http://isijournal.info/journals/index.php/ISIJ/article/view/252/197
Abstract
This review takes a deep look at increases in the incidence of cancer and heart disease after
the introduction of industrial vegetable oils in the world. Most vegetable oils are highly
processed and refined products, which completely lack the essential nutrients. Omega-6
Linoleic acid from vegetable oils increases oxidative stress in the body of humans, contributing
to endothelial dysfunction and heart disease. The consumption of these harmful oils which are
high in mega-6 polyunsaturated fats results in changing the structure of cell membrane which
contribute to increasing inflammation and the incidence of cancer.
Niknamian, S., & Kalamian, M. (2016). Vegetable Oils Consumption as One of the Leading Cause of Cancer and Heart Disease. International Science And Investigation Journal, 5(5), 157-168. Retrieved from http://isijournal.info/journals/index.php/ISIJ/article/view/252/197
Vetenskapen om vad ska man äta för att hålla sig frisk! The science on what to eat to stay healthy!
lördag 4 februari 2017
onsdag 25 januari 2017
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
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
Etiketter:
Ketogenic Diet
måndag 9 januari 2017
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.
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
lördag 24 december 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. | Niknamian | International Science and Investigation journal
http://www.isijournal.info/journals/index.php/ISIJ/article/view/237
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
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
Etiketter:
Ketogenic Diet
söndag 11 december 2016
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.
Etiketter:
Gluten
onsdag 23 november 2016
tisdag 22 november 2016
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.
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.
söndag 20 november 2016
lördag 12 november 2016
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
"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
Etiketter:
Statin
torsdag 3 november 2016
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
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
onsdag 28 september 2016
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
"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."
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
Etiketter:
Ketones,
Oxidative stress
söndag 25 september 2016
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.
"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.
fredag 26 augusti 2016
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.
"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
Vitamin A intake was inversely associated with gastric cancer risk, while no significant association was found with retinol intake or blood retinol level"
"CONCLUSIONS:
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
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