I am writing this letter in response to the most recent editorial by Floegel and Pischon on the newest epidemiological study by Lagiou and colleagues. Taking aside the sensationalised and “concluded” results of the study for one minute, we turn our attention to what can only be described as, in my opinion, a completely unjustified and extremely biased editorial which has, at best, only summed up the conclusions of the paper, with complete disregard to actually critiquing. As a general rule, results from any observational based study (of which the Lagiou paper is) should never bring or be the basis of hard conclusions however, this is exactly what the authors of this editorial have so inappropriately and crudely come to. Granted, epidemiological studies do have their place in allowing scientists to understand associations between disease and risk and permit the development of certain hypotheses. They do not however, allow any control over the exposure and so direct causality can never be determined from this kind of work. The present study has leaped from what may have been an appropriate hypothesis to outright concluding causality; the evidence of the current study is by no means strong enough to determine this and in fact there will be many other hypotheses which could counter this argument. For example, at one point in the editorial they conclude that:
“A high protein diet may indicate higher intake of red and processed meat and thus higher intakes of iron, cholesterol and saturated fat. These single factors have previously been linked to a higher risk of major chronic diseases, in observational studies.”

Again they conclude this kind of statement based on an observational study which was published back in 2002 however, a meta-analysis which was published in 2010 (Siri-Tarino et al 2010) by the same group conclude the opposite results of this study stating that there is in fact, “no significant evidence for concluding that dietary saturated fat is associated with increased risk of CHD or CVD”. This further emphasises that how simply agreeing with the conclusion of papers, although it may make interesting and read-worthy news, is not good or responsible scientific practice. To take this one step further and looking at the issue of CVD risk and the most “well-known” risk factor for it being saturated fat, we draw your attention to a study conducted by Volek et al (2008). This study looked to compare the level of saturated fat in the blood of those on an isocaloric fat restricted or carbohydrate restricted diet and what was found, was that those on the low carbohydrate diet had a lower level of saturated fat in the blood, despite having a three-time greater intake compared to those on the low fat arm. Again this and many other pieces of work could easily refute the very broad claims which both authors are trying to make, that following a low-carbohydrate/high protein diet will increase mortality due to increased CVD risk. Likewise data from The Woman’s Health Initiative showed that after 8 years of following a dietary intervention that reduced total fat and increased intakes of fruit, vegetables and grains, did not reduce the risk of CHD or CVD as stated by the editorial (TWHI. 2006).

This takes us one step-further onto the actual study itself which, due to the sensationalised stories and noise around the world which have materialised as a result of it, warrants the in-depth critique of the study. There are many flaws with this study, the first being the actual recording of the food intake of the women participants. The intake was self-reported with no attempt made to assess the validity or accuracy of this. Furthermore, the researchers only took a food frequency at the start of the study and then again at follow-up, 15 years later. This in no way can be a true representation of eating habits over time if at no other time point was intake measured again as it is highly known that at any given time, approximately 40% of women can be trying to lose weight (Ware et al 2003). Secondly, the scoring system which they have employed again only allows for certain assumptions of carbohydrate and protein intake and nowhere does it take into account the quality of either carbohydrate or protein which was actually consumed. It is this scoring system which has allowed for the generalisation and assumption of this editorial, that if people follow the “Atkins” style diet, due to the “dose-response relation” observed, they will have an even higher incidence of CVD and mortality. However, the actual clinical and randomised evidence which exists could easily dispute this claim as it is known that if followed correctly, actual CVD markers and overall risk can be reduced (Nordmann et al 2006; Foster et al 2010). Finally, although the researchers will have adjusted for other risk factors such as smoking and hypertension, there is no way to determine or adjust for the myriad differences which will occur from individual to individual.

In conclusion, the way in which this editorial is written and because it is placed in such a prestigious journal, the impact that it could have may be very damning because of its generalised recommendations to clinicians not to recommend a low-carbohydrate diet. As we well know the figures of obesity are at epidemic proportions and unless we halt the growing trends, the cost to the economy and society, although already great, will likewise reach epidemic proportions. There is enough evidence to indicate that this dietary approach is effective at promoting weight loss and improving many health conditions such as type 2 diabetes (Westman et all 2008), metabolic syndrome (Volek et al 2008) and CVD (Gardner et al 2007), all of which are associated co-morbidities of obesity. We would therefore stress that although this study by Lagiou must be acknowledged and will warrant further studies and investigations, that such conclusions on the safety and efficacy of such diets cannot be concluded.

Competing interests: Go Lower is a commercial diet company based on low carbohydrate principles

The advice against low carbohydrate diets in this editorial is not justified by the article to which it refers. The two commentators misread the evidence and exaggerate its implications.

They contend that the “long term health effects” of such diets override the short-term weight losses that make them so popular. In support, they interpret the article by Lagiou et al as showing “adherence” to such diets over 15 years.

It does no such thing. Even the authors do not claim that. They imply that subjects maintained their low carbohydrate diets, but never say so explicity.

They could not demonstrate “adherence” for a simple reason. They only measured food intakes once, at the beginning of the study. Over the following decade and a half, they never even attempted to assess what subjects were eating.

This is an extreme example of a fundamental problem in most diet studies, the inadequate measurement of food intakes (1). The commentators disregard or fail to see the limitations of the study.

Their comments carry a sharp irony. They dispagage “lay people” who find low carbohydrate diets “appealing”, without having full information about them. They should apply the same standards to themselves.

The flaws in the primary data mean that the Lagiou article does not allow us to draw any conclusions about the long-term effects of low carbohydrate diets, for or against. Thus, the commentators’ conclusions are premature, excessive, perhaps even wrong.

(1) Winkler J, The fundamental flaw in obesity research, Obesity Reviews, (2005), 6, 199-202. jtw@blueyonder.co.uk

Competing interests: None declared

Many studies are suggesting that high-carbohydrate diets, particularly in the form of high-glycemic index load, may activate the sympathetic nervous system with deleterious effects to human health (1). On the other hand, protein or fat ingestion has no significant sympathoexcitatory effect (2,3,4).

Also, sympathetic activation has been linked in several studies to obesity, hypertension, insulin resistance, diabetes, and even atherosclerosis (5, 6).

If the above studies are right, continuing to give support to high carbohydrate diets is both a wrong choice as well bad advice.

References:
1) Koop W. Chronically increased activity of the sympathetic nervous system: our diet-related“evolutionary” inheritance. The Journal of Nutrition, Health & Aging Volume 13, Number 1, 2009
2) Welle S, Ulavivat U, Campell G. Thermic effect of feeding in men: Increased plasma norepinephrine levels following glucose but not protein or fat consumption. Metabolism 1981; 30: 953-958
3) Welle SL, Lilavivathana U,Campell RG. Increased plasma nor epinephrine concentrations and metabolic rates following glucose ingestion in man. Metabolism 1980; 29: 806-09
4) Tentolouris N, Tsigos D, Perea E et al. Differential effect of high-fat and high carbohydrate isoenergetic meals on cardiac autonomic nervous system activity in lean and obese women. Metabolism 2003; 52: 1426-32
5) Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf
6) Book "Acidity Theory of Atherosclerosis: New Evidences", 2012, Amazon.com http://tinyurl.com/7KK4a78

Competing interests: None declared