Abstract
Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.
Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.
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| Based on Wiki Eye |
Diets high in refined starches such as breads and cereals increase insulin levels. This affects the development of the eyeball, making it abnormally long and causing short-sightedness, suggests a team led by Loren Cordain, an evolutionary biologist at Colorado State University in Fort Collins, and Jennie Brand Miller, a nutrition scientist at the University of Sydney.
The theory could help explain the dramatic increase in myopia in developed countries over the past 200 years. It now affects 30 per cent of people of European descent, for example.
“The rate of starch digestion is faster with modern processed breads and cereals,” says Brand Miller. In response to this rapid digestion, the pancreas pumps out more insulin. High insulin is known to lead to a fall in levels of insulin-like binding protein-3, the team points out.
That could disturb the delicate choreography that normally coordinates eyeball lengthening and lens growth. And if the eyeball grows too long, the lens can no longer flatten itself enough to focus a sharp image on the retina, they suggest.
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But while reading may play a role, it does not explain why the incidence of myopia has remained low in societies that have adopted Western lifestyles but not Western diets, says Cordain.
“In the islands of Vanuatu they have eight hours of compulsory schooling a day,” he says, “yet the rate of myopia in these children is only two per cent.” The difference is that Vanuatuans eat fish, yam and coconut rather than white bread and cereals.
The theory is also consistent with observations that people are more likely to develop myopia if they are overweight or have adult-onset diabetes, both of which involve elevated insulin levels. The progression of myopia has also been shown to be slower in children whose protein consumption is increased.
Journal reference: Acta Ophthalmologica Scandinavica (vol 80, p 125)
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| Probably not true! |
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| Who is a bastard who wrote "why"? |
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| Magic rocks! :) |
- "results in healthier gut microbiome long term"
- "may do best for ApoE4 carriers"
- "may be able to restore and heal glucose tolerance which does not happen on the high fat..."
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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.
Ramsden, of the National Institutes of Health, unearthed raw data from a 40-year-old study, which challenges the dogma that eating vegetable fats instead of animal fats is good for the heart. The study, the largest gold-standard experiment testing that idea, found the opposite, Ramsden and his colleagues reported on Tuesday in BMJ (formerly the British Medical Journal).
Although the study is more than just another entry in the long-running nutrition wars—it is more rigorous than the vast majority of research on the topic—Ramsden makes no claims that it settles the question. Instead, he said, his discovery and analysis of long-lost data underline how the failure to publish the results of clinical trials can undermine truth.
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The coleader of the project was Dr. Ancel Keys, author of the Seven Countries Study, Time cover subject, and the most prominent advocate of replacing saturated fat with vegetable fat. “The idea that there might be something adverse about lowering cholesterol [via vegetable oils] was really antithetical to the dogma of the day,” Bob Frantz said.
His father, he said, “was always committed to discovering the truth. He would be pleased this is finally coming out.”
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| From The Telegraph "Modern dunce's cap" |
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"Global dietary guidelines should be reconsidered in light of these findings."
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| Source link , design by Trey Cox |
Findings
During follow-up, we documented 5796 deaths and 4784 major cardiovascular disease events. Higher carbohydrate intake was associated with an increased risk of total mortality (highest [quintile 5] vs lowest quintile [quintile 1] category, HR 1.28 [95% CI 1.12–1.46], ptrend=0.0001) but not with the risk of cardiovascular disease or cardiovascular disease mortality. Intake of total fat and each type of fat was associated with lower risk of total mortality (quintile 5 vs quintile 1, total fat: HR 0.77 [95% CI 0.67–0.87], ptrend<0.0001; saturated fat, HR 0.86 [0.76–0.99], ptrend=0.0088; monounsaturated fat: HR 0.81 [0.71–0.92], ptrend<0.0001; and polyunsaturated fat: HR 0.80 [0.71–0.89], ptrend<0.0001). Higher saturated fat intake was associated with lower risk of stroke (quintile 5 vs quintile 1, HR 0.79 [95% CI 0.64–0.98], ptrend=0.0498). Total fat and saturated and unsaturated fats were not significantly associated with risk of myocardial infarction or cardiovascular disease mortality.
Compared with people who ate the lowest 20 percent of carbohydrates, those who ate the highest 20 percent had a 28 percent increased risk of death. But high carbohydrate intake was not associated with cardiovascular death.
People with the highest 20 percent in total fat intake - an average of 35.3 percent of calories from fat - had about a 23 percent reduced risk of death compared with the lowest 20 percent (an average of 10.6 percent of calories from fat). Consuming higher saturated fat, polyunsaturated fat and monounsaturated fat were all associated with lower mortality. Higher fat diets were also associated with a lower risk of stroke.
Results: ...The most significant dietary correlate of low CVD risk was high total fat and animal protein consumption. Additional statistical analyses further highlighted citrus fruits, high-fat dairy (cheese) and tree nuts. ... The major correlate of high CVD risk was the proportion of energy from carbohydrates and alcohol, or from potato and cereal carbohydrates.
Conclusion: Our results do not support the association between CVDs and saturated fat, which is still contained in official dietary guidelines. Instead, they agree with data accumulated from recent studies that link CVD risk with the high glycaemic index/load of carbohydrate-based diets. In the absence of any scientific evidence connecting saturated fat with CVDs, these findings show that current dietary recommendations regarding CVDs should be seriously reconsidered.
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| by Cecilia Bleszynski (C) 2017 |
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high fat
First, last fall, experts on the committee that develops the country’s dietary guidelines acknowledged that they had ditched the low-fat diet. On Thursday, that committee’s report was released, with an even bigger change: It lifted the longstanding caps on dietary cholesterol, saying there was “no appreciable relationship” between dietary cholesterol and blood cholesterol.
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Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists overstated the significance of their studies.
Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health. In 2011, directors of the National Institute of Statistical Sciences analyzed many of Harvard’s most important findings and found that they could not be reproduced in clinical trials.
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In 2013, government advice to reduce salt intake (which remains in the current report) was contradicted by an authoritative Institute of Medicine study[*]. And several recent meta-analyses have cast serious doubt on whether saturated fats are linked to heart disease, as the dietary guidelines continue to assert.
Uncertain science should no longer guide our nutrition policy. Indeed, cutting fat and cholesterol, as Americans have conscientiously done, may have even worsened our health. In clearing our plates of meat, eggs and cheese (fat and protein), we ate more grains, pasta and starchy vegetables (carbohydrates). Over the past 50 years, we cut fat intake by 25 percent and increased carbohydrates by more than 30 percent, according to a new analysis of government data. Yet recent science has increasingly shown that a high-carb diet rich in sugar and refined grains increases the risk of obesity, diabetes and heart disease — much more so than a diet high in fat and cholesterol.
It’s not that health authorities weren’t warned. “They are not acting on the basis of scientific evidence, but on the basis of a plausible but untested idea,” Dr. Edward H. Ahrens Jr., a top specialist at Rockefeller University and prominent critic of the growing doctrine on dietary fats and cholesterol, cautioned back in the ’80s.
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Since the very first nutritional guidelines to restrict saturated fat and cholesterol were released by the American Heart Association in 1961, Americans have been the subjects of a vast, uncontrolled diet experiment with disastrous consequences. We have to start looking more skeptically at epidemiological studies and rethinking nutrition policy from the ground up.
Until then, we would be wise to return to what worked better for previous generations: a diet that included fewer grains, less sugar and more animal foods like meat, full-fat dairy and eggs.
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Objectives National dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. ...
Conclusions
Dietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.
Discussion
The main findings of the present meta-analysis of the six RCTs [Randomized Controlled Trials] available at the time of issuing dietary guidelines in the US and UK indicate that all-cause mortality was identical at 370 in the intervention and control groups. There was no statistically significant difference in deaths from CHD. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.
It is a widely held view that reductions in cholesterol are healthful per se. The original RCTs did not find any relationship between dietary fat intake and deaths from CHD or all-causes, despite significant reductions in cholesterol levels in the intervention and control groups. This undermines the role of serum cholesterol levels as an intermediary to the development of CHD and contravenes the theory that reducing dietary fat generally and saturated fat particularly potentiates a reduction in CHD.
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There was best practice, randomised controlled trial, evidence available to the dietary committees, which was not considered and should have been. The results of the present meta-analysis support the hypothesis that the available RCTs did not support the introduction of dietary fat recommendations in order to reduce CHD risk or related mortality. Two recent publications have questioned the alleged relationship between saturated fat and CHD and called for dietary guidelines to be reconsidered.31 ,32 The present review concludes that dietary advice not merely needs review; it should not have been introduced.
The studies’ own conclusions. These are the verbatim conclusions from each of the studies:
1965 Rose Corn and olive oil: “It is concluded that under the circumstances of this trial corn oil cannot be recommended as a treatment of ischaemic heart disease. It is most unlikely to be beneficial, and it is possibly harmful.” (ref 9)
1965 Research Committee Low-fat diet: “A low-fat diet has no place in the treatment of myocardial infarction” (ref 10) [heart attack].
1968 MRC soya-bean oil: “There is no evidence from the London trial that the relapse-rate in myocardial infarction is materially affected by the unsaturated fat content of the diet used.” (ref 11)
1969 Dayton LA Veterans study: “Total longevity was not affected favorably in any measurable or significant degree… For this reason, and because of the unresolved question concerning toxicity, we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (ref 12)
1970 Leren Oslo Diet Heart study: “Epidemiological studies have demonstrated several factors associated with the risk of developing first manifestations of coronary heart disease. Blood lipids, blood pressure and cigarette smoking are such risk variables… In spite of the small numbers this observation lends some support to the view that the multi-factorial approach is the best way to the solution of the coronary heart disease problem.”(ref 13)
1978 Woodhill Sydney Diet Heart Study: “Survival was significantly better in the P [control] Group.” “It must be concluded that the lipid hypothesis has gained little support from secondary intervention studies.” (ref 14)
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A dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons.
Those who reported the highest carbohydrate intake at the beginning of the study were 1.9 times likelier to develop mild cognitive impairment than those with the lowest intake of carbohydrates. Participants with the highest sugar intake were 1.5 times likelier to experience mild cognitive impairment than those with the lowest levels.
But those whose diets were highest in fat - compared to the lowest - were 42 percent less likely to face cognitive impairment, and those who had the highest intake of protein had a reduced risk of 21 percent.
When total fat and protein intake were taken into account, people with the highest carbohydrate intake were 3.6 times likelier to develop mild cognitive impairment.
"A high carbohydrate intake could be bad for you because carbohydrates impact your glucose and insulin metabolism," Dr. Roberts says. "Sugar fuels the brain - so moderate intake is good. However, high levels of sugar may actually prevent the brain from using the sugar - similar to what we see with type 2 diabetes."
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