Niacin has been investigated for its potential impact on lipid metabolism and cardiovascular health. This meta-analysis aims to systematically evaluate the effects of niacin interventions on apo A1 and apo B levels, key regulators of lipoprotein metabolism and markers of cardiovascular risk. A comprehensive search of the literature was performed on five databases of PubMed, Scopus, Web of Science, Embase and Cochrane library, from inception up to 15 July 2023. This search identified 1452 publications, from which twelve randomised controlled trials met the inclusion criteria. The intervention dosages ranged from 500 to 3000 mg/d, and the study durations spanned from 6 to 102·8 weeks. The niacin intervention demonstrated a significant reduction in apo B levels (weighted mean differences (WMD): −24·37 mg/dl, P = 0·01). Subgroup analyses indicated that intervention duration played a role, with trials of ≤ 16 weeks showing a greater reduction in apo B. Regarding apo A1, niacin significantly increased its levels (WMD: 8·23 mg/dl, P < 0·001). Subgroup analyses revealed that the beneficial effects of niacin on apo A1 were observed at a dosage of > 1500 mg/d (P < 0·001), and extended-release niacin was more effective compared with other forms (P < 0·001). According to the Begg’s regression test, no publication bias was observed in this systematic review and meta-analysis. This meta-analysis highlights niacin’s potential role in improving lipid profiles and cardiovascular health. Further well-designed clinical trials are needed to elucidate and confirm optimal dosages and durations of niacin interventions for influencing apo A1 and B.

Niacin deficiency causes pellagra, the symptoms of which include dermatitis, diarrhoea and dementia. Investigating the mechanism underlying these phenotypes has been challenging due to the lack of an appropriate animal model. Here, we report a mouse model of pellagra-related nausea induced by feeding mice a low-niacin diet and administering isoniazid (INH), which is thought to induce pellagra. Mice fed a normal or low-niacin diet received INH (0·3 or 1·0 mg/mg per animal, twice daily, 5 d), and nausea was evaluated based on pica behaviour, which considered the rodent equivalent of the emetic reflex. Furthermore, the effect of therapeutic niacin administration on nausea was evaluated in this model. Urinary and hepatic metabolite levels were analysed by LC coupled with MS. INH-induced pica was observed in mice fed a low-niacin diet but not in those fed a normal diet. Levels of urinary metabolites, such as 1-methyl-2-pyridone-5-carboxamide, kynurenic acid and xanthurenic acid, were significantly reduced in the mice treated with INH compared with those that did not receive INH. Furthermore, niacin supplementation prevented pica and restored the levels of some metabolites in this mouse model. Our findings suggest that INH-related nausea is pellagra-like. We also believe that our newly established method for quantifying pica is a useful tool for investigating the mechanisms of pellagra-related nausea.

As the precursor to NAD+ and NADP+, niacin is important for catabolic and anabolic redox reactions. In addition, niacin is known for its anti-lipolytic action via a hydroxycarboxylic acid-2-receptor-dependent mechanism. The anti-lipolytic effects of traditional free niacin supplementation during transition periods had been studied extensively, but the reported effects are ambiguous. In the past decade, a series of studies were conducted to evaluate the effects of rumen-protected niacin (RPN) on production performance and metabolic status in early lactation and on heat stress in dairy cows. Feeding RPN seems more effective than free niacin regarding increasing circulating niacin concentration. The rebound of plasma NEFA was found after termination of niacin abomasal infusion. Feeding RPN or infusion of niacin via the abomasum could suppress lipolysis and reduce insulin resistance in early lactation. Additionally, RPN supplementation could possibly relieve heat stress through vasodilation during moderate to severe heat stress condition. However, these beneficial effects of niacin supplementation have not always been observed. The inconsistent results across studies may be related to dosages of niacin supplementation, rebound of plasma NEFA concentration, stage of lactation or severity of heat stress. Overall, the current review is to present updated information on niacin nutrition in dairy cows and the recommendations are given for future research.

Experimental studies suggest that B vitamins such as niacin, folate, riboflavin, vitamin B6 and vitamin B12 may protect against DNA damage induced by ionising radiation (IR). However, to date, data from IR-exposed human populations are not available. We examined the intakes of these B vitamins and their food sources in relation to the frequency of chromosome translocations as a biomarker of cumulative DNA damage, in eighty-two male airline pilots. Dietary intakes were estimated by using a self-administered semi-quantitative FFQ. Translocations in peripheral blood lymphocytes were scored by using fluorescence in situ hybridisation whole-chromosome painting. Negative binomial regression was used to estimate rate ratios and 95 % CI, adjusted for age and occupational and lifestyle factors. We observed a significant inverse association between translocation frequency and dietary intake of niacin (P = 0·02): adjusted rate ratio for subjects in the highest tertile compared with the lowest tertile was 0·58 (95 % CI 0·40, 0·83). Translocation frequency was not associated with total niacin intake from food and supplements as well as dietary or total intake of folate, riboflavin or vitamin B6 or B12. However, the adjusted rate ratios were significant for subjects with ≥ median compared with < median intake of whole grains (P = 0·03) and red and processed meat (P = 0·01): 0·69 (95 % CI 0·50, 0·96) and 1·56 (95 % CI 1·13, 2·16), respectively. Our data suggest that a high intake of niacin from food or a diet high in whole grains but low in red and processed meat may protect against cumulative DNA damage in IR-exposed persons.

In the present study, eighty-four breast cancer patients were randomized to receive a daily supplement of 100 mg co-enzyme Q10, 10 mg riboflavin and 50 mg niacin (CoRN), one dosage per d along with 10 mg tamoxifen twice per d. A significant increase in poly(ADP-ribose) polymerase levels and disappearance of RASSF1A DNA methylation patterns were found in patients treated with supplement therapy along with tamoxifen compared to untreated breast cancer patients and tamoxifen alone-treated patients. An increase in DNA repair enzymes and disappearance of DNA methylation patterns attributes to reduction in tumour burden and may suggest good prognosis and efficacy of the treatment.

Due to the incorporation of niacin into the coenzymes NAD and NADP, niacin is of great importance for the metabolism of man and animals. Apart from niacin in feed and endogenous formation, microbial niacin synthesis in the rumen is an important source for dairy cows. But the amount synthesised seems to differ greatly, which might be influenced by the ration fed. Many studies revealed a positive impact of a niacin supplementation on rumen protozoa, but microbial protein synthesis or volatile fatty acid production in the rumen showed inconsistent reactions to supplemental niacin. The amount of niacin reaching the duodenum is usually higher when niacin is fed. However, not the whole quantity supplemented reaches the duodenum, indicating degradation or absorption before the duodenal cannula. Furthermore, supplementation of niacin did not always lead to a higher niacin concentration in blood. Effects on other blood parameters have been inconsistent, but might be more obvious when cows are in a tense metabolic situation, for example, ketosis or if high amounts are infused post-ruminally, since ruminal degradation appears to be substantial. The same is valid for milk parameters. In the few studies where blood niacin and milk parameters have been investigated, enhanced niacin concentrations in blood did not necessarily affect milk production or composition. These results are discussed in the present review, gaps of knowledge of niacin's mode of action on the metabolism of dairy cows are identified and directions for future research are suggested.

The pyridine nucleotide NAD+ is derived from dietary niacin and serves as the substrate for the synthesis of cyclic ADP-ribose (cADPR), an intracellular Ca signalling molecule that plays an important role in synaptic plasticity in the hippocampus, a region of the brain involved in spatial learning. cADPR is formed in part via the activity of the ADP-ribosyl cyclase enzyme CD38, which is widespread throughout the brain. In the present review, current evidence of the relationship between dietary niacin and behaviour is presented following investigations of the effect of niacin deficiency, pharmacological nicotinamide supplementation and CD38 gene deletion on brain nucleotides and spatial learning ability in mice and rats. In young male rats, both niacin deficiency and nicotinamide supplementation significantly altered brain NAD+ and cADPR, both of which were inversely correlated with spatial learning ability. These results were consistent across three different models of niacin deficiency (pair feeding, partially restricted feeding and niacin recovery). Similar changes in spatial learning ability were observed in Cd38− / −  mice, which also showed decreases in brain cADPR. These findings suggest an inverse relationship between spatial learning ability, dietary niacin intake and cADPR, although a direct link between cADPR and spatial learning ability is still missing. Dietary niacin may therefore play a role in the molecular events regulating learning performance, and further investigations of niacin intake, CD38 and cADPR may help identify potential molecular targets for clinical intervention to enhance learning and prevent or reverse cognitive decline.

The guinea-pig was previously reported as being sensitive to a niacin-deficient (ND), high-protein diet, suggesting that it is a suitable model for the low tryptophan to NAD+ conversion observed in human subjects. However, these studies were based on growth rates and mortality. The objective of the present study was to determine whether guinea-pigs are suitable for ND studies based on measurements of blood and bone marrow NAD+. Using a 20 % casein diet, ND decreased blood NAD+ after 4 weeks, but this parameter returned to normal after 9 weeks of feeding, while bone marrow was decreased by 35 % at this time point. Using a 15 % casein diet, 7 weeks of ND caused 44 and 42 % decreases in blood and bone marrow NAD+. Using a 10 % casein diet, ND decreased NAD+ by 32 % in blood and 62 % in bone marrow at 7 weeks. Growth rates were directly related to the dietary tryptophan content, with the lowest growth rates seen with the 10 % casein diet. Changes in guinea-pig NAD+ are comparable with the rat model at similar levels of dietary tryptophan, while mortality rates were dramatically higher in the guinea-pig model. The present study concludes that mortality in ND guinea-pigs is not indicative of poor tryptophan conversion, but is due to environmental stresses in guinea-pigs that are not observed with rats. We conclude that guinea-pigs are not suitable for research on niacin deficiency and they present challenges for any study requiring purified diets and wire-bottomed cages.

Niacin (nicotinic acid) in its non-physiological dose level is known to be an effective lipid-lowering agent; its potential risk as a therapeutic agent, however, has not been critically considered. Since niacin is excreted predominantly as methylated pyridones, requiring methionine as a methyl donor, the present study was undertaken to examine whether metabolism of the amino acid is altered in the presence of large doses of niacin. Male Sprague–Dawley rats were given a nutritionally adequate, semi-synthetic diet containing niacin at a level of either 400 or 1000 mg/kg diet (compared to 30 mg/kg in the control diet) for up to 3 months. Supplementation with niacin (1000 mg/kg diet) for 3 months resulted in a significant increase in plasma and urinary total homocysteine levels; this increase was further accentuated in the presence of a high methionine diet. The hyperhomocysteineaemia was accompanied by a significant decrease in plasma concentrations of vitamins B6 and B12, which are cofactors for the metabolism of homocysteine. The homocysteine-raising action of niacin, in particular, has an important toxicological implication, as hyperhomocysteineaemia is considered to be an independent risk factor for arterial occlusive disease. The niacin-associated change in homocysteine status may be an important limiting factor in the use of this vitamin as a lipid-lowering agent.