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"Sugar Industry and Coronary Heart Disease Research/A Historical Analysis of Internal Industry Documents" Cristin E. Kearns, Laura A. Schmidt, and Stanton A. Glantz, JAMA Intern Med. 2016 Nov 1; 176(11): 1680–1685.Results
SRF’s [Sugar Research Foundation] Interest in Promoting a Low-Fat Diet to Prevent CHD Sugar Research Foundation president Henry Hass’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet:...
If the carbohydrate industries were to recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.
The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.” ..
Growing Evidence That Sucrose Elevates Serum Cholesterol Level
... Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”
... Finally, here commended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.” ...
SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD
... Nine months into the project, in April 1966, Hegsted told the SRF that the review had been delayed because of new evidence linking sugar to CHD: “Every time the Iowa group publishes a paper we have to rework a section in rebuttal [emphasis added].”44 The “Iowa group” included Alfredo Lopez, Robert Hodges, and Willard Krehl, who had reported a positive association between sugar consumption and elevated serum cholesterol level.
Discussion
These internal documents show that the SRF initiated CHD research in 1965 to protect market share and that its first project, a literature review, was published in NEJM in 1967 without disclosure of the sugar industry’s funding or role. The NEJM review served the sugar industry’s interests by arguing that epidemiologic, animal, and mechanistic studies associating sucrose with CHD were limited, implying they should not be included in an evidentiary assessment of the CHD risks of sucrose. Instead, the review argued that the only evidence modality needed to yield a definitive answer to the question of how to modify the American diet to prevent CHD was RCTs that exclusively used serum cholesterol level as a CHD biomarker. Randomized clinical trials using serum cholesterol level as the CHD biomarker made the high sucrose content of the American diet seem less hazardous than if the entire body of evidence had been considered.
Following the NEJM review, the sugar industry continued to fund research on CHD and other chronic diseases “as a main prop of the industry’s defense.”51 For example, in 1971, it influenced the National Institute of Dental Research’s National Caries Program to shift its emphasis to dental caries interventions other than restricting sucrose.8 The industry commissioned a review, “Sugar in the Diet of Man,” which it credited with, among other industry tactics, favorably influencing the 1976 US Food and Drug Administration evaluation of the safety of sugar.51 These findings, our analysis, and current Sugar Association criticisms of evidence linking sucrose to cardiovascular disease6,7 suggest the industry may have a long history of influencing federal policy.
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"The fructose–copper connection: Added sugars induce fatty liver and insulin resistance via copper deficiency", James J. DiNicolantonio, Dennis Mangan, James H. O'KeefeThe overconsumption of sugar may be one of the biggest drivers of NAFLD.4 Several factors may be involved in sugar-driven NAFLD, including bacterial translocation from the gut to the liver and advanced glycation end products.8 However, low hepatic copper levels are also implicated in NAFLD; thus sugar consumption can lead to low copper.9 This suggests that the overconsumption of sugar may lead to NAFLD and insulin resistance via hepatic copper deficiency.
In a rat model of NAFLD, dietary sucrose and copper deficiency increased inflammation, fibrosis and lipogenesis.9 Compared to a control diet in which rats were fed with sufficient copper and 10% sucrose, either a high-sucrose diet or a low copper diet increased the hepatic expression of genes regulating inflammation and fibrosis. The low copper diet led to low serum and hepatic copper, increased lipid peroxidation and histopathology similar to that found in NAFLD. The combined low copper and high sugar diet led to all of these changes as well as hepatic insulin resistance and liver damage, but neither low copper nor high sugar caused weight gain. Low copper and high sugar promoted gene expression and physiological processes typical of NAFLD as well as non-alcoholic steatohepatitis (NASH) even without weight gain.
The fructose component of dietary sucrose, in particular, can induce copper deficiency. In rats, a diet of only 3% fructose from beverage intake – a rather modest fructose consumption that is lower than typical intake of Americans – impaired copper status and led to a significant induction of hepatic injury, iron overload and fat accumulation.10 Therefore, fructose-induced copper deficiency could be an important mechanism behind fructose-induced NAFLD. Ultra-high consumption of fructose is not necessarily required for fructose-induced fatty liver with levels lower than the average American consumption capable of inducing it in rats.
Abstract
In animal studies, sugar has been found to produce more symptoms than is required to be considered an addictive substance. Animal data has shown significant overlap between the consumption of added sugars and drug-like effects, including bingeing, craving, tolerance, withdrawal, cross-sensitisation, cross-tolerance, cross-dependence, reward and opioid effects. Sugar addiction seems to be dependence to the natural endogenous opioids that get released upon sugar intake. In both animals and humans, the evidence in the literature shows substantial parallels and overlap between drugs of abuse and sugar, from the standpoint of brain neurochemistry as well as behaviour.
The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show.
The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry.
“They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA Internal Medicine paper.
The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat.
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In 1965, Mr. Hickson enlisted the Harvard researchers to write a review that would debunk the anti-sugar studies. He paid them a total of $6,500, the equivalent of $49,000 today. Mr. Hickson selected the papers for them to review and made it clear he wanted the result to favor sugar. Harvard’s Dr. Hegsted reassured the sugar executives. “We are well aware of your particular interest,” he wrote, “and will cover this as well as we can.”
Abstract
Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in theNew England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.
...
RESULTS
SRF’s Interest in Promoting a Low-Fat Diet to Prevent CHD
Sugar Research Foundation president Henry Hass’s 1954 speech, “What’s New in Sugar Research,”12 to the American Society of Sugar Beet Technologists identified a strategic opportunity for the sugar industry: increase sugar’s market share by getting Americans to eat a lower-fat diet: “Leading nutritionists are pointing out the chemical connection between [American’s] high-fat diet and the formation of cholesterol which partly plugs our arteries and capillaries, restricts the flow of blood, and causes high blood pressure and heart trouble… if you put [the middle-aged man] on a low-fat diet, it takes just five days for the blood cholesterol to get down to where it should be… If the carbohydrate industries were to recapture this 20 percent of the calories in the US diet (the difference between the 40 percent which fat has and the 20 percent which it ought to have) and if sugar maintained its present share of the carbohydrate market, this change would mean an increase in the per capita consumption of sugar more than a third with a tremendous improvement in general health.”12
The industry would subsequently spend $600 000 ($5.3 million in 2016 dollars) to teach “people who had never had a course in biochemistry… that sugar is what keeps every human being alive and with energy to face our daily problems.”12
...
The SRF’s vice president and director of research, John Hickson, started closely monitoring the field.15
In December 1964, Hickson reported to an SRF subcommittee15 that new CHD research was a cause for concern: “From a number of laboratories of greater or lesser repute, there are flowing reports that sugar is a less desirable dietary source of calories than other carbohydrates, eg,—Yudkin.”15 Since 1957, British physiologist John Yudkin16 had challenged population studies singling out saturated fat as the primary dietary cause of CHD and suggested that other factors, including sucrose, were at least equally important.17,18
Hickson proposed that the SRF “could embark on a major program” to counter Yudkin and other “negative attitudes toward sugar.”15 He recommended an opinion poll “to learn what public concepts we should reinforce and what ones we need to combat through our research and information and legislative programs” and a symposium to “bring detractors before a board of their peers where their fallacies could be unveiled.”15 Finally, he recommended that SRF fund CHD research: “There seems to be a question as to whether the [atherogenic] effects are due to the carbohydrate or to other nutrient imbalance. We should carefully review the reports, probably with a committee of nutrition specialists; see what weak points there are in the experimentation, and replicate the studies with appropriate corrections. Then we can publish the data and refute our detractors.”15
In 1965, the SRF asked Fredrick Stare, chair of the Harvard University School of Public Health Nutrition Department19 to join its SAB as an ad hoc member.20 Stare was an expert in dietary causes of CHD and had been consulted by the NAS,1 National Heart Institute,21 and AHA,22 as well as by food companies and trade groups.19 Stare’s industry-favorable positions and financial ties would not be widely questioned until the 1970s.23
....
SRF Funds Project 226: A Literature Review on Sugars, Fats, and CHD
On July 13, 1965, 2 days after the Tribune article, the SRF’s executive committee approved Project 226,31 a literature review on “Carbohydrates and Cholesterol Metabolism” by Hegsted and Robert McGandy, overseen by Stare.10 The SRF initially offered $500 ($3800 in 2016 dollars) to Hegsted and $1000 ($7500 in 2016 dollars) to McGandy, “half to be paid when you start work on the project, and the remainder when you inform me that the article has been accepted for publication.”31 Eventually, the SRF would pay them $650032 ($48 900 in 2016 dollars) for “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose.”31
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Is sugar dangerous because it’s calories? Or because it’s sugar?
...we took the added sugar away from 43 obese children who were already sick, to see if they got well. But if they lost weight, critics would argue that the drop in calories or the loss in weight was the reason for their improvement. Therefore, the study was “isocaloric”; that is, we gave back the same number of calories in starch as we took away in sugar, to make sure they maintained their weight.
For nine days we catered their meals to provide the same fat, protein, and total carbohydrate content as their home diet; but within the carbohydrate fraction we took the added sugar out and substituted starch. We took the pastries out, we put the bagels in; we took the yoghurt out, we put the baked potato chips in; we took chicken teriyaki out, we put turkey hot dogs in. We gave them processed food – kid food – but “no added sugar” food. We reduced their sugar consumption from 28% to 10% of their calories. They weighed themselves every day; if they were losing weight, we told them to eat more.
We were astonished at the results. Diastolic blood pressure decreased by five points. Blood fat levels dropped precipitously. Fasting glucose decreased by five points, glucose tolerance improved markedly, insulin levels fell by 50%. In other words we reversed their metabolic disease in just 10 days, even while eating processed food, by just removing the added sugar and substituting starch, and without changing calories or weight. Can you imagine how much healthier they would have been if we hadn’t given them the starch?
This study establishes that all calories are not the same (“a calorie is not a calorie”); substituting starch for sugar improved these children’s metabolic health unrelated to calories or weight gain.
In spite of these difficulties, such studies have already shown that sucrose, in proportions within the range found in current human dietaries, produces an increase in plasma lipids, uric acid, insulin and cortisol; abnormalities in platelet behavior; reduction in glucose tolerance; tissue resistance to insulin; damage to the liver and the kidney, and an increase in lipid in the aorta.
It is our opinion that the potential mechanisms underlying the epidemic should be carefully reappraised. On the basis of both he experimental studies performed in our laboratories and an extensive review of the literature, we revisit an old hypothesis hat a simple dietary substance may have a significant role in driving the epidemic. Interestingly, reappraising the role of sugar nd its influence in the development of cardiorenal disease may lead to a new understanding of why certain populations, such as African Americans, Native Americans, Maori, and Australian Aborigines, are at greater risk of developing the disease. Similar to the relation between high intakes of salt or protein and the risk of developing kidney disease or to the relation between a high-fat diet and the atherosclerotic phenotype, we propose that sugars containing fructose may play a major role in the development of hypertension, obesity, and the metabolic syndrome and in the subsequent development of kidney disease. Although physical inactivity and overeating are major contributors to the obesity epidemic, we present evidence that fructose may be the "caries" to the epidemic’s root.
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One unique aspect of fructose is that it is the only sugar that raises uric acid concentrations, and this can be shown in both humans (56) and rodents (57). Fructose enters hepatocytes and other cells (including tubular cells, adipocytes, and intestinal epithelial cells), where it is completely metabolized by fructokinase with the consumption of ATP; unlike in glucose metabolism, there is no negative regulatory mechanism to prevent the depletion of ATP. As a consequence, lactic acid and uric acid are generated in the process, and uric acid concentrations may rise by 1–4 mg/dL after the ingestion of a large fructose-based meal (58). Although the rise in uric acid concentrations has historically been viewed as simply a potential risk factor for inducing gout, recent studies suggest that this may be a key mechanism to explain how fructose causes cardiovascular disease. In addition, it also provides a mechanism to explain why rodents are relatively resistant to the effects of fructose (see below).
FRUCTOSE-INDUCED HYPERURICEMIA AS A MECHANISM FOR CARDIORENAL DISEASE
Nakagawa et al (51) recently showed in experimental animals that lowering uric acid concentrations could largely prevent features of the metabolic syndrome induced by fructose, including weight gain, hypertriacylglycerolemia, hyperinsulinemia and in-
sulin resistance, and hypertension. The protective effect of lowering uric acid concentrations on the development of the metabolic syndrome was shown regardless of whether the uric acid concentrations were lowered by using a xanthine oxidase inhibitor or a uricosuric agent (51). These studies were surprising, because most authorities had considered uric acid to be either biologically inert or an important antioxidant in the plasma (59). However, uric acid was found to have numerous deleterious biologic functions. For example, uric acid stimulates both vascular smooth muscle cell proliferation and the release of chemotactic and inflammatory substances (60–62), induces monocyte chemotaxis (63), inhibits endothelial cell proliferation andmigration (64, 65), and causes oxidative stress in adipocytes, which results in the impaired secretion of adiponectin (66).
In animals, the effect of elevated uric acid concentrations is even more pronounced. For example, mildly hyperuricemic rats develop hypertension because of the inhibition of nitric oxide synthase in themacula densa, the stimulation of intrarenal renin, and a reduction in endothelial nitric oxide bioavailability (67). Over time, hyperuricemic rats develop renal arteriosclerosis that then causes the animals to develop a salt-sensitive form of hypertension.
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WHY ARE AFRICAN AMERICANS SUSCEPTIBLE TO CARDIOVASCULAR DISEASE?
It is well known that African Americans have higher rates of obesity, hypertension, diabetes, kidney disease, and heart disease. ... Recent studies also have documented that the sugar intake of African Americans is greater than that of whites (110, 111). Similar high sugar intakes were noted in studies of Australian Aborigines and Samoans living in New Zealand (112,113). Furthermore, it is known that African Americans have higher concentrations of uric acid (114); in the African American Study of Hypertension and Kidney Disease, the average uric acid concentration was 8.3 mg/dL (115).
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If the hypothesis is correct that fructose has a role in the epidemic of cardiovascular disease, then a number of predictions should arise from future studies. First, fructose intake will be a risk factor for hypertension, insulin resistance, hypertriacylglycerolemia, obesity, type 2 diabetes, preeclampsia, chronic kidney disease, stroke, cardiovascular disease, and mortality. Second, reducing uric acid in patients with uric acid concentrations [greater than] 6.0 mg/dL will improve endothelial dysfunction, decrease systemic vascular resistance, lower blood pressure, lower triacylglycerol concentrations, improve body weight, lower the risk of the progression of renal disease, and reduce cardiovascular disease risk. Third, low-fructose diets coupled with mild purine restriction will improve weight and reduce cardiovascular disease risk. Fourth, fructokinase will be identified as a key enzyme mediating the cardiorenal disease syndrome; genetic polymorphisms will be associated with cardiovascular disease risk, and blocking the enzyme will provide a novel way to prevent cardiorenal disease. Clearly, much more work needs to be done to prove or disprove this hypothesis.
