Feeding geese nicotnic acid improves muscle & fat tone, bone density, lipid metabolism. 80mg/kg per day was found to be optimal dose for improving quality of geese tibia ( longest bone in leg ).
In 58 patients with fatty liver disease, the ones with the most niacin in their diet had the most favorable outcome, with a 37% reduction in liver fat after 9 months of lifestyle interventions, vs only 10% reduction in the patients eating the least niacin.
In rats, supplementing with high levels of nicotinic acid in diet before experiencing cell damage (induced by tert-butyl hydroperoxide injections) helped protect the liver, preserving its normal structure and improving its ability to absorb zinc, a beneficial element. This effect was less pronounced if the NA was increased after the cell damage had occurred. Rats with a deficiency of nicotinic acid in their diet exhibited the highest level of liver damage.
Iron deficiency impairs body converting tryptophan to niacin. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks had linear growth responses to either nicotinic acid or tryptophan supplementation. Low bio-available iron contributes to niacin deficiency in populations.
Out of 26 patients with moderate ulcerative colitis (inflammation of the colon) who were unresponsive to conventional treatments, 92.3% responded positively and 88.5% went into remission after receiving a daily niacin enema treatment for 6 weeks. The had no serious side effects, showed notable improvements in intestinal healing, reduced symptoms like rectal bleeding and stool frequency. Niacin is a promising, well-tolerated alternative for inducing clinical remission of ulcerative colitis.
A study in mice found that niacin supplementation increased NAD+ levels in the testes, which led to an improvement in sperm count and sperm motility. NAD+ deficient mice have ~30% smaller testes (balls) than the control mice (~1.5g vs ~2.17g). NAD+ is essential for spermatogenesis and that NAD+ deficiency leads to male infertility.
Niacin supplementation may prevent premature menopause. Women with premature menopause have significantly lower levels of niacin. Niacin levels lowest in women most severe symptoms.
Review of many clinical trials concludes niacin supplementation can improve lipid profiles without affecting the glycemic levels for patients with Type 2 diabetes.
Rats where split into 2 groups, one group was injected with a single does of streptozotocin at a dose of 60 mg/kg body weight, which is a chemical that is used to induce diabetes. After 12 weeks it was found that the diabetes group was only able to convert half as much tryptophan to niacins as the control group. The rats in the diabetic group had twice the excretion of xanthurenic acid in their urine. Xanthurenic acid is a waste product that is produced when tryptophan is not converted into niacin.
Rats in group 1 received no treatment. Rats in group 2 received daily 100 mg/kg body weight niacin injections. Rats in group 3 received daily 50 mg/kg body weight vitamin C injections. Rats in group 4 received both niacin and vitamin C injections. Blood sugar levels were measured before and after treatment. The results showed that niacin and vitamin C both lowered blood sugar levels in normal rats. Niacin was more effective than vitamin C in lowering blood sugar levels in diabetic rats. The combination of niacin and vitamin C was the most effective in lowering blood sugar levels in diabetic rats.
24 healthy men and women with a mean age of 35 years, where injected Intravenously w/ 1g of niacin or placebo for 2 weeks. The niacin group ended up with acutely lower levels of FFAs (free fatty acids, fats floating around in the bloodstream) and significantly higher levels of triglyceride stored in visceral adipose tissue. This may help to reduce the amount of fat that is stored in the liver and other organs, which can help to improve insulin sensitivity and reduce the risk of metabolic complications. IE niacin may help people with diabetes and obesity to lose weight and improve their health.
Dyssebacia ( reddening, greasy, flaky scales often around nose and mouth ) is a sign of niacin deficiency.
23 hypertriglyceridaemic men took 4g/day of niacin for 6 weeks and saw very significant improvements in lipoprotein concentrations (reducing very low density cholesterol and triglycerides by ~50%) as well as reduced blood clotting and thrombosis factors.
In cultured skin cells, nicotinic acid supplementation 1.3-fold up-regulated intracellular NAD+ level significantly and its metabolites nicotinic acid mono nucleotide also increased NAD+ level by 1.5-fold with 100 μM application. Surprisingly, NAM and its derivatives could not up-regulate cellular NAD+ levels in keratinocytes.
People with acne often have abnormal lipid profiles and elevated oily secretion on their skin. Foam cells are an important pathological change in acne lesions. Acne is not a skin disease induced by infection, because no bacteria, fungi or parasites can be seen in early phase of acne lesion. The foam cells in acne lesions are white blood cells that have ingested large amounts of lipids. Niacin is the only vitamin that promotes the ability of HDL to scoop up cholesterol particles from plaques in the heart's blood vessels and move those particles to the liver for disposal, which prevents foam cell formation. Foam cells in acne lesions suggest that patients with acne are deficient in niacin and that acne can be considered a type of pellagra (niacin deficiency).
Study of 4,269 people that take niacin or have Seborrheic dermatitis finds no cases of Seborrheic dermatitis in people who take niacin.
Summary of GPR109A (niacin receptor) role in inflammation of the nervous system, especially the brain, and how activation of GPR109A plays a role in healing may conditions such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, stroke, and pathological pain.
Niacin improves organ function and survival following hemorrhagic shock. Rats and mice where bled 60% of their blood volume, and replaced with Ringers lactate solution to induce hemorrhagic shock ( deprive tissue of oxygen and blood ). After 10 minutes of shock the animals where split into 3 groups and injected with nicotinic acid, NMN or DMSO, at 3 levels of dosing. Niacin at 10mg/kg, which was the highest dose given, had by far the best level of survivability. Rats, given NMN even at a 5x higher dose than niacin at 50mg/kg did not achieve a survival rate to the level observed in the 10mg/kg or the even 5mg/kg treated mice. Use of GPR109A knockout mice confirmed that the niacin GPR109A receptor plays a major role in the survivability enhancing effect of niacin.
Axon degeneration from NMN accumulation can be prevented by bypassing the NAD+ salvage pathway (which is associated with the production of NMN) by providing nicotinic acid riboside (a precursor to nicotinic acid mononucleotide) as substrate for the body to make NAD+ via the primary Preiss Handler pathway instead.
Nicotinamide mononucleotide (NMN) accumulation in the extra cellular environment contributes to the breakdown of axons (nerve fibers).
Gut bacteria play an important role in NAD production. NAD boosting effect of oral NAM (nicotinamide) NR (nicotinamide riboside) is largely dependent on gut bacteria breaking them down to nicotinic acid, and that nicotinic acid being processed via Preiss Handler pathway. Nicotinic acid highly efficient at boosting NAD in mammals.
This research used stable isotope tracing and microbiota-depleted mice to reveal that salvage NAD+ precursor supplements like nicotinamide (NAM) and nicotinamide ribose (NMR) don't actually boost NAD+, but depend on bacteria to first convert them into nicotinic acid. And that the resulting nicotinic acid is the converts to NAD+ via the Preiss Handler pathway.
Higher levels of nicotinic acid in blood are strongly correlated with better hearing ability in 42 Japanese senior men.
25 individuals with CKD (chronic kidney disease) stages 2-4 treated with a combination of supplements, including 500mg niacin 3x/day for three months, improved the disease by at least one stage.
Authors hypothesis that antidepressants tilt tryptophan metabolism towards making serotonin instead of niacin, which in turn can lead to niacin/NAD+ deficiency that exacerbates common psychiatric problems.
Dogs with severe niacin deficiency required folic acid to be administered in tandem with niacin in order to recover and avoid death.
Nicotinic acid mimics the effect of a ketogenic diet in activating HCA2, which induces a neuroprotective phenotype in bone marrow-derived macrophages that infiltrate the brain and that this results in an improved outcome in a mouse model of stroke.
Loss of fertility is associated with lower NAD+ levels. Restoring NAD+ in aged mice by putting nicotinamide mononucleotide (NMN) in their drinking water at 2g/L restored their fertility as well as the adverse effect of old age on the development of the embryo.
The effects on cholesterol of modified "sustained release" niacin was compared to immediate release niacin (aka nicotinic acid) and showed that sustained release tends to lower LDL more, while immediate release raises HDL more at all dosage levels. The key takeway though is that 52% of the patients taking sustained release developed signs of liver toxixity, while 0% of the ones taking immediate release did.
Feeding normal and diabetic rats 800mg of niacin per kg of diet increased testicular weight in all rats and decreased testicular MDA (a biomarker for cancer). Normal rats, but not diabetic ones, also had an increase in sperm count and serum testosterone.
Taking niacin ~1-3g daily clears up liver collagen and fat deposits which are associated with liver disease. It also prevents them from forming.
This study showed depressed males have a narrower preference for female photographs (only preferring good looking ones) which is a marker for lower cognitive flexibility. The less nicotinic acid in their body, the narrower their preference. This indicates nicotinic acid may regulate human social decision-making (especially preference-related behaviors) by acting on the HCAR2 in microglia (the resident immune cells of the brain and spinal cord which constantly patrol the cerebral microenvironment to respond to pathogens and damage).
The 1906 to 1940 epidemic of pellagra was around 3 million cases, with 1 in 30 resulting in death. A Dr Goldberger was appointed to study the cause. Even though correctly identified the root cause as a nutritional deficiency (later to be confirmed as niacin specifically) his prognosis was rejected by politicians in affected regions since they basically didn't want to admit that a diet consisting of largely degerminated cornmeal (which was a key economic export) was not appropriate for human wellbeing. The invention of degerminating corn, which removes nutrients but prolongs shelf-life, coincided with the appearance of the disease. Goldberger would cure orphans suffering from pellagra by feeding them a more varied diet including fresh milk and meat.
The de novo production of NAD+ in the cell nucleus is central to the DNA repair capacity of aging cells and thus against preventing tumors.
Rats being poisoned with methylmercury have less adverse effects when their diet is supplemented with niacin (50md/day).
Participants in an open label study at Kaiser Permanente in San Francisco supplemented ~3g niacin a day. After about 1 year, 81% of patients had an by an average reduction of 27% in intra-abdominal fat. The degree of fat loss was associated with the degree of increase in HDL cholesterol and a reduced Total Cholesterol/HDL cholesterol ratio.
In depth review of NAD+, how its made in the human body, how it becomes deficient, and how its deficiency is a causal factor of a wide range of diseases. And how boosting NAD+ via enhancing agents like niacin ( especially niacin since it is the primary, so called Preiss–Handler pathway of manufacture ) can help cure a wide range of diseases.
Niacin reduces inflammation caused by low levels of oxygen in tissue that is associated with obesity.
Piglets separated from their mother in agriculture tend to struggle health wise. Supplementing their diet with niacin significantly improves their survivability via factors like improved colonic microbial diversity, intestinal health, reduced intestinal inflammation and improved overall immunity.
Relief of the asthma attacks was obtained in 21 out of 30 cases with niacin either via intravenous injection (16 out of 21 patients relieved) or orally (5 out of 9 patients relieved). A series of 50 or 100 mg doses used. Relapse was common once niacin was discontinued.
~30% of Gulf War veterans got Gulf War Illness, which is likely caused by toxic exposure to pesticides and chemical warfare agents. There is no known medical treatment. A regimen of niacin, sauna and exercise cured 11 of 22 participants.
This study grafted malignant gliomas cells (which are one of the most common types of primary brain tumors) into rat brains to see if nicotinic acid administration would help regulate the implanted tumor. ~70% of the allografted rats that were continuously administered with nicotinic acid were still alive on day 58. 100% of control group died by day 24. Biopsy showed much less tumor spread in nicotinic acid rats. Their results suggest that niacin the helps prevent the invasion of other kinds of malignant cells such as melanoma ( skin cancer ) cells and that this points to a general role of nicotinic acid in regulating tumor invasion.
Reports of patients successfully managing or curing various forms of arthritis via nicotinic and/or nicotinamide supplementation. A daily dosage of about one gram per 50 lb. body weight is necessary.
Case report of a patient with bipolar disorder who had been on lithium and other bipolar meds who was able to get off all meds after starting taking 1g niacin 3 times a day. He has been stable for 11 years on this niacin supplementation regimen. Stopping niacin leads a return of his symptoms within 2-3 days and clears up in one day after resuming the niacin regimen.
The antiviral activities of noncanonical PARP isozyme activities are limited by the availability of NAD and that nutritional and pharmacological interventions to enhance NAD levels may boost innate immunity to coronaviruses.
Niacin reduces blood viscosity through a variety of mechanisms, thus improving blood flow and perfusion through choke points of the vasculature. Finally, niacin has cardioprotective effects that may limit ischemia–reperfusion injury. By preserving glycolysis during periods of inadequate blood supply and improving blood flow to the heart after a stroke, niacin can improve the functional recovery of the muscular tissue of the heart.
Many of the beneficial and adverse effects of niacin are mediated via GPR109, which is highly expressed in adipose tissue and macrophages. Multiple infectious and inflammatory stimuli stimulate GPR109A expression in adipose tissue and in macrophages.
Niacin, a pharmacological Gpr109a agonist, suppressed colitis and colon cancer in a Gpr109a-dependent manner in mice. Thus, Gpr10a has an essential role in mediating the beneficial effects of gut microbiota and dietary fiber in colon.
Cultural cell study indicates the lifespan extension ability of niacin depends on whether the intracellular NAD+ level was lower than the sirtuin-saturating concentration.
Low dose niacin (50 mg/kg diet and 250 mg/kg diet) when supplemented in combination with leucine (24 g/kg diet) has a similar effect on lowering cholesterol in mice than standard therapeutic dose (1000 mg/kg diet) of niacin without leucine supplementation. Leucine amplifies niacin effect on lipid metabolism, hyperlipidemia and atherosclerosis in mice, at least in part by activation of the AMPK/Sirt1 axis.
Curcumin is an anticancer agent, it has demonstrates potent anti-proliferative activity in a wide range of cancer cells, including liver, breast, lung, stomach, colon, prostate, head and neck cancers. This study modified curcumin by adding 2 niacins molecules to it to make Curcumin Nicotinate. They tested it out on some cancer cell cultures and it showed that the Curcumin Nicotinate improved the anti cancer effect of curcumin by improving its cell selectivity.
42 people drank a 10g mixture of glycine, glutamine and niacin daily for 3 weeks saw an increase in serum growth hormone (GH) levels by 70%, but this GH increase was not associated with improvement in mood or memory. Circulating Insulin-like growth factor 1 (IGF-I) levels did not change.
Niacin pretreatment of skin cells protects against UV-induced cell death and apoptosis by enhancing the pro-survival pathways including AKT, mTOR and S6 in skin keratinocytes. Oral and external niacin is safe and appears to be a promising chemo-preventive supplement for reducing the mutagenic, immunosuppressive and cell damage effects of sunlight. This is also the first study providing a molecular mechanism to support that niacin can be utilized as a skin photo-damage protective agent.
GPR109A expressed in immune cells as well as in colonic tissue is necessary for protection against colitis and colon carcinogenesis. Niacin suppresses colitis and colon cancer in a GPR109A-dependent manner. GPR109A is key in mediating the beneficial effects of gut microbiota and dietary fiber in colon. Niacin suppresses atherosclerosis by activating GPR109A in immune cells. GPR109A mediates butyrate effects in colon and is a critical molecular link between colonic bacteria and dietary fiber and the host.
Many microbial metabolites, especially butyrate, found in the intestinal flora, are extremely important in regulating systemic and pulmonary immune and inflammatory responses and have a wide range of anti-inflammatory and immunity enhancing functions. Improving intestinal micro-ecology via like butyrate supplementation may partially mediate the effects of SARS-CoV-2 on the both local gastrointestinal response and systemic immune response of the host, and thus be a target for COVID-19 prevention and treatment.
People with Myalgic Encephalomyelitis / Chronic Fatigue Syndrome have a deficit in the butyrate-producing capacity of the gut microbiome. The relationships observed among symptom severity and gut microbiome disturbances suggests a causal linkage and support research into interventions that boost butyrate production.
In depth review of how deficiency of butyrate and melatonin compromise gut and overall mitochondrial function and lead to lower levels of other key molecules in cellular metabolism like sirtuins, PGC-1α and NAD+.
People with psoriasis tend to have lower levels of melatonin than average at 2 a.m and higher than average at 6am, 8 am & noon.
Melatonin supplementation benefits male hypertensive and female obese rats due to suppression of metabolic disorders and lethal arrhythmia risk. Arrhythmia is a problem with the rate or rhythm of your heartbeat. Protection against arrhythmia may attributed, at least in part, to up-regulation of myocardial Cx43, which is a protein that is essential for the formation of heart structures.
Single-center, open-label, randomized clinical trial done on Covid patients in Iraq to study melatonin supplementation for Covid treatment. All 158 patients got standard care, 82 of those patients ate 10mg melatonin each night. Thrombosis and sepsis developed significantly less in melatonin group. 13 patients in control group died vs 1 person in the melatonin group.
Oxidized Low Density Cholesterol, oxLDL induced inhibition of macrophage migration may be reversed by Niacin, which explains part of Niacin's atheroprotective effects on cardiovascular disease independent of its effects on plasma lipids. Macrophage foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls. Niacin also inhibited the formation of peroxynitrite (which is a powerful oxidant exhibiting a wide array of tissue damaging effects)
The role of TRPV4 channel present in human ciliary body epithelial cells in AANAT production was studied. AANAT, Aralkylamine N-acetyltransferase seems to be the key enzyme involved in producing melatonin from serotonin. In rodents, transcriptional activation of aanat gene is the classical mechanism to induce melatonin biosynthesis. TRPV4 is present in the human ciliary body and ciliary body epithelial cells. Activating TRPV4 channel increases the expression of AANAT, which elevates the concentration of NAS and melatonin
Looked into how niacin and nicotinamide cross blood brain barrier in control, Huntington & Alzheimer patients. Nicotinamide had higher uptake in brain tissue than niacin. No statistical difference in concentrations across the groups. It was observed that niacin and nicotinamide concentrated in red blood cells vs plasma over time.
NA activates the capsaicin receptor TRPV1 by lowering the activation threshold for heat, causing channel activation at physiological body temperature. Conversely it inhibits TRPV4 by raising activation temp to above body temp, ~41 celsius. Overall, the effects on TRPV1 and TRPV3 are potentiating while those on TRPV2 and TRPV4 are inhibitory. Little is known about the detailed structures of TRPV2-4. The TRPV receptors play a role in the flushing response.
Explores protective effect of niacin on lung tissue by dosing mouse lung white blood cells with niacin and exposing them to inflammatory toxins (Lipopolysaccharides). This demonstrated strong anti-inflammatory effects of niacin ( reduced levels of TNF-α, IL-6 and IL-1β) and that the protective effect depends on expression of GPR109A.
Niacin has multi-faceted anti inflammatory properties that act in both localized and systemic ways. A major area of its activity is in tissue related to fat storage via the GPR109A receptor. Dosing cells with TNF-alpha ( an inflammatory substance ) showed that niacin treated cells increased the atheroprotective hormone adiponectin and reduced macrophage chemotaxis
Rats injected with e coli bacteria to induce lung inflammation survived better with high dose (~1% of diet) niacin supplementation. The reduced lung inflammation and damage was associated with downregulation of the NF-κB (Nuclear Factor Kappa B) pathway.
In various studies where patients are treated for gastric ulcers, those on melatonin did better.
Nicotinamide, Nicotinic acid (niacin) and the related aromatic amides have been shown to have striking indications of possessing anticarcinogenic properties.
Mice subjected to high dose ultraviolet light for about 6 months while fed a diet supplemented with 0%, 0.1%, 0.5%, or 1.0% (by dry weight of feed) of niacin showed 68%, 60%, 48%, and 28% rates of skin cancer respectively, indicating a protective effect. Elevated levels of NAD found in niacin supplemented mice. NAD modulates the function of DNA strand scission surveillance proteins p53 and poly(ADP-ribose) polymerase, two proteins critical in cellular responses to UV-induced DNA damage.
Statistical analysis of 82 airline pilots showed a 42 % decrease in the frequency of chromosome translocations (ie DNA damage from higher rates of ionizing radiation while flying) for those with high compared with low dietary niacin.
Melatonin plays a key role in intracellular membrane integrity, especially when a cell is in under stress. Melatonin plays role in maintaining a high ATP:ADP ratio, which suppresses glycolysis. Supplemental melatonin shown to accumulate in all cells, accumulates 10x in membrane compared to mitochondria. Plays unique role in fat/water interfaces, as it can combine with both. Biomolecular condensates play a big role in brain disorders and are shaped by complex relationships between membraneless organelles, membranes/lipid rafts, ATP, RNA, and most of all, stress. Melatonin’s intimate association with each of these decisive influencers may position it as an important mediator of sorting out of these condensates in health and disease via ATP-dependent mechanisms.
Red blood cells exposed to oxidative stress will consume melatonin and use it for protect against deterioration.
Rats where given unlimited access to food and a controlled amount of exercise. Those taking niacin + melatonin lost statistically significantly more weight, compared to control, niacin only and melatonin only groups. Suggests a synergy between niacin & melatonin supplementation for anti-obesity. It's noted that mice lacking the niacin receptor GPR109A had progressive weight gain and liver fat accumulation.
Psoriatic skin has reduced GPR109A expression, topical sodium butyrate increases GPR109A expression in skin and is potentially useful in psoriasis therapy.
The expression of niacin receptor GPR109A is decreased by over 70% in breast cancer samples. It's reduced in early stages, and almost undetectable in advanced stages. Increasing expression of GPR109A seems to act as a tumor suppressor in breast tissue, but interestingly can also acts as tumor protective in other tissues like skin, mechanism of differentiation unknown.
When mice are induced with pulmonary hypertension via drugs and low oxygen, those on niacin have less severe outcomes, due to enhanced macrophage activity and release of PGD2.
Niacin via its ability to enhance macrophage and microglia is great for repairing (myelin) sheaths that protect nerve fibers, which deteriorate in diseases like multiple sclerosis.
Ca2+ is one of the major ways that cells communicate and is involved in the regulation of many important cellular processes from proliferation to apoptosis. Ca2+ regulation is involved in many autoimmune conditions and nicotinic acid (niacin) and is key to this signaling.
Niacin treatment of mice bearing intracranial brain tumor initiative cells increased macrophage representation within the tumor, reduced tumor size, and prolonged survival.
Adipose tissue (body tissue used for the storage of fat) is major site of action for niacin. When adding a white blood cell attractant to adipose tissue, niacin suppresses the pro-atherogenic (plaque inducing) chemokines and upregulates the atheroprotective (protective against plaque and improves metabolism of sugar) adiponectin.
An overview of the evidence for using niacin to treat headaches. Mechanisms explored are vasodilation, improvement of mitochondrial energy metabolism, improved oxygenation, lowering of lactic acid.
Long covid is due to changes in the metabolism of tryptophan and the lack of niacin (NAD/NADH+). Tryptophan has its metabolism altered by the lack of intestinal absorption due to internalization of ACE-2 and hypoxemia and inflammation, diverting its products to the formation of toxic Kynurenine metabolites. The longer time under hypoxemia, the less niacin and the more tryptophan will deviate to Kynurenine in an inflamed environment
Computer modeling shows niacin a key to therapy for covid via enhancing the immune system, inhibiting inflammation and regulating cellular microenvironment.
It's inferred that the majority of melatonin is created inside the mitochondria, independent of the pineal daylight associated melatonin. Melatonin has a 3 billion year history of use inside cells as a highly efficient anti-oxidant. It functions as an anti-oxidant for both plants and animals. It stimulates synthesis of other antioxidants like glutathione. It's the "swiss army knife" of anti-oxidants and uniquely positioned as the "fox in the hen house" inside the mitochondria where many free radicals originate. Melatonin reverses the Warburg effect and aids in arresting cancer cell growth.
Supplementing melatonin is safe. Melatonin is a potent anti-oxidant and anti-inflammatory agent, it's found in all cells and can easily cross all physiological barriers in body. Melatonin levels decreases with age. Melatonin therapy looks promising for a wide range of health issues in newborn babies.
Feeding rabbits Niacin up-regulated SIRT1 expression, which is involved with DNA repair. Rabbits where then subjected to stress via a collar on an artery in their neck and it was shown that niacin protects against blood vessel inflammation via the SIRT1/CD40-dependent signaling pathway.
Studies show that melatonin ameliorates hyperinsulinemia, insulin resistance, and insulin sensitivity.
In depth review of how niacin and its metabolites play a key role in brain and nerve health. Alzheimers and Niacin intake are inversely correlated. Niacin helps cells stay alive when blood supply is cutoff.
Niacin involved with over 400 NAD+ dependent reactions. Essentially all cancer patients are deficient in niacin. Exposing mice to high levels of UVB radiation to induce skin cancer showed that mice on the highest doses of niacin had the lowest rate of skin cancer at 28% compared to 68% in the control group.
Peripheral blood mononuclear cells (diverse mix of highly specialized immune cells) supplemented with nicotinic acid (niacin) and then blasted by x-ray radiation showed increased NAD+ levels, improved DNA repair efficiency and enhanced genomic stability compared to control.
Patients with mitochondrial myopathy (which is associated with NAD+ deficiency) received ~1g niacin daily for 4 months. This resulting in increasing blood NAD+ levels in all patients, up to 8x, improved muscle strength, improved respiratory chain activity and reduced fatty liver.
Disruption of NAD synthesis caused a deficiency of NAD and birth defects in humans and mice. Niacin supplementation during pregnancy prevented the birth defects in mice.
Talks about how intracellular niacin depletion along leads to tryptophan depletion as the body attempts to compensate by synthesizing niacin from tryptophan. And how this imbalance impairs the immune system in HIV.
9 years after the conclusion of a long term study on various drugs to reduce risk of death of people who had a heart attack, only the niacin group showed a statistically significant, 11% reduction in mortality than in the placebo group. This was after they stopped taking the niacin 9 years earlier, indicating a long term benefit.
Overview of how niacin and its metabolites like NAD, NADP, NADPH play a key role in cellular signaling, apoptosis, balancing intestinal flora and gene expression. Without external supply of supply of niacin, the genome becomes unstable via the antioxidant system no longer functioning efficiently, which ultimately leads to cell death.
Supplementing mice with melatonin increases butyrate production in their gut via bacteria, conversely antibiotics severely impair this butyrate production. When mice are poisoned with titanium nanoparticles to induce bone deterioration, butyrate has a protective effect against bone loss. This protective effect is specifically dependent on the GPR109A receptor that seems to be activated by the butyrate enriched gut microbiota.
Low niacin in diet leads to higher (~125%) rates of severe gum infection.
GPR109A (aka HCA2) is highly expressed in immune cells and together with niacin seems to inhibit proinflammatory aspects of immune cell activity.
A study from 1937 showing supplementing niacin cures black tongue in dogs just as well as feeding them liver. Other studies from the time are also mentioned such as one that shows rats supplementing nicotinic acid (niacin) lived longer.
The GPR109A receptor and its agonists (niacin and butyrate) have anti-inflammatory actions in the skin, gut and retina. For Parkinson's disease, niacin supplementation may have 3 benefits: lower inflammation via GPR109A-related mechanisms, increase dopamine production in the brain by supplying NADPH and boosting mitochondrial functions by increasing the NAD/NADH ratio.
GPR109A plays an essential role in gut health. GPR109A deficiency worsens colitis and colonic inflammation in mice. GPR109A expression is necessary for immune health. Antibiotics mess up butyrate producing gut bacteria, thus reducing GPR109A.
When fed a high fat diet + niacin, mice deficient in niacin receptor GPR109A got fat and had fatty livers. While mice with normal GPR109A receptors didn't get fat and didn't end up with fatty livers.
Rats fed high niacin diet and then poisoned with ethylnitrosourea (a potent mutagen) survived for longer and had increase amounts of NAD+ (1-1.5x) and ADP-ribose in their bone marrow.
Mice fed 3x the Niacin of a standard mouse diet increased zinc absorption by 70.9%, they also seemed to have more protein mass and denser skeletons.
An overview of research showing supplementing niacin lowers the risk of heart attack frequency and severity.
39 patients taking 2g/day extended release niacin for ~6 months had a ~40% reduction in liver fat. Other markers of inflammation such as CRP (C-reactive protein) where also reduced.
The focus is on how niacin and its metabolites enable white blood cells to react to a changing microenvironment (macrophage plasticity). It also discusses the anti-oxidant and anti-inflammatory aspects of niacin.
This paper investigates the production melatonin in the gut, notably it being unrelated to the day/light cycle and how eating patterns affect its production, and what the produced melatonin may be used for.
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