Definition of a tolerable upper intake level of niacin: a systematic review and meta-analysis of the dose-dependent effects of nicotinamide and nicotinic acid supplementation

Minto, Clara; Vecchio, Maria Gabriella; Lamprecht, Manfred; Gregori, Darío

doi:10.1093/nutrit/nux011

Cited by 24 publications

(21 citation statements)

References 62 publications

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“…Second, the use of wild type mice may also prove the potential benefits of niacin and/or fatty acids in HFDs in a non‐genetically modified cohort. From a translational point of view and given the undesirable flushing at therapeutic doses of niacin, it is probable that an HFD in wild type mice could be the most appropriate control in a study design that did not involve niacin.…”

Section: Discussionmentioning

confidence: 99%

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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Scope Obesity is a principal causative factor of metabolic syndrome. Niacin potently regulates lipid metabolism. Replacement of saturated fatty acids by MUFAs or inclusion of omega‐3 long‐chain PUFAs in the diet improves plasma lipid levels. However, the potential benefits of niacin in combination with MUFAs or omega‐3 long‐chain PUFAs against white adipose tissue (WAT) dysfunction in the high fat diet (HFD)‐induced metabolic syndrome are unknown. Methods and results Male Lepob/obLDLR−/− mice are fed a chow diet or HFDs based on milk cream (21% kcal), olive oil (21% kcal), or olive oil (20% kcal) plus 1% kcal from eicosapentaenoic and docosahexaenoic acids, including immediate‐release niacin (1% w/v) in drinking water, for 8 weeks. Mice are then phenotyped. Dietary MUFAs are identified as positive regulators of adipose NAD+ signaling pathways by triggering NAD+ biosynthesis via the salvage pathway. This coexists with overexpression of genes involved in recognition of NAD+ and fatty acids, a surrounding lipid environment dominated by exogenous oleic acid and an alternatively activated macrophage profile, which culminate in a healthy expansion of WAT and improvement of several hallmarks that typify the metabolic syndrome. Conclusion Niacin in combination with dietary MUFAs can favor WAT homeostasis in the development of HFD‐induced obesity and metabolic syndrome.

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Section: Discussionmentioning

confidence: 99%

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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“…Our data suggesting that high dietary niacin intake may be associated with osteoporosis is in contrast with the concept that there are no adverse effects from naturally occurring niacin from food . In agreement with the idea that dietary intake of niacin needs to be considered with respect to disease states, a recent meta‐analysis suggested that the limits of nicotinic acid for nutritional supplements should be reconsidered, and that appropriate limits may differ for healthy versus disease states . Our findings in CHS suggest that trials including niacin intake for diseases of the aging, in particular, studies including patients at high risk for fracture, should include assessments of BMD and incident fractures and measure concentrations of niacin to understand more about the apparently complex association of niacin with BMD and osteoporosis, with careful consideration of different levels of dietary intake of niacin.…”

Section: Discussionmentioning

confidence: 99%

Association of Dietary Niacin Intake With Incident Hip Fracture, BMD, and Body Composition: The Cardiovascular Health Study

Carbone

Bůžková

Fink

et al. 2019

Journal of Bone and Mineral Research

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Interest in niacin has increased in the setting of reports suggesting that niacin plays a role in diseases of aging. No study to date has examined the association of dietary niacin intake with multiple skeletal health parameters including bone mineral density (BMD), hip fractures, and body composition, and none have included both African American and white men and women. Participants included 5187 men and women ≥65 years from the Cardiovascular Health Study (CHS). Mean daily dietary niacin intake was 32.6 mg, with quartiles 1 through 4 defined as 3.6 to 21.8 mg/day, 21.9 to 30.2 mg/day, 30.3 to 40.9 mg/day, and 41.0 to 102.4 mg/day, respectively. Risk of incident hip fracture per 10 mg increment of daily dietary niacin intake was estimated using proportional hazards models. During a median follow‐up of 13 years, 725 participants had an incident hip fracture. In models adjusted for demographic and clinical characteristics and diet, dietary niacin intake was significantly associated with an increased risk of hip fractures (hazard ratio [HR] 1.12; 95% CI, 1.01 to 1.24) with spline models suggesting a U‐shaped association. In post hoc analyses, both the lowest (HR 1.31; 95% CI, 1.04 to 1.66) and highest (HR 1.53; 95% CI, 1.20 to 1.95) quartiles of niacin intake were associated with an increased risk of incident hip fracture versus quartiles 2 and 3. There was a trend for a significant inverse association of dietary niacin intake with hip BMD (p = 0.06), but no significant association with total body BMD or any body composition measures. In this cohort of elderly, community‐dwelling African American and white men and women, both high and low dietary niacin intakes were associated with a significantly increased risk of subsequent hip fracture, suggesting a possible U‐shaped association. By comparison, dietary niacin may have an inverse linear association with hip BMD. © 2018 American Society for Bone and Mineral Research.

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“…It is a trace nutrient known as vitamin B3 (Lanska, 2012), available in certain foods (dairy products, fish, eggs, and vegetables) (Minto et al, 2017), nutritional supplements and fortified foods (Colbourne et al, 2013). Its effects are associated with energy metabolism and neuroprotection (Chi and Sauve, 2013).…”

Section: Precursors Of Nad +mentioning

confidence: 99%

Antioxidant Alternatives in the Treatment of Amyotrophic Lateral Sclerosis: A Comprehensive Review

et al. 2020

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that produces a selective loss of the motor neurons of the spinal cord, brain stem and motor cortex. Oxidative stress (OS) associated with mitochondrial dysfunction and the deterioration of the electron transport chain has been shown to be a factor that contributes to neurodegeneration and plays a potential role in the pathogenesis of ALS. The regions of the central nervous system affected have high levels of reactive oxygen species (ROS) and reduced antioxidant defenses. Scientific studies propose treatment with antioxidants to combat the characteristic OS and the regeneration of nicotinamide adenine dinucleotide (NAD +) levels by the use of precursors. This review examines the possible roles of nicotinamide riboside and pterostilbene as therapeutic strategies in ALS.

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Definition of a tolerable upper intake level of niacin: a systematic review and meta-analysis of the dose-dependent effects of nicotinamide and nicotinic acid supplementation

Cited by 24 publications

References 62 publications

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Association of Dietary Niacin Intake With Incident Hip Fracture, BMD, and Body Composition: The Cardiovascular Health Study

Antioxidant Alternatives in the Treatment of Amyotrophic Lateral Sclerosis: A Comprehensive Review

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