Many health authorities are now introducing and implementing district food policies, drawing upon the recommendations of the NACNE and COMA Committees. There is, however, no authoritative advice about the particular needs of pregnant women and young children.
It was because of this lack of information that the Institute of Obstetrics and Gynaecology and the CPG, whose interest in this subject stems from an awareness that the seeds of coronary heart disease are sown in childhood, decided to organise this conference. It brought together experts from different but related areas in nutrition and health care to discuss and recommend ways in which nutrition could be improved during these important periods of life.
Director,
March, 1986
ACKNOWLEDGEMENTS
We would like to thank the organisers – Dr. Donald Gau, general practitioner, member of the Cot Council of Management; Caroline Walker, nutritionist, member of the Nutrition Sub-Committee; Dr. Gillian Gau of Queen Charlotte’s Maternity Hospital – without whom there would have been no symposium.
Acknowledgement is also made to the speakers, both for their presentation on the day and their subsequent help in editing their papers for publication in this report.
Particular thanks must go to Patricia Hawkins of the Institute of Obstetrics and Gynaecology for her invaluable assistance during table Symposium and after.
CONTENTS
2. EARLY NUTRITION AND ERAIN DEVELOPMENT: Michael Crawford, Professor of Nutritional Biochemistry, The Institute of Zoology
3. WHAT DO BRITISH MOTHERS EAT?: Wendy Doyle, State Registered Dietitian, The Institute of Zoology, London
4. THE MANAGEMENT AND PREVENTION OF ALLERGY BY INFANT FEEDING (Summary): John Soothill, Professor of Immunology, Institute of Child Health, London
5. WHY ARE BRITISH TEETH SO BAD?: Aubrey Sheiham, Department of Community Dental Health and Dental Practice, University College, London
6. DIET: THE BEGINNING OF ATHEROMA: Christine Marenah, Lecturer in Chemical Pathology and Metabolic Disorders, St. Thomas’ Hospital, London
7. HOW SAFE ARE LOW FAT DIETS FOR CHILDREN?: Andrew Tomkins, Senior Lecturer, Department of Human Nutrition, London School of Hygiene
8. NUTRITION IN PREGNANCY AND EARLY CHILDHOOD: Philip James, Director, The Rowett Research Institute, Aberdeen
9. PRACTICAL GUIDELINES: Maggie Sanderson, Dietitian, St. Leonard’s Hospital, London
10. PANEL DISCUSSION. CHAIRMAN: Caroline Walker, Nutritionist, London
1. EPIDEMlOLOGY AND DIET – Professor David L. Miller
It is surprising that epidemiologists have not given mar the problems of nutrition and the relationship between nutrition and health. It is a truism that we are what we eat, and that the foetus and the breast-fed infant is what the mother eats. It is also clear the seeds of ill health may be sown very early in life, perhaps prenatally, and that balanced nutrition promotes health. Children in Britain are without doubt healthier than they were a hundred years ago they die lass often in infancy and they grow taller. What, then, is the problem.
To begin with, in this field we are strong on assertion but weak on evidence – at least evidence that is sufficiently convincing to command respect and action by health professionals and politicians. The subject receives scant attention in most medical education, both for doctors and other health professionals. Indeed, there is a general lank of commitment to disease prevention, or indeed to any action treat involves deferred rather than immediate benefits in medicine. This too, I suppose, is partly a reflection of our lack of knowledge and, therefore uncertainty about what action should be taken.
I looked at two recently published textbooks on community medicine for medical students. Each of them devotes only about two pages out of more than 200 to the subject of nutrition and health. The only reference that I could find to the question of child and maternal health and nutrition in another such book, just received, was a statement that free or reduced priced foods in child health clinics are considered by some to provide an important incentive to attendance. That was all it had to say on the subject. A book of which I was co-author also had a section of only two pages. Its first sentence reads: “Although the relationship between diet and health is complex, the importance of good nutrition in the prevention of disease and in the promotion of health is beyond doubt”, but there followed little information of real importance. If the matter is “beyond doubt”, why is not more attention paid to the subjects?
What is the basis of this certainty? We know that the consequences of severe malnutrition can be disastrous. We know something of the consequences of specific deficiencies. We know that there is a correlation between maternal nutrition and prenatal mortality. We know there is a correlation between nutrition and infant mortality rates, possibly due to the fact that poorly-nourished children are more susceptible to infection and that there is a correlation between nutrition and children’s stature. But gross nutritional deficiencies of the kind that produce recognisable clinical syndromes are rare, if not unknown, in British children. Our problems tend to be obesity and over-eating, although there is perhaps some malnutrition in the poorest and largest families. We know of the protective effect of breast-feeding against the risks of infection in infants and the superior nutritional value of breast milk. However, the principal constituents of breast milk are well buffered against the maternal diet, and it would take severe maternal malnutrition to have any adverse influence on the constituents of breast milk. We know that the seeds of diseases such as atheroma may be sown by excessive fat intakes even very early in life. During the day you will be hearing all of this and much more about what we know, but in the light of current knowledge, what can we do practically?
Dr. Richard Turner, who was one of the founding fathers of the CPG, said in a symposium held a few years ago; “Those who maintain the philosophy that dietary advice should not be given without conclusive evidence that benefit will result should ponder what they are waiting for and how long they are prepared to wait.”
Professor Geoffrey Rose of the London School of Hygiene, a distinguished cardiovascular epidemiologist has advocated energetic action in dietary matters without waiting for proof of efficacy, which he believes to be an unreasonable precondition for action in this area. An important impediment to action is that people want to enjoy their food and are not very amenable to prescription on the choices they should make on health grounds. Also, there are competing cultural taboos and social customs and commercial pressures, which probably influence diet more than anything else.
As an epidemiologist approaching disease prevention, I am most comfortable if it is possible to establish the cause of disease and identify a specific agent that can be removed, or against which we can protect ourselves. But in dietary matters we are not dealing with an external agent. Nevertheless, I believe that epidemiologists could and should contribute more vigorously to the subject by identifying specific nutritional risk factors in relation to disease, and by defining Cadre accurately the normal ranges of the various parameters of nutrition, as well as the natural history of nutritionally related diseases. They might try to draw together two strands: the levels of nutritionally significant parameters and the natural history of the disease. Next, they should be evaluating interventions, not in individuals because that is an almost impossible task – the time-scale of cohort or population studies would be far too long to be practicable. But it is possible to test the consequences of trying to shift the population distribution of various disease-related nutritional factors, such as obesity. We can test the efficacy of various health education methods, and the contents of educational packages. It is also important that we do our best to dispel some of the myths surrounding diet and health. For example, it was long thought that school milk was of value in promoting child growth until studies by Professor Holland and his colleagues showed that this was not the case.
It has been said that the pharmacy of prevention is in the House of Commons, but it is not only there; it lies also with us. We need to persuade our colleagues of the importance of nutrition for health, and to teach our patients good dietary practices. We should be trying to influence politicians in the formulation of national policies in agriculture, food production, food labelling, in the subsidies offered to food producers and in public diet and health education messages. In such ways perhaps we may be able to achieve the promotion of health and of disease prevention to which we all committed.
2. EARLY NUTRITION AND BRAIN DEVELOPMENT
– Professor Michael Crawford
I want to discuss the role that nutrition, particularly fats, plays in early development, especially the development of the brain and of the vascular system. If you think about the differences between animal species, the outstanding difference between man and other species is unquestionably the degree to which the brain develops. It is interesting again, that whenever there is evidence of the evolution of a sophisticated nervous system it is associated with a fairly sophisticated evolution of the vascular system. In fact, both systems seem to go together throughout biology.
It is particularly interesting in the case of the human species, when we consider the anatomy of the brain, that a very large and disproportionate amount of the brain is concerned with the hand. In the fine structure of the capillary network in the hand an incredible vascular network is required to feed many muscles involved in hand movement. There are, too, many nerve endings enabling the hand to function properly.
The point I want to make is that the evidence given in relation to cardiovascular disease, which is effectively a vascular problem, now strongly implicates dietary fats as one of the major causes. That being the case, it is interesting that the brain itself is made up of 60% fat. The experimental evidence that is emerging in relation to brain growth and development indicates -that the same principles operating in the growth and function of the vascular system are also operating in the context of the brain. The difference is that the brain is perhaps the most carefully protected of all the organs in the body and therefore it is very difficult to manipulate.
There are many examples in the literature of people who dissect out brains and weigh and measure them. From the facts given it is simply obvious that brain development is the province of foetal and early neonatal growth and development. A large part of the structural material used to build the brain is fat. To put it in simple terms, 60% of solid structural matter in the adult brain is fat or lipid. It is interesting to find out where that comes from, and its nutritional relevance. The trouble with understanding fat and nutrition is, that most of the writings are by those who refer to the damage that fat causes to people. That is primarily because fat studies have been related to triglyceride, cholesterol and adipose tissue.
There are two types of fat in the body – storage and structural. Storage is what is called visible fat. Invisible fat inside the cells is used for cell structures Inevitably, this structural fat is the most important component of the brain and nervous system, and the second most important in all soft tissues of the body, where it is used for cell membranes, in collaboration with protein. Fat is an integral part of the cell organism. Structural lipids and fats at cell level require essential fatty acids that have to be part of the diet.
Probably the difference between essential fatty acids and the other nutrients is that they are stored in fats. consequently it is difficult to deprive animals of essential fatty acids because of that factor. Linoleic has two double bonds in the molecule and alpha-linolenic has three double bonds in the molecule. Double bonds cannot be inserted in the position where they are found in essential fatty acids. Linoleic acid occurs in seed material and alphalinolenic acid primarily in green leaf material.
We now know a great deal about the metabolism of the essential fatty acids. Linoleic acid is unsaturated and chain elongated to a carbon chain length with three double bonds and four double bonds in the molecule. Similarly, alphalinolenic acid is desaturated and chain elongated to twenty-two carbon chain length fatty acids with five and six double bonds in the molecule.
They provide for the liquidity requirements in cell membranes. This type of operation that biology employs enables nature to have a great variety of different qualities of building bricks for cell membranes. For example, the myelin sheath requires a relatively rigid structure, so nature can choose saturated and mono-unsaturated fats preferentially for building the myelin sheath. On the other hand, if we consider the synaptic junction or the outer segments of the rods in the retina, these respond to single photons of light and a high degree of liquidity is needed in the cell membranes involved in the game. In that case docosa hexanoic acid with a twenty-two carbon chain length and six double bonds is the most highly unsaturated of the polyunsaturated fatty acids used to build tile receptor mechanisms of the outer segments of the rods of the retina.
The fatty acids are not just used for structural purposes. They are used in a way analogous to essential amino acids for hormone-like reasons. For example, the amino acid tryptophan is converted to serotonin; thyroxine and adrenaline are by-products of the phenylalanine and tyrosine metabolism. In exactly the same way, essential fatty acids produce by-products of their twenty carbon chain length derivatives. These are the prostaglandins, leukotrienes and lipoxins which are responsible for regulating functions such as the prevention of platelet adhesion to the blood vessel walls, vascular responsiveness and tone immune system function. They are probably closely related to blood pressure control and are important in the reproductive system – pregnancy and parturition. They have wide-ranging hormone-like functions of this nature.
It is interesting that neither of the parent essential fatty acids – that is linoleic or alpha-linoleic acids – are found in significant amounts in the brain. Instead the twenty and twenty-two carbon chain length derivatives are present. This composition is a highly specialised feature of the central nervous system and its attributes.
It is also interesting that the rate at whichtheselong chain derivatives can be synthesised from the parent fatty acids is limited by the desaturation rate. That is an important matter, which I shall return to later. From 1973 studies of rat brain development the acquisition by the developing brain of arachidonic and docosa hexanoic acids closely follows the early developmental period of the brain associatedwith the phase of cell division. On the other hand, acquisition of the long chain saturated and mono-unsaturated fatty acids follows much closer on the development of myelinatlon, whilch takes place after the cells have appeared in bulk: it is a question of making the connections between the cells.
The brain has such a heavy investment in fat because, in the human brain, it has 1012 cells. Each cell will make something like 10,000 connections with other cells which explains the very high requirement for membrane systems in the brain and hence for lipids. What happens in the human brain is that it has acquired 70% of the total long-chain fatty acids before a child is horn, which fits in roughly with the total cell count at birth. After birth there is a switch to myelination, but there is still a fat requirement for the completion of the 30%, which occurs mostly in the first six to twelve months.
We know that specific provision of these long-chain highly unsaturated fatty acids for brain development is being achieved by the placenta. We have studied human placenta profusion and found the placenta actively selects arachidonic acid as opposed to linoleic acid and passes arachidonic acid and docosa hexanoic acid on to the foetus. There is a deliberate selection of those highly unsaturated essential fatty acid derivatives destined for brain cell development.
Although the brain is the most carefully protected system in the body and is difficult to manipulate in any way whatsoever, there is clear experimental evidence that the brain is vulnerable during this period of rapid growth. John Dobbing compared a small litter with a large litter of rats: the pup’s large litter grew slower than the small litter. The interesting thing was that brain development takes place postnatally in the rat and was retarded in the large litter pups in an irrecoverable way. There was no change in the velocity at which the brain grew as a result of the manipulation of litter size and difference in nutrition when many pups compared to few pups were trying to suckle from one mother. But there was microcephaly as a consequence of under-nutrition in that period in the large litter.
We were able to design an experiment in which we gave rat mothers about 0.3% of their energy as essential fatty acids – that is about on the borderline compared to 5% of the energy. In the third generation, where the experiment stopped, we found that there was a 25% reduction in brain cell count at birth in the low essential fatty acid group. Although the same number of pups were bone, tile mortality was also severely affected. Thus there appears to bea specific effect of lipid under-nutrition creating a precise retardation in the brain cell development.
One wants to take these messages into the human sphere to see whether we can find anything relevant to a role for lipids, especially in relation to pregnancy when 70% of the human brain cells divide. In collaboration with the Queen Elizabeth Hospital for Children and the Salvation Army Mothers’ Hospital in the East End of London we set out to examine this question in a group of mothers in Hackney. The results were published in 1982 and I shall refer to them briefly.
First, I should like to highlight the fact that protein intakes were not significantly different in the mothers of the tow birthweight group. But there was a substantial difference in calorie intakes. Of the vitamins, pyridoxine was also strongly correlated with low birthweight in agreement with previous reports. The protein intakes met the recommended daily allowances of the Department of Health. However, almost nothing else did!
The mean birthweight in the Salvation Army Mothers’ Hospital group was just over 3,000 grams hut the low birthweight mothers had intakes in the region of 1,400 kcals. We were so worried about the extent of the calorie intake deficits in the Hackney group that we did a smaller study at the Royal Free Hospital where we found the birthweight mean and calorie intakes were higher. 50% of the Salvation Army Hospital birthweights were at or below 3,000 grates. Chamberlain has emphasised that that is the point below which mortality starts to rise.
Mean calorie intakes obtained for 7 days in each of the 3 trimesters from the Salvation Army and the Royal Free Hospitals showed that the calorie deficits of the low birthweight group were especially in the first trimester. It was interesting that the first trimester was the most severely affected.
In relation to the calorie deficits, it was clear that a lower fat intake made the biggest contribution. Suffice it to say that where there is a lower fat intake in the lower birthweight group there would have been expected ipso facto, a lower essential fatty acid intake, and this is what we found. The second point to note is that as fats are used as energy reserves, it would not be unreasonable to expect that a significant proportion of such essential fatty acids going in, even in this low intake situation, would be burnt for energy.
We did some studies in relation to the question of concentrations of fatty acids in the blood as well as in the food. We found the low in-food intakes correlated with maternal and cord blood up to a birthweight of 3,000 grams. There was also a relationship between birthweight, placental weight and head circumference at birth. It is interesting that in the cord blood the plasma phosphoglyceride level of arachidonic acid was 10.9% in the low compared to 15.6% in the high placental weight group. Similar quite significant differences were found in relation to birthweight and head circumference.
One point I want to make is that when we consider the programming during pregnancy the growth of the placenta and the deposition of fat precedes foetal growth that does not accelerate until about the twentieth week. Fat deposition and placental development occur in advance of the time when the foetus exercises its demands. Biology is preparing in advance for nutritional requirements of the growing foetus. In view of the data from hackney it was significant that the biggest calorie deficit was in the first trimester! It seems clear knowing the function of the placenta in feeding the growing infant, that this differential timing of events must be a key issue in relation to feeding the foetus.
After birth, human milk – although quite a different story to cord blood has nevertheless significant quantities of long-chain derivatives of essential fatty acids. Triglyceride is the major component in human milk and accounts for about 96% of the lipid. Phosphoglycerides are also present and are much richer in longer chain derivatives. People seem to think that the essential fatty acids are present in only small amounts in human milk. Fat is the major energy provider, at between 50 and 60% of the total energy in milk. Consequently fatty acids should be put into perspective in terms of total energy rather than simply fat. The proportion of total energy at 6% essential fatty acids is roughly the same as the protein delivered on an energetic basis – i.e. between 6% and 7% in human milk.
As this symbiosis has relevance to coronary heart disease, I shall refer to our studies in Africa of infants born with different or similar blood cholesterol levels to European infants. Europeans have d high mortality rate from cardio-vascular disease whereas Africans do not. We found no difference in blood cholesterol levels between European and African children studies, at birth. However there was a significant difference between the two groups by the gage of seven or eight years: they could be separated simply on the basis of clearly identifiable blood cholesterol levels. In other words, one of the major risk factors is clearly identifiable by the age of seven to eight years.
Data in the United States showing differences between Mexican and Wisconsan children highlighted precisely the same effect at the early age of five to nine years. The two populations could be clearly identified. Blood pressure data shows that pressure does not rise significantly in African Communities in the way that it does in American or European ones, with age. At what age does blood pressure start to rise? It is now well documented that the upward movement begins at six to eight years of age in children from high-risk populations. I find the evidence very compelling and somewhat in contradiction to the message of the Department of Health’s report on cardio-vascular disease, which gave the impression that we should not worry too much about the nutrition of children, and that nutritional advice should be left to adults.
The data in fact means that the processes leading to the emergence of the two nest important risk factors of blood pressure and blood cholesterol levels are operating at an age predating six years of age. If they can be measured by the age of six then the forces that lead to the emergence of the two most serious risk factors have been operating beforehand. There is also clear evidence of early vascular changes in infants and children who died from accidental causes.
Bearing in mind nature’s strategy of preparing in advance, it is important to look beyond the nutrition of adults if we are concerned about cardio-vascular disease, to the nutrition of mothers and children. The interaction between mother and child must be one of the most important factors determining a start to life in the right biological framework. The question of lipid nutrition was one of the key issues focused on by the COMA committee, and in other reports. The recommendations by FAO and WHO in 1978 clearly specified recommendations for children and mothers. It is important to understand that the period during which systems are vulnerable is duringgrowth and development. It is biological nonsense to set aside this critical early period of development when there is so much evidence that the systems that Wet are most concerned with are vulnerable at this early period.
References
1. Dobbing, J. (1972) Vulnerable periods of brain development. IN Lipids, malnutrition and the developing brain. Ed. Elliott, K. and Knights, J. Ciba Foundation Symposium. Elsevier/North-Holland: pp 1-7.
2. Chamberlain, R. et al. (1975) British births 1970. Vol 1. The first weeks of life. Chapter 3. London: William Heinemann Medical.
3. WHAT DO BRITISH MOIHERS EAT? – Mrs Wendy Doyle
In the past few years, between the study referredto by Dr. Michael Crawfordand the present study, I have coded about 700 records of weekly diet intakes, which represent about 13½ years of one person’s food intake. The analyses presented some interesting facts.
I shall be showing how mothers in Hackney measure up to the current recommendations or guidelines on healthy eating and the prevention of heart disease. The first section will deal with the practical side of things: fled patterns, what mothers eat and what they like in terms of the common foods. Secondly, I shall analyse the food recordsin terms of nutrient intake.
I have not looked in detail at the social class distribution of Hackney mothers, although Hackney has changed considerably in the past four to six years. It is probably much more representative of the total population than it was six years ago. It is still part of London, but houses are relatively cheap. Many more young professional people such as barristers, doctors, archive journalists and even dietitians are buying houses in the area, which is lending to a wider distribution of social class.
i) The Intervention Study
We are doing an intervention study in Hackneyin which it is hoped that persistent nutrition counselling, as opposed to one-off booking in a clinic, will help to reduce the incidence of low birthweight, which has been higher in Hackney than in most other parts of England. I recruit the mothers for my study at their first visit to the clinic at the Salvation Army Mothers’ Hospital. After a preliminary talk on a one-to-one basis, I suggest that it might be a good idea for them to compile a diet record for a week. The intakes of particular foods are not weighed but they are shown in household measurements.
My aim is to identify any problems and deficiencies in the diets,workings from a week’s food intake. Most of the records are done at about 12 or 13 weeks’ gestation. The only criterion of the studyis that mothers should enteris during their first trimester, in the hope that they can go through most of their pregnancy with an improved diet. I concentrateon the very important balance that needs to be struck between differentnutrients, especially vitamins mad minerals, and the total calorie intake.
ii) Food Patterns
Today I shall be considering the NACNE and COMA recommendations, in particular the total fat, saturated fat and fibre intakes, and refined sugars, alcohol and salt. To look at the food patterns I have taken those foods most likely to alter intake of these nutrients, i.e. bread, fruit, milk, eggs, puddings, cakes, biscuit, and processed meats (which are much higher in salt and often in saturated fats). I shall also be dealing with fish, cheese, vegetables, sugar, confectionery, sweetened drinks, alcohol and the types of oils and fats used. Throughout, I shall be referring to a total of 437 food records unless stated otherwise.
Bread
A high proportion of the mothers used white bread (71%), with only 24% using wholemeal. Bread is one of the most difficult foods to change; the usual excuse being that their husbands or children do not like wholemeal bread. It was striking that many of those eating wholemeal bread seemed to be from the higher social classes. Another interesting finding was the number of people who ate wholemeal bread and also drank alcohol – 55%! The benefits or otherwise of women drinking alcohol during pregnancy is beyond the scope of this discussion, but I shall be talking about the amounts consumed.
Cakes, sweets, sweetened drinks
Consumption of sweet biscuits, cakes and puddings will influence refined sugar intake as well as saturated fat and total fat intakes. A high proportion of mothers ate biscuits, with the amounts varying between a moderate amount and a very large number. 69% ate cakes, some as many as fourteen a week. Those are the mothers whom we need to be concerned about. Many of the mothers ate puddings – including schoolteachers having school dinners! 66%take sugar in coffee, tea or other hot drinks. Half the mothers ate sweets or chocolates. Again the average was very skewed: some individuals had as many as sixteen portions a week. One mother ate 16 Mars bars during the week of her assessment, as well as 27 sweetened drinks. I have excluded Ribena as it does contribute some vitamin C to the diet.
Milk and eggs
It was striking that 95% of the mothers drank whole milk, although milkmen deliver skimmed and semi-skimmed milk we can try to influence mothers on this – any suggestions for keeping their calories under control will get same co-operation. The average number of eggs eaten was just over 4 but the top of the range was very high at 16 eggs per week.
Meat and fish
The mothers ate an average of just over four portions of processed meats a week. They tended to have pies, sausages and burgers during the week and eat more fresh foods at weekends. There were an increasing number of vegetarian mothers – 6% of those under consideration. Many of those who were not vegetarian did not eat many portions of meat during the week. The good news is that 71% ate fish. The bad news is that a high proportion of that came from fish and chip shops, so it would be fried in batter. Otherwise, the most usual source of fish were fish fingers or tinned fish like tuna fish.
Fruit and vegetables
An average of almost one portion of fruit a day was eaten, although the range shows that some people had much more than this, while 57% ate less than one portion a day. 11% did not have fresh fruit during the week fresh or cartoned orange juice has become much more popular, perhaps because the lower price has brought it within more people’s reach. Almost 60% of mothers have orange juice at least once a week.
The average number of portions of vegetables, excluding potatoes, included very many more fresh vegetables than tinned. Of the fresh vegetables, tomatoes were the most popular. Beans, baked beans, frozen peas, tinned peas, cabbage and carrots were also fairly popular. 56% of the mothers ate fresh or frozen vegetables every day; but 2.3% did not eat any fresh or frozen vegetables.
Chips were very popular: 76% had one or more portions of chips during the week. 23% had three or more portions and 1% had chips every day. Crisps were also popular, with 55% having at least one bag a week, arid 11% having four or more bags. Of those who ate crisps, the range was from one to fifteen bags.
Alcohol
37.5% consumed one or more alcoholic drinks per week. Only 3.4% had more than seven alcoholic drinks. We need to be concerned about tile range of consumption: some had as many as 21 drinks a week.
Fats and oils
Margarine was the fat used predominantly for spreading – used by 62% -, 35% used butter and only 2% were on low-fat spreads. Of the 191 people who had margarine, 44.58 had a medium quality and 25% had a margarine rather low in the essential (polyunsaturated) fatty acids. These percentages are basely on a total of 308 because I have excludedone of the four groups being studied as they were given freemargarine and oil,high in polyunsaturated fats. It is interesting that the total amount of fat eaten by that group was similar to the other groups. This suggests that we eat fat to our own levels.
iii) Analysis of the Food Records
The NACNE and COMA reports give some guidelines for the total population, but not specifically for pregnant women. The short-term guidelines designed for the 1980s in NACNE are that we should reduce our total fat intakes to 34% of energy, saturated fat to 158 and sucrose to 12%. Salt should be reduced lay 1 gram and alcohol to 58 of total energy. Fibre should be increased to 20g a day. COMA emphasises total fat and saturated fat levels. It does not make specific recommendations on fibre, but suggests that simple sugars and Sally should not be increased further. It states that “excessive” alcohol should be avoided but the levels it specifies are high. Excessive consumption for men is defined as 80 grams of alcohol a day. This represents 10 spirits, 5 pints of beer or 7 glasses of wine. The suggested “excessive” limit for women, 52 grams a day, would amount to 7 glasses of spirits, 2 pints of beer or 4½ glasses of wine.
In relation to fibre, only 16.5% ate more than 25 grams, and 8.1% achieved 30 grams, which is the long-term NACNE guideline. Mothers and women in general, may find that 30 grams a day is rather difficult to achieve. It as much easier for a man eating 3,400 calories a day to get 30 grams of fibre than for a woman eating perhaps 2,250 calories a day. The mean intake of fibre was 18 grams a day. The range was very wide – from 5 to 50 grams.
I was surprised at the high proportion (69%) who were within the NACNE short term guidelines for added sugar at 12% of energy. Even 54% achieved the long term NACNE guidelines but the range was rather wide, with one mother getting 36.4% of her energy from refined sugars.
In relation to fat, 12% were within the short-term guidelines, but only 2.3% achieved the long-term guidelines. The mean intake was rather high at 40% and the range was quite wide (24 – 54%). For saturated fat, 39% took less than 15% of their calories from saturated fat and only 2% achieved the long-term guideline of 12%. The range was wide (8 – 25%) and the mean intake was 15.8%. A point worth making here is that COMA suggested that trans fatty acids should Lee included in saturated fat figures, we have not yet included trans fatty acids in our analysis and this will mean even fewer will be within the guidelines set.
44% had achieved a P:S ratio above 0.32, the suggested NACNE short term level: 36% achieved the COMA figure. The range was again very wide, from 0.1 to 1.1. Again if the trans figures had been included there would have been considerably fewer “achievers”.
An alcohol intake of more than 5% of calories was recorded for 5.6%. That figure may be due partly to some people not having a large total calorie intake so that their alcohol intake appears to be high. The mean calorie intake of these mothers worked out at just over 2000, but the range was again rather wide, from about 1300 to 3200 calories a day.
Sodium intake was more difficult to interpret but the number who managed to achieve the recommended intake surprised me. Professor James and Sanchez-Castillo did an interesting study of salt in which they showed that only 11.6% of salt came from addition at table or in cooking. The remainder came from other sources. Although I advised people to avoid adding extra salt to their food, I think it is probably more important to advise them to have more fresh foods in place of refined foods. Processed foods do not just have high contents of sodium: they tend to be much higher in saturated fat, total fats, sugars and refined carbohydrate than the natural, whole foods.
iv) Conclusion
To sum up, we can see that some of the guidelines are more difficult to achieve than others, with total fat appearing to be the most difficult to achieve.
A final comment: I was asked by Dr. Gau to analyse a hospital record where there was a choice of menu. It was rather like the outside world: there was a huge choice hut it was a case of the consumer knowing which choice to make. Careful choices from a hospital menu enable patients to keep within the short-term guidelines, but it does mean choosing with great care. A poor choice could be well outside the guidelines. It is a matter of educating people to make that right choice. That is our difficulty.
Reference
1. Sanchez-Castillo, Claudia and James, W P T (1984) Epidemiological assessment of sodium sources in the diet by use of the lithium-marker technique. 398th meeting of the Nutrition Society, London. (Published in the Proceedings of the Nutrition Society, Cambridge University Press).
4. PREVENTION OF ALLERGY BY INFANT FEEDING (Summary)
– Professor John Soothill
Feeding is an emotional subject, and therefore food allergy has been a contentious subject. Epidemiology and Clinical observations provide instant aetiological clues, but double-blind randomised Controlled studies are needed to establish causality.
Atopic allergy, affecting one in three of the population, is highly familial and inheritable, affecting more than half of the offspring of two allergic parents. It is antigen non-specific in that most atopics react to many different antigens. Although it is highly familial, it is not simply genetic, as can be seen from studies of identical twins. In one such ease, a sustained difference in response was shown by a boy with, first, infantile eczema, and then asthma; his identical twin was unaffected. Skin prick tests and IgE antibodies were identical. The concordance rate for atopic disease in identical twins is about 50%.
Epidemiological studies have demonstrated that season and place of birth affect future development of atopic allergy. The widespread introduction of artificial feeding of infants in the 1930s was paralleled in the USA by increased rates of eczema.
rib test the association of artificial feeding with atopic disease, we conducted prospective studies in children of atopic parents. Double-blind Controlled trials were of course impossible. Of a group of affected parents, about half accepted the advisability of breast-feeding. In this grouptherewas a reduction in tile incidence of infantile eczema before the age of 6 months. About half of subsequent prospective studies have shown a protective effect from breast-feeding. Mother’s milk may also protect against respiratory allergy.
The WHO has recommended that for the prevention of allergy in genetically Vulnerable people, exclusive breast-feeding, or feeding with Pregestumil should Ill continued up to 6 months, with Selective weaning.
Smoking, pets, animal products and house mites should all be avoided if possible.
There is some evidence that the mother’s diet can act as a primary sensitiser in her breast-fed baby but this is rare. Finally, an already sensitised child may be made ill when it takes foreign antigens from mother’s milk. Perhaps sensitisation can occur antenatally, but this is still a poorly studied areas of particular relevance here is the way health professionals encourage mothers to drink extra cows’ milk during pregnancy, for which I am aware of no established indication. Calcium tablets can be a useful alternative.
Food allergy in older children is also difficult to study. It may involve empirical diets, avoiding a few foods (e.g. milk, eggs) or many foods, which require the individual to eat an extremely limited diet until foods have been reintroduced one by one. We have established in randomised controlled trials that eczema, migraine, hyperactivity behaviour disorder and a range of accompanying symptoms can be prevented by dietary manipulation.
Diet treatment is socially disruptive and sometimes dangerous. The disease must be worse than all the effects of treatment. Approaches to treatment include the prevention of sensitisation in the genetically vulnerable, the avoidance of antigens to which a patient is already sensitised and, in selected cases, manipulation uptake of the antigen by pharmacological means.
5. WHY ARE BRITISH TEETH SO BAD? – Professor Aubrey Shetham
I shall be dealing with the more practical side of nutrition to put the doubters in the picture about sugar and dental disease. Much of what I shall be referring to should be beneficial also in terms of general health, if guidelines are followed. Just as we might be worried about excessive fat consumption in childhood, excess refined sugars can lead to high triglyceride levels that might affect the arteries. In addition, of course, we are concerned about obesity.
I am concentrating on sugar in relation to dental disease because there is no evidence that any other nutritional factor has an effect on dental health, apart from sugar and fluoride. Fluoride is very much a preventive whereas sugar is a causative factor in disease. It always surprises me that a food damaging a part of the body to the extent that Sugar damages the teeth is not banned. We have become immured to the idea that the substance causes holes in the hardest structure of the human body, and we eat that substance so freely. That is the main point that I want to make.
There are a number of primary recommendations about sugar. A World Health Organisation meeting in Oslo concluded that dental caries is a sugar-induced disease for which treatment should be undertaken as a major responsibility. The group recommended that one should discourage the frequent use of Sugar as a food, for instance by labelling certain foodstuffs with warnings as to their potential hazards for dental health. They recommended removing all added sugars from infant and baby foods, paediatric medicines, fruit juices and vitamin preparations; reduce the levels of added sugars in commonly-used foods such as breakfast cereals and jams; and make available more sugar-free foods and reduce the sugar content of confections and drinks. They recommended sugar-free snacks and drinks and research into alternative uses for this high-energy substance. In other words we could run motorcars on it rather than ruin our bodies with it.
The Centre for Agricultural Strategy in their report on National Food Policy in the UK, said that of all foods considered a health risk, sugar is the one on which there is probably the most general consensus. For those quoting the COMA report I should like to put the record straight. COMA said that sugar intake should be reduced for conditions such as dental caries. It is very important to stress that point, especially because of the absence of specific reference to sugar in labelling recommendations. In these, sugar is being referred to as a carbohydrate we shall be no better off knowing how much sugar there is in a product if the current recommendations on labelling are enforced.
The Health Education Council says that the basic mechanism of caries is beyond doubt; the central cause of caries is sugar, particularly sucrose, in our diet. Many influential bodies hold a consensus that sugar causes caries. A letter published in the British Dental Journal in response to the Sugar Bureau’s booklet “Sweet Reason”, quoted Professor Cohen as one of those who do not believe that sugar is the main factor. He replied that in all the experiments he had carried out he had never found caries in monkeys without the presence of added sucrose in the diet.
It is important to consider this link – especially if one reads the press – as there seems to be controversy about sugar. We should recognise what is happening because the mechanism and strategy used by the food industry to confuse the public is to create a controversy. What is not pointed out in the media is that one person might disagree with the consensus view whereas the impression is of a fifty-fifty split. For instance, there is said to be no unanimity about the relationship between sugar and tooth decay. But unanimity on any issue is rare. There is a consensus that frequent intake of sugary foods promotes caries.
When considering the mechanism of caries it is important to refer to the mother’s diet and how that will influence the decay experience of the child. The organisms – the bacteria – that induce the decay are introduced into the child’s mouth by the parents. An example can be found in a study by Kohler in Sweden. She found that the mother’s streptococcae count correlated very highly with those of her child. When mothers’ bacterial counts were reduced by reducing the sugar in the diet, the bacterial count decreased in the children. That is not surprising. When the mother was feeding her child and tasting its food, she was actually transmitting her bacteria to the child. Why does the mother have a high Streptococcus mutans count? She is eating a high sugar diet during pregnancy. So the microis determined by the substrate. The organisms that form acid in the presence of sugar also form polysaccharide that makes them stick to the teeth. That will act as a source of nutrient when sugar is not present and reduce the buffering action of saliva. When there is sticky bacterial plaque it takes longer for the saliva to neutralise the acid.
In comparative terms, a study done at the London Zoo showed that Streptococcus mutans did not appear in any of the mammals except sugar-eating monkeys. It is quite clear that the bacteria are closely related to diet.
One of the ways people are told to get rid of these bacteria is to brush their teeth. But a toothbrush bristle is no match for a fissure in the biting surface of a tooth. The bacteria will wave at the bristles as it goes by. So, brushing teeth will not in fact reduce decay. A clean tooth will not decay, it is true, but it is impossible to get a clean tooth. The bristles do not get into the fissures between the teeth where most decay occurs.
The central reaction when sugars are taken is a very rapid drop in the pH; acid is formed very rapidly. It is a sort of “sprinter’s curve”.
You have to get to the bathroom within four minutes before the critical level of pH for decalcification of the tooth is reached, at about 5.7. Brushing teeth after a meal does little good, even if you got there on time. To be effective, you must get to the bathroom within four minutes.
The sugar is converted into acid and it will demineralise the interprismatic substance of the tooth and a lesion occurs. One of the interesting and most exciting findings is that a lesion can remineralise or heal. One of the factors to help that healing is fluoride in toothpaste or drinking water. Fluoride enhances the remineralisation process. The topical or local effect is now considered important. Water fluoridation will give a topical effect for the whole population.
I want to highlight some important evidence on sugar in medicines. Children taking liquid sugary medicines have much higher decay levels than a control group in a study who were given the same medicines in tablet form. It is important not to add to the problems of chronically ill children by giving them syrupy medicines that will damage their teeth. A recent article published in the Journal of Community Dental Health makes recommendations to the industry about reducing the number ofmedicines with sugar in them.
The critical relationship between sugar and decay is an S-shaped curve. A certain level of sugar is compatible with not getting decay. The decay rate will rapidly increase beyond that level where sugar is taken frequently in young children with newly erupted teeth (which are more prone to decay than mature teeth, which have been in the mouth for four years or more). People over the age of 18, with the exclusion of their wisdom teeth, get little decay. Adults are not decay-prone. That is not to say that they should eat as much sugar as they want. Decay is possible. Parents may pass on bacterial and the threshold of taste for sweets to their children. That is important information to pass on to parents.
A very high level of sugar intake in the child population now faces us. NACNE made recommendations to halve sugar consumption, especially sugars taken in snacks and soft drinks between meals.
The sugar consumption pattern in young children has not been studied recently. The last study of pre-school children suggested that the pre-school child was eating an average of 2 ounces of sugara day. An article published in New Health some months ago suggested that the average British child in the first year of life had 1,486 teaspoons of sugar. That is a very high quantity of sugar. From evidence of teenager’s aged 11 to 14 in Newcastle, the group took 21% of its energy intake from sugar. The NACNE guidelines suggest that the level should be 10%.
The frequency distribution of the sugar intake of children shows that many of them are taking in very large quantities of sugar. We have along way to go in reducing sugar consumption in the child population.
There are, however, hopeful trends in dental health. One of them is that dental decay is decreasing. The decay rate has dropped from 1.37 to 0.52 in eight years in three-year-old children – a 60% decrease. The level of bottle caries has dropped from 8% to 1%. The percentage caries-free has increased considerably. The main factor thought to be responsible for the decrease is a change in breast-feeding patterns. The percentage of mothers in the town where the decrease occurred, who breast-fed entirely, increased from 6% to 26%. In that period milk formulae which needed added sugar were taken off the market. It led to a big change in feeding patterns of children. The mothers were concerned, when they were interviewed, not to have fat babies. There has been a trig shift in concern about what is good for the young child.
This improvement in dental health is occurring in all ages of the population. There was a decrease in decay rates in the five to fifteen age range between 1973 and 1983. Nevertheless the average fifteen year-old had about six decayed teeth; a considerable amount of pain and suffering in the child population. 93% of fifteen-year-olds had one or more decayed teeth. As the Sugar Bureau says that we do not need to worry about sugar because decay is decreasing – their latest theme – I would like to remind them that fifteen-year-old children still have six holes in their teeth on average, and that 93% of fifteen-year-olds have had their teeth attacked by sugar-induced disease.
There is a big social class difference in dental decay. In nursery school Children in Edinburgh there was a large difference in decay between non-deprived and deprived children; 3.2 compared to 0.8 decay rate. One of the significant factors was the sort of food given to children by their mothers after leaving nursery school; 75% of the deprived mothers gave their children sweets whereas only 32% of the nondeprived children were given sweets.
I should like to move on to consider the reasons why children have bad teeth. It is not so much a question of the direct cause being sugar, but why we eat so much sugar. Minter, which is a market research organisation, prepared a report for the sugar industry. According to lintel, marketing has played a minor role in the sugar business, and knowledge of the Whitehall corridors of power has often been more important to the sugar industry than any understanding of the needs of the consumer.
A Senate Select Committee in America said that a close watch should be kept on the slanted and often blatantly misleading advertising practices of tile sugar authorities, who suggest on a world-wide scale based on the role of glucose in the body’s energy pathways, that humans should therefore consume more table sugar. That was thought to be very little short of ethical dishonesty.
Advertisements for Ribena, for example, suggest that sugar or artificial sweeteners are not used. Baby Ribena is therefore claimed to be not too sticky or sweet and made only with special glucose syrups. They say that sugar was taken out of Ribena but glucose was put in to replace sucrose. Who would guess that low-sugar Farley’s rusks have 15% sugar, but that the next item is dextrose? The rusks contain about 23; sugars, which is the equivalent of feeding a young child a doughnut. That is said to be a low-sugar product.
The sort of information that goes to schools includes a sugar resource study kit produced by the Sugar Bureau. It contains the pseudo-science that the sun gives energy, and sugar gives energy. It is quite obvious that you need it. The whole conflation of carbohydrates is into tall especially when we are dealing with labelling. Putting Sugar Beth other carbohydrates that are important suggests that it is essential food. There are many more examples, for instance statements t at tee body can store only a small proportion of energy; if that is not maintained, starvation and death will follow’ That material is gains out to schoolchildren. We wonder at the confusion of the public, and we wonder where it comes from. The confusing of sugar and energy is played upon strongly. Sugar is said to be instant energy for manual Workers and brings extra energy and warmth to the elderly who need it so much.
In a publication about dieting, sugar is presented as the everyday food with the least calorific value in the selection. One teaspoon of sugar is compared with a ham-and-cheeseburger and two ounces of double cream, which are much more calorific than one teaspoonful of sugar. That is produced by the food and sugar industry and widely distributed. Currently, there is a £5 million campaign called Energywise – Sugarwise, designed to promote the consumption of sugar because sugar sales are dropping. In addition, the three main confectioners spend a great deal of money on advertising; Cadbury, Mars and Rowntree Mackintosh spend £23 million to £26 million a year.
Let us go back to the recommendations of the World Health Organisation and consider what we can do about them. They suggest that we should discourage the frequent use of sugar as a food and label certain foodstuffs to warn of their potential hazards to dental health. I do believe that is a possibility. Cigarettes are labelled as a potential health hazard. Confectioners already put quite a lot of information about their products on the labels. It is not beyond practical possibility to do something about that.
WHO suggests removing all added sugars from infant and baby foods, paediatric medicines, fruit juices and vitamin preparations. It is unfair to ask a mother to shop around for so-called sugar-free foods. Now it is a question of foods being sugars-free because sucrose and glucose are equally harmful to teeth. More high-fructose syrups are being introduced. The different names for sugar such as corn syrup, or other euphemisms, make it difficult for the consumer to know what does or does not constitute sugar. Mothercare puts “No Sugar (sucrose)” on its products. The contents have added glucose.
The manufacturers need to reduce the level of added sugar in commonly used foods such as breakfast cereals and jams, according to WHO, and make available sugar-free foods. That is not impossible because manufacturers in this country, such as Quaker, have a large range of sugar-free products available in America, which are not sold here. Many confections that are made by companies with outlets in Britain and on the Continent are sugar-free on the Continent. We need to talk to the soft drinks industry, in particular, to persuade them to reduce sugar in soft drinks. They are a major source of sugar for a large group of the population, especially those who believe that orange squash is a good source of vitamin C.
The Oral Research Advisory Group of the WHO recommends that the frequency of sugar intake is a valid procedure for the reduction of the occurrence of dental caries. Why do we not have strong statements about that? One of the things to consider, because advertising of sugar-containing foods is so common, is the role of the Advertising Standards Authority. Its rule 4.2 says that advertisements should not contain statements or visual representations which directly or by implication, by ommission, ambiguity or exaggeration, are likely to mislead the consumer about the product advertised. As a group concerned about health, you are in a very good position – to write to the manufacturers, the Advertising Standards Authority or to other bodies concerned with food and health complaining about misleading advertisements. Many dietitians and health visitors send material to us that they are given by representatives. Their health claims are quite appalling.
An example of what is possible is a symbol meaning tooth-friendly. A smiling tooth with an umbrella appears on confections in Switzerland that have passed a test and do not lower the pH in plaque below 5.7 for half an hour after the child has eaten them. We could have available a range of confections safe at least for teeth. That would avoid the killjoy aspect that people complain of and the problem of deciding what to give a child who always wants sweets. If you provide a range of products that children can eat that makes it much easier.
I want to emphasise again the point about sugary medicines. We should press for the removal of sugars from medicines, especially from those taken on a long-term basis by young children. Some books still show a child’s visit to the clinic being rewarded by sweets. Many health professionals are still rewarding children by giving them sweets. If it has their approval it is very difficult for you or me to say that it is wrong.
The Health Education Council says that glucose is not an acceptable sugar substitute and its use in infant health drinks and sweets should be condemned, together with the use of sugar in medicines.
About health warnings, why not have a warning that says: “The frequent use of this product contributes to dental decay and other health problems”? The health problem that I am talking about is caused by sugar. Why not say: “Sugar can seriously damage your health” or “This product contains more than 50% sugar and should be regarded as a confection rather than a food.” Lots of children eat breakfast cereals as a confection rather than a food, while they are watching television.
We should remember that there is no physiological requirement for sugar. All human nutritional needs can be met in full without taking a spoonful of white or brown sugar on its own or in food or drink. We area talking about a food without a physiological use in the body. Nobody has ever died from sugar deficiency.
6. DIET: THE BEGINNING OF ATHEROMA – Dr. Christine B. Marenah
This is a somewhat unusual experience for me in that when I received the invitation to talk at a symposium entitled “Nutrition in Pregnancy and Early Childhood”, I wondered very much what Contribution I could mate since neither of these groups of patients form a substantial proportion of my experience. On reflection however, I realised just how pertinent it would be to talk to such a group, since it is in the early years of Childhood that prevention of atheroma really has to begin.
In talking about lipids and atheroma it is all too easy to be insular, but hyperlipidaemia is only one risk factor. Two other major risk factors for the development of atheroma, hypertension and obesity are both profoundly influenced by diet. These three risk factors do not have merely additive effects. Considering just two of these variables, that is serum cholesterol and systolic blood pressure; from the Framingham Study it is evident that in asymptomatic males (with normal ECG at entry) as the serum cholesterol increases from 6.1mmol/1 to 8.1mmol/1 at a systolic blood pressure of 105mm of mercury, so the probability of developing coronary heart disease within eight years doubles; at a systolic blood pressure of 180mm of mercury and a cholesterol of 8.1mmol/1 the risk is seven times that of an individual’s with a systolic blood pressure of 105mm of mercury and a cholesterol of 6.1mmol/1. Furthermore, this is true throughout the range of serum cholesterol and systolic blood pressure and is not only true for hypertensive and hypercholesterolaemic individuals.
Initially, I would like to briefly outline how lipids are transported in the blood and hence remind you of the meaning of some of the abbreviations, which I will be using later. Fat and water do not mix, and in order for the blood fats (cholesterol and triglyceride) to be transported in the blood they must be made water soluble; this is achieved by packaging the litid in spherical particles (lipoproteins) varying size whereby the lipid forms a fatty core which is surrounded by a water soluble layer of protein and phospholipid.
The largest lipoproteins are the chylomicrons: these are produced in the intestine and are predominantly triglyceride of dietary origin. They circulate in the blood stream and become progressively triglyceride depleted by the action of the enzyme lipoprotein lipase to form so-called chylomicron remnant particles. These chylomicron remnants are taken up by the liver.
The lipoprotein class, which is next in terms of size and density to chylomicrons, is Very Low Density Lipoprotein (VLDL). VLDL is also triglyceride-rich; it is synthesised in the liver from endogenous triglyceride. VLDL is catabolised in viva via Intermediate Density Lipoprotein (IDL) to Low-Density lipoprotein (LDL). LDL is the major cholesterol-carrying lipoprotein in normal individuals.
The smallest, densest, lipoprotein, High Density Lipoprotein (HDL), is actually made up of two sub-classes; the minor sub-class HDL2 being slightly bigger and less dense than the major Subclass HDL3. The importance of this sub-division is that the protective role ascribed to HDL in the earlier epidemiological studies is in fact a property of the minor HDL2 sub-class.
Thus, simplistically, there are good and bad lipids. HDL and specifically HDL2 are inversely related to coronary heart disease risk and hence are protective; LDL correlates directly with total serum cholesterol and coronary heart disease risk.
Atheroma is a continuous process starting in childhood and proceeding throughout life. By the time patients are symptomatic, for example at presentation with myocardial infarction, they have already reached a point on their “life curve” whereperhaps 80% of their coronary artery is occluded. Even with sensitive techniques, for example, coronary angiography, 50% occlusion has occurred before it is demonstrable. In order to have an effect on the atheromatous process it is necessary to attack at a much earlier stage, that is during the long silent period of the disease when patients are asymptomatic and preferably when there is no occlusion or only minimal occlusion. In order to do this we need to start way back in childhood.
Much of the evidence of the role of cholesterol in the development of atheroma is circumstantial and this circumstantial evidence may be summarised under the following headings:
- Observations of the nature of the atherosclerotic lesion
- Animal models
- Longitudinal epidemiological studies
- Cross-cultural studies
- Investigation of unusual populations
I. The nature of the atherosclerotic lesion itself
At the age of 3 years all infants have demonstrable fatty streaks in the aorta, and by the age of 10, fatty streaks can be demonstrated in the coronary arteries. The predominant lipid in these fatty streaks is cholesterol. Children in both industrialised and under-developed countries exhibit these fatty streaks. What appears to be important in terms of the development of atheroma therefore is not the appearance of these fatty streaks but their progression into fibrous plaques; since it is these that are the real precursors of occlusive vascular disease.
The major component of the occlusive atherosclerotic lesion is cholesterol. At every stage of the atheromatous lesion therefore, from fatty streaks through to occlusive vascular disease, cholesterol is the major component.
II. Experiments with Animal Models
It has been shown possible to induce atherosclerosis in all aninbal species so far tested by appropriate dietary manipulation.
Furthermore, in animal studies it has been shown that with reversion to a non-atherogenic diet regression of atherona is possible. Armstrong demonstrated that 60% occlusive lesions of the coronary arteries in male rhesus monkeys, produced by feeding with a high cholesterol diet, could be shown to regress so that there was only 15-20% occlusion after 19 months on their normal low cholesterol diet. There is, of course, the question as to whether such experimentally induced atherosclerosis in animals is equivalent in all respects to naturally occurring atherosclerosis in man, and hence whether we could extrapolate from these studies that regression of atheromatous lesions in man is possible.
III. Longitudinal Epidemiological Studies
Numerous studies during the past thirty years have addressed the question of the relationship between serum cholesterol and the risk of developing cardiovascular disease. The Framingham study, one of the major such studies, showed that of all the parameters serum cholesterol at entry was one of the most powerful predictive factors for future development of myocardial infarction; serum cholesterol being on a par in its predictive value with systolic blood pressure. From the Framingham data it appears that total serum cholesterol is the best predictor of subsequent myocardial infarction and that this is true throughout the whole range of serum cholesterol; that is even in the mid-range a value just below the mean for total serum cholesterol carries a lower risk than does the mean value. Serum cholesterol has also been shown to contribute to risk independently of other useful predictors, e.g. blood pressure, smoking and family history of cardiovascular disease. The effect of cholesterol as a risk factor was shown to be not merely additive with other risk factors, but multiplicative.
IV. Cross-Cultural Studies
There are three types of cross-cultural studies that have a bearing on the diet-cholesterol-atheroma hypothesis.
Firstly, study of populations in non-industrialised countries. It has been repeatedly shown that the incidence and prevalence of cardiovascular disease in primitive, non-technological societies are significantly lower than in industrialised Societies. In general, serum cholesterol levels in infants are similar in all cultures, the levels in non-technological societies increase during infancy and then stabilise during childhood, whilst in affluent societies, the serum cholesterol level continues to rise throughout adolescence and adult life. The incidence of fatty streaks in children is similar in all societies but the progression of these to established atheromatous plaques is what is responsible for differing coronary heart disease risk in the differing populations.
Secondly, studies on industrialised populations. Although the incidence of coronary heart disease is high in such populations, it does vary fairly widely between countries Ancel Keys in the Seven Countries Study showed strong correlation’s between heart disease incidence rates in the populations studied and the mean serum cholesterol level, as well as equally strong relationships between disease rates and the percentage of calories the populations consumed as saturated fat.
Thirdly, studies on migrating populations throw light on whether it is the differing gene pool, which is responsible for the differing levels of coronary heart disease in different populations, or whether it is an environmental factor. The correlation of morbidity indices and serum lipid patterns across cultures is suggestive of causation; however, another possible explanation is that different gene pools are involved. Migrating populations eliminate this latter possibility for, provided there is insignificant intermarriages if both serum cholesterol and coronary heart disease incidence change when a population moves, it is highly likely that this results from environmental factors superimposed on a static gene pool. We know that when an individual changes his diet the serum cholesterol level changes quickly in response and then stabilises at a new level within a matter of weeks.
Atherosclerosis however, as we have seen, is a slow process with a time scale of years; bearing this in mind, it is still possible to see whether a migrating population shares the characteristics of its country of origin or its country of adoption.
Ancel Keys studied Japanese men in Japan and also those who had emigrated to Hawaii and Los Angeles. He found that the percentage of dietary calories derived from fat, serum cholesterol level and the incidence of coronary heart disease was different in the three groups; all three parameters being highest in those living in Los Angeles, and lowest in those remaining in Japan. However, comparing first generation Japanese in Los Angeles with indigenous Los Angeles citizens, although their diet and serum cholesterol levels were similar their coronary heart disease incidence was lower. But, second generation Japanese in Los Angeles acquired their adopted home’s coronary heart disease incidence. This adds weight to the hypothesis that serum cholesterol level is a good predictor of risk only if diet is not changed markedly in the lifetime of the individual.
From his extensive studies of diet Ancel Keys suggested, in 1969, that the change in serum cholesterol produced by dietary manipulation can be estimated from the following formula:
^C = 1.3 (2^S – ^P + ^Z)
^C = Change in Serum Cholesterol Level
S = Percentage of calories supplied by dietary saturated fat
P = Percentage of calories supplied by dietary polyunsaturated fat
Z = Sq. Root of dietary cholesterol in up/1,000 Kcals.
This has been found to be widely applicable.
V. Unusual Populations
As in most spheres in medicine, much has been learned about the normal by Studying the abnormal; this also applies to atheroma research in which a lot has been learnt from studying patients with genetically (ietennined hyperlipidaemia. Some of these conditions are associated with an increased risk of developing coronary heart disease.
Three monogenic disorders of lipid metabolism predispose to the development of premature coronary heart disease. Firstly, Familial Hypercholesterolaemia, which is probably the most “malignant” of the hyperlipidaemias. 50% of males with this autosomal dominant condition suffer a myocardial infarction before the age of 45 years. The second hyperlipidaemiat Remnant Hyperlipoproteinaemia or Type III hyperlipoproteinaemia, often presents with early onset peripheral vascular disease in addition to premature coronary heart disease. The third condition, much less well defined than the other two, is Familial Combined Hyperlipidaemia. This condition was first described following a study in Seattle of myocardial infarction survivors. This showed that 30% of such patients demonstrate high levels of VLDL, LDL or both, and one or both of these lipoproteins is elevated also in a first degree relative.
Thus, you can see that the circumstantial evidence for linking dietary fat, serum cholesterol and the development of atheroma is strong. However, considering the vast literature relating to diet and lipid levels, very little has been done in terms of children’s diets and their serum lipids. A notable exception to this is the Bogalusa Heart Study that addressed the problem of coronary heart disease risk factors from birth to 18 years of age. This study demonstrated that if the children were divided into three groups on the basis of their total serum cholesterol level, the first group having serum cholesterol levels less than the 25th percentile, the second group having a level between the 25th and 75th percentile, and the third group a value greater than the 75th percentile, then total fat, animal fat and saturated fatty acid content of the diet is significantly lower in the first group than in the other two groups. A further important finding of this study is “tracking” of the serum cholesterol level throughout childhood; that is children found to be in the last group (greater than the 75th percentile) at an early age if followed up in subsequent years, remain greater than the 75th percentile. The same tracking phenomenon has been demonstrated to apply to the systolic blood pressure. Thus, as far as these two major risk factors are concerned, their levels in early childhood may be predictive of risk much later in life.
At St. Thomas’ over the last few years, we have looked at the relationship between diet and its possible manipulation, serum cholesterol levels and the development of atheroma in a fairly small way. The first study, which I would like to describe, looked at the effect of dietary manipulation on serum cholesterol levels. In this study a typical Western diet (Diet A, 40% energy derived from fat with a P:S ratio of 0.27) was compared with a conventional fat-modified diet (Diet B. with 27% of its energy from fat and a P:S ratio of 1.0), a fat-modified diet Supplemented with fruit, vegetable and cereal fibre (Diet C) and a diet which was really a hybrid between Diet A and Diet C (Diet D providing 40% energy from fat with a P:S ratio of 1.0 and supplemented with fibre). on Diet B there was a mean reduction in serum cholesterol of 22%and a mean reductionof 27% in LDL cholesterol. By increasing the fibre content to 55g/2,000 Kcal, as in Diet C a mean fall in cholesterol of 29% and a 35% mean reduction in LDL cholesterol was achieved. Thus the effect of adding fibre was additive to the effect of fat reduction. As a bonus the mean HDL cholesterol was reduced less on Diet C (12%) compared to a mean reduction of 35% on Diet B.
The above-described study was performed in an institutional setting, but one would be a supreme optimist to think that such startling results could be achieved in a free-living population. So, the next step was to prescribe this fat-modified high fibre diet to hospital outpatients to see what was possible in this setting. Mean reductions of 22% and 25% in total cholesterol and LDL cholesterol were achieved. But no significant change in mean EMIL or HDL2 cholesterol level. Thus, it appears, by appropriate dietary manipulation we can have a very significant effect on patients’ total serum cholesterol and LDL cholesterol, without having an adverse effect on the protective HDL2.
In conclusion, I would like to describe a study that addressed the question of whether regression in established atheroma is possible. In this study patients with symptomatic peripheral vascular disease, who were unfit for surgery, were randomised into treatment and usual care groups. The two groups were well matched in terms of their base-line characteristics and both groups received identical advice to stop smoking and to lose weight when appropriate. The treatment group were treated with a fat-modified diet and, in addition, one or two lipid lowering drugs in order to render them normolipidaemic. Biplanar femoral arteriography was performed before and after the treatment period, which extended for a mean period of 19 months. The rate of progression of atheroma was reduced by approximately 60% by hypolipidaemic treatment. Within this relatively short study period, only a minority of arterial segments showed radiological improvement, but twice as many segments in the treatment group as in the usual care group demonstrated lack of progression of the atherosclerotic lesion. Thus, it has been shown both in this study and by other workers that in late, symptomatic atherosclerosis, reducing serum cholesterol level cam slow progression of the arterial lesion. Whether this is true in the asymptomatic stage of the disease we do not know, nor do we know whether actual regression occurs, although it has been claimed by other workers. Furthermore, we do not know whether or not extrapolation from what we have seen to occur in the femoral artery is applicable to what is occurring in the coronary artery: studies addressing this latter problem are currently underway.
I also think there is convincing evidence that what we eat from early childhood onwards is reflected in our cholesterol level and that, even in early childhood, the coronary heart disease risk factor status of an individual can be determined. Furthermore, even in adult life dietary changes will be reflected in a reduction or increase in the serum cholesterol concentration and this in turn can be shown to affect a reduction or increase in the rate of progression of even established symptomatic atheroma. I think the signs are rood in that if we can get the message across to sufficient numbers ofpeople (especially the young) that dietary modification does work, we may prevent the laying down of atheroma before it lays us down.
7. HOW SAFE ARE LOW FAT DIETS FOR CHILDREN?
– Dr Andrew Tomkins
There is currently an increasing awareness of the link between dietary fat intake and certain diseases such as coronary heart disease and colon cancer. Current recommendations to reduce the fat intakes by adults in the U.K. until they constitute about 30-35% of total calories consumed have not really addressed the question of the needs of the growing child. There have been objections to these fat/energy ratios by dietitians and paediatricians with responsibility for advising on diets that ensure that otherwise healthy Children achieve their genetic potential for growth. Those with experience of managing children who are underweight because of illness have inferred that 30-35% is too low. However it is really not clear whether such objections are justified. It would be helpful if there was data on cohorts of British children who had been brought up on low fat diets in order to see if they were shorter or thinner than their classmates who had consumed a more typical “British diet”. Unfortunately there is no such information.
It may therefore be helpfulto examine dietary fat consumption in different population groups throughout the world and to compare these values with anthropometric measurements and in order to do so I shall examine data on five populations in W. Africa, not because they are more special than anywhere else but because the quality of the data is reasonable.
The first group, the Tuareg, are a pastoralist people who, until the recent drought at any rate, possess large numbers of cows and goats from which they are supplied with considerable volumes of milk. Their milk consumption varies considerably throughout the year, being greatest during the rainy season when t pasture is lush and least during the hot dry months when the terrain is dusty and devoid of vegetation. At this time they are dependent on millet Or rice for their energy supplies. The average fat/calories proportion consumed by children age 2-4 years throughout the year is high by African standards at 32%, Nutritional status assessed by weight/age, height/age, weight/height and body mass index (Wt/Ht2) was very similar to the N.C.H.S. international reference standards which are made up of healthy N. American children.
The second group, the Fulani, are also migrant pastoralists with herds of cattle and goats but they spend a considerable proportion of the agricultural year in a single site where they plant and harvest a cereal crop, usually millet. They have a similar increase in milk consumption during the rainy season to the Tuareg but overall their fat/calorie intakes are lower with average levels of around 20%. They have a lean stature reflected in a lower body mass index than other population groups in Africa – this may be genetic. However; their growth rates, in terms of weightgain per month, are similar to N.C.H.S. standards during the rainy season and only falter a bit during the dry months on average the weight gain of children age 2-4 years of age is around 190g/month (i.e. virtually identical to the N.C.H.S. standard of around 200g/month for children age 12-60 months).
A third groups Bambara millet farmers, are a settled community living in villages surrounded by fields which are laboriously prepared for cultivation of sorghum and millet. Again, there are seasonal changes in food intake but these relate to differences in food quantities available rather than changes in type of food. The “hungry season” at the end of the rains when the crop has yet to be harvested can be a devastating time of food shortage, for children just as much for adults. On an annual average the fat/calorie ratio for young children is around 15%. This is associated with quite marked changes in rate of weight gain. During the hungry season many children will stop growing though they do achieve remarkable catch up growth once the harvest is gathered in. On average their child growth rates are around 170g/month.
A fourth group, the Hausa sorghum and millet farmers, have similar quantities and seasonal availability of cereals to the Bambara farmers but their diet is much more varied with greater availability of stews of groundnuts, meat and fish which provide an average intake of around 30%. Their growth rates (averaged throughout the year – 190g/month) were only just below the N.C.H.S. standard.
A fifth group, of urban children in W. Africa of mixed Mandinka and Wolof tribal stock, had a fat/calorie ratio intake of around 32% and they grew at similar rates to the children in Hausa families although both groups showed marked differences in rates of growth at different months of the year.
What can these figures tell us about the safety of low levels of fat in the diets of British children? Obviously they have to be approached with great caution. There are enormous methodological problems in assessing diet in children. However, as similar methods were used in each community we have some confidence in the data. Comparisons between the groups have to allow for the considerable differences in lifestyle between the groups. This may affect energy requirements considerably.
However it seems that all five population groups are capable of growing very adequately (by British or N. American standards) despite the fact that they are eating much less fat than their British counterparts. Indeed most of these children were eating far less than the values of 30-35% fat/calorie ratios that have attracted criticism
Perhaps we will be able to be more certain of how safe a low fat diet is when we know more about the growth and nutritional status of children who have been brought up in families which have provided food which is lower in fat/calorie ratios than is traditionally eaten in U.K. These studies need to concentrate on healthy children in the Community rather than the sick children in hospital clinics.
Whatever the safe level for adequate nutrition for British children, it is worth bearing in mind that recent evidence suggests that many of the metabolic conditions and degenerative disorders associated with a diet that contains excessively high fat content are established during childhood and adolescence. Unless we concentrate on improving the diet of children, we may find that we have missed the boat, in terms of health promotion and disease prevention in adults.
8. ATTRITION IN PREGNANCY AND EARLY CHILDHOOD
Professor Philip James
The problem of nutrition in pregnancy is not simple when one considers the processes which are taking place during the nine months. There area remarkable series of changes in a variety of organs. We are not simply considering a selective accumulation of nutrients in the uterus and foetus but all metabolic changes which occur in the nether. The problem is how to begin to sort out the nutrient needs of pregnant women and relate them to government policy making and the current debate about health.
Let us first consider the energy needs of pregnancy and assess what the emerging report on energy and protein requirements (produced by WHO, FAO and the United Nations University) proposes. Unfortunately we discover that this advanced text has to rely on the Classic Calculations by Doctor Hytten many years ago building up estimates of energy need on the basis of theory rather than observation. We have to distinguish between the amount of energy laid down in the mother and child and the extra energy cost of being pregnant, growing a baldly and maintaining a variety of physical activities. This sounds and is complicated and we should not be impressed by simple figures of the energy needs of am “average” woman to which we add the costs of pregnancy. Thus official reports suggesting that women need 9.2 MJ (2,200 kcal) daily are unhelpful energy requirements vary by weight, sex and age and depend predominantly on the body composition of the individual. There is also individual variability in metabolism as well as different degrees of physical activity. To claim therefore that one has an unusually low energy requirement because one needs 1-1.5 MJ (250-360 kcal) less than an average value is meaningless. The new WHO/FAO/UNU report specifies a method for estimating a person’s quiescent, i.e. basal metabolic rate (SMR). Then one can estimate a sedentary individual’s total needs as about 1.5 times this figure but normal people may be expected to have a need within ± 20% of this final value.
What then of pregnancy? We know now that the BMR of the pregnant woman goes up but we know little of her metabolic response to food nor whether the efficiency with which she undertakes physical exercise improves. If the BMR is expressed on a weight basis then the cost of maintaining her tissues does appear on this crude analysis to have fallen and this may reflect a true adaptation to pregnancy.
It now seems therefore that the scientific evidence is inadequate forassessing a pregnant mother’s real energy requirements. The FAO/WHO reportestimates that perhaps 1.2 MJ (290kcal) extra energy is needed daily with less in the probable event of women cutting down their activity as pregnancy advances. Changes in efficiency and activity may account for the increasingly numerous observations that pregnant women seem to eat the same amount as normal and certainly do not “eat for two”.
The subject of protein requirements in pregnancy is only a little easier than that of energy. In the 1970s the picture seemed clear: we knew what normal women needed and could add specified extra needs for the pregnant state. Unfortunately we now realise that the experiments contributing to the view of the ’70s were badly designed and that normal protein needs are higher than we at first thought. A figure of 0.75 g/kg/day for the protein requirement of a normal woman needs to be increased by an extra 3.3g per day to cover an appropriate increase in body protein as part of a weight gain of 12.5 kg. The figure of 3.3 is, however, only a value for the average person and when it comes to women who biologically need lore protein to cope properly, then we have to add 30% to this value. With the addition of an absorbality and use factor the experts calculate an extra average daily protein need of about 6g.
Now let us come to the subtle problem of vitamins. How do we assess the need for water-soluble vitamins during pregnancy? Indian researchers in Bangalore laboratories have shown that pregnancy is a most unusual condition as far as vitamins are concerned. A series of proteins are included for secretion into the blood from the liver in response to the surge in female sex hormones during pregnancy. These proteins bind specific vitamins and then transport them selectively to the uterus so that the foetus has first call on the inflow of dietary vitamins. Thus the mother may appear to be deprived of vitamins when her babe is being provided for. These examples serve to illustrate the complicated response by the body to pregnancy and caution against simple conclusions about the needs of the pregnant mother.
The story on mineral needs is as complicated as that on vitamins and we remain in a muddle. If, however, we accept the Nicholls’ recent summary, they conclude that increased amounts of both vitamins and minerals are needed in pregnancy. For instance, in the USA experts suggest a doubling of the folio acid requirements and, fond as they are of vitamin C, suggest normal intakes should increase from 60 to 80 mg in pregnancy. Calcium needs rise from 800 to an astonishing 1,200mg – this intake to continue throughout lactation. Intakes of phosphorus, magnesium, iron and zinc also should increase.
It may be said that the Americans are over-zealous in their concern for vitamins and minerals. Let us then consider the British figures, taken from DHSS reports. These are assessed on a reasonable estimate of what we think normal people need, with an allowance for individual variation. In pregnancy women seem to need more of most things except – perhaps energy. During lactation nutrient requirements increase, for obvious reasons. There is also a selectively increased need, for instance, for vitamin A.
Now let us take the ordinary British diet and assume that we should not attempt to meddle with such a wonderful institution but simply, in the case of pregnant women, add one or two marvellously healthy foods. My first choice must obviously be milk since it is nutritious and simple to take. If we assume that we need to provide an extra 840 kJ for the sedentary pregnant woman with a daily extra of 6 protein and 700 mg extra of calcium, we find that we cannot match our new demands by simply providing an extra pint of milk. It contains plenty of protein, nearly enough calcium but far too much energy. Skimmed milk, however, meets almost all these estimated requirements.
Unfortunately an extra pint of skimmed (or whole) milk will not cope with the demand for extra water-soluble vitamins. In other words, we come to the astonishing conclusion that we have to change the diet of a normal woman once she becomes pregnant and enters that unusual state where she is attempting to grow a foetus which demands the best of nutrient supply. Perhaps this is as good a biological test of optimal nutritional needs as we are likely to get pending decades of worthy nutritional research. We now see why most health visitors and dietitians encourage their “patients” to change to an unusual diet for this abnormal state of pregnancy!
One can do a number of calculations based on adding single nutrients and show that it is difficult to devise a system where a single or a few foods are added to the average British diet in order to meet the demand of experts. We are led to the inexorable conclusion that pregnant women should eat a NACNE-type diet, low in fat and sugar, if they are to fulfil the nutrient needs of themselves and their children.
The problem with dealing with the pregnant woman’s nutrition once she is registered in an antenatal clinic is that thereis increasing evidence that this will be too late for a crucial phase of her nutritional needs. There is steadily mounting evidence that subtle vitamin deficiencies, such as those encountered in the poorer sections of the population, lead to neural tube defects as the embryo goes through its critical early phase of development. Some women are more prone than others to these devastating effects for reasons that relate either to genetics, dietary intake or other reasons. Preliminary evidence suggests that if these women are given advice to improve their diet before their next conception they can reduce the risk of another abnormal child from about 5% to 1% or even 0.6%. This is powerful but unconfirmed evidence that diet is the key to preventing a lifetime of disability. The Medical Research Council is now conducting a trial in an effort to assign a specific vitamin to this story. Unfortunately for science, women’s diets seem to be improving and many doctors favour preventive action at this stage rather than waiting for the hard evidence.
Whatever one’s views it is unlikely that many would quibble with the view that any woman contemplating pregnancy should be advised to “eat well”. This, in practice, means eating a low fat, low sugar diet if an adequate minerals and vitamins intake is to be achieved on our current energy intakes.
Given these considerations of pregnancy and the needs of the pre-pregnant state we find grounds for proposing that young women should be on a NACNE or COMA style diet as well as their husbands who are more prone to coronary artery disease.
So what of the children? COMA specifically excluded from its new recommendations children aged 1-5 years. This, in practice, was not the view of the main panel but reflected advice from the group dealing with children, a group who perhaps by virtue of training and experience has less concern for the problem of coronary disease. Nevertheless the group was rightly concerned with the possibility that children dependent on milk would be placed on low fat milk and thereby suffer. There seems little doubt that the breast fed babe should transfer to properly constituted infant milk formulae and in addition begin a diet conducive to the present and long-term Welfare of the child.
It will be difficult to implement the COMA policy which implies that at least 75% of people should change their diet whilst maintaining the present diet of those less than 5 years of age.
A more refined policy for children may eventually emerge but in the meanwhile we find ourselves obliged to note that the COMA/NACNE recommendations are suitable for pregnant and lactating mothers and for their growing older children. Those who yearn for the pre-NACNE days now at least have to accept that these nutritionally vulnerable groups are likely to be benefited by the currently acceptable policies.
9. PRACTICAL GUIDELINES
– Miss Maggie Sanderson
My brief this afternoon is to look at what recommendations can be made for nutrition in childhood and how these can be translated into practical terms for mothers. The main concerns in adult nutrition, have been centred around four main components of the diet: fat, fibre, sugar and salt. But how applicable are these recommendations for children, and is there any specific advice for this age group?
In the last two years, three major reports have been published:
Present Day Practices in Infant Feeding (1983); DHSS
NACNE Report (1983); HEC
COMA Report on Diet and Cardiovascular Disease (1984); DHSS
The first only considers the diets of infants under one year old, the Second and third specifically excluded Children under five from their recommendations.
To try and augment the lack of UK data in this area, a group of community dietitians have recently been searching through all the scientific literature published over the last five years. The most striking result of this activity has been the discovery of how few published recommendations there are and how little data there is available on the actual nutrient intake of healthy children under five. I will therefore present here what recommendations these are and suggest same tentative recommendations where there are none.
Fat Recommendations
The most widely accepted recommendations for infants are those given by Fomon (1974) who recommends that infants should derive between 30-30% of their energy from fat.
The COMA report recommends that the Kcalories from fat in the adult diet should not exceed 35% of energy.
Children up to the age of three to four months receive all their Kcalories and nutrients from milk. About 50% of this energy comes from fat. As the infant becomes older, milk becomes a less important source of Kcalories due to the increasing contribution of other foods during and after weaning, lentil at eighteen months, it only provides 36% of Kcalories.
TABLE I
Contribution of Milk to Fat Intake (Yeunq 1983)
| Up to 6 months 7 months 18 months | 82-99% 73% 36% |
However, it is at six months when babies are changed from bottle or breast-feeding to a cup that mothers may be worried about which milk to give. Should they continue to give proprietary baby milks, whole milk or, in view of the increasing worry about fat in relation to heart disease, give semi-skimmed milk (2% milk)?
Yeung (1983) found in his study of Canadian children that 51% were taking semi-skimmed milk (2% milk) at six months while 49% were using whole milk (or 4% milk).
He found no difference in the Kcalorie intake between the two groups and found that many of the nutrients were significantly higher in the grouper taking the 2% milk. While this may be beneficial for some nutrients Yeung concluded that the raised sodium and protein intake in the groups taking 2% milk may be inadvisable in children under twelve months. He was also concerned that the low fat intake of the infants in the 2% group at six months may reduce their essential fatty acid intake. He therefore recommended that it would be prudent not to give any reduced fat milk to children under one year, but found no contradiction from then on.
Fibre
The only recommendation on fibre intake that we could find was one issued by the American Paediatric Society. They stated that children under one year do not need any fibre. We could find no recommendation for children between the ages of one and five. The recommendation for adults is 30g of fibre a day.
Information on the actual intake of fibre in children under five is also Scarcest In the last five years, there appears to have been only one paper published on the dietary fibre intake of this group, and this was from Australia. We did however find some unpublished data (see Table III).
The Community Nutrition Group of the British Dietetic Association carried out a small-scale survey on children under five. The results of this survey showed a range of 8-19g of fibre per day, which was slightly higher than the other UK studies. Perhaps this difference reflects the time differences between the studies. Black’s figures were collected in 1979, the Community Nutrition Group’s survey in the spring of 1985.
TABLE IIMean Food and Nutrient Intakes Fed 2% and Non-defatted Milks
| Age | ||||||||
| 6 months | 8 months | 10 months | 12 months | |||||
| 2% Milk | Non- defatted Milk | 2% Milk | Non- defatted Milk | 2% Milk | Non- defatted Milk | 2% Milk | Non- defatted Milk | |
| Amourt of Food (g) | 1139* | 1016 | 1197** | 1103 | 1225 | 1184 | 1218 | 1207 |
| Energy (Kcal) | 713 | 714 | 800 | 827 | 877 | 898 | 922 | 950 |
| Protein (K) | 35.1* | 22.2 | 38.0* | 31.4 | 40.6* | 35.5 | 42.1** | 38.6 |
| Fat (g) | 19.3* | 28.9 | 22.0* | 30.5 | 26.2* | 32.5 | 29.5* | 36.0 |
| Carbohydrate (g) | 99.6** | 91.7 | 112.9 | 107.7 | 120.9 | 117.3 | 122.9 | 120.1 |
| Canciurn (mg) | 1098* | 727 | 1109* | 848 | 1045* | 853 | 986* | 850 |
| Phosphorous (mg) | 939* | 607 | 992* | 763 | 875* | 818 | 960* | 848 |
| Iron (rag) | 12.2 | 12.3 | 12.2 | 12.7 | 11.0 | 10.1 | 9.7 | 8.1 |
| Sodium (mg) | 588* | 323 | 671* | 501 | 850* | 679 | 938 | 888 |
| Potassium (mg) | 1800* | 966 | 1874* | 1369 | 1925* | 1565 | 1921* | 1678 |
| Vitamin A (JU) | 6402 | 6287 | 6441** | 7512 | 6626 | 7005 | 5753* | 7348 |
| Thiamin (mg) | 0.77 | 0.75 | 0.81 | 0.80 | 0.78 | 0.73 | 0.73 | 0.73 |
| Riboflavin (mg) | l.91* | 1.30 | 1.98* | 1.60 | 1.89* | 1.60 | 1.76** | 1.61 |
| Niacin (mg) | 7.73 | 8.23 | 9.21 | 9.49 | 9.99 | 9.62 | 10.41 | 10.41 |
| Vitamin C (mg) | 73.2 | 74.6 | 78.0 | 86.0 | 90.7 | 93.3 | 97.4 | 101.6 |
| Calorie Density (cal/100 gm) | 62.9* | 70.6 | 67.4* | 75.2 | 72.2** | 75.9 | 76.8 | 79.0 |
* significantly different from non-defatted milk group at P 0.001
** significantly different from non-defatted milk group at P 0.05
| Published Data | Age | Mean | Range |
| Australian Study(Magarey & Boulton, 1984) | 4 years | 12 | 2.8-28g |
| Unpublished Data | |||
| United Kingdom(Black) | 2 years3 years | 7.38.5 | |
| United Kingdom(Nelson) | 3-5 years | 10 | 2-15g |
Raising children’s fibre intake has been shown to be beneficial as it can raise nutrient density and relieve constipation. A report by Davis (unpublished) shows that the iron and zinc content of the diet goes up as the fibre intake is increased. In all the fibre reports on constipation in children published in the past five years, one of the main recommendations was to increase dietary fibre.
What possible recommendations could we give for fibre intake in children? If we assume that the NACNE recommendation for adults is made on the basis of an average Kcalorie intake, recommendations might be made on a proportional basis.
TABLE IV
| Possible fibre recommendations | ||
| Age | Calories | Fibre |
| 1 to 3 year olds | 1200 Kcals | 14g |
| 1300 Kcals | 15g | |
| 3 to 6 year olds | 1600 Kcals | 19g |
| 6 to 9 year olds | 2000 Kcals | 24g |
We found in our own small study that children did quite happily take these quantities, without suffering ill effects. At present, however, these are only offered as tentative upper limits until more evidence is available from much larger and more extensive studies.
There are two main objections frequently made, to raising children’s fibre intake. Firstly, that it may cause malabsorbtion of the micronutrients such as zinc and iron. In fact, there is very little evidence in the literature to support the malabsorption of zinc in diets where fibre is derived from wheat or corn. There also appears to be little evidence about iron when the fibre is derived from whole grain rather than bran.
The second objection raised is that a higher fibre diet will lead to a reduction in Kcalories. From the literature, this does not seem to be substantiated. Instead, healthy children eat to Kcalorie requirements and therefore consume more food, so increasing the nutrient density of the diet.
Sugar
The recommendations for sugar for the under one year olds are quite clear. Present-Day Practices in Infant Feeding (1983) states that sugar should not be added to infants’ foods, but what about older children? Professor Sheiham (1983) recommends that if fluorides present in toothpaste and drinking water, sugar consumption should not exceed 15kq per head.
Why are we so concerned about sugar? Professor Sheiham has amply illustrated the case from the dental point of view. However, many dietitians are concerned that the higher the percentage of Kcalories consumed from sugar, the less nutrients will be taken by children for the same number of Kcalories. Table V shows two ways in which a five to six year old may be getting a third of their calories, and this may have an effect on other nutrients.
| Example A: | during the day: | 15g boiled sweets200mil fizzy drink3 cups of tea with 2 teaspoons of sugar |
| this provides: | 1/3 total Kcalories negligible minerals and vitamins | |
| Example B: | during the day: | 1 slice fruit cake200ml pure orange juice1 slice wholemeal bread with butter or margarine |
| this provides: | 1/3 total Kcals all vitamin C 1/3 RDA Iron 1/3 RDA Fibre* 1/3 RDA Zinc** |
(RDA = Recommended Daily Amount, *=tentative recommendation, **=USA RDA)
Substituting Example B for A could hardly be called a draconian measure and would considerably increase the nutrient density of the child’s diet.
Salt
Again, Present Day Practices in Infant Feeding (1983) categorically recommends that no salt should be added to infant food. While the COMA report recognises that the salt issue is debatable it does state that: “Salt intake is needlessly high…consideration should be given to ways and means of decreasing it.” As a taste for salt is formed in childhood, if we wish to decrease the salt intake in the adult population, surely childhood is the time to train palates.
The major source of salt in the British diet is from processed foods. It accounts for over 80% of all sodium consumed. Mothers could therefore be advised about the sorts of foods that are high in sodium as part of a health education programme for the whole family, not just the children.
The importance of breakfast in the diet has often been a subject for debate, not only between scientists, but also often between mother and chil! Data published by Morgan et al (1981) from the USA would suggest that training children in the habit of eating breakfast, especially breakfast cereal, should be encouraged. (See Table VI)
Breakfast Cereal Contribution to the Diet
Children eating breakfast cereals, 3 out of 7 days per week:
| Consumed – twice as much | fibre niacin vitamin A |
| Consumed – one and a half times as much | thiamine riboflavine vitamin B12 pymdoxine |
It was found that the non-breakfast eating group rarely made up the difference from other meals in the rest of the day.
In summary, therefore, the evidence indicates that we ought to be lowering the fat, added sugar and salt content of children’s diets, and raising the fibre. One of the major criticisms of this proposal has been that the result of such changes would increase the bulk of the diet to such an extent that children’s Kcalorie intake would drop. It is suggested this in turn would lead to a multitude of problems, including failure to grow.
To test this hypothesis, I took a standard diet from a paediatric textbook recommended for a child of between three and six years old, and applied the recommendations. The standard diet supplied 1560 Kcalories:
45% of Kcals derived from Carbohydrate
12% of Kcals derived from Protein
38% of Kcals derived from Fat
(2.7% of Fat derived from EFA*)
The changes made were to:
change all bread to wholemeal and increase the amount by one slice
change milk to 2%
remove sweetened drinks and substitute with fruit juice
remove jams and marmalade and substitute low-sugar products and peanut butter
This resulted in a diet that provided 153S Kcalories:
50% of Kcals derived from Carbohydrate
15% of Kcals derived from protein
35% of Kcals derived from Fat
3.5% of Fat Kcals derived from EFA (using butter)
8.5% of Fat Kcals derived from EFA (using polyunsaturated margarine)
(*EFA = Essential Fatty Acids)
Changing children’s diets in terms of the reports that have been published need not therefore lead to children having to eat vast quantities of food, or making major changes in their dietary habits.
How can we pass this information on to mothers?
In our own district we have developed teaching aids for health visitors and others around the four food group system Each of the groups is illustrated by photographs mounted on large boards.
Milk group – choose 1 portion
Illustrating milk, cheese, yoghurt and giving the low-fat alternatives
Meat find alternative group – choose 2 portions
Illustrating leaner meat, emphasising chicken and fish and showing 1 selection of vegetarian alternatives.
Fruit and vegetable group – choose at least 3 portions
Illustrating a wide range of fruit and vegetables used in Hackney. It also includes canned fruit in natural juice, salt-free and frozen vegetables.
Cereal group – choose at least 4 portions
Illustrating different breads, pastas and breakfast cereal. Potatoes are also shown in this group.
There are no boards to illustrate fats or sugar products. This omission is used to promote discussion about the role of these products in the diet.
In designing these boards, we have made sure that all the products photographed are available in local supermarkets. By using these boards, we can get over to mothers the modern nutritional messages of increasing the fibre and decreasing the fat, sugar and salt content of their families’ diets.
References
1. Fomon, S.J. (1974) Infant Nutrition. Eastbourne: Saunders & co. 2nd edition.
2. Yeung, D.L. (1983) Infant Nutrition: a study of feeding practices and growth from birth to 18 months. Ottawa: The Canadian Public Health Association.
3. Magarey, A. and Boulton, T.J.C (1984) Nutritional studies during childhood; IV. Energy and nutrient intake at age 4. Aust. Paediatr. J. 20: 187-194.
4. Morgan, Karen J et al (1981) The role of breakfast in nutrient intake of
5-12 year old children. American Journal of Clinical Nutrition. 34: 1418-1427.
10. PANEL DISCUSSION
– Caroline Walker (Chairman)
The DHSS COMA Committee recommended in 1984 that children under 5 years should receive full-fat milk. Later, in May 1985, the DHSS announced the setting up of a new working party whose brief is as follows:
“It will review the whole range of current practices in feeding infants and young children and will look particularly at the extent of breast-feeding in Britain, what foods older babies and toddlers need and the importance of cow’s milk in toddlers’ diet. It will also take into account the findings of a new survey of infant feeding practices which is to be carried out in 1986 by the Office of Population Censuses and Surveys.”
In the light of these two developments, what should toddlers and young children eat?
The panel discussion focused on the following main areas:
i) The qualitv of the scientific evidence. Do we have proof that Changing food intake alters disease patterns?
‘Proof’ of the kind expected in physics or chemistry is impossible to achieve in the human sciences. The ‘ideal’ human experiment cannot be carried out because we cannot manipulate individual behaviour from birth until death. Studies indicate that arterial changes begin in childhood, and it is therefore reasonable to promote a healthy lifestyle from infancy onwards. While agreeing that this was not his area of expertise, Professor Soothill remained personally unconvinced that eating habits cause heart disease, and said that more randomised- controlled trials of dietary modification were necessary. However, he agreed that added sugars should be cut out of diets in the interests of healthy teeth.
ii) Healthy food for mothers
Poorer women can follow recommendations given by NACNE and COMA. Skimmed and semi-skimmed milks are preferable to full fat milk; the energy density of the diet can be better increased by the use of polyunsaturated oils Ms Sanderson pointed out that the deep seated aversion to bread and potatoes among poorer women needs to be tackled by education programmes. Fresh f Kit and vegetables, fish, lean meat, low-fat dairy foods and whole grain cereals should form the basis of healthy meals. Polyunsaturated oils should be used. Added sugars and saturated fats should be reduced. Low birthweight is linked with low energy intake during pregnancy, and the above advice is compatible with increasing energy intakes and increasing the nutrient density of the diet.
iii) Zinc
There is no British Recommended Daily Amount (RDA) for zinc. Dr. Meadows reported that mothers in East London had leukocyte zinc levels of 30mg (the normal population level was around 60mg, he reported). Low zinc levels, which can be attributed to generally poor diet, may be linked with low birth weight. The American RDA is 15mg/day for adults, 20mg during pregnancy, and 25mg during lactation. Average zinc intake in the UK is around 10mg/day.
iv) Recommended Daily Amounts (RDAs) of nutrients
How useful are the official RDAs issued in Britain by the DHSS? Two concerns were expressed. First, that any figure for an RDA is rather arbitrary from a Scientific point of view. Second, that British recommendations are for a relatively small number of nutrients known to be of public health relevance. American recommendations generally set higher targets and are more comprehensive. Should health professionals in the UK perhaps use these?
v) Sugars
The British Nutrition Foundation has said that eating an apple is as damaging to teeth as eating chocolates. What advice should mothers be given?
Experiments on animals where rats are fed individual foods such as apples and Cabanas up to 15 times a day, are not relevant to human eating habits. Caries do not develop unless sucrose is added to the diet. Sucrose-intolerant children (a genetic abnormality) do not eat sucrose, and do not develop caries. In all populations where sucrose is absent from the diet, individuals have heartily teeth.
‘Health’ drinks containing added sugars (whether glucose or sucrose) are damaging to children’s teeth.