Are some diets “mass murder”?
BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g7654 (Published 15 December 2014) Cite this as: BMJ 2014;349:g7654
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Richard Smith’s article Are some diets “mass murder”? uses a work of a popular commentator to reach his conclusions in this article.
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Smith’s conclusion that Teicholz demolishes the saturated fat hypothesis fails with just a little scrutiny. Below are several paragraphs from Smith’s editorial, followed by a brief commentary.
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Teicholz begins her examination by pointing out that the Inuit, the Masai, and the Samburu people of Uganda all originally ate diets that were 60-80% fat and yet were not obese and did not have hypertension or heart disease.
According to Teicholz, Mann found that “he could identify almost no heart disease at all” in the Maasai. Mann’s paper, Atherosclerosis in the Masai, stated, “Measurements of the aorta showed extensive atherosclerosis with lipid infiltration and fibrous changes but very few complicated lesions. The coronary arteries showed intimal thickening by atherosclerosis which equaled that of old U.S. men.” [1] Smith’s and Teicholz’s assertion that heart disease was non-existent in the Maasai is clearly false.
* * * * *
<<“[Keys is] possessing a very quick, bright intelligence” but also “direct to the point of bluntness, and critical to the point of skewering.” >>
The actual quote from Blackburn is “Ancel Keys has a quick and brilliant mind, a prodigious energy, and great perseverance. He can also be frank to the point of bluntness, and critical to the point of sharpness.” [2] Blackburn’s words of “can be” has been transformed into “as being”. Participants in the Minnesota starvation experiment spoke of Keys’s compassion.
* * * * *
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According to Truswell, USA male mortality reached its peak in 1967 or 1968 – 15 years after Teicholz claims. Truswell also states that heart disease reached its peak in 1978 in England and Wales and Scotland in 1973. [3] These dates are nowhere near the unsupported date of 1952 as claimed be Teicholz.
Smith is confusing the later Seven Countries Study with Keys’s minor discussion paper of 1953. Keys did not gather the data for this paper but used data from a number of existing sources.
Y&H criticised the 1953 paper in a document published in 1957. [4]
The Y&H paper (which uses FAO data from 1951-1953 that was published in 1956) shows the correlation between heart disease and total calories consumed, animal fat consumption and animal protein consumption at approximately 70%. They were disputing the classifications of heart disease and Keys’s methodology – not the lack of correlation.
Even if data from all the 22 countries are included, it still shows:
• positive correlations between heart disease and total calories consumed, fat consumption, animal fat consumption, and animal protein consumption, and
• negative correlations with heart disease and carbohydrate consumption, vegetable protein consumption, and vegetable fat consumption.
The above correlations are clearly noted in Y&H’s paper.
Note that Keys first presented his discussion paper in Amsterdam in 1952 which is before the time that the data used by Y&H was available.
Tobacco is not mentioned in this paper. Possibly Smith and Teicholz are confused by a later disagreement that Yerushalmy had with researchers who claimed that women who smoked had lower birth-weight infants. He suggested that smoking was not the cause of low-birth weight but the result of “mode of life” differences between the smoking population and non-smoking populations.
In recent years, far too much attention is paid to one page of a discussion paper written in the early 1950s. Keys writes, “the fact that the present high rate from degenerative heart disease in the United States is not inevitable is easily shown by the comparison with some other countries.” This was the purpose of the paper.
The comment that Keys could have gathered data from many more countries and people (women as well as men) obviously refers to Keys’s later Seven Countries Study – not the 1953 discussion paper. Keys explained why women were not involved – the invasiveness of the physical examinations and the fact that heart disease is much less prevalent in women.
An average of 95.9% of all eligible men participated in the Seven Countries Study — excluding the cohorts in the Netherlands and the U.S.
* * * * *
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Banting was 165 cm tall and weighed 92 kg at the start of his high-fat, low-carbohydrate diet. Over twelve months he lost 21 kg resulting in a weight of 76 kg. It was a big improvement but not exactly slim. He is still overweight with a BMI of 28.
Smith states that the Ornish Diet requires fewer than 10% energy from saturated fat. This simple view assumes that a criteria for a healthy diet is defined by the macronutrient ratio by energy intake. A person consuming a whole-food, plant-based diet as advocated by Ornish will consume about 10% fats, 10% protein and 80% carbohydrate. This diet will also be high in fibre, phytonutrients and low in saturated fats. Added oils are absent.
The Gardner study [5] referenced by Smith completely misrepresented the Ornish Diet. The diet consumed by the participants comprised of 52% carbohydrate, 30% fat and 52% carbohydrate. The amount of fibre consumed was very low at 19.3 g/d. Ornish wrote a letter to the editor of the journal complaining about the misrepresentation of his diet but it was not published.
* * * * *
Unfortunately, both Smith and Teicholz have numerous mistakes, For example, Teicholz describes cholesterol as being “yellow”—it is white. Lent is a 40-day period – not 48 days as described by Teicholz.
From the conclusion of The Big Fat Surprise, Teicholz proclaims:
< Moreover, we now know that there are many good reasons to eat animal foods like red meat, cheese, eggs, and whole milk: they are particularly dense in nutrients— far more so than fruits and vegetables. […] And after all, red meat, cheese, and cream are delicious! Not to mention eggs fried in butter, cream sauces, and the drippings from a pan of roasted meats.>> * * * * * According to Ancel Keys, who originated the term, the best Mediterranean diet is “almost vegetarian (or lactovegetarian)” and consists of “pasta in many forms, leaves sprinkled with olive oil, all kinds of vegetables in season, and often cheese, all finished off with fruit, and frequently washed down with wine.” * * * * Perhaps Smith’s conclusion could be extended to, “it’s surely time for better science and for humility among popular commentators.” [1] Mann, G. V. et al. (1972) Atherosclerosis in the Masai. American Journal of Epidemiology. 95 (1), 26. [2] Truswell, A. S. (2010) Cholesterol and Beyond: The Research on Diet and Coronary Heart Disease 1900-2000. Sections 31.1, 31.4 [3] Yerushalmy, J. & Hilleboe, H. E. (1957) Fat in the Diet and Mortality from Heart Disease. New York State Journal of Medicine. 57 (14), 2343–2354. [4] Gardner, C. D. et al. (2007) 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. 297 (9), 969–977. [5] Keys, A. (1995) Mediterranean diet and public health : personal reflections. American Journal of Clinical Nutrition. 61 (6), 1321S–1323S.
Blackburn, H. (n.d.) Ancel Keys - by Henry Blackburn, MD [online]. Available from: http://mbbnet.umn.edu/firsts/blackburn_h.html.
Competing interests: Author of Low-Carbohydrate Mania: The Delusions, Myths and Fantasies
In his thoughtful commentary on “mass murder by diet” 1, Richard Smith implied that much of the blame for the harmful increase in carbohydrate intake was attributable to the promotion of the Cretan Mediterranean diet by Ancel Keys.
However, the Mediterranean diet put forward by Keys is not a low-fat diet at all; it is a diet high in beneficial fat (~40% of calories from fat, mainly olive oil)2, low in harmful animal fat and cholesterol, high in fruits, vegetables and legumes; and with its focus on whole grains, it is a low glycemic diet.
Saturated fat by itself is much less harmful than saturated fat when consumed in combination with cholesterol: dietary cholesterol has a permissive effect on the adverse effects of saturated fat on fasting lipids3. So analyzing saturated fat on its own is overly simplistic. This has been called the “bacon and egg effect”4: the bacon is much more harmful when consumed with egg yolk. (One large egg yolk contains more than the 200 mg daily intake of cholesterol recommended for patients at risk of cardiovascular events5.)
The biggest problem with much of what is written about diet is a misplaced focus on fasting lipids. Diet is about the post-prandial state, which occupies about 2/3 of the day6. Much of this misplaced focus results from the sustained propaganda campaign of the egg industry following their conviction for false advertising4. To understand this, please view the videos to which links are shown below.
The high carbohydrate intake that Smith rightly points out is a problem resulted not from promotion of the Mediterranean diet, but from the endorsement by the American Heart Association of the low-fat diet, pulled, as Willett and Stampfer said, from thin air2, by a committee trying to design a diet that would lower fasting cholesterol levels.
In the Israeli diet study7 comparing a Cretan Mediterranean diet with a low-fat diet and a low-carbohydrate diet, the Mediterranean diet was much better in diabetics than either a low-fat or a low-carb diet – there was a greater reduction of fasting blood glucose, insulin and insulin resistance on the Mediterranean diet. Furthermore, weight loss was better than on the low-fat diet, and identical, on the Mediterranean diet and low carbohydrate diet.
A low-carb diet that is high in cholesterol and saturated fat would truly result in mass murder by diet.
Video links:
http://nutritionfacts.org/video/eggs-and-cholesterol-patently-false-and-...
http://nutritionfacts.org/video/eggs-vs-cigarettes-in-atherosclerosis/
http://nutritionfacts.org/video/egg-cholesterol-in-the-diet/
http://nutritionfacts.org/video/how-the-egg-board-designs-misleading-stu...
Also see: http://www.athero.org/commentaries/comm1145.asp
References
(1) Smith R. Are some diets "mass murder"? BMJ 2014; 349:g7654.
(2) Willett WC, Stampfer MJ. Rebuilding the food pyramid. Sci Am 2003; 288(1):64-71.
(3) Fielding CJ, Havel RJ, Todd KM, Yeo KE, Schloetter MC, Weinberg V et al. Effects of dietary cholesterol and fat saturation on plasma lipoproteins in an ethnically diverse population of healthy young men. J Clin Invest 1995; 95(2):611-618.
(4) Spence JD, Jenkins DJ, Davignon J. Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease. Can J Cardiol 2010; 26(9):e336-e339.
(5) Reiner Z, Catapano AL, De BG, Graham I, Taskinen MR, Wiklund O et al. ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur Heart J 2011; 32(14):1769-1818.
(6) Spence JD. Fasting lipids: the carrot in the snowman. Can J Cardiol 2003; 19:890-892.
(7) Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008; 359(3):229-241.
Competing interests: No competing interests
Dear Editor
I commend the BMJ on publishing more debate on dietary advisories in ‘Are some diets “mass murder”?’ by Richard Smith. He has penned papers such as ‘Medical Journals Are an Extension of the Marketing Arm of Pharmaceutical Companies’ which is relevant to diet related disease. More and more medication is prescribed to treat the risk markers (not causes) of hypertension, dyslipidaemia and hyperglycaemia for diabetes, liver, and cardiovascular (CV)and neurodegenerative diseases, and cancer. Nutraceuticals, vitamins as well as medication is sold to manage obesity. There is less and less emphasis on real, high nutrient food as being preventative of, and probably able to ameliorate, much obesity related metabolic syndrome (MetS).
However, although Smith’s overall ideas, and those of the popular and scientific authors he cites probably lie in the correct direction, none acknowledges some very basic and highly likely scientific theory about diet in humans.
It would seem eminently sensible, and remiss not to start, to look at human evolution and most importantly to review the metabolic oddities that we find in large brained human mammals1.
Evidence that humans have evolved some intriguing interrelated pathways in energy metabolism2 and micronutrient nutrition3 4, including fat turnover and storage5, should not come as surprise to scientists. Furthermore unique human brain neurotransmitter biology6 relates to strong behavioural drives for finding or producing energy dense food, and in fact for ‘perseveration’ in many human endeavours. These factors together should indicate that reliance on studies of small nocturnal, short-lived, rodents (lab rats and mice) which are bred or engineered to live outside their natural habitat, will not yield appropriate science on diets for humans.
Once humans got to the stage of devising and building technology that changed their physical, chemical and dietary environment, development tended to proceed under pressure from technology-commodity driven industry. Evidence again indicates that once humans started farming, approximately 10,000 years ago7, energy dense, preserveable, rather than nutrient dense, food was produced and traded, and human health and robustness declined8 9.
As Smith’s articles allude to, the current food and drug industry has picked up parts of medical science that it can profit from and dissuaded researchers from pursuing solid, hypothesis driven biological science, using basic principles, such as Bradford Hill’s criteria10 11.
Ironically, the science on appropriate food for humans has largely been undertaken, albeit accidentally, in studies where the right questions were not asked and results poorly interpreted; we just have to apply real scientific hypothesis and start from the beginning of this science – human evolution - which we can now do12 13. Studies on human diet and health can no longer be single-item, reductionist, randomised controlled trials (RCT) alone.
Smith has critiqued a meta-analyses of RCT type studies, which commonly do not produce clear results, when the questions of what was studied, and how, were not appropriate. He has spent much time in the past, when he was the BMJ editor involved in investigating a single researcher in India, who was at least investigating a difficult area (multi-nutrient food effects on cardiovascular health) in difficult conditions before the correct tools were developed, and at worst fabricating data.
In fact, a more robust meta-analysis of high nutrient, low toxicity diets 14, and studies of the traditional Mediterranean diet 15-30, along with systems modelling that are starting to be used in energetics and epidemiology of nutrition31 show that whole food diets will likely lead to improved health at the population level. Further evolutionary and epidemiological data collection, together with prospective clinical and community studies, and human physiological studies all augmented with sophisticated mathematical systems modelling, is urgently required.
Oddly, the free internet has now become a repository of extremes – well thought out science that the major journals rarely publish, and crackpot opinion. These are what the public read – and many people can see the value of pre-agricultural forager type-diets for conferring health. Increased efforts are being made by some to move to ‘paleo diets’.
However, high nutrient, uncontaminated, whole food based diets will likely suffice if it is the nutrient density that is important, and this is the scientific debate that public health researchers and policy makers need to air in high profile journals, without industrial interference.
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5. Cunnane SC, Crawford MA. Survival of the fattest: fat babies were the key to evolution of the large human brain. Comp. Biochem. Physiol. 2003;136(1):17-26.
6. Shumay E, Fowler JS, Volkow ND. Genomic features of the human dopamine transporter gene and its potential epigenetic states: Implications for phenotypic diversity. PLoS ONE 2010;5(6):1-17.
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8. Mummert A, Esche E, Robinson J, Armelagos GJ. Stature and robusticity during the agricultural transition: Evidence from the bioarchaeological record. Econ. Hum. Biol. 2011;9(3):284-301.
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10. Hill AB. The Environment and Disease: Association or Causation? Proc. R. Soc. Med. 1965;58:295-300.
11. Phillips CV, Goodman KJ. Causal criteria and counterfactuals; nothing more (or less) than scientific common sense. Emerg Themes Epidemiol 2006;3:5.
12. McGill A-T. Past and future corollaries of theories on causes of metabolic syndrome and obesity related co-morbidities part 2: a composite unifying theory review of human-specific co-adaptations to brain energy consumption. Arch. Public Health 2014;72(1):31.
13. McGill A-T. Causes of metabolic syndrome and obesity-related co-morbidities Part 1: A composite unifying theory review of human-specific co-adaptations to brain energy consumption. Arch. Public Health 2014;72(1):30.
14. Barański M, Średnicka-Tober D, Volakakis N, Seal C, Sanderson R, Stewart GB, et al. Higher antioxidant and lower cadmium concentrations and lower incidence of pesticide residues in organically grown crops: a systematic literature review and meta-analyses. Br. J. Nutr. 2014;112(05):794-811.
15. Grosso G, Pajak A, Mistretta A, Marventano S, Raciti T, Buscemi S, et al. Protective role of the Mediterranean diet on several cardiovascular risk factors: evidence from Sicily, southern Italy. Nutrition, metabolism, and cardiovascular diseases : NMCD 2014;24(4):370-7.
16. Busko M. Mediterranean Diet Reverses Metabolic Syndrome in PREDIMED. Medscape.com 2014;October (14):http://www.medscape.com/viewarticle/833218_print.
17. Estruch R, Ros E, Salas-Salvadó J, Covas M-I, Corella D, Arós F, et al. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. N. Engl. J. Med. 2013;DOI: 10.1056/NEJMoa1200303.
18. Issa C, Darmon N, Salameh P, Maillot M, Batal M, Lairon D. A Mediterranean diet pattern with low consumption of liquid sweets and refined cereals is negatively associated with adiposity in adults from rural Lebanon. Int. J. Obes. 2011;35(2):251-8.
19. Tangney CC, Kwasny MJ, Li H, Wilson RS, Evans DA, Morris MC. Adherence to a Mediterranean-type dietary pattern and cognitive decline in a community population. Am. J. Clin. Nutr. 2010;93(3):601-7.
20. Elhayany A, Lustman A, Abel R, Attal-Singer J, Vinker S. A low carbohydrate Mediterranean diet improves cardiovascular risk factors and diabetes control among overweight patients with type 2 diabetes mellitus: a 1-year prospective randomized intervention study. Diabetes Obes. Metab. 2010;12(3):204-09.
21. Esposito K, Maiorino M, Ciotola M, Palo CD, Scognamiglio P, Gicchino M, et al. Effects of a Mediterranean-Style Diet on the Need for Antihyperglycemic Drug Therapy in Patients With Newly Diagnosed Type 2 Diabetes - A Randomized Trial. Ann. Intern. Med. 2009;151:306-14.
22. Caudwell P, Hopkins M, King NA, Stubbs RJ, Blundell JE. Exercise alone is not enough: weight loss also needs a healthy (Mediterranean) diet? Public Health Nutr. 2009;12(9A):1663-6.
23. Mackenbach JP. The Mediterranean diet story illustrates that "why" questions are as important as "how" questions in disease explanation. J. Clin. Epidemiol. 2007;60(2):105-9.
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26. Gerber M. Biofactors in the Mediterranean diet. Clin. Chem. Lab. Med. 2003;41(8):999-1004.
27. de Lorgeril M, Salen P, Martin JL, Monjaud I, Boucher P, Mamelle N. Mediterranean dietary pattern in a randomized trial: prolonged survival and possible reduced cancer rate.[see comment]. Arch. Intern. Med. 1998;158(11):1181-7.
28. De Lorgeril M, Salen P, Martin JL, Mamelle N, Monjaud I, Touboul P, et al. Effect of a mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease. Insights into the cardioprotective effect of certain nutriments.[see comment]. J. Am. Coll. Cardiol. 1996;28(5):1103-8.
29. Ulijaszek SJ. Human dietary change. Philos. Trans. R. Soc. Lond. B Biol. Sci. 1991;334(1270):271-8; discussion 78-9.
30. Dunn FL. Epidemiological Factors: Health and Disease in Hunter-Gatherers. In: Lee R, DeVore I, editors. Man the Hunter. Chicago Aldine, 1968.
31. Leonard WR, Ulijaszek SJ. Energetics and evolution: an emerging research domain. Am. J. Hum. Biol. 2002;14(5):547-50.
Competing interests: No competing interests
I'm trying to come to grips with this as an educated lay person. I'm used to seeing good hypothesis move to theory through the incremental increase in experimental data, a good theory being improved as decimal places of precision are added, interesting corner cases being discovered and elaborated but everybody knowing that these are the edges not the big fat middle.... This is science!
After reading the article and reading the responses I'm more confused with the state of affairs than ever the only facts I can glean from all this are :
* If people followed worlds best dietary advice they would have reduced morbidity and mortality from heart disease and some cancers.
* Almost nobody in the west can or will follow worlds best dietary advice.
* Eating any manufacturers pre-prepared food will mean you are not following best dietary advice.
* The original studies were flawed and legislators were pushed into before a benefit could be clearly shown.
* Some of the original recommendations for replacements of animal fats were later shown to be far worse than animal fats.
* The concept of disproving the null hypothesis is lost on both sides of the argument and everybody is cherry picking data to support there position.
* The signal to noise ratio may be too low to with regard to animal fats and heart disease to call, if a link is made it will be in the small percentages not a doubling (or for smoking a 9 to 1 increase in lung cancer : ~20db = really clear signal)
* Large food manufactures, acting in their own best interests, made things worse (trans fats?)
So the big question to the community :
* When choosing what form of excess calories I should have in my tasty treat, which is least bad, simple carbs (aka sugar) or animal fats? The article suggests animal fats now appear to be less bad than sugar. Is this correct, currently unknown, or a bald faced lie that is currently fashionable in our science hating anti-vaxer world.
Competing interests: No competing interests
The Mediterranean diet has passed the tests of long-term sustainability, nutritional adequacy, and clinical effectiveness demonstrated in long-term randomized trials using hard clinical end-points (myocardial infarction, stroke, cardiovascular death).[1]
Please double-check in detail the reference on the Mediterranean diet that you are using. Despite belonging to a collaboration that I regard in high consideration, it is severely flawed. Suffice it to say that they excluded the most important studies and, even worse, they included studies that in no way represent the traditional Mediterranean diet. The highest weight in that meta-analysis was given to a study that never claimed to use a "Mediterranean-type" diet.
A more balanced international review on the definition and the potential health benefits of the Mediterranean diet [2] can be found in:
http://www.biomedcentral.com/1741-7015/12/112
References
1. Martínez-González MA, Salas-Salvadó J, Estruch R. Intensive lifestyle
intervention in type 2 diabetes. N Engl J Med. 2013;369:2357.
2. Trichopoulou A, Martínez-González MA, Tong TY, Forouhi NG, Khandelwal S,
Prabhakaran D, Mozaffarian D, de Lorgeril M. Definitions and potential health
benefits of the Mediterranean diet: views from experts around the world. BMC Med.
2014;12:112.
Competing interests: No competing interests
Richard Smith’s article1 draws attention to the paucity of evidence supporting the arguments of those advocating dietary change. One dietary change that did have a pronounced impact was that taking place during the Mesolithic-Neolithic transition in which the change from a hunter-gatherer to an agricultural mode of food production had profound effects on the nutrition and disease susceptibility of the population concerned2.
Members of genus Homo had evolved a hunter gatherer lifestyle over a two million year time period and study of extant hunter gatherers suggests that Mesolithic man’s access to game meat would have resulted in a greater intake of animal protein than would have been available to Neolithic society3.
The Neolithic farmers who entered central Europe around 7500 BP4 achieved rapid population increase, made possible by an increasingly positive energy balance due to the high calorie mostly cereal diet of relatively sedentary farmers compared to the more low calorie food of mobile foragers5. However, this was often associated with a decrease in health status as demonstrated by the increase in evidence of nutritionally based diseases seen in many early Neolithic skeletons6 2.
Although the lifestyle of Neolithic farmers has been described as “sedentary” in comparison to that of Mesolithic hunter-gatherers5 and we do not know the effect, if any, either would have had on the incidence of cardiovascular disease, both lifestyles would have been be likely to involve far greater calorie expenditure than that of twenty first century European man.
1. Smith, R. Gastroenterological tracts: Are some diets mass murder? BMJ 2014,349:g7654
2. Harper, K., Armelagos, G. The changing disease-scape in the third epidemiological transition. Int. J. Environ. Res. Public Health 2010; 7:675-697.
3. Gluckman, P., Beedle, A., Hanson, M. Principles of evolutionary medicine. Oxford: Oxford University Press, 2009; 182-191.
4. Price, T.D., Bentley, R.A., Luning, J., Gronenborn, D., Wahl, J. Prehistoric human migration in the Linearbandkeramik of central Europe. Antiquity 2001; 75:593-603.
5. Bocquet-Appel, J-P. (2011) When the world’s population took off: the springboard of the Neolithic demographic transition Science 2011; 333:560-561
6. Wittwer-Backofen, U., Tomo, N. From health to civilization stress? In search for traces of a health transition during the early Neolithic in Europe. In: Bocquet-Appel, J-P., Bar-Yosef, O., eds. The Neolithic Demographic Transition and its Consequences. Dordrecht: Springer, 2008; 501-538.
Competing interests: No competing interests
It is disappointing to see the BMJ publish a paper largely based on a bestselling diet book rather than solid scientific information.
Competing interests: No competing interests
Many thanks to Dr. Richard Smith for his wonderful paper published on Feature section last 15th December. We recommend to read it to all BMJ family members around the globe. To read it, it’s a good form of ending this 2014th year. We want to take this opportunity for thanking to all members of the BMJ Editorial Staff for their continuous helping to us during all this year, and for wishing them Merry Christmas and Happy New Year. The best for you and yours!
We think that is better to direct the accusation of “mass murderers” nor to diets but to those barbaros, unscrupulous people, scientists, salesmen, big food manufacturers, governments, and associations, who promote through massive information and communication media or through political processes bad changes in human behavior or diets and lifestyles based on fragile science to poor and bad illustrated in health societies. That kind of advertisement is absurd, unacceptable; it’s a complete horror in the humanism new world era.
Although it’s very difficult to measure the association between a bad diet and chronic disease Basic Biochemistry gives us the necessary elements for understanding that for instance the excessive intake of carbohydrates or the organic over saturation with alcohol, at long term, produces substantial damage, mainly in the normal functioning of the nervous system, and must lead to terrible bad outcomes such as heart disease or stroke. Mass adoption of bad cultures in health lead to increases in blood triglycerides, cholesterol, and other lab parameters, that are good markers of chronic diseases. We think that is one of the main problems suffering by our contemporary society; that is another form of massive violence. It is something like mental, emotional, institutional violence. Its final effect is similar to that produced by a killer or a terrorist against society, but at long term. It is a disaster as a flood or a tsunami that destroys the people bodies little by little. As consequence of the corrupt promotion made by those death’s merchants people don’t immediately die; the daily consumption of insane bad foods, of very low biological value cause suffering to people for many years, an evil living and lead them to an inevitable death. The number of victims caused by the traditional and classical social violence is nothing in comparison with the number of illnesses, diseases, and deaths caused as a logical result of bad publicity in health, and the promotion of insane diets and lifestyles.
It is urgent and indispensable to make a good quaternary prevention against those wild acts, harmful to the human mind and body, acts that buy the people dreams, hopes and desires for ever living healthy, acts that ravage large world populations. Educational authorities must play an important role in quaternary prevention. It is necessary to educate better people in health aspects, from preschool to higher education. It is also important to create serious control entities that daily look for the people’s security and ensure them a life with dignity.
Competing interests: No competing interests
In response to Dr. Cooper. The NEJM reference is Medline 17554120 and where the authors explain the 50-54% age-adjusted U.S. coronary heart disease [CHD] mortality rate drop between 1980 and 2000 by putting the old culprits, interventions and drugs into a statistics package. They generously credit the medical world for about half that drop and the balance to other reduced "risk factors". This is a bizarre exercise. It does not explain why women had rates 50% lower than men in 1980 and in 2000. Didn't women have the same diets, conventional risk factors and medical care?
Not considered was the fact that women during their reproductive years [the time period when men experience much of the decline of their arterial structure] have much lower homocysteine [~10%, U.K. NDNS V4 2004 T 4.21], a risk factor totally ignored as potentially causal but one that declined during that period, especially in the U.S.
In the "risk factor" categories they attribute 44% of the reduced mortality rate to about 5% lower cholesterol and blood pressure levels. Based on what evidence does that save lives? Is blood pressure a result of declining arterial function or a cause thereof; is it chicken or egg? There has never been a placebo controlled cholesterol or blood pressure trial in women that ever found a mortality benefit. In population studies, people over age 50 in the bottom quartile for cholesterol tend to die first while cholesterol is found not to be a risk factor for CHD death in women [Medline 15006277].
Clearly this statistical exercise, having to explain a massive amount of "deaths prevented or postponed" LACKED variables.
That some with PCSK9 loss-of-function mutations [allowing better internalization of that nutrient emulsion particle called LDL] live with less CHD is interesting [reference?] but I predict that the ongoing "K9" injectable inhibitor trials will save nobody; The jury is out, far out.
A 2015 update: in 2412 Norwegian heart patients 5 yr follow-up: total coronary events RR=0.83 in the top saturated fat quartile and RR=1.02 for all cause deaths, vs quartile 1, multivariate adjusted. Nothing significant. [doi 10.3945/jn.114.203505]
Competing interests: No competing interests
Re: Are some diets “mass murder”?
1. I see that so far Dr Smith has not responded to any of the criticisms in the rapid responses.
2. Nobody has considered the possibility that SOME of us may prefer dying of heart attacks rather than of, say, a painful cancer.
3. I am 85. I shall continue to eat (as I have done all my life) as much and whatever I feel like, and until satiety prevails.
( I have known very brief episodes of hunger when no food was available).
I am not fat. Indeed I am slim.
4. No one has considered (or at least voiced the possibility) that some fat persons (not just fat, female, fecund immortalised in gall-stone surgery) might have inherited their peculiar metabolism.
5. No one has considered the possiblity that in some people, indeed in some populations, a prolonged period of deprivation followed by surfeit for a long period might have resulted in first, an altered metabolism, followed by excess intake (purely psychological, a fear of return of deprivation) for a long period, then an established habit of over-eating. I have known people who passed through such phases. Some ended up with diabetes (the mellitus variety).
6. No one has considered the possibilty that SOME long-lived populations in the apricot rich, goat herding areas of Central Asia, where wheat too used to be in short supply and people subsisted on millet to make up the meal did not have the Mediterranean olive oil. Nor fish. Besides apricots they also had mulberries, Goats supplied meat, milk, LIVE yoghurt.
Never been there myself. And now they may all be eating steak, chips, and drinking champagne. Their life-span might now be more like that of the French in NICE?
Competing interests: No competing interests