haidut

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Comparisons with treatment with niacin to raise HDL and lower LDL has been considered the gold-standard for all new statin drugs. However, it has been shown that both niacin and niacinamide have the same protective effects on cardiovascular disease (CVD) despite the fact that niacinamide has little to no effect on cholesterol levels. This study shows that the positive effects of the vitamin B3 varieties on CVD are NOT due to effects on cholesterol levels but due to vitamin B3 directly blocking inflammation of blood vessels through a specialized "receptor" unique to vitamin B3. So, treating CVD is achievable by lowering inflammation, rather than cholesterol that is only present in blood vessels as a protective reaction. This simple fact has been known for over 100 years and yet is still overlooked clinically by medical "experts" who are often on the payroll of Pfizer and Co.
Finally, the potent anti-inflammatory effect of vitamin B3 may explain its positive impact on other inflammatory conditions like MS and RA.

Nicotinic acid blocks immune cells in atherosclerosis
"...In genetically modified mice, Max Planck researchers were able to demonstrate that nicotinic acid strongly inhibits the progression of atherosclerosis, just as in humans. In mice that lacked the nicotinic acid receptor GPR109A, the agent had no effect on atherosclerosis. In contrast to human cholesterol levels, the cholesterol levels of mice remain constant despite the administration of nicotinic acid. “This suggests that nicotinic acid does have an anti-atherosclerotic effect via its receptor, but that this is not due to a change in the lipid concentration”, says Stefan Offermanns, Director at the Max Planck Institute in Bad Nauheim. Further studies showed that the nicotinic acid receptor is present in different immune cells. For example, the receptor was found in macrophages in atherosclerotic blood vessels. When the scientists intentionally blocked the receptor in the cells of the immune system, the effect of the nicotinic acid disappeared. This suggests that the receptor expressed by immune cells transmits the anti-atherosclerotic effect. Finally, experiments showed that nicotinic acid keeps macrophages from entering the atherosclerotic vascular wall by activating its receptor, thereby halting chronic inflammation. Furthermore, nicotinic acid changes the gene expression in the immune cells of the vascular wall and thereby stops the inflammatory activity of these cells. They thus become more efficient at removing cholesterol stored in the atherosclerotic vascular wall. These findings suggest that the beneficial impact of nicotinic acid, one of the oldest agents used against atherosclerosis, inhibits inflammation in vascular walls. Targeted anti-inflammatory measures are therefore generally an efficient principle for treating atherosclerosis and preventing cardiovascular diseases. “Moreover, the effects of nicotinic acid on different cells in the immune system point to new possibilities for treating other diseases which are associated with excessive immune reactions or chronic inflammation”, says Offermanns."
 

drk

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Any references you are aware of that offer guidance re dose of naicinamide?
 

ddjd

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Jul 13, 2014
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Comparisons with treatment with niacin to raise HDL and lower LDL has been considered the gold-standard for all new statin drugs. However, it has been shown that both niacin and niacinamide have the same protective effects on cardiovascular disease (CVD) despite the fact that niacinamide has little to no effect on cholesterol levels. This study shows that the positive effects of the vitamin B3 varieties on CVD are NOT due to effects on cholesterol levels but due to vitamin B3 directly blocking inflammation of blood vessels through a specialized "receptor" unique to vitamin B3. So, treating CVD is achievable by lowering inflammation, rather than cholesterol that is only present in blood vessels as a protective reaction. This simple fact has been known for over 100 years and yet is still overlooked clinically by medical "experts" who are often on the payroll of Pfizer and Co.
Finally, the potent anti-inflammatory effect of vitamin B3 may explain its positive impact on other inflammatory conditions like MS and RA.

Nicotinic acid blocks immune cells in atherosclerosis
"...In genetically modified mice, Max Planck researchers were able to demonstrate that nicotinic acid strongly inhibits the progression of atherosclerosis, just as in humans. In mice that lacked the nicotinic acid receptor GPR109A, the agent had no effect on atherosclerosis. In contrast to human cholesterol levels, the cholesterol levels of mice remain constant despite the administration of nicotinic acid. “This suggests that nicotinic acid does have an anti-atherosclerotic effect via its receptor, but that this is not due to a change in the lipid concentration”, says Stefan Offermanns, Director at the Max Planck Institute in Bad Nauheim. Further studies showed that the nicotinic acid receptor is present in different immune cells. For example, the receptor was found in macrophages in atherosclerotic blood vessels. When the scientists intentionally blocked the receptor in the cells of the immune system, the effect of the nicotinic acid disappeared. This suggests that the receptor expressed by immune cells transmits the anti-atherosclerotic effect. Finally, experiments showed that nicotinic acid keeps macrophages from entering the atherosclerotic vascular wall by activating its receptor, thereby halting chronic inflammation. Furthermore, nicotinic acid changes the gene expression in the immune cells of the vascular wall and thereby stops the inflammatory activity of these cells. They thus become more efficient at removing cholesterol stored in the atherosclerotic vascular wall. These findings suggest that the beneficial impact of nicotinic acid, one of the oldest agents used against atherosclerosis, inhibits inflammation in vascular walls. Targeted anti-inflammatory measures are therefore generally an efficient principle for treating atherosclerosis and preventing cardiovascular diseases. “Moreover, the effects of nicotinic acid on different cells in the immune system point to new possibilities for treating other diseases which are associated with excessive immune reactions or chronic inflammation”, says Offermanns."
apart from its serotonin, prostaglandin, histamine raising, what is the main drawback to regular niacin. I have heard its helpful for NAFLD in ways niacinamide isnt
 

haidut

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apart from its serotonin, prostaglandin, histamine raising, what is the main drawback to regular niacin. I have heard its helpful for NAFLD in ways niacinamide isnt

First time I hear about this. What would be the mechanism through which niacin is beneficial for NAFLD while niacinamide is not?
 

aguilaroja

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Comparisons with treatment with niacin to raise HDL and lower LDL has been considered the gold-standard for all new statin drugs. However, it has been shown that both niacin and niacinamide have the same protective effects on cardiovascular disease (CVD) despite the fact that niacinamide has little to no effect on cholesterol levels. This study shows that the positive effects of the vitamin B3 varieties on CVD are NOT due to effects on cholesterol levels but due to vitamin B3 directly blocking inflammation of blood vessels through a specialized "receptor" unique to vitamin B3. ..
Nicotinic acid blocks immune cells in atherosclerosis
"...These findings suggest that the beneficial impact of nicotinic acid, one of the oldest agents used against atherosclerosis, inhibits inflammation in vascular walls. Targeted anti-inflammatory measures are therefore generally an efficient principle for treating atherosclerosis and preventing cardiovascular diseases. “Moreover, the effects of nicotinic acid on different cells in the immune system point to new possibilities for treating other diseases which are associated with excessive immune reactions or chronic inflammation”, says Offermanns."

The niacinamide metabolite, its methylated form, N1-methylnicotinamide (MNAM), has been getting attention as a posited beneficial agent. MNAM’s alleged helpful actions of increasing prostacyclin and nitric oxide go counter to Dr. Peat’s ideas but conform to recent trends in commercial pharmacology. There’s still much speculation about pathways and actions, nudged along commerce-driven dogma.

I suspect that MNAM niacinamide metabolite more significantly shunts PUFA droplets away from more harmful places, a kind of PUFA harm reduction as adaptive response.

N1-methylnicotinamide (MNAM) as a guardian of cardiovascular system. - PubMed - NCBI
“Atherosclerosis is identified as the formation of atherosclerotic plaques, which could initiate the formation of a blood clot in which its growth to coronary artery can lead to a heart attack. N-methyltransferase (NNMT) is an enzyme that converts the NAM (nicotinamide) to its methylated form, N1-methylnicotinamide (MNAM). Higher levels of MNAM have been reported in cases with coronary artery disease (CAD). Further, MNAM increases endothelial prostacyclin (PGI2) and nitric oxide (NO) and thereby causes vasorelaxation. The vasoprotective, anti-inflammatory and anti-thrombotic roles of MNAM have been well documented; however, the exact underlying mechanisms remain to be clarified. Due to potential role of MNAM in the formation of lipid droplets (LDs), it might exert its function in coordination with lipids, and their targets. In this study, we summarized the roles of MNAM in cardiovascular system and highlighted its possible mode of actions.”

“...existence of LDs[lipid droplets] in the endothelial cells has recently been reported (Kuo, Lee, & Sessa, 2017; Majzner et al., 2016). The main functions of endothelial LDs are prevention of lipotoxocity and transfer of FA to neighboring cells .… The uptake of polyunsaturated fatty acids (PUFAs) like arachidonic acid (AA) induces formation of LDs in the endothelial cells as unsaturation degree of endothelial LDs is associated to environment… High concentration of PUFAs along with MNAM boosts generation of endothelial LDs (Majzner et al., 2016). The exact role of MNAM in the context of PUFAs uptake has not yet been determined. However, it is believed that it acts as a cationic carrier either for membrane or for fatty acids negative charge… On the other hand, TNFα induces formation of endothelial LDs with unsaturated nature…, and also up regulates NNMT expression in skeletal myoblasts .… It has been indicated that unsaturated LDs are generated in pathological states and contain arachidonyl lipids, which are linked to prostaglandin synthesis…”
 
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