Interesting Studies: Probably low carb related in one way or another

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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    "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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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.

    Source
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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 tissues
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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    b3tz4h9t1053.jpg
    (Graph and article via Ted Naiman)
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    Autophagy Pioneer Wins Nobel Link
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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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  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    This guest blog post in Scientific American is a few years old but I never read it: The fat-fueled brain: unnatural or advantageous? Link
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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.

    Article
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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
    Media
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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.

    Source
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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

  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    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.

    Source
  • governatorkp
    governatorkp Posts: 89 Member
    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.
  • AlabasterVerve
    AlabasterVerve Posts: 3,171 Member
    Blog
    Saturated fat and heart disease -Dr. Malcolm Kendrick