Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes | SpringerLink

http://link.springer.com/article/10.1007/s10545-016-0011-5


Conclusion

Ketogenic diet was an effective and safe treatment for the majority of patients. Treatment effect was mainly determined by disease phenotype and attainment and maintenance of ketosis.

Sofou, K., Dahlin, M., Hallböök, T. et al. J Inherit Metab Dis (2017). doi:10.1007/s10545-016-0011-5

Multiomics reveal non-alcoholic fatty liver disease in rats following chronic exposure to an ultra-low dose of Roundup herbicide : Scientific Reports

http://www.nature.com/articles/srep39328





Abstract:

The impairment of liver function by low environmentally relevant doses of glyphosate-based herbicides (GBH) is still a debatable and unresolved matter. Previously we have shown that rats administered for 2 years with 0.1 ppb (50 ng/L glyphosate equivalent dilution; 4 ng/kg body weight/day daily intake) of a Roundup GBH formulation showed signs of enhanced liver injury as indicated by anatomorphological, blood/urine biochemical changes and transcriptome profiling. Here we present a multiomic study combining metabolome and proteome liver analyses to obtain further insight into the Roundup-induced pathology. Proteins significantly disturbed (214 out of 1906 detected, q < 0.05) were involved in organonitrogen metabolism and fatty acid β-oxidation. Proteome disturbances reflected peroxisomal proliferation, steatosis and necrosis. The metabolome analysis (55 metabolites altered out of 673 detected, p < 0.05) confirmed lipotoxic conditions and oxidative stress by showing an activation of glutathione and ascorbate free radical scavenger systems. Additionally, we found metabolite alterations associated with hallmarks of hepatotoxicity such as γ-glutamyl dipeptides, acylcarnitines, and proline derivatives. Overall, metabolome and proteome disturbances showed a substantial overlap with biomarkers of non-alcoholic fatty liver disease and its progression to steatohepatosis and thus confirm liver functional dysfunction resulting from chronic ultra-low dose GBH exposure.

• Scientific Reports 7, Article number: 39328 (2017)

• doi:10.1038/srep39328

Nutritional Ketosis Condition and Specific Ketogenic Diet, May Benefit Cancer Patients as an Alternative Treatment by Sudden Change in the Metabolic State of Cancer Cells. | Niknamian | International Science and Investigation journal

http://www.isijournal.info/journals/index.php/ISIJ/article/view/237

Abstract

Cancer disease is the second cause of death in the United States and world-wide. Most Researchers estimate that 595,690 of American people will die from cancer at the end of the year 2017. That means 1,600 deaths/day approximately.³⁹ Cancer in modern societies is commonly treated with the combination of organ surgery, chemotherapy and radiotherapy. Many kinds of diet strategies have been experimented. However, none of them have been particularly effective. Interestingly, there is some applied research suggesting that a very low-carb, high fat diet may help.^{40, 41, 42} According to Otto Warburg hypothesis, the cause of cancer is the change in the metabolism of mitochondrion in human cells. Low oxygen in tissues in combination with high blood glucose will change the cell respiration from aerobic to anaerobic which leads to fermentation type of respiration. In this perspective and prospective research, I have shown the very low carbohydrate ketogenic diet and mostly ketosis, may benefit cancer patients in reducing and weakening cancer cells. Although further researches are needed, this perspective article could be beneficial in future perspective of alternative treatments of cancer.




Niknamian, S. (2016). Nutritional Ketosis Condition and Specific Ketogenic Diet, May Benefit Cancer Patients as an Alternative Treatment by Sudden Change in the Metabolic State of Cancer Cells.. International Science And Investigation Journal, 5(5), 28-48. Retrieved from http://www.isijournal.info/journals/index.php/ISIJ/article/view/237

Bread and Other Edible Agents of Mental Disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809873/

Abstract

Perhaps because gastroenterology, immunology, toxicology, and the nutrition and agricultural sciences are outside of their competence and responsibility, psychologists and psychiatrists typically fail to appreciate the impact that food can have on their patients’ condition. Here we attempt to help correct this situation by reviewing, in non-technical, plain English, how cereal grains—the world’s most abundant food source—can affect human behavior and mental health. We present the implications for the psychological sciences of the findings that, in all of us, bread (1) makes the gut more permeable and can thus encourage the migration of food particles to sites where they are not expected, prompting the immune system to attack both these particles and brain-relevant substances that resemble them, and (2) releases opioid-like compounds, capable of causing mental derangement if they make it to the brain. A grain-free diet, although difficult to maintain (especially for those that need it the most), could improve the mental health of many and be a complete cure for others.

Bressan P, Kramer P. Bread and Other Edible Agents of Mental Disease. Frontiers in Human Neuroscience. 2016;10:130. doi:10.3389/fnhum.2016.00130.

β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms. - PubMed - NCBI

https://www.ncbi.nlm.nih.gov/m/pubmed/27826689/

The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709725/



Abstract

Until recently, multiple sclerosis has been viewed as an entirely inflammatory disease without acknowledgment of the significant neurodegenerative component responsible for disease progression and disability. This perspective is being challenged by observations of a dissociation between inflammation and neurodegeneration where the neurodegenerative component may play a more significant role in disease progression. In this review, we explore the relationship between mitochondrial dysfunction and neurodegeneration in multiple sclerosis. We review evidence that the ketogenic diet can improve mitochondrial function and discuss the potential of the ketogenic diet in treating progressive multiple sclerosis for which no treatment currently exists.



Storoni M, Plant GT. The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis. Multiple Sclerosis International. 2015;2015:681289. doi:10.1155/2015/681289.

Which diet is the best for weight loss? - Black Belt Nutrition

http://www.blackbeltnutrition.org/diet-best-weight-loss

Intensity of Statin Therapy and Mortality | Cardiology | JAMA Cardiology | The JAMA Network

http://jamanetwork.com/journals/jamacardiology/fullarticle/2580531?JamaNetworkReader=True


"Mortality
Patients receiving high-intensity statin therapy had a 1-year mortality rate of 4.0% compared with 4.8% for those receiving moderate-intensity statin therapy, 5.7% (1632 of 28 765) for those receiving low-intensity statin therapy, and 6.6% (4868 of 73 728) for those receiving no statin therapy (P < .001)."


Rodriguez F, Maron DJ, Knowles JW, Virani SS, Lin S, Heidenreich PA. Association Between Intensity of Statin Therapy and Mortality in Patients With Atherosclerotic Cardiovascular Disease. JAMA Cardiol. Published online November 09, 2016. doi:10.1001/jamacardio.2016.4052

Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries | Grasgruber | Food & Nutrition Research

http://www.foodandnutritionresearch.net/index.php/fnr/article/view/31694



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


Food & Nutrition Research 2016, 60: 31694 - http://dx.doi.org/10.3402/fnr.v60.31694

Grasgruber, P., Sebera, M., Hrazdira, E., Hrebickova, S., & Cacek, J. (2016). Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries. Food & Nutrition Research, 60. doi:http://dx.doi.org/10.3402/fnr.v60.31694

Ketone bodies are protective against oxidative stress in neocortical neurons - Kim - 2007 - Journal of Neurochemistry - Wiley Online Library

http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2007.04483.x/full


"Abstract

Ketone bodies (KB) have been shown to
prevent neurodegeneration in models of Parkinson’s and Alzheimer’s diseases,
but the mechanisms underlying these effects remain unclear. One possibility is
that KB may exert antioxidant activity. In the current study, we explored the
effects of KB on rat neocortical neurons exposed to hydrogen peroxide (H2O2) or diamide – a thiol oxidant
and activator of mitochondrial permeability transition (mPT). We found that:
(i) KB completely blocked large inward currents induced by either H2O2 or diamide; (ii) KB
significantly decreased the number of propidium iodide-labeled cells in
neocortical slices after exposure to H2O2 or diamide; (iii) KB significantly decreased
reactive oxygen species (ROS) levels in dissociated neurons and in isolated
neocortical mitochondria; (iv) the electrophysiological effects of KB in
neurons exposed to H2O2 or diamide were mimicked by bongkrekic acid and cyclosporin A, known
inhibitors of mPT, as well as by catalase and DL – dithiothreitol, known
antioxidants; (v) diamide alone did not significantly alter basal ROS levels in
neurons, supporting previous studies indicating that diamide-induced neuronal
injury may be mediated by mPT opening; and (vi) KB significantly increased the
threshold for calcium-induced mPT in isolated mitochondria. Taken together, our
data suggest that KB may prevent mPT and oxidative injury in neocortical
neurons, most likely by decreasing mitochondrial ROS production."

Kim, D. Y., Davis, L. M., Sullivan, P. G., Maalouf, M., Simeone, T. A., Brederode, J. v. and Rho, J. M. (2007), Ketone bodies are protective against oxidative stress in neocortical neurons. Journal of Neurochemistry, 101: 1316–1326. doi:10.1111/j.1471-4159.2007.04483.x

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. - PubMed - NCBI

https://www.ncbi.nlm.nih.gov/m/pubmed/20071648/?i=3&from=Siri-Tarino%20PW,%20Sun%20Q,%20Hu%20FB,%20Krauss%20RM



"CONCLUSIONS: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat."


Siri-Tarino PW, Sun Q, Hu FB,
Krauss RM. Meta-analysis of prospective cohort studies evaluating the
association of saturated fat with cardiovascular disease. Am J Clin
Nutr 2010;91:535-46.

Estimated intake of vitamin D and its interaction with vitamin A on lung cancer risk among smokers

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293152/



"Total vitamin D intake ≥400 versus <400 IU/d was associated with a lower risk of total lung cancer among participants who received the CARET active intervention (HR=0.56, 95% CI=0.32–0.99) and among those who had total vitamin A intake ≥1,500 μg/d Retinol Activity Equivalent (RAE; HR=0.46, 95% CI=0.23–0.91). The beneficial associations were attenuated among those who did not receive the CARET active intervention or who had total vitamin A intake <1,500 μg/d RAE (P-interaction=0.02 for current smokers). Our observation suggests that vitamin A may assist vitamin D in preventing lung cancer among smokers."



Cheng T-YD, Goodman GE, Thornquist MD, et al. Estimated intake of vitamin D and its interaction with vitamin A on lung cancer risk among smokers.International journal of cancer Journal international du cancer. 2014;135(9):2135-2145. doi:10.1002/ijc.28846.

Association between vitamin A, retinol intake and blood retinol level and gastric cancer risk: A meta-analysis. - PubMed - NCBI

http://www.ncbi.nlm.nih.gov/pubmed/25008141

"CONCLUSIONS:

Vitamin A intake was inversely associated with gastric cancer risk, while no significant association was found with retinol intake or blood retinol level"

Association between vitamin A, retinol intake and blood retinol level and gastric cancer risk: A meta-analysis.Wu Y, Ye Y, Shi Y, Li P, Xu J, Chen K, Xu E, Yang J.Clin Nutr. 2015 Aug;34(4):620-6. doi: 10.1016/j.clnu.2014.06.007. Epub 2014 Jun 23.PMID: 25008141

EU har godkänt tre genmodifierade sojabönor

http://www.livsmedelsverket.se/om-oss/press/nyheter/pressmeddelanden/eu-har-godkant-tre-genmodifierade-sojabonor/



EU:s register över godkända GMO-produkter