theory which gives the reason for vitamin B1 in the stack (right below the figure in the
original post). If you are not seeing the full relief after the orgasm:
- It might be worth getting your vitamin D3 levels checked and then adjusting the dose accordingly.
- Make sure you take the second dose. You mentioned that sometimes you don't take the second dose. On an orgasm day I always make sure to get the second dose in, because if I miss the 2nd dose then I too would have some lingering symptoms.
- Reducing arachidonic acid (AA) intake is just as important as increasing omega-3 intake. Plants (fruits, vegetables, nuts) don't produce. This means that all your arachidonic acid (AA) is coming from animal fat. Eat leaner cuts of meat or reducing meat consumption are two strategies. Humans don't have a dietary requirement for AA. We can produce all the AA we need from the omega-6, linoleic acid.
Without knowing how you have modified the stack, this is the best answer I can give.
Hi
Shep, cortisol and progesterone both use a similar mechanism to work in synergy with
vitamin D3 (1,25(OH
2)D
3) to reduce inflammation [1]. In the figure below vitamin D3 (1,25(OH
2)D
3) binds to the vitamin D receptor (VDR) and cortisol binds to the glucocorticoid receptor (GCR). Both actions are required for cortisol to have an anti-inflammatory effect. When D3 levels are low cortisol has a pro-inflammatory effect.
Figure 1 from [1]: Inhibition of the p38 MAP kinase pathway by 1α,25(OH)2D3 and a mechanism for the synergistic anti-inflammatory effects of 1α,25(OH)2D3 and glucocorticoids. Proinflammatory stimuli lead to p38 MAP kinase phosphorylation and activation which subsequently induces expression of many proinflammatory proteins such as IL-6 and TNFα. Vitamin D3 induces MKP1 expression which dephosphorylates and inactivates p38 MAP kinase. Vitamin D3 stimulates glucocorticoid-induced MKP1 expression via enhanced expression of Med14. When vitamin D levels are low, the body tries to compensate by producing more progesterone levels [2]. So if someone has high cortisol and progesterone levels,
this could mean that there is a vitamin D deficiency. Also, if inflammation is high, the body may require more vitamin D3 than the usually daily recommendation. But I think both vitamin D3 and cortisol (or progesterone) are required for the anti-inflammatory effect shown in the above figure.
Vitamin D3 is a strong inhibitor of inflammatory cytokines and NF-kB with an IC50=0.1 uM (roughly 4000 IU per day) [3]. For details about why cytokines, NF-kB and COX-2 are important, see the figure in the
original post. For information on the IC50 value see
Cost effective alternatives for omega-3One last word on vitamin D3. Because of the process depicted in the figure above, it is required for mast cell stabilization [4]. And when there is a vitamin D3 deficiency, mast cells will automatically destablize/degranulate without any external inflammatory stimulus[4].
Hi
dwight_schrute, I don't know much about olive oil, but I know it contains COX-1 and COX-2 inhibitors. The figure in the
original post explains why I would think a COX-2 inhibitor would be beneficial. You can increase the production of DAO with vitamin C, but I personally haven't found this to be useful.