Not only is obesity an indepndent disease. Also, the different forms of obesity (subcutaneous vs omental) have completely different manifestations. Abdominal obesity is associated with increased omental fat which releases inflammatory factors and fatty acids through the portal vein to the liver with all the adverse metabolic consequences associeted with increased abdominal fat mass. On the other hand subcutaneous obesity (the more protective form) is associated with insulin resistance.

Obesity can be considered as a risk factor , rather than as a disease . It is abdominal obesity , which is considered more important than increased BMI . Even in metabolic syndrome , measurement of abdominal circumference is considered an important criteria . This highlights that there is a view that diabetes mellitus , hypertension , lipid disorders & abdominal obesity is more relevant than obesity . It is very essential to look for these risk factors in every obese person . Obesity without these associated risk factors can be considered as metabolically healthy state . Therefore , obesity is an indication for screening for cardiovascular risk factors & prognosis is based on the presence of associated co morbid risk factors .

Fernando: You mean: obesity is the consequence of ¨adipositis¨? Inflammation of adipous tissue that produces chemical mediators of inflammation and fibrosis? What is th definition of disease?

Singh: Heathy obesity exists? If so what is the proportion of heathy obese individuals?

The following article ' Metabolically healthy Obesity and risk of all - cause and cardiovascular disease mortality ' in J Clin Endocrin Metab. July 2012 , 97(7): 2482-2488 has discussed this concept . This is for your reference .

obesity is an independant disease representing the epigenetic aspects of in utero development that is metaphysiologic but pathologic in adults commonly.

EHsidibé endocrinologist in tropical area/pobox 5062 DAKAR FANN 99000

Singh: Thank you for your reference. It is clear that around 5-10% of obese patients do not have some metabolic abnormalities such as high blood pressure, high-density lipoprotein-cholesterol, diabetes ,  triglycerides, high waist circumference, etc. These condition  is  arbitrarily called ¨healthy obesity¨ (definition used: if they have at least one of these metabolic abnormalities). In these individuals it is expected to observe low incidence of cardiovascular complications. Nevertheless, the long term clinical history or evolution of these patients is not known. I mean the incidence of relevant metabolic abnormalities obesity- related at 1,3,5,10 years of follow-up  and the morbidity of the new situation. The problem I see in this issue, is that in those studies dealing with  ¨healthy obese¨ individuals,  adiposity (the morbid state of adipous tissue) is not evaluated. The most precise way for doing it is by means of determination of adipokines (leptin, TNF system, resistin, adiponectin, etc.). In my opinion ,Unless the above mentioned factors are not cleared, the term ¨healthy obese¨ is controversial and  it has to be used with caution.

What do you think about the growing number of studies which correlate obesity to the composition of intestinal microbiota? Facts or fantasy?

I agree with you , Diego garcia-compean that obesity is definitely a health problem . The reference which I mentioned , highlights that in a subset , complications do not occur & they are healthy , in terms of not having any metabolic disease . But , obesity is a life style risk factor , which occurs due to poor food habits & lack of exercise . Therefore , maintaining ideal weight is definitely essential for good health . Measurement of adipokines would definitely predict future complications in obese persons .

I agree with Jumana with the finger crossed for those group of obese people who got protected somehow from developing 'inflammation'...like the so-called 'lean-NAFLD'...

Individuals with lean-NAFLD according to a recent 20 year-follow up study by Paul Angulo and whose results were exposed in the last DDW in Chicago have significantly higher mortality than NAFLD- obese patients. The prevalence is around 3-5% . These results have  to be confirmed by other groups. Results  may suggest that in this small group of patients, factors that mediate NAFLD are different than in obese patients. And of course they may be more aggresive. According to Angulo,  results of these studies are very difficult to explain in simple terms. And adipokines and other chemical mediators have not been determined in these patients yet. Indeed it is a very interesting issue that demands clarification in big sample size prospective studies including investigation of multiple risk factors and measurements  of chemical mediators of liver disease.

It is clear that, in this type of NAFLD ,  obesity does not ¨protect¨the patients. Conversely, mortality  may be the effect of unknown noxious factors not related to obesity.

The most important reason why obesity should be classified as a separate disease entity is that it is a recently developed 'scourge' plaguing the modern world and expected to tighten its sinister grip in future  with multiple pathogenetic mechanisms involving gastro, endocrine, lipidology, nutrition and having bad impact on practically all body systems. I feel it is basically due to exposure of "energy-thrifty" genes (which developed due to repeated exposure to famines in past) being exposed to the multifarious cuisines of the modern world in the poorer countries. In rich countries it is due to overeating, sedentary behaviour involving lavish lifestyles and not much mental or physical work

Obesity is a risk factor factor developing other diseases. Obesity cuases serious problems like rise of inflammatory markers. Type 2 diabetes and hypertension more likely to occur and finally ends up with metabolic syndrome

The role of gut microbiota in pathophysiology of obesity is a non resolved issue. It has been observed,  that fecal transplantation from obese rats with metabolic syndrome to  non obese germ-free rats resulted in transfer of metabolic syndrome-associated features from the donor to the recipient. It is suggested that increase of energetic availability produced by fermentation of carbohydrates by means of microbiota activity, stimulation of gut  hormones,  increased intestinal permeability causing elevated systemic levels of lipopolysaccharides (LPS). This metabolic endotoxemia is suggested to contribute to low-grade inflammation, a characteristic trait of obesity and the metabolic syndrome. Nowadays, although there is ample evidence for a role of gut microbiota in the development of obesity in rodents, its contribution to human obesity is unknown.

This is a "How long is a piece of string" question that invites but does not accept dogmatic answers. We need hard data and plausable mechanisms.

A few years ago an Indian chap noticed that the spread of obesity resembled the spread of an infectious disease and moved to the USA to get funding to track down the organism. I do not know what followed. Unfortunately the pattern of spread can not distinguish between an infection and the spread of of a social meme for overeating. Fei and Zhao recently implicated Klebsiella mobilis as causative in one case of morbid obesity. The small sample size makes this little more than annecdote except there is a plausable mechanism. The mouse paw oedema assay is used for Klebsiella sp. which means that there is at least one O-linked N-acetylglucoseamine transferase (OGT) toxin. Almost all the apetite regulation hormoes are mediated by a hexamine pathway which would be disrupted by an OGT toxin. Although the evidence is suggestive, we still do not know. What we need is:-

1) An exhaustive list of organisms having an OGT toxin

2) Assays which could reliably tell us the percentage of these organisms in the gut flora.

3) Large scale surveys of gut flora and types and degree of obesity to find those correlations that exist.

4) The biochemistry on how these OGT toxins affect the hormone production. and balance.

The lifestyle model blames the victim. This is dangerous for human beings who find it difficult to resist that dangerous mind-bending drug, righteousness. What else could induce men who have sisters and daughters to shoot a schoolgirl in the head for wanting to go to school. I am on the low end of normal for BMI. If my trousers get tight I stop eating and get some exercise. I have a neighbour who is eating himself to death. It would be easy to blame him for lackig my moral viitue but he and his family may be the victims of an infection and, there but for the grace of God, go I.

There is evidence that change in lifestyle causes increases in metabolic disorders. The famous data for post war Japan and T2DM is often cited. However, before accepting the  "just so" stories of the righteous healthy eaters we need to look more closely. In this context, words like,multifactorial and holistic, are simply expressions of total ignorance.  What is it in the "Western Lifestyle" that are causative agents or factors for the ills this causes?

One that springs to mind is intensively farmed meat much of which is contaminated with Clostridium novyii type A with its OGT alpha-toxin. There is a vaccine which gives two years protection but the advice in the pig farming literature is to only use it on valuable breeding stock. It is a slow developing disease which will not cause the pigs to sicken and die before slaughter. It does cost in terms of reduced food conversion but this is less than the cost of the vaccine. I have seen pigs liver with the characterisic "areo- chocolate" appearance on sale in my local supermarket. Which brings us back full circle to a dangerous organism with a plausable mechanism but not enough known to be sure.

Is any one up for a collaboration to start attacking the sea of ignorance. I have no lab facilities but can assist with literature searches.

At least in infants, prepubertal and pubertal subjects I think it is convenient to talk in terms of "Pediatric Obesities". In effect, in addition to exogenous obesity, a number of syndromes, chromosomopathies, endocrinopathies and monogenic diseases develop obesity; however, the characteristics, evolution and approach to treating and understanding this weight gain will be different.

I think the term "obesity" is somewhat ambiguous. It is true that we define obesity according to body mass index, but this is very poor informative about the underlying processes to weight gain. What is certain is that it is an individually ongoing situation; in DRECE study (unpublished data) more than 80% of individuals categorized as obese, still are obese after 15 years of follow-up, although they have changed other comorbidities.

Moreover, not all obese population may be considered at risk. Unrecognized certain genetic combinations that result in overweight and obesity does not increase the cardiovascular risk of individuals, while in others, particularly if accompanied by cardiometabolic syndrome, the risk is clearly increased. In NAFLD- obese patients we dont know what is the cause and what the effect.

It has something to do with all this the microbiota? I think it's early to have clear ideas about it, but it seems that food intolerance to certain elements could favor a proinflammatory state and some insulin resistance by TNF alpha and IgG3. I do not think that everything is reduced to a simple equation between food intake and energy expenditure. In my opinion it is necessary to progress further in understanding obesity, its causes and the "effective" way to intervene; Simple diet is usually not efficient, and the surgical procedures do not provide a clear guarantee of good health, especially if do not know the cause of obesity.

Dear All,

I d like to ask for your advice regarding a weight loss RCTrial.

If the interventional weight loss  trial is only for 12 weeks long  would you suggest to measure leptin, adiponectin, cortisol, insulin, or other markers ? (Pre and post trial)

And if yes, which ones ?

Would you suggest this if he trial is for a year ?

I would really appreciate the advise as reading the literature is fairly inconclusive to me.

Can you please drop an email to my address bujpet(AT)yahoo.co.uk if you have a good idea and suggestion ?

It's good possible method of psychological influence on the patient in a case alimentary-constitutional obesity type - "if it's the disease (diagnosis), hence it is necessary to search the probable reason and to influence it". Before development steatosis, arterial hypertensia, diabetes mellitus and etc. it's especially actually for some patients.

When there will be accurate data, for example, about the infectious nature of obesity, we will use target therapy.

Zmicar,

When Ben Longo-Mbenza was in Kinshasa he was treating obese women with antibiotics. He paper with his protocols and results is on the internet. Ben has moved arround since then but you can find him through Skillpages.

It is difficult to be sure whether obesity changed the gut microbiota or the reverse. Hepatic steatosis may be the confounding variable related to both. But of course different microbiota cause different metabolic alterations. There are a lot of juvenile obesity in developed countries. One can study the microbiota in obese infants and toddlers from developed countries and compare them to that of non obese infants and obese adults