Sugar and the heart: old ideas revisited
BMJ 2013; 346 doi: https://doi.org/10.1136/bmj.e7800 (Published 15 January 2013) Cite this as: BMJ 2013;346:e7800All rapid responses
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Sir,
Recent attention in the journal on the role of sugar in generating disease is welcome and perhaps overdue. And the re-issue of Yudkin’s book (Pure, white and deadly), which has been almost impossible to obtain until recently is particularly welcome. But by focussing on heart disease and the sugar hypothesis, Truswell’s response to Watts’ ‘Sugar and the heart: old ideas revisited’ has, for me, missed the point (1, 2).
Sucrose in particular, but highly glycaemic carbohydrates in general, appear to be involved in the genesis of Type 2 Diabetes, something not mentioned in his letter but of considerable importance in both western medicine and society. Foods and drinks that evoke excessive glycaemic responses after ingestion, now so consumed so excessively, necessarily evoke a supra-physiological insulin response. Insulin, the hormone of storage, shunts free fatty acids into adipocytes and blocks their release, promoting and maintaining obesity. Insulin in excess is also a cause of Non-Alcoholic Fatty Liver, Polycystic Ovarian Syndrome among other things, and would appear to be the principle underlying driver for the Metabolic Syndrome. An insulin-dominated metabolism promotes an adverse lipid profile and raises triglycerides. Chronic dietary hyperglycaemia is a significant cause of health problems.
I am sure the quality and quantity of fats consumed is important for health, as is exercise and the daily dietary calorific load, but glycaemia and hyper-insulinism may be more important in the long run. Perhaps the rule we all learned during biology lessons at school could be re-written. Insulin is not just the body’s response to increases in blood sugar; it is in fact it’s last defence!
And finally, in response Truswell’s report that Yudkin’s peers were concerned and embarrassment at his hypothesis, I wonder if the colleagues of August Semellweis, James Lind and John Snow shared the same feelings. Sadly prophets as well as charlatans may be a source of embarrassment.
Chris Barclay
GP, Saxmundham, UK.
csbarclay@btinternet.com
Competeing Insterests: none
1. Watts G. Sugar and the heart: old ideas revisited. BMJ 2013;346:e7800 (15 January)
2. Truswell AS. Sugar hypothesis never gathered supportive data. Letters. BMJ 2013;346:f811 (16 February)
Competing interests: No competing interests
Ideas about diet and disease coexist in two worlds, the world of popular culture and myth, and the world of science. Though “sugar causes heart disease” might become a little more fashionable after “Pure, White and Deadly”is reissued, the scientific data and constructs will not change. Evidence for the fat hypothesis is massive and has increased since Yudkin’s book went out of print.
I think Geoff Watts conveys two wrong impressions about John Yudkin’s disappointment that the sugar hypothesis did not get confirmed. I was there. I followed him as head of Nutrition at Queen Elizabeth College, London, in 1971. Yudkin WAS a conviction nutritionist. Most scientists on a government panel on diet and heart disease, after 12 meetings, manage to reach a compromise set of conclusions and recommendations. But the DHSS 1974 Report on Prevention of Coronary Heart Disease [1], which had 13+7 members, has an unusual Note of Reservation by Professor J Yudkin, providing his belief that the Report exaggerated the possible role of dietary fat in causing IHD, and minimized the possible role of dietary sucrose.
The conservatism of this report has been thought to explain why coronary heart disease [CHD] mortality [age standardized] stayed the same in England and Wales until 1978, while it fell substantially from 1964 in USA, Finland, Australia and New Zealand. [2]
The official UK advice was brought in line with growing scientific evidence by the Royal College of Physicians/ British Cardiac Society Working party in 1976. [3]
The sugar hypothesis did not lose its force because of protests by the sugar industry. The more powerful meat and dairy industries were happy with it at the time. The sugar hypothesis simply never gathered supportive data, starting with the fact that sucrose does not ordinarily raise plasma cholesterol and has not been found an independent risk factor for CHD in prospective studies. Leading nutritionists in USA and Europe never took up sugar and CHD. In the UK Yudkin’s peers were concerned and sometimes embarrassed.
By the time the BMJ’s best selling “ABC of Nutrition” was first published in 1986, sugar does not appear in the 4 page chapter, on CHD written for general practitioners .
I think it would have been more useful if Penguin had reissued a different Yudkin classic, “This Slimming Business”[1958]. It’s beautifully written and the messages are [in general] still needed.
A Stewart Truswell
University of Sydney
Email:stewart.truswell@sydney.edu.au
[1] Department of Health and Social Security. Diet and Coronary Heart Disease. Report of the Advisory Panel of the Committee On Medical Aspects of Food Policy [Nutrition] on Diet in relation to Cardiovascular and Cerebrovascular Disease. HM Stationary Office, London.
[2] Mirzaei M, Truswell A S, Taylor R and Leeder S R. Coronary heart disease epidemics: not all the same. Heart 2009;95:740-746.
[3] Report of a Joint Working Party of the Royal College of Physicians of London and the British Cardiac Society. Prevention of Coronary Heart Disease. J Roy Coll Physicians London 1976; 10:213-275.
[4] Truswell A S. ABC of Nutrition. BMJ Books, London, 1986, 1992, 1999, 2003.
Competing interests: No competing interests
We should not forget that Surgeon Captain T L Cleave RN published his book "Diabetes, Coronary Thrombosis and the Saccharine Diseases" in 1966 some five years before that of Professor Yudkin. Surgeon Captain Cleave believed that refined carbohydrates were the underlying cause of many diseases.
Cleave T L. Diabetes, Coronary Thrombosis and the Saccharine Diseases. 1966. John Wright and Sons, London.
Competing interests: No competing interests
The debate about fat or sugar keeps constantly mixing up two different things: prevention of obesity and prevention of cardiovascular disease (1). Too many calories, be it from sugar or fat, lead to overweight. Intake of saturated fat often leads to higher plasma cholesterol level which is a causal factor of atherosclerotic disease.
While overweight and obesity predispose to many ills and ailments, they do not necessarily lead to cardiovascular disease if dyslipidemia and hypertension do not develop (of course they often do).
In Finland the pendulum has indeed swung: decades-long decrease in the population cholesterol levels has stopped, even increased (2). The likely culprit is the strong promotion of low-carb diets curiously promoting an increase of the consumption saturated fat. Sugar industry loses, dairy industry wins, clinical consequences will be seen in the future. I would bet on an increase in cardiovascular disease.
By the way, Ancel Keys included not only saturated fat but also sugar and exercise in his health advice 50 years ago (3). So far, I haven’t discovered better and simpler advice if we want to prevent both cardiovascular disease and obesity.
1. Ornish D. Eating for health, not weight. New York Times, Sunday Review 22 Sep, 2012.
2. Vartiainen E et al. Cholesterol levels in the Finnish population have increased after decades of de-cline Finnish Medical Journal 2012;67:2364
3. Time Magazine, http://www.time.com/time/covers/0,16641,19610113,00.html
Competing interests: No competing interests
Re: Sugar and the heart: old ideas revisited
Dear Editor,
Like John Yudkin, we are sympathetic to his belief that sugar plays an important role as a cause of cardiovascular disease (CVD), and that the official story, popularized by documents such as the most recent 2013 Australian Dietary Guidelines (1), have it wrong. Further, we suggest that the evidence presented in these guidelines actually supports sugar much more so than saturated fat as a cause of CVD, but the authors of the report do not recognise it.
The guidelines emphatically state (p77) that:
“There is no new evidence that sugars play a causal role in the development or moderation of cardiovascular risk factors.”
One study linking serum triglycerides and sugar is referenced from 1972, implying that nothing has been published in the forty years since. Much has been, in fact the reader can find evidence on the same page; yet the authors don’t recognise it as such. The next bullet point offers an example. It describes statistical evidence linking sugar intake with type-2 diabetes, itself a well-known risk factor for CVD:
“However, more recent studies indicate that sugar-sweetened drinks may increase the risk of developing type 2 diabetes.762 A recent meta-analysis also supports an increased risk of type 2 diabetes and the metabolic syndrome from consumption of sugar-sweetened drinks.”
Later, the authors report that sugar is likely to cause dental caries, apparently isolated from other diseases. However, dental decay, in observational studies, is strongly associated with cardiovascular disease (2) and diabetes (3). In a Finnish case-control study, for example, the mean number of teeth among cases with angiographically confirmed coronary heart disease was 8.8 (standard deviation (SD)=9.1) compared with 17.0 (SD=10.5) among age and gender matched surgery patients from the same hospital catchment (4). In the CVD group, 35% of patients were edentulous, compared to 14% of controls. This difference was not explained by smoking, since the prevalence of this behaviour was very similar in both groups. We have argued in previous publications (5,6) that sugar intake is likely to act as a confounder of the relationship between dental decay and cardiovascular disease, since indices of sugar intake have been linked directly to both conditions (figure).
Evidence which links sugar intake with CVD has been reported elsewhere (5). Although some of the evidence here was published after the date of studies which were available to the guideline writing team (2009), the majority were available, yet were not reported. To briefly summarise, an American cohort study found a positive association between intake of sugared drinks and incident coronary heart disease (7). Statistical evidence of association is also found between indices of sugar intake and other diseases or risk factors for CVD: such as gout, hyperuricaemia (8), raised blood pressure (9) and dyslipidaemia (10).
In the guidelines, however, the authors have already allocated this role, that is the dietary cause of CVD, to another dietary factor. They state that:
“The evidence indicates that replacing dietary saturated fat with monounsaturated and polyunsaturated fats is associated with improved blood lipid profiles and reduced risk of cardiovascular disease”.
However, as the authors point out, apart from the link between saturated fat and low density lipoprotein cholesterol, itself a relatively weak risk factor for CVD, there is little other evidence with which to support their assertion.
Specifically, they state that no study shows evidence linking hypertension with fat intake (of any type). Similarly, the guideline writing team found little evidence to support the notion that reducing saturated fat improves biochemical indices of diabetes. Then, they pointed to evidence that replacing saturated with poly and monounsaturated fats reduces diabetes risk, referenced the 2010 U. S. dietary guidelines (11). But they seemed unable to cite the original studies. Neither could we, after thoroughly searching the American guideline. The authors also agreed that no evidence linked reducing dietary fat to weight loss.
From this brief treatment, and like another author today (12), or Yudkin over 40 years ago (13), we believe that overwhelming evidence supports excess sugar intake as a leading dietary cause of CVD and its risk factors, over that which implicates saturated fat. The authors of these recent Australian guidelines are swimming against an accumulating tide of studies which contradict their stance. In fact, the evidence presented in their own document undermines their position. By pointing out these inconsistencies, our hope is that debate about this important subject is informed by reasoned use of evidence rather than selective and inaccurate reporting. With such contradictions, another section of the report, which reads:
“Health professionals and the public can be assured that the process of assessing the scientific evidence provides for the best possible advice.”
has a distinctly hollow ring. John Yudkin was ignored then, and now, with peril.
References
1. National Health and Medical Research Council. Australian Dietary Guidelines. Canberra: National Health and Medical Research Council., 2013.
2. Scannapieco FA, Bush RB, Paju S. Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. Ann. Periodontol. 2003;8(1):38-53.
3. Loe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care 1993;16(1):329-34.
4. Janket S-J, Qvarnstrom M, Meurman JH, Baird AE, Nuutinen P, Jones JA. Asymptotic Dental Score and Prevalent Coronary Heart Disease. Circulation 2004;109(9):1095-100.
5. Thornley S, Tayler R, Sikaris K. Sugar restriction: the evidence for a drug-free intervention to reduce cardiovascular disease risk. Intern. Med. J. 2012;42 Suppl 5:46-58.
6. Thornley S, McRobbie H, Jackson G. The New Zealand sugar (fructose) fountain: time to turn the tide? N. Z. Med. J. 2010;123(1311):58-64.
7. de Koning L, Malik VS, Kellogg MD, Rimm EB, Willett WC, Hu FB. Sweetened beverage consumption, incident coronary heart disease, and biomarkers of risk in men. Circulation 2012;125(14):1735-41, S1.
8. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ 2008;336(7639):309-12.
9. Winkelmayer WC, Stampfer MJ, Willett WC, Curhan GC. Habitual caffeine intake and the risk of hypertension in women. JAMA 2005;294(18):2330-5.
10. Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB. Caloric Sweetener Consumption and Dyslipidemia Among US Adults. JAMA: The Journal of the American Medical Association 2010;303(15):1490-97.
11. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary guidelines for Americans, 2010. 7th Edition. Washington DC: U.S. Government Printing Office, 2010.
12. Hu FB. Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity-related diseases. Obes. Rev. 2013;14(8):606-19.
13. Yudkin J. Sugar consumption and myocardial infarction. The Lancet 1971;297(7693):296-97.
Competing interests: No competing interests