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.The data is not fully verified. I used the reference links and borrowed some words from this post Comment by Captain Sunset on Hyperlipid
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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The energy-producing organelle mitochondrion contains its own compact genome, which is separate from the nuclear genome. In nearly all mammals, this mitochondrial genome is inherited exclusively from the mother, and transmission of paternal mitochondria or mitochondrial DNA (mtDNA) has not been convincingly demonstrated in humans. In this paper, we have uncovered multiple instances of biparental inheritance of mtDNA spanning three unrelated multiple generation families, a result confirmed by independent sequencing across multiple unrelated laboratories with different methodologies. Surprisingly, this pattern of inheritance appears to be determined in an autosomal dominantlike manner. This paper profoundly alters a widespread belief about mitochondrial inheritance and potentially opens a novel field in mitochondrial medicine.
The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness. As one participant put it, “poor methods get results”. The Academy of Medical Sciences, Medical Research Council, and Biotechnology and Biological Sciences Research Council have now put their reputational weight behind an investigation into these questionable research practices. The apparent endemicity of bad research behaviour is alarming. In their quest for telling a compelling story, scientists too often sculpt data to fit their preferred theory of the world. Or they retrofit hypotheses to fit their data. Journal editors deserve their fair share of criticism too. We aid and abet the worst behaviours. Our acquiescence to the impact factor fuels an unhealthy competition to win a place in a select few journals. Our love of “significance” pollutes the literature with many a statistical fairy-tale. We reject important confirmations. Journals are not the only miscreants. Universities are in a perpetual struggle for money and talent, endpoints that foster reductive metrics, such as high-impact publication. National assessment procedures, such as the Research Excellence Framework, incentivise bad practices. And individual scientists, including their most senior leaders, do little to alter a research culture that occasionally veers close to misconduct.
Consider a report published last year in The Lancet that studied nutrition among more than 135,000 people across 18 different countries — making it the largest-ever observational study of its kind. The researchers found that people who ate the least saturated fat — about the same amount currently recommended for heart patients — had the highest rates of heart disease and mortality. Meanwhile, people who consumed the most saturated fat had the lowest rate of strokes.
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| Identify what is bad for you ... (Wiki Bacon) |
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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| (from Dairy Council of California) |
They observed that in Alzheimer’s, immune cells that normally protect the brain instead begin to consume a vital nutrient called arginine.
Really? Dr. Pickett must be a very wise man knowing that upfront and thus excluding that therapeutic option by his statement, without doing any testing!
Arginine is an amino acid and an essential nutrient for several bodily processes, including cell division, healing and immune responses.
It is found in food, including dairy products, meat, nuts and chickpeas, but the team at Duke said that their study did not suggest eating more arginine would have an impact on Alzheimer’s risk. The blood-brain barrier regulates how much arginine can enter the brain, and the immune response that breaks down arginine would remain the same even if confronted with higher levels of the nutrient.
“The study suggests that low levels of arginine in the brain could contribute to the death of nerve cells in Alzheimer’s, but there is much more we still need to understand about how and why nerve cells die in the disease,” she added.
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| Wiki |
Results The mean (SD) age of participants was 73.6 (2.9) years, 51.2% were female, 61.7% were of white race, and 38.3% were black. After 10 years, 881 participants had died, 572 had developed CVD, and 398 had developed HF. In adjusted Cox proportional hazards regression models, sodium intake was not associated with mortality (hazard ratio [HR] per 1 g, 1.03; 95% CI, 0.98-1.09; P = .27).
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Underfunded Scientists Force Lipstick-Covered Rat With Cancer To Run Through Maze |
"... 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)
