Requirements

Thiamin is involved in using carbohydrates as kilocalories; the requirement is based on total caloric need. The recommended dietary allowance (RDA) for men (≥14 years old) is 1.2 mg/day and for women (≥19 years old) is 1.1 mg/day (Table 11-1). Participation in rigorous physical activity uses more energy, so more thiamin is required. Also, requirements are increased by pregnancy and lactation, hemodialysis or peritoneal dialysis, fever, hyperthyroidism, cardiac conditions, alcoholism, and the use of loop diuretics. No known adverse effects are evident from excessive thiamin intake, including supplements. Although a tolerable upper intake level (UL) is not established for thiamin, care should be taken when consumption routinely exceeds the RDA.

Sources

Thiamin is widely distributed in foods, and intake of a variety of foods, including enriched grains or whole grains, can ensure adequate amounts (Table 11-2). Approximately 40% of thiamin intake is provided by enriched breads, cereals, and pasta. (Because of enrichment, enriched breads may contain almost twice as much thiamin as whole grains). In the meat group, pork is an exceptionally good source. Other good sources include nuts and legumes. Following the guidelines for MyPlate and eating a variety of foods ensures adequate intake.

Table 11-2

Thiamin content of selected foods

Food	Portion	Thiamin (mg)
Total, whole grain	1 cup	2.0
Wheaties	1 cup	1.0
Trail mix, tropical	1 cup	0.63
Lean pork chop, broiled	3 oz	0.44
Green peas, cooked	1 cup	0.41
Bagel, wheat	-4 inches	0.40
White rice, enriched, cooked	1 cup	0.26
Bread, white, enriched	1 slice	0.15
Bread, whole-wheat	1 slice	0.13
Sweet potato, baked	1 cup	0.12
Peanuts, dry roasted	1 oz	0.12

Data from U.S. Department of Agriculture, Agricultural Research Service. USDA national nutrient database for standard reference, release 26, 2013. Nutrient Data Laboratory Home Page. Accessed August 30, 2013. Available at: http://www.ars.usda.gov/nutrientdata

Hypo States

Thiamin is required for metabolism of carbohydrates, proteins, and fats; insufficient intake adversely affects most organ systems. Primary dietary deficiency usually occurs in developing countries where polished rice is the staple diet. In developed countries, thiamin deficiency is secondary to alcoholism, ingestion of raw fish containing microbial thiaminase (an enzyme that inactivates thiamin), chronic febrile states, and total parenteral nutrition (TPN). Cooking deactivates thiaminase.

Thiamin is called the “morale vitamin” because short-term deficiency causes patients to become depressed, irritable, anorexic, fatigued, and unable to concentrate. The brain and central nervous system, almost entirely dependent on glucose for energy, are seriously impaired when thiamin is unavailable.

Severe thiamin deficiency results in beriberi, which causes extensive damage to the nervous and cardiovascular systems. Beriberi means “I cannot”; patients with this severe thiamin deficiency cannot move easily. The classic chronic form of beriberi manifests with impairment of sensory and motor function without involvement of the central nervous system. Other symptoms include muscular wasting (dry beriberi), edema (wet beriberi), deep muscle pain in the calves, peripheral paralysis, tachycardia (rapid heartbeat), and an enlarged heart.

Whether or not a thiamin deficiency is evident in oral tissues is controversial. Some clinicians have associated a flabby, red, and edematous tongue with thiamin deficiency (Fig. 11-4). The fungiform papillae become enlarged and hyperemic (engorged with blood).

Wernicke-Korsakoff syndrome is another thiamin deficiency disease, typically associated with alcoholism, which is characterized by mental confusion, nystagmus (involuntary rapid movement of the eyeball), and ataxia (a gait disorder characterized by uncoordinated muscle movements). These symptoms occur most frequently in malnourished alcoholics. Alcohol intake increases thiamin requirement, yet total nutrient intake is usually poor in alcoholics. Early diagnosis is essential to initiate thiamin therapy early in the course of the disease to prevent permanent damage and death.

Requirements

As shown in Table 11-3, the Institute of Medicine (IOM) recommends an intake of 1.3 mg/day for men (14 years old and older) and 1.1 mg/day for women (19 years old and older). This level is influenced by individual energy requirements. Additionally, when nitrogen balance is positive, more riboflavin is retained. No UL has been established.

Sources

Although milk and milk products are excellent sources of riboflavin, approximately 30% of the dietary intake is furnished by foods in the grain group (Table 11-4). Meat, poultry, and fish also provide about one-fourth of the dietary requirement.

Hypo States

The body carefully guards its limited riboflavin stores. Even in severe deficiency, one-third of the normal amount is present in the liver, kidney, and heart. Primary riboflavin deficiency is uncommon, but is encountered in patients with multiple nutrient deficiencies as a result of poor nutrient absorption or use. Because riboflavin is essential in vitamin B₆ and niacin functions, riboflavin deficiency leads to symptoms related to secondary deficiency of these nutrients.

Symptoms associated with riboflavin deficiency, or ariboflavinosis, include angular cheilitis (Fig. 11-5), glossitis (Fig. 11-6), dermatitis, and anemia. With consistently inadequate intake, these symptoms may be observed within 8 weeks. Along with angular cheilosis, the lips may become extremely red and smooth. Fungiform papillae become swollen and slightly flattened and mushroom-shaped during early stages of riboflavin deficiency; the tongue has a pebbly or granular appearance. Severe chronic deficiencies lead to progressive papillary atrophy and patchy, irregular denudation of the tongue. The tongue may become purplish red or magenta in color because of vascular proliferation and decreased circulation. In more advanced cases, the entire tongue may become atrophic and smooth (Fig. 11-6). These symptoms, especially glossitis and dermatitis, may be secondary to vitamin B₆ deficiency.

Requirements

The body obtains niacin not only directly from food, but also indirectly from conversion of an amino acid, tryptophan, and from synthesis by intestinal microorganisms. RDAs are given in terms of niacin equivalents, which include dietary sources of niacin plus its precursor, tryptophan. Approximately 1 mg of niacin may be formed from 60 mg of dietary tryptophan. Niacin requirements are related to caloric intake. The RDA niacin equivalents for adults are 14 to 16 mg daily (Table 11-5). The UL for adults is 35 mg daily. There is no known adverse effect related to naturally-occurring niacin in foods.

Table 11-5

Institute of Medicine recommendations for niacin

Life Stage	EAR (mg/day)*†		RDA (mg/day)‡		AI (mg/day)§	UL (mg/day)
	Male	Female	Male	Female
0-6 months					2	ND¶
7-12 months					4	ND¶
1-3 years	5	5	6	6		10
4-8 years	6	6	8	8		15
9-13 years	9	9	12	12		20
14-18 years	12	11	16	14		30
≥19 years	12	11	16	14		35
Pregnancy
14-18 years		14		18		30
≥19 years		14		18		35
Lactation
14-18 years		13		17		30
≥19 years		13		17		35

^*EAR (estimated average requirement)—the intake that meets the estimated nutrient needs of half of the individuals in a group.

^†Niacin equivalents.

^‡RDA (recommended dietary allowance)—the intake that meets the nutrient needs of almost all (97% to 98%) individuals in a group.

^§AI (adequate intake)—the observed average or experimentally set intake by a defined population or subgroup that seems to sustain a defined nutritional status, such as growth rate, normal circulating nutrient values, or other functional indicators of health. An AI is used if insufficient scientific evidence is available to derive an EAR. For healthy human milk–fed infants, the AI is the mean intake. The AI is not equivalent to a RDA.

Preformed niacin.

^¶ND—not determinable because of lack of data of adverse effects in this age group and concern with regard to lack of ability to handle excess amounts. Source of intake should be from food and formula to prevent high levels of intake.

Data from Institute of Medicine (IOM), Food and Nutrition Board: Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B₆, folate, vitamin B₁₂, pantothenic acid, biotin, and choline, Washington, DC, 1998, National Academy Press.

Sources

Niacin is widely distributed in plant and animal foods. Good sources include meats, cereals, legumes, seeds, and nuts (Table 11-6). Approximately 65% of the niacin in the U.S. diet is obtained from meat and milk. Tryptophan is found mainly in milk, eggs, and meats. The RDA for niacin equivalents is easily met by consuming foods high in niacin and foods containing tryptophan.

Hyper States and Hypo States

Supplemental doses of nicotinic acid (3 to 6 g/day) are effective in reducing low-density lipoprotein (LDL) cholesterol and triglycerides, while increasing high-density lipoprotein (HDL) cholesterol. (Nicotinamide does not function in this role.) Despite positive changes in serum lipid levels, a large study funded by National Institutes of Health using a combination of niacin supplements and statin did not reduce risk of CHD (heart attacks and strokes), causing the study to be terminated early.1,2

The use of 50 mg of niacin taken daily can function as a vasodilator, producing flushing of the skin, itching, tachycardia, nausea and vomiting, and severe liver damage. Extended-release niacin is associated with few gastrointestinal symptoms without increasing liver damage. Because the body is able to store some niacin, larger doses associated with supplements may lead to serious problems, including abnormal liver function and gout.

Niacin deficiency is usually associated with a maize (corn) diet because corn products contain all the essential amino acids except tryptophan. This diet increases the body’s requirements for tryptophan and niacin. A deficiency is also seen in alcoholics but is unlikely in individuals who consume adequate protein. Niacin deficiency results in degeneration of the skin, gastrointestinal tract, and nervous system, a condition known as pellagra. Symptoms of pellagra have been referred to as “the 4 Ds”—dermatitis, diarrhea, depression or dementia, and death. The term pellagra is derived from the Latin word for animal hide; the skin may become rough and resemble goose flesh. The most striking and characteristic sign of pellagra is a reddish skin rash, especially on the face, hands, or feet, which is always bilaterally symmetrical (i.e., appears on both sides of the body at the same time) (Fig. 11-7A). It flares up when skin is exposed to strong sunlight. Neurological symptoms include depression, apathy, headache, fatigue, and loss of memory. If untreated, it may lead to death.

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