Fructose-copper connection

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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'Keefe

Quote:

The 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.

Fat and cholesterol-heart disease theory - worldwide hoax perpetrated by American Sugar Association!

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This is now official, documents found and published! If one thinks about the implications, scale and the length of time, it would probably not be surprizing if this were followed by some some serious Crime Against Humanity type investigation against the officials that were involved, and named!

NY Times: How the Sugar Industry Shifted Blame to Fat

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.”

JAMA paper: Sugar Industry and Coronary Heart Disease Research
A Historical Analysis of Internal Industry Documents

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.

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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

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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

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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

Just a spoonful of sugar (with CO2) helps the medicine go down

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http://en.wikipedia.org/wiki/Sugar

http://ajph.aphapublications.org/doi/abs/10.2105/AJPH.2014.302151

Quotes:

Objectives. We tested whether leukocyte telomere length maintenance, which underlies healthy cellular aging, provides a link between sugar-sweetened beverage (SSB) consumption and the risk of cardiometabolic disease.
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Results. After adjustment for sociodemographic and health-related characteristics, sugar-sweetened soda consumption was associated with shorter telomeres (b = –0.010; 95% confidence interval [CI] = −0.020, −0.001; P = .04). Consumption of 100% fruit juice was marginally associated with longer telomeres (b = 0.016; 95% CI = −0.000, 0.033; P = .05). No significant associations were observed between consumption of diet sodas or noncarbonated SSBs and telomere length.
Conclusions. Regular consumption of sugar-sweetened sodas might influence metabolic disease development through accelerated cell aging. (Am J Public Health. Published online ahead of print October 16, 2014: e1–e7. doi:10.2105/AJPH.2014.302151)

Notice the lack of correlation for non-carbonated sugar-sweetened beverages!

More on the carbohydraty poison, today's news.  Skim milk anyone?

Quote:

In women the adjusted mortality hazard ratio for three or more glasses of milk a day compared with less than one glass a day was 1.93 (95% confidence interval 1.80 to 2.06). For every glass of milk, the adjusted hazard ratio of all cause mortality was 1.15 (1.13 to 1.17) in women and 1.03 (1.01 to 1.04) in men. For every glass of milk in women no reduction was observed in fracture risk with higher milk consumption for any fracture (1.02, 1.00 to 1.04) or for hip fracture (1.09, 1.05 to 1.13). The corresponding adjusted hazard ratios in men were 1.01 (0.99 to 1.03) and 1.03 (0.99 to 1.07). In subsamples of two additional cohorts, one in males and one in females, a positive association was seen between milk intake and both urine 8-iso-PGF2α (a biomarker of oxidative stress) and serum interleukin 6 (a main inflammatory biomarker).

Interestingly, detrimental effects seem to be related to the milk lactose contents rather than fat or proteins, because consumption of milk products that are high in fat and lower in lactose, such as fermented milk, cheese or cream, seem to correlate with more favorable biomarkers profile.

Comparing milk with other dairy products
Particularly noteworthy is that intake of fermented milk products such as yogurt and soured milk and cheese were associated with lower rates of fracture and mortality. Furthermore, we observed a positive association only between milk intake and markers of oxidative stress (urine 8-iso-PGF2α) and inflammation (serum interleukin 6). Previously, we found a negative relation between bone mineral density and 8-iso-PGF2α.42 63 Interleukin 6 seems to be causally related to cardiovascular disease64 and may influence bone loss and osteoporosis.65 Importantly, those who consume high amounts of non-fermented milk have a more non-favourable cardiovascular risk factor profile, with higher blood pressure, lower high density lipoprotein cholesterol levels, and higher insulin resistance.18 In contrast, intake of cheese and fermented milk products is related to higher high density lipoprotein cholesterol levels, less insulin resistance, and a lower risk of myocardial infarction.18 22 23 24 In addition, a recent small randomised cross over study indicated that the intake of a fermented dairy diet seemed to provide a more favourable biomarker profile than that of a non-fermented dairy diet.66

46% sugar diet causes breast cancer...

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Underfunded Scientists Force Lipstick-Covered Rat With Cancer To Run Through Maze

... in mice, as medical "scientists" have recently discovered in this study.   Strangely, that is not what they officially concluded, that's why I put the word in quotes!   The lethal mice diet consisted of 46% of sugar (31% sucrose + 10% maltodextrin + 5% dextrin), 21% of milk fat and 19% of casein.   Read more about that in this post by Denise Minger.

Heretic

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"... a flea without legs cannot jump when told, because it cannot hear - concluded the leading biologist Professor Lysenko"  (old Soviet joke) 

"You need a computer to obfuscate things properly but to really foul things up you need a scientist!" (anonymous, 1960-ties)