Obesity (Again).

Being overweight remains in the news, with bulk of opinion being slanted toward the view that people who are in this state (obesity and the UK) are largely responsible for their own predicament. I not only find that somewhat cruel, but also founded in poor or even bad science.

I've already said in my previous post that is unlikely to be the fault of the 'fatties' but more of those who are advising them to eat a 'healthy diet' which in the DH 'speak' will largely be carbohydrate based and 'low fat'. In the latter's case that will be monounsaturated fats and polyunsaturated fats instead of saturated fats. Plant based oils (generally) then, in lieu of animal fats. This last bit of advice seems to fly in the face of the fact that homo-sapiens have some problems in metabolising some fats with CIS bonds (and even more problems with fats containing trans bonds). Animal fats such as lard, tallow and dripping, also contain quite large amounts of mono and polyunsaturated fats despite their undeserved reputation for being  entirely 'saturated'. Yet, it is patently obvious that this advice to avoid saturated fats and animal fats in particular, has done nothing to reduce the incidence of obesity and the associated risks of Diabetes, CHD, CVD and Cancer, because it continues to increase.

Looking in more depth at Nutrition and it's relationship with obesity we have to consider the mechanisms involved in becoming overweight. 'Hyperphagia' is synonymous with obesity, that is over-eating in simple terms. It can be a result of some genetic disorders or Diabetes, especially in Type 1's who inject insulin. It also manifests itself in Type 11's who are in advanced stages of the disease. High Carbohydrate diets typically can bring about this problem due to increased gene expression of the neuropeptide Y(NPY) in the hypothalamus, and causing a reduction in the expression of the hormone (CRH). What that means is that the brain is increasing its output of orexigenic (hunger generating) agents and decreasing output of anorectic (hunger suppressing) agents. This is how the brain stimulates our nutritional needs of hunger and satiety. So, it is evident that early stage diabetics (metabolic syndrome), Type 11 diabetics and the obese subjects will be permanently hungry. If, however we feed them a diet of fats and proteins and eliminate most carbohydrates, this phenomena is suppressed in a more 'normal' manner and appetite is curtailed at a much earlier stage in eating.

Forcing people then, to eat a 'healthy diet', two thirds of which is carbohydrate based, if we include the vegetables and fruit, is contributing to the obesity that it is meant to be reducing! Once we become 'insulin resistant' as well, we can arrive at a position where almost all intake is rapidly stored as fat, despite the fact that we are hungry, even starving, and our ability to 'feel full' is almost non-existent. Low carb diets, especially in the context of this section of society, are proven to have a considerable success in enabling obese and diabetics to attain an optimal weight and, more importantly, to maintain it. The mechanism is not fully understood, and there is considerable conjecture amongst biochemists that it may be down to ' metabolic advantage' with fats and proteins, or the satiety afforded by this food group actually reducing the calorie intake, or even the fact that increasing saturated fat intake, replaces vegetable/seed oil intake (generally Omega-6's) and that in itself helps to reduce obesity. Many hypotheses are propounded, reputations impugned, the science examined, re-examined and much that is known is based upon animal studies, not humans, but whatever the mechanism, it is certain that for most, a low or minimal diet of carbohydrates does bring about considerable weight loss and a 'normalisation' of blood sugars in most diabetics (Type 11's). Dogmatic views about diet and nutrition, without examining the science involved and ignoring outcomes, is what has brought about the ever rising tide of obesity and diabetes.

Those of us who are 'insulin resistant' respond to this more readily than any other cohort, and it is not a panacea for all, by any means, because all of us reach a plateau with our bodies, some quicker or slower than others. In fact being slightly over weight has some advantage for humanoids and was likely a defence mechanism against famine or periods when food was not abundant. The body in fact conserves energy in fat reserves and is quite loath to give them up, which is why so many dieters fail in their endeavours to lose weight because basal metabolism 'slows' as we begin to diet, especially with low fat/low calorie diets. Your body is attempting to 'save' you from yourself.

Completely Unnecessary Picture of Low Carber J- Lo

So why does mainstream advice for lowering the risk of obesity and the morbidity's that stem from it, continue to advocate measures, that are most likely to fail either in the short or long term? Well having your beliefs undermined, no matter how much evidence exists to prove you are wrong , is hard to bear, even for Doctors and Scientists.Being told what you want to hear, is comforting and reinforces preconceptions at the expense of the truth. Selection bias is something we are all guilty of at some time and I admit to it myself. We should not defend the indefensible but all too often the truth becomes clouded by hyperbole. Scientists delight in the rigour of 'peer review' often tearing quite good studies to pieces because 'they can' rather than due to any poverty of evidence. Equally as well they often lose the ability to reflect that 'correlation (and observation) does not prove causation' in the data they present. Which is why we get 'scare' stories extrapolated from views and opinions of Scientists, rather than hard evidence of harm.

It should not be countenanced and I have always believed that all of us  need to be as objective as possible in our search for truth, even when that truth challenges our basic and long held belief system. 'On the word of no-one' (Nullias in Verba), only the proof, is what we need.

This post has been devoid of links thus far. I've saved them  to the end. I've used some before, so don't be surprised to see them again. They all possess the 'gold standard' of trials, they are RC T's.

1. Brehm BJ, et al. A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. J Clin Endocrinol Metab 2003;88:1617–1623.
2. Samaha FF, et al. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. N Engl J Med 2003;348:2074–81.
3. Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr. 2003 Mar;142(3):253–8.
4. Aude YW, et al. The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial. Arch Intern Med. 2004;164:2141–2146.
5. Volek JS, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism 2004, 1:13.
6. Yancy WS Jr, et al. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial. Ann Intern Med. 2004;140:769–777.
7. Nichols-Richardsson SM, et al. Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet. J Am Diet Assoc. 2005;105:1433–1437.
8. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial. JAMA. 2007;297:969–977.
9. Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabet Med. 2007 Dec;24(12):1430-5.
10. Shai I, et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med 2008;359(3);229–41.
11. Krebs NF, et al. Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents. J Pediatr 2010;157:252-8.
12. Summer SS, et al. Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet. Obesity (Silver Spring). 2011 Mar 31. [Epub ahead of print]
13. Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial. Diabet Med. 2006 Jan;23(1):15–20.

Lies, damned lies, and statistics.

Attributed to Mark Twain, about Disraeli, this phrase has received considerable use, in decrying statistics as a means of bolstering an argument, and indeed, sometimes in the support of one. However, when statistics are used, in the support of a drug or treatment in Medicine, or a lifestyle change or recommendation, we are into a different 'ballgame' altogether. It is best policy then to treat them with healthy scepticism.

The The Jobbing Doctor recently referred to the increase in oesophageal cancer, from an anecdote about his own practise. This is in fact borne out by the statistics. In the period between 1995 and 2008 there has been an increase of nearly 50%! But that only means, an absolute risk of 14.4 persons per 100,000 as opposed to the previous 8.8 persons per 100,000. That's no consolation to those with adenocarcinoma of that organ, but the risk is still quite low. And that brings me to the crux, of my railing against, studies that prove very little, but grab headlines and frighten and confuse the populace by mixing up relative and absolute risk, often to sell us a drug, a lifestyle change or a treatment protocol that has little to no effect on survival, or the progress of an illness.

There has been much publicity, about the trials of various drugs recently, highlighting the pro's and the con's (literally) of their worth. The use of statin's, for example, was initially believed to be a panacea for low risk (should that be no risk?) patients in the prevention, of future heart disease. But this has been clearly shown to be of little benefit, whilst at the same time as increasing risks for other diseases such as diabetes. The use of statin's in primary prevention is now pretty much a 'dead parrot', but will GP's stop prescribing them for the achievement of a highly dubious surrogate end point? Well, err, no, because they are paid to achieve them by the QOF (Quality Outcomes Framework). And let not the science, get in the way of a nice little earner!

Trials, generally have been the basis of evidenced based Medicine since 1946, when Austin Hill designed the 'randomised control trial', for tuberculosis treatment with antibiotics, which were in their infancy. I suppose it was easier then, because there was not much in the way of groundbreaking science or drugs around, but as 'Pharma' became bigger and richer, the stakes got much higher, and the opportunities for 'massaging' the results became ever easier, especially once the baffling science of statistics, became a science in itself. So we are today, beset by statistics, that are 'mangled', to produce the right outcome, for a drug, a lifestyle or dietary change, or the cessation of something, that may be vaguely enjoyable.

Until only relatively recently, there was no compulsion to reveal all the results of a particular trial, but now 'Pharma' is compelled to do so, bringing to light a number, that showed particular drugs, to be less effective than previously thought. 'Pharma' had been guilty then, of 'hiding' from public (and other scientists) view, those trials that showed some drugs, had little to no effect, or did harm. This is termed 'selection bias' and has long been used to influence outcomes, in favour of that which was needed to justify, a particular protocol or drug's use. But, random chance, has a part to play, and as most RCT's are designed to ensure at least a 5% success ratio, then 1 in 20 completely useless one's will register as positive. These and others, are those they did not wish us to see, but no longer, they are now compelled to show all.

Another trick, often used, especially when, you can hide the data behind a 'paywall' such as the BMJ, or 'The Lancet' or many of the other journals, is to mix up relative and absolute risk within the 'abstract'. For example; I can double your chance of winning the Lottery. How; buy another ticket! Your relative chance has doubled, but only to 2 in 14 million, your absolute chance. If one extrapolates that into scientific study, as is often done, a somewhat distorted view, is given to the unsuspecting reader (journalist usually). As I have also said, many times, in my posts, correlation does not prove causation. And, as many trials are observational they simply correlate facts about the cohort under observation. The whole of the vegetarian revered book, 'The China Study', was no more than a complex and detailed correlation of observed data. Denise Minger wrote an extremely well researched and devastating critique of that testament to a vegan diet, that blew it out of the water, in my view.

This co-relationship (correlation) between several factors can be co-incidental. For example; many fat people are diabetic, but not all are, and in fact quite a few thin people are also diabetic. But it is not an absolute fact that all diabetics are fat; unless of course you ply them with drugs from 'Pharma', when they almost certainly, will get fat. That was a hypothesis, by the way, borne out by a considerable amount of evidence, and more importantly, the proof implicit, in the biological mechanism of insulin, which is generally enhanced by hypoglycemic drugs, of being an agent of fat storage.


An example of how society has been hoodwinked by both 'Big Pharma' and the GP's is the ever lowering of blood pressure targets, both for those at any risk, and those at 'allegedly' known risk, ( people with a history of CHD/CVD), who are prescribed anti-hypertensives of one kind or another. This is yet another 'surrogate end point', viewed as a possible marker for heart disease, but not actual heart disease. Well, the QOF for prevention, is for GP's to prescribe these appalling drugs, to lower blood pressure, in the targeted cohort, for which they get paid, on a 'payment by results' system. However, it turns out that the QOF for this had no discernible effect at all, on outcomes for the lowering of BP in patients being treated in primary care. There is even an implication, if you click on the whole study (amazingly free), that other 'payment by results' treatment protocols, for other diseases of society are also not effective, except for the pay of GP's. Some Doctors say, that they were already achieving high levels of compliance prior to QOF's institution, so these rewards are simply retrospective. I think that's a cynical manipulation of the facts to suit events. Either way, it's hardly value for money, or indeed of any real use to the patient, who is taking medication to fulfill a 'tick' list, often at cost to their well being.

Have then Doctors, taken the money, despite their efforts having produced no tangible result, or is the whole exercise pointless anyway? Because, further study will show that although the various drugs do lower BP to an extent, in some, but not all patients, the outcomes for the cohort taking them remains unchanged. Exactly the same number die, whether they take drugs or not. This review from Cochran highlights the inadequacies of both the studies and interventions in use, and is pretty damning, in its conclusions.

So, long suffering reader, I would urge scepticism in all data, that is presented to you as 'proof' of anything, especially a drug or treatment, that has been provided as a preventative measure by your 'hard pressed' GP. Was the study an RCT? Was it reproduced in a number of trials ( at least three), with a significant time scale (at least a year), for each? Was it interventional (the drug or device/protocol being designed to change an outcome)? Was it 'blinded' (the cohort and the trial personnel have no knowledge of who is getting what)? Was it longitudinal (over a long time) and if so the time must be long and the cohort large, such as the Framingham Study (60 years). This latter study, interestingly, has been criticised by many as both observational, self reported for many of its facts (by the cohort) and that much of the adverse data was suppressed. However, Michael Eades found that it was reported, just not very prominently.

Finally, be a sceptic, and believe only that, which is proven by real science, not Daily Mail headline drivel, or advocacy research, or perhaps worse, what your Doctor tells you (if it's QOF'ed).