Correct. As the lactic acid gets you only like 400m, really fast
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Posted 23 December 2013 - 11:06 PM
Posted 23 December 2013 - 11:13 PM
Edited by Ukko, 23 December 2013 - 11:14 PM.
Posted 23 December 2013 - 11:26 PM
Edited by Ukko, 24 December 2013 - 12:00 AM.
Posted 24 December 2013 - 03:04 AM
aberration in mitochondrial complex I NADH dehydrogenase activity can profoundly enhance the aggressiveness of human breast cancer cells
And complex I NADH dehydrogenase is...
http://en.wikipedia....se_(ubiquinone)Complex I (EC1.6.5.3) (also referred to as NADH:ubiquinone oxidoreductase or, especially in the context of the human protein, NADH dehydrogenase (ubiquinone)) is an enzyme of the respiratory chains of myriad organisms from bacteria to humans. It catalyzes the transfer of electrons from NADH to coenzyme Q10 (CoQ10) and, in eukaryotes, it is located in the innermitochondrial membrane. It is one of the "entry enzymes" of oxidative phosphorylation in the mitochondria.[1]
I wonder if this can help explain the effects of C60/EVOO due to possible positive effects by C60 on the electron transfer chain in the inner mitochondrial membrane? We may have already solved this NAD+ issue with C60/EVOO.....
When NADH is reduced to NAD, the electron transport chain accepts the electrons from the molecules. As the electrons are transferred to each carrier within the electron transport chain, free energy is released and is used to form ATP. Oxygen is the final acceptor of electrons in the electron transport chain. Without oxygen, the electron transport chain becomes jammed with electrons. Consequently, NAD cannot be produced.
Posted 24 December 2013 - 04:10 AM
Posted 24 December 2013 - 04:52 AM
Edited by trance, 24 December 2013 - 04:53 AM.
Posted 24 December 2013 - 04:57 AM
Posted 24 December 2013 - 05:43 AM
Posted 24 December 2013 - 07:35 AM
Posted 24 December 2013 - 07:37 AM
Posted 24 December 2013 - 05:53 PM
I think Darryl mentioned sublingual NR and NAD. Anybody try this? Do they readily absorb sublingually?
Edited by Ukko, 24 December 2013 - 06:01 PM.
Posted 26 December 2013 - 07:08 PM
Posted 26 December 2013 - 07:38 PM
Rats received 2 h ischemia by intraluminal filament and were then reperfused. Taurine (50 mg/kg) was administered intravenously 1 h after ischemia. Treatment with taurine markedly reduced neurological deficits, lessened brain swelling, attenuated cell death, and decreased the infarct volume 72 h after ischemia. Our data showed the up-regulation of PARP and NF-κB p65 in cytosolic fractions in the core and nuclear fractions in the penumbra and core, and the increases in the nuclear poly (ADP-ribose) levels and the decreases in the intracellular NAD+ levels in the penumbra and core at 22 h of reperfusion; these changes were reversed by taurine. Moreover, taurine significantly reduced the levels of tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and intracellular adhesion molecule-1, lessened the activities of myeloperoxidase and attenuated the infiltration of neutrophils in the penumbra and core at 22 h of reperfusion.
In this study the PARP-1 inhibiting capacity of caffeine and several metabolites as well as other (methyl)xanthines was tested using an ELISA-assay with purified human PARP-1. Caffeine itself showed only weak PARP-1 inhibiting activity, whereas the caffeine metabolites 1,7-dimethylxanthine, 3-methylxanthine and 1-methylxanthine, as well as theobromine and theophylline showed significant PARP-1 inhibiting activity. Further evaluation of these compounds in H2O2-treated A549 lung epithelial and RF24 vascular endothelial cells revealed that the decrease in NAD+-levels as well as the formation of the poly(ADP-ribose)polymer was significantly prevented by the major caffeine metabolite 1,7-dimethylxanthine. Furthermore, H2O2-induced necrosis could be prevented by a high dose of 1,7-dimethylxanthine.
In this study, the in vitro PARP-1-inhibiting effect of various flavonoids was investigated. The flavonoids myricetin, tricetin, gossypetin, delphinidin, quercetin, and fisetin were identified as significant inhibitors of the purified enzyme. Further evaluation of these compounds in N-methyl-N′-nitro-N-nitrosoguanidine-treated human pulmonary epithelial cells showed that the formation of the poly(ADP-ribose) polymers, as well as the decreased NAD+ levels, was reduced by quercetin, fisetin, and tricetin. Finally, IL-8 production of LPS-stimulated human pulmonary epithelial cells could be significantly reduced by these flavonoids.
PARP-1 activation by hydrogen peroxide decreased intracellular NAD+ levels in human pulmonary epithelial cells, which was found to be prevented in a dose-dependent manner by theophylline, a widely used compound in the treatment of COPD. This enzyme inhibition by theophylline was confirmed in an ELISA using purified human PARP-1 and was found to be competitive by nature.
The active metabolite of vitamin D, 1α,25-dihydroxy-vitamin D3, is a PARP inhibitor. UV irradiation-mediated PARP activation in human keratinocytes can be inhibited by treatment with vitamin D, 7-dehydrocholesterol or 1α,25-dihydroxyvitamin D3. Inhibition of cytochrome P450 reversed the PARP inhibitory action of vitamin D and 7-dehydrocholesterol, indicating that conversion to 1α,25-dihydroxyvitamin D3 mediates their PARP inhibitory action. Vitamin D may protect keratinocytes against over-activation of PARP resulting from exposure to sunlight. PARP inhibition may contribute to the pharmacological and anti-inflammatory effects of vitamin D.
Various vitamins and vitamin-like substances inhibited the activity of poly(ADP-ribose) synthetase in vitro. The most potent were essential fatty acids, i.e. arachidonic acid, linoleic acid, and linolenic acid; their 50% inhibitory concentrations (IC50) were 44–110 μM, indicating a higher potency than nicotinamide, a well-known vitamin inhibitor (IC50 = 210 μM). Vitamins K3, K1, and retinal were the next strongest inhibitors, followed by α-lipoic acid, coenzyme Q10, and pyridoxal 5-phosphate.
Edited by Darryl, 26 December 2013 - 08:36 PM.
Posted 26 December 2013 - 07:55 PM
Posted 26 December 2013 - 08:11 PM
Posted 26 December 2013 - 08:21 PM
@bocor: Sublingual NADH lozenges might work (at a much higher cost than nicotinic acid or nicotinamide riboside), but something like the Source NaturalsCoenzymated B3 will be hydrolysed to nicotinamide during digestion.
Posted 26 December 2013 - 08:21 PM
Posted 26 December 2013 - 08:33 PM
im still not understanding all this talk about NAD precursors supplementing with NAD is direct makes more sense right?Im still waiting for my Coenzymated b3 (NAD) in the mail will update
Posted 26 December 2013 - 08:53 PM
Posted 26 December 2013 - 09:32 PM
Posted 26 December 2013 - 10:58 PM
Edited by Darryl, 26 December 2013 - 11:05 PM.
Posted 27 December 2013 - 12:01 AM
Posted 27 December 2013 - 04:01 AM
Edited by Darryl, 27 December 2013 - 04:55 AM.
Posted 27 December 2013 - 03:45 PM
Posted 27 December 2013 - 06:05 PM
Edited by trance, 27 December 2013 - 06:07 PM.
Posted 27 December 2013 - 07:06 PM
Posted 28 December 2013 - 03:26 AM
In The H Factor Solution, James Braly, 2009, says that more than 1000 mg of niacin can boost homocysteine. "... the removal of niacin from the body requires it to become methylated." He recommends matching niacin doses with an equal amount of TMG if you take more than 500 mg niacin.
Posted 28 December 2013 - 04:24 AM
As I reported earlier, I've been taking 250mg NR daily for the last 6 months. There's no flushing from this dose if I take it alone, and it's completely "survivable" -- why wouldn't it be? I doubt there would be any noticeable difference at 500mg.
I haven't eaten yet, I'll give a 500mg dose a try right now.
Posted 28 December 2013 - 05:01 AM
Posted 28 December 2013 - 06:50 AM
Sure, I understood that.
I was interested if any flush occurred, or any other effect was noticed, at double the recommended dose of NR on an empty stomach. There was nothing discernible from norm, as noted.
The other dosing protocol suggested would still be prohibitive at today's retail cost, and non-sustainable from that aspect for most.
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