Since 2014 I've been using niacin ER as a sublingual to induce a flush and increase mobility.
600-800 mg niacin is what I take as sublingual to generate a flush, which allows to go from wheelchair only to walking with walker up to 100 ft. Exercise for 60 min (peddling, core strength, arm weights). Stiffness is gone from legs.
If you try this start small with 50 mg and work your way up. Use a pill crusher, put the power under tongue. It's very intense, so be careful. You will get used to it eventually, but at first it is an uncomfortable, itchy sunburn feeling.
Managed to time the flush right last week and blew back my neuro's hair when I jumped up and headed down the hall with a walker for 50 feet. The doc kept saying "I've never heard of this"
The clinical pharmacist suggested Prozac as a vasodilator (that's why Raynaud's patients use it). It does have 2 MS trials but they reported MRIs, not mobility results.
So have I found a way to unlock the NAD fire hose, or is it vasodilation, and the oxygen allows better mobility?
So is it
A) As a precursor to NADH, niacin provides electrons for ATP synthesis that fuels mitochondria & energy.
“Any condition associated with poor mitochondrial function, such as chronic fatigue syndrome… may well benefit from niacinamide supplementation.”
But can NAD+ create such a dramatic energy increase in just 20 minutes, enough to get me walking?
Or is it
B) The mechanism and mitigation of niacin-induced flushing
Niacin activates the arachidonic acid cascade to induce vasodilatation. Niacin activates the G-protein coupled receptor 109A (GPR109A) to increase cAMP and releases arachidonic acid from cell membranes. Arachidonic acid is metabolised to produce prostaglandins, ...
There is some historical info on the flush effect. Richard Brickner's original paper "Phenomenon of relief by flush in multiple sclerosis" from the 1950's, they mainly used Amyl Nitrite, CO2 and histamine phosphate USP to achieve the flush, but they did occasionally use Nicotinic Acid. I found a paper that summarized all the subsequent work done in this direction, but the authors dismiss it because it was observational reports; controlled studies weren't as common in the 1950's. Also they seemed to building a case towards the end argument that expanding veins to treat CCSVI was pointless.
'On the historical succession of vessel-based therapies in the treatment of multiple sclerosis'
https://www.academia.edu/attachments/45 ... ?s=regpath
Yes, I think that the vasodilation got blood flowing more efficiently in my brain. Nitroglycerin is usually prescribed to heart failure patients. I've read that long-term use of nitroglycerin can interfere with the body's own vasodilation process through endothelial nitric oxide synthase, eNOS. In a sense, one can become dependent on it. It was an interesting experiment, but I don't know if I could I could talk a doctor into a prescription. By the way, the nitro was in the form of a small sublingual tablet about 4 mm or so in diameter. It was pretty fast acting. I've done some preliminary research into natural vasodilators, but haven't yet found something for a more permanent solution. Though, over the summer I like to eat fresh cherries and watermelon and find that it helps with my blood pressure.SammyJo wrote:NHE, do yo think the vasodilation from the nitro patch enlivened you with oxygen?
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype.
Cell Metab. 2016 Feb 9;23(2):303-14.
- Cellular senescence permanently arrests cell proliferation, often accompanied by a multi-faceted senescence-associated secretory phenotype (SASP). Loss of mitochondrial function can drive age-related declines in the function of many post-mitotic tissues, but little is known about how mitochondrial dysfunction affects mitotic tissues. We show here that several manipulations that compromise mitochondrial function in proliferating human cells induce a senescence growth arrest with a modified SASP that lacks the IL-1-dependent inflammatory arm. Cells that underwent mitochondrial dysfunction-associated senescence (MiDAS) had lower NAD+/NADH ratios, which caused both the growth arrest and prevented the IL-1-associated SASP through AMPK-mediated p53 activation. Progeroid mice that rapidly accrue mtDNA mutations accumulated senescent cells with a MiDAS SASP in vivo, which suppressed adipogenesis and stimulated keratinocyte differentiation in cell culture. Our data identify a distinct senescence response and provide a mechanism by which mitochondrial dysfunction can drive aging phenotypes.