Nutrition

Chapter 5 Nutrition




Introduction


In developing countries, lack of food and poor usage of the available food can result in protein-energy malnutrition (PEM); 50 million pre-school African children have PEM. In developed countries, excess food is available and the most common nutritional problem is obesity.


Diet and disease are interrelated in many ways:



In the UK, dietary reference values for food and energy and nutrients are stated as reference nutrient intakes (RNIs), on the basis of data from the Food and Agriculture Organization (FAO-WHO), United Nations University (UNU) expert committee, and elsewhere. The RNI is sufficient or more than sufficient to meet the nutritional needs of 97.5% of healthy people in a population. Most people’s daily requirements are less than this, and so an estimated average requirement (EAR) is also given, which will certainly be adequate for most. A lower reference nutrient intake (LRNI) which fails to meet the requirements of 97.5% of the population is also given. The RNI figures quoted in this chapter are for the age group 19–50 years. These represent values for healthy subjects and are not always appropriate for patients with disease.




Water and electrolyte balance


Water and electrolyte balance is dealt with fully in Chapter 13. About 1 L of water is required in the daily diet to balance insensible losses, but much more is usually drunk, the kidneys being able to excrete large quantities. The daily RNI for sodium is 70 mmol (1.6 g) but daily sodium intake varies in the range 90–440 mmol (2–10 g). These are needlessly high intakes of sodium which are thought by some to play a role in causing hypertension (see p. 778).



Dietary requirements




Energy


Food is necessary to provide the body with energy (Fig. 5.1). The SI unit of energy is the joule (J), and 1 kJ = 0.239 kcal. The conversion factor of 4.2 kJ, equivalent to 1.00 kcal, is used in clinical nutrition.






Energy requirements

There are two approaches to assessing energy requirements for subjects who are weight stable and close to energy balance:





Energy expenditure

Daily energy expenditure (Fig. 5.2) is the sum of:




Total energy expenditure can be measured using a double-labelled water technique. Water containing the stable isotopes 2H and 18O is given orally. As energy is expended carbon dioxide and water are produced. The difference between the rates of loss of the two isotopes is used to calculate the carbon dioxide production, which is then used to calculate energy expenditure. This can be done on urine samples over a 2–3-week period with the subject ambulatory. The technique is accurate, but it is expensive and requires the availability of a mass spectrometer. An alternative tracer technique for measuring total energy expenditure is to estimate CO2 production by isotopic dilution. A subcutaneous infusion of labelled bicarbonate is administered continuously by a minipump, and urine is collected to measure isotopic dilution by urea, which is formed from CO2. Other methods for estimating energy expenditure, such as heart rate monitors or activity monitors, are also available but are less accurate.


Basal metabolic rate. The BMR can be calculated by measuring oxygen consumption and CO2 production, but it is more usually taken from standardized tables (Table 5.1) that only require knowledge of the subject’s age, weight and sex.


Table 5.1 Equations for the prediction of basal metabolic rate (in MJ/day)























































Age range (years) Equation for predicting BMRa 95% confidence limits

Men


 


 


 10–17


0.0740 × (wt) + 2.754


±0.88


 18–29


0.0630 × (wt) + 2.896


±1.28


 30–59


0.0480 × (wt) + 3.653


±1.40


 60–74


0.0499 × (wt) + 2.930


N/A


 75+


0.0350 × (wt) + 3.434


N/A


Women


 


 


 10–17


0.0560 × (wt) + 2.898


±0.94


 18–29


0.0620 × (wt) + 2.036


±1.00


 30–59


0.0340 × (wt) + 3.538


±0.94


 60–74


0.0386 × (wt) + 2.875


N/A


 75+


0.0410 × (wt) + 2.610


N/A


Data from Department of Health, 1991. BMR, basal metabolic rate. aBodyweight (wt) in kg.


Physical activity. The physical activity ratio (PAR) is expressed as multiples of the BMR for both occupational and non-occupational activities of varying intensities (Table 5.2).


Table 5.2 Physical activity ratio (PAR) for various activities (expressed as multiples of BMR)

































  PAR

Occupational activity


 


 Professional/housewife


1.7


 Domestic helper/sales person


2.7


 Labourer


3.0


Non-occupational activity


 


 Reading/eating


1.2


 Household/cooking


2.1


 Gardening/golf


3.7


 Jogging/swimming/football


6.9


Total daily energy expenditure = BMR × [Time in bed + (Time at work × PAR) + (Non-occupational time × PAR)].


Thus, for example, to determine the daily energy expenditure of a 69-year-old, 50 kg female doctor, with a BMR of 4805 kJ/day spending one-third of a day sleeping, working and engaged in non-occupational activities, the latter at a PAR of 2.1, the following calculation ensues:



image



In the UK, the estimated ‘average’ daily energy requirement is:



This is at present made up of about 50% carbohydrate, 35% fat, 15% protein ± 5% alcohol. In developing countries, however, carbohydrate may be >75% of the total energy input, and fat <15% of the total energy input.


Energy requirements increase during the growing period, with pregnancy and lactation, and sometimes following infection or trauma. In general, the increased BMR associated with inflammatory or traumatic conditions is counteracted or more than counteracted by a decrease in physical activity, so that total energy requirements are not increased.


In the basal state, energy demands for resting muscle are 20% of the total energy required, abdominal viscera 35–40%, brain 20% and heart 10%. There can be more than a 50-fold increase in muscle energy demands during exercise.





Protein


In the UK, the adult daily RNI for protein is 0.75 g/kg, with protein representing at least 10% of the total energy intake. Most affluent people eat more than this, consuming 80–100 g of protein per day.


The total amount of nitrogen excreted in the urine represents the balance between protein breakdown and synthesis. In order to maintain nitrogen balance, at least 40–50 g of protein are needed. The amount of protein oxidized can be calculated from the amount of nitrogen excreted in the urine over 24 h using the following equation:


Grams of protein required = Urinary nitrogen × 6.25 (most proteins contain about 16% of nitrogen).


In practice, urinary urea is more easily measured and forms 80–90% of the total urinary nitrogen (N). In healthy individuals urinary nitrogen excretion reflects protein intake. However, excretion does not match intake in catabolic conditions (negative N balance) or during growth or repletion following an illness (positive N balance).


Protein contains many amino acids:



Animal proteins (e.g. in milk, meat, eggs) contain a good balance of all indispensable amino acids, but many proteins from vegetables are deficient in at least one indispensable amino acid. In developing countries, protein intake derives mainly from vegetable proteins. By combining foodstuffs with different low concentrations of indispensable amino acids (e.g. maize with legumes), protein intake can be adequate provided enough vegetables are available.


Loss of protein from the body (negative N balance) occurs not only because of inadequate protein intake, but also because of inadequate energy intake. When there is loss of energy from the body, more protein is directed towards oxidative pathways and eventually gluconeogenesis for energy.




Fat


Dietary fat is chiefly in the form of triglycerides, which are esters of glycerol and free fatty acids. Fatty acids vary in chain length and in saturation (Table 5.3). The hydrogen molecules related to the double bonds can be in the cis or the trans position; most natural fatty acids in food are in the cis position (Box 5.1).


Table 5.3 The main fatty acids in foods































































Fatty acid No. of carbon atoms : No. of double bonds Position of double bondsa

Saturated


 


 


 Lauric


C12:0


 


 Myristic


C14:0


 


 Palmitic


C16:0


 


 Stearic


C18:0


 


Monounsaturated


 


 


 Oleic


C18:1


(n-9)


 Elaidic


C18:1


(n-9 trans)


Polyunsaturated


 


 


 Linoleic


C18:2


(n-6)


 α-Linolenic


C18:3


(n-3)


 Arachidonic


C20:4


(n-6)


 Eicosapentaenoic


C20:5


(n-3)


 Docosahexaenoic


C22:6


(n-3)


a Positions of the double bonds (designated either n as here or ω) are shown counted from the methyl end of the molecule. All double bonds are in the cis position except that marked trans.



The essential fatty acids (EFAs) are linoleic and α-linolenic acid, both of which are precursors of prostaglandins. Eicosapentaenoic and docosahexaenoic acid are also necessary, but can be made to a limited extent in the tissues from linoleic and linolenic acid, and thus a dietary supply is not essential.


Synthesis of triglycerides, sterols and phospholipids is very efficient. Even with low-fat diets subcutaneous fat stores can be normal.


Dietary fat provides 37 kJ (9 kcal) of energy per gram. A high-fat intake has been implicated in the causation of:



The data on causation are largely epidemiological and disputed by many. Nevertheless, it is often suggested that the consumption of saturated fatty acids should be reduced, accompanied by an increase in monounsaturated fatty acids (the ‘Mediterranean diet’) or polyunsaturated fatty acids. Any increase in polyunsaturated fats should not, however, exceed 10% of the total food energy, particularly as this requires a big dietary change.





Polyunsaturated fatty acids

The n-6 polyunsaturated fatty acids (PUFA) are components of membrane phospholipids, influencing membrane fluidity and ion transport. They also have antiarrhythmic, antithrombotic and anti-inflammatory properties, all of which are potentially helpful in preventing cardiovascular disease.


The n-3 PUFA increase circulating high-density lipoprotein (HDL) cholesterol and lower triglycerides, both of which might reduce cardiovascular risk. Some of the actions of n-3 PUFA are mediated by a range of leukotrienes and eicosanoids, which differ in pattern and functions from those produced from n-6 PUFA.


Epidemiological studies and clinical intervention studies suggest that n-3 PUFA may have effects in the secondary prevention of cardiovascular disease and ‘all-cause mortality’ (e.g. 20–30% reduction in mortality from cardiovascular disease according to some studies). The benefits, which have been noted as early as 4 months after intervention, have been largely attributed to the antiarrhythmic effects of n-3 PUFA, but some work suggests that n-3 PUFA, administered as capsules, can be rapidly incorporated into atheromatous plaques, stabilizing them and preventing rupture. Whether these effects are due directly to n-3 PUFA or other changes in the diet is still debated.


The GISSI Prevention Trial, which followed over 11 000 patients for 3.5 years after a myocardial infarction, administered fish oils (eicosapentaenoic acid, EPA and docosahexaenoic acid, DHA) in the form of capsules and demonstrated a striking benefit in reducing mortality. The effects of vitamin E (300 mg α-tocopherol/day) were also studied, but no benefit was found.



Recommendations for fat intake

The British Nutrition Foundation and the American Heart Association presently recommend a two-fold increase of the current intake of total n-3 PUFA (several fold increase in the intake of fish oils, and a 50% increase in the intake of α-linolenic acid). Implementing this recommendation will mean either a major change in the dietary habits of populations that eat little fish, or ingestion of capsules containing fish oils. Some government agencies have warned of the hazards of eating certain types of fish, which increase the risk of mercury poisoning and possibly other toxicities.


The current recommendations for fat intake for the UK are shown in Box 5.2.






Carbohydrate


Carbohydrates are readily available in the diet, providing 17 kJ (4 kcal) per gram of energy (15.7 kJ (3.75 kcal) per gram monosaccharide equivalent). Carbohydrate intake comprises:



Carbohydrate is cheap compared with other foodstuffs; a great deal is therefore eaten, usually more than required.




Dietary fibre

Dietary fibre, which is largely non-starch polysaccharide (NSP) (entirely NSP according to some authorities), is often removed in the processing of food. This leaves highly refined carbohydrates such as sucrose which contribute to the development of dental caries and obesity. Lignin is included in dietary fibre in some classification systems, but it is not a polysaccharide. It is only a minor component of the human diet.


The principal classes of NSP are:



None of these are digested by gut enzymes. However, NSP is partly broken down in the gastrointestinal tract, mainly by colonic bacteria, producing gas and volatile fatty acids, e.g. butyrate.


All plant food, when unprocessed, contains NSP, so that all unprocessed food eaten will increase the NSP content of the diet. Bran, the fibre from wheat, provides an easy way of adding additional fibre to the diet: it increases faecal bulk and is helpful in the treatment of constipation.


The average daily intake of NSP in the diet is approximately 16 g. NSP deficiency is accepted as an entity by many authorities and it is suggested that the total NSP be increased to up to 30 g daily. This could be achieved by increased consumption of bread, potatoes, fruit and vegetables, with a reduction in sugar intake in order not to increase total calories. Each extra gram of fibre daily adds approximately 3–5 g to the daily stool weight. Pectins and gums have also been added to food to slow down monosaccharide absorption, particularly useful in type 2 diabetes.


Eating a diet rich in plant foods (fruits, vegetables, cereals and whole grain – the main sources of dietary fibre) is generally recommended for general health promotion, including protection against ischaemic heart disease, stroke and certain types of cancers. This has been attributed to a lipid lowering effect, the presence of protective substances, such as vitamin and non-vitamin antioxidants and other vitamins such as folic acid, which is linked to homocysteine metabolism, a risk factor for cardiovascular disease. Fermentation of fibre in the colon may protect against development of colonic cancer. However, associated lifestyle factors such as low physical activity may also help explain some of those associations.



Health promotion


Many chronic diseases – particularly obesity, diabetes mellitus and cardiovascular disease – cause premature mortality and morbidity and are potentially preventable by dietary change. This is a global problem, e.g. obesity affects one in nine adults in the world with the BMI being now similar in high- and middle-income groups. Reduction in salt and fat intake, combined with exercise and stopping smoking, would have a major effect on the health of the population.


Box 5.2 suggests the composition of the ‘ideal healthy diet’. The values given are based on the principle of:



Reductions in dietary sodium and cholesterol have also been suggested. There would be no disadvantage in this, and most studies have suggested some benefit.





Nutrient goals and dietary guidelines

The interests of the individual are often different from those associated with government policy. A distinction needs to be made between nutrient goals and dietary guidelines:



Since dietary habits in different countries vary, dietary guidelines may also differ, even when the nutrient goals are the same. Nutrient goals are based on scientific information that links nutrient intake to disease. Although the information is incomplete, it includes evidence from a wide range of sources, including experimental animal studies, clinical studies and both short-term and long-term epidemiological studies.




Protein-energy malnutrition (PEM)



Developed countries


Starvation uncomplicated by disease is relatively uncommon in developed countries, although some degree of undernourishment is seen in very poor areas. Most nutritional problems occurring in the population at large are due to eating wrong combinations of foodstuffs, such as an excess of refined carbohydrate or a diet low in fresh vegetables. Undernourishment associated with disease is common in hospitals and nursing homes, and Table 5.4 gives a list of conditions in which malnutrition is often seen. Surgical complications, with sepsis, are a common cause. Many patients are admitted to hospital undernourished, and a variety of chronic conditions predispose to this state (Table 5.5).


Table 5.4 Common conditions associated with protein-energy malnutrition


















Sepsis Dementia

Trauma


Malignancy


Surgery, particularly of GI tract with complications


Any very ill patient


GI disease, particularly involving the small bowel


Severe chronic inflammatory diseases


 


Psychosocial: poverty, social isolation, anorexia nervosa, depression


Table 5.5 Nutritional consequences of disease and the underlying risk factors (physical/psychosocial problems)







The majority of the weight loss, leading to malnutrition, is due to poor intake secondary to the anorexia associated with the underlying condition. Disease may also contribute by causing malabsorption and increased catabolism, which is mediated by complex changes in cytokines, hormones, side-effects of drugs, and immobility. The elderly are particularly at risk of malnutrition because they often suffer from diseases and psychosocial problems such as social isolation or bereavement (Table 5.5).





Pathophysiology of starvation (Fig. 5.4)

In the first 24 h following low dietary intake, the body relies for energy on the breakdown of hepatic glycogen to glucose. Hepatic glycogen stores are small and therefore gluconeogenesis is soon necessary to maintain glucose levels. Gluconeogenesis takes place mainly from pyruvate, lactate, glycerol and amino acids, especially alanine and glutamine. The majority of protein breakdown takes place in muscle, with eventual loss of muscle bulk.



Lipolysis, the breakdown of the body’s fat stores, also occurs. It is inhibited by insulin, but the level of this hormone falls off as starvation continues. The stored triglyceride is hydrolysed by lipase to glycerol, which is used for gluconeogenesis, and also to non-esterified fatty acids that can be used directly as a fuel or oxidized in the liver to ketone bodies.


Adaptive processes take place as starvation continues, to prevent the body’s available protein being completely utilized. There is a decrease in metabolic rate and total body energy expenditure. Central nervous metabolism changes from glucose as a substrate to ketone bodies. Gluconeogenesis in the liver decreases as does protein breakdown in muscle, both of these processes being inhibited directly by ketone bodies. Most of the energy at this stage comes from adipose tissue, with some gluconeogenesis from amino acids, particularly from alanine in the liver, and glutamine in the kidney.


The metabolic response to prolonged starvation differs between lean and obese individuals. One of the major differences concerns the proportion of energy derived from protein oxidation, which determines the proportion of weight loss from lean tissues. This proportion may be up to three times smaller in obese subjects than lean subjects. It can be regarded as an adaptation which depends on the composition of the initial reserves (Fig. 5.3). This means that deterioration in body function is more rapid in lean subjects. Furthermore, survival time is much less in lean subjects (~2 months), compared to the obese (can be at least several months).


Following trauma or shock, some of the adaptive changes do not take place. Glucocorticoids and cytokines (see below) stimulate the ubiquitin-proteasome pathway in muscle, which is responsible for accelerated proteolysis in muscle in many catabolic illnesses. In starvation, there is a decrease in BMR, while in inflammatory and traumatic disease the BMR is often increased. These changes all result in continuing gluconeogenesis with massive muscle breakdown, and further reduction in survival time.







Clinical features


Patients are sometimes seen with loss of weight or malnutrition as the primary symptom (failure to thrive in children). Mostly, however, malnourishment is only seen as an accompaniment of some other disease process, such as malignancy. Severe malnutrition is seen mainly with advanced organic disease or after surgical procedures followed by complications. Three key features which help in the detection of chronic protein-energy malnutrition (PEM) in adults are listed in Box 5.3.



Other factors that may suggest PEM include:



The factors listed in Box 5.3 act as a link between detection and management (Fig. 5.5, the ‘Malnutrition Universal Screening Tool’). If the underlying physical or psychosocial problems are not adequately addressed, treatment may not be successful.



PEM leads to a depression of the immunological defence mechanism, resulting in a decreased resistance to infection. It also detrimentally affects muscle strength and fatigue, reproductive function (e.g. in anorexia nervosa, which is common in adolescent girls; p. 1188), wound healing, and psychological function (depression, anxiety, hypochondriasis, loss of libido).


In children, growth failure is a key element in the diagnosis of PEM. New WHO standards for optimal growth in children 0–4 years have been adopted by developing and developed countries. They aim to reflect optimal rather than prevailing growth in both developed and developing countries, since they involved a healthy pregnancy and children born to non-smoking, relatively affluent mothers who breast-fed their children exclusively or predominantly for the first 6 months of life. The general principles of management of severe PEM in children are similar in developed and developing countries but resources are required to manage the problems once identified (see p. 205).



Treatment


When malnutrition is obvious and the underlying disease cannot be corrected at once, some form of nutritional support is necessary (see also pp. 221, 223). Nutrition should be given enterally if the gastrointestinal tract is functioning adequately. This can most easily be done by encouraging the patient to eat more often and by giving a high-calorie supplement. If this is not possible, a liquefied diet may be given intragastrically via a fine-bore tube or by a percutaneous endoscopic gastrostomy (PEG). If both of these measures fail, parenteral nutrition is given.



Developing countries


The International Union of Nutritional Sciences, with support from the International Pediatric Association, launched a global Malnutrition Task Force in 2005 to ensure that an integrated system of prevention and treatment of malnutrition is actively supported.


In many areas of the world, people are on the verge of malnutrition due to extreme poverty. In addition, if events such as drought, war or changes in political climate occur, millions suffer from starvation. Although the basic condition of PEM is the same in all parts of the world from whatever cause, malnutrition resulting from long periods of near-total starvation produces unique clinical appearances in children virtually never seen in high-income countries. The term ‘protein-energy malnutrition’ covers the spectrum of clinical conditions seen in adults and children. Children under 5 years may present with the following:



image Kwashiorkor occurs typically in a young child displaced from breast-feeding by a new baby. It is often precipitated by infections such as measles, malaria and diarrhoeal illnesses. The child is apathetic and lethargic with severe anorexia. There is generalized oedema with skin pigmentation and thickening (Fig. 5.6b). The hair is dry, sparse and may become reddish or yellow in colour. The abdomen is distended owing to hepatomegaly and/or ascites. The serum albumin is always low. The exact cause is unknown, but theories related to diet (low in protein, and high in carbohydrate) and free radical damage in the presence of inadequate antioxidant defences have been proposed.


image Marasmus is the childhood form of starvation, which is associated with obvious wasting. The child looks emaciated, there is obvious muscle wasting and loss of body fat. There is no oedema. The hair is thin and dry (Fig. 5.6a). The child is not so apathetic or anorexic as with kwashiorkor. Diarrhoea is frequently present and signs of infection must be looked for carefully.



A classification of severe malnutrition by the World Health Organization (WHO) (Table 5.6) makes no distinction between kwashiorkor and marasmus, because their approach to treatment is similar. The WHO classification of chronic undernutrition in children is based on standard deviation (SD) scores. Thus, children with an SD score between −2 and −3 (between 3 and 2 standard deviation scores below the median – corresponding to a value between 0.13 and 2.3 centile) can be regarded as being at moderate risk of undernutrition, and below an SD score of −3, of severe malnutrition. A low weight-for-height is a measure of thinness (wasting when pathological) and a low height-for-age is a measure of shortness (stunting when pathological). Those with oedema and clinical signs of severe malnutrition are classified as having oedematous malnutrition.


Table 5.6 Classification of childhood malnutrition



















  Moderate malnutrition Severe malnutritiona

Symmetrical oedema


No


Yes: oedematous malnutritionb


Weight-for-height SD score


−3 to −2 (70–79%)c


<−3 (<70%)c (severe wasting)d


Height-for-age SD score


−3 to −2 (85–89%)c


<−3 (<85%)c (severe stunting)


a The diagnoses are not mutually exclusive.


b Older classifications use the terms kwashiorkor and marasmic-kwashiorkor instead.


c Percentage of the median National Centre for Health Statistics/WHO reference.


d Called marasmus (without oedema) in the Wellcome classification and grade II in the Gomez classification.


Starvation in adults may lead to extreme loss of weight depending upon the severity and duration. They may crave for food, are apathetic and complain of cold and weakness with a loss of subcutaneous fat and muscle wasting. The WHO classification is based on body mass index (BMI), with a value <18.5 kg/m2 indicating malnutrition (severe malnutrition if <16.0 kg/m2).


Severely malnourished adults and children are very susceptible to respiratory and gastrointestinal infections, leading to an increased mortality in these groups.




Investigations


These are not always practicable in certain settings in the developing world.






Resuscitation and stabilization

The severely ill child will require:



The standard WHO oral hydration solution has a high sodium and low potassium content and is not suitable for severely malnourished children. Instead, the rehydration solution for malnutrition (ReSoMal) is recommended. It is commercially available but can also be produced by modification of the standard WHO oral hydration solution.


Infection is common (Box 5.4). Diarrhoea is often due to bacterial or protozoal overgrowth; metronidazole is very effective and is often given routinely. Parasites are also common and, as facilities for stool examination are usually not available, mebendazole 100 mg twice daily should be given for 3 days. In high-risk areas, antimalarial therapy is given.



Large doses of vitamin A are also given because deficiency of this vitamin is common. After the initial resuscitation, further stabilization over the next few days is undertaken, as indicated in Table 5.7.


Table 5.7 Timeframe for the management of the child with severe malnutrition (the 10-step approach recommended by the WHO)












Prevention


Prevention of PEM depends not only on adequate nutrients being available but also on education of both governments and individuals in the importance of good nutrition and immunization (Box 5.5). Short-term programmes are useful for acute shortages of food, but long-term programmes involving improved agriculture are equally necessary. Bad feeding practices and infections are more prevalent than actual shortage of food in many areas of the world. However, good surveillance is necessary to avoid periods of famine.



Food supplements (and additional vitamins) should be given to ‘at-risk’ groups by adding high-energy food (e.g. milk powder, meat concentrates) to the diet. Pregnancy and lactation are times of high energy requirement and supplements have been shown to be beneficial.




Vitamins


Deficiencies due to inadequate intake associated with PEM (Table 5.8) are commonly seen in the developing countries. This is not, however, invariable. For example, vitamin A deficiency is not seen in Jamaica, but is common in PEM in Hyderabad, India. In the West, deficiency of vitamins is less common but prominent in the specific groups shown in Table 5.9. The widespread use of vitamins as ‘tonics’ is unnecessary and should be discouraged. Toxicity from excess fat-soluble vitamins is occasionally seen.



Table 5.9 Some causes of vitamin deficiency in developed countries








Fat-soluble vitamins



Vitamin A


Vitamin A (retinol) is part of the family of retinoids which is present in food and the body as esters combined with long-chain fatty acids. The richest food source is liver, but it is also found in milk, butter, cheese, egg yolks and fish oils. Retinol or carotene is added to margarine in the UK and other countries.


Beta-carotene is the main carotenoid found in green vegetables, carrots and other yellow and red fruits. Other carotenoids, lycopene and lutein, are probably of little quantitative importance as dietary precursors of vitamin A.


Beta-carotene is cleaved in the intestinal mucosa by carotene dioxygenase, yielding retinaldehyde which can be reduced to retinol. Between a quarter and a third of dietary vitamin A in the UK is derived from retinoids. Nutritionally, 6 µg of β-carotene is equivalent to 1 µg of preformed retinol; vitamin A activity in the diet is given as retinol equivalents.





Vitamin A deficiency

Worldwide, vitamin A deficiency and xerophthalmia (see below) is the major cause of blindness in young children despite intensive preventative programmes.


Xerophthalmia has been classified by the WHO (Table 5.10). Impaired adaptation followed by night blindness is the first effect. There is dryness and thickening of the conjunctiva and the cornea (xerophthalmia occurs as a result of keratinization). Bitot’s spots – white plaques of keratinized epithelial cells – are found on the conjunctiva of young children with vitamin A deficiency. These spots can, however, be seen without vitamin A deficiency, possibly caused by exposure. Corneal softening, ulceration and dissolution (keratomalacia) eventually occur, superimposed infection is a frequent accompaniment and both lead to blindness. In PEM, retinol-binding protein along with other proteins is reduced. This suggests vitamin A deficiency, although body stores are not necessarily reduced.


Table 5.10 Classification of xerophthalmia by ocular signs






























Ocular signs Classification

Night blindness


XN


Conjunctival xerosis


XIA


Bitot’s spot


X2


Corneal xerosis


X2


Corneal ulceration/keratomalacia <image corneal surface


X3A


Corneal ulceration/keratomalacia >image corneal surface


X3B


Corneal scar


XS


Xerophthalmic fundus


XF


From WHO/UNICEF/IVACG 1988. X, xerophthalmia.


Mar 31, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Nutrition
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