Interesting Studies: Probably low carb related in one way or another
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Drastic Calorie Restriction for the Treatment of Massive Obesity
This regimen has always been well tolerated, without any major complaint, since appetite is initially attenuated and then suppressed by increased ketone production induced by caloric restriction [3].
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Sugar Industry and Coronary Heart Disease Research
A Historical Analysis of Internal Industry Documents
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.
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Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss program versus hypocaloric diet in patients with type 2 diabetes mellitus
Results:
No significant differences in the laboratory safety parameters were found between the two study groups. Changes in the urine albumin-to-creatinine ratio in VLCK diet were not significant and were comparable to control group. Creatinine and blood urea nitrogen did not change significantly relative to baseline nor between groups. Weight loss and reduction in waist circumference in the VLCK diet group were significantly larger than in control subjects (both P<0.001). The decline in HbA1c and glycemic control was larger in the VLCK diet group (P<0.05). No serious adverse events were reported and mild AE in the VLCK diet group declined at last follow-up.
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"Contrary to expectations, when challenged with a high-fat diet (HFD) to induce obesity, Ctrp1-KO mice had increased physical activity and reduced body weight, adiposity, and expression of lipid synthesis and fibrotic genes in adipose tissue..."
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Increased liver fat and glycogen stores following high compared with low glycaemic index food: a randomized cross over study
Results
Plasma glucose and insulin peak values and AUC were significantly greater following the HGI test meal compared with LGI test meal as expected. Hepatic glycogen concentrations increased more following the HGI test meal (P < 0.05) and peak levels were significantly greater after 7 days of HGI dietary intervention compared to that at the beginning of the intervention (P < 0.05). Liver Fat fractions increased significantly following the HGI dietary intervention compared with the LGI dietary intervention (two way repeat measures ANOVA, P ≤ 0.05).
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Short-term benefits of an unrestricted-calorie traditional Mediterranean diet, modified with a reduced consumption of carbohydrates at evening, in overweight-obese patients.
In conclusion, MeD with a restriction of carbohydrates in the evening significantly ameliorates obesity and associated metabolic complications.
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Does eating too much sugar cause type 2 diabetes?
Insulin is a key hormone that regulates blood glucose after eating. Insulin resistance, when the body's metabolic tissues stop responding normally to insulin, is one of the earliest detectable changes in the progression to diabetes.
However, according to this study, the cause of insulin resistance may have little to do with defects in insulin signaling and might actually be caused by a separate process triggered by excess sugar in the liver that activates a molecular factor known as carbohydrate-responsive element-binding protein, or ChREBP.
The ChREBP protein is found in several metabolic organs in mice, humans and other mammals. In the liver, it is activated after eating fructose, a form of sugar naturally found in fruits and vegetables, but also added to many processed foods including soft drinks. The study found that fructose initiates a process that causes the liver to keep making glucose and raising blood glucose levels, even as insulin tries to keep glucose production in check.
"For the past several decades, investigators have suggested that there must be a problem in the way the liver senses insulin, and that is why insulin-resistant people make too much glucose," Herman said. "We found that no matter how much insulin the pancreas made, it couldn't override the processes started by this protein, ChREBP, to stimulate glucose production. This would ultimately cause blood sugar and insulin levels to increase, which over time can lead to insulin resistance elsewhere in the body."
Herman is new to Duke and led the research over the past four years at Beth Israel Deaconess Medical Center at Harvard University with collaborators from the University of Massachusetts Medical School and Pfizer Inc.
To test their hypothesis, researchers studied mice that were genetically altered so their liver insulin signaling pathways were maximally activated -- in other words, their livers should not have been able to produce any glucose.
The researchers found that even in these mice, eating fructose triggered ChREBP-related processes in the liver, causing it to make more and more glucose, despite insulin signals telling it to stop.
Previous studies have reported that high fructose diets can cause multiple metabolic problems in humans and animals, including insulin resistance and fatty liver disease. Because most people found to be insulin-resistant also have fatty liver, many investigators have proposed that the fructose-induced fatty liver leads to liver dysfunction, which causes insulin resistance, diabetes and high risk for heart disease.
The new findings suggest fatty liver disease may be a red herring, Herman said. The likely cause of insulin resistance may not be the buildup of fat in the liver, as commonly believed, but rather the processes activated by ChREBP, which may then contribute to the development of both fatty liver and increased glucose production.
Although much more research is required, the scientists believe they better understand a key mechanism leading to pre-diabetes and can now explore how to possibly interrupt that chain of events.
Media: New theory on how insulin resistance, metabolic disease begin
Science: Fructose, but not glucose, impairs insulin signaling in the three major insulin-sensitive tissues0 -
Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries
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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Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss program versus hypocaloric diet in patients with type 2 diabetes mellitus
Our data show that VLCK diet (a low-calorie-ketogenic diet <50 g of carbohydrate daily) as part of a interventional weight loss program including lifestyle and behavioral modification support over a 4-month period is a safe, well tolerated, and accepted medical nutritional therapy option for subjects with T2DM. Furthermore, VLCK diet intervention in subjects with T2DM is associated with significantly larger weight loss along with amelioration of glycemic control as compared with a standard care nutritional intervention based on the ADA guidelines.
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(Graph and article via Ted Naiman)0 -
Autophagy Pioneer Wins Nobel Link1
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Heritability of high sugar consumption through drinks and the genetic correlation with substance use1,2
The positive association between high sugar consumption and high substance use was partly due to unique environmental factors (e.g., social situations). Genetic factors were also of influence, suggesting that neuronal circuits underlying the development of addiction and obesity are related. Further research is needed to identify genes that influence sugar consumption and those that overlap with substance use.
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This guest blog post in Scientific American is a few years old but I never read it: The fat-fueled brain: unnatural or advantageous? Link0
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Nearly 100 national health and medical groups — including the American Heart Association, the American Diabetes Association and the Centers for Disease Control and Prevention — enjoy sponsorships by Coca-Cola Co. or PepsiCo, according to a new study by two Boston University researchers.
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High-Protein Intake during Weight Loss Therapy Eliminates the Weight-Loss-Induced Improvement in Insulin Action in Obese Postmenopausal Women
In this study, we compared the effects of ∼10% WL with a hypocaloric diet containing 0.8 g protein/kg/day and a hypocaloric diet containing 1.2 g protein/kg/day on muscle insulin action in postmenopausal women with obesity. We found that HP intake reduced the WL-induced decline in lean tissue mass by ∼45%. However, HP intake also prevented the WL-induced improvements in muscle insulin signaling and insulin-stimulated glucose uptake, as well as the WL-induced adaptations in oxidative stress and cell structural biology pathways.
Notes: 34 postmenopausal women with obesity, HP group given a protein supplement
Science
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The 5th epidemiology review that finds no link between saturated fats and CHD mortality.
Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis.
Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines.
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With past studies commonly focusing on gluten and its impact on digestive health, this new research, presented at UEG Week 2016, turns the spotlight onto a different family of proteins found in wheat called amylase-trypsin inhibitors (ATIs). The study shows that the consumption of ATIs can lead to the development of inflammation in tissues beyond the gut, including the lymph nodes, kidneys, spleen and brain. Evidence suggests that ATIs can worsen the symptoms of rheumatoid arthritis, multiple sclerosis, asthma, lupus and non-alcoholic fatty liver disease, as well as inflammatory bowel disease.
Media:
New study links protein in wheat to the inflammation of chronic health conditions
Wheat proteins may cause inflammation beyond the gut
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3-Hydroxybutyrate Regulates Energy Metabolism and Induces BDNF Expression in Cerebral Cortical Neurons
During fasting and vigorous exercise, a shift of brain cell energy substrate utilization from glucose to the ketone 3-hydroxybutyrate (3OHB) occurs. Studies have shown that 3OHB can protect neurons against excitotoxicity and oxidative stress, but the underlying mechanisms are unclear. Neurons maintained in the presence of 3OHB exhibited increased oxygen consumption and ATP production, and an elevated NAD+/NADH ratio. We found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons.
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So, you posted a ton of links here.
However, did you check the reliability of the sources?
Who set up the study? Do they gain any profit at all from the presented result?
Were reliable research methods used and respected?
Was the information accurately interpreted?
I recommend collecting both PRO and CON content to compare.
I also recommend using a Databank such as PubMed or NCBI.1 -
Blog
Saturated fat and heart disease -Dr. Malcolm Kendrick0 -
Why the MFP forum refrain "there's no reason to track sugar in your diet unless you have a medical condition" is not the best advise - especially for those with overweight and obesity.
Glucose intolerance and insulin resistance link to unfavorable cardiac function, structure
"Our findings inform and extend the clinical concept of diabetic cardiomyopathy—adverse changes in cardiac structure and function commonly observed among patients with diabetes mellitus in two ways," said lead author Ryan Demmer, PhD, assistant professor of Epidemiology at the Mailman School of Public Health. "First, they confirm that diabetes mellitus—both controlled and uncontrolled—is related to the worse measures of cardiac structure and function among Hispanics. Second, they demonstrate that these relationships emerge early in the natural history of diabetogenesis and prior to diabetes development."
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‘Nutrition Heretic’ Gary Taubes on the Long Road Back From a Big, Fat Public Shaming
"While the orthodoxy has yet to embrace Atkins and low-carb, high-fat diets, or ketogenic diets as they’re technically called, as healthful diets, let alone ideal, they’re getting there. Hundreds if not thousands of physicians now preferentially prescribe them to their patients, and the bookstores are overflowing with diet books and cookbooks, promoting variations on these themes. There’s even a yearly international meeting of academic researchers and physicians just to discuss what they consider the somewhat remarkable clinical efficacy of ketogenic diets in treating an ever-increasing spectrum of rare to common disorders. The world has certainly changed. We are making progress."
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Effect of type and amount of dietary carbohydrate on biomarkers of glucose homeostasis and C reactive protein in overweight or obese adults: results from the OmniCarb trial
Conclusions Reducing carbohydrate, regardless of high or low GI, decreased GA and fructosamine. This suggests that reducing carbohydrate content, rather than GI, is a better strategy for lowering glycemia in adults at risk for diabetes.
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Big news. The BMJ stands behind Nina Teicholz's September 2015 article that argued the US Dietary Guidelines Advisory Committee (DGAC) used weak scientific methods to develop the guidelines.
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Saturated fat could be good for you
Re: Visceral adiposity and metabolic syndrome after very high–fat and low-fat isocaloric diets: a randomized controlled trial
"The very high intake of total and saturated fat did not increase the calculated risk of cardiovascular diseases," says professor and cardiologist Ottar Nygård who contributed to the study.
"Participants on the very-high-fat diet also had substantial improvements in several important cardiometabolic risk factors, such as ectopic fat storage, blood pressure, blood lipids (triglycerides), insulin and blood sugar."
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"The alleged health risks of eating good-quality fats have been greatly exaggerated. It may be more important for public health to encourage reductions in processed flour-based products, highly processed fats and foods with added sugar," he [Simon Nitter Dankel] says.
Media | Science (see COI) | Simon Dankel0 -
If salt increases your blood pressure, you're likely insulin resistant; IR increases salt and water retention.
Salt sensitivity is associated with insulin resistance in essential hypertension.
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Insurance underwriters review the science and look towards the future and how the changing views on saturated fat and carbohydrate might impact their business.
Challenging 40 years of dietary guidelines
"These findings highlight a new chapter in the fight against obesity and diabetes. We may eventually see the tide turning now that saturated fat is no longer seen as harmful and we can advise those with deranged carbohydrate metabolism to replace energy from carbohydrate with fats, hence substantially reducing the one nutrient that is in fact driving their disease process.
Underwriting these ex diabetics and ex obese individuals will pose the same problem we face with bariatric surgery. How sustainable is the weight loss or reversed (“cured”) diabetes? And how should we underwrite the harms the years of being obese and diabetic might have had, despite now being normoglycemic and having a “standard” BMI."0 -
Petition signed by 200 Canadian doctors -- times are a changing. via Dr. Malcolm Kendrick's blog post:
The diet heart hypothesis suffers another attack – hoorah!
Points for Change
The Canadian Dietary Guidelines should:
- Clearly communicate to the public and health-care professionals that the low-fat diet is no longer supported, and can worsen heart-disease risk factors
- Be created without influence from the food industry
- Eliminate caps on saturated fats
- Be nutritionally sufficient, and those nutrients should come from real foods, not from artificially fortified refined grains
- Promote low-carb diets as at least one safe and effective intervention for people struggling with obesity, diabetes, and heart disease
- Offer a true range of diets that respond to the diverse nutritional needs of our population
- De-emphasize the role of aerobic exercise in controlling weight
- Recognize the controversy on salt and cease the blanket “lower is better” recommendation
- Stop using any language suggesting that sustainable weight control can simply be managed by creating a caloric deficit
- Cease its advice to replace saturated fats with polyunsaturated vegetable oils to prevent cardiovascular disease
- Stop steering people away from nutritious whole foods, such as whole-fat dairy and regular red meat
- Include a cap on added sugar, in accordance with the updated WHO guidelines, ideally no greater than 5% of total calories
- Be based on a complete, comprehensive review of the most rigorous (randomized, controlled clinical trial) data available; on subjects for which this more rigorous data is not available, the Guidelines should remain silent.
2 - Clearly communicate to the public and health-care professionals that the low-fat diet is no longer supported, and can worsen heart-disease risk factors
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Calories Proper: These dudes ate a ton of sat fats and nothing bad happened
Visceral adiposity and metabolic syndrome after very high–fat and low-fat isocaloric diets: a randomized controlled trial
Conclusions: Consuming energy primarily as carbohydrate or fat for 3 mo did not differentially influence visceral fat and metabolic syndrome in a low-processed, lower-glycemic dietary context. Our data do not support the idea that dietary fat per se promotes ectopic adiposity and cardiometabolic syndrome in humans.
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Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review
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