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
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
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
tisdag 9 augusti 2016
måndag 8 augusti 2016
Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention. - PubMed - NCBI
http://www.ncbi.nlm.nih.gov/pubmed/21450549
RESULTS:
"Urine levels of BPA and DEHP metabolites decreased significantly during the fresh foods intervention [e.g., BPA geometric mean (GM), 3.7 ng/mL preintervention vs. 1.2 ng/mL during intervention; mono-(2-ethyl-5-hydroxy hexyl) phthalate GM, 57 ng/mL vs. 25 ng/mL]. The intervention reduced GM concentrations of BPA by 66% and DEHP metabolites by 53-56%. Maxima were reduced by 76% for BPA and 93-96% for DEHP metabolites."
CONCLUSIONS:
"BPA and DEHP exposures were substantially reduced when participants' diets were restricted to food with limited packaging."
Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention.
Rudel RA, Gray JM, Engel CL, Rawsthorne TW, Dodson RE, Ackerman JM, Rizzo J, Nudelman JL, Brody JG.
Environ Health Perspect. 2011 Jul;119(7):914-20. doi: 10.1289/ehp.1003170. Epub 2011 Mar 30.
PMID: 21450549
RESULTS:
"Urine levels of BPA and DEHP metabolites decreased significantly during the fresh foods intervention [e.g., BPA geometric mean (GM), 3.7 ng/mL preintervention vs. 1.2 ng/mL during intervention; mono-(2-ethyl-5-hydroxy hexyl) phthalate GM, 57 ng/mL vs. 25 ng/mL]. The intervention reduced GM concentrations of BPA by 66% and DEHP metabolites by 53-56%. Maxima were reduced by 76% for BPA and 93-96% for DEHP metabolites."
CONCLUSIONS:
"BPA and DEHP exposures were substantially reduced when participants' diets were restricted to food with limited packaging."
Food packaging and bisphenol A and bis(2-ethyhexyl) phthalate exposure: findings from a dietary intervention.
Rudel RA, Gray JM, Engel CL, Rawsthorne TW, Dodson RE, Ackerman JM, Rizzo J, Nudelman JL, Brody JG.
Environ Health Perspect. 2011 Jul;119(7):914-20. doi: 10.1289/ehp.1003170. Epub 2011 Mar 30.
PMID: 21450549
The contribution of diet to total bisphenol A body burden in humans: results of a 48 hour fasting study. - PubMed - NCBI
http://www.ncbi.nlm.nih.gov/pubmed/23026348
The contribution of diet to total bisphenol A body burden in humans: results of a 48 hour fasting study.
Christensen KL, Lorber M, Koslitz S, Brüning T, Koch HM.
Environ Int. 2012 Dec 1;50:7-14. doi: 10.1016/j.envint.2012.09.002. Epub 2012 Sep 29.
PMID: 23026348
onsdag 6 juli 2016
Targeting insulin inhibition as a metabolic therapy in advanced cancer: a pilot safety and feasibility dietary trial in 10 patients. - PubMed - NCBI
http://www.ncbi.nlm.nih.gov/m/pubmed/22840388/
CONCLUSION: "Preliminary data demonstrate that an insulin-inhibiting diet is safe and feasible in selected patients with advanced cancer. The extent of ketosis, but not calorie deficit or weight loss, correlated with stable disease or partial remission."
Nutrition. 2012 Oct;28(10):1028-35. doi: 10.1016/j.nut.2012.05.001. Epub 2012 Jul 26.
CONCLUSION: "Preliminary data demonstrate that an insulin-inhibiting diet is safe and feasible in selected patients with advanced cancer. The extent of ketosis, but not calorie deficit or weight loss, correlated with stable disease or partial remission."
Nutrition. 2012 Oct;28(10):1028-35. doi: 10.1016/j.nut.2012.05.001. Epub 2012 Jul 26.
Prenumerera på:
Kommentarer (Atom)