British Medical Bulletin (1981) Vol. 37, No. 1, pp.



but they do not, in any way, distinguish causes in the same
manner that the term protein-energy malnutrition quite
specifically suggests a dietary cause.
We can therefore make clinical distinctions between kwashi-
THE BIOCHEMISTRY AND orkor and marasmus, but the object of many experimental
PHYSIOLOGY OF KWASHIORKOR studies, and of dietary surveys in different parts of the world,
has been to find differences in their dietary aetiology. It is well
AND MARASMUS known that it is necessary to feed experimental animals
unrestricted amounts of diets low in protein to produce a
W A COWARD PhD syndrome resembling kwashiorkor; restricting the intake of any
diet will result in severe wasting. Survey work in Uganda
P G LUNN PhD (Whitehead et al. 1977) also showed that, when diets with a
wide range of protein: energy ratios are available within a
University of Cambridge
and community, it is the children who habitually consume diets from
Medical Research Council the low end of the range (protein: energy, 0.04-0.06) who are at
Dunn Nutritional Laboratory, Cambridge risk of developing kwashiorkor. These observations contrast
with others typified by those of Gopalan (1968). He showed
that, in Indian children eating cereal-based diets with a relatively
Concepts and definitions: protein-energy malnutrition, constant protein: energy ratio (0.08), either kwashiorkor or
kwashiorkor and marasmus marasmus could emerge if energy intakes were low. Taking
Adaptation to a deficiency of energy: the pathogenesis of extreme views would therefore suggest that kwashiorkor and
marasmus marasmus represent different aspects of the same disease (as the
Failure of adaptation to protein deficiency: the pathogenesis
term protein-energy malnutrition suggests) or that they are
of kwashiorkor
Pathogenesis of intermediate forms of protein-energy different diseases with distinguishable aetiologies.
malnutrition Protagonists of each idea have ample support for their
Regulation of body fluid volumes in protein-energy arguments but it is unrewarding to initiate a discussion of the
malnutrition aetiology of kwashiorkor and marasmus by emphasizing one
a The distribution of extracellular fluid volume theory to the exclusion of the other. A more realistic approach
b Sodium and water balance is to accept that each idea makes a worthwhile contribution in a
c Membrane defects and the sodium pump
worldwide context but that causes can differ in individual,
Plasma proteins in kwashiorkor and marasmus
References regional circumstances.

It is just four years since Alleyne et al. (1977) published their 2 Adaptation to a Deficiency of Energy: the Pathogenesis
comprehensive treatise on protein-energy malnutrition. In this of Marasmus
paper we will focus on a few developments in biochemistry and
physiology that we believe are important for our understanding It is now widely accepted that the severe wasting seen in
of how the clinical features of the disease emerge in children marasmic children represents the end-product of metabolic
subjected to a hostile environment and inadequate diet. adaptation to an inadequate energy intake, mediated by changes
in hormonal pattern. Although a child is not clinically identified
as a case of marasmus until weight-for-age falls below 60%, the
1 Concepts and Definitions: Protein-Energy Malnutrition,
relevant metabolic changes can be detected, within a community
Kwashiorkor and Marasmus
where marasmus occurs, well before this stage is reached.
In recent years it has been customary to use the term Whitehead et al. (1977) and Lunn et al. (1979a) showed that
"protein-energy malnutrition" to describe a group or spectrum fasting plasma cortisol and growth hormone (GH) levels were
of diseases that often affect children living in poor communities high but insulin concentrations were low in Gambian children
in most developing countries. The expression suggests impor- with faltering growth rates, and insulin: cortisol ratios were
tant concepts. These are that inadequate intakes of energy or strongly correlated with growth velocities (Lunn et al. 1979a).
protein, or both, are causative factors and that there is a The changes seen when children are admitted to hospital
continuous connection in terms of biochemistry and physiology (reviewed by Alleyne et al. 1977) are only more exaggerated
between the extreme forms of protein-energy malnutrition, examples of the same pattern.
which are kwashiorkor and marasmus. A reduction in plasma insulin concentration is a normal
For comprehensive clinical descriptions of the two syndromes response to a reduced food intake and extremely low values are
the reader may refer to Alleyne et al. (1977), but for the present seen in marasmic children admitted to hospital. Cahill (1970)
it will be sufficient to use a series of internationally accepted suggested that a decreased level of this hormone is the main
definitions suggested by a Wellcome Trust Working Party regulator for the release of energy metabolites from endogenous
(Lancet, 1970). The crucial diagnostic features are the degree sources. Raised plasma cortisol concentrations will augment
of body wasting and the presence of oedema. Thus, when the effect on the mobilization of skeletal muscle protein,
Harvard weight standards (Stuart & Stevenson, 1959) are used, releasing amino acids for gluconeogenesis and perhaps for the
children of 60-80% expected weight-for-age are called cases of hepatic synthesis of plasma proteins. Adipose tissue
kwashiorkor if oedema is present. Below 60% the diagnosis is mobilization will be enhanced by changes in GH concentra-
marasmic kwashiorkor if they have oedema or marasmus if tions, and free fatty acids will become available as alternative
oedema is absent. These definitions have the merit of simplicity sources of energy (Parra et al. 1973).


Vol. 37 No. 1

that there are other more (Coward et al. in South African children. from an early stage. plasma insulin concentrations The study of Lunn et al.BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn Reductions in the plasma concentration of thyroid hormones cance of a high variability in the unrelated individual require- have also been reported for marasmic children admitted to ments for protein and energy. but there are some features not Plasma cortisol and GH levels were not elevated. and much higher than those found in Gambian changes described are in most cases the expected responses to pre-school children of the same age (Whitehead et al. 1970). (1975) have shown that. This view is substantially different from the eostasis and oedema. to produce including albumin and apo-proteins for (J-lipoprotein synthesis. it has been demonstrated that they fall after in children. hied. This change can be regarded as A child admitted to hospital with kwashiorkor is usually an effective adaptation. Locking away cortisol may be a feature of kwashiorkor. 1977) and a markedly elevated tri-iodothyronine likely explanations (see section 4). feedback stimulus for GH release (Mohan & Jaya Rao. however. 1974. blood Although plasma cortisol concentrations are elevated • in glucose concentrations will tend to rise and result in hyper. 1981 . it would explain to a fatty liver. 1967). but this was not found to be the case in Egyptian children school children indicates that the first of these possible pathways (Carter et al. is the one adopted. only by feeding diets virtually free of protein (Edozien. If the excess energy is not removed. The malnutrition. By promoting muscle protein found in marasmic children with the same degree of anorexia synthesis. the appearance of kwashiorkor in children who. endemic. The those involved in the development of obesity and. malnutrition. then the situation described by Gopalan somatomedin concentrations are low in children with kwashi- (1968) in India. 1973. (1973) showed that this response occurs Enwonwu & Sreebny. becomes easier to understand. Anthony & even after a single meal. 1977). marasmus because they fail. If true. and certainly it has been therefore. 20 Br. Lunn el al. 1968). There need. 1979) can this adaptation between GH levels and the severity of protein deficiency as be overcome. level (Edozien et al. might otherwise be expected to become instead have a much reduced plasma insulin concentration marasmic. 1973) that impaired somatomedin production might cause a Waterlow (1974) has previously pointed out the likely signifi. 1975. be no hypoglycaemic stress and consequently no shown that short-term fasting in healthy subjects results in elevation of plasma cortisol or GH to cause wasting. as values 3 Failure of Adaptation to Protein Deficiency: the will be influenced by the duration and severity of the clinical Patbogenesls of Kwashlorkor phase of the illness. and deficiencies in (J-lipoprotein synthesis dietary ideas we have already outlined. 1981) also exists in the response of children discussed by Pimstone et al. Thus the rat is a poor model for kwashiorkor and a few days of feeding meals containing protein (Pimstone el al. metabolism is geared to survival. 1973). (1973). if the mechanisms regulating plasma GH concentrations in kwashi- considerable degree of individual variation to over-eating orkor have not been identified. 1968). The course taken may ultimately faster return to a normal insulin respose. These non-essential amino acids typical of the developmental phases of results suggest that a defect in the adrenals' ability to produce kwashiorkor (Grimble & Whitehead. 1967. This latter Plasma GH concentrations are high in children with response enables the animals to "burn-off' any energy excess kwashiorkor and are not reduced by glucose loads (Pimstone et and will prevent the development of changes we have described al. assessed by plasma albumin concentrations (Pimstone el al. and by inhibiting Synacthen (synthetic P'~24 adrenocorticotrophic hormone) gluconeogenesis will cause an accumulation of alanine and other results in a poor response (Jaya Rao et al. The considerable variation that exists between reports is not surprising. Children with all forms of protein-energy malnutrition have a When the low protein content of a diet limits growth there poor insulin response to a glucose load (Alleyne et al. 1979). In general. because of in- Rats do not respond to low-protein diets in this way and adequate food intakes. there is no evidence to support the suggestion (Grant el al. 1977). Fasting plasma insulin concentrations in these GH concentration is elevated and thyroid hormone concentra- children were higher than in children who had recovered from tions are either normal or reduced (Alleyne et al. very different from that which existed earlier in his illness but much more like that found in marasmus. Mann et al. Data from Jordan determine the kind of protein-energy malnutrition that even. Bull. Kajubi & Okel. information on thyroid hormone concentrations was obtained. 1968). 1977). effect. since lowering the basal metabolic rate described as apathetic and anorexic and the hormone profile is will conserve the meagre supplies of energy available. There can be only two options: energy can be stored as fat or it potassium supplementation of rehabilitation diets results in a can be removed by oxidation. (1973) in Uganda remains the most are reduced but can be normal. It must be a relative excess of energy. problem of adaptation is how to deal with the energy excess. 1971. even when energy intakes could be argued that this might be expected in a child whose are lower than recommended requirements. 1979). 1978. We believe. but no fully understood. hospital (Alleyne et al. high insulin concentrations will deplete the plasma of and infection. but a number of possibilities are (James & Trayhurn. 1979). Tulp et al. The mechanisms we have discussed are clearly similar to 1968. Robinson et al. Although plasma to low-protein diets. 1974). 1968). Jaya Rao (1974) essential amino acids in muscle when protein intake is low is proposed that some children develop kwashiorkor rather than likely to produce a fall in hepatic synthesis of export proteins. However. and stimulation of the adrenal cortex with essential amino acids. 1968. 1968) and Turkey (Giirson & Saner. or marasmus on identical diets. they are usually lower than those insulinaemia and fat deposition. amounts of cortisol adequate for adaptation to protein-energy Hypoalbuminaemia could lead to defects in body fluid homo. Fiorotto & Coward. Philbrick & Hill. 1971) tually develops (see MacLean & Graham. anorexia and hypoglycaemia. There is also an inverse relationship Edozien. Lunn et al. 1977). cortisol values are often elevated complete source of information on the hormonal profiles of and correlate with the degree of wasting and the severity of pre-school children living in an area where kwashiorkor is intercurrent infections (Abbassy et al. children with kwashiorkor. already in short supply. However. The impaired glucose tolerance (Vance et al. (Hopkins et al. indicate that adding chromium to the diet produces a similar The endocrine pattern in non-hospitalized Ugandan pre. where children can develop either kwashiorkor orkor.

was maintained by a reduction in the colloid Westhuysen et al. (1975a) found increased plasma renin content of interstitial fluid that matched the changes in plasma. irrespective of the presence of oedema. 1979b) that and suggests that. sodium loads. severe wasting could be induced in b Sodium and Water Balance children who are otherwise likely to present as cases of The alternative. 1973). Furthermore. although Van der water filtration. when a malnourished child develops sodium there may be another important way in which marasmic and water retention. or protein deficiencies. or perhaps complementary. the distribution of extracellular fluid between the vascular and (1973) found either normal or increased aldosterone secretion interstitial spaces. experi- example of a failure of homoeostasis that specifically dis. in practice. 1973) and baboons (M tinguishes kwashiorkor from other forms of malnutrition. again. while these 5 Regulation of Body Fluid Volumes In Protein-Energy changes will undoubtedly limit the potential for salt and water Malnutrition excretion. in preparation) showed that further reduction in plasma protein content will produce an changes in aldosterone concentration and plasma renin activity imbalance of the transcapillary forces and the organism's can precede the appearance of oedema by many months. It was proposed that the incidence of infections that of any other plasma protein. Klahr & Alleyne (1973) identified factors that causes of such losses are a measles infection or the presence of could impair the ability of malnourished children to excrete intestinal helminths. excessive salt and water retention. Alternatively. 37 No. However. because albumin synthesis admitted to hospital with oedema have the underlying rates are unalterably low (Patrick. idea begins with kwashiorkor. Worthington et range of plasma protein concentrations. While protein-energy malnutrition have elevated plasma renin ac- this adaptation to hypoproteinaemia is effective over a large tivities. Active renal salt and water retention might then occur to of the development of kwashiorkor (Lunn et al. by the recognition that the contribution of albumin to the total A conventional view was outlined by Whitehead & Lunn colloid osmotic pressure of plasma (>50%) is greater than that (1979). Likely renal function. cumstances the task is to identify the reasons for phases of oedema and hypoproteinaemia have appeared precipitously as a sodium retention in malnourished children. 1968). They observed that. published data show that renal plasma flow (RPF) and glomerular filtration rate (GFR) are decreased but. preventing excessive those with kwashiorkor. plasma albumin concentrations will fall kwashiorkor can develop. not In a review of the effects of protein-energy malnutrition on compensated for by increased rates of protein synthesis. it is more insistence that changes in plasma albumin concentration are likely that non-nutritional factors modulate the effects of the functionally important in the development of kwashiorkor and diet. because in normal animals the Westhuysen et al. al. the same group of workers (Van der fluid protein concentration. but other abnormalities occur and elevate plasma glucocorticoid concentrations will alter the their importance has to be considered. However. At the tubular level. This idea indicates that blood and plasma volumes will be reduced in kwashiorkor and the most recent observations with labelled erythrocytes (Viart. 1975b) showed that children suffering from plasma: interstitial fluid concentration ratio is about 2. the concept that children with kwashiorkor are over-hydrated We have also recently suggested (Lunn et al. For example. 1967). Srikantia (1968) postulated a role for antidiuretic 21 Vol. result of an increased gastrointestinal loss of plasma proteins. evidence for a specific association with the believe that the most important factors are those that determine presence of oedema is ambiguous. interstitial volume expansion will occur. We believe that many children with the development of oedema. 1979). In these cir- metabolic features of marasmus. two distinctly different views can now be low-protein diets and are not associated with evidence of identified. contradicting much of the Malnutrition earlier work. activity in oedematous malnourished rats but not in non- This represented a proportionally larger change in interstitial oedematous animals. the homoeostatic mech. further early pathogenesis of this disease. ments with sheep (Rabinowitz et al. and it is theoretically volumes measured with protein-bound tracers could be mis- possible that. Migeon et al. marasmic kwashiorkor might emerge The development of these ideas was stimulated by an (Whitehead & Alleyne. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward & P G Lunn Since plasma GH concentrations rise only in the terminal stages lost. it is prevent plasma volume contraction but. a normal balance of normal in children with marasmus and elevated in only half of transcapillary colloid osmotic pressures. (1977) measured plasma aldosterone concentrations in anism does not possess infinite gain because. 4 Pathogenesis of Intermediate Forms of Protein-Energy 1977) show that this is the case. effects of diet and accelerate wasting in children developing marasmus. when plasma monkeys fed low-protein diets and found elevated levels when protein concentration is reduced by half. but Fiorotto and W A Coward. In addition. interstitial fluid protein oedema was present. they are not specifically associated with the presence The appearance of oedema in malnourished children is an of oedema in children (Alleyne. as a result of the alternating dominance of energy leadingly large. 1972). in preparation) have shown that until recently little progress had been made in identifying its reductions in RPF and GFR are early effects of feeding cause. but our own serial studies with baboons concentrations reach values close to zero. At this stage any (M Fiorotto & W A Coward. in the face of the unlikely that GH-mediated changes are directly involved in the circulation's reduced ability to hold retained fluid. With only one exception (Srikantia. 1 . Superimposed on these. Viart suggested that in malnutrition plasma determine how available nutrients are used. when plasma protein rates in malnourished children but plasma concentrations were concentrations fall in protein-deficient rats. sodium retention could result from a The Distribution of Extracellular Fluid Volume elevated plasma aldosterone levels and increased plasma renin Coward & Fiorotto (1979) and Fiorotto & Coward (1979) activity but. The differences could be attributed to different We have suggested that the endocrine response to a diet can methodologies. control over the distribution of extracellular fluid volume will be Finally.

In this way it is possible to build normal children. 1975). 1975. total body water from 64% to over 70% of body weight in 14 Plasma RBP and TBPA have also been proposed as sensitive days but oedema does not appear. pp. 1978. It is unlikely that changes in only one aspect of universally accepted. (1971) showed that low transferrin concentrations were could cause increased fractional sodium resorption. We have therefore often found it distal tubule fluid. other workers report even indicators of nutritional status (Ingenbleek et al. the problem of the relationship of these and Reeds & Laditan (1976) extended this observation to changes to dietary and environmental causes of kwashiorkor.and length-for-age in under- significant dietary component. 1973) is not clear.—ED. higher values in oedema-free marasmic children (Hansen et al. 1975. The connection between these observations and those 6 Plasma Proteins in Kwashiorkor and Marasmus showing that fractional sodium reabsorption can be decreased in malnourished oedematous children (Alleyne. For also on utilization and catabolism. Ingenbleek et al. Wright & Briggs (1979) have recently reviewed the butes to oedema formation. rates of intravascular- leucocytes it was shown that there were dramatically increased extravascular exchange and the degree of hydration. PP. Bull. 1972. (1969). 22 Br. There associated with a poor prognosis in children with kwashiorkor. 1980). produce substantial changes in rates of plasma protein synthesis. but this idea has not been 1965). are compatible with these McFarlane et al. 1979) may be relevant. However. kwashiorkor but not in marasmus. recognized. However. It is the transport rates of sodium in kwashiorkor. 1981 . al. Fondu et al. showed that serum transferrin concentrations were linearly 1980) or. S « Nirumg* R«o. Furthermore. because their concentrations are greatly 1 1 See Golden & Golden. Our general view is that malnutrition because of its rapid response to refeeding in there is a need to separate the influence of those factors malnourished children. 1979) and erythrocytes synthesis (the diet. 1980). 1971. changes in its plasma environment in the renal medulla needed for salt and water concentration should be meaningful in terms of the ultimate reabsorption in later segments. if we accept water losses could be prevented only by reductions in RPF and that a low plasma albumin concentration specifically contri- GFR. ouabain-sensitive Na-K adenosinetriphosphatase activity is thyroxine-binding prealbumin (TBPA) and retinol-binding pro- increased (compared with normal and recovery values) in tein (RBP). the the interstitium and cells. never elevated in malnourished children. Thus. 31-36 of this Bulletin. where the functional significance c Membrane Defects and the Sodium Pump of changes in the concentration of a plasma protein is In following up lines of thought developed by Metcoff (1975). include those with marasmus. (1970) and Gabr et observations and. remains. where it was found that have consistently attracted attention: these are transferrin. malnutrition. and those controlling the general frequency with which iron-deficiency anaemia2 occurs in degree of hydration. essentially because urine osmolality is regulative physiology will be able to explain these findings. Delpeuch et al. Observations made by Patrick et al. In these circumstances the manner in which convenient to classify children according to their albumin the kidney regulates salt and water balance in relationship to concentration and to relate other biochemical changes to these intake may not have the precision of response available in values (Whitehead et al. Delpeuch et al. in experimental animals (Olusi et al. The protein-energy malnutrition. Children with kwashiorkor can that a decrease in transferrin concentration caused by mal- lose their oedema and decrease their total body water from 77% nutrition can be masked by an increase due to a lack of iron to 63% of body weight when they are fed diets not known to (Ismadi et al. 1973). In the first instance it should be responsive to synthesis would lead to the dissipation of the hypertonic changes in nutrient intake and. the latter workers Trace element deficiencies1 could provide the link (Patrick. which could be balance between these processes that determines whether the achieved only by an increase in membrane permeability to concentration of a specific protein reflects the degree of sodium and subsequent stimulation of the sodium pump. a thermogenic response involving nourished children although albumin concentrations were not increased sodium pumping might be relevant Others have also advocated the use of plasma transferrin It will be clear that we are some way from integrating all these concentration as a most sensitive index of protein-energy observations into a concise framework.and substrate-dependent component) but (Kaplay. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn hormone in oedema formation. Nichols et There are a multitude of reports on the usefulness of the al. It could be argued (Fiorotto. up a comprehensive picture of the development and resolution of kwashiorkor. secondly. but before discussing them it is peritubular capillaries would limit sodium reabsorption in the necessary to develop a concept that describes an ideal marker proximal tubules. There is no information on this aspect of renal This strategy is inevitably empirical. McFarlane et al. we can describe the "sensitivity" of a particular Patrick (1979) commented on the significance of changes in protein in malnutrition without simultaneously considering membrane permeability and the activity of the sodium pump in nutrient intake or the final form of malnutrition that emerges. if mirrored at the level of the renal tubule. Thus excessive sodium and pathology of protein-energy malnutrition. marasmic children fed high-energy diets increase their are likely to be less ambiguous. and in protein deficiency reduced rates of urea for malnutrition. but it is suggested that centration of any protein is dependent not only on rates of findings for leucocytes (Patrick.23-30 of thiiBuBttm. 1980) that measurement of plasma protein concentrations for the assess- hypoproteinaemia and low plasma oncotic pressure in the ment of nutritional status. 1965. if an energy intake in excess of requirements is a related to deficits in weight. since the plasma con- tubule cell physiology in malnutrition. it is clear that its measurement is evidence for the existence of a mechanism by which GFR in a useful in communities where kwashiorkor is the predominant single nephron is regulated by the composition or rate of flow of form of malnutrition. malnourished children can complicate the situation to the extent (1978) illustrate the problem. and sensitivity to reduced protein intake responsible for the distribution of body water between plasma. hied. however. three plasma proteins results obtained for erythrocytes.—ED. and in these circumstances other indices of malnutrition However. In contrast to this situation.

marasmus and marasmic kwashiorkor. The peak levels were lowest in kwashi. marasmus appears. or to their sites of synthesis. / . Zeitoun M M & Ragab M (1967)/. Stanfield J P & Whitehead R G (1977) deficiencies and protein deficiencies.1313-1319 Coward W A S Fiorotto M (1979) Proc. Chim. Davis I T . Nutr. plasma levels of holo-RBP (native homoeostasis. Coward W A. REFERENCES Abbassy A S. April 1967). 32. recognizes that kwashiorkor and marasmus are marasmus (Smith et al. The theory. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward & P G Lunn reduced in malnourished children admitted to hospital and tion and more appropriate to suggest instead that they are rapidly return to normal with refeeding. Nutr. Churchill. Ingenbleek Y. it is possible that a balanced relationship hours after treatment. (1978).375-379 Hopkins L L Jr. London Anthony L E & Edozien J C (1975) / . Trop. Med. Fondu P. identified as diet-independent plasma proteins. Clin. Afr. 1977. RBP and TBPA) and those this reason we have biased our discussions towards re- requiring larger protein intakes (albumin.721-722 Alleyne G A O (1965) Renal and cardiac function In severely malnourished Gabr M.501-514 Clin. Experimental studies on obese women (Shetty et al. Med. 24.918-921 Patwardhan V N (1968) Am. Schrieck Van den H-G. (1980) have also shown that TBPA concentrations decrease Another group of proteins that has recently attracted with increasing severity of malnutrition assessed anthropo. (1980) metabolically distinct diseases. J. University of London 216-221 Alleyne G A O (1967) Pediatrics (Springfield) 39. Ransome-Kuti O & Majaj A S (1968) Am. 282. 1978. awakening an interest in the latter disease. J. e d Calorie Alleyne G A O. 2. many aspects of the biochemistry and tion when only 1 g protein/kg body weight per day was fed physiology of kwashiorkor have not yet been explained. is most important. children with marasmic to disturbances in homoeostasis such as those found in kwashiorkor had intermediate values. RBP from the liver. Nutr. Edozien J C (1968) Nature (London) 220. Fiorotto M & Coward W A (1979) Br. However. 1975). The immunoglobulins (IgA. Clin. Niehaus N. 21. Nuxr. In this respect. For (prothrombin. Nutr. 101. 1974) that in a universal context it is necessary groups of proteins on the basis of the responsiveness to dietary to appreciate that a lack of nutrients in general. most concisely outlined by Schelp et are equally low in kwashiorkor.195-202 Gurson C T & Saner G (\91\)Am. Workers in metrically. rather than kwashiorkor.J. 37 No. since vitamin A deficiency inhibits the release of children in other developing countries. transferrin. 668-675 48. De Nayer P & De Visscher M (1975) Enwonwu C O & Sreebny L M (1971)/. Olson (1975) found it possible to distinguish view (McLaren. Mar M-H. 105. but it needs related to the accumulated surplus of native RBP in the liver experimental investigation and further studies on malnourished before dosing. following intramuscular for the synthesis of proteins (e. This result therefore indicates that RBP synthesis is less affected in marasmus than in We recognize that marasmus. Susheela T P & Narasinga Rao B S (1971) Indian J.596-600 Carter J P. Res. 21. It would be wrong to suggest stresses interact to produce the diseases identified as kwashi- that RBP and TBPA are better indices than albumin concentra. between proteinases and their inhibitors is destroyed.J. Ada. Nutr. Abd-FJ-Hadi K. peaking at 3 result of infection. Large et al. albumin) essential for injection with vitamin A. but lead to improvements in the prevention and treatment of the differences illustrate the difficulties that exist when the nutritional disease. The values achieved are kwashiorkor. Nutr. Nutr. Soc. Thailand (Schelp et al. This is an intriguing. Becker D & Pimstone B L (1973) Arch. Hay R W. Ogunshina & Hussain different indices from the dietary and metabolic points of view.106-109 108. 43. Med. IgG and IgM) were gap rather than a protein gap. Nutr. Whitehead R G & Lunn P G (1977) Br. 38. B Gholmy A & GrimbleR F & Whitehead R G (1970) Lancet.87-95. When proteinase inhibitor levels are high as a protein with the ligand retinol attached) increased. Nutr.g.400-411 Gopalan C (1968) In: McCance R A & Widdowson E M. Elucidation of the mechanisms involved will not only or absolute rates of synthesis. orkor. 49—58 (Proceedings of a Protein-energy malnutrition. Hyg. Cornu A & Chevalier P (1980) Br.(1971) / . diet-dependent although we may have an adequate knowledge of how and why proteins were subdivided into those that increased in concentra. 38. Mikhail M. However. El-Hawary M F S & El-Dali M. Brinkman G L & Bowie M D (1965) S. University of Cambridge 59.917-919 203-211 Edozien J C. proconvertin. but suggests that proteinase have recently investigated RBP and TBPA in children suffering inhibitor levels determine the extent to which a malnourished the combined effects of vitamin A deficiency and protein-energy child can mobilize endogenous proteins to provide amino acids malnutrition and have shown that. 1 . 1767-1776 Ingenbleek Y. Arnold. with an energy therapy. Child. CahiU G F Jr (1970) New Engl. Makoui T & Switzer B R (1978)/. so the authors considered that the peak concentrations provided some measure of the liver's ability to synthesize RBP from the outset. Dis. It was not possible convincingly minority of the world's malnourished children are likely to suffer to relate these differences in responsiveness to normal fractional from it.61-67 Fiorotto M (1980) Studies on oedema/unction in experimental protein-energy Ismadi S D. 42. J. 39. Trop. Hambley J. J. De Visscher M & De Nayer P (1972) Lancet. this leads orkor and highest in marasmus. London colloquium held in Cambridge. nutritional problem most frequently encountered by doctors In reviewing the relationship between diet and plasma protein working in developing countries. Nutr. / .1581-1587 23 Vol. Kattab A. Mandelbaum I M & Vis H L (1979) Am. 1. even though only a lipoprotein and complement). Med. but will also provide a more complete usefulness of an index for malnutrition is defined only in terms of understanding of how nutritional and other environmental sensitivity to a dietary change. Picou D I. (3. we accept the concentrations. pp.631-648 Grant D B. 21-31 13. Clin. Clin. 74.51-59 Hansen J D L. marasmic kwashiorkor and al. 63. 1979) attach crucial 1979) indicate that TBPA and RBP concentrations are sensitive metabolic importance to changes in the plasma concentration of to changes in either energy or protein intake and this finding a1-antitrypsin and a1-antichymotrypsin in the development of supports the observations that TBPA and RBP concentrations malnutrition. is the kwashiorkor. malnutrition (Thesis for PhD degree). Pediatr. novel idea. J. Jamaican children (Thesis for MD degree).115—126 491-195 Delpeuch F. attention are the plasma proteinase inhibitors.

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