Dietary Defiency and Excess UPDATES

Anorexia And Illness —

It is good to read papers which look at mechanism rather than describe phenomena. This a good paper describing why anorexia is a feature of acute illness.

Anorexia is part of the body’s acute-phase response to illness. Microbial products such as lipopolysaccharides. which are also commonly used to model acute illness, trigger the acute-phase response and cause anorexia mainly through pro-inflammatory cytokine

Lipopolysaccharide stimulate cytokine production through the cell-surface structural molecule CD14 and toll-like receptor-4. Cytokines ultimately change neural activity in brain areas controlling food intake and energy balance. The blood-brain barrier endothelial cells (BBB EC) are an important site of cytokine action in this context. BBB EC and perivascular cells (microglia and macrophages) form a complex regulatory interface that modulates neuronal activity by the release of messengers (e.g. PG. NO) in response to peripheral challenges. Serotonergic neurons originating in the raphe nuclei and glucagon-like peptide-1-expressing neurons in the hindbrain may be among the targets of these messengers, because serotonin (5-HT). acting through the 5-HT2C receptor, and glucagon-like peptide-l have recently emerged as neurochemical mediators of lipopolysaccharides anorexia. The central melanocortin system, which is a downstream target of serotonergic neurons, also appears to be involved in mediation of lipopolysaccharide anorexia. Interestingly. Lipopolysaccharides also reduce orexin expression and the activity of orexin neurons in the lateral hypothalamic area of fasted mice. As the eating-stimulatory properties of orexin are apparently related to arousal, the inhibitory effect of lipopolysaccharides on orexin neurons might be involved in lipopolysaccharide-induced inactivity and anorexia.

In summary, the immune signalling pathways of lipopolysaccharides -induced. and presumably acute illness-induced, anorexia converge on central neural signalling systems that control food intake and energy balance in healthy individuals

Langhans 2007 Signals generating anorexia during acute illness Proceedings of the Nutrition Society vol 66 p 321-330 food intake: Acute-phase response: Cytokines

Benefits of Weight Reduction —

The Nutrition Research Review of 2009 contains an interesting review and meta-analysis of the effect of weight loss on all-cause mortality risk

Overweight and obesity are associated with increased morbidity and mortality, although the range of body weights that is optimal for health is controversial. It is less clear whether weight loss benefits longevity and hence whether weight reduction is justified as a prime goal for all individuals who are overweight (normally defined as BM! > 25 kg/m2).

The review examines the evidence base for recommending weight loss by diet and lifestyle change as a means of prolonging life. An electronic search identified twenty-six eligible prospective studies that monitored subsequent mortality risk following weight loss by lifestyle change, published up to 2008.

The Data were analysed by meta-analysis, giving particular attention to the influence of confounders. Moderator variables such as reason for weight loss (intentional, unintentional), baseline health status (healthy, unhealthy), baseline BM! (normal, overweight, obese), method used to estimate weight loss (measured weight loss, reported weight loss) and whether models adjusted for physical activity (adjusted data, unadjusted data) were used to classify subgroups for separate analysis.

Intentional weight loss per se had no positive effect on all-cause mortality (relative risk (RR) 1•01; P = 0•89), while weight loss which was unintentional or ill-defined was associated with excess risk of 22 to 39 %. Intentional weight loss had a small benefit for individuals classified as unhealthy (with obesity-related risk factors) (RR 0•87 (95 % Cl 0•77, 0•99); P = 0•028), especially unhealthy obese (RR 0•84 (V5 % Cl 0•73, 0•97); P = 0•018), but appeared to be associated with slightly increased mortality for healthy individuals (RR 1•11 (95 % Cl 1•00, 1•22); P = 0•05), and for those who were overweight but not obese (RR 1•09 (95 % Cl 1•02, 1•17); P = 0•008).

There was no evidence for weight loss conferring either benefit or risk among healthy obese. In conclusion, the available evidence does not support solely advising overweight or obese individuals who are otherwise healthy to lose weight as a means of prolonging life. Other aspects of a healthy lifestyle, especially exercise and dietary quality, should be considered. However, well-designed intervention studies are needed clearly to disentangle the influence of physical activity, diet strategy and body composition, in order to define appropriate advice to those populations that might be expected to benefit.

Harrington et al A review and meta-analysis of the effect of weight loss on all-cause mortality risk

Weight loss: All-cause mortality: Meta-analyses

Biology Of Obesity —

A review in Proceedings of the Nutrition Society (2005), 65, 31-38 Trayburn P

Obesity is a preoccupation of modern nutrition. The founding fathers of our science would never have believed that the eradication of some major nutritional problems would lead to this particular epidemic.

The biology of obesity includes]

The fundamental mechanisms of energy balance and its regulation, genes, appetite, endocrine factors.

The biological basis for the development of obesity

Adipose tissue function

The biological description of the obese state ( particularly physiological adaptations)

The pathological consequences of obsess, i.e. associated disorders

The physiological basis of treatment strategies

Energy balance

It has always been axiomatic that obesity is fundamentally a problem of energy balance. That obesity can only develop when energy intake is in excess of energy expenditure, differences in input and output being buffered primarily by changes in fat stores.

There are two immutable ” Laws of Obesity”.

That for obesity to develop, intake must be in excess of expenditure
obese subjects have a higher energy expenditure and therefore a higher average energy intake than lean subjects. They have a larger relative mass to move about.
Appetite. It is understood that the central hypothalamus controls food intake. Several peripheral signals are recognised in the regulation of food intake eg ghreli, peptide YY and leptin. Leptin is secreted from the white adipose tissue.

The attractive work on thermogenesis of 20 to 30 years ago, has not stood the examination of time. That is the uncoupling of oxidative phosphorylation by brown adipose tissue mitochondria.

White Adipose tissue. The buffering of energy intake and expenditure is through triacylglycerol deposition in White Adipose Tissue. Obesity is due the laying down of white fat mass ( >85%). Adipose tissue is the source of endocrine signals e.g. leptin. There is a rich array of different glucose transporters more than 8 different types.

White Adipose Tissue is also an important endocrine system. Secreting adipokines.

Inflammation A number of inflammation related proteins e.g. nerve growth factor (NGF) are released by white adipocytes. It has been suggested that obesity and diabetes are associated with chronic low grade inflammation. This tissue related inflammation may play a role in the development of insulin resistance and associated pathologies.

Several thoughts come to mind in reading this very interesting review albeit somewhat tardily

There has always been the aphorism that within every fat person is a thin person struggling to get out. Maybe that within every thin person there is a fat person at risk of struggling in. Are we all at risk or only certain people.
If one goes round a super market , the fattest people are to be found in the crisp and confectionary isles tossing goodies into their trolleys. Cheap delicious high energy foods. Greed has been carefully cultivated in our society either for readily eaten food or alcohol
The concept of low grade inflammation is fascinating. I was reared in Gastroenterology where the pre-occupation was duodenal ulcer disease. Everyone knew that this was a result of too much acid produced by the stomach. Everyone knew that this was due to stress. Reduce acid and stress and all would be ok. The chronic low grade inflammation in the stomach duodenum was ignored until the Helicobacter that causes gastric and duodenal inflammation was found. Eradication of the helicobacter led to a disappearance of duodenal ulceration. Maybe there is a message here for diabetes and obesity.
Appetite preferences are also important. The heavy consumption of sweets, crisps and alcohol is an exaggeration of appetite needs. Who are those who can so indulge themselves.?
That exercise is so important. The reduction of the involvement of schools in games and the reduced time given to energy expending games eg soccer, rugby and running cannot be good. Playing fields being lost for housing developments cannot be good for exercising children.

Chewing The Fat —

In the May 21st 2007, Nature vol 447, pp 525-7 Kendall Powell gives a chatty account of fat metabolism

It is worth reading

One thing that did occur to me was a result of the reminder that adipose tissue produces TNFά, and cytokine interleukin both indicators of low grade inflammatory processes. In addition macrophages invade fat tissue, macrophages are associated with an inflammatory response.

In this article coherent arguments are made for the inflammatory response being part of the complications of obesity.

I worked as a Gastroenterologist. For most of my working life duodenal ulcers were seen to be a consequence of excess gastric acid secretion and that stress was the basis of this. Then it was shown that the causal agent was infection of the gastric and duodenal mucosa by Helicobacter pylorides. Everyone until then everyone assumed that no bacteria could survive in the hostile environs of the stomach. Since it was possible to eradicate the Helicobacter by antibiotics duodenal ulceration has ceased to be a problem.

What if obesity is the consequence of an infection . Not necessarily primarily in the adipose tissue. It is easy to dismay such a silly idea out of hand but remember the duodenal ulcer story and the inflammatory process was thought to be due to the acid.

Childhood Obesity —

Childhood and adult obesity is a real problem. There are so many bottoms around which require two seats to fit their shape.

There is a brilliant review on the aetiology of childhood obesity in the Nutrition Research Review, 2007, 20, 29-45 by KL Procter..

Of the models suggested to account for this increase the one chosen is an ecological one which discusses individual, social and cultural and physical environment.

A genetic reason as a prime cause is dismissed out of hand. The environment must be the prime contributor regardless of the genetic predisposition.

The factors discussed are

Physical activity children exercise less and watch television more

Diet , this is not clear cut as more food is not necessarily being eaten

Eating patterns , snacking and missing main meals. Meals are less defined and grazing is the norm.

Diet composition again a complex topic.

Consumption of unhealthy foods fast foods and soft drinks.

Obesogenic environment

Foetal environment birth weight, maternal smoking, is associated with childhood obesity

Infant environment regarded by some as critical

Family structure

School environment

Neighbourhood environment

And others, the food industry, TV adverts and general attitudes and policies.

Dietary Defiency and Excess
Choir And Obesity

It is interesting to make observations on common conditions and groups. When I first came to Edinburgh as a student in 1954 there were groups of elderly people with rickets sitting on the benches alongside a main thoroughfare.

Last weekend I went to a Christmas Choir concert here in Fife. There must have been over 50 children mostly girls aged 10-12years singing in a choir. There are many quoted figures for obesity rates but in this group only 2 or at the most 3 who were obese. The remainder were slim children. This is in contrast to the young people using those aisles in the supermarket which carry biscuits, sweets, drinks, alcoholic or non alcohol where fat people abound.

Does this mean that singing prevents obesity? Or that the type of child who sings in a choir comes from a social group wee nutrition is important.

Drugs For Obesity —

In a study in the Lancet the value of the drug tesofensine which is an inhibitor of the presynaptic uptake of noradrenaline, dopamine and serotonin in weight reduction is reported. A dosage of 0.5 mg once daily along with an energy intake reduction could result in a weight loss over 24 weeks of 10%. The adverse effects were dry mouth, nausea, constipation hard stools diarrhoea and insomnia.. 21% withdrew from the trial.

The more unfortunate side effects of earlier drugs e.g agitation and anxiety were not seen.

An interesting study worth following and seeing the long term consequences, are these successes maintained?.

Astrup et al (2008) Effects of tesofensine on body weight loss, body composition and quality of life in obese patients: a randomised double blind , placebo controlled trial. Lancet. Vol 372 pp 1906-1913.

Bray 2008 Is new hope on the horizon for obesity? Lancet vol 372 1859-60.

Early Life Nutrition —

Undernutrition in early life and body composition on reaching adolescence in males.

Gigante et al, British Journal of Nutrition 2007, 97, 949-954

In middle- and high-income countries there is an epidemic of excess weight and obesity. This has attracted a number of studies to determine the early determinants of adult size. One possibility is that individuals who have suffered under nutrition in early life, followed by Western-type diets might be at risk of overweight and chronic disease.

The association between stunting and overweight in children has been shown in a cross-sectional study in four countries in nutritional transition (Russia. Brazil. South Africa and China). The risk of being overweight for a stunted child ranged from 1-7 to 7-8. In a review of early nutrition and later-life, adiposity and high birth weight was associated with subsequent obesity, whereas the evidence for poor nutrition in early life as a risk factor for increased fatness later in life was inconclusive. In a more recent review, the increase in weight or BMI and rapid growth during infancy were associated with obesity in childhood and adulthood.

In Brazil, stunted boys accumulated more body fat and gained less lean mass than non-stunted boys, and stunted girls showed a significantly higher percentage of fat mass at the end of follow-up, whereas non-stunted girls showed no significant differences in the percentage of fat mass over time

In this study in British Journal of Nutrition ( Gigante et al 2007, 97, 949-954 ) a cohort of boys aged 18 years was studied in Pelotas. a city in Southern Brazil since their birth. The aim of the present analysis was to study the associations between stunting, wasting and underweight at 2 and 4 years of age, and the body composition of male adolescents. This is part of a long term study of boys identified at birth. It is note worthy that the population are boys. That 5% of the group died and those who were poor, with low birth weight and malnourished were most at risk.

The conclusions of this study which included body composition indices was that under nutrition in early life is not a risk factor for over weight or obesity. These boys had lower fat, lean and body mass indices.

The results suggest that under nutrition is not a risk factor for overweight and obesity in later life population and may partially protect against fatness in adolescence.

This is a remarkable study and illustrated the merit of long term studies.

Eating Practices —

Eating meals as a family around a table may well be a practice or habit which is changing. People eat at a table in cafes and restaurants but less so in homes where the meal may be grazed or at the TV.

The benefits of a meal eaten around a table is that it has ritual, the food may be eaten slowly and there is a community feeling. It is also more rewarding to the cook when the food is appreciated rather than gulped down.

Slowly eaten food has advantages and glycaemic indices etc pale into insignificance compared to eating slowly.

Eating And Obesity —

Maruyama and colleagues in Osaka Japan have reported a fascinating study on eating quickly and eating until full ( Maruyama et al 2008 The joint impact on being overweight of self reported behaviours of eating quickly and eating until full: cross sectional survey BMJ vol 337 pp 1091-1093

Eating quickly, gorging and binge eating have been associated with total energy intake satiety, insulin resistance and being overweight and obesity. This combination increases the risk of being obese 3 fold.

The show in heir study that eating until full and eating quickly were associated with being overweight in Japanese men and women.

There may well have been a radical change in social behaviour and eating patterns over the period that obesity has been a problem.

The paper was accompanied by and editorial

Denney-Wilson and Campbell 2008 Eating behaviour and obesity. Eating fast and until full trebles the risk. BMJ vol 337 pp 1064-5

Excess Weight —

David Rose in the Times Thursday 13th November writes on the value of measuring waistline and BMI in assessing excess weight.

If one has a waist measurement in the top 20 % then there is a substantial increase in mortality. In a large study ( 350,000 ) from Imperial College London, German Institute of Nutrition and elsewhere individuals aged from 25 to 79 were followed for 9.7 years and 14,723 died during this period. .

For men a waist line over 47.2 ins was associated with a doubling of death rate compared with 37.2 ins. The same is true of women ( 39.4 ins compared with 25.6 ins )

The waist to hip ratio was more sensitive ( range 0.78-1.10 for men and 0.66 to 0.98 for women ), a 0.1 increase was associated with a 34% increase in mortality for men and 24% for women.

Accumulating fat between the midriff is not good for one.

This was reported in the New England Journal of Medicine November 13th 2008.

Fat Cell Count —

Two factors contribute to an increase in fat mass: the number of fat cells and how much fat each of these cells stores (their volume). Spalding and colleagues studied the dynamics of fat-cell number in some 700 adults, both lean and obese, and combined their data with previous observations in children and adolescents.

Irrespective of weight, the number of fat cells seems to rise steadily from birth to the early twenties, but remains constant thereafter. In patients observed before and up to two years after surgical treatments that facilitate weight loss by reducing stomach size, no decrease in fat-cell numbers was detected, although their volume did drop.

Fat cells have a high turnover: new cells are continually being produced to replace their dead predecessors. The average age of a fat cell seems to be about 10 years in both lean and obese individuals, and the number of fat cells as a proportion of all cells remains constant in each weight group. But the total number of new fat cells was higher in obese subjects, suggesting that they are replenishing an existing larger pool.

In lean individuals the fewer fat cells can still store large amounts of fat

Fat people can still reduce the volume, it not the number of their fat cells.

Shadan (2008), What’s your fat allowance? Nature vol 453, p 169

(K.L. Spalding et al .( 2008 ) Nature vol 453 18th May .

Fat Therapy —

Few safe and effective drugs are currently available for the treatment of obesity. This interesting paper looks at the use of liraglutide, a drug used in diabetic control on weight reduction. The aim of the study was to assess the effect on bodyweight of liraglutide (at doses up to 3•0 mg per day), in combination with an energy-deficit low-fat diet and physical activity

Liraglutide is a glucagon-like peptide-l (GLP-1) analogue with a 97% structural homology to human GLP-1, a gut-derived incretin hormone. Liraglutide has a long half-life of about 13 h and is given once a day by subcutaneous injection. Liraglutide is used for the treatment of type 2 diabetes mellitus and has benefits for glycaemic control at doses up to 1• 8 mg a day.

Because liraglutide also causes a dose-dependent weight loss, and benefits to the concentration of glycosylated haemoglobin (HbA,,) and systolic blood pressure, and has the potential as an attractive treatment option for both type 2 diabetes and obesity.

The underlying mechanisms for the effects on weight reduction of liraglutide are probably through effects on the gastrointestinal tract and the brain. Native GLP-l suppresses appetite and energy intake in both normal-weight and obese individuals, as well as in people with type 2 diabetes, and delays gastric emptying.

GLP-l receptors are expressed in several brainstem nuclei involved in appetite regulation, and subcutaneously administered liraglutide might also reach these sites.

The study was a double-blind, placebo-controlled 20-week trial, with 564 individuals (18-65 years of age, body-mass index 30-40 kg/ml) who were randomly assigned, to one of four liraglutide doses (1•2 mg, 1•8 mg, 2•4 mg, or 3-0 mg, n=90-95) or to placebo (n=98) administered once a day subcutaneously, or orlistat (120 mg, n=95) three times a day orally. Orlistat blocks intestinal lipase activity. All individuals had a 500 kcal per day energy-deficit diet and increased their physical activity throughout the trial, including the 2-week run-in.

Mean weight loss with liraglutide 1•2-3•0 mg was 4•8 kg, 5•5 kg, 6•3 kg, and 7•2 kg compared with 2•8 kg with placebo and 4•1 kg with orlistat, and was 2•1 kg to 4•4 kg (2•9-6•0) greater than that with placebo.

Liraglutide reduced blood pressure at all doses, and reduced the prevalence of prediabetes (84–96% reduction).

Nausea and vomiting occurred more often in individuals on liraglutide than in those on placebo, but adverse events were mainly transient and rarely led to discontinuation of treatment.

Liraglutide treatment over 20 weeks is well tolerated, induces weight loss, improves certain obesity-related risk factors, and reduces prediabetes.

Astrup, et al (2009 ) Effects of liraglutide in the treatment of obesity:

a randomised, double-blind, placebo-controlled study . The Lancet vol 374 pp1606-16


Bray 2009 Gastrointestinal hormones and weight management . Lancet vol 374 pp 1570-1

Fetal Growth —

Fetal growth in the first trimester has far reaching implications

What happens to babies in the womb has implications way beyond birth. The first trimester seems particularly important. A link has been established between poor growth in the first trimester and adverse birth outcomes in 1631 pregnant women with reliable dates. They also recorded accelerated growth in infancy for these babies, who seemed to be “catching up” growth they had missed in the first trimester. Rapid growth in infancy is a well known risk factor for cardiovascular disease in adults. A poor intrauterine environment in early pregnancy may have lifelong implications, say the researchers.

They used crown-rump length between the 10th and 13th week of pregnancy as a proxy for early fetal growth. Smoking and failing to take folic acid supplements were both inde¬pendently associated with shorter crown-rump length in the first trimester. So were increases in diastolic blood pressure and maternal hae¬matocrit. After multiple adjustments, babies with a crown-rump length in the bottom fifth had more than twice the odds of being born preterm, at low birth weight , or small for gestational age compared with other babies.

lAMA 2010;303:527-34

Forbes Equation —

There is great attachment to biological modelling. When it works it is great but many have fallen by the way side

Hall in Brit J of Nutrition 2007, 97, 1059-63 ( Body fat and free fat mass inter-relationships :Forbes theory revisited.

Twenty years ago Forbes suggested that body fat mass and fat free mass are in a sense companions and a change in one induces a change in the other and in the same direction. That there is an empirical, non-linear relationship between Free Fat Mass and body Fat Mass using cross-sectional body composition data and that longitudinal changes of body composition were described by movement along the cross-sectional curve

From this hypothesis Forbes expressed a mathematical expression for the Free Fat Mass proportion of body weight change as a function of the initial body Fat Mass. Forbes’s mathematical expression is strictly valid only for infinitesimal weight changes.

Hall has looked at this to account for macroscopic weight changes. The new equation predicts that the composition of weight change depends on both the direction and magnitude of the weight change in addition to the initial body fat mass.

The new equation was compared with experimental data from underfeeding and overfeeding in humans.

Hall also discusses the relationship between Forbes’s theory and an alternative representation of body composition change that assumes the existence of an energy partitioning parameter, called the P-ratio. The P-ratio defines the fraction of an energy imbalance accounted for by changes of the bodv’s protein reserves. The P-ratio depends on the initial body composition s well as the direction and magnitude of weight change.

Genetics and Obesity —

Genetic link to obesity

Obesity is a highly heritable disorder but the genetic associations reported to date account for only a small percentage of the inherited variation in body mass index,

In Nature 2010 volume 463 two groups have reported deletions on chromosome16p11.2 that may explain part of the ‘missing heritability’ in terms of , high-penetrance mutations that are rare but when present are often associated with severe obesity.

This contrasts to more common gene defects less closely associated with clinical symptoms. Bochukova (2010 ) Large rare chromosomal deletions associated with severe early onset obesity vol 463 pp 666-670. identified copy number variants in 300 patients with severe early-onset obesity, caused by deletions involving genes including SH2Bl, known to be involved in leptin and insulin signalling. Many of the patients also suffered neurodevelopmental disorders.

Walters et al.( 2010 A new highly penetrant form of obesity due to deletions on chromosome 16p11.2 Nature vol 463 671-675 identified deletions of at least 593 kilobases in 31 patients with a previously unrecognized type of extreme obesity.

Hospital Malnutrition —

In a study looking at malnutrition as an independent predictor of 1-year mortality following acute illness, Gariballa and Forster studied four hundred and forty-live randomly selected hospitalised patient. Their nutritional status was assessed from anthropometric, haematological and biochemical data. Nutritional status was compared between survivors and non-survivors at baseline, 6 weeks and 6 months. Using Cox’s proportional hazard analysis, they measured the association between nutritional assessment variables and 1 -year mortality after adjusting for disability, chronic illness, medications, smoking and tissue inflammation. Nutritional status was significantly worse amongst non-survivors compared with survivors, and non -survivors showed marked and significant deterioration in all measures of nutritional status compared with survivors. After adjusting for poor prognostic indicators the hazard ratios of death in the fourth, third and second quarters of both baseline serum albumin and mid-upper arm circumference distributions relative to the first were 0-68, 0-77 and 0-58 and 0-61. 1-0 and 0-87 respectively. Intervention studies are needed to determine whether the relationship between malnutrition and the poor outcome highlighted by the present study is causal or a mere association.

Gariballa and Forster 2007 Malnutrition is an independent predictor of 1-year mortality following acute illness Proceedings of the Nutrition Society vol 98, 332-336.

How To Slim —

I bought a sandwich from BON Appetit and found this advise on how to slim. I was such common sense that I thought it was worth handing on. I have not contacts with the firm and only occasionally eat sandwiches but this is such good advise.


We interviewed loads of French women (of all ages). A few Spanish and a couple of Italians as well. Here’s their advice on eating well (and keeping a good figure):

Insist on nutritious, fresh, natural, quality food without any nasties in it


Eat three times a day and don’t pig out No grazing Don’t count calories. Simply eat with your head. Think about what your’re eating (before you eat it]


Lay the table, sit down, get a plate. And when you’re nearly full, stop eating


Don’t diet , diets are rubbish. Being on a diet is a constant losing battle. Crisps, cookies and candy are not ‘treats’. Eat them at your peril. Drink lots and lots (and lots) of water every day and, dare we say it, less alcohol?

If you hate exercise don’t worry (don’t feel guilty).

Eat and drink properly and you’ll be fine


Behave slim and you’ll stay slim. Slim is a state of mind




Hunger Strikes —

Hunger strikes are the terrible consequences of a deeply felt conviction. This form of protest, often the only one available has been used over the years. In India, by the Suffragettes , Irish IRA prisoners and Guantanamo Bay. One of my ancestors survived this form of protest in Holloway Prison as a Suffragette.

The Offender Health section of the UK Department of Health is publishing a guideline for the care of these protesters.

Care is complicated as there is electrolyte imbalance, vitamin and mineral depletion infection, hypothermia and renal failure. Failure can lead to Wernicke-Korsakoff syndrome

Sometimes a prisoner may survive for as long as 19 months. It would be a terrible and important comparison with the prisoners in German Concentration camps during the 1938-45 period..

Doctors are sometimes called upon to force feed .This is forbidden by the World Health Association in Declarations.

Editorial Lancet 2008 Clinical Care of hunger strikers vol 372 p777

Lipid Profile —

Osteoporosis is a major public health problem through its association with age-related fractures. Bone mineral density (BMD) is an important determinant of fracture risk, with an approximate doubling of fracture risk for every 1 SD reduction in BMD. Low bone mineral density is also associated with an increased risk of cardiovascular mortality in postmenopausal women, and several drugs, the statins, hormone replacement therapy and bisphosphonates alter bone density and lipid synthesis.

Furthermore osteoblasts and adipocytes share a common progenitor from stromal cells in bone marrow. This has led investigators to study the relationship between cholesterol concentration and bone mass, and to suggest a relationship between hyperlipidaemia and BMD as a link between atherosclerosis and osteoporosis.

E.M. Dennison et al in their paper Lipid profile, obesity and bone mineral density: the Hertfordshire Cohort Study, Q.J.Med 2007, 100, 297-303 have looked at this possible association in a population of 1000 men and women living in Hertfordshire. This population has already provided a wealth of information thanks to detailed information at birth allowing studies on birth weight and health events in later life.

The new study showed was that people with high triglyceride concentrations had better bones, and at least part of the explanation for this was that people with higher triglyceride concentrations tended to be ‘fatter’, which is apparently good for bones for many reasons. By contrast, people with high concentrations of HDL cholesterol, tended to have thinner bones. The reason for this is not clear, but it would appear that in in this group, people with high concentrations of HDL cholesterol tended to be slimmer, so this may be important.

Measures of Malnutrition —

On May 22, WHO and UNICEF change the definition of new case severe acute malnutrition based on the 2006 WHO growth standards. Before the global food crisis, a 2006 review estimated that 13 million children had such malnutrition. By January, 2009, aid agencies reported about 19 million affected. Calls were made for the disease-burden demand to be met with increased supply of treatment services.

Numbers of children diagnosed as malnourished vary greatly depending on which case definition is used. Each has advantages and disadvantages, and is useful for particular purposes. Malnutrition for admission to feeding programmes was originally defined by low weiqht-for-aqe. This definition was changed to weiqht-for-heiqht to better identify children who would benefit most from treatment. Weight-for¬ height expressed as Z scores is useful for surveys, yet many treatment programmes admit children with conceptually simpler %-of-median measures. (Minus 1 Z score=l standard deviation below a normally distributed population median. Nutritional oedema is also part of the case definition for severe acute malnutrition.) More recently, focus has been on mid-upper-arm circumference.’

WHO growth standards are an international gold standard describing how children should grow when measured by weight and height. Previously, severe acute malnutrition was defined as weight-for-height <70% or ?3 Z scores below the National Centre for Health Statistics (NCHS) median. The new case definition is weight-for-height ?3 Z scores below the WHO growth standards median. The diagnostic threshold of mid-upper-arm circumference has also been changed from 110 mm to 115 mm.

Increases in the diagnoses of severe acute malnutrition with the new WHO weight¬-for-height criteria have been noted. As different countries use different case definition it is difficult to know the true extent of severe acute malnutrition.

Most countries currently use %-of-median. Changing from

Kerac et al 2009 New WHO growth standards: roll-out needs more resources. Lancet vol 374 pp 100-101

Metabolic Syndrome US —

In the Lancet 27th June 2008 the clinical usefulness of the Metabolic Syndrome. is challenged.

The metabolic syndrome is a collection of risks for insulin resistance and vascular disease under two principle headings

Cardiovascular risk.

Global diabetes or cardiovascular risk.

Smoking, physical inactivity , unhealthy eating


Inflammation, hypercoagulation

Age, race, sex, family history

Abnormal lipid metabolism

Overweight and obesity

Insulin resistance syndrome.

Genetics and age

Increased lipids


Increased blood glucose.

The response of the clinical world is

Criteria are ambiguous or incomplete and the rationale for thresholds ill-defined.

Is adding diabetes useful

No clear basis for including or excluding other cardiovascular risk factors.

Cardiovascular risk factors are variable.

Treatment of this syndrome is no different from the sum of its parts.

Most importantly the medical value of diagnosing the syndrome is unclear.

This review clearly reflects the day to day experience of clinicians rather than the needs of nutrition scientists.

Kahn R 2008 Metabolic syndrome – what is the clinical usefulness The Lancet vol 371 pp 1892-3

Sattar et al 2008 Can metabolic syndrome usefully predict cardiovascular disease and diabetes? Outcome data from two prospective studies Lancet vol 371 pp1927-35

Dietary Defiency and Excess
Metabolic Syndrome —

Sarcopenia that is the loss of muscle mass and strength with age, and is also a feature of type 2 diabetes in the older person .

In diabetes there is a relationship between increased glucose concentration and weaker muscle strength.

In the Hertfordshire cohort study impaired grip strength runs in parallel with the features of the metabolic syndrome.

The paper suggests that there may be place for the use of the grip test in the clinic.

Sayer et al 2007 Grip strength and the metabolic syndrome: findings from the Hertfordshire Cohort study Q.J.Med vol 100, 707-713

Metabolic Syndrome G —

This is an interesting Review of the Metabolic syndrome: from epidemiology to systems biology

The Metabolic syndrome is a group of metabolic conditions that occur together and promote the development of cardiovascular disease and diabetes. Recent genome-wide association studies have identified several novel susceptibility genes for Metabolic syndrome traits, and studies in rodent models have provided important molecular insights. However, as yet, only a small fraction of the genetic component is known. Systems-based approaches that integrate genomic, molecular and physiological data are complementing traditional genetic and biochemical approaches to more fully address the complexity of Metabolic syndrome.

Lusis, Attie & Reue2008 Metabolic syndrome: from epidemiology to systems biology Nature Reviews Genetics 9, 819-830 (November 2008) |

Metabolic Syndrome —

The BMJ has interesting debates on contentious topics and in the 22 March 2008 the question of the value of the diagnosis of the metabolic syndrome is discussed.

The International Diabetes Federatioi definition of the metabolic syndrome4

Presence of central obesity—Waist circumference varies with ethnicity.

If body mass index is >30 central obesity can be assumed

Plus any two of the following: Triglyceride concentration >1.7 mmol/l or receiving specific treatment for this lipid abnormality High density lipoprotein cholesterol

Systolic blood pressure >130 mm Hg or diastolic >85 mmol/l, or treatment for hypertension

Fasting plasma glucose >5.6 mmol/l or previously diagnosed glucose type 2 diabetes. If >5.6 mmol/l, oral glucose tolerance test is strongly recommended but is not necessary to diagnose the syndrome

Two groups of experts are asked “Should we dump the metabolic syndrome ?

Professor Gale of Bristol argues whilst the diagnosis is a useful label but is too Imprecise

for clinical usage..

George Alberti and Dr Zimmet argue for its use and value in deciphering the multifactorial

nature of the problem..

Gale, Alberti and Zimmet 2008, Should we dump the metabolic syndrome BMJ vol 336

pp 640-641.

Nutrition Screening —

The identification of patients coming to hospital as being under or over weight is very important. Especially the underweight.

There are many methods and Body Mass Index is the hall mark measure.

Matos et al write in EJCN that handgrip strength is a good indicator of underweight patients.

This is an easy method in principle and fun if a happy person teases the patient into a good test.

However the test may be compromised by arthritis, strokes, anxiety ( not another bloody test ) and inattention

My own feeling is look at the person are they thin, fat or normal size?

Matos LC et al (2007) handgrip strength as a hospital admission nutrition risk screening method. European Journal Clinical Nutrition vol 61, 1128-35.

Obesity 15.01.07 —

Rennie KL et al have written a review on The effect of physical activity on body fatness in children and adolescents ( Proceedings Nutrition Society, 2006, 65, 393-402) and discuss the lack of consistency between studies that have investigated the relationships between measurements of physical activity and energy expenditure and body fatness in children. This may be because energy intake is more important. Or that the methodology for measuring activity and body composition does not adjust physical activity energy expenditure and differences in body composition, or body fat is not appropriately adjusted for body size. It may be more important to measure the amount and intensity of physical activity required to prevent fat-mass gain than the energy expended in physical activity. A clearer understanding of the psycho-social, behavioural and environmental factors that influence activity is needed, including the interactions between physical activity and other behaviours such as time spent sedentary, sleeping and eating.

Obesity Worldwide —

Scotland is the second-fattest nation in the developed world, with only the United States having higher obesity levels, a report revealed yesterday.

Figures show for the first time the full extent of the link between obesity and serious illness in Scotland, with obese people 18 per cent more likely to receive hospital treatment than those of normal weight

Women are particularly likely to develop serious health problems from being obese, according to the report by the Scottish Public Health Observatory, a collaboration of public health information bodies in Scotland.

Obese women are nearly 13 times more likely to develop type 2 diabetes than women of normal weight, more than four times as likely to suffer from high blood pressure, and about three times as likely to develop cancer of the colon. They are nearly 30 per cent more likely to suffer a stroke.

Obese men are more than five times as likely to develop type 2 diabetes than those of normal weight, 2.6 times as likely to suffer from high blood pressure and about twice as likely to develop osteoarthritis. Their chances of suffering a stroke are also 30 per cent higher.

Based on 2003, the most recent year for which figures are available, nearly 500,000 cases of high blood pressure, 36 per cent of the total, and more than 50,000 cases of coronary heart disease were a direct result of obesity, according to the report About 900 cases of cancer, mostly of the colon, were also attributed to obesity.

Under new rules for Schools in Scotland , at least two portions of fruit and vegetables will be served every lunchtime, oily fish will he served once every three weeks, while deep-fried food will be limited to three items a week. Sweets and fizzy drinks will be removed from schools and chips will be served only as part of a balanced meal.

Top of the table (per cent)

United States 32. 2

Scotland .25.5

Mexico 242

UK (as a whole) 23

England. 22.5

Canada 22.4

Greece 219

Australia _ 217

New Zealand 20.9

Hungary 18.8

Czech Republic

And at the bottom

Germany 12.9

France. ~ 9.5

Italy -9

Norway 8.3

Times Sept 26th 2007 p 11

Dietary Defiency and Excess
Obesity 2010″,document.location))
Obesity is a very busy topic.

This review in Critical Reviews in Food science and Nutrition makes a thorough evaluation of the 10 putative contributors to the obesity epidemic. The review is comprehensive and well worth reading

The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear.

The eating energy-dense foods and reduced physical activity are the alleged causes of the epidemic, despite a lack of solid evidence to demonstrate their causal role.

The writers accept that these may contribute to obesity, but propose several alternative putative contributors that would benefit from equal consideration and attention.

Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein.

Their questioning of the big two stems from two points. First, the evidence supporting various elements of the big two as contributors to individual or population levels of obesity is often quite weak. Second, even though some elements of the big two do very likely play some role in influencing obe¬sity levels, we believe that an unquestioned assumption of their pre-eminence has led to the possibly ill-advised expenditure of public effort and funds on programs aimed at reducing popu¬lation levels of obesity that has also reduced the exploration of other potential causes and the alternative obesity reduction programs that might stem from their identification.

The big two seem to they have an appeal based, in part, on their simplicity and the fact that they require little specialized knowledge to comprehend and deal with easily observable as¬pects of life with which all of us are familiar.

What are some of the specific facts that enhance our scepticism of the big two as near-omnipotent causes of the obesity epidemic?

1. Papers on Restaurant Dining, Physical education , urban life, high fructose corn syrup consumption and vending machines do not support these attractive ideas.

2. Infections and obesity. A number of bacterial infections have been shown in animal experiments to increase weight in the infected host. Fat cells and macrophages have many similar functions and affecting macrophages by infection may influence adipocyte response

3. Epigenetics and obesity There may be environmental influences on our genetic make up.

4. Maternal age older mums, fatter offspring

5. Fat people or rather individuals with a genetic predisposition have more children than those with a lover level of adiposity.

6. Human adiposity levels have a genetic component.

7. Decreased Sleep may influence the mediators of appetite and energy homeostasis

8. Endocrine disrupters and obesity, including plasticizers ( bisphenyl ether and bisphenol A ) which are stable in the environment.

9. Pharmaceutical drugs

10. Ambient temperature

McAllister et al 2009 Ten putative contributors to the obesity epidemic . Critical Reviews in Food science and Nutrition vol 49, 868-913

Obesity And Activity —

It is a axiom that obesity and lack of activity go together. There are three interesting papers in the International Journal of Obesity on this topic. Overall the pointers substantiate the axiom.

The first examined the longitudinal relationship between occupational and domestic sources of physical activity and body weight in a sample of Chinese adults. In a population-based longitudinal observational study of Chinese adults (4697 women and 4708 men) aged 18–55 from the 1991, 1993, 1997, and 2000 waves of the China Health and Nutrition Survey. The study measured height and weight and detailed self-reported energy expenditure from multiple occupational and domestic sources were assessed over a 9-year period.. Increased occupational physical activity resulted in overall lower body weight for both men and women and increased domestic physical activity resulted in overall lower body weight in men

A second study did not entirely support this. They analyzed whether elderly Iranians in Sweden have a higher mean body mass index (BMI) and are less physically active than elderly Swedes after adjustment for possible confounders. A total of 402 men and women (167 Iranian-born and 235 Swedish-born) aged 60–84 years residing in Stockholm, Sweden, were included in this population-based survey. Iranian participants were weighed and their height was measured. BMI values from the Swedish participants were based on self-reported data adjusted for the known discrepancy between objectively measured and self-reported weight and height. Overall, Iranian women had the highest mean BMI (29.2) of all subgroups. There was no significant difference in BMI between Swedish men and Swedish women or Iranian men. In contrast, Iranian women had significantly higher BMI than the reference group after adjustment for age, education and marital status. Iranians and Swedes had almost the same odds of once-weekly leisure-time physical activity.

The third was very interesting and assessed whether frequency of television viewing in adolescence (11 and 16 years) or early adulthood (23 years) affected subsequent changes in body mass index (BMI) through to mid-adulthood life, and waist–hip ratio in mid-adulthood. The 1958 British birth cohort includes all births in 1 week in March 1958 in England, Scotland and Wales. The main analyses included at least 11 301 participants. Outcome measures included BMI at 16, 23, 33 and 45 years and waist–hip ratio at 45 years. Watching television ‘often’ at 16 years (but not 11 years) was associated with a faster gain in BMI between 16 and 45 years in males. More frequent television viewing at 11, 16 and 23 years was associated with a faster gain in BMI between 23 and 45 years in females, but not in males. Television viewing at 23 years was associated with waist–hip ratio at 45 years: participants watching more than 5 times per week had a waist–hip ratio 0.01 higher than those watching less often. At 45 years, those watching television for 4 h per day had a waist–hip ratio 0.03–0.04 higher than those watching for less than1 h per day

K L Monda, L S Adair, F Zhai and B M Popkin (2008 ) Longitudinal relationships between occupational and domestic physical activity patterns and body weight in China European Journal of Clinical Nutrition 62, 1318–1325;

A Koochek, S-E Johansson, T O Kocturk, J Sundquist and K Sundquist

(2008) Physical activity and body mass index in elderly Iranians in Sweden: a population-based study. European Journal of Clinical Nutrition 62, 1326–1332;

T J Parsons, O Manor and C Power ( 2008 ) Television viewing and obesity: a prospective study in the 1958 British birth cohort European Journal of Clinical Nutrition 62, 1355–1363;

Obesity And Cancer —

Gillian Reeves and her colleagues have studied if there is a relationship between body mass index (kg/m1) and cancer incidence and mortality. They studied a large group of 1.2 million UK women recruited into the Million Women Study, aged 50-64 during 1996-2001, and followed up, on average, for 5.4 years for cancer incidence and 7.0 years for cancer mortality. They looked at the Relative risks of incidence and mortality for all cancers, and for 17 specific types of cancer, according to body mass index, adjusted forage, geographical region, socioeconomic status, age at first birth, parity, smoking status, alcohol intake, physical activity, years since menopause, and use of hormone replacement therapy.

45 037 incident cancers and 17 203 deaths from cancer occurred over the follow-up period. Increasing body mass index was associated with an increased incidence of endometrial cancer (trend in relative risk per 10 units=2.89, 95% confidence interval 2.62 to 3.18), adenocarcinoma of the oesophagus (2.38,1.59 to 3.56), kidney cancer (1.53, 1.27 to 1.84), leukaemia (1.50,1.23 to 1.83), multiple myeloma (1.31,1.04 to 1.65), pancreatic cancer (1.24, 1,03 to 1.48), non-Hodgkin’s lymphoma (1.17,1.03 to 1,34), ovarian cancer (1.14,1.03 to 1.27), all cancers combined (1,12,1.09 to 1.14), breast cancer in postmenopausal women (1.40, 1.31 to 1.49) and colorectal cancer in premenopausal women (1.61,1.05 to 2.48). In general, the relation between body mass index and mortality was similar to that for incidence. For colorectal cancer, malignant melanoma, breast cancer, and endometrial cancer, the effect of body mass index on risk differed significantly according to menopausal status.

They concluded that increasing body mass index is associated with a significant increase in the risk of cancer for 10 out of 17 specific types examined. Among postmenopausal women in the UK, 5% of all cancers (about 6000 annually) are attributable to being overweight or obese.

They suggest that for endometrial cancer and adenocarcinoma of the oesophagus, body mass index represents a major modifiable risk factor; about half of all cases in postmenopausal women are attributable to overweight or obesity

Association with adenocarcinoma of the oesophagus makes sense as acid reflux will be a potent irritant and hence a stimulus for malignant change. The endometrial cancer

Reeves et al 2007 Cancer incidence and mortality in relation to body mass index in the million women study: cohort study. BMJ vol 335 pp 1134-9

Calle2007 Editorial Obesity and cancer BMJ vol 335, pp 1107-8

Maybe the other side of this story is important. Malignant change is reduced by decreased energy intake. That it is not so much the obesity but the nutritional load and the metabolic stress incurred.

Obesity And Diet —

Obesity has reached epidemic proportions in the USA and affects one in three adult women aged 20 years or older, 62 % of women are overweight or obese (BMI more than 25 kg/m2). Obesity will soon surpass tobacco and become the leading cause of preventable death in the USA Women may be at greater risk of obesity than men. The sex difference is possibly related to differences in dietary patterns as well as physiological and behavioural (for example, reduced physical activity) changes associated with ageing, higher levels of body fat and the ability to store more fat, fluctuations in sex hormone concentrations, dysregulation of serotonin and higher leptin levels.

Women may also experience a larger burden of obesity related disease, including CVD, hypertension, dyslipidaemia, respiratory dis¬turbances, type 2 diabetes and osteoarthritis.

There is a requirement for innovative nutrition intervention strategies based on the links between the characteristics and quality of habitual long-term eating behaviours and obesity-related out¬comes, such as dietary patterns and diet quality indices.

This study by Wolongevicz et al prospectively examined the relationship between diet quality a sand the development of overweight or obesity in women over a broad age range, The authors evaluated whether a previously validated, global diet index, the Framingham nutritional risk score predicted the development of overweight or obesity over 16 years in healthy, normal-weight (BMI < 25 kg/m2) women.

They identified a link between diet quality, assessed using the Framingham nutritional risk score, and risk of becoming overweight or obese in women.

Focusing on food intake behaviour is essential. A nutritional risk score that is comprehensive and nutrient-based, like the Framingham nutritional risk score allows assessment of overall nutrient intake patterns of indi¬viduals to identify areas for translation to dietary changes in food patterns, rather than using a more uniform set of inter¬vention guidelines that are potentially irrelevant or more restrictive than appropriate to the individual.

Wolongevicz et al (2010) Diet quality and obesity in women: the Framingham Nutrition Studies Brit J Nutr vol 103 1223-1229

Obesity and dietary predictors —

This study looks for the dietary predictor of visceral adipose tissue area in overweight young adults. A total of 109 young adults (fifty males and fifty-nine females) ate ad libitum in a university cafeteria for 14 d. All food and beverages consumed in the cafeteria were measured using observer-recorded weighed plate waste. Food consumption ontside the cafeteria (i.e. snacks) was assessed by multiple-pas 24 h recall procedures. Visceral adipose tissue was determined using computed tomography. Stepwise regression demonstrated that the best predictor of visceral adiposity in women was total dietary fat (P~0•05). In men, the model for predicting visceral adiposity included Ca and total dietary fat. They concluded that total dietary fat is the best predictor of Visceral adipose tissue area in both men and women. While this relationship was independent in women, in men there was a synergistic relationship between dietary fat consumption and Ca consumption in predicting Visceral adipose tissue.

Bailey et al 2010 Dietary predictors of visceral adiposity’ in overweight young adults . Brit Journal Nutrition vol 103, 1702-1705

Obesity And Exercise —

Twin studies are an elegant method of resolving complex problems, comparing like with like with one variable different.

Exercise is thought to reduce high-risk body fat, but intervention studies are frequently limited by short follow-ups and observational studies by genetic selection. In this elegant study for Finland Leskinen and colleagues studied the effects of a physically inactive or an active lifestyle on high-risk (visceral, liver and intramuscular) fat in twin pairs differerence in leisure-time physical activity habits for over 30 years.

Sixteen middle-aged (50–74 years) same-sex twin pairs (seven monozygotic (MZ), nine dizygotic (DZ)) with long-term difference in physical activity habits during the 32-year-long follow-up.were identified from the Finnish Twin Cohort (TWINACTIVE study).

In within-pair analyses carried out after the adult life-long discordance in physical activity habits, the physically inactive co-twins had 50% greater visceral fat area compared with the active co-twins (mean difference 55.5 cm2. The liver fat score was 170% higher and the intramuscular fat area 54% higher among the inactive co-twins. All the trends were similar for MZ and DZ pairs. Peak oxygen uptake was inversely associated with visceral and intramuscular fat area, with similar trends in intrapair difference correlations. The intrapair difference correlation between visceral and intramuscular fat was also high.

The authors concluded that regular physical activity seems to be an important factor in preventing the accumulation of high-risk fat over time, even after controlling for genetic liability and childhood environment. Therefore, the prevention and treatment of obesity should emphasize the role of regular leisure-time physical activity.

Leskinen et al (2009) Leisure-time physical activity and high-risk fat: a longitudinal population-based twin study International Journal of Obesity 33, 1211–1218;

Obesity And Genes —

There is a growing interest in evolutionary models of human adiposity, ‘thrifty genes’ or ‘thrifty phenotypes’, a variety of metabolic or behavioural traits which gives frugality in the expenditure or storage of energy.

At the broadest level, humans represent a thrifty species relative to other mammals, indicating that metabolic adaptations had a crucial role in the emergence of the Homo lineage, in particular in buffering reproduction from ecological stochasticity.

Some variability in adiposity may be due to genotypes systematically favoured in certain ecological settings.
Genetic variability is also present within populations, and may be considered bet hedging (distributing risk across offspring to increase parental fitness). Bet hedging is an alternative to genetic drift to account for genetic variability in the absence of strong selective pressures. Contrasting with genetic variability emerging over the long-term, thrifty phenotypes represent a response to short-term ecological variability. Physiological plasticity allows the emergence of variability in response to ecological cues experienced directly or by very recent ancestors.

Cultural norms or individual preferences allow voluntary behavioural manipulation of thrift in individuals. Overall, there is a range of factors and processes both favouring and opposing thrifty genes, which may reflect moderate bet hedging rather than systematic adaptation. Plasticity protects the genome from selective pressures by tailoring the organism to ongoing ecological conditions. The fact that obesity can occur in different individuals through different genotypes, life histories and behaviours indicates that different treatments are also likely to be required.

Wells (2009 ) Thrift: a guide to thrifty genes, thrifty phenotypes and thrifty norms

International Journal of Obesity (2009) 33, 1331–1338.

Obesity And Genetics —

Complex human diseases result from the interplay of many genetic and environmental factors. To build up a picture of the factors contributing to one such disease, obesity, gene expression was evaluated as a quantitative trait in blood and adipose tissue samples from hundreds of Icelandic subjects aged 18 to 85. The results reveal a tendency to certain characteristic patterns of gene activation in the fatty tissues — though to a much lesser extent in the blood —of people with a higher body mass index. A transcriptional network constructed from the adipose tissue data has significant overlap with a network based on mouse adipose tissue data.

Experimental support for the idea that complex diseases are emergent properties of molecular networks influenced by genes and environment comes from a study in mice. Mice were examined for disturbances in genetic expression networks that correlate with metabolic traits associated with obesity, diabetes and atherosclerosis. Three genes — Lpl, Lactb andPpm1l— were identified as previously unknown obesity genes. This ‘molecular network’ approach raises the prospect that therapies might be directed at whole ‘disease networks’, rather than at one or two specific genes.

This is such interesting work. There must be a range of disease liabilities from the direct relationship of gene change and Haemophilia or Thalassaemia to the consequences of a complex web of interconnecting genes and an accumulated liability prompted by the environment being conducive to such developing obesity and atheroma.

Emilsson et al 2008, Genetics of gene expression and its effect on disease Nature vol 453 pp 423-428

Chen et al 2008, Variations in DNA elucidation molecular networks that cause disease. Nature vol 452 pp 429-435

Obesity And Shape —

Where I live in Scotland obesity is a real problem. It is so sad to see young women waddling along with considerable difficulty.

What is odd to me is that the old fashioned fat woman was equally fat all over, this new epidemic seems to concentrate the fat around the bottom, and result in a very broad beam person. Often the grace and prettiness of the face is left intact.

Many believe the pandemic is due to a massive increase in the eating of processed food. Could this be that the other contents of the food eg the preservative sodium nitrate could play a role n in affecting the distribution of the fat by influencing body signals and distribution controls. Crisps come to mind though there may be other chemicals and does not explain the effect of soft drinks though these may just ad to the energy input.

Obesity Book —

A recent book “The evolution of obesity” by Power and Schulkin is a very comprehensive survey of the possible causations of this complex problem. It identifies many weight-regulation mechanisms and possible evolutionary reasons for why these can fail. The book uses an evolutionary framework al to analyse a major body of neuroendocrine knowledge about obesity.

They point out that no simple description can be accurate.

Attributing one function to a hormone is attractive, but often wrong. There is a strong correlation of leptin concentrations with body-fat mass, suggesting that leptin limits body weight. But administering leptin to people who are obese does not reduce appetite or weight. Low leptin levels signal the need to seek food, but leptin is only one part of the complex system that regulates eating.

The authors come to similar conclusions for dozens of information molecules that are involved in feeding regulation – including the hormones ghrelin, corticotropin-releasing hormone and cholecystokinin.

The book covers nearly all the main issues in obesity research, the ‘thrifty genotype’ – shaped to store fat to cope with food scarcity, adipose tissue, where fat is stored, as an endocrine organ that secretes at least ten information molecules, and describe the role of cytokines as mediators of the tissue damage associated with abdominal obesity.

The epidemiology of the recent obesity epidemic, a threefold increase in obesity in the United States in just 50 years is discussed.

Power and Schulkin ask why humans eat meals instead of feeding continuously, quoting from explanations from behav¬ioural ecology with the brain mechanisms responsible and with the social functions of sharing meals. They review changes in diet since the Palaeolithic era and the interactions between meat eating and brain evolution.

Other possible contributors to obesity are fructose-based beverages and exercise

The book is reviewed by Randolph Nesse in Nature 2009, vol 40 page 461

Power and Schulkin 2009. The evolution of obesity . John Hopkins University pp 408

Obesity Book —

Dietary counselling is a short term solution to obesity

Dietary counselling is the mainstay of many weight loss programmes. To measure how well this works in practice a meta-analysis of 16 randomised controlled trials was made in the USA (Ann Intern Med 2007; vol 147 pp :41-50. Forty two of the trials included exercise as part of the programme. When compared with what they described as usual care, dietary counselling helped overweight and obese people lose just under two units of body mass index, or 6% of their initial body weight in one year. But weight increased once counselling finished. They regained about half their initial weight loss in three years. Weight gain accelerated towards the end of follow up starting with 0.02 to 0.03 units of body mass index a month between 12 and 18 months and increasing to 0.04 units a month between 24 and 30 months.

Whether these small benefits make a lasting difference to people’s risk of cardiovascular events or death is unclear. The researchers found no trials of dietary counselling with clinically useful end points.

The trials were generally of average or poor quality and tested a mixed bag of interventions. So there’s likely to be some uncertainty around the final combined result.

Obesity Drugs —

In a study in the Lancet the value of the drug tesofensine which is an inhibitor of the presynaptic uptake of noradrenaline, dopamine and serotonin in weight reduction is reported. A dosage of 0.5 mg once daily along with an energy intake reduction could result in a weight loss over 24 weeks of 10%. The adverse effects were dry mouth, nausea, constipation hard stools diarrhoea and insomnia.. 21% withdrew from the trial.

The more unfortunate side effects of earlier drugs e.g agitation and anxiety were not seen.

An interesting study worth following and seeing the long term consequences, are these successes maintained?.

Astrup et al (2008) Effects of tesofensine on body weight loss, body composition and quality of life in obese patients: a randomised double blind , placebo controlled trial. Lancet. Vol 372 pp 1906-1913.

Bray 2008 Is new hope on the horizon for obesity? Lancet vol 372 1859-60.

Obesity In Woman —

Ryan explains the disadvantages of obesity with in a stark list of outcomes at

every stage of life ( Ryan 2007 Obesity in women: a life cycle of medical risk:

International Journal of Obesity , 31, S3-S&.

Obesity can have an adverse affect at each stage of a woman’s life cycle.

In young women, obesity has an impact on psycho social health and, as they grow older

and become parents, on their reproductive health. Obesity is also associated with a number

of serious risks during pregnancy.

In older women , obesity is associated with a number of chronic diseases. E.g. type 2

diabetes and cardiovascular disease, and possibly increased risk for almost all types of


The elderly obese woman, should she live that long is at risk for dementia and Alzheimer’s


Obesity has a marked impact on life expectancy.

The medical risks associated with obesity in women are also important for the woman’s

children and future generations.

There is emerging evidence that nutrition during foetal and early life can influence risk for

obesity and chronic diseases for both sexes.

Obesity Measures —

David Rose in the Times Thursday 13th November writes on the value of measuring waistline and BMI in assessing excess weight.

If one has a waist measurement in the top 20 % then there is a substantial increase in mortality. In a large study ( 350,000 ) from Imperial College London, German Institute of Nutrition and elsewhere individuals aged from 25 to 79 were followed for 9.7 years and 14,723 died during this period. .

For men a waist line over 47.2 ins was associated with a doubling of death rate compared with 37.2 ins. The same is true of women ( 39.4 ins compared with 25.6 ins )

The waist to hip ratio was more sensitive ( range 0.78-1.10 for men and 0.66 to 0.98 for women ), a 0.1 increase was associated with a 34% increase in mortality for men and 24% for women.

Accumulating fat between the midriff is not good for one.

This was reported in the New England Journal of Medicine November 13th 2008.

Obesity Polymorphisms —

Obesity and polymorphisms in genes regulating human adipose tissue


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Obesity is the result of imbalance between food intake and energy expenditure-resulting in the storage of energy as fat. Adipose tissue contains the largest store of energy in the body and plays an important role in regulating energy partitioning. Developments in genomics, in particular microarry-based expression profiling, have provided scientists with ■ number of new candidate genes whose expression in adipose tissue is regulated by obesity. Integrating expression profiles with genome-wide linkage and/or association analyses is a promising strategy to identifv new genes underlying susceptibility to human obesity

This article provides a comprehensive review of adiposaMissue-expressed genes implicated in predisposition to human obesity. The authors consider the following genes of particular interest: peroxisome proliferator-activated receptor gamma and. potentially, INSIG2 acting in ■dipogenesis; the adrenoreeeptors beta 2 and 3. as well as hormone-sensitive lipasc acting on lipolysis: uncoupling protein £ acting in mitoeho«lria energy expenditure: and among secreted molecules the cvtokim- tumor nccrost. farter alpha and the hormone leptin. With the rapid development in genome research, we predict that additional allcles in genes regulating adipose tissue function will be established as risk factors for common obesity in the coming years. This has important implications for the prevention of obesity and may also offer new therapeutic targets.

Obesity Prevention —

There have been a number of obesity prevention schemes for children in schools. The reasonable premise is the young are receptive and they have a life ahead to be influenced

A Cochrane report found that in 27 intervention schemes success was meagre. Possibly because they were too short term

An intervention scheme in the South of England concentrated on carbonated drinks and health talks. The results were encouraging at 12 months. However at 3 years the benefit had disappeared. Suggesting that there can be no let up in the programme.

One third of the children were lost to follow up.

This is a life long project

James et al 2007 Preventing childhood obesity: two year follow-up results from the Christchurch obesity prevention programme in schools (CHOPPS) BMJ vol 335 pp 762-764

Obesity and sex —

Obesity and sex are subjects that doctors find especially difficult to discuss with patients, despite evidence that such discussions help. Although short conversations (three to five minutes) during routine Visits can contribute to changes in behaviour, such as increasing physical activity, eating less fat, and losing weight, most primary care professionals do not talk to their patients about weight.

Bajos and colleagues’ study of 12 364 French men and women aged 18-69 found that obese men and women are at greater risk of negative sexual outcomes than their non¬obese counterparts. This was particularly true for obese women, who were 30% less likely to report a sexual partner in the past 12 months, whereas obese men were 70% less likely to report more than one partner in the same period and 2.6 times as likely to report erectile dysfunction. Although no other differences were found in indices of sexual function in existing relationships, obese women were five times as likely to have met their partner on the internet, more likely to have an obese partner, and less likely to view sex as important for personal life balance.

The factors that underlie these observations of self reported sexual experience and the directions of causal¬ity cannot be determined from a cross sectional study,

Obese women in the 18- 29 year old age group were less likely to report that they used oral contraception or sought contraceptive advice in the past year, and, most startling of all, they were 4.3 times more likely to report unintended pregnancy. Obesity in pregnancy is a major public health concern. Obesity in pregnancy is associated with markedly increased maternal and neonatal morbidity and mortality, and increased healthcare costs. It is the principal maternal health project of the Centre for Maternal and Child Enquiries (CMACE) for 2008- 2011, and it is the subject of a new joint guide¬line from CMACE and the Royal College of Obstetricians and Gynaecologists. So if the message of this paper-that obese women have nearly five times the risk of unwanted pregnancies reproducible in other populations, this shoul.d be a matter of concern for public health and prac¬titioners in reproductive health.

The data on contraception need cautious interpreta¬tion, however, because they focus purely on oral contraception and condoms, ignoring long acting reversible contraceptives, which the UK’s National Institute for Health and Clinical Excellence (NICE) recommends as particularly suitable for obese women.

Goldbeck-Wood (2010) Obesity and poor sexual health outcomes BMJ vol 341 pp 56-7

Bajos (2010) Sexuality and obesity, a gender perspective: result from French national randomn probability survey of sexual behaviours. BMJ vol 340, p 84

Obesity Surgery —

In the June/July 2007 American Gastroenterology Perspectives there are two very interesting articles. One on the future of treatment of Crohns disease

The second is Technologies in the pipeline for obesity., by Susan Yanovski. P 9 and 15.

Obesity is a scourge of Western affluent society. The surgeons have inevitably something to offer.

The laparoscopic banding of the stomach.

Intragastric balloons

Implantable gastric electrical stimulators

Vagal pacemakers

Vagal blockers

Deep brain stimulation with electrode pacemakers

The food industry is looking at nice food with little calorie content ( fruit and vegetables ?)

Games industry

Video games which stimulate exercise..

Obesity Surgery (2) —

Bariatric surgery, or weight-loss surgery, are the various surgical procedures to treat obe¬sity by modification of the gastrointestinal tract to reduce nutrient intake and/or absorption. This review discusses how appetite and levels of gastrointestinal hormones are altered after bariatric surgery.

Surgical removal of.body fat such as liposuction or abdo¬minoplasty are not considered bariatric surgical proce¬dures.

Surgical pro¬cedures can be grouped in two main categories:

Restrictive procedures, e.g. gastric banding reducing the volume of the stomach and physically preventing excessive consumption of food

Or bypass proce¬dures, e.g. Roux-en- Y gastric bypass , a small stomach pouch is created with a stapler and bypasses the stomach remnant.

Gut hormones are an important element in appetite regulation as a result of the signals from the periphery to the brain. Such hormones include ghrelin, peptide YY, glucagon-like peptide-l and gastric inhibitory polypeptide, all of which are currently being investigated as potential obesity treat¬ments.

Bariatric surgery is currently the most effective therapy for substantial and sustained weight loss. Understanding how levels of gut hormones are modulated by such procedures has greatly contributed to the comprehension of the underlying mechanisms of appetite and obesity.

Bueter and le Roux 2009 Bariatric surgery as a model to study appetite control , Proceedings of the Nutrition Society vol 68 , 227-233

Obesity Therapy —

The ingenuity that has been devoted to obesity is boundless. Whether this be psychological, surgical or therapeutic .

As weight losses, achieved with lifestyle intervention are modest and limited by high rates of recidivism and compensatory slowing of metabolism there is a potential for even greater use of drug treatment. In a meta analysis review by Rucker the use of the long term efficacy of anti-obesity drugs in reducing weight and improving health status is looked at.

The trials (30 trials of one to four years duration) were reviewe, all lasted for over a year. .

The drugs studied were

Orlistat, a gastrointestinal lipase inhibitor

sibutrarnine. a central!) acting monoamine reuptake inhibitor,

rimonabant an endocannabinoid receptor antagonist,

Compared with placebo, orlistat reduced weight by an average of 2.9 kg ,

sibutramine by 4.2 kg

rimonabant by 4.7 kg.

Patients receiving active drug treatment were significantly more likely to achieve 5% and 10% weight loss than control subjects.

Ortistat reduced the incidence of diabetes and improved concentrations of total cholesterol and low density

lipoprotein cholesterol, blood pressure, and glycaemic control in patients with diabetes but increased rates of

gastrointestinal side effects and slightly lowered concentrations of high density lipoprotein.

Sibutramine improved concentrations of high density lipoprotein cholesterol and triglycerides but raised

blood pressure and pulse rate.

Rimonabant improved concentrations of high density lipoprotein cholesterol and triglycerides, blood

pressure, and glycaemic control in patients with diabetes but increased the risk of mood disorders.

Rucker et al2007, Long term pharmacotherapy for obesity and overweight: updated meta-analysis BMvol 335, 1194-9

Dietary Defiency and Excess
Obesity Thought —

In a previous blogg I pondered on the aetiology of obesity and wonderedif there was an infective element.

Interesting there is a paper in New Engl J Med 2007, 357, 370-9 which describes the social nature of obesity. Close contacts tend to be obese together. Obesity gathers in clusters. Siblings, husbands and wives but not to neighbours. Might fit with an infection.

Another thought is that obesity and snacking go together. To snack usually means to eat crisps, biscuits and other high energy foods. It is of course possible that the E number compounds in these foods may have a deleterious effect on the eaters and have an influence on intake , metabolism and storage of fat.

Origins of obesity —

The explanations for the epidemic of obesity that is such a problem to modern man are varied and ingenious. They range from the genetic to the endocrine, amount of exercise and diet.

All of these are probably based in fact.

One contribution to obesity, which may be central to the problem, is the availability of inexpensive prepared food. Our ancestors until the 1970s bought raw foods and cooked them. This required much work by the housewife and therefore there was a limit to how much was available. Confectionary was limited in availability. Now the advances in transport means that large containers can move foods around the world. Commercial modern cooking and baking facilities and practices mean that our shops are full of ready to eat food. Which are delicious. This availability is expanded by the huge supply of sweets, chocolates and potato crisps. No time is spent cooking them and a limiting factor is removed.

Protein Diets and Satiety —

In the management of obesity the effect of diet compo¬sition on feeding behaviour is clearly important to encourage weight loss in the short term and weight maintenance in the longer term. Isoenergetic amounts of the dietary macronutri¬ents are not equal in terms of their effect on appetite and motivation to eat.

The diet com¬position strongly affects ad libitum energy intake with protein being the most satiating macronutrient, independent of energy density, relative to carbohydrate and fat. The protein-induced satiety is important as hunger is one of the main reasons why subjects do not comply with a weight-loss regimen. Are such diets safe ?.

For example, recent studies have indicated greater weight loss can be achieved on high-protein diets when compared with high-carbohydrate, low-fat alternatives for periods up to 6 months, but by 12 months, all diets were equally effective. However high-protein low-carbohydrate diets are high in fat, and often the contributions of fruit, vegetables and whole grains is low, which runs counter to current healthy eating advice. There is also some recent evidence that high-protein low-carbohydrate diets may have implications for gut health. But many studies show improvements in fasting lipidaemia and/or glycaemic con¬trol on such diets. High-protein diets could be a powerful tool to promote weight loss in the short term.

It is not known how much protein is required to maximise protein-induced satiety or whether there is a relationship with the energy density of the diet. Normal protein intake is about 15 % of energy intake, which, for a sedentary adult male, is approximately 76-88 g/d. The high-protein diets reported for weight-loss studies often include about 30 % of energy intake as protein. This does not mean that protein intake (g) is doubled, as energy intake is reduced. Often the protein intake is increased only by 30-40 % over habitual levels.

It is not clear if protein promotes satiety (inter-meal interval) or satia¬tion (meal termination) or, indeed, both. Humans eat and over¬consume energy for a variety of reasons, often not related to hunger.

Johnstone 2009 High-protein diets for appetite control and weight loss-the “holy grail “ of dieting British J of Nutrition vol 101 pp 1729-1730

Protein Malnutrition —

Pancreatic ß-cells and skeletal muscle act in a synergic way in the control of systemic glucose homeostasis.

Several pyruvate-dependent and pyruvate -independent shuttles increase tricarboxylic acid cycle intermediate anaplerosis and increase ß -cell ATP:ADP ratio, triggering insulin exocytotic mechanisms.

Mitochondrial tricarboxylic acid cycle intermediate cataplerosis gives rise to the so-called metabolic coupling factors, which are also related to insulin release.

Peripheral insulin resistance seems to be related to skeletal muscle fatty acid accumulation and oxidation imbalance. Exercise increases skeletal muscle tricarboxylic acid cycle intermediate anaplerosis, increasing fatty acid oxidation and restores insulin sensitivity.

Protein malnutrition reduces ß -cell insulin synthesis, release and peripheral sensitivity. Despite little available data concerning mitochondrial metabolism under protein malnutrition, evidence points towards reduced ß-cell and skeletal musc1e mitochondrial capacity.

The observed decrease in insulin synthesis and release may reflect reduced anaplerotic and cataplerotic capacity.

Furthermore, insulin release is tightly coupled to ATP:ADP increase which in turn is related to tricarboxylic acid cycle intermediate anaplerosis. The effect of protein malnutrition upon peripheral insulin resistance is time-dependent and directly related to fatty acid oxidation capacity. In contrast to ß -cells, tricarboxylic acid cycle intermediate anaplerosis and cataplerosis pathways in skeletal muscle seem to control fatty acid oxidation and regulate insulin resistance.

Mitochondrial metabolism: Skeletal muscle: Pancreatic islets

Zoppi et al 2010 Insulin release, peripheral insulin resistance and muscle function in protein malnutrition: a role of tricarboxylic acid cycle anaplerosis. British Journal of Nutriton vol 103, 1237-1250

Sarcopenia —

Ageing is associated with a gradual loss of skeletal muscle mass, known as sarcopaenia. These age-related changes in skeletal muscle mass are attributed to a disruption in the regulation of skeletal muscle protein synthesis and/or degradation

Protein turnover in skeletal muscle tissue is highly responsive to nutrient intake in healthy, young individuals. In the elderly, the muscle protein synthetic response to food intake seems to be blunted, which is likely due to impaired anabolic signalling in skeletal muscle tissue and may be a key factor in the aetiology of sarcopaenia.

In addition to food intake, physical activity can effectively modulate muscle protein metabolism, stimulating both muscle protein synthesis and breakdown. However, post-exercise net protein balance will remain negative in the absence of food intake Recently, Koopman and colleagues have reported that co-ingestion of protein and leucine with carbohydrate following physical activity can increase muscle protein synthesis to the same extent in young and elderly lean men

The latter indicates that the combined ingestion of carbohydrate and protein with additional free leucine might indeed represent an effective strategy to further increase muscle protein synthesis and/or to inhibit protein degradation following physical activity. Follow-up studies have shown that leucine has the ability to function as a nutritional signalling molecule that stimulates muscle protein synthesis at the level of translation initiation through the activation of mTOR

In addition, leucine has also been shown to have the potential to affect muscle protein metabolism by decreasing the rate of protein degradation. most likely by stimulating insulin secretion.

In previous studies, Koopman et al have shown that the combined ingestion of carbohydrate, protein and leucine is more effective than the-ingestion of only carbohydrate in stimulating muscle protein synthesis in vivo in man. More recent data suggest that the intake of amino acid mixtures or proteins with additional leucine can further enhance muscle protein synthesis in the elderly. However, the proposed surplus value of leucine co-ingestion under normal living conditions, in which physical activity is followed by food intake, has not yet been assessed.

In a study reported in the British Journal of Nutrition , Koopman et al determined the potential surplus value of free leucine co-ingestion on post-exercise muscle protein synthesis in elderly men (about 75 years old) under conditions where large amounts of whey protein and carbohydrate are being ingested.

However the ingestion of leucine, carbohydrate and protein following physical exercise in the elderly does not increase muscle protein .

Koopman et al 2008 Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men British Journal of Nutrition vol 99 57-580.

Dietary Defiency and Excess
Ebrahimi-Mameghaniet al Changes in weight and waist circumference over 9 years in a Scottish population

European Journal of Clinical Nutrition (2008) 62, 1208–1214; doi:10.1038/sj.ejcn.1602839; published online 11 July 2007

This study looked at patterns of measured weight and waist circumference (WC) change and the increase in overweight and obesity over a 9-year period in a Scottish population..

A total of 1044 subjects from two age-defined cohorts aged 39 and 59 in 1991. Height, weight and WC were measured in 1991, 1995 and 2000 and body mass index (BMI) was calculated. Pattern of weight and WC change was studied over approximately 9 years.

The prevalence of overweight and obesity increased markedly and the younger cohort showed greater increases in weight and WC than the older cohort. There was no significant difference in mean BMI and/or mean 9-year weight change between men and women in either age cohort, and mean weight gain was similar for all occupational groups. Only 20% of subjects maintained a stable weight (2 kg), while 42.2 and 17.6% gained greater than 5 and 10 kg over the 9-year period, respectively. The rate of weight gain appeared to be relatively steady over the 9 years among younger subjects but declined in the older subjects in the second half of the observation period.

Health promotion strategies to prevent weight gain need to be population-based, targeting all social and age groups, but particularly those in their early middle-age.

Starvation —

The response of the body to starvation is a complex process. This paper is interesting, because if there is loss of ribosomes, then refeeding has to be a cautious process until the cellular synthetic processes are restored to full.

Autophagy is a process in which cytoplasmic components are broken down to supply materials for the synthesis of essential molecules under nutrient-limiting conditions. Because this process involves random sequestration of the cytoplasm by large membrane vesicles, considerable amounts of molecules, such as ribosomes, are necessarily degraded by autophagy. However, starving cells also promote additional selective degradation of ribosomes as a requirement for survival.

Hitoshi Nakatogawa and Yoshinori Ohsumi (2008) Starved cells eat ribosomes Nature Cell Biology vol 10 pp 505 7

Starvation 2 —

Alex de Waal has written a very thoughtful review of starvation and the practical political elements in this.

Starvation can come in various forms and causes.

Absolute starvation is rare, this is often a technique in warfare where a group of people are surrounded by hostile forces and denied food and water. This is pure starvation. This has happened in Darfur and Ethiopia

Where the supply of food is drastically educed by climatic, food supply Government inaction or error or other reasons than the cause of death is often a secondary event an superimposed disease e.g. infectious diarrhoea or pneumonia.

Amartya Sen wrote that famines do not occur in countries which have a free press and democratic elections. India has been relatively free of famines since independence whereas during Chairman Mao’s Great Leap Forward ( 1958-61) some 30 million died.

More recently the expectation of life in China has exceeded India.

Lancet 2008 The Art of Medicine. On famine crimes and tragedies vol 372, pages 1538-1539

Starving —

This article by Tegegne in Medicine Conflict and Survival 2008, The primary solution of global poor health and poverty vol 24, pp 107-114 is a thoughtful discussion of this massive problem.

There is a huge global burden of disease and mortality. The principal underlying cause is regarded as poverty. This is associated with a global order of fear, over-consumption, over-population and violence, which can interact in a vicious circle. It is proposed that the solution to the problem is not only the relief of poverty, but the institution of a new order in which the individual is sovereign. This in turn requires a trinity of ideals for the individual: self-control to avoid over-consumption, altruism to cope with fear, and peace to manage violence.

Stunted Children —

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 follow 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.

Surgery For Obesity —

Obesity may be difficult to overcome and in these situations the surgeons as always have explored surgical management of the problem.

In the Journal of the Royal College of Physicians of Edinburgh Witherspoon and Galloway review surgical procedures useful for obesity control.

Medical treatment for the grossly obese is not always effective in the long term.

In these situations bariatric surgery has much to offer.

The operations may be

restrictive procedures.
reducing the functional capacity of the stomach by reducing the capacity of the stomach with a band across the upper stomach

2 . operations resulting in malabsorption

These reduce the absorptive capacity of the intestine , either by bypassing part of the intestine or removing small bowel.

A mix of 1 and 2. Laparoscopic small gastric pouch with bypass of remaining stomach , duodenum and variable length of jejunum.
Weight loss may be very good, 50 to 75 %.

The gastric banding complications are mechanical, band erosion and slippage.

The creation of malabsorption requires very careful follow up as very severe complications may result. Apart from the malnutrition some patients will have disabling diarrhoea and incontinence.

Overall restrictive procedure s are the best.

Witherspooon and Galloway 2008 Surgery for severe obesity: an effective cure for a difficult problem J R Coll Physicans Edin vol 38, 129-30

Weight Loss and HIV —

HIV is a grave problem in sub-Saharan and the basic treatment is antiretroviral therapy. Mortality is high during the first few months of treatment, significantly associated with weight loss i.e. reduced BMI. How can the BMI be increased?

The most commonly used supplement in food aid programmes is corn-soy blended flour, a cheap fortified cereal-legume combination that requires cooking.

The results are disappointing.

A controlled trial using an energy dense ready to use fortified pre-cooked lipid paste made from peanuts that resists bacterial contamination is reported in the BMJ of May 30th 2009. And works, increases BMI and lean body mass but does not change mortality.

Which challenges the underlying concepts and ideas. Is weight loss the entire cause of death? There was no increase in micronutrient content of the supplement above normal recommendations. More is not necessarily better.

The editorial quotes Kleiber’s law, that in the face of competitive functional demands, how specific nutrients are used eg energy and pattern of protein deposition will be determined by the relative availability of all other nutrients. A wise thought.

In the resuscitation of inmates of freed concentration camp inmates in 1944 much had to be learnt about the way in which food was reintroduced.

MacDonald et al 2009 Supplementary feeding with either ready o use fortified spread or corn soy blend in wasted adults starting antiretroviral therapy in Malawi: randomised , investigator blinded controlled trail BMJ vol 338 pp 1309-1312

Rollins in Editorial Food supplements and HIVBMJ vol 338 pages 1282-3


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