What if sugar is worse than just empty calories? An essay by Gary Taubes
BMJ 2018; 360 doi: https://doi.org/10.1136/bmj.j5808 (Published 04 January 2018) Cite this as: BMJ 2018;360:j5808
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Although excessive sugar is considered unhealthy, this article does not make the case that sugar is the only major etiological dietary factor for type 2 diabetes or ischemic heart disease. Neither is the case made that saturated fat and a high fat intake do not play a major role in these diseases. Perhaps a more scientific article would be better received or at least we could hear the arguments from the other side of the debate. This article is very one sided and lacks any convincing evidence.
"What can be asserted without evidence can also be dismissed without evidence" to quote Christopher Hitchens.
Competing interests: No competing interests
There are many factual errors and misrepresentations in this text, staring with the sugar being the prime suspect. Taubes refers to a text authored by Emerson and Larimore that examines the relationship between diabetes and pre- and post-war food consumption. He states they blamed sugar, and produces this quote: “’Rises and falls in sugar consumption,’ Emerson and Larimore wrote, ‘are followed with fair regularity . . . by similar rises and falls in the death rates from diabetes.’” However, in the text the authors make clear that sugar is actually NOT the prime suspect: “The food shortage expressed itself not so much in the lack of sugar and carbohydrates as in lack of fats, which should make one suspect that it is not the quality but the gross quantity of food (calories) that plays the chief part in development of a high diabetes death rate in a community where more food is eaten than is required.” So, the sugar shortage, in effect, was the shortage of all foods. Sugar consumption was used only as a proxy. This is repeated in the text: “One index of the tendency of our people to use larger amounts of food is the record of per capita consumption of sugar, which is offered here not as an explanation of the increased death rates from diabetes in recent years, but more as a sign of the tendency to excesses in the use of foods of all kinds, beyond the needs of persons for foods in proportion to their expenditure of energy at the different ages of life, and in particular in the later decades.” (1) If any prime suspect is fingered by the authors, it is the difference in physical activity between those that have diabetes and those that do not. This point is brought up many times in the text and is the closing sentence from Emerson.
Taubes then makes a series of leaps that go from fructose is lipogenic to sugar is the cause of diabetes: “and from there, by this hypothesis, to the insulin resistance that is the fundamental biochemical disturbance in type 2 diabetes.” Note that the statement sugar causes diabetes is explicitly claimed and cited with appropriate evidence but it is assumed for the duration of the editorial, and Taubes poses questions of why sugar was missed until recently when he wrote The Case Against Sugar claiming so.
Taubes writes: “By 1993, the American Journal of Clinical Nutrition dedicated an entire issue to the possible deleterious effects of sugar consumption. “Further studies are clearly needed to determine the metabolic alteration that may take place during chronic fructose or sucrose feeding,” the Swiss physiologists Luc Tappy and Eric Jéquier wrote. This research still needs be done” In fact, the entire issue was not dedicated to sugar consumption, only the supplements were dedicated to fructose, and indeed there is an article in that very supplement titled Diabetes and Fructose Metabolism that states: “In summary, detrimental effects of fructose on carbohydrate metabolism were not reported in any of these studies, and there may be a beneficial effect short-term.” (2) And another article titled The Public Health Significance of Dietary Fructose that concludes “On the basis of currently available information, as reviewed in this monograph, fructose is a valuable, traditional source of food energy, and there is no basis for recommending increases or decreases in its use in the general food supply on in special dietary use products.” (3)
“[I]f the hypothesis that the fructose content of sugar and high fructose syrups makes them uniquely toxic is found to be correct then the dietary prescriptions of the past 40 years have been very wrong.” What advice? Have the dietary guidelines recommended increasing intakes of high fructose corn syrup? Have doctors been telling their patients they need to eat more sugar?
In the article Taubes states that industry was too involved in research, that long-term human trials need to be conducted, it’s difficult to tease out the role of weight loss vs sugar, and research needs to focus on “hard endpoints such as mortality and cardiovascular events.” Immediately after this statement Taubes declares that “diabetes can be reversed” in low-carb diets, and cites a study that was funded by Atkins Nutritionals, is only 10 weeks in length, did not examine CVD or death but instead looked at HBA1c, and where the patients lost significant weight so it’s impossible to tell if the weight loss contributed more to the HBA1c levels that the low-carb diet. Nevertheless, Taubes states “This is consistent with the hypothesis that sugar is a cause of diabetes.”
In the sidebar, Taubes takes some potshots at Joslin and Himsworth stating: “So a population that ate a carbohydrate rich diet and had low rates of diabetes provided compelling reason to believe, so Joslin argued, that sugar was not a cause. (Neither Joslin nor Himsworth apparently considered the fact that the Japanese diet also contained relatively little sugar.) Actually, Himsworth did consider the Japanese. (4)
Also in the sidebar, Taubes states “By 1985 the guidelines stated dogmatically that ‘too much sugar in your diet does not cause diabetes.’” I don’t know what is dogmatic about that statement, considering it was based on the available evidence at the time, and is still consistent with the scientific literature.
1. Emerson H, Larimore L. Diabetes mellitus: A contribution to its epidemiology based chiefly on mortality statistics. Arch Intern Med [Internet]. 1924 Nov;34(5):585–630. Available from: http://dx.doi.org/10.1001/archinte.1924.00120050002001
2. Gerrits PM, Tsalikian E. Diabetes and fructose metabolism. Am J Clin Nutr [Internet]. 1993 Nov;58(5):796S–799S. Available from: http://ajcn.nutrition.org/content/58/5/796S
3. Glinsmann WH, Bowman BA. The public health significance of dietary fructose. Am J Clin Nutr [Internet]. 1993 Nov;58(5):820S–823S. Available from: http://ajcn.nutrition.org/content/58/5/820S
4. Himsworth HP. Diet and the incidence of diabetes mellitus. Clin Sci. 1935;2:117–48.
Competing interests: No competing interests
Gary Taubes came back against the dominant paradigm in nutrition. Let’s have a look at this crusade.
1/ Despite campaigns against obesity and T2D, epidemiology demonstrated that more children and adults are overweight or diabetic. This is not only a US issue, it occurs in every country where access to food is cheap and industrial foods available. The story is known and physicians usually reiterate their advice without great conviction. Their feedback is often irrational because of poor education on this topic. They usually incriminate excess of calories, lack of exercise or non-observance of dietary guidelines. However, both the majority of patients and health professionals agree on one point: fat is the culprit. Therefore people reduced their fat intake. By the way, since meat fed with corn has an increase fat content and/or is cooked with fat, they reduce meat consumption. Statistics showed it (http://www.bmj.com/content/348/bmj.g2272). Exceptions exist. Since WWII Japan kept essential of its food model. Switzerland and France followed the same path. This is associated with high life expectancy, less obesity and CVD. But if Japanese diet is high in fish, seafood, omega 3 fatty acids and algae and low in calories, it is not the case of those European countries with low CVD rates, where saturated fats from fermented cheeses and meats are largely consumed. One can conclude that those people have had a lot of good sense to avoid the state policies that are not efficient elsewhere and that present dietary guidelines don’t work.
2/ "Saturated fats are the ones in your belly and arteries". We heard that from our mom and our faculty. Tough to eat a butter cuck without culpability. Indeed science helps:
- saturated fats are neutral for CVD and even associated with a lower rate of stroke (http://ajcn.nutrition.org/content/91/3/535.long ). There is no convincing evidence that fat leads to weight gain. No major difference exists between the source of saturated fats despite the fact that small differences exist according to the main fatty acids in terms of blood profile.
- industrial trans fats are very harmful for health. They increase CVD, distort blood lipid profile and increase the incidence of metabolic syndrome.
- fats in their matrix (it is the whole food which contains it) appear to be not only essential for some of them but very efficient in terms of energy needs and metabolism signalling. So fat is not the culprit of the present diabesity epidemic as dietary fat does not go in your belly or arteries, fat goes in your liver and its fate depends on a lot of factors. Fat does not make your body store energy nor your brain eat more of it.
3/ In this long time lapse since WWII a huge increase in wealth allowed a historical downfall of food prices. Calories intake increased and expenditure fell with mechanisation and sitting. The sum increases but this positive balance hides a distortion. Carbohydrates increased more than those from other groups of nutrients through different incentives (for instance: external one is added sugar in industrial products and internal one the trend of compulsory eating that follows pure sugar consumption). I don't buy the idea that calories don't matter, but we have solid evidence that a calorie is not a calorie. Our body is not a calorimeter but a set of billions of cells specialised in complex tasks, communicating together and receiving signals from outside and inside. Food is signalling through hormones. And one important food signalling in our environment is the rise of insulin after carbohydrates intake (http://journals.lww.com/co-endocrinology/Abstract/2012/04000/What_causes... ). This pathway is very linked to survival in times of food scarcity. The final result is a chronic increase of insulin in the setting of low exercise which leads to more storage than in the past. This mechanism is modulated by genomics and some people are more sensitive to insulin than others. Wealth and abundance play a major role in obesity and T2D but once more time there is a distortion because of the sugary wave.
4/ Carbohydrates or sugar? Taubes is right to emphasize the role of sugar in the US obesity epidemic. Sugary foods and beverages are everywhere in the US diet. Elsewhere other carbs are involved. Especially the refined ones present in industrial products like breakfasts and desserts. Taubes is right to point out this nutrient and to vilify it instead of empty calories. Indeed the metabolic signal and addictive behaviour attached to pure sugar are at the first rank in the diabesity epidemics because it drives the body in a permanent state of storage with no risk of future famine (http://clinchem.aaccjnls.org/content/clinchem/64/1/192.full.pdf ). But does Gary Taubes harden the line? On the contrary, I found him prudent, as he asks for clinical well-designed studies. Indeed when we look at low carbohydrate diet studies it is very disappointing. Either they are not low carb, or they are too short or they are about too few people or they measure only lipid parameters... For sure, we need quality studies. On the other hand, numerous physicians all over the world are advising their family, their related and themselves to follow a low carb diet. Not because they are foolish, but because they have strong anecdotal evidence about this. In this setting we have to think of glycemic load and not only amount of added sugar per a day.
5/ Is the train of sugar hiding other trains? Is Taubes "radicalised" about sugar? An open editorial is not the place to be too cautious or too soft. However, empty calories do matter and one can interestingly complete his advice to avoid sugar by an ancestral approach of diet as advocated by Cordain in Paleo diet or even recently Campbell in Whole.
Finally, it is urgent to conduct alternatives studies on carbohydrates and fat in human diet and to upgrade the knowledge based on those results in order to teach correctly medical students and current medical doctors. This knowledge should be put in perspective with evolutionary data and present trends of chronic diseases. It is why this editorial helps.
Competing interests: Authors eat mainly a whole food diet, practice different sports weekly and are involved in the treatment of CVD.
I ask as I am ignorant.
Has anyone published any account of frequency - or scantiness - of
1. Diabetes
2. Obesity
3. Dental caries
over the past five or six scores of years in
a. British Guyana, Guyana
b. Surinam
c. Jamaica
d) Trinidad
e) Northern Pakistan area where sugar cane is grown
d) North Western India where sugar cane is grown.
In the areas noted ahove, I guess the farmers and others engaged in the trade of sugar cane did not and may be still do not wait for sugar " sugar, pure, white and deadly" to reach them in packets. They do, perhaps consume sugar cane juice as mood takes them ( squeezed in the jaws, or in an okd-fashioned machine, or use "Shakkar" or "Gur".
Hoping for enlightenment
JK Anand
Competing interests: No competing interests
In the article in BMJ current issue, Gary Taubes writes: "This research (Stanford University, my note!), mostly in animals, supported John Yudkin’s contention that consuming large doses of sugar could cause a cluster of metabolic abnormalities that associate with heart disease: insulin resistance and type 2 diabetes, hepatic lipogenesis, dyslipidaemia, ectopic fat accumulation, and perhaps visceral fat accumulation as well.9".
This is my question: "Do you think that consuming large doses of sugar could cause a cluster of metabolic abnormalities that associate with heart disease in all individuals, rather than possibly in subjects involved by relative constitution-dependent, Inherited Real Risk, I've discovered 20 years ago?".
Sergio Stagnaro and Simone Caramel. Inherited Real Risk of Type 2 Diabetes Mellitus: bedside diagnosis, pathophysiology and primary prevention. Front Endocrinol (Lausanne). 2013; 4: 17. Published online 2013 Feb 26. doi: 10.3389/fendo.2013.00017 http://www.frontiersin.org/Review/ReviewForum.aspx [MEDLINE]
Stagnaro S., West PJ., Hu FB., Manson JE., Willett WC. Diet and Risk of Type 2 Diabetes. N Engl J Med. 2002 Jan 24;346(4):297-298. [MEDLINE]
Sergio Stagnaro and Simone Caramel. The Key Role of Vasa Vasorum Inherited Remodeling in QBS Microcirculatory Theory of Atherosclerosis. Frontiers in Epigenomics and Epigenetics. http://www.frontiersin.org/Epigenomics_and_Epigenetics/10.3389/fgene.201... [MEDLINE]
Sergio Stagnaro and Simone Caramel. The Inherited Real Risk of Coronary Artery Disease, Nature PG., European Journal of Clinical Nutrition 67, 683 (June 2013) | doi:10.1038/ejcn.2013.37 [MEDLINE]
Caramel S., Marchionni M., Stagnaro S. Morinda citrifolia Plays a Central Role in the Primary Prevention of Mitochondrial-dependent Degenerative Disorders. Asian Pac J Cancer Prev. 2015;16(4):1675. http://www.ncbi.nlm.nih.gov/pubmed/25743850 [MEDLINE]
Stagnaro Sergio. Epidemiological evidence for the non-random clustering of the components of the metabolic syndrome: multicentre study of the Mediterranean Group for the Study of Diabetes. Eur J Clin Nutr. 2007 Feb 7; [MEDLINE]
Stagnaro Sergio. Pre-Metabolic Syndrome, Classic And Variant, Precedes For Decades The Metabolic Syndrome. April20, 2009. http://sciphu.com, and at URL http://wwwshiphusemeioticscom-stagnaro.blogspot.com/
Stagnaro Sergio. Pre-Metabolic Syndrome and Metabolic Syndrome: Biophysical-Semeiotic Viewpoint.International Atherosclerosis Society. www.athero.org, 29 April, 2009. http://www.athero.org/commentaries/comm904.asp
Stagnaro S., Singh RB. Influence Of Nutrition On Pre-Metabolic Syndrome And Vascular Variability Syndrome. Editorial, The Open Nutrition Journal. Bentham Sci. Publish. Nutraceuticals Journal, 2009, Volume 2, http://www.benthamscience.com/open/tonutraj/articles/V002/118TONUTRAJ.pdf
Competing interests: No competing interests
Dear editor
in this article by Gary Taubes there is an explicit argument and an implicit argument. The explicit argument resumes the author's theories set out in his book “The case against sugar”. This argument, reflected in the title, can be summed up as Gary Taubes refers to sugar as the perfect culprit and the sole cause of almost all the diseases (obesity, diabetes cardio-vascular diseases) that afflict humanity today.
The perfect culprit is a bit like the panacea or the magic bullet. It’s somewhat simplistic. But life, nature and science are complex.
But if sugar, and carbohydrates are the only culprits then we can exonerate all other causes, and that is the implicit argument. The implicit argument is revealed in sentences like this:” Evidence suggests that when people severely restrict carbohydrate intake–not just sugars, but also grains and starchy vegetables–diabetes can be reversed or disappears.”
There we are, and in reality Gary Taubes is defending the same theories as in his book “ Godd Calorie Bad Calories” about the low carb high fat (LCHF) diet.
Since the whole argumentation is based on narrative rather than rigorous and solid science, we must ask ourselves the following question: can we trust Gary Taubes' rigorous interpretation of the authors he quotes?
For me the answer would be no. And I base this opinion on a careful review of this author's books, made by someone who has a degree in nutrition and who took care to check the references in support of the author's assertions [1].
In this review the author shows that the book from Gary Taubes is full of contradictions, omissions, incomplete citations, false quotes and sophisms.
I will not go into details, everyone can read.
For this reason, and since we already know that eating too much sugar is not a healthy diet I think this article does not add anything to the current debate about the origin of the epidemic of obesity, diabetes and cardiovascular disease.
[1] https://thescienceofnutrition.wordpress.com/tag/gary-taubes/
Competing interests: No competing interests
A most interesting debate. Would it be useful to study a cohort of people with stable normal BMI and high refined sugar diet and explore their incidence of Type 2 diabetes ? Should be simple to allow for population risk factors and other lifestyle factors. It seems that obesity obscures the study of dietary sugars since it has a indendent drive on endocrine disturbance and lipid metabolism.
Competing interests: No competing interests
I disagree with Gary Taubes, whom I hold in the highest regard. Let’s analyze this physiologically rather than epidemiologically. The slippery slope between “associated” and “caused” is all too familiar.
Glucose:
Mr. Taubes speaks of “disassociating any deleterious effect of sugar from that of the calories it contains,” but is not alarmed by fructose’s seemingly amiable companion - glucose. After all, those beta cells done in by diabetes are designed to cope with glucose, not fructose.
Conventionally, type 2 diabetes is attributed to obesity and to insulin resistance. In fact, some go so far as to say that insulin resistance is type 2 diabetes. However, while insulin resistance does cause higher blood glucose, it is not the root problem; it is dead beta cells that are the irreversible and progressive essence of type 2 diabetes. Insulin resistance is just reversible adaptations to too much blood glucose, too often; causing chronically overstuffing of muscle cells and the liver’s glucose fuel tank. Insulin resistance was branded the villain in Type 2 diabetes because it seemed disease-like, while the ubiquitous consumption of dietary carbs (glucose) seemed natural.
Obesity so often catches the eye when seeing type 2 diabetes patients that the association seems causal, but many have tried to physiologically connect obesity to type 2 diabetes, without success. One does not cause the other, but they have a common progenitor, dietary glucose, both in quantity and in transient peak effects.
Human evolution expects almost all glucose to be released little by little from the liver, just as needed. So blood glucose never rises very much or very fast and our beta cells are never overtaxed. But, when you eat carbs, blood glucose rises massively and quickly, triggering massive and quick insulin secretion; and even transient peaks, unknown during evolution, seem like massive glucose loads to beta cells which then try to respond with excess insulin production. Insulin resistance in liver and muscles further aggravates this by requiring even more insulin to force in even more glucose.
This threatens the very survival of our beta cells. The main trigger of apoptosis is failure of a cell to perform its function, but requiring beta cells to massively and quickly secrete insulin tempts them into failure and triggers apoptosis. Most type 2 diabetes beta cells have suffered apoptosis - that is diabetes.
If, eight hours after eating, the pancreas is unable to supply enough insulin to push fasting blood glucose below 90, there must be few surviving beta cells - and each of those few survivors now are asked to secrete even more insulin. Thus an avalanche effect, fewer beta cells, more asked from each cell, faster apoptosis - progressively worsening diabetes.
Treatment: Over the course of one month, reduce carbs to near zero. Rescue failing beta cells by injecting insulin during their recovery.
Fructose:
This indictment of glucose in type 2 diabetes does not let fructose off the hook in NAFLD and atherosclerosis. Fructose causes de novo lipogenic production of VLDL (triglycerides) which cause fatty liver, and, with the help of CETP, produces small, dense LDL particles capable of piercing the arterial endothelium and, with contributions from the immune system, atherosclerosis.
Chronically excessive glucose may have a similar effect - stay tuned.
Adapted (with too little context) from my paper in progress, “Unified Physiology of Obesity and the Metabolic Syndrome.”
Competing interests: No competing interests
Re: What if sugar is worse than just empty calories? An essay by Gary Taubes
A recent extensive systematic review and meta-analysis resulted in 44% increase in coronary heart disease (CHD) for people whose daily dietary glycemic load (GL) got increased by only 65 gr.
Reference
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6410335/
Competing interests: No competing interests