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

19-24

BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS WA Coward&PGLunn

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).

19

Vol. 37 No. 1

The malnutrition. plasma insulin concentrations The study of Lunn et al. (1973) in Uganda remains the most are reduced but can be normal. already in short supply. in South African children. 1968). There need. indicate that adding chromium to the diet produces a similar The endocrine pattern in non-hospitalized Ugandan pre. If the excess energy is not removed. This change can be regarded as A child admitted to hospital with kwashiorkor is usually an effective adaptation. amounts of cortisol adequate for adaptation to protein-energy Hypoalbuminaemia could lead to defects in body fluid homo. 1977). 1979). because of in- Rats do not respond to low-protein diets in this way and adequate food intakes. effect. 1977). The impaired glucose tolerance (Vance et al. anorexia and hypoglycaemia. 1967. blood Although plasma cortisol concentrations are elevated • in glucose concentrations will tend to rise and result in hyper. feedback stimulus for GH release (Mohan & Jaya Rao. 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. the appearance of kwashiorkor in children who. 1968. If true. assessed by plasma albumin concentrations (Pimstone el al. high insulin concentrations will deplete the plasma of and infection. 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. However. 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. or marasmus on identical diets. 1979). endemic. hied. but a number of possibilities are (James & Trayhurn. 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. This view is substantially different from the eostasis and oedema. it has been demonstrated that they fall after in children. 1975. becomes easier to understand. there is no evidence to support the suggestion (Grant el al. 1973) that impaired somatomedin production might cause a Waterlow (1974) has previously pointed out the likely signifi. Data from Jordan determine the kind of protein-energy malnutrition that even. The considerable variation that exists between reports is not surprising. 1970). Bull. then the situation described by Gopalan somatomedin concentrations are low in children with kwashi- (1968) in India. 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. they are usually lower than those insulinaemia and fat deposition. (1973) showed that this response occurs Enwonwu & Sreebny. 1977). 1968). The course taken may ultimately faster return to a normal insulin respose. very different from that which existed earlier in his illness but much more like that found in marasmus. and stimulation of the adrenal cortex with essential amino acids.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. 1968). from an early stage. 1968). only by feeding diets virtually free of protein (Edozien. but there are some features not Plasma cortisol and GH levels were not elevated. 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. Thus the rat is a poor model for kwashiorkor and a few days of feeding meals containing protein (Pimstone el al. Fiorotto & Coward. Robinson et al. malnutrition. Locking away cortisol may be a feature of kwashiorkor. metabolism is geared to survival. 1979) can this adaptation between GH levels and the severity of protein deficiency as be overcome. 1978. marasmus because they fail. problem of adaptation is how to deal with the energy excess. is the one adopted. It must be a relative excess of energy. however. 1981) also exists in the response of children discussed by Pimstone et al. We believe. that there are other more (Coward et al. 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. 1971) tually develops (see MacLean & Graham. 1967). 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. The mechanisms we have discussed are clearly similar to 1968. The those involved in the development of obesity and. hospital (Alleyne et al. 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. 20 Br. 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. to produce including albumin and apo-proteins for (J-lipoprotein synthesis. 1968) and Turkey (Giirson & Saner. might otherwise be expected to become instead have a much reduced plasma insulin concentration marasmic. Tulp et al. 1974. Philbrick & Hill. (1973). even when energy intakes could be argued that this might be expected in a child whose are lower than recommended requirements. it would explain to a fatty liver. 1977). if the mechanisms regulating plasma GH concentrations in kwashi- considerable degree of individual variation to over-eating orkor have not been identified. Kajubi & Okel. 1973. However. but no fully understood. Anthony & even after a single meal. In general. and deficiencies in (J-lipoprotein synthesis dietary ideas we have already outlined. where children can develop either kwashiorkor orkor. Although plasma to low-protein diets. Lunn et al. level (Edozien et al. information on thyroid hormone concentrations was obtained. By promoting muscle protein found in marasmic children with the same degree of anorexia synthesis. There is also an inverse relationship Edozien. 1981 . 1971. 1979). Mann et al. Lunn el al. since lowering the basal metabolic rate described as apathetic and anorexic and the hormone profile is will conserve the meagre supplies of energy available. 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. 1973). (Hopkins et al. children with kwashiorkor. 1974). (1975) have shown that. and certainly it has been therefore. 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. 1977) and a markedly elevated tri-iodothyronine likely explanations (see section 4).

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

It is unlikely that changes in only one aspect of universally accepted. remains. We have therefore often found it distal tubule fluid. because their concentrations are greatly 1 1 See Golden & Golden. 31-36 of this Bulletin. 22 Br. and those controlling the general frequency with which iron-deficiency anaemia2 occurs in degree of hydration. However. in experimental animals (Olusi et al. 1978. 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. if we accept water losses could be prevented only by reductions in RPF and that a low plasma albumin concentration specifically contri- GFR. 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.and length-for-age in under- significant dietary component. 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. 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. 1981 . 1972. 1973). kwashiorkor but not in marasmus. BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn hormone in oedema formation. In contrast to this situation. produce substantial changes in rates of plasma protein synthesis. the the interstitium and cells. 1975). never elevated in malnourished children. Delpeuch et al. There is no information on this aspect of renal This strategy is inevitably empirical. S « Nirumg* R«o. (1969). if mirrored at the level of the renal tubule. (1970) and Gabr et observations and. It could be argued (Fiorotto. but this idea has not been 1965). The protein-energy malnutrition. al. PP. 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). Thus excessive sodium and pathology of protein-energy malnutrition. include those with marasmus. 1975. It is the transport rates of sodium in kwashiorkor. 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. However. Thus. 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. In this way it is possible to build normal children. malnutrition. McFarlane et al. 1965. 1973) is not clear. 1971. 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). if an energy intake in excess of requirements is a related to deficits in weight. 1979) may be relevant. Nichols et There are a multitude of reports on the usefulness of the al.23-30 of thiiBuBttm. 1979) and erythrocytes synthesis (the diet. three plasma proteins results obtained for erythrocytes. and in protein deficiency reduced rates of urea for malnutrition. Fondu et al. 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. secondly. For also on utilization and catabolism. up a comprehensive picture of the development and resolution of kwashiorkor. and sensitivity to reduced protein intake responsible for the distribution of body water between plasma. higher values in oedema-free marasmic children (Hansen et al. hied.and substrate-dependent component) but (Kaplay. 1980). where it was found that have consistently attracted attention: these are transferrin. 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. showed that serum transferrin concentrations were linearly 1980) or. the problem of the relationship of these and Reeds & Laditan (1976) extended this observation to changes to dietary and environmental causes of kwashiorkor. Furthermore. (1971) showed that low transferrin concentrations were could cause increased fractional sodium resorption. 1980). Wright & Briggs (1979) have recently reviewed the butes to oedema formation. malnourished children can complicate the situation to the extent (1978) illustrate the problem. but it is suggested that centration of any protein is dependent not only on rates of findings for leucocytes (Patrick.—ED. marasmic children fed high-energy diets increase their are likely to be less ambiguous. 1980) that measurement of plasma protein concentrations for the assess- hypoproteinaemia and low plasma oncotic pressure in the ment of nutritional status. Delpeuch et al. are compatible with these McFarlane et al. 1975. Ingenbleek et al. other workers report even indicators of nutritional status (Ingenbleek et al. Bull. rates of intravascular- leucocytes it was shown that there were dramatically increased extravascular exchange and the degree of hydration. essentially because urine osmolality is regulative physiology will be able to explain these findings. the latter workers Trace element deficiencies1 could provide the link (Patrick. however. Observations made by Patrick et al. In the first instance it should be responsive to synthesis would lead to the dissipation of the hypertonic changes in nutrient intake and. recognized. There associated with a poor prognosis in children with kwashiorkor. 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. pp. since the plasma con- tubule cell physiology in malnutrition. 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. 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. and in these circumstances other indices of malnutrition However.—ED.

The values achieved are kwashiorkor. Fiorotto M & Coward W A (1979) Br. Nutr. pp. Nutr. Nutr. This result therefore indicates that RBP synthesis is less affected in marasmus than in We recognize that marasmus. 63.106-109 108. 38. J. orkor.J. since vitamin A deficiency inhibits the release of children in other developing countries. The peak levels were lowest in kwashi. nutritional problem most frequently encountered by doctors In reviewing the relationship between diet and plasma protein working in developing countries. Med. Schrieck Van den H-G. peaking at 3 result of infection. 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. Picou D I. 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. J. The immunoglobulins (IgA. However. but it needs related to the accumulated surplus of native RBP in the liver experimental investigation and further studies on malnourished before dosing. novel idea. Pediatr. Workers in metrically. 1975). El-Hawary M F S & El-Dali M. 21-31 13. most concisely outlined by Schelp et are equally low in kwashiorkor. Cornu A & Chevalier P (1980) Br. Ogunshina & Hussain different indices from the dietary and metabolic points of view. Ada. or to their sites of synthesis. Becker D & Pimstone B L (1973) Arch. Arnold. Makoui T & Switzer B R (1978)/. malnutrition (Thesis for PhD degree). Soc. 42. Nuxr. Afr. Child. For (prothrombin. Edozien J C (1968) Nature (London) 220. Davis I T . 21. (3. Nutr. 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. marasmic kwashiorkor and al. Large et al. Trop. However. Coward W A. Whitehead R G & Lunn P G (1977) Br. (1980) have also shown that TBPA concentrations decrease Another group of proteins that has recently attracted with increasing severity of malnutrition assessed anthropo. In this respect. IgG and IgM) were gap rather than a protein gap. even though only a lipoprotein and complement). Med. The theory. Med. Clin. RBP from the liver. Nutr. Dis. Thailand (Schelp et al. London Anthony L E & Edozien J C (1975) / .g. Nutr. e d Calorie Alleyne G A O.195-202 Gurson C T & Saner G (\91\)Am. REFERENCES Abbassy A S. Ransome-Kuti O & Majaj A S (1968) Am. Nutr. B Gholmy A & GrimbleR F & Whitehead R G (1970) Lancet. 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. transferrin. identified as diet-independent plasma proteins. 105.400-411 Gopalan C (1968) In: McCance R A & Widdowson E M. 24.918-921 Patwardhan V N (1968) Am.501-514 Clin. Ingenbleek Y. rather than kwashiorkor. Nutr. children with marasmic to disturbances in homoeostasis such as those found in kwashiorkor had intermediate values. 668-675 48. 1. Hay R W. / .721-722 Alleyne G A O (1965) Renal and cardiac function In severely malnourished Gabr M. Jamaican children (Thesis for MD degree). is the kwashiorkor. Hyg. attention are the plasma proteinase inhibitors. marasmus and marasmic kwashiorkor. 1978. 74. albumin) essential for injection with vitamin A. it is possible that a balanced relationship hours after treatment.87-95.917-919 203-211 Edozien J C. De Visscher M & De Nayer P (1972) Lancet. 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. Mikhail M. Stanfield J P & Whitehead R G (1977) deficiencies and protein deficiencies. Zeitoun M M & Ragab M (1967)/. Elucidation of the mechanisms involved will not only or absolute rates of synthesis.J. 32. 101. Mar M-H. 43. 39. Clin. 38. Res. J. Clin. University of London 216-221 Alleyne G A O (1967) Pediatrics (Springfield) 39.61-67 Fiorotto M (1980) Studies on oedema/unction in experimental protein-energy Ismadi S D.375-379 Hopkins L L Jr. diet-dependent although we may have an adequate knowledge of how and why proteins were subdivided into those that increased in concentra. 21. recognizes that kwashiorkor and marasmus are marasmus (Smith et al. University of Cambridge 59. we accept the concentrations. De Nayer P & De Visscher M (1975) Enwonwu C O & Sreebny L M (1971)/.115—126 491-195 Delpeuch F. Med. (1978). awakening an interest in the latter disease. This is an intriguing. Brinkman G L & Bowie M D (1965) S.596-600 Carter J P. Nutr. 1767-1776 Ingenbleek Y. Clin. this leads orkor and highest in marasmus. (1980) metabolically distinct diseases. 1977. J. but lead to improvements in the prevention and treatment of the differences illustrate the difficulties that exist when the nutritional disease. Abd-FJ-Hadi K.51-59 Hansen J D L. Hambley J. Niehaus N. 2. following intramuscular for the synthesis of proteins (e. RBP and TBPA) and those this reason we have biased our discussions towards re- requiring larger protein intakes (albumin. marasmus appears.1581-1587 23 Vol. 49—58 (Proceedings of a Protein-energy malnutrition. 37 No. with an energy therapy. CahiU G F Jr (1970) New Engl. 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. When proteinase inhibitor levels are high as a protein with the ligand retinol attached) increased. Nutr. is most important. Mandelbaum I M & Vis H L (1979) Am.1313-1319 Coward W A S Fiorotto M (1979) Proc. / . J. 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. Chim. 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. Trop. between proteinases and their inhibitors is destroyed. Kattab A. Susheela T P & Narasinga Rao B S (1971) Indian J. Fondu P.631-648 Grant D B. plasma levels of holo-RBP (native homoeostasis.(1971) / . Churchill. Olson (1975) found it possible to distinguish view (McLaren. 282. Experimental studies on obese women (Shetty et al. proconvertin. so the authors considered that the peak concentrations provided some measure of the liver's ability to synthesize RBP from the outset. April 1967). London colloquium held in Cambridge. 1 .

4.393--W2 Schdp F P. J.BIOCHEMISTRY AND PHYSIOLOGY OF KWASHIORKOR AND MARASMUS W A Coward & P G Lunn James W P T & Trayhurn P (1981) Br. Hay R W & Baker B A (1973) Br. 33. Alvarado 1. Clin.Med. Ahmed S I & Jacobton K L (1977) Nutr. ed. 38. Adcock K J. Barbezat G. Cuellar A Soc. Neal G. Clin. Hyg. 32. Afr. Soc. J. 1. Santa Ynez. Supawan V. Lunn P G. Academic Press. Whitehead R G. Clin. J. Nutr. Thanangkul O.1200-1201 Pimstone B L. Glover J. 28. Migasen* P. Jackson A A.268-270 Srikantia S G (1968) In: McCtnce R A & Widdowson E M. Calorie McLaren D S (1974) Lancet. Med Bull.4m. Nutr. Schreura W H P & Supawan V (1977) Lunn P G. Nutr.43-^8 Pimstone B.189-195 & Nichols B L (1973) pp. ed. Garza C.794-800 Waterlow J C (1974) Lancet. PA Metcoff J (1975) In: Olson R E. Shoji E S.J. 2. 129-141 Kidney Int. ed. Reddy S. Coward W A & Lunn P G (1973) Lancet. ed. 2. 31-43* Worthington B S. Nutr.349-354 Ogunshina S O & Hussain M A (1980) Am. Trop. Barbezat G. 732-738 (1970) Br. 43.302-303 Reeds P J & LadiUn A A O (1976) Br. held in May 1973).1381-1387 colloquium held in Cambridge. Nutr. Clin. & Amacher P.1415-1422 Med. Saunders. 109. Chim.1799-1803 Mohan P S & Jaya Rao K S (1979)^rcA. Hansen J D L & Murray P (1968) Am. 73. Whitehead R G. Goodman D S & Olson McFariane H. New York 1321-1332 Migeon C J. London Mann M D. 28. Int. Clin. Protein-calorie malnutrition. Cocks T. Hansen J D L & Murray P (1967) Lancet. Rev. J. Med. Suttajit M. Whitehead R G. 31. Afr. Seakins A & Picou D I M (1978) Br. 365-367 Nutr.579-584 Rabinowitz L. Suskind R. Clin. 49. Nutr.813-818 ' For full bibliographic*] daaflj tec Migeon et at. 49. 2. 399—424 (Proceedings of a Van der Westhuysen J M. Osunkoya B O & Adesina H (1975) Clin. Patrick J (1979) Proc. J.55-61 pediatrics. R. 21. Danforth E Jr & Horton E S (1979) /. Buchanan K D & Williams R H (1968) /. Jones J J & Van Niekerk C H Nichols B L. Robinson H. Jones J J & Van Niekerk C H (1975a) S. J. Becker D J. Med. Garcia G.72-79 275-297. (1975b) S. 30. Lab. 39. 31. Academic Press. 59.J. (1973) 24 Br. Thanangkul O & Olson R E (1980) Br. J.1217 Smith F R. 38. 27.31-38 399-422 Schelp F P. 203-211 (Proceedings of a MacLean W C Jr & Graham G G (1979). Jung R T & James W P T (1979) Lancet. Adcock K J. Coward W A. J. Nutr. Dls. Trop. /.62-64 Van der Westhuysen J M.712 Olson R E (1975) In: Olson R E. Soc.4m. Parra A. 12-61. Pimpantha R. 65-85. Canseco L. Churchill. 2. 29.J./. Adeshina H.188-207 Lancet (1970) 2. Nutr. Tulp O L. 1981 . 38. Bull. Jaya Rao K S (1974) Lancet. pp. 290-297 kwashlorkor and psychosocial deprivation. 73-90* Kaplay S S (1978) Am. McFarlane H. ed. pp. 37. 4. 34. Freedland R A & Avery E H (1973) Klahr S & Alleyne G A O (1973) Kidney Int.Nutr. Pongpaew P & Schreurs W H P (1978) Am. Whitehead R G & Coward W A (1979b) Trans. Meyers C.766-767 Wright F S & Briggs J P (1979) Physiol. Becker D J & Hansen J D L (1973) pp.1729-1731 363-398* Viart P (1977) Am. Pongpaew P & Migasena P (1979) Am. Child. Hazlewood C F & Viteri F (1973) pp. Kanengoni E. New York Whitehead R G & Lunn P G (1979) Proc. Reddy S. 230-232 1. April 1967). Kroc Foundation. Med.. /. Rep.482^*87 Kajubi S K & Okel R M (1974) Am. CA J. Nutr. 7th ed. Clin. Dis.93-96 deficiencies and protein deficiencies. Cooke A R & Akene J R E (1975) Am. Nutr. J. Stuart H C & Stevenson S S (1959) In: Nelson W E. 1. 27. Nutr. Pongpaew P.958-1006 Patrick J. Philadelphia.438-^44 Shetty P S. 62. Klish W. Protein-calorie malnutrition. Kowarski A & Graham G G (1973) In: Gardner LI Vance J E. J.69-76 Olusi S O. 72. Br. Gunther R A.61-68 751-760 Patrick J (1980) Lancet.255-263 Large S. Child. Med. Lunn P G. 3. pp. Srikantia S G & Gopalan C (1968) Arch. J. Nutr. Kimzey S L. McFarlane H. Clin. Cole T J & Austin S (1979t) Br. Nutr. Nutr. Med. Argote R M.417-424 Phflbrick D J & Hill D C (1974) . Nutr. 32. Pimstone B L. Cooke A & Gumey J M (1969) Lancet. 16. 45-72* 43. Soc. Leitzmann C. Kerr D & Picou D (1973) pp. 41.451-456 73-84 Schelp F P. Nutr. symposium. 1. Clin. Bull. 36. 709-711 1333-1334 Jaya Rao K S. Beitins I Z. Thanangkul O. 71. pp. Watrasiewicz K E. Med. Migasen* P. J. Nulr. Clin.107-116 Whitehead R G. Nutr. Endocrine aspects of malnutrition: marasmus. Whitehead R G & Alleyne G A O (1972) Br. Pimstone B L & Hansen J D L (1975) Br. pp. Reeds P J. Clin. Krupp P P. Lunn P G A Rutishauser I (1977) Trans R.63-66 Ada. J.Hyg. Textbook of 33.

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