Type I and type II deficiencies
Type I and type II deficiencies Michael Golden 26.03.2000
Re: type I and type II deficiencies: Part 2 Ian Darnton-Hill 30.04.2000
Re: type I and type II deficiencies Michael Golden 04.05.2000
Re: type I and type II deficiencies Ian Darnton-Hill 08.05.2000
First phase diet in severe malnutrition Liana Steenkamp 17.05.2000


Date: Sun, 26 Mar 2000 12:34:19 +0100

From: Michael Golden <m.goldenatabdn.ac.uk>

Subject: Type I and type II deficiencies.

 

Dear NGONUTS,

I have received the following message from Tor Strand in Nepal, about type I and II deficiencies. As I am asked this same question very frequently, I add a full explanation to the bottom of this message. It is consequently now quite long and I will need to send it in two parts: for this I apologise.

Nevertheless, I do think that this concept indicates where we may have gone wrong in the past with nutritional intervention and where we could go in the future.

Mike Golden

 

--------------------------------

To: Nutri <ngonutatabdn.ac.uk>

Message-ID: <B50378FE.3A29%Toratwlink.com.np>

 

Can anybody explain me the difference (again) between type 1 and type 2 micronutrients?

Thank you

 

Dr. Tor A Strand

Centre for International Health, University of Bergen, Norway

Current address. (from February 6 till May 22 2000) P.O. Box 1045, Jawlakhel, Kathmandu, Nepal

Phone: 00-977-1-53 02 98, Fax: 00-977-1-53 87 20

Email: tor.strandatcih.uib.no, http://www.uib.no/People/mihtr

-------------------------------------

 

Type 1 and type II nutrient deficiency

By Michael H. N. Golden

 

A child responds to a deficiency of an essential nutrient in one of two quite different ways.

First, he can continue growing, consume the body stores and then have a reduction in the specific bodily functions that depend upon the deficient nutrient. Or, second, he can stop growing, avidly conserve the nutrient in the body and, if necessary, loose weight to make the nutrient internally available and thus maintain the concentration of the nutrient in the tissues. The difference between these two responses is fundamental and can be seen in experimental and farm animals, bacteria and even in plants grown on soils that have the same nutrient deficiencies.

The nutrients whose deficiencies give rise to a type I or a type II response I have called type I and type II nutrients. A list of the nutrients that fall into each category is given in table 1 and a summary of the differences in the type of response in table 2.

Why is it important to distinguish these two classes of nutrient?

We all usually think about nutrient deficiencies as if they gave a type I response; because we very rarely recognise type II deficiency these nutrients have been ignored by nutritionists and their deficiencies remain largely uncorrected. I have argued (1,2) that type II nutrient deficiency is responsible for stunting in height. If this is correct then half the children in the world have unrecognized type II nutrient deficiency. Let us compare and contrast the type I and type II nutrients and explore the implications of the different ways in which we respond to a dietary lack of these nutrients.

 

TYPE I nutrient deficiency.

These are the nutrients (table 1) which are required principally for specific metabolic functions in the body, rather than for metabolism in general. They are stored in the body. With a deficient diet the person continues to grow normally. The body store is consumed first and then the concentration of the nutrient in the tissues falls so that the specific metabolic function (biochemical pathway) that depends upon the nutrient declines until the person becomes ill. The illness is recognized by particular and characteristic signs and symptoms; after this stage is reached growth may, or may not, be affected secondary to the overt illness.

The diagnosis of a deficiency of a type I deficiency is relatively straightforward. We can usually recognise the clinical picture; then we either measure the concentration of the nutrient itself or measure the protein/enzyme that depends upon the presence of the nutrient or test the relevant metabolic pathway or physiological function. For example, with iron deficiency we recognise anaemia, examine the red cells and then measure ferritin, iron, transferrin or protoporphyrin. Similarly, with iodine we recognise the goiter and the signs of hypothyroidism and then measure iodine, thyroxine or other thyroid related hormones. As doctors, nurses and nutritionists we learn to recognise, diagnose and treat all the type I nutrient deficiencies listed in table 1. Because their deficiencies are common we make sure that there are adequate amounts in the diet, we supplement or fortify foods where deficiency is common and we develop specific programmes to alleviate the problems.

It is important to realise that because growth failure is not a necessarily part of the clinical picture of a type I nutrient deficiency, fat or tall people can be severely deficient of these nutrients without an anthropometric change. Anthropometric surveys do not tell us about the status of any of these nutrients in a population.

 

TYPE II nutrient deficiency

With type II deficiency, there are no characteristic signs or symptoms that differentiates one type II deficiency from another. They all give the same picture of poor growth, stunting and wasting. This concept is important because a person can easily have a deficiency that goes uncorrected because the actual nutrient that is deficient is not recognized.

When there is a deficiency of one of the `type II' or `growth' nutrients the person stops growing, the body starts to conserve the nutrient so that its excretion falls to very low levels and there is no reduction in the tissue concentration. With continued or severe deficiency the body starts to break down its own tissues to release the nutrient for use by the rest of the body; this process is associated with a reduction of appetite.

There are no body stores of these nutrients that can be called upon in an emergency and into which excess nutrients can be deposited. Thus, as the tissue is broken down to release the deficient nutrient, the excess of all the others is excreted from the body and lost. During reversal (convalescence or catch-up) they will all have to be given to the person to make good these losses as well as replacing the deficient nutrient. These deficiencies do not affect at any organ or tissue in particular, except, perhaps, in relation to those with very a high mitotic and synthetic rate such as the immune system and the intestinal mucosa, rather all tissues and organs are affected.

These have always been the `problem' nutrients without clearly defined diagnostic tests or determination of human requirements. With animals the requirements have been assessed with "growth" assays. In other words the experimental animal has been given a diet with graded amounts of the nutrient and the point at which there is no increase in growth rate is taken as the requirement. As such experiments have not been performed in humans for ethical reasons, we are not clear about the precise requirements for man. Nevertheless, it is clear that the desired rate of growth is the major determinant of the dietary requirement for all the type II nutrients.

They all need to be supplied in greatly increased amounts when rapid weight gain is required, for example during convalescence from illness, and also when catch-up in weight or height is needed.

There are major conceptual and practical difficulties when we try to understand these deficiencies. Thus, for example, it is difficult to comprehend how an animal can die from zinc deficiency when it has a normal concentration of zinc in its tissues (3); yet such an animal will die without zinc and it will respond rapidly and dramatically to small amounts of dietary zinc. The same applies to the other type II nutrients. To appreciate how this comes about is to understand these nutrients. They form part of the structure and fundamental metabolic machinery of each and every cell; they form the structure of the body and are concerned in practically every metabolic pathway and all the fundamental process such as protein and nucleic acid synthesis, metabolite transport and ionic gradients.

The strategy that the body uses for dealing with day to day fluctuations in intake is different for the two classes of nutrient. With the type I nutrients the body maintains a store that is added to and drawn upon to buffer changes in supply. In contrast, with the type II nutrients some of the dietary intake is incorporated into functional tissue during its "turnover" and the rest, which is in excess, is excreted. In the face of a low intake the body homeostatically reduces the excretion to minute amounts and recycles the nutrient, within the body. However, this conservation and re-use strategy means that growth (which increases the total pool of the nutrient if the concentration is to be maintained) cannot occur during a period of limited intake; the body maintains the concentration of the nutrient in the tissues mainly by stopping growth as soon as there is a dietary limitation of any one of these nutrients. The child's body goes into a `maintenance mode', with all the functions, apart from growth, continuing normally. If the low dietary intake continues for a sufficient time then, as the individual 'maintains' himself, he falls further and further behind his peers to eventually present as growth failure.

As the response to a deficiency - growth failure - is the same for each of the nutrients, when we observe growth failure it could be caused by a lack of any one of the type II nutrients and we cannot be sure which is responsible - is it phosphorus or potassium, magnesium or zinc, nitrogen or sulphur?

This is not a major problem in practice for treatment ,because we should treat type II deficiency by giving a diet which contains sufficient amounts of all of these nutrients in a balanced way. It is a major problem for prevention - in one society the limiting type II nutrient may be zinc and in another protein or phosphorus - giving the wrong ones will have no effect.

The mechanisms by which the body ceases growth in response to nutritional lack (by reducing the production of the hormonal mediators of growth, down-regulation of receptors, reducing protein synthesis, etc.) gives a similar hormonal picture to that seen in endocrine disease. Apart from poor growth, no feature reproducibly corresponds with deficiency, indeed there does not need to be any `defect' in the animal's metabolic pathways that can be related to the diet and held responsible for the growth delay; only the adaptive hormonal changes mediating the slow growth need be present. Growth failure, and growth failure alone, is the effect of a diet deficient in protein, zinc, magnesium, phosphorus, potassium etc..

The response to a long standing mild deficiency is a diminutive person, with the body in proportion. The extent of the stunting will be in relation to the integral of the degree of shortfall of the nutrient and time. With a mild deficiency there will be no clinical signs, except maybe a poor appetite, until growth failure becomes apparent: if the diet is restored before growth failure is diagnosed the deficiency will go completely undetected.

With a severe deficiency,there may be loss of tissue leading to wasting, without necessarily time for stunting to become apparent; again the nutritional nature of the wasting may remain undiagnosed and be ascribed to toxins, infection, worms, or another pathological agent altogether. The balance between the severity of the deficiency and its duration will also determine the relative amounts of stunting and wasting that are produced.

Mild, chronic deficiencies are expected to be more common than severe, acute deficiencies so that stunting would be predicted to be more common than wasting: this is what is observed.

As a consequence of not having a store for type II nutrients, when there is a negative balance for one of these nutrients, implying tissue catabolism, there is a negative balance for all the components of lean tissue. Thus protein, zinc or potassium deficiency, for example, will each lead to a negative balance of the other type II nutrients, in proportion to their relative concentrations in the tissues that are being broken down. This was shown elegantly by Rudman et al in parenterally fed adults (4).

Nutrient balance studies are thus unreliable in predicting which nutrient is deficient in the diet. When we observe a negative balance for any one nutrient such as nitrogen, we should consider a type II nutrient deficiency as a possible cause. During treatment, as whole tissue has been lost, all the components for that tissue to be resynthesised need to be given irrespective of the cause of the negative balance and weight loss.

Because of the avid metabolic conservation possible, it is extremely difficult to produce a deficiency of one of these nutrients in the non-growing child or adult by dietary means alone; there usually has to be a pathological loss of the nutrient from the body. Thus, it is almost impossible to produce sodium deficiency in the normal adult (5) unless there is excess sodium loss in sweat or diarrhoea. Depletion of the type II nutrients sufficiently severe to cause loss of function are thus usually found in association disease such as persistent diarrhoea and are probably the reason that persistent diarrhoea is associated with anorexia and weight loss (instead of an increased appetite as one would expect with energy deficiency).

Because the type II nutrients are fundamental to basic biological processes throughout the plant as well as the animal kingdom, they tend to have similar concentration ratios in many foods. It is not, therefore, unusual for diets to be deficient in several of these nutrients. These nutrients are dietary 'fellow travellers'. It is very difficult or impossible to determine if a particular type II nutrient is causing growth failure in the individual (2), however, it is relatively simply to find out if a child with low weight-for-height or height-for-age has a deficiency of one of these nutrients. The growth response to a trial of a complete and balanced diet should form part of the assessment of all such children.

Apart from growth failure the other response which is common with a deficiency of each of these nutrients is anorexia; this is corrected if the nutrient is supplied. Thus, if a child with zinc deficiency is supplemented with zinc, he will regain his appetite and have an increased intake of protein, energy, potassium, and even non-supplemental zinc, in response to the specific supplement (6). Clearly with these nutrients it is impossible to interpret dietary intake data for single nutrients or energy as the increase, or decrease, in the intake and utilization of the nutrient under consideration may be caused by a dietary variation of a different nutrient altogether. In the study by Krebs et al (6), protein intake was low; if supplemental protein (without zinc) had been given there would have been no response (except perhaps an increase in anorexia) and the conclusion possibly drawn that the short stature was not nutritionally based at all. As growth will be limited by the most deficient nutrient, it is only possible to have a `deficiency', in the classical sense, with one type II nutrient at a time - the limiting one. Thus, even if a diet contains very reduced quantities of a particular nutrient, protein for example, no response to supplementation and no specific consequences are to be expected, if another type II nutrient is even more limiting. When a poor appetite is seen in a patient it is a signal that there may be a type II nutrient deficiency.

The concepts of a type II nutrient have been accepted with respect to the essential amino acids being properly balanced each in its appropriate amount to make a protein with a high 'score' - it might be easiest if this concept is expanded to include all the other type II nutrients as if they were essential amino acids in dietetic terms although, of course, they are nothing like amino acids in metabolic terms.

When a dietary supplement is given, which does not contain all the nutrients required for new tissue synthesis, the rate of growth and the efficiency of growth will be determined by the most limiting nutrient in the new diet (basic diet plus supplement), not in the original diet or in the supplement alone, indeed by diluting the original diet an incomplete supplement can make a deficiency worse. Clearly, if an unbalanced supplement is given the other nutrients in the supplement will be used inefficiently; just as a diet with protein which has an amino acid score of zero, because it lacks an essential amino acid, is totally useless and is wasted. The degree of inefficiency is related to the magnitude of the imbalance between the actual limiting nutrient in the diet as a whole and the nutrient under consideration. When we observe an inefficient use of nutrients or energy we can infer that the diet may be imbalanced with respect to one of the type II ingredients that is limiting growth and efficiency. This may be one useful measure of the adequacy of a diet as a whole - the efficiency of use of its energy for growth. Gross inefficiency is almost universal in reported supplementation trials (7). This is not surprising as all these supplementation trials concentrated on supplying extra protein and energy whilst ignoring the other type II nutrients, particularly potassium, magnesium, zinc and available phosphorus.

More recently, zinc has become fashionable as an additive. Some investigators, if they do not get a response from a small dose, increase the dose to unphysiological levels. Others initially add excess "to be sure of a response". They thus give very unbalanced diets and the excess of the supplemented nutrient cannot be used and may well be toxic. There are now examples of trials of zinc where detrimental effects of high doses are being reported. We should not be surprised - the concepts underlying these experiments are flawed and the investigators perceive the zinc as if it is a type I nutrient whose excess will be benignly put into some mythical store.

As a further complication, the response to the supplement, and the required balance of nutrients in the supplement, will depend upon the precise mix of tissues that the person is trying to lay down. This will depend, in turn, upon the age of the subject, the degree of wasting and stunting that has to be made good, and the composition of the required new tissues. Clearly, the dietary requirement for skeletal growth, for muscle synthesis, for adipose tissue and for skin synthesis are likely to differ - but, by how much, in what way and whether this is ever a major factor has not been explored. It is likely that giving a diet with the same balance of nutrients as that which constitute the tissues themselves, with adjustments made for intestinal absorption, is likely to be the best starting point in prescribing an appropriate intake to prevent undernutrition, promote rapid recovery from illness and shorten convalescence.

Supplementation studies have shown that substantial numbers of children may have a type II deficiency in affluent as well as developing countries.

Early investigations in Scotland (8) and Alabama (9) showed a growth response to adding milk to poor children's diets, the same response was shown by Malcolm in New Guinea (10). In Africa there are consistent height differences between tribes that have different staple foods (11). And differences between the growth of western infants with different formulae (12-14). In a series of studies in Colerado, Hambidge has shown a height spurt with zinc supplementation of short children (15). Similarly, in Ontario, 25% of short children responded to zinc supplementation with a height spurt (16). It is likely that the children that did not respond to zinc had their height limited by one of the other type II nutrients. It would seem that the human response to a deficiency is the same as in experimental animals and that unsuspected nutritional limitation is a common cause of short stature.

I would emphasise that the examples chosen to illustrate the nature of deficiency of these nutrients have been largely drawn from work with zinc.

This is because there has been a lot of interest and data published on the effect of zinc whereas the magnesium, potassium and phosphorus, for example, have been ignored by nutritionists. However, the same principles apply to all of them and not just to the nutrients studied in the experiments reported. The crucial thing is to have the right balance of type II nutrients in the diet: this rarely happens and most of the supplemental diets we currently give to malnourished children or adults are limiting in one or other of the type II nutrients.

The type I,type II concept can also be applied to breast milk. The type II nutrients tend to have a physiologically determined concentration that does not change with the mother's nutritional status. In contrast the breast-milk concentration of type I nutrients goes up and down depending upon the mother's status. Thus, breast milk thiamine, riboflavin, pyridoxine, B12, vitamin A, iodine etc can be very low if the mother is taking a deficient diet, Yet, because the mother can be fat and look quite well nourished in spite of the type I deficiency, we do not ascribe the illness in the child to a nursing mother's nutrient deficiency. Thus, for example, infants can die from what is diagnosed as meningo-enchephaitis when it is actually infantile beri-beri, or be anaemic due to unsuspected B12 deficiency due to the fat mother having a low thiamine or B12 intake.

We cannot assume that because the mother is not wasted that her breast milk is perfect. Breast milk is by far the best food for an infant - but this has to come from a well nourished mother. In this respect, anthropometric assessment of the mother is not a guarantee that the breast milk does not have a major deficiency of a type I nutrient. All mothers should have a balanced diet.

The concept of type I and II nutrients also applies to foetal growth - the small-for-gestational age infant is the first casualty of a diet deficient in type II nutrients - we should not be tackling this problem by only giving type I nutrients (micronutrient bullets) some protein and energy.

The forgotten type II nutrients are critical.

The type I nutrients give rise to biochemical abnormalities without any necessary anthropometric changes whereas the type II nutrients give rise to anthropometric abnormalities without specific or diagnostic biochemical changes. Clearly both are needed to assess the nutritional status of an individual patient. Nevertheless, it is ironic that anthropometric criteria are used to diagnose undernourished and malnourished individuals who are then treated with a diet that has energy and all the type I nutrients whose deficiencies are prevalent whilst the deficiencies that gave the wasting and stunting in the first place remain uncorrected. Because the unbalanced supplements that are given have such little effect it is then assumed that the growth problems are not nutritional and effort is diverted to other activities - or stated to be all due to "poverty" about which little can be done without major political change.

There is a pressing need for a new way of addressing the nutritional problems of the malnourished of all ages in a balanced and rational way.

References

1. Golden, M.H. (1988) The role of individual nutrient deficiencies in growth retardation of children as exemplified by zinc and protein. In: Linear growth retardation in less developed countries, pp. 143-163. Ed. Waterlow, J.C. Raven press, New york.

2. Golden, M.H. (1991) The nature of nutritional deficiency in relation to growth failure and poverty. Acta Paediatrica Scandanavica, 374, 95-110.

3. Williams, R.B. & Mills, C.F. (1070) The experimental production of zinc deficiency in the rat. British Journal of Nutrition, 24, 989-1003.

4. Rudman, D., Millikan, W.J., Richardson, T.J., Bixler II, T.J., Stackhouse, W.J. & McGarrity, W.C. (1975) Elemental balances during intravenous hyperalimentation of underweight adult subjects. Journal of Clinical Investigation, 55, 94-104.

5. McCance, R.A. (1936) Experimental human salt deficiency. Lancet, 1, 823-830.

6. Krebs, N.F., Hambidge, K.M. & Walravens, P.A. (1984) Increased food intake of young children receiving a zinc supplement. American Journal of Diseases of Childhood, 138, 270-273.

7. Beaton, G.H. & Ghassemi, H. (1982) Supplementary feeding programs for young children in developing countries. American Journal of Clinical Nutrition, 35, 864-916.

8. Orr, J.B. (1928) Milk consumption and the growth of school children. Lancet, 1, 202-203.

9. Spies, H., Dreizen, S., Snodgrasse, R.M., Arnett, C.M. & Webb-Peploe, H. (1959) Effect of dietary supplement of non fat milk on human growth failure. American Journal of Diseases of Childhood, 98, 187-197.

10. Lampl, M., Johnston, F.E. & Malcolm, L.A. (1978) The effects of protein supplementation on the growth and skeletal maturation of New Guinean school children. Annals of Human Biology, 5, 219-227.

11. Nicol, B.M. (1959) The protein requirements of Nigerian peasant farmers. British Journal of Nutrition, 13, 307-320.

12. Fomon, S.J., Filer, L.J., Thomas, L.N., Anderson, T.A. & Nelson, S.E. (1975) Influence of formula concentration on caloric intake and growth of normal infants. Acta Paediatrica Scandanavica, 64, 172-181.

13. Fomon, S.J., Filer, L.J., Ziegler, E.E., Bergmann, K.E. & Bergmann, R.L. (1977) Skim milk in infant feeding. Acta Paediatrica Scandanavica, 66, 17-30.

14. Salmenpera, L., Perheentupa, J. & Siimes, M.A. (1985) Exclusively breast fed healthy infants grow slower than reference infants. Pediatric Research, 19, 307-312.

15. Walravens, P.A. & Hambidge, K.M. (1976) Growth of infants fed a zinc supplemented formula. American Journal of Clinical Nutrition, 29, 1114-1121.

16. Gibson, R.S., Vanderkooy, P.D.S., MacDonald, A.C., Goldman, A., Ryan, B.A. & Berry, M. (1989) A growth-limiting, mild zinc-deficiency syndrome in some Southern Ontario boys with low height percentiles. American Journal of Clinical Nutrition, 49, 1266-1273.

 

TABLE 1

Classification of nutrients according to whether the response to a deficiency is a reduced concentration in the tissues and specific signs or a reduced growth rate with non-specific signs.

TYPE I response

TYPE II response

iron

water

copper

potassium

manganese

sodium

iodine

magnesium

selenium

zinc

calcium

phosphorus

fluorine

Protein

thiamine

nitrogen

riboflavin

carbon skeletons of essential amino acids

pyridoxine

threonine

nicotinic acid

lysine

cobalamin

sulphur

folate

oxygen

ascorbic acid

 

retinol

 

tocopherol

 

vitamin D

 

vitamin K

 

 

TABLE 2

The differences between a type I and a type II deficiency response

TYPE I (Specific Function Nutrients)

TYPE II (Growth Nutrients)

growth continues in early stages

growth failure first response

specific clinical signs develop

no specific clinical signs

body store

no body store of these nutrients

concentrated in particular tissues

not concentrated in any particular tissue

specific enzymes affected

general effect on metabolism

not usually anorexic

anorexia common response

tissue concentration independent of the other type nutrients

dependant upon all the other type II nutrients

tissue concentration drops with deficiency

tissue concentration maintained with deficiency

tissue concentration maintained in different metabolic states

tissue concentration may change (drop) with metabolic state

food sources very variable

ratio in foods not very variable

diagnosed by biochemical tests

Do not give specific biochemical abnormalities

Anthropometric abnormality only appears late in the deficiency

Diagnosed by anthropometric abnormality

 

Prof. Michael H.N.Golden
Dept of Medicine and Therapeutics
Univ of Aberdeen, Foresterhill, AB9 2ZD. Scotland, (UK)
Tel +44 (1224) 681 818 ext 52793/53014, Tel(direct) +44 (1224) 663 123 527 93, Fax +44 (1224) 699 884
INTERNET
m.goldenatabdn.ac.uk


Date: Sun, 30 Apr 2000 15:12:53 -0400

From: "Ian Darnton-Hill" <IDarnton-HillatHKI.Org>

Subject: Re: type I and type II deficiencies: Part 2

 

Dear Mike:

I have been meaning to get back to this for a while but catching up after the week in DC has been a challenge.

I think this is a very interesting concept and seems reasonable from my limited animal and other research experience. However, I am less clear about the programmatic implications of it.

At one point you say, "All mothers should have a balanced diet". Well sure, no one's arguing with that. So should all children. It also suggests that growth at different stages, and even for different organ systems would require particular constituents in the nutrient make-up of their diets at different times (as I understood it). Doesn't this suggest (especially given the Nicol 1959 ref. re some African diets), that some/many diets clearly are not appropriate (as the vast numbers of under-nourished children would suggest). Then what is the alternative? You suggest supplementary feeding is very inefficient - and imply if wrongly constituted could even be detrimental.

Reading through, it seemed like a recommendation (in the absence of balanced and adequate diets for all the world) for preventative multimicronutrient supplements with adequate energy and protein. While this may not be perfect, if the net was truly wide enough to cover virtually every known micronutrient, then this should be done- while at the same time, working for dietary adequacy and accessibility.

However, I would be interested to hear your response. And if not suggesting mutlimicronutirents, what is the practical alternative in such populations?

Thanks and regards,

Ian

(Will start working on some of the ACC/SCN stuff soon but just haven't had time yet. Hope you will be able to help again- this coming year will be the r reeal transition)


Date: Thu, 04 May 2000 17:15:24 +0100

From: Michael Golden <refugeesatabdn.ac.uk>

Subject: Re: type I and type II deficiencies

 

Dear Ian,

It is indeed likely that there are differences in the nutrient balance for growth that is needed in different situations. This has been known for years in animal production.

This comes up when we consider the differences between stunting and wasting - which reduces to the difference between the nutrient requirements for longitudinal (skeletal) and for ponderal (soft tissue) growth.

Longditudinal growth occurs in cartilage which then ossifies. The major components of cartilage are collagen (low content of essential amino-acids) and glycoseaminoglycans which are mainly complex carbohydrates with a sulphate group on most of the carbohydrate rings. The essential bulk nutrient needed for longitudinal growth is thus sulphur. The major source of sulphur are the amino-acids methionine and cystine.

It is of great interest therefore when we look at the classic photographs of McCance & Widdowson's pigs that they had on a low protein diet, that they are very stunted, but their jaw-bones are almost as large as the control pigs and because of this they seem misshapen. The Jaw is peculiar in that it grows directly from membrane and does not require cartilage. I have often wondered if this is the reason that very stunted children seem to have changes in face shape that are much less retarded than their longitudinal growth. At any rate, you are right - there are likely to be different requirements at different stages of growth.

I hold it as self evident that the nutrients that we need to supply are the ones that the person does not have in adequate amounts. There are about 40 essential nutrients, and without all of them the individual will fail to achieve health. Further, a diet which is sufficiently poor to be deficient in one is likely to be deficient in a whole range of nutrients. So, yes, I am asking for multi-micronutrients - but also some of the not-so-micronutrients, what I have termed the "forgotten nutrients" such as magnesium, potassium and phosphorus, that are not classified with either the fat-carbohydrate-protein macronutrients or with the micronutrients.

There are some type I nutrients for which there is no alternative to bringing in exogenous supplies (either as fertiliser, animal-feed, fortificants or supplements) because they are low in the soil (environment) and the level in plants reflects the level in the soil - so that LOCAL diet diversification will only give a range of deficient foods - iodine and selenium would be examples. On the other hand for most of the type II nutrients and the organic type I nutrients dietary diversification is the way forward in my opinion.

There are traditional culinary practices, such as adding ash from burnt plants to food, germination and fermentation that have often been lost, and are frequently "discouraged" that have evolved to circumvent many of these problems. Doris Calloway described deterioration in the Hopi when they were given "government corn" and abandoned their practice adding ash from specific plants to their food - ash which was high in the type II minerals when she analysed it.

The reason why supplemental feeding programs have made little difference, again in my conception, is that the diets that have been used have all been incomplete, particularly with respect to type II nutrients.

In animal studies the deleterious effects of giving a defined diet missing an essential amino acid, but normal amounts of all the other amino-acids is much worse than giving a low protein diet (balanced) - this is equivalent to having the animal on a deficient diet and supplementing with everything except one amino-acid - this has been elegantly shown by Alf Harper, in many of his early studies. This effect I have generalised from the amino-acids to all type II nutrients. There are examples of detrimental effects of supplementation with single type II nutrients in humans as well.

The effect of (very) high levels of zinc or protein in isolation on pregnancy outcome has been reported to be deleterious. In some of the initial studies of zinc supplementation in Iran, the control group (which got a supplement without zinc - ie it was unbalanced) did much worse than the group that got no supplement at all. So yes certainly, giving and unbalanced type-II nutrient supplement can indeed be deleterious - I would not give high levels of any of the type II nutrients alone without the others.

Mike Golden

Prof. Michael H.N.Golden
Dept of Medicine and Therapeutics
Univ of Aberdeen, Foresterhill, AB9 2ZD. Scotland, (UK)
Tel +44 (1224) 681 818 ext 52793/53014, Tel(direct) +44 (1224) 663 123 527 93, Fax +44 (1224) 699 884
INTERNET
m.goldenatabdn.ac.uk

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Date: Mon, 08 May 2000 19:22:11 -0400

From: "Ian Darnton-Hill" <IDarnton-HillatHKI.Org>

Subject: Re: type I and type II deficiencies

 

Thanks Mike:

We forget the earlier (and on-going) animal experiments at our peril. I also of course agree about traditional practices to obtain a 'balanced' diet. Almost by definition, where availability and accessibility are adequate, a particular traditional diet must have been adequate. One wonders if it is only when there is some change in the status quo- and this could be very subtle- when malnutrition, or 'imbalance' occurs.

cheers,

Ian


Date: Wed, 17 May 2000 14:03:24 +0100

From: "Liana Steenkamp" <lianastatiafrica.com>

Subject: First phase diet in severe malnutrition

 

I have three questions relating to this discussion: 1. A report in 1989 in the American Journal of Clinical Nutrition indicated that when inorganic Zn is added to Soy based diets, the body would utilize this source of Zn. Would this still be an issue (impact of phytate on Zn bioavailability) in soy/maize supplements with added inorganic ZN?

2. What about the phytate content of maize which is very much similar to a high quality soy protein isolate. Would that not have a similar effect on Zn bioavailibility?

3. Are there any recent bioavailability studies available - it seems that most of the studies were done more that 20 years ago when the quality of soy protein isolates used in products were poor and the phytate content higher than in products currently available?

Regards

 

Liana Steenkamp, M Sc Dietetics
South Africa

 

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Note added:

Inorganic zinc added to the diets can indeed make sufficient zinc available: but this means that the diet has to be fortified with the correct amount - and not used directly.

You are correct there is also a major problem with maize in the treatment of severe malnutrition. It should never be used in the first phase. The problems with maize for the later management of severe malnutrition is not entirely explicable on the basis of zinc chelation alone (other cereals give better results) - but the reasons are unclear.

Modern soy protein isolates are mainly used as ingredients in formulations prepared for use in rich countries.