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NUTRITIONAL DISORDERS By Dr Runsewe-Abiodun T.I

NUTRITIONAL DISORDERS By Dr Runsewe-Abiodun T.I. Introduction. Nutritional disorders may result from eating too little or too much food. Or they may result from eating too little or too much of a particular nutrient, such as a vitamin or mineral.

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NUTRITIONAL DISORDERS By Dr Runsewe-Abiodun T.I

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  1. NUTRITIONAL DISORDERSBy Dr Runsewe-Abiodun T.I

  2. Introduction • Nutritional disorders may result from eating too little or too much food. • Or they may result from eating too little or too much of a particular nutrient, such as a vitamin or mineral. • Nutritional disorders may also develop when the body cannot use the nutrients it gets, regardless of whether a person eats appropriate amounts of a variety of foods

  3. Nutritional Disorder Can result from • Excessive or deficient macronutrient • Excessive or deficient micronutrient

  4. Micronutrient deficiency • The life and vitality of human beings depend crucially on certain vitamins and minerals that help determine the efficient functioning of the brain, the immune system, reproduction and energy metabolisms.

  5. Micronutrient deficiency (2) • The body needs only small amount of these nutrients g or mg/day – but it cannot manufacture them. They must be part of the diet or taken as supplement.

  6. Micronutrient deficiency (3) • Deficiency of any of them leads to learning disabilities, impaired work capacity, preterm deliveries, complications in pregnancy etc. • This is most devastating for preschool children and pregnant women amongst others. • It is also debilitating for the national economy as well.

  7. Micronutrient deficiency • Vitamin A • Vitamin B1 (Thiamine) • Vitamin B2 (Riboflavin) • Vitamin C • Vitamin D*** • Niacin • Zinc • Iron**** • Iodine

  8. Introduction • Nutritional disorders may result from eating too little or too much food. • Or they may result from eating too little or too much of a particular nutrient, such as a vitamin or mineral. • Nutritional disorders may also develop when the body cannot use the nutrients it gets, regardless of whether a person eats appropriate amounts of a variety of foods

  9. Nutritional Disorder Can result from • Excessive or deficient macronutrient • Excessive or deficient micronutrient

  10. Micronutrient deficiency • The life and vitality of human beings depend crucially on certain vitamins and minerals that help determine the efficient functioning of the brain, the immune system, reproduction and energy metabolisms.

  11. Micronutrient deficiency (2) • The body needs only small amount of these nutrients g or mg/day – but it cannot manufacture them. They must be part of the diet or taken as supplement.

  12. Micronutrient deficiency • Deficiency of any of them leads to learning disabilities, impaired work capacity, preterm deliveries, complications in pregnancy etc. • This is most devastating for preschool children and pregnant women amongst others. • It is also debilitating for the national economy as well.

  13. Historical background • Vitamin A was discovered in 1913 when experiments showed that if the only fat present in diets of young animals was lard, their growth was retarded, and when butter was substituted the animals grew and thrived. A substance in butter but not in lard was found also in egg yolk and cod-liver oil. It was named vitamin A.

  14. Vitamin A • Carotenes or carotenoids can act as a provitamin. There are many carotenoids in plants, but the most important for human nutrition is beta-carotene, which can be converted to vitamin A by enzymatic action in the intestinal wall. • Breastmilk is an important source of vitamin A for infants.

  15. Vitamin A Deficiency (VAD) • Deficiency of vitamin A constitutes the most widespread and serious nutritional disorders in developing countries. • Many tissues are affected, but mainly the cornea – blindness • VAD found mainly in children 6months –6years • VAD-in 5% of children in some parts of the country

  16. VAD • Dietary deficiency of vitamin A most commonly and importantly affects the eyes, and it can lead to blindness. • Xerophthalmia, meaning drying of the eyes (from the Greek word xeros, meaning dry), is the term now used to cover the eye manifestations resulting from vitamin A deficiency. • The serious eye manifestations of vitamin A deficiency leading to corneal destruction and blindness are mainly seen in young children. This condition is sometimes called keratomalacia.

  17. VADefficiency (VAD) • Includes not only Xerophthalmia but also other conditions in which Vit A status is subnormal. • *Keratomalacia-seen in infants and preschool children often in association with PEM • *Xerosis of the skin • *Follicular hyperkeratosis

  18. Xerophthalmia It covers all ocular manifestation of vitamin A deficiency including night blindness, conjuctival and corneal lesion. • Clinical features • *Bitot –spots: white foamy patches bilateral and on temporal parts of the eyes- indicate chronic deficiency. • *Conjunctival Xerosis • *Corneal Xerosis

  19. VAD • Vitamin A deficiency also has a role in a variety of clinical conditions not related to the eyes, and it may contribute to higher child mortality rates, especially in children who develop measles as measles act in synergism with VAD to inc. mortality rates in childhood.

  20. VAD • Vitamin A is involved in the functioning of the immune system. • Mild deficiency states stunted growth, increased infections and high level of childhood mortality.

  21. VAD • Vitamin A deficiency also adversely affects epithelial surfaces apart from the eye. • Deficiency of Vitamin A has been associated with increased rates and severity of infections.

  22. VAD • Vitamin A deficiency was neglected in the developing world for some time • However, the World Summit for Children (1991) and the International Conference on Nutrition (1992) called for the virtual elimination of vitamin A deficiency and its consequences, including blindness, by the year 2000. • Much more emphasis is now being placed on the control of vitamin A deficiency.

  23. Causes • An inadequate intake of carotene or preformed vitamin A, • poor absorption of the vitamin or • an increased metabolic demand. Of these three, dietary deficiency is by far the most common cause of xerophthalmia.

  24. Good sources of Retinol • Good sources of retinol, or preformed vitamin A, are liver, fish-liver oils, egg yolks and dairy products. • In most non-industrialized countries, however, the majority of poor people get most, often 80 percent or more, of their vitamin A from carotene in foods of vegetable origin.

  25. Daily dietary requirement • The biological activity of vitamin A is now usually expressed as retinol equivalents (RE) rather than in international units (IU). One RE is equal to 1 µg of retinol or 6 µg of beta-carotene. • The World Health Organization (WHO) has recommended an intake of 300 RE daily for infants and 750 RE for adults.

  26. Daily dietary requirement (2) Daily req. G Retinol/day • 0-6yrs. 300 • 7-10yrs. 4000 • Adolescents 750 • *For -carotene x6

  27. Epidemiology • The most common cause of blindness in children in many endemic areas. • Xerophthalmia occurs almost entirely in children living in poverty. • Extremely rare in more affluent families, even in areas where xerophthalmia is prevalent. • It is related to low socio-economic status, low levels of female literacy, land shortages, inequity, poor availability of curative and preventive primary health care, high rates of infectious and parasitic diseases and grossly inadequate family food security.

  28. Xerophthalmia as a significant health problem • Prevalence rates of five different signs have been recommended as criteria for judging whether xerophthalmia is a significant public health problem in a given population. • It is suggested that if the prevalence of any one sign (i.e. the percentage of children examined having the sign) in children aged six months to six years in a vulnerable population is above the cut-off, then xerophthalmia should be considered a public health problem in that population.

  29. Prevalence criteria for determining public health significance of vitamin A deficiency Sign Prevalence above (%) Night blindness 1 Bitot's spots 0.5 Corneal xerosis/corneal ulceration/keratomalacia 0.01 Corneal scar 0.05 Plasma vitamin A <10 µg/dl 5

  30. Clinical manifestations • WHO and others have accepted a classification of the disease according to certain signs. The classification is now widely used in surveys.

  31. Non-ocular effects of VAD • Non-ocular effects of vitamin A deficiency have been described better in experimental animals than in humans. • In young animals growth retardation is marked. • Providing vitamin A to children with measles is highly beneficial. • Research in several countries showed that providing vitamin A supplements reduced young child mortality by 20 to 40 percent.

  32. Laboratory tests • Since vitamin A is stored in the liver, a diet deficient in vitamin A results eventually in low hepatic stores. Thus the best way to judge vitamin A nutritional status is to obtain an estimate of the level of vitamin A in the liver. This level can be measured easily only at autopsy. • Determination of serum vitamin A levels is useful for community surveys. • Conjunctival impression cytology • Dark room adaptation etc

  33. Treatment • Effective treatment depends on early diagnosis, immediate dosing with vitamin A and proper treatment of other illnesses such as PEM, tuberculosis, infections and dehydration. • Severe cases with corneal involvement should be treated as emergencies. • Sometimes hours, and certainly days, may make the difference between reasonable vision and total blindness.

  34. Treatment • Treatment for children one year of age or over should be 200 000 IU of vitamin A orally or 100 000 IU of water-miscible vitamin A (retinyl palmitate) by intramuscular injection. • Vitamin A in oil should not be used for injection. • The oral dose should be repeated on the second day and again on discharge from hospital or seven to 30 days after the first dose. • These doses should be halved for infants.

  35. Xerophthalmia -Tx • When there is corneal involvement it is desirable to apply an antibiotic ointment such as topical bacitracin to both eyes six times per day. • Appropriate systemic antibiotics should also be administered.

  36. Treatment contd. • Night blindness and conjunctival xerosis are completely reversible and respond quickly to treatment using oral doses of vitamin A on an out-patient basis. • Corneal ulceration is arrested by treatment and will heal within a week or two but will leave scars. • The case fatality rate is often high because of accompanying PEM and infections.

  37. Prevention • As with PEM, three essentials for prevention of vitamin A deficiency are adequate food security, care and health.

  38. Prevention • Increasing the production and consumption of foods rich in vitamin A and carotene by at-risk populations. • Nutrition education- eat vit A rich foods e.g. green leafy vegetables provides  carotene. • Massive dose programme 200000 IU of vit A • Food fortification e.g fortified sugar in Central America or dried skimmed milk.

  39. IODINE DEFICIENCY DISORDERS (IDD) • Iodine deficiency is responsible not only for very widespread endemic goitre and cretinism, but also for retarded physical growth and intellectual development and a variety of other conditions. • These conditions together are now termed iodine deficiency disorders (IDD).

  40. IDD (2) They are particularly important because: · perhaps one-quarter of the world's people consume inadequate amounts of iodine; · the disorders have a major impact on the individual and on society; · of the four major deficiency diseases, IDD is the easiest to control.

  41. IDD- A CRIME • In fact, as H.R. Labouisse wrote in 1978 when he was Executive Director of the United Nations Children's Fund (UNICEF), "Iodine deficiency is so easy to prevent that it is a crime to let a single child be born mentally handicapped for this reason" (quoted in Hetzel, 1989). Nonetheless this crime persists.

  42. IDD • It describes better than goitre the extent of I2 deficiency. • Focussing on the extremes – goitre and Cretininism would seem to obscure the socioeconomic impact of I2 deficiency which affects over 400million people in Africa alone. • Prevalence rate in Nigeria 15 – 35%.

  43. IDD-tip of iceberg • Endemic goitre and severe cretinism –IDD iceberg. • They can be diagnosed relatively easily by health professionals without the use of laboratory or other tests.

  44. IDD-Submerged part The smaller, less visible enlargements of the thyroid gland and an array of other abnormalities are the submerged and larger part: • Mental retardation • Children's failure to develop psychologically to their full potential. • Higher rates of foetus loss (including spontaneous abortions and stillbirths), • deaf-mutism, • certain birth defects and neurological abnormalities.

  45. Effects of IDD • It affects all stages of fetal development, abortions, still birth, infertility, congenital malformation and neonatal morbidity • NB. Affected mother may have no overt sign of I2 deficiency.

  46. Cause of IDD • A less important cause of IDD is the consumption of certain foods which are said to be goitrogenic or to contain goitrogens. • Goitrogens are "antinutrients" which adversely influence proper absorption and utilization of iodine or exhibit antithyroid activity. • Foods from the genus Brassica such as cabbage contain goitrogens, as do certain root crops such as cassava • Unlike goitrogenic vegetables, cassava is a staple food in certain parts of Africa and it has been implicated as an important cause of goitre in these areas.

  47. Iodine deficiency occur in all areas where sea food is not eaten, mountainous areas and areas where iodine is periodically washed away by heavy rainfall or flood. • Other factors that would facilitate IDD include: • Ingestion of thiocyanate – as in cassava, maize bamboo shoots, sweet potatoes and lima beans – these block the thyroid uptake of I2. • Thioureas in millet, sorghum and groundnut impair the organification of I 2. • Bacterial and Chemical contamination of the H2O sources.

  48. Epidemiology • Any enlargement of the thyroid gland is called a goitre. • The thyroid is an endocrine gland centrally situated in the lower front part of the neck. • It consists of two lobes joined by an isthmus. In an adult, each lobe of the normal thyroid gland is about the size of a large kidney bean. • Endemic goitre is almost certainly caused by iodine deficiency, and where goitre is endemic other iodine deficiency disorders can also be expected to be prevalent.

  49. Epidemiology • Where goitre is endemic, often large numbers of people have an enlargement of the thyroid gland, and some have enormous unsightly swellings of the neck. • The condition is usually somewhat more prevalent in females, especially at puberty and during pregnancy, than in males.

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