23: Nutritional and Metabolic Disorders

Nutritional and Metabolic Disorders

Shubha B.N. Sairam and Praveen

Nutriology as per Dorland’s Medical Dictionary is the science of nutrition. It is the science of how the body utilizes food to meet requirements for development, growth, repair, and maintenance. Nutrients are biochemical substances that can be supplied only in adequate amounts from an outside source, usually from food.

The relationship between nutrition and oral health is multifaceted. Nutrition has both local and systemic impacts on the oral cavity. While diet and eating patterns have a local effect on the teeth, saliva and soft tissues, the systemic impact of nutrition also has considerable implications and it too merits assessment as a component of comprehensive care. The systemic effect is the impact of the nutrients consumed as they assume their biological functions in relation to the development and maintenance of the extra- and intraoral structures and secretions. The oral cavity is often one of the first sites where nutrient deficiencies can be clinically noted.

Clinical manifestations of nutrient deficiencies can have a significant impact on the function of the oral cavity. Functional properties of the oral cavity include taste, salivation, mastication and swallowing food. Any alterations in the structure and function of the oral cavity may compromise intake and contribute to the development of a nutrient-deficiency state. When the associated oral structures are affected, these alterations may be compounded even further, leading to subsequent inadequate dietary intake and compromised nutritional status.

There are six classes of nutrients: water, carbohydrates, proteins, fats, minerals and vitamins. Nutrients work together and interact in complex metabolic reactions. Proteins, carbohydrates and fats provide energy for body needs. However, the body cannot use this energy without adequate amounts of vitamins and minerals.

Nutritional Requirements of Indians

Energy requirement is defined as the amount that will balance the energy expenditure of the individual (as determined by body size and composition and level of physical activity) consistent with long-term good health. This intake will allow for the maintenance of economically necessary and socially desirable physical activity. In children and pregnant/lactating women, the energy requirement will include energy needed for deposition of tissue and secretion of milk at the rate consistent with good health. All estimates of requirement are based on habitual intakes though these are expressed as daily intake.

Recommended dietary allowance (RDA) is the amount of selected nutrients considered adequate to meet the known nutrient needs of healthy people. The Canadian equivalent is the recommended nutrient intakes (RNIs). The energy needs of men and women for different activity levels computed on the basis of recommendations made by a Joint Expert Consultation of the World Health Organization (WHO)/Food and Agricultural Organization (FAO)/United Nations University (UNU) in 1985 and by an Expert Committee constituted in 1988 by the Indian Council of Medical Research (ICMR) are as shown in Tables 1 and 2. The ICMR’s RDA is higher than those recommended by the WHO/FAO/UNU.

Table 1

ICMR’s recommended dietary allowance for energy

Source: Dr BS Narasinga Rao–Gopalan Oration (2001).

Table 2

Recommended dietary allowance of infants and children

Source: ^*WHOIFAO/UNO (1985); ^†ICMR (1988).

For computing RDA, the ICMR has taken body weight of ‘reference man’ as 60 kg and that of ‘woman’ as 50 kg. Average weight of Indian men is 52 kg and women 44 kg. For children and adolescents, weight for age from National Center for Health Statistics (NCHS), USA/well-to-do Indian children have been utilized by ICMR for deriving the RDA so that energy intake enables optimum growth. However, as in adults, majority of children and adolescents weigh substantially less and hence their energy requirement is lower.

Carbohydrates

Carbohydrates have been the major sources of energy since the dawn of history and furnish up to 90% of energy needs. Carbohydrates provide about 4 kcal/g. The average adult stores about 300 g of carbohydrate in the liver and muscle tissue as glycogen.

Functions

Mainly provides fuel for the body, especially the central nervous system.

Adequate consumption has a protein sparing function, i.e. proteins consumed are used for anabolic function rather than as an energy source.

In the absence of carbohydrates, fat metabolism is incomplete and leads to formation of ketone bodies.

Carbohydrates are required for the formation of structural components such as cartilage, nervous tissue and bone.

Carbohydrates are required for the formation of non–essential amino acids.

Non-starch polysaccharides constitute dietary fibers that are required to prevent constipation, reduce blood cholesterol and give satiety.

It is recommended that 55–60% of total energy intake should be obtained from carbohydrates.

Sources

Grains (wheat, corn, rice, oats, rye, barley, buckwheat and millet) provide complex carbohydrates and starches. Vegetables, especially root and seed varieties (potatoes, sweet potatoes, beet and peas) contain considerable amounts of starch. Milk is a good source of lactose. Dietary fiber can be obtained from whole grain breads and cereals and legumes.

Dental considerations

For decades, dietary carbohydrates have one of the major constituents incriminated in the causation of caries. The occurrence of caries depends upon the frequency of consumption, chemical constitution, route of administration, and physical properties of carbohydrates.

Sugar substitutes have been claimed to be non-cariogenic due to their inability to act as substrates for the enzyme glucosyltransferase. Xylitol is one such commonly used sugar substitute. It has been found to be non-cariogenic. Some studies also show that chewing xylitol gum has cariostatic properties. Other sugar substitutes, sorbitol, aspartame, sucralose have been found to have a negligible effect on the development of caries.

Proteins

Second to water, proteins are the most abundant substances in the body. The structural units of proteins are amino acids. Of the 20 amino acids present in nature, nine are considered essential, i.e. these are to be supplied by the diet.

Functions

Generation of new body tissues

Repair of body tissues

Production of enzymes, hormones, immunoglobulins

Regulation of fluid balance

Transport of insoluble fats

Provide energy—4 kcal/g.

Sources

Meat and milk food groups provide most of the dietary proteins. Soy is also a good source of proteins.

Deficiency

Protein energy malnutrition

This term covers the spectrum of clinical conditions seen in undernutrition. The two clinical forms of protein energy malnutrition (PEM) include kwashiorkor and marasmus.

Kwashiorkor occurs when a child is fed on a diet with very low protein content relative to energy. This results in a high level of plasma insulin and low levels of plasma cortisol. This hormonal pattern leads to an uptake of amino acids in muscle, diverting these from liver, leading to decreased albumin synthesis and therefore edema.

Thus a child with kwashiorkor shows apathy, lethargy and severe anorexia. There is generalized edema, muscle wasting in shoulders and upper arms. The child may have a ‘moon face’. Potbelly due to weakness of abdominal muscles occurs. Skin changes in the form of thickening, cracking and areas of denudation occur. Hair changes color and becomes sparse.

Marasmus occurs when there is inadequate food intake resulting in energy deficiency. This leads to low insulin and high plasma cortisol levels. This results in amino acids being released from muscles making them available for protein synthesis.

A child with marasmus presents with no subcutaneous fat and wasted muscles. The body weight is severely reduced. There is no edema, and skin and hair changes are mild or absent.

Studies have shown that the incidence of PEM among Indian children could be as high as 51.6–70%.

Dental considerations

During tooth development, mild-to-moderate protein deficiency results in smaller molars, chemical alterations of the exposed enamel surface, significantly delayed eruption and retardation of mandibular development. Smaller salivary glands develop resulting in decreased salivary flow. This saliva has a different protein, amylase and aminopeptidase activity, thereby compromising its immune function. Delayed eruption and decreased salivary flow lead to increased incidence of dental caries. Epithelium, connective tissue and bone may be poorly developed. Insufficient intake of protein results in negative nitrogen balance, decreased levels of secretory IgA. This leads to a lowered resistance to infections, reduced ability to withstand the stresses of injury or surgery, and prolonged recovery time. PEM may be a major reason for the occurrence of necrotizing ulcerative gingivitis (NUG) and noma.

Lipids

Lipids provide more energy per gram than either carbohydrates or proteins and are an essential component of tooth enamel and dentin.

Chemistry and sources

The structural units of lipids are fatty acids. Saturated fatty acids contain only single bonds. Examples include palmitic and stearic acids found in animal fat, butter, coconut oil, chocolate, etc.

Monounsaturated fatty acids contain only one double bond. The most abundant of these is oleic acid found in olive, peanut oil and animal products.

Polyunsaturated fatty acids (PUFAs) contain two or more double bonds. Three PUFAs that are considered to be essential fatty acids include linoleic, linolenic and arachidonic acids. These are found in safflower, soybean, fish and corn oils, nuts and seeds.

Deficient consumption of fats leads to loss of weight. Deficiency of linoleic acid leads to growth retardation, skin lesions, and reproductive failure.

Over consumption of fats leads to excessive fat stores and obesity. Other conditions related to fat consumption include diabetes mellitus, hyperlipidemia, fatty infiltration of liver, and certain types of cancer.

Dental considerations

Epidemiological and laboratory studies indicate that fats have a cariostatic effect. Dietary fats probably have local rather than systemic influence. Hypotheses for anticariogenicity include:

1. Some fatty acids, such as oleic acid act as growth factors for lactobacilli, others, such as lauric acids inhibit the growth of streptococci.

2. Long-chain fatty acids may decrease the dissolution of hydroxyapatite by acids.

3. Oral food retention decreases with increased fat intake.

4. Fats may lubricate the tooth and prevent acid penetration into enamel.

5. Fats may produce a film on food particles and prevent partial digestion of food particles in the mouth.

6. Dietary fat delays gastric emptying, enhancing fluoride absorption and increasing tissue fluoride concentration.

Vitamins

Vitamins are catalysts for all metabolic reactions using proteins, fat and carbohydrates for energy, growth and cell maintenance. Vitamins are vital to life, but are required in minute amounts.

Vitamins are classified as fat soluble—vitamins A, D, E, K and water soluble—vitamins B, C.

Characteristics of fat-soluble vitamins

These are soluble in fats or fat solvents. Chemically, these are organic substances and do not contain nitrogen. These are absorbed in the intestines in the presence of bile. These are fairly stable to heat, as in cooking. Larger amounts of these vitamins can be stored in the body and for long periods of time. Thus, symptoms of deficiencies appear late. Increased intake may lead to toxicity.

Vitamin A

Vitamin A (retinol) is an essential nutrient needed in small amounts by humans for the normal functioning of the visual system; growth and development; and maintenance of epithelial cellular integrity, immune function, and reproduction. These dietary needs for vitamin A are normally provided as preformed retinol (mainly as retinyl ester) and provitamin A carotenoids or β-carotene.

Functions

Vitamin A functions at two levels in the body: the first is in the visual cycle in the retina of the eye; and the second is in all body tissues where it systemically maintains the growth and soundness of cells.

In the visual system, carrier bound retinol is transported to the retina. Rhodopsin, the visual pigment critical to dim-light vision, is formed in rod cells after conversion of all-trans-retinol to retinaldehyde, isomerization to the 11-cis-form, and binding to opsin. Alteration of rhodopsin through a cascade of photochemical reactions results in the ability to see objects in dim light. The speed at which rhodopsin is regenerated is related to the availability of retinol. A deficient intake of vitamin A thus leads to night blindness.

The growth and differentiation of epithelial cells throughout the body is especially affected by vitamin A deficiency. In addition, goblet cell numbers are reduced in epithelial tissues and as a consequence, mucous secretions (with their antimicrobial components) diminish. Cells lining protective tissue surfaces fail to regenerate and differentiate, hence they flatten and accumulate keratin. Both factors—the decline in mucous secretions and loss of cellular integrity—reduce the body’s ability to resist invasion from potentially pathogenic organisms. Pathogens can also compromise the immune system by directly interfering with the production of some types of protective secretions and cells. Classical symptoms of xerosis (drying or non-wettability) and desquamation of dead surface cells as seen in ocular tissue (i.e. xerophthalmia) are the external evidence of the changes also occurring to various degrees in internal epithelial tissues.

Current understanding of the mechanism of vitamin A action within cells outside the visual cycle is that cellular functions are mediated through specific nuclear receptors. Binding with specific isomers of retinoic acid (i.e. all-trans-and 9-cis-retinoic acid) activates these receptors. Activated receptors bind to DNA response elements located upstream of specific genes to regulate the level of expression of those genes. These retinoid-activated genes regulate the synthesis of a large number of proteins vital to maintaining normal physiologic functions. There may, however, be other mechanisms of action that is as yet undiscovered.

Dietary sources

Preformed retinal is found in milk, cheese, butter, eggs, meat, cod liver oil and liver. (β-Carotene is also present in yellow, orange and green leafy vegetables (spinach, turnip greens, broccoli).

To express the vitamin A activity of carotenoids in diets on a common basis, a Joint FAO/WHO Expert Group in 1967 introduced the concept of the retinol equivalent (RE) and established the following relationships among food sources of vitamin A:

1 μg retinol = 1 RE

1 μg β-carotene = 0.167 μg RE

1 μg other provitamin A carotenoids = 0.084 μg RE.

Older literature describes the International Unit of vitamin A. This may be converted to RE as depicted in Table 3:

Table 3

Estimated mean requirement and safe level of intake for vitamin A

Group	Mean requirement (mg RE/day)	Recommended safe intake (mg RE/day)
Infants and children
0–6 months
7–12 months	180	375
1–3 years	190	400
4–6 years	200	400
7–9 years	200	450
	250	500
Adolescents
10–18 years	330–400	600
Adults
Females
19–65 years	270	500
65+years	300	600
Males
19–65 years	300	600
65+years	300	600
Pregnant women	370	800
Lactating women	450	850

Source: Vitamin and mineral requirements in human nutrition, WHO.

1 IU retinol = 0.3 μg retinol

1 IU β-carotene = 0.6 μg β-carotene

1 IU retinol = 3 IU β-carotene.

Deficiency

Vitamin A deficiency leads to xerophthalmia and night blindness due to degeneration of epithelial cells. Xeroderma can also occur. Mild deficiency may be related to a depressed immune response.

Dental considerations

Vitamin A is necessary for growth of both soft tissue and bone. It is required for resorption of old bone and synthesis of new bone, formation of ameloblasts, odontoblasts, and maintenance of the integrity of epithelial tissues.

Severe deficiency of vitamin A may result in enamel hypoplasia and defective dentin formation in developing teeth. Odontoblasts lose the ability to arrange themselves in normal parallel linear formation leading to altered dentin deposition. This further leads to degeneration and atrophy of ameloblasts. This results in enamel hypoplasia characterized by defects in enamel matrix and incomplete calcification.

Clinical applications

Carotenoids possess antioxidant properties and are very efficient in scavenging singlet oxygen and peroxyl radicals. These free radicals are known to damage the structure and function of cell membranes. Thus a diet rich in antioxidants is associated with a lower risk of cancer and heart disease.

Stich and colleagues gave large quantities of (β-carotene and sometimes vitamin A to chewers of betel quids in Kerala, India, and to Canadian Inuits with pre-malignant lesions of the oral tract and witnessed reductions in leukoplakia and micronuclei from the buccal mucosa.

However, the amount of supplements used in these studies have been large and hence, not advisable other than increasing consumption of fruits and vegetables.

Retinoids have been used in oral precancer, cancer and immunologically mediated diseases such as lichen planus. Retinoids have a potent growth inhibiting effect on cancer in vivo and in vitro. They can induce apoptosis and regulate the function of the immune system. On this basis, retinoids have been used as chemopreventive agents in oral squamous cell carcinoma (SCC). However, clinical trials of retinoids have not yielded significant results. Retinoids have been used in the treatment of oral leukoplakia, and has been shown to cause temporary remission, but also causes toxicity. Retinoids have been used as an adjunctive treatment in the management of oral lichen planus. Retinoids eliminate reticular and plaque-like lesions but these recur following withdrawal of therapy.

Toxicity

Because vitamin A is fat soluble and can be stored, primarily in the liver, routine consumption of large amounts of vitamin A over a period of time can result in toxic symptoms, including liver damage, bone abnormalities and joint pain, alopecia, headaches, vomiting, and skin desquamation. Other clinical symptoms include diplopia, alopecia, dryness of mucous membranes, reddened gingiva, thinning of epithelium, cracking and bleeding lips, and increased activity of osteoclasts. Overconsumption of β-carotene leads to hypercarotenemia and yellow pigmentation of skin.

Vitamin D

Functions

Vitamin D is required to maintain normal blood levels of calcium and phosphate, which are in turn needed for the normal mineralization of bone, muscle contraction, nerve conduction and general cellular function in all cells of the body. Vitamin D achieves this after its conversion to the active form 1,25-dihydroxy vitamin D (1,25-(OH)₂D), or calcitriol. This active form regulates the transcription of a number of vitamin D-dependent genes that code for calcium-transporting proteins and bone matrix proteins. Vitamin D also modulates the transcription of cell cycle proteins, which decrease cell proliferation and increase cell differentiation of a number of specialized cells of the body (e.g. osteoclastic precursors, enterocytes, keratinocytes). This property may explain the actions of vitamin D in bone resorption, intestinal calcium transport and skin.

Sources

The most physiologically relevant and efficient way of acquiring vitamin D is to synthesize it endogenously in the skin from 7-dehydrocholesterol by sunlight (UV) exposure. In most situations, approximately 30 minutes of skin exposure (without sunscreen) of the arms and face to sunlight can provide all the daily vitamin D needs of the body (Table 4).

Table 4

Recommended nutrient intakes (RNIs) for vitamin D

Group	RNI (mg/day)
Infants and children
0–6 months	5
7–12 months	5
1–3 years	5
4–6 years	5
7–9 years	5
Adolescents
10–18 years	5
Adults
19–50 years	5
51–65 years	10
65+ years	15
Pregnant women	5
Lactating women	5

Units: For vitamin D, 1 I U = 25 ng, 40 IU = 1 mg, 200 IU = 5 mg, 400 IU = 10 mg, 600 IU = 15 mg, 800 IU = 20 mg.

Source: Vitamin and mineral requirements in human nutrition, WHO.

Skin synthesis of vitamin D may be influenced by:

Latitude and season—both influence the amount of UV light reaching the skin

The aging process—thinning of the skin reduces the efficiency of this synthetic process

Skin pigmentation—the presence of darker pigments in the skin interferes with the synthetic process because UV light cannot reach the appropriate layer of the skin

Clothing—virtually complete covering of the skin for a medical, social, cultural or religious reasons leaves insufficient skin exposed to sunlight

Sunscreen use—widespread and liberal use of sunscreen, though reducing skin damage by the sun, deleteriously affects synthesis of vitamin D.

It is recommended that individuals not synthesizing vitamin D should correct their vitamin D status by consuming the amounts of vitamin D appropriate for their age group.

Other food sources include cod liver oil, catfish, salmon, turnip greens, tuna, milk, egg yolk and butter.

Deficiency

Rickets is a clinical syndrome that occurs when there is a deficiency of vitamin D in the growing skeleton. Infants with rickets exhibit delayed development and muscle hypotonia, craniotabes (small non-calcified areas in skull bones), bossing of frontal and parietal bones, swelling of the rib costochondral junctions (rickety rosary). Severe rickets may be associated with hypocalcemic tetany, giving rise to laryngeal stridor when the vocal cords are affected.

Vitamin D deficiency in the adults is termed osteomalacia. Osteomalacia is characterized by bone pain, pathologic fractures. Muscle weakness and a waddling gait may be present.

Dental considerations

Patients with rickets also have involvement of alveolar bone resulting in its weakening. Patients with severe vitamin D deficiency develops enamel hypoplasia. This is characterized by pitting of surface enamel. These surfaces are prone to adherence of plaque. However, studies of susceptibility to caries among these teeth reveal conflicting results.

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