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TABLE 1 Dietary Reference Intakes for Niacin by Life Stage Group DRI values (mg/day) EARa,b RDAa,c AIa,d ULe,f males females males females Life stage group NDg 0 through 6 mo 2 7 through 12 mo 4 ND 1 through 3 y 5 5 6 6 10 4 through 8 y 6 6 8 8 15 9 through 13 y 9 9 12 12 20 14 through 18 y 12 11 16 14 30 19 through 30 y 12 11 16 14 35 31 through 50 y 12 11 16 14 35 51 through 70 y 12 11 16 14 35 > 70 y 12 11 16 14 35 Pregnancy £ 18 y 14 18 30 19 through 50 y 14 18 35 Lactation £ 18 y 13 17 30 19 through 50 y 13 17 35 a As niacin equivalents (NE). 1 mg of niacin = 60 mg of tryptophan; 0â6 months = preformed niacin (not NE). b EAR = Estimated Average Requirement. c RDA = Recommended Dietary Allowance. d AI = Adequate Intake. e UL = Tolerable Upper Intake Level. Unless otherwise specified, the UL represents total intake from food, water, and supplements. f The UL for niacin applies to synthetic forms obtained from supplements, fortified foods, or a combination of the two. The UL is not expressed in NEs. g ND = Not determinable. This value is not determinable due to the lack of data of adverse effects in this age group and concern regarding the lack of ability to handle excess amounts. Source of intake should only be from food to prevent high levels of intake.
PART III: NIACIN 263 NIACIN T he term niacin refers to nicotinamide (nicotinic acid amide), nicotinic acid (pyridine-3-carboxylic acid), and derivatives that exhibit the bio- logical activity of nicotinamide. Niacin is involved in many biological reactions, including intracellular respiration and fatty acid synthesis. The amino acid tryptophan is converted in part into nicotinamide and thus can contribute to meeting the requirement for niacin. The primary method used to estimate the requirements for niacin intake relates intake to the urinary excretion of niacin metabolites. The requirements are expressed in niacin equivalents (NEs), allowing for some conversion of the amino acid tryptophan to niacin (1 mg niacin = 60 mg tryptophan). The Toler- able Upper Intake Level (UL) is based on flushing as the critical adverse effect. The UL applies to synthetic forms obtained from supplements, fortified foods, or a combination of the two. (The UL is in mg of preformed niacin and is not expressed in NEs.) DRI values are listed by life stage group in Table 1. Meat, liver, poultry, and fish are rich sources of niacin. Other contributors to niacin intake include enriched and whole-grain breads and bread products and fortified ready-to-eat cereals. The classic disease of niacin deficiency is pel- lagra, which in industrialized nations generally only occurs in people with chronic alcoholism or conditions that inhibit the metabolism of tryptophan. There are no adverse effects associated with the excess consumption of naturally occur- ring niacin in foods, but they can result from excess intakes from dietary supple- ments, fortified foods, and pharmacological agents. The potential adverse ef- fects of excess niacin intake include flushing, nausea, vomiting, liver toxicity, blurred vision, and impaired glucose tolerance. NIACIN AND THE BODY Function The term niacin refers to nicotinamide, nicotinic acid, and derivatives that ex- hibit the biological activity of nicotinamide. Niacin acts as a donor or acceptor of a hydride ion in many biological reductionâoxidation reactions, including intracellular respiration, the oxidation of fuel molecules, and fatty acid and steroid synthesis. The amino acid tryptophan is converted in part into nicotina- mide and thus can contribute to meeting the requirement for niacin.
DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 264 Absorption, Metabolism, Storage, and Excretion Absorption of niacin from the stomach and intestine is rapid. At low concentra- tions, absorption is mediated by sodium ionâdependent facilitated diffusion. At higher concentrations, absorption is by passive diffusion. Niacin is stored in various body tissues. The niacin coenzymes NAD (nicotinamide adenine di- nucleotide) and NADP (nicotinamide adenine dinucleotide phosphate) are syn- thesized in all body tissues from nicotinic acid or nicotinamide. The bodyâs niacin requirement is met not only by nicotinic acid and nico- tinamide present in the diet, but also by conversion from dietary protein con- taining tryptophan. DETERMINING DRIS Determining Requirements The requirements for niacin are based on the urinary excretion of niacin me- tabolites. The EAR and RDA are expressed in niacin equivalents (NEs), allow- ing for some conversion of the amino acid tryptophan to niacin (1 mg niacin = 60 mg tryptophan). Special Considerations Individuals with increased needs: The RDAs for niacin are not expected to be sufficient to meet the needs of people with Hartnupâs disease, liver cirrhosis, or carcinoid syndrome, or the needs of individuals on long-term isoniazid treat- ment for tuberculosis. Extra niacin may also be required by those being treated with hemodialysis or peritoneal dialysis, those with malabsorption syndrome, and women who are carrying more than one fetus or breastfeeding more than one infant. Criteria for Determining Niacin Requirements, by Life Stage Group Life stage group Criterion 0 through 6 mo Human milk content 7 through 12 mo Extrapolation from adults 1 through 18 y Extrapolation from adults 19 through > 70 y Excretion of niacin metabolites Pregnancy £ 18 y through 50 y Age-specific requirement + increased energy utilization and growth needs during pregnancy
PART III: NIACIN 265 Lactation £ 18 y through 50 y Age-specific requirement + energy expenditure of human milk production The UL The Tolerable Upper Intake Level (UL) is the highest level of daily nutrient intake that is likely to pose no risk of adverse effects for almost all people. Members of the general population should not routinely consume more than the UL. The UL for niacin represents preformed niacin and is based on flushing as the critical adverse effect. The UL developed for niacin applies to all forms of niacin added to foods or taken as supplements (e.g., immediate-release, slow- or sustained-release nicotinic acid, and niacinamide [nicotinamide]). Individu- als who take over-the-counter niacin to treat themselves, such as for high blood cholesterol, for example, might exceed the UL on a chronic basis. The UL is not meant to apply to individuals who are receiving niacin under medical supervi- sion. Niacin intake data indicate that only a small percentage of the U.S. popu- lation is likely to exceed the UL for niacin. Special Considerations Individuals susceptible to adverse effects: People with the following condi- tions are particularly susceptible to the adverse effects of excess niacin intake: liver dysfunction or a history of liver disease, diabetes mellitus, active peptic ulcer disease, gout, cardiac arrhythmias, inflammatory bowel disease, migraine headaches, and alcoholism. Individuals with these conditions might not be pro- tected by the UL for niacin for the general population. DIETARY SOURCES Foods Data from the Continuing Survey of Food Intakes by Individuals (CSFII, 1994â 1996) indicated that the greatest contribution to the niacin intake of the U.S. adult population came from mixed dishes high in meat, fish, or poultry; poul- try as an entree; enriched and whole-grain breads and bread products; and fortified ready-to-eat cereals. Most flesh foods are rich sources of niacin. Dietary Supplements In the 1986 National Health Interview Survey (NHIS), approximately 26 per- cent of all adults reported taking a supplement containing niacin. For adults who took supplements and participated in the Boston Nutritional Status Sur-
DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 266 vey (1981â1984), median supplemental niacin intakes were 20 mg/day for men and 30 mg/day for women. Supplements containing up to about 400 mg of niacin are available without a prescription in the United States. Bioavailability Niacin from meat, liver, beans, and fortified or enriched foods appears to be highly bioavailable, whereas niacin from unfortified cereal grains is bound and only about 30 percent available (although alkali treatment of the grains in- creases the percentage absorbed). Niacin added during enrichment or fortifica- tion is in the free form of niacin; foods that contain this free form include beans and liver. The conversion efficiency of tryptophan to niacin, although assumed to be 60:1, varies depending on a number of dietary and metabolic factors. The effi- ciency of conversion is decreased by deficiencies in some other nutrients (see âDietary Interactionsâ). Individual differences also account for a substantial dif- ference in conversion efficiency. Dietary Interactions There is some evidence that inadequate iron, riboflavin, or vitamin B6 status increases niacin needs by decreasing the conversion of tryptophan to niacin. Data were not available to quantitatively assess the effects of these nutrientâ nutrient interactions on the niacin requirement. INADEQUATE INTAKE AND DEFICIENCY The classic disease of severe niacin deficiency is pellagra, which is characterized by the following signs and symptoms: ⢠Pigmented rash ⢠Vomiting, constipation, or diarrhea ⢠Bright red tongue ⢠Depression ⢠Apathy ⢠Headache ⢠Fatigue ⢠Memory loss Pellagra was common in the United States and parts of Europe in the early 20th century in areas where corn or maize (low in both niacin and tryptophan) was the dietary staple. Now it is occasionally seen in developing nations, such as in India, China, and Africa. In industrialized nations, it is generally only
PART III: NIACIN 267 associated with chronic alcoholism and in individuals with conditions that dis- rupt the metabolism of tryptophan. Deficiencies of other micronutrients, such as pyridoxine and iron, which are required to convert tryptophan to niacin, may also contribute to the appearance of pellagra. EXCESS INTAKE There is no evidence of adverse effects associated with the excess consumption of naturally occurring niacin in foods. But adverse effects may result from ex- cess niacin intake from dietary supplements, pharmaceutical preparations, and fortified foods. Most of the data concerning adverse effects of niacin has come from studies and case reports involving patients with hyperlipidemia or other disorders who were treated with pharmacological preparations that contained immediate-release nicotinic acid or slow- or sustained-release nicotinic acid. The potential adverse effects of excess niacin intake include the following: ⢠Flushing (the first observed adverse effect observed; generally occurs at lower doses than do other adverse effects) ⢠Nausea and vomiting ⢠Liver toxicity ⢠Blurred vision ⢠Impaired glucose tolerance
DRIs: THE ESSENTIAL GUIDE TO NUTRIENT REQUIREMENTS 268 KEY POINTS FOR NIACIN Niacin is involved in many biological reactions, including 3 intracellular respiration and fatty acid synthesis. The amino acid tryptophan is converted in part into nicotinamide and thus can contribute to meeting the requirement for niacin. The requirements for niacin are based on the urinary excretion 3 of niacin metabolites. The UL is based on flushing as the critical adverse effect. The requirements are expressed in niacin equivalents (NEs), 3 allowing for some conversion of the amino acid tryptophan to niacin (1 mg niacin = 60 mg tryptophan). The UL for niacin represents preformed niacin (the UL is not 3 expressed in NEs) and applies to synthetic forms obtained from supplements, fortified foods, or a combination of the two. Niacin intake data indicate that only a small percentage of the 3 U.S. population is likely to exceed the UL for niacin. People with an increased need for niacin include those with 3 Hartnupâs disease, liver cirrhosis, carcinoid syndrome, and malabsorption syndrome, as well as those on long-term isoniazid treatment for tuberculosis or on hemodialysis or peritoneal dialysis. Also, pregnant females who are carrying more than one fetus or breastfeeding more than one infant may require additional niacin. Meat, liver, poultry, and fish are rich sources of niacin. Other 3 contributors to niacin intake include enriched and whole-grain breads and bread products and fortified ready-to-eat cereals. The classic disease of severe niacin deficiency is pellagra, 3 which in industrialized nations generally only occurs in people with chronic alcoholism or conditions that inhibit the metabolism of tryptophan.
PART III: NIACIN 269 There is no evidence of adverse effects associated with the 3 excess consumption of naturally occurring niacin in foods. But adverse effects may result from excess niacin intake from dietary supplements, pharmaceutical preparations, and fortified foods. The adverse effects of excess niacin intake include flushing, 3 nausea and vomiting, liver toxicity, and impaired glucose tolerance. However, most of the data on adverse effects has come from research with patients with special conditions who were treated with pharmacological preparations.