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DSM in Animal Nutrition & Health


Properties and Metabolism

Chemically, niacin is one of the simplest vitamins, having the empirical formula C6H3O2N (Illus. 13-1). Nicotinic acid and nicotinamide correspond to 3-pyridine carboxylic acid and its amide, respectively. There are antivitamins or antagonists for niacin. These compounds have the basic pyridine structure. Two of the important antagonists of nicotinic acid are 3-acetyl pyridine and pyridine sulfonic acid. Nicotinic acid and nicotinamide (niacinamide) generally possess the same activity, although one report with lactating cows suggested that the nicotinamide form has slightly higher activity (Jaster and Ward, 1990). Nicotinic acid is converted to the amide form in the tissues, and Erickson et al. (1991) suggests this occurs in the rumen. Nicotinamide functions as a component of two coenzymes: nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).


Illustration 13-1


Both nicotinic acid and nicotinamide are white, odorless, crystalline solids soluble in water and alcohol. They are very resistant to heat, air, light and alkali and thus are stable in feeds. Niacin is also stable in the presence of the usual oxidizing agents. However, it will undergo decarboxylation at a high temperature, when in an alkaline medium. An important source of niacin for ruminants is ruminal synthesis. Synthesis of niacin in the rumen has been demonstrated in sheep (Rérat et al., 1959), cattle (Hungate, 1966) and goats (Porter, 1961). This synthesis also has been suggested to be under metabolic control; e.g., more is synthesized when small amounts are provided in the ration and vice versa (Porter, 1961; Abdouli and Schaefer, 1986). Nicotinic acid and its amide are readily and very efficiently absorbed by diffusion at either physiological or pharmacologic doses. Nicotinic acid and nicotinamide are rapidly absorbed from the stomach and the intestine (Nabokina et al., 2005; Jacob, 2006). The mechanism by which nicotinamide nucleotides present in animal feeds are absorbed, however, is unknown. Whether the coenzyme is hydrolyzed in the lumen or after it is taken up by the mucosa is unclear. In animals, absorption from the small intestine seems to be the major route by which niacin is made available to the host. Although direct absorption from the rumen is possible, normally it is thought to be limited because only a small portion (3% to 7%) of the vitamin is in the supernatant fraction of rumen fluid; most is bound within the microbes themselves (Rérat et al., 1959). Niacin in foods occurs mostly in its coenzyme forms, which are hydrolyzed during digestion, yielding nicotinamide, which seems to be absorbed as such without further hydrolysis in the gastrointestinal tract. The intestinal mucosa is rich in niacin conversion enzymes such as NAD glycohydrolase (Henderson and Gross, 1979). Nicotinamide is released from NAD in the liver and intestines by glycohydrolases for transport to tissues that synthesize NAD as needed. In the gut mucosa, nicotinic acid is converted to nicotinamide (Steinet al., 1994). Nicotinamide is the primary circulating form of the vitamin and is converted into its coenzyme forms in the tissues. Blood transport of niacin is associated mainly with red blood cells. Niacin rapidly leaves the blood stream and enters kidney, liver and adipose tissues. The tissue content of niacin and its analogs, NAD and NADP, is a variable factor, dependent on the diet and a number of other factors, such as strain, sex, age and treatment of animals (Hankes, 1984). Although niacin coenzymes are widely distributed in the body, no true storage occurs. The liver is the site of greatest niacin concentration in the body, but the amount stored is minimal. Urine is the primary pathway of excretion of absorbed niacin and its metabolites. The principal excretory products in humans, dogs, rats, and pigs is the methylated metabolite N1-methylnicotinamide or as two oxidation products of this compound, the 4-pyridone or 6-pyridone of N1-methylnicotinamide. On the other hand, in herbivores, niacin does not seem to be metabolized by methylation, but large amounts are excreted unchanged. In the chicken, however, nicotinic acid is conjugated with ornithine as either alpha- or delta-nicotinyl ornithine or dinicotinyl ornithine. The measurement of the excretion of these metabolites is carried out in studies of niacin requirements and niacin metabolism.

The amino acid tryptophan is a precursor for the synthesis of niacin in the body. There is considerable evidence that synthesis can occur in the intestine. There is also evidence that synthesis can take place elsewhere within the body. The extent to which the metabolic requirement for niacin can be met from tryptophan will depend first on the amount of tryptophan in the diet and second on the efficiency of conversion of tryptophan to niacin. The pathway of tryptophan conversion to nicotinic acid mononucleotide in the body is shown in Figure 13-1. Protein, energy, vitamin B6 and riboflavin nutritional status and hormones affect one or more steps in the conversion sequence shown in Figure 13-1, and hence can influence the yield of niacin from tryptophan. Iron is required by two enzymes for the conversion of tryptophan to niacin with a deficiency-reducing tryptophan utilization. At low levels of tryptophan intake, conversion efficiency is high. It decreases when niacin and tryptophan levels in the diet are increased.


Figure 13-1: Conversion of Tryptophan to Nicotinic Acid Mononucleotide Plus Some Side Reactions


Animal species differ widely in ability to synthesize niacin from tryptophan, but all are relatively inefficient. From a variety of experiments, approximately 60 mg tryptophan is estimated to be equivalent to 1 mg niacin in humans, while the rat is more efficient at a conversion rate of 35 to 50 mg tryptophan required. Conversion efficiency of tryptophan to niacin in the chick is estimated to be 45:1 (Baker et al., 1973; Chen and Austic, 1989) and relatively efficient, whereas in the turkey it is inefficient, with conversions ranging from 103 to 119:1 (Ruiz and Harms, 1990). Ruminants would be less efficient in this conversion than most species. Conversion efficiency is probably due to inherent differences in liver levels of picolinic acid carboxylase, the enzyme that diverts one of the intermediates (2-amino, 3-acroleylfumaric acid) to the picolinic acid pathway instead of allowing this compound to condense to quinolinic acid, the immediate precursor of nicotinic acid. Picolinic acid carboxylase activity in livers of various species has a positive correlation to experimentally determined niacin requirements. The rat diverts very little of its dietary tryptophan to carbon dioxide and water, and thus is relatively efficient in converting tryptophan to niacin. Picolinic acid carboxylase activity of various species is presented in Table 13-1. The cat has been shown to have 30 to 50 times as much picolinic acid carboxylase activity than the rat. Thus, the cat has so much of this enzyme that it cannot convert any of its dietary tryptophan to niacin. The cat, therefore, has an absolute requirement for niacin itself. The duck has a very high niacin requirement (approximately twice as high as chickens), with considerably higher levels of picolinic acid carboxylase activity (Scott et al., 1982).



The major function of niacin is in the coenzyme forms of nicotinamide, NAD and NADP. Enzymes containing NAD and NADP are important links in a series of reactions associated with carbohydrate, protein and lipid metabolism. They are especially important in the metabolic reactions that furnish energy to the animal. The coenzymes act as an intermediate in most of the H+transfers in metabolism, including more than 200 reactions in the metabolism of carbohydrates, fatty acids and amino acids. These reactions are of paramount importance for normal tissue integrity, particularly for the skin, the gastrointestinal tract and the nervous system. Like the riboflavin coenzymes, the NAD- and NADP-containing enzyme systems play an important role in biological oxidation-reduction systems due to their capacity to serve as hydrogen-transfer agents. Hydrogen is effectively transferred from the oxidizable substrate to oxygen through a series of graded enzymatic hydrogen transfers. Nicotinamide-containing enzyme systems constitute one such group of hydrogen transfer agents. Important metabolic reactions catalyzed by NAD and NADP are summarized as follows (McDowell, 2000; Jacob, 2006; Kirkland, 2007):

a. Carbohydrate metabolism:

  1. Glycolysis (anaerobic and aerobic oxidation of glucose)

  2. TCA (Krebs) cycle


b. Lipid metabolism:

  1. Glycerol synthesis and breakdown

  2. Fatty acid oxidation and synthesis

  3. Steroid synthesis


c. Protein metabolism: 

  1. Degradation and synthesis of amino acids

  2. Oxidation of carbon chains via the TCA cycle


d. Photosynthesis


e. Rhodopsin synthesis


Niacin-dependent poly (ADP-ribose) is involved in the post-translational modification of nuclear proteins. The poly ADP-ribosylated proteins seem to function in DNA repair, DNA replication and cell differentiation (Carson et al., 1987). Poly (ADP-ribose) is synthesized in response to DNA strand breaks. Rat data have shown that even a mild niacin deficiency decreases liver poly (ADP-ribose) concentrations and that poly (ADP-ribose) levels are also altered by food restriction (Rawling et al., 1994). Zhang et al. (1993) suggest that a severe niacin deficiency may increase the susceptibility of DNA to oxidative damage, likely due to the lower availability of NAD. Turnover rates of protein in Japanese quail have been related to niacin deficiency. A high turnover rate due to the deficiency was primarily attributed to enhanced degradation rate of proteins rather than enhanced synthesis rate of proteins (Park et al., 1991).

For ruminants, niacin is particularly required for unique features involving protein and energy metabolism, including liver detoxification of portal blood NH3 to urea and liver metabolism of ketones in ketosis. It is apparent that niacin can increase microbial protein synthesis (Girard, 1998). It may result in an increased molar proportion of propionate in rumen volatile fatty acids and may cause an increased rate of flow of material through the rumen. The primary function of interest for lactating dairy cows deals with the role of niacin in fatty acid oxidation and glucose synthesis, particularly as a preventive and possible treatment for clinical and subclinical ketosis.



Wide variations in niacin requirements of animals have been reported. Cunha (1982a) identified a number of factors that influence niacin requirements in swine, including the following:

  • Genetic differences that can influence niacin needs and selection for swine with increased production levels.
  • The ability to synthesize niacin from tryptophan.
  • Limited bioavailability of niacin in feeds.
  • Increased stress and subclinical disease level on the farm because of closer and more frequent contact among pigs in confinement.
  • Trend toward more intensified operations, which may lessen opportunity for coprophagy.
  • Trend toward earlier weaning, which increases the need for higher niacin levels in milk-substitute diet (pre-starter and starter feeds).
  • Newer methods of handling and processing feeds, which may affect niacin and tryptophan level and availability.
  • Various nutrient interrelationships, including amino acid imbalances.
  • Molds and antimetabolites in feeds that can increase niacin and tryptophan needs.


Metabolic conversion of excess dietary tryptophan to niacin by all classes of swine except the newborn pig has complicated the determination of the niacin requirement (Luecke et al., 1948). Firth and Johnson (1956) estimate that each 50 mg of tryptophan in excess of the tryptophan requirement yields 1 mg of niacin; therefore, tryptophan can be a source of niacin in niacin-deficient diets. Swine niacin requirements generally range between 7 and 20 mg per kg (3.2 and 9.1 mg per lb) of diet (NRC, 1998). Firth and Johnson (1956) estimated the available niacin requirement for 1 to 8 kg (2.2 to 17.6 lbs) body weight pigs to be about 20 mg per kg (9.1 mg per lb) for a diet with no excess tryptophan. When tryptophan is fed to meet the requirement, Harmon et al. (1969) concluded, the weanling pig needs approximately 13.2 mg of available nicotinic acid per kg 6 mg per lb of diet. Harmon et al. (1970) reported that in comparison with unsupplemented pigs, young swine that received corn-based diets formulated to contain the marginal requirement for tryptophan had improved rate of gain and gain: feed ratio when either 0.01% l- or dl-tryptophan or 13.2 ppm nicotinic acid was added. Powick et al. (1947b) found that the level of nicotinic acid required for optimal growth of pigs between the ages of three and nine weeks was 0.6 to 1.0 mg per kg (0.27 to 0.45 mg per lb) live weight per day. However, Copelin et al. (1980) found no benefit of 5, 10 or 22 mg of niacin per kg diet (2.3, 4.5 or 10 mg per lb) versus the control with no added niacin when growing-finishing swine were fed corn-soybean meal diets formulated to provide 17.46% and 14.66% crude protein in the grower (up to 60 kg) and finisher (to 100 kg) diets, respectively. Findings of Yen et al. (1978) support the results of Copelin et al. (1980). Yen et al.(1978) fed 0, 5, 10 or 15 ppm of niacin in a typical fortified corn-soybean meal diet that contained 4.45% or more soybean meal (44% protein) and found no benefit of niacin on finishing-pig performance. There is limited information available for establishing the niacin requirement of pregnant and lactating sows. An estimated requirement of 10 mg per kg (4.5 mg per lb) has been extrapolated from growing-pig data (NRC, 1998). Goodband et al. (1987) evaluated the effects of supplemental niacin on sow and litter performance through two parities. Sows received a corn-soybean meal diet that provided the following niacin supplementation during gestation and lactation, respectively: 50 and 100, 250 and 500 or 500 and 1000 mg per day. Results of this study suggested a tendency for higher pig survivability for primiparous sows fed additional niacin. Sows fed additional niacin also weaned heavier pigs. Goodband et al. (1987) suggested that these results may have been due to improved milk production of sows receiving additional niacin. Similar results have been reported (Hutjens, 1990) in dairy cows supplemented with 6 to 10 gm of niacin daily with respect to increases in total milk yield and fat content of milk. Goodband et al. (1987) suggested that optimum daily niacin requirements for sows based on sow and litter performance appear to be 250 to 500 and 500 to 1000 mg per day for gestation and lactation diets, respectively. Not all research findings have supported the addition of niacin beyond that available in typical sow rations. Ivers et al. (1993) concluded that a corn-soybean meal-oat diet with 12.8% crude protein provides adequate niacin without further supplementation with crystalline niacin for gestating and lactating sows. The basal diet contained 23 mg of niacin per kg (10.4 mg per lb). Sows assigned to the treatment group received 33 mg of supplemental niacin per kg (15 mg per lb) added to the basal diet, and their performance did not differ from those provided just the basal diet. Ivers et al. (1993) concluded that adequate niacin was available from the feed ingredients in addition to niacin from excess tryptophan in the diet or niacin synthesis by intestinal tract bacteria. The results of investigations by Goodband et al. (1994) suggest that sow productivity may influence the niacin requirement. In this report, primiparous sows fed 250 or 500 mg of niacin per day versus 50 or 100 mg of supplemental niacin per day during gestation and lactation, respectively, had increased pig survival from birth to weaning and increased pig and litter weaning weights. However, Goodband et al. (1994) reported that second parity sows receiving niacin supplements showed no improvements in sow or litter performance.



Niacin is widely distributed in foods of both plant and animal origin. Animal and fish by-products, distiller’s grains and yeast, various distillation and fermentation solubles and certain oilseed meals are good sources. Most species can use the essential amino acid tryptophan and synthesize niacin from it. Because tryptophan can give rise to body niacin, niacin and tryptophan content should be considered together in expressing niacin values of foods. However, since there is a preferential use of tryptophan for protein synthesis before any becomes available for conversion to niacin (Kodiceket al., 1974), it seems unlikely, given the low tryptophan content in many animal feedstuffs, that tryptophan conversion greatly contributes to the niacin supply. Luecke et al. (1947) investigated the relationship of nicotinic acid, tryptophan and protein when fed to swine. They reported that lowering the protein content of a corn ration deficient in nicotinic acid elevated the severity of nicotinic acid deficiency symptoms produced in the large intestine. However, when 200 mgdl-tryptophan was supplied daily to this ration, the pigs had only mild symptoms and grew rapidly. Powick et al. (1948) confirmed the findings of Luecke et al. (1947). Powick et al. (1948) produced a nicotinic-deficient status in pigs receiving a diet composed of primarily corn (40%). Deficiency symptoms were overcome by the addition of nicotinic acid. However, nicotinic-acid could only partly prevent deficiency symptoms in a similar diet that was lower in tryptophan content. However, dl-tryptophan (0.25% of the diet) prevented symptoms of nicotinic acid deficiency except for some diarrhea in the pigs fed a low-nicotinic acid, low-tryptophan diet. Powick et al. (1947a) also found that although tryptophan was for the most part a satisfactory substitute for nicotinic acid, nicotinic acid did not serve as an adequate substitute for tryptophan in the conditions of this experiment. Powick et al. (1947a) reported that corn-based diets that supplied at least 0.7 to 0.8 mg of nicotinic acid per kg (.32 to .36 mg/lb) live weight per day prevented the nicotinic acid deficiency. Braude et al. (1946) found that between 5 and 10 mg nicotinic acid supplied as either food yeast or in a crystalline form in combination with the experimental diet would prevent or cure nicotinic acid deficiency induced in their experiment.

Oilseeds contained about 40% of their total niacin in bound form, while only a small proportion of the niacin in pulses, yeast, crustaceans, fish, animal tissue, or milk is bound. By use of a rat assay procedure, Carter and Carpenter (1982) showed that for eight samples of mature cooked cereals (corn, wheat, rice, and milo) only about 35% of the total niacin was available. Much of the niacin in grains and their mill by-products is in a bound form, which is not totally biologically available to animals (Manoukas et al., 1968; Yen et al., 1978). For example, Luce et al. (1966) reported that niacin in hard red winter wheat is not appreciably available to swine. Thus, although the bioavailability of niacin is 100% in soybean meal, it is zero in wheat and sorghum and varies from 0 to 30% in corn. In a related study, Luce et al. (1967) indicated that the niacin in both yellow corn and milo is predominantly unavailable to growing swine. Luecke et al. (1947) determined that weanling pigs fed a high-protein, low-nicotinic acid corn ration exhibited mild symptoms of nicotinic acid deficiency. If the corn in the ration was replaced with oats, no symptoms of nicotinic acid deficiency were noted.

Some bound forms of niacin are biologically available. The niacin in corn, however, is particularly unavailable and is implicated in the etiology of pellagra in societies that consume large quantities of the grain. The bioavailability of niacin is 100% in soybean meal but zero in wheat and sorghum and varies from 0 to 30% in corn (McDowell and Ward, 2008).

In immature seeds, niacin occurs as part of biologically available coenzymes necessary for seed metabolism. Binding of niacin to carbohydrates by ester linkages may cause it to be retained in the mature seed until it is utilized. The vitamin availability for man and animal is thus impaired. In rat growth assays for available niacin, corn harvested immaturely (“milk stage”) gave values from 74 to 88 µg/g, whereas corn harvested at maturity gave assay values of 16 to 18 µg/g (Carpenter et al., 1988). In the calculation of the niacin content of formulated diets, probably all niacin from cereal grains should be ignored or at least given a value no greater than one-third of the total niacin.

Niacin is commercially available in two forms, niacinamide and nicotinic acid, with both forms providing about the same niacin biologic activity. However, a recent report showed that niacinamide significantly increased (P<0.05) in milk, milk fat and 4% fat-corrected milk over controls during lactation. These production parameters were also higher compared to nicotinic acid-supplemented animals, but not significantly (P<0.05). An additional source of supplemental niacin would be from the vitamin K supplement menadione nicotinamide bisulfite (MNB). Results with chicks suggest that MNB is fully effective as a source of vitamin K and niacin activity (Oduho et al., 1993). Crystalline products are used in feeds and pharmaceuticals and dry dilutions in feeds.



Deficiency of niacin is characterized by severe metabolic disorders in the skin and digestive organs. The first signs to appear are loss of appetite, retarded growth, weakness, digestive disorders and diarrhea. Burroughs et al. (1950) observed these signs of niacin deficiency in rations that were calculated to contain less than 15 mg of niacin per kg of diet (6.8 mg per lb). However, the weanling pigs supplied with the same rations plus an additional 60 mg of niacin daily grew and developed normally. Cartwright et al. (1948) reported that pigs fed a low-protein diet without niacin developed a moderately severe, normocytic anemia that could be relieved by supplementation of niacin or protein. When fed this same low-protein diet but with supplemental niacin, the pigs did not develop significant anemia. Niacin deficiency is found in both human and animal populations that are overly dependent on foods (particularly corn) low in available niacin and its precursor tryptophan. Niacin is one of the B vitamins that would be expected to be deficient for typical swine diets, particularly when corn, which is low in available niacin and tryptophan, is fed. Wide variation has been observed in the severity of clinical signs of niacin deficiency in pigs with similar breeding and environmental backgrounds. Occasionally, animals appear to thrive with no niacin, and other animals appear to vary in their requirement (Cunha, 1977). During gestation and lactation, it was not possible to produce niacin deficiency with sows fed a purified diet with either 18% or 26.1% casein (Ensminger et al., 1951). Evidently the diet contained enough tryptophan to supply niacin needs, or the duration of the experiment was not sufficient for the animals to develop a niacin deficiency. Signs of niacin deficiency include poor appetite, decreased growth rate (Illus. 13-2), stomatitis, normocytic anemia and achlorhydria, followed by a severe diarrhea, occasional vomiting and an exfoliate type of dermatitis and hair loss (Cunha, 1977). Nervous system degenerative changes are reported to occur in the ganglion cells in the posterior root with extensive chromatolysis in the dorsal root (Wintrobe et al., 1945). Powick et al. (1947b) and Braude et al. (1946) observed deficiency symptoms that were similar but not identical to those reported by Cunha (1977).


Illustration 13-2: Niacin Deficiency


The pig has not received adequate niacin. The difference is less growth and conditionthan the pervious pig.

Coutesy of D.E. Becker, Illinois Agriculture Experiment Station


Niacin-deficient pigs have inflammatory lesions of the gastrointestinal tract. Ulcerative necrotic lesions of the large intestine swarm with fusiform bacteria and spirochetes (Illus. 13-3). Diarrhea with foul-smelling feces particularly involve the large intestine, which thickens, is very red and appears weak and “rotten.” Enteric conditions may be due to niacin deficiency, bacterial infection or both. Deficient pigs respond readily to niacin therapy, but infectious enteritis is not benefited. However, adequate dietary niacin may aid the pig in maintaining its resistance to bacterial invasion.


Illustration 13-3: Niacin Deficiency


Fortification Considerations

Niacin supplementation should be considered for all classes of swine. Much of niacin contained in common feeds (plant sources) is in a bound form that is not available to animals. In formulating swine diets, therefore, niacin values for corn and other cereal grains and their by-product feeds should be disregarded. It is best to assume that these feeds provide no available niacin for the pig or chick (Cunha, 1982b). Kodicek et al. (1956) determined that nicotinic acid could be liberated by alkali treatment of maize. This approach was suggested to have practical applications for the production of cereals. The work by Kodicek et al. (1956) and their subsequent study (Kodicek et al., 1959) further confirmed that without treatment, the nicotinic acid in maize is bound and unavailable to pigs. Kodicek et al. (1959) determined that if maize was treated with 1% lime water and baked into tortillas, nicotinic acid-deficient pigs recovered from their deficiency. Kodicek et al. (1959) suggested, with regard to the beneficial effect of curing the nicotinic acid deficiency in these pigs, that release of nicotinic acid from an unavailable bound form was involved. The pig and most species can use the essential amino acid tryptophan to synthesize niacin, but they cannot convert niacin back to tryptophan. Therefore, if a diet contains enough niacin, the tryptophan is not depleted for niacin synthesis. Most swine diets do not contain large excesses of tryptophan, particularly diets based on corn. Tryptophan concentrations in corn are not only low but largely unavailable. Therefore, one should ensure that swine diets are adequate in niacin, since it is inexpensive and it would be poor economics to satisfy niacin needs by the more expensive tryptophan (Cunha, 1982a). The most critical time for supplementation is during early growth, when requirements are the highest. Niacin requirements, as recommended by the NRC (1998) for swine, may be insufficient. Supplementation of niacin for swine is important to provide a reasonable safety factor, and higher niacin levels are recommended when subclinical disease level, stress and high production rates are expected. Nutritionists must set niacin fortification objectives in relation to the type of diet, class of pigs, stress conditions present and other factors that may influence the need by swine for niacin supplementation. Cunha (1982a) recommends two levels of niacin supplementation for each class of swine, an “average” level and a “high” level. The high level is to account for factors that increase niacin needs considerably. Increased swine requirements recommended by Cunha (1982b) are more than double (up to 44 mg per kg; 20 mg per lb of diet) those of the NRC (1998) for growing swine under more stressful conditions, with breeding and lactating animals needing a four-fold increase (44 mg per kg; 20 mg per lb of diet). Real et al.(2002) fed supplemental niacin to pigs receiving a corn-soybean meal based diet. Results indicated that 13 to 55 mg per kg (5.9 to 25 mg per lb) added dietary niacin can be fed to pigs in a commercial environment to improve feed efficiency. Pork quality, as measured by drip loss, pH and color were improved by higher concentrations of added dietary niacin. In addition to the critical time of early growth, especially with early weaning and the use of prestarter feeds, gestation is a period of special supplemental vitamin needs. Gestation is critical especially when feed intake is restricted to 1.4 to 2 kg (3 to 4.5 lbs) of feed per sow daily. The low level of feed intake is used to keep sows from becoming fat. However, this diet requires a higher concentration of niacin (as well as other nutrients) to provide the sow with the total niacin it needs daily (Cunha, 1982a).

Some producers have removed vitamin and trace mineral premixes from finishing diets 3 to 6 weeks prior to slaughter. This is often not advisable in relation to the risk of reduced performance. Shaw et al. (2002) removed the vitamin premix 28 days prior to slaughter, this withdrawal significantly reduced niacin in the longissimus dorsi muscle.

Commercially produced niacin is quite stable compared with most other vitamins. Niacin and niacinamide were found to be stable for three months in premixes with or without minerals (Verbeeck, 1975). Gadient (1986) reports niacin to be insensitive to heat, oxygen, moisture and light. As a general rule, the retention of niacin activity in pelleted feeds after three months at room temperature is 95% to 100%.


Vitamin Safety

Harmful effects of nicotinic acid occur at levels far in excess of requirements. Limited research has indicated that nicotinic acid and nicotinamide are toxic at dietary intakes greater than 350 mg per kg (160 mg per lb) of body weight per day (NRC, 1998). Nicotinic acid and niacinamide tolerance in swine has not been determined. Campbell and Combs (1991) fed up to 68 gm niacin per kg (30.8 gm/lb) of feed to starting pigs and reported a significant decrease in feed intake and average daily gain in comparison with pigs fed diets containing 34 g niacin per kg feed.