Niacin was the third B vitamin to be identified as a dietary essential for its role in treating the deficiency disease “black tongue” in dogs and a disease with a similar etiology, pellagra, in humans. The discovery was tied to pets and humans consuming diets nearly monopolized by grains and deficient in quality proteins.
Since the late 1930s, incidence of these diseases is almost unheard of. Today, while no significant consumer controversies are prevalent on pet enthusiast blogs or customer service hotlines regarding niacin in petfood, we can’t become complacent and overlook its importance.
In the older nutrition literature, niacin may be referred to as vitamin B3—for its place behind thiamine (B1) and riboflavin (B2)—or vitamin PP (PP for pellagra preventive factor). The term “niacin” is actually a coined word used to describe several vitamers with biological activity associated with nicotinamide, nicotinic acid and a couple of select pyridine nucleotides.
Structurally, niacin is one of the simplest of the vitamins. Nicotinic acid is based on a pyridine ring (nitrogen-containing 6-sided ring) and a carboxyl side group (carbon with an OH and a double bonded oxygen). If the OH is replaced with an NH (amide), the molecule becomes nicotinamide.
In metabolism, niacin is converted to the co-enzyme nicotinamide adenine dinucleotide (NAD) and its phosphorylated form (NADP). The NAD and NADP co-enzymes function as electron transport intermediates in energy transfer reactions. They play a central role in carbohydrate metabolic pathways like glycolysis and the Krebs cycle, fatty acid oxidation, protein metabolism and many other tissue specific functions. These are vital factors for healthy maintenance of nervous tissues, the gastrointestinal tract and skin functions.
Deficiency symptoms are typically secondary to dietary insufficiency of quality meat-based proteins and manifest as anorexia, weight loss, inflammation around the mouth and throat, salivation, blood in the saliva and bloody diarrhea. The reason protein quality factors into niacin deficiency is that tryptophan can be converted to niacin in most species. However, in pet diets, tryptophan is often the first-limiting amino acid.
Further, the cat is unable to convert tryptophan to niacin. While cats possess all the biosynthetic pathways necessary for the conversion, they also possess a super-high picolinic carboxylase activity (the highest reported in the animal kingdom). This competing bifurcation in the path steals tryptophan away from niacin production in favor of acetyl-CoA and CO2. One can surmise that during the evolution of the cat, since the felid diet was sufficient in pre-formed niacin from its prey, the metabolic machinery to convert tryptophan was marginalized in deference to other more critical needs. Because of this, today most modern cat diets must be fortified with niacin.
Meats, especially organ meats like liver, are rich sources of the pre-formed niacin-containing co-enzymes NAD and NADP. Yeast and fermentation products can also provide a significant supply. Plant sources contain primarily nicotinic acid, which is not an issue by itself; but the bio-availability of nicotinic acid can be compromised in plant sources due to strong chemical bonds with peptides (e.g., the so-called niacinogens) or carbohydrates (e.g., niacytin found in wheat bran). The net result is that bioavailability in grains and oilseeds is low, ranging from 0 to 50%.
However, the bound niacin can be released by extensive cooking. For example, Mexican foods use a process called nixtamalization where corn is cooked in limewater (saturated calcium hydroxide). This process adds many beneficial properties to the food and also releases the niacin, but this is not a practical step for petfood production. So, the general recommendations are to ignore the niacin contribution from the base dietary ingredients or at most only consider one-third of the niacin as nutritionally available, then provide supplemental sources to fill the gap.
These supplemental dietary sources are merchandised by the primary vitamin manufacturers in the wholesale ingredients market channel. Besides modest amounts that have been promoted from so-called “green” sources, most are chemically synthesized using several routes. In general, nicotinic acid is produced by oxidation of 5-ethyl-2-methylpyridine and nicotinamide is produced via 3-methylpyridine. These compounds are derived from two carbon sources such as acetaldehyde and formaldehyde or from acrolein and ammonia.
Both nicotinic acid and niacinamide moieties of niacin are commercially available for use in petfoods. These are ultra-concentrated vitamins with nearly 100% active content that are required by the animal at only part per million levels. Thus, these white to off-white crystalline powders are commonly mixed with other vitamins into a vitamin premix. Petfood manufacturers will specify whether they prefer nicotinic acid or niacinamide in their premix depending on the type of petfood application.
Nicotinic acid is moderately soluble in polar solvents like water and alcohol but insoluble in non-polar solvents like ether. Niacinamide, on the other hand, is highly soluble in water and soluble in ether. While niacin is supposedly an odorless, tasteless compound in its most pure state, the supplemental forms often carry with them the strong medicinal odor that one often attributes to the B vitamins.
From a labeling perspective, the Association of American Feed Control Officials’ Official Publication (2011) equates niacin with nicotinic acid and niacinamide with nicotinamide. Nutritionally, they are interchangeable, and according to AAFCO (Section 90.16), both can be lumped under the term “niacin supplement.” Regardless of form, they are relatively stable in petfood processes.
One should be aware that around 75% of such a supplement will survive processing and persist for the full shelf-life of the product; so generous overages should be considered. As a practical matter, there is no safe upper limit established for dogs or cats. It has been established that niacin is toxic at levels in excess of 350 mg/kg body weight per day for most animals (NRC, 1987). So, in the end, it is important to be liberal with supplementation because a deficiency can be devastating and a substantial margin of safety exists should excess be included.
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