Dietary Defiency and Excess

Weight, morbidity and life expectation —

Fat distribution differs between species and individuals. It is stored inside the abdomen in amphibians and reptiles. In mammals and many birds the fat is distributed around the body in discrete compartments in close contact with other tissues. The deposition, size and site of individual fat deposits is a constant variable in humans. Intermuscular depots of fat are the most metabolically active. Fat cell volume and activity is peculiar to any one site. Gender , appetite and exercise are important in dictating the distribution and abundance of fat tissue.

Excessive fat is stored in the white adipose tissue, when energy intake persistently exceeds energy output. It is reasonable to define obesity as a body mass index (BMI; weight/height2) greater than 30. It is not known why people become fat. Biological inheritance accounts for only 5 % of the chances of having a particular BMI index and amount of subcutaneous fat, but for 20 % of the propensity for the manner in which the fat is distributed. There is very little evidence to suggest a genetic basis for human obesity. The condition has a strong cultural and social background. In most obese patients high leptin concentrations have been found, interpreted as a reduced sensitivity to leptin’s physiological effects..

The type of obesity is important, whether the fat is distributed around the waist which is dangerous or gluteofemoral region which is not. Visceral adipose tissue is drained by the portal vein and directly drains into the liver. The release of free fatty acids from the waist, ie portal vein drained fat can be rapid and is a consequence of regional differences in the activity of lipolysis regulating hormones , catecholamines and insulin. Central obesity is associated with increased glucocorticoid production and the number of glucocorticoid receptors is greater in the visceral than in subcutaneous fat depots, whereas leptin gene expression is greatest in the subcutaneous tissue.

Little is known about the effect of weight change on longevity. In the adult who changes weight there are often concomitant changes in smoking habits and exercise levels. In a long study of weight changes and longevity in Harvard graduates, the lowest all-cause mortality was in individuals who maintained a stable body weight over 15 years. If there was an increase or decrease in weight of over 5 kg during that period then there was an increase in mortality. This was primarily due to an increase in coronary heart disease rather than to deaths from cancer. These changes in mortality were not influenced by smoking habits or exercise levels.

A long-term study between 1922 and 1935 followed up adolescents aged 13–18 who were overweight (BMI greater than 75th percentile). Mortality rates were compared with lean contemporary subjects with a BMI between the 25th to 75th percentile. In middle age (analysed in 1968) the only health risk from adolescent obesity was diabetes mellitus. When the group became elderly, then there was an increased mortality among those males who had been fat in adolescence. There was an increase in death from all causes, including coronary heart disease, stroke and colorectal cancer. The morbidity associated with early obesity in women included an increased incidence of coronary heart disease, atherosclerosis and arthritis.

Weight loss is a complex dietary management problem. A high fat and consequently high energy diet can be delicious and difficult to resist. Red pepper, chilli and mustard increase the thermogenic properties of a meal. The capsaicinoids in red peppers also increase the lipid oxidation properties of a meal in women, not unrelated to their sympathoadrenal system effects.


A definition of health should include the concept of sustainability or the ability of the ecosystem to support life in quantity and quality. Entrapment occurs when a community exceeds the food-carrying capacity of the land, when it lacks the ability to obtain food to sustain its population, or when its people are forced to migrate from a bad to a worse situation. Entrapment leads to dependence on outside aid, forced migration, starvation and possibly civil war. Increased mortality rate, continuing high birth rates, decreased longevity, poor uptake of contraception and precarious food sources raise the question of whether populations are in danger of entrapment.

1. The causes of starvation are many, but lack of food, especially energy and protein are critical deficiencies.

2. During starvation there is adaptation to the new dietary restrictions. The adaptation is both genetically and biologically determined, with physiological, metabolic, behavioural and social changes. There is considerable inter-individual variation in adaptation; children are particularly vulnerable.

3. Physiological efficiency is important in determining successful adaptation.

4. The effects of starvation are weight loss, changes in metabolism, and increasing dependence upon available nutrient stores. The specificity of such release of stores causes some metabolic imbalances, e.g. ketone body production.

5. Adaptations to low energy and low protein intakes are different. Low energy intake leads to weight loss and reduced energy. Dietary protein reduction has a profound effect on protein structure in all forms throughout the body.

6. Protein energy malnutrition (PEM) is a group of deficiency conditions where all combinations and degrees of energy and protein deficiency are represented.

7. Marasmus is a lack of dietary energy, protein and other nutrients, and is found in total starvation. Kwashiorkor is a deficiency of dietary protein with sufficient calorie intake.

8. In PEM the organs essential for life are conserved if possible at the cost of the expendable tissues.

9. Feeding can restore growth in the young, but intellectual recovery may not be complete.

Further Reading —

Blackburn GL ( 2001) Pasteur’s quadrant and malnutrition Nature 409, 397-401
Smith, R. (1993) Over population and over consumption. British Medical Journal, 306, 1285–6.
Weaver, L.T. and Beckerleg, S. (1993) Is health a sustainable state; a village study in the Gambia? Lancet, 341, 1327–30.
Allahbadia, G.N. and Shah, N. (1992) Begging eunuchs of Bombay. Lancet,339, 48–9.
American Gastroenterological Association Medical Position Statement ( 1996) Guidelines for the management of malnutrition and cachexia, chronic diarrhoea and hepatobiliary disease in patients with human immundeficiency virus infection. Gastroenterology 111, 1722-1752.
Ben-Tovin DI, Walker K, Gilchrist P, Freeman R. Kalucy R, Esterman A ( 2001) Outcome in patients with eating disorders: a 5 year study. Lancet. 357,1254-57.
Black JA (1997) Two hundred years since Malthus. British Medical Journal315, 20-27.
Burges, R.C. (1956) Deficiency disease in prisoners of war at Changi, Singapore. Lancet, ii, 411–18.
Collins S ( 2001) Changing the way we address severe malnutrition during famine. Lancet. 358, 498-501.
Dulloo AG, Jacqueet J ( 1999) The control of partitioning between protein and fat during human starvation: its internal determinants and biological significance. British Journal of Nutrition 82, 339-356.
Ferro-Luzzi A, James WPT ( 1996) Adult malnutrition: simple assessment techniques for use in emergencies. British Journal of Nutrition. 75, 3-10.
Henry CJK ( 2001) The biology of human starvation: some new insights. British Nutrition Foundation Nutrition Bulletin 26, 205-211.
Hoare S, Poppitt SD, Prentice AM, Weaver LT ( 1996) Dietary supplementation and rapid catch up growth after acute diarrhoea in childhood. British Journal of Nutrition, 76, 479-490.
Leader (1992) Insights into fasting. Lancet, 339, 152–3.
Leather S (1996) The making of modern malnutrition .The Caroline Walker Trust. London
McCarrison, R. (1921) Studies in Deficiency Disease, Oxford Medical Publications, Oxford.
McConnell AA, Reid DT ( 1998) The Irish Famine : a century and a half on . Proceedings of the Royal College of Physicians of Edinburgh 28, 383-394.
Olubodon, J.O.B., Jaiyesimi, A.E.A., Fakoya, E.A. and Olasoda, O.A. (1991) Malnutrition in prisoners admitted to a medical ward in a developing country.British Medical Journal, 303, 693–4.
Payne, PR, and Dugdale, A.E. (1977) Model for the prediction of energy, balance and bodyweight. Annals of Human Biology, 4, 425–35.
Smith DA, Woodruff MFA ( 1951) Deficiency diseases in Japanese Prison Camps. Medical Research Council. London. Special Report no 274.
Symposium. Clinical Nutrition in childhood ( 2000) Proceedings of the Nutrition Society. 59, 135-162.
Symposium. Nutrition in Clinical management : malnutrition in our midst. ( 1998) Proceedings of the Nutrition Society 55, 841-862.
Vaz M, Thangam S, Prabhu A, Shetty PS ( 1996) Maximum voluntary contraction as a functional indicator of adult chronic under nutrition. British Journal of Nutrition 76, 9-15.
Waterlow, J.C. and Stephen, J.M.L. (eds) (1981) Nitrogen Metabolism in Man, Applied Science Publishers, London.
Waterlow, J.C. (1986) Metabolic adaptation to low intakes of energy and protein. Annual Review of Nutrition, 6, 495–526.
Waterlow, J.C. (1994) Childhood malnutrition in developing nations. Annual Review of Nutrition, 14, 1–20.
Williams, C.D. (1933) A nutritional disease of child-hood associated with a maize diet. Archives of Disease in Childhood, 8, 423–33.
World Health Organization (1981) The Treatment and Management of Severe Protein Energy Malnutrition, WHO, Geneva.


Back to top