inflammation
Pathways
Studies (51)
Relationship between dietary niacin intake and erectile dysfunction: a population-based study
A large U.S. study found men with higher dietary niacin (vitamin B3) intake had a lower risk of erectile dysfunction (ED). Men in the highest third of niacin intake were 56% less likely to have ED compared to those in the lowest third. This link held true even after accounting for other factors like age, weight, and health conditions.
Dietary nicotinic acid supplementation improves hepatic zinc uptake and offers hepatoprotection against oxidative damage
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.
Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation
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.
Deficiency of metabolite sensing receptor HCA2 impairs the salutary effect of niacin in hemorrhagic shock
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.
Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway
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.
Reversing Chronic Kidney Disease with Niacin and Sodium Bicarbonate
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.
Effect of Different Levels of Niacin on Serum Biochemical Parameters, Antioxidant Status, Cytokine Levels, Inflammatory Gene Expression and Colonic Microbial Composition in Weaned Piglets
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.
NAD+ homeostasis in human health and disease
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.
Protective effects of niacin against methylmercury-induced genotoxicity and alterations in antioxidant status in rats
Rats being poisoned with methylmercury have less adverse effects when their diet is supplemented with niacin (50md/day).
Treatment of Asthma by Nicotinic Acid
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.
Action of nicotinic acid on the reversion of hypoxic-inflammatory link on 3T3-L1 adipocytes
Niacin reduces inflammation caused by low levels of oxygen in tissue that is associated with obesity.
Treatment of Arthritis by Nicotinic Acid and Nicotinamide
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.
Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity
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.
Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages
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.
Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis
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.
Antiatherothrombotic effects of nicotinic acid
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.
Deficient butyrate-producing capacity in the gut microbiome of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients is associated with fatigue symptoms
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.
Niacin protects against UVB radiation-induced apoptosis in cultured human skin keratinocytes
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.
Activation of Gpr109a, Receptor for Niacin and the Commensal Metabolite Butyrate, Suppresses Colonic Inflammation and Carcinogenesis
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.
Intestinal Flora as a Potential Strategy to Fight SARS-CoV-2 Infection
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.
Gut dysbiosis dysregulates central and systemic homeostasis via decreased melatonin and suboptimal mitochondria functioning: pathoetiological and pathophysiological implications.
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+.
Melatonin supplementation ameliorates myocardial connexin-43 disorders and arrhythmia risk of hypertensive and obese rats
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.
The Effect of Melatonin on Thrombosis, Sepsis and Mortality Rate in COVID-19 Patients
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.
Niacin Reverses Migratory Macrophage Foam Cell Arrest Mediated by oxLDL In Vitro
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)
Nicotinic Acid is a Common Regulator of Heat-Sensing TRPV1-4 Ion Channels
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.
Anti-inflammatory effects of nicotinic acid
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
Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms
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 attenuates lung inflammation and improves survival during sepsis by downregulating the nuclear factor-κB pathway
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.
Melatonin Treats H Pylori and Gastric Ulcers
In various studies where patients are treated for gastric ulcers, those on melatonin did better.
Melatonin protects human red blood cells from oxidative hemolysis: new insights into the radical-scavenging activity
Red blood cells exposed to oxidative stress will consume melatonin and use it for protect against deterioration.
Niacin Attenuates Pulmonary Hypertension Through H-PGDS in Macrophages
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.
Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin
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.
Network Pharmacology and bioinformatics analyses identify intersection genes of niacin and COVID-19 as potential therapeutic targets
Computer modeling shows niacin a key to therapy for covid via enhancing the immune system, inhibiting inflammation and regulating cellular microenvironment.
The COVID-19 Burden or Tryptophan Syndrome: Autoimmunity, Immunoparalysis and Tolerance in a Tumorigenic Environment
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
The treatment of migraines and tension-type headaches with intravenous and oral niacin (nicotinic acid): systematic review of the literature
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.
Decreased expression of G-protein-coupled receptors GPR43 and GPR109a in psoriatic skin can be restored by topical application of sodium butyrate
Psoriatic skin has reduced GPR109A expression, topical sodium butyrate increases GPR109A expression in skin and is potentially useful in psoriasis therapy.
Melatonin as a master regulator of cell death and inflammation: molecular mechanisms and clinical implications for newborn care
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.
Melatonin in Mitochondria: Mitigating Clear and Present Dangers
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.
Nicotinic acid inhibits vascular inflammation via the SIRT1-dependent signaling pathway
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.
The NAD + precursor nicotinic acid improves genomic integrity in human peripheral blood mononuclear cells after X-irradiation
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.
Open AccessReview Minireview Exploring the Biological Cycle of Vitamin B3 and Its Influence on Oxidative Stress: Further Molecular and Clinical Aspects
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.
Niacin Cures Systemic NAD + Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy
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.
The oxidative stress-induced niacin sink (OSINS) model for HIV pathogenesis
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.
Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway
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.
A novel treatment target for Parkinson's disease
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 brain by supplying NADPH and boosting mitochondrial functions by increasing the NAD/NADH ratio.
Periodontitis and intake of thiamine, riboflavin and niacin among Korean adults
Low niacin in diet leads to higher (~125%) rates of severe gum infection.
Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization
GPR109A (aka HCA2) is highly expressed in immune cells and together with niacin seems to inhibit proinflammatory aspects of immune cell activity.
Activation of the receptor (Gpr109a) for niacin and the commensal metabolite butyrate suppresses colonic inflammation and carcinogenesis
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.
Niacin for treatment of nonalcoholic fatty liver disease (NAFLD): novel use for an old drug?
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.
Niacin and its metabolites as master regulators of macrophage activation
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.
Gut melatonin: A potent candidate in the diversified journey of melatonin research
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.