In a human trial, niacin (vitamin B3) significantly raises NAD+, which has anti-aging effects. - Longevity and Supplements (Live healthy naturally)


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Saturday, August 6, 2022

In a human trial, niacin (vitamin B3) significantly raises NAD+, which has anti-aging effects.

Niacin, a very old vitamin discovered more than 80 years ago, was used in a human study that showed it might boost the presence of an energy component necessary for cellular function. 

NAD+ and niacin

Since it was discovered in 1937 by American researcher Conrad Elvehjem, niacin is a type of water-soluble vitamin B3.
Because it can be made by oxidizing nicotine with nitric acid, niacin was formerly known as nicotinic acid.
The name niacin, which is derived from the words NIcotinic ACid vitamIN, was however used since people are aware that nicotine is the addictive ingredient in tobacco. 

Niacin is one such substance that can enhance NAD+ levels, and there has been a lot of interest in supplements that can accomplish this in recent years.
Before delving into the findings of a recent human study that we want to highlight today, we should talk about NAD+ and why it is significant in the context of metabolism and aging. NAD+ biology plays a crucial role in energy metabolism. 

All live cells contain nicotinamide adenine dinucleotide (NAD), a coenzyme.
Since it is a dinucleotide, two nucleotides are bonded together by their phosphate groups.
Adenine bases are present in one nucleotide while nicotinamide is present in the other. 

NAD transports electrons from one redox reaction to another throughout metabolism, facilitating redox processes.
This indicates that NAD exists in two states in the cell: NAD+, an oxidizing agent, and NADH, its reduced state, which is formed by stealing electrons from other molecules.
The electrons that NADH carries can then be donated by turning it into a reducing agent.
NAD conducts a variety of biological operations, including serving as a substrate for enzymes that modify proteins post-translationally by adding or removing chemical groups, in addition to its primary role in the transfer of electrons.

NAD+ is made from basic building blocks like the amino acid tryptophan, as well as in a more complex manner when nicotinic acid (also known as niacin) or other NAD+ precursors are consumed through diet.
Finally, a salvage pathway receives the products of these several pathways and transforms them back into the active NAD+ form. 


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Niacin's function in NAD+ biology has been clarified by the findings of a recent human study .

Niacin was administered to study participants in doses that increased gradually over a 4-month period, from 250 mg/day to 750–1000 mg/day, followed by a 10-month follow-up treatment period.
The participants were split into two groups: a study group made up of people with mitochondrial myopathy and a control group made up of two healthy people for every person with the disease.
Everyone who took part in the trial started taking niacin supplements at the same time. 

Niacin treatment, according to the researchers, boosted muscle NAD+ levels in the study group by 1.3 times after 4 months and 2.3 fold at 10 months.
The fact that NAD+ levels in the control group did not rise suggests that NAD+ levels in skeletal muscle tissue are tightly regulated and that NAD+ levels will only rise in patients who have lower than normal levels due to diseases like mitochondrial myopathy or, possibly, aging, which also affects mitochondrial function.
This is crucial because it was previously unclear whether niacin administration boosted NAD+ in muscle or if it was simply filtered out and increased NAD+ in the liver. 

After 4 months, supplementation increased the level of whole blood NAD+ by 7.1 fold in the study group and 5.7 fold in the control group in comparison to the participants' baseline levels.
The rise was 8.2 times greater than the baseline after 10 months.
This demonstrates that niacin pills do not merely pass through the liver unprocessed; rather, large amounts of them enter the bloodstream and raise NAD+ levels there. 

Supplementing with niacin also seems to improve body composition.
Participants observed an increase in muscle mass in both the control and study groups, as well as a decrease in whole-body fat % in the controls.
The patients' muscle strength improved after 10 months of niacin administration.

Additionally, the researchers saw that visceral fat was lowered by 25% and hepatic fat was cut in half.
Both of these fat deposits have been associated with a higher risk of developing metabolic syndrome.
Niacin had little effect on the body's surface fat, but it had a considerable influence on the harmful fat that surrounded the organs. 

Niacin has also been associated with elevated blood glucose levels, which is a risk factor for developing diseases like diabetes.
The study's findings demonstrated that, after four months of supplementation, niacin did raise fasting glucose levels in both the study and control groups.
Glycosylated hemoglobin, a measure of long-term blood sugar levels, was unaffected.

According to the findings of this study, niacin does appear to raise blood glucose levels; however, as other studies have shown [2], the advantages seem to vastly exceed any potential drawbacks of a modest increase in blood glucose.

The individuals' hemoglobin concentration did slightly fall after 4 months of niacin administration, although this level never dropped below typical healthy ranges throughout the trial. This is another negative effect worth noting. 

NAD+ is a redox-active metabolite whose depletion has been linked to mice' accelerated aging and development of degenerative illnesses.
NAD+ repletion may help patients with degenerative illnesses feel better, but it is unclear whether NAD+ depletion happens in those people.
Here, we describe patients with adult-onset mitochondrial myopathy who also have a systemic NAD+ deficit.
Niacin, a vitamin B3 form, was given to patients and their matched controls for either 10 or 4 months at an escalating dose (up to 750–1,000 mg/day; NCT03973203).
All participants experienced blood NAD+ increases of up to 8 times, and patients' muscle NAD+ levels matched those of their controls.
While all individuals' muscle strength and mitochondrial biogenesis increased, several patients displayed a predisposition toward anemia. Muscle metabolome in patients changed in favor of controls, and liver fat even dropped by 50%.
Our research suggests that blood tests can be used to detect NAD+ shortage and that niacin is a potent NAD+ enhancer for the treatment of mitochondrial myopathy. 


When we think about NAD+ biology in the context of metabolism and aging, these findings are thought-provoking.
Other precursor supplements that could raise NAD+ in people, including NR and NMN, are relatively expensive in comparison to niacin, which is affordable and widely available.
These findings demonstrate that niacin can increase human NAD+ levels in blood and muscle, as well as possibly in other tissues.

Unsurprisingly, despite the exciting nature of these findings, we do not support the use of supplements or any particular supplement seller, and the discussion presented here is only for scholarly purposes.

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