Book On Growth Disorders —

Disorders of growth either too little or too much are of great importance to clinical nutritionists. This book is an important source of information in this field. Such a topic covers so many fields, social, nutritional, genetic , public health, emotional to mention but a few.

Growth is one marker of health within and between communities. Though why height matters is another discussion. Small men Nelson, Napoleon and others were not tall but very important in their field.

Growth disorders, Kelnar CJH, Savage MO, Saenger MO, Cowell CT 2ndedition

Hodder Arnold London


Does Size Matter —

Size rules biology to a great.extent. When things get bigger, their length increases linearly but their surface area increases by the square and their volume by the cube. So when the proportions, properties and performances of organisms, such as body shape, life span or speed of movement, are plotted against size or weight in log-log graphs, they fall on straight lines. The relationship between weight and strength dates back to Galileo, who calculated the effect of increases in animal size on body proportion.

In general life is shorter, hence the time flies faster, the smaller the organism. And the bacteria zipping around in the water sample under a microscope are not an optical illusion; rather, they are moving at more than a hundred body lengths a second — equivalent to 720 kilometres per hour for a 2-metre-sized organism like humans. The same rate as planes .

What made size matter in the first place? Selection by predators is the most obvious reason, with increasing size. Selection by predators with increasing size a way to escape. Also there is always room at the top, implying that organisms can always get bigger. But the bigger they are, they harder they fall, so it is the small ones that are less vulnerable in the long run.

Victor Smetacek Nature vol 445, February 22 9 821 writing about the book

Why Size matters, from Bacteria to blue whales John Tyler Bonner Princeton University Press.

Height may be of importance, but much more important from the health point of view is obesity and the corollary of this anorexia nervosa. Will people born in the developed world in the 1990s have shorter lives than those born 60 years ago? The upward trend in life expectancy over the past century is set to reverse unless the life style of young people dramatically improves. The steady rise of childhood obesity in the USA is likely to reduce life expectancy by 2 to 5 years by the middle of the century, with enormous increases in morbidity from type 2 diabetes, heart disease and other vascular disorder. Obesity during pregnancy may well have consequences for the foetus.

The average stature and physique of humans from different parts of the world reflect the local nutritional regime by processes that are established in utero and transmitted to succeeding generations. It seems that obesity and its consequences are likely to emerge when there is freely available food.

In the developing world, those released from the grip of historic poverty are most affected, whereas in the developed world, for reasons that are less well understood, the victims are the least educated and the least affluent.

The Pima Indians of Arizona and the inhabitants of the Pacific island of Nauru until a few decades ago were lean and fit and free of diabetes. Now the majority of their young adults are obese, develop diabetes and die prematurely of heart disease. There may be a genetic predisposition to diabetes but the abrupt decline in strenuous physical activity along with the loss of the traditional foods by energy-dense food is the real cause.

We have to return to a different way of life, in our new context. The food styles of our ancestors, clean food, water and decent sanitation, accompanied by exercise appropriate to our age and stage of life.

Michael Sargent reviewing Mismatch: Why Our World No Longer Fits Our Bodies

by Peter Gluckman & Mark Hanson ; Oxford University Press. 2006. 304 pp in Nature vol 445, pp 600

The terrible scourge of obesity in children is reviewed in the BMJ 2006, vol 33 pp1207-10 in a review article ( JJ Reilly and D Wilson )

They define obesity as an excessive body fat content with an increased risk of morbidity. BMI is probably the best measure of obesity, overweight being a BMI > than 91st percentile using the UK BMI charts and obesity > 98thcentile. The epidemic of childhood obesity began in the UK in the 1980s.In 2004 14% of 2-11 year old children are obese and 25 % of 11-15 year olds obese.

The health consequences of this is wide. Psychological health health , cardiovascular overload, asthma, diabetes, orthopaedic problems,

And these persist into adult life with worsening seriousness and added the risk of diabetic problems.

Guide lines to prevention are complex and must be introduced with compassion and care.

The family as an entity must be treated and overall dietary changes are needed. A restriction in high energy foods to eating only at meals especially low energy containing foods is important.

Growth equations —

Predicting the magnitude and rate of weight gain for a given increase of energy intake requires a model of whole-body energy expenditure that includes the energy cost of tissue deposition.


An alternative approach uses the theoretical biochemical efficiencies for protein and fat synthesis in combination with models of energy expenditure that include body fat and protein turnover costs. He illustrates this alternative approach using a simple mathematical model applied to previously published data from growing rats and human infants and compare the simple model results with the classical Kielanowski model.

While both models fit the data reasonably well (R 2 > 0•87 in rats and R 2 > 0•67 in infants), the Kielanowski method resulted in parameter estimates that varied widely across experiments, had poor precision, and occasionally produced efficiency estimates greater than 1. In contrast, the new method provided precise parameter values and revealed consistencies across different experiments. The proposed mathematical framework has implications for interpreting studies of animal nutrition as well as providing a roadmap for future modelling efforts.

Hall 2010 Mathematical modelling of energy expenditure during tissue deposition Brit J Nutrition vol 104 4-7

Height And Culture —

In most surveys quantitative data are gathered with questionnaires and interviews. A comparison of such self reported data

with measured equivalents shows that people systematically underestimate or overestimate frequencies (cigarettes smoked daily, age of onset, time to pregnancy) or clinical parameters (height, weight, blood pressure). This may occur because participants intentionally or unintentionally round figures to a preferred end digit. Bopp et al analysed the preference for the end digits zero and five when reporting height. Since height is overestimated in almost all cultures (with variable magnitude) people who round to zero and five probably overestimate rather than underestimate their height .

Their results show shows similarities between languages belonging to the same family. People speaking Germanic (and possibly Slavic) languages indicated the end digits zero or five consistently less frequently than did people speaking a Romance, Greek, or Semitic language. In a large and representative Swiss sample, people kept the end digit preference characteristic for their native language even when living in a region using a different language, suggesting that such preferences are inherent in culture. This cultural bias might be particularly important when analysing trends in countries with high cultural preferences for rounding numbers and this could mask or exaggerate real differences between populations and could also explain why differences between measured and self reported estimates vary between cultures.

This is a real lesson for international surveys where countries are compared.

Bopp et Faeh 2008. Who gives me fives? BMJ vol 337, 1463

Nutrients And Growth —

How cells sense nutrients to control growth is largely unknown. I fact the selection of nutrients between cells whether they be in the brain, muscle or elsewhere is a knowledge desert.

When we eat a meal how does the food get distributed before the eventual cell receives the nutrient.

There is also the distribution of carbohydrate, amino acids and lipids as well as the essential trace elements and vitamins.

It is possible to understand that when the cell requires trace elements or vitamins, the deficit is sent as a message to the cell surface and than the receptor signal needy to the blood and things happen.

How does the cell signal that amino acids or sugars or lipids are needed?

In mammalian cells, nutrients (such as amino acids), growth factors and cellular energy together trigger a molecular signalling pathway, mediated by the protein TOR, that controls cell growth. TOR inhibition by the anticancer drug rapamycin prevents unruly cell growth.

TOR (‘target of rapamycin’) is protein kinase found in two functionally and structurally distinct multiprotein complexes: TORC1 and TORC2. TORC1 controls many cellular processes that ultimately determine cell growth, including protein synthesis, ribosome formation, nutrient transport and autophagy (a survival mechanism that kicks in in response to starvation).

Activation of TORC1 requires simultaneous availability of amino acids, growth factors and energy. Inputs from growth factors (such as insulin) and energy contribute to the determination of that amino acids trigger TORC1 activation. Amino-acid depletion results in rapid dephosphorylation of two molecules downstream of TORC1, S6K and 4E-BP, whereas addition of amino acids leads to rapid, TORC1 -dependent phosphorylation of these molecules. But what is the molecular link between the amino-acid signal and TORCl activation?

Rag GTPases, heterodimers of RagA or RagB and RagC or RagD are involved in TORCl activation in response to this nutrient signal. By binding to TORCl, Rag GTPases mediate its transfer to intracellular membranes that contain another GTPase, Rheb. There, other signals such as cellular energy and growth factors (insulin) integrate with the amino-acid signal, leading to Rheb-mediated activation of TORCl and phosphorylation of its downstream effectors S6K and 4E-BP, which ultimately lead to protein synthesis and cell growth.

An very interesting start to understanding a key elements of nutrition.

Zinzalla and Hall 2008 Linking nutrients to growth Nature vol 454 287-8

Pubertal Growth —

The onset of puberty is a wonderful event for the child if not the parents. The curiosity is why it happens at this age. Why is the latent growth delayed. It is also interesting that the age of puberty and the so called growth spurt varies form child to child. Some children continue growing long after others and after a slow start grow more that expected.

Indian, Japanese and US children have similar growth patterns up to the age of 9 years. Thereafter a growth gap develops during the remaining years of growth between the first two nationals and the US adolescents. It is not clear whether this difference is environmental or genetic. The Indian and Japanese diet is largely cereal-derived and there may be dietary deficiency or dietary antinutrients which cause the lack of growth. A survey by the Japanese Ministry of Education in 1992 of 700,000 children aged between 4 and 18 years showed they had grown significantly in height compared with their parents. Boys aged 13–14 years old were 9.5 cm taller and 9 kg heavier than their parents at the same age. At 17–18 years these Japanese in 1992 were 5 cm taller than 30 years ago. Much of this difference was in leg length.

In the Netherlands, there is a tradition of monitoring children’s height that goes back to the 19th century. During the last century and the early part of this century differences of 5–11 cm at various ages were noted between those children whose fathers had a ‘low’ as compared with a ‘high’ occupational status. This gap is now reduced to differences of 1–3 cm. Similar reduction in height differentials between socially and economically disadvantaged and rich children have been observed in India. A British tradition, unproven except in folklore, is that the child’s height at 2 years 6 months is half that of the final growth achievement.

A curious feature of the development of the stunted child is the anatomy of the deficient height. This may be the sitting height, that is, coccyx to top of head or standing height where leg length is important. In stunted USA blacks and Australian Aborigines the sitting height is deficient; in Japanese, standing height is deficient and in Indians the deficit is symmetrical. Possibly some complicating micronutrient is deficient or the timing of the deficiency at some vulnerable period occurs primarily affecting trunk or leg growth.

Stunted Children, Body Composition —

Prolonged under nutrition during inter uterine and early child hood development is common in developing countries and causes stunting. ( Martin et al British J Nutrition , 92, 819-825 ,2004 ). The prevalence in stunting world wide is 33%. Stunting in adults reflects the adequacy of nutrition during the pregnancy, breast feeding and subsequent feeding. Stunting paradoxically is related to increased body fat and overweight. The metabolic response of stunted children is different to normal build children with diets when fed a diet with a higher fat content. The result is a greater increase in weight and waist:hip ratio.

In the study of Martin et al 2004, they analysed changes in body composition of stunted children during a fellow up period in poor children in Sao Paulo Brazil. The stunted girls developed with less lean mass and greater body fat than normal controls.

One explanation is a preferential utilisation of protein stores as an energy store. The problem is one of biological adaptation to better metabolic efficiency.

It also raises an interesting point for our own populations. There has been a impoverished population in our society for ever. There is at the present time a more bountiful provision of cheap food. The impoverished now have ready access to cheap food and this is leading to obesity in a population metabolically ill prepared for the present abundance.

UK-WHO Growth Charts —

In April 2006 the World Health Organization published a new growth standard for children aged under 5 years. They were based on the growth patterns of healthy infants in United States, Norway, Oman, Brazil, India , Ghana, born at full term whose mothers were non-smoking, relatively affluent whose pregnancy was healthy. The results for each country were very consistent with the other countries..

The United Kingdom was one of the first developed coun¬tries to adopt it, and the Department of Health commissioned the Royal College of Paediatrics and Child Health to design new growth charts and develop new evidence based instructions and supporting educational materials. These charts (known as the UK-WHO growth charts) are now in use for monitoring the growth of children aged under 4 years.

An article by Wright and colleagues discusses the use of these very user friendly charts which replace the previous charts. They give clear instructions on gestational corrections, and include a new chart for infants born before 3 weeks gestation.

The charts also contain a tool to determine body mass index from weight and height and an aid fo predicting adult height.

Wright et al Using the UK-WHO growth charts. BMJ vol 340 pp647-650

Value of Growth Monitoring in Infants —

The value of growth monitoring is discussed at length in an important review by Ashworth et al (2008) Maternal & Child Nutrition vol 4 pp 86–117

The rationale for growth monitoring and promotion is almost self evident , but is it?. The concerns are based on low participation rates, poor health worker performance and inadequacies in health systems minimizing what can be done to alleviate the problem.

The launch of the new World Health Organization growth standard and charts has reopened the debate. Growth monitoring programmes should improve nutritional status, increase utilization of health services and reductions in mortality.

There is evidence from small-scale studies in Nigeria, Jamaica, India, and from large programmes in Tanzania India, Madagascar and Senegal that children whose growth is monitored and whose mothers receive nutrition and health education and have access to basic child health services have a better nutritional status and/or survival than children who do not. There is evidence from India and Bangladesh that growth monitoring has little or no effect on nutritional status in large-scale programmes unlesss there is good nutrition counselling.

Good nutrition counselling is important for growth promotion and is often done badly. Effort must be made to promote exclusive breastfeeding and appropriate complementary feeding, irrespective of decisions about growth monitoring. There is no controversy about the need for growth-promotion activities, and weighing children is desirable to assess health and nutrition status. The debatable question is whether weights need to be monitored monthly and plotted on a chart. Even if there is a policy for growth monitoring, if a child has grown well in the first year of life then it would appear that little is gained by monitoring weight beyond the age of 12 months, and that the time spent monitoring older children might be better spent improving the counselling given to caregivers of infants. Growth monitoring may not be the best use of limited resources in countries with weak economies and inadequate health budgets: a limited package of health and nutrition interventions including good nutrition counselling may be preferable, aiming for good coverage and effective health worker performance, and prioritizing infants and children

Combine growth monitoring with other health intervention channels such as immunization for the convenience of caregivers, and ensure consistent message delivery. Target younger children and use the time gained to improve services. Monitor weight until 12 months of age. If there are episodes of growth faltering, continue to monitor until 18 months. Training, supervision and support will need to be improved if health workers are to be equipped with the necessary knowledge and communication skills to promote healthy growth. Impact will be related to coverage, intensity of contact, health worker performance, adequacy of resources and the ability and motivation of families to follow advice.

Ann Ashworth, Roger Shrimpton, Kazi Jamil (2008) Growth monitoring and promotion: review of evidence of impact Maternal & Child Nutrition 4 (s1) , 86–117


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