NADH can enter the Blood Brain Barrier and thus was mostly used for Parkinsons and Alzheimer to give an immediate boost. I only benefit from NADH myself (especiallyas brain fog buster) but dont benefit from NAD+ at all.
Other people are the opposite way around. You will have to try it yourself I think.
NADH:
Oral supplementation with NAD+ and
NADH has not shown any significant elevation in plasma or tissue levels of NAD+ , potentially due to inefficient metabolism of NAD+ through the gut, thus leading to poor bioavailability (177). In addition,
oral NADH may not be oxidized to NAD+ in the body, may not be efficiently absorbed by the gastrointestinal system, or may be converted to a product before absorption that cannot yield NAM (34, 35)
NAD+ serves as an electron acceptor, and its reduction leads to the generation of
NADH,
which can be subsequently oxidized by complex I of the ETC to produce NAD+
The
cytosolic/nuclear NAD+ pool is replenished when NADH is converted back to NAD+ in the reactions of the aforementioned shuttles, including the conversion of pyruvate to lactate. NAD+ levels in nuclear, cytosolic, and mitochondrial compartments are also replenished via specific de novo and salvage pathways that are discussed in the text and overviewed in
Fig. 2.
Within mitochondria, NADH is oxidized to NAD+ in the electron transport chain (ETC).
One study investigated the
effect of NADH, the reduced form of NAD+ , on proliferation, cytokine release, and cell redox status of lymphocytes collected from healthy aged subjects (40). Cells exposed to
NADH (500 lM/L) showed increased levels of GSH, and catalase activities, while malondialdehyde and carbonyl proteins are markedly decreased (40),
suggesting a decline in oxidative stress. Recently, it has been shown that treatment with 1 mM NADH increased the expression of nuclear Nrf2, catalase activity,
and total GSH by increasing SIRT2 function (69).
The reduced form of NAD+ and NADP are
NADH (
Fig. 2, Step t) and NADPH (
Fig. 2, Step s), respectively.
These nucleotides serve as hydride donors, in over 400 enzymatic reactions throughout the body involving dehydrogenases, hydroxylases, and reductases (
219). These reduced and phosphorylated forms can interconvert,
but do not alter the levels of NAD+.
Supplementation with either NAD+ and its reduced form
NADH or its precursors
represents a potential therapeutic strategy to slow down the aging process and/or improve the management of age-related degenerative disease.
We found that
NADH dose-dependently increased the levels of GSH, GSSG, and total glutathione (Fig. 3A). The time-course study regarding the effects of NADH treatment on glutathione synthesis showed that NADH increased the GSH and GSSG levels at both 8 and 12 h after the NADH treatment (Fig. 3B), while it did not affect the GSH and GSSG levels at either 2 or 4 h after the NADH treatment
NADH oxidation to NAD+ back and forth:
Its ability to switch between these two forms is what allows NAD to carry out its main function—carrying electrons from one reaction to another in the process of metabolism and energy production.
The electron transporters embedded in the mitochondrial membrane are oxidoreductases that shuttle electrons from NADH to molecular oxygen, another electron acceptor. This loss of electrons is called oxidation. NADH undergoes a reverse reaction, converting back to NAD+
If oxygen is present, the cell can extract substantial chemical energy by breaking down pyruvate through the citric acid cycle, which converts NADH back to NAD+.
In Excercise:
Without oxidation, the cell must use fermentation to oxidize NADH before it builds up to unhealthy levels.
The cytosolic/nuclear NAD+ pool is replenished when NADH is converted back to NAD+ in the reactions of the aforementioned shuttles, including the conversion of pyruvate to lactate. NAD+ levels in nuclear, cytosolic, and mitochondrial compartments are also replenished via specific de novo and salvage pathways that are discussed in the text and overviewed in Fig. 2. Within mitochondria, NADH is oxidized to NAD+ in the electron transport chain (ETC).
Caution:
Multiple studies have also suggested that NADH can affect the oxidative stress state of cells. For example, NADH can produce direct antioxidant effects, while excessive intracellular NADH can induce ‘reductive stress’ [23–25]. Our previous study has also indicated that NADH treatment can increase the intracellular oxidative stress and decrease the survival of glioma cells, which can be prevented by antioxidants [26]. Other studies have suggested that NADH may produce beneficial effects on PD [19,27].
