kcal /g
Protein 4
Fat 9
Carbohydrate 4
Dietary fibre 2
lundi 31 août 2015
Even the NYT makes the mistake between cholesterol and LDL particles
"The new drugs are approved for use by people with heart disease who cannot control their LDL, the dangerous cholesterol, by other means. "
Free cholesterol, free oxy-cholesterol, or cholesterol esters of fatty acids are Cholesterol
LDL are particles which are assembled by the liver according to several metabolic signals with proteins around for solubility in the plasma and lipids in the core. Cholesterol, esters of cholesterol, triglycerides are the lipids in LDL particles.
Antibiotics overuse and D2: a very high concern
http://press.endocrine.org/doi/pdf/10.1210/jc.2015-2696
"Conclusions
Patients with type 2 diabetes, compared to control subjects free of type 2 diabetes, are overexposed to antibiotics be- fore their diagnosis with type 2 diabetes as defined by the first redemption of a prescription on an oral glucose-low- ering agent. This may represent an increased demand for antibiotics from an increased risk of infections in patients with yet-undiagnosed diabetes, prediabetes, or manifest type 2 diabetes. However, the possibility that antibiotics exposure increases diabetes risk cannot be excluded and deserves further investigation in interventional studies. Thus, our results call for new investigations of the long- term effect of antibiotics on lipid and glucose metabolism and body weight gain. In particular, we suggest investi- gation of commonly used narrow-spectrum penicillins be- cause these drugs are frequently prescribed and showed the highest OR for type 2 diabetes risk. "
Patients with type 2 diabetes, compared to control subjects free of type 2 diabetes, are overexposed to antibiotics be- fore their diagnosis with type 2 diabetes as defined by the first redemption of a prescription on an oral glucose-low- ering agent. This may represent an increased demand for antibiotics from an increased risk of infections in patients with yet-undiagnosed diabetes, prediabetes, or manifest type 2 diabetes. However, the possibility that antibiotics exposure increases diabetes risk cannot be excluded and deserves further investigation in interventional studies. Thus, our results call for new investigations of the long- term effect of antibiotics on lipid and glucose metabolism and body weight gain. In particular, we suggest investi- gation of commonly used narrow-spectrum penicillins be- cause these drugs are frequently prescribed and showed the highest OR for type 2 diabetes risk. "
vendredi 28 août 2015
Intensive statin therapy in AMI patients: disappointing results at 12 months
The results after 12 months in this RCT which was blinded only for radiologists who made the plaque evaluation are rather disappointing or at best mitigated.
Comparatively to the standard regime the intensive statin therapy showed:
-no depletion in the fatty content of the plaque, indeed the two regimes led to an increase in the total plaque volume.
-an increase of the calcium content of the plaque in the intensive group
-no decrease in the MACE
-a decrease the "vulnerability" of the predetermined vulnerable plaques as assessed by total volumes but only for the patients treated with an intensive regime. The vulnerable patients were 18/96/140 and 18 plaques , 8 in the conventional regime and 10 in the intensive one.
Table 1
Size of the cohort 140 patients recruted 96 evaluable patients
Treatment Rosu +/- Ezetimibe Standard dose
LDL-C < 1.8 mmol 40 mg Simvastatin
Duration of treatment (m) 12 12
Table 2
Treatment regime Intensive Conventional
Number of patients 48 48
MACE
AMI 2 1
Unstable Angina 6 8
Vulnerable plaques 10 8
http://ac.els-cdn.com/S0021915015013593/1-s2.0-S0021915015013593-main.pdf
And another disappointing result with different parameters:
http://eurheartj.oxfordjournals.org/content/early/2014/08/28/eurheartj.ehu373.full
Table 1
Size of the cohort 140 patients recruted 96 evaluable patients
Treatment Rosu +/- Ezetimibe Standard dose
LDL-C < 1.8 mmol 40 mg Simvastatin
Duration of treatment (m) 12 12
Table 2
Treatment regime Intensive Conventional
Number of patients 48 48
MACE
AMI 2 1
Unstable Angina 6 8
Vulnerable plaques 10 8
http://ac.els-cdn.com/S0021915015013593/1-s2.0-S0021915015013593-main.pdf
And another disappointing result with different parameters:
http://eurheartj.oxfordjournals.org/content/early/2014/08/28/eurheartj.ehu373.full
jeudi 27 août 2015
High carb diet linked to high non fasting TG
http://www.jlr.org/content/41/4/595.full.pdf+html
Look at table 3!
And the link is: fructose metabolism in a positive balance of calories.
http://www.hindawi.com/journals/jnme/2015/823081/
Hudgins, L. C., M. Hellerstein, C. Seidman, R. Neese, J. Diakun, and J. Hirsch. 1996. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J. Clin. Invest. 97: 2081– 2091.
Hudgins, L. C., C. E. Seidman, J. Diakun, and J. Hirsch. 1998. Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar. Am. J. Clin. Nutr. 67: 631–639.
Hellerstein, M .K. 1996. Regulation of hepatic de novo lipogenesis in humans. Annu. Rev. Nutr. 16: 523–557.
From the study of fructose metabolism quoted supra:
"
4. Atherosclerosis
It appears that high fructose intake can create an unfavorable lipid profile in blood via DNL [94]. The main product of DNL is palmitic acid [95], a fatty acid specifically shown to increase the risk of atherosclerosis [96]. Fatty acids formed by DNL will mainly be packed in VLDLs delivered into the bloodstream. This may, in turn, increase the level of low-density lipoproteins (LDLs) in the blood. In several studies, fructose has to a greater extent than glucose increased blood levels of triglycerides [51, 65, 97, 98] and LDLs [65, 99–103]. Aeberli et al. [104] showed that fructose increased the small dense LDLs, the type of LDLs that may in particular be linked to cardiovascular risk [105]. The level of high-density lipoproteins (HDLs) in blood does not seem to be affected by fructose [100, 101]. In most studies, an intake of fructose >100 g/day has been necessary to observe the adverse effects on lipid profiles [51, 65, 85, 98, 100, 106–108]. However, in a recent study by Aeberli et al. [109], a daily intake of about 77 g fructose and 34 g glucose for 3 weeks resulted in increased levels of total cholesterol and LDLs in the blood of healthy young men, compared with a daily intake of approximately 109 g glucose and 28 g fructose over the same time period. The fact that both groups also ingested an unknown amount of starch and the fact that food intake was not controlled reduce the solidity of these results. Maersk et al. [90] found that intake of 50 g fructose per day together with 50 g glucose could have a negative effect on blood triglyceride level. The lack of a control group ingesting glucose makes it difficult to conclude that this is an effect of fructose. Conversely, Lowndes et al. [110] found no negative effect on lipid profile in overweight or obese individuals consuming HFCS or sucrose incorporated in a eucaloric diet for ten weeks at levels corresponding to the 25th and 50th percentiles of adult fructose consumption. Using the current knowledge, it does not appear that the consumption of moderate amounts of fructose (<50 d="" g="" i="" nbsp="">alone will result in an unfavorable blood lipid profile [86, 111].
Due to the insignificant levels of fructose in peripheral blood, as described above, only glucose has the potential to be a substrate for DNL in adipose tissue. Although DNL in adipose tissue seems to be small as earlier discussed, glucose will, because of its presence in blood and by raising blood insulin level, probably to a higher extent than fructose, stimulate DNL in adipose tissue. Intake of glucose, in amounts that exceed the total capacity for glycogen storage and glucose oxidation, may thus increase DNL in adipose tissue more than the same amount of fructose. While fat formed in the liver has to be transported as lipoproteins in blood, this is avoided if the fat is formed directly in adipose tissue. Considering known negative health effects of lipoprotein residues, DNL occurring in adipose tissue may be preferable compared with DNL in the liver. This may illustrate a metabolic difference between glucose and fructose when consuming large amounts of sugars.
Another possible difference between fructose and glucose on risk factors for atherosclerosis is the effect of these sugars on blood uric acid level. Increased uric acid level has been associated with atherosclerosis in epidemiological studies, but the causality is uncertain [112–114]. Fructose appears to increase uric acid levels in the blood to a higher extent than glucose, especially at high intakes and when consumed as excess energy [86, 115, 116]. Intake of 0.5 g fructose/kg body weight is the lowest quantity shown to result in uric acid formation [117]. An increased blood level of uric acid can theoretically lead to elevated blood pressure because uric acid inhibits an enzyme in the endothelial cells of the arteries called endothelial nitric oxide synthase (eNOS). Activated eNOS leads to increased production of nitric oxide (NO), an important vasodilator. Thus, inhibition of eNOS may lead to vasoconstriction. Although only 0.5 g fructose/kg body weight has been shown to give uric acid formation and increased uric acid level theoretically could increase blood pressure, results from studies of the effect of fructose on blood pressure are very inconsistent [65, 72, 118, 119]. An average intake of fructose does not seem to lead to increased blood pressure [111, 120, 121]. The lack of causal link between uric acid level and atherosclerosis makes it difficult to draw conclusions on this effect of fructose."
Look at table 3!
And the link is: fructose metabolism in a positive balance of calories.
http://www.hindawi.com/journals/jnme/2015/823081/
Hudgins, L. C., M. Hellerstein, C. Seidman, R. Neese, J. Diakun, and J. Hirsch. 1996. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J. Clin. Invest. 97: 2081– 2091.
Hudgins, L. C., C. E. Seidman, J. Diakun, and J. Hirsch. 1998. Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar. Am. J. Clin. Nutr. 67: 631–639.
Hellerstein, M .K. 1996. Regulation of hepatic de novo lipogenesis in humans. Annu. Rev. Nutr. 16: 523–557.
From the study of fructose metabolism quoted supra:
"
4. Atherosclerosis
It appears that high fructose intake can create an unfavorable lipid profile in blood via DNL [94]. The main product of DNL is palmitic acid [95], a fatty acid specifically shown to increase the risk of atherosclerosis [96]. Fatty acids formed by DNL will mainly be packed in VLDLs delivered into the bloodstream. This may, in turn, increase the level of low-density lipoproteins (LDLs) in the blood. In several studies, fructose has to a greater extent than glucose increased blood levels of triglycerides [51, 65, 97, 98] and LDLs [65, 99–103]. Aeberli et al. [104] showed that fructose increased the small dense LDLs, the type of LDLs that may in particular be linked to cardiovascular risk [105]. The level of high-density lipoproteins (HDLs) in blood does not seem to be affected by fructose [100, 101]. In most studies, an intake of fructose >100 g/day has been necessary to observe the adverse effects on lipid profiles [51, 65, 85, 98, 100, 106–108]. However, in a recent study by Aeberli et al. [109], a daily intake of about 77 g fructose and 34 g glucose for 3 weeks resulted in increased levels of total cholesterol and LDLs in the blood of healthy young men, compared with a daily intake of approximately 109 g glucose and 28 g fructose over the same time period. The fact that both groups also ingested an unknown amount of starch and the fact that food intake was not controlled reduce the solidity of these results. Maersk et al. [90] found that intake of 50 g fructose per day together with 50 g glucose could have a negative effect on blood triglyceride level. The lack of a control group ingesting glucose makes it difficult to conclude that this is an effect of fructose. Conversely, Lowndes et al. [110] found no negative effect on lipid profile in overweight or obese individuals consuming HFCS or sucrose incorporated in a eucaloric diet for ten weeks at levels corresponding to the 25th and 50th percentiles of adult fructose consumption. Using the current knowledge, it does not appear that the consumption of moderate amounts of fructose (<50 d="" g="" i="" nbsp="">alone will result in an unfavorable blood lipid profile [86, 111].
Due to the insignificant levels of fructose in peripheral blood, as described above, only glucose has the potential to be a substrate for DNL in adipose tissue. Although DNL in adipose tissue seems to be small as earlier discussed, glucose will, because of its presence in blood and by raising blood insulin level, probably to a higher extent than fructose, stimulate DNL in adipose tissue. Intake of glucose, in amounts that exceed the total capacity for glycogen storage and glucose oxidation, may thus increase DNL in adipose tissue more than the same amount of fructose. While fat formed in the liver has to be transported as lipoproteins in blood, this is avoided if the fat is formed directly in adipose tissue. Considering known negative health effects of lipoprotein residues, DNL occurring in adipose tissue may be preferable compared with DNL in the liver. This may illustrate a metabolic difference between glucose and fructose when consuming large amounts of sugars.
Another possible difference between fructose and glucose on risk factors for atherosclerosis is the effect of these sugars on blood uric acid level. Increased uric acid level has been associated with atherosclerosis in epidemiological studies, but the causality is uncertain [112–114]. Fructose appears to increase uric acid levels in the blood to a higher extent than glucose, especially at high intakes and when consumed as excess energy [86, 115, 116]. Intake of 0.5 g fructose/kg body weight is the lowest quantity shown to result in uric acid formation [117]. An increased blood level of uric acid can theoretically lead to elevated blood pressure because uric acid inhibits an enzyme in the endothelial cells of the arteries called endothelial nitric oxide synthase (eNOS). Activated eNOS leads to increased production of nitric oxide (NO), an important vasodilator. Thus, inhibition of eNOS may lead to vasoconstriction. Although only 0.5 g fructose/kg body weight has been shown to give uric acid formation and increased uric acid level theoretically could increase blood pressure, results from studies of the effect of fructose on blood pressure are very inconsistent [65, 72, 118, 119]. An average intake of fructose does not seem to lead to increased blood pressure [111, 120, 121]. The lack of causal link between uric acid level and atherosclerosis makes it difficult to draw conclusions on this effect of fructose."
 |
| http://www.wjgnet.com/1007-9327/full/v19/i8/1166.htm |
 |
| http://www.wjgnet.com/1007-9327/full/v19/i8/1166.htm |
If there is health claims why would there be different guidelines for nutritional supplements vs pharmaceutical drugs?
http://www.nutraingredients.com/Ingredients/Omega-3s-Nutritional-oils/What-degree-of-evidence-is-required-to-make-an-EU-health-claim/?utm_source=newsletter_product&utm_medium=email&utm_campaign=18-Aug-2015&c=dC5HnbRQjql21K9TeCAWSyv5nTSeb3u1
Si il ya des allégations de santé pourquoi y aurait-il des lignes directrices différentes pour les suppléments nutritionnels vs médicaments pharmaceutiques?
http://www.hsa.gov.sg/content/dam/HSA/HPRG/Complementary_Health_Products/Overview_Framework_Policies/Health_Supplements/HSGuidelines.pdf
http://www.fda.gov/Food/DietarySupplements/QADietarySupplements/ucm191930.htm
Si il ya des allégations de santé pourquoi y aurait-il des lignes directrices différentes pour les suppléments nutritionnels vs médicaments pharmaceutiques?
http://www.hsa.gov.sg/content/dam/HSA/HPRG/Complementary_Health_Products/Overview_Framework_Policies/Health_Supplements/HSGuidelines.pdf
http://www.fda.gov/Food/DietarySupplements/QADietarySupplements/ucm191930.htm
mercredi 26 août 2015
Hey parents Let them eating micro-organisms
http://m.pediatrics.aappublications.org/content/135/3/e590.full#sec-7
Le figaro fait la pub du vin
http://sante.lefigaro.fr/actualite/2015/08/21/24030-vin-est-bon-pour-coeura-faible-dose
Mais pas une seule citation!
Argument d'autorité d'un cardiologue
http://www.sciencedirect.com/science/article/pii/S0024320515001526
http://www.atlantico.fr/decryptage/desole-non-aucune-etude-serieuse-jamais-prouve-que-boire-vin-maintenait-en-meilleure-sante-guy-andre-pelouze-1738503.html
So HDL-C does not increase after wine consumption either white or red ones. If you look at the slides only 2 times a week exercise improve the so-called markers of atheroma...
http://www.atlantico.fr/decryptage/desole-non-aucune-etude-serieuse-jamais-prouve-que-boire-vin-maintenait-en-meilleure-sante-guy-andre-pelouze-1738503.html
| In Vino Veritas (IVV) Study: Randomized trial comparing long-term effects of red and white wines on markers of atherosclerosis and oxidative stress | ||||||||||||||||||||||||||||||||||||||||||||||||||
Authors:
M. Taborsky1, P. Ostadal2, T. Adam3, D. Rihova2, 1Palacky University, Faculty of Medicine and Dentistry, 1st Dept of Internal Medicine-Cardiology - Olomouc - Czech Republic, 2Na Homolce Hospital - Prague - Czech Republic, 3Palacky University, Faculty of Medicine and Dentistry, Clinical Biochemistry - Olomouc - Czech Republic, | ||||||||||||||||||||||||||||||||||||||||||||||||||
On behalf: Czech National Telemedicine Center
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| Topic(s): Epidemiology, lipids | ||||||||||||||||||||||||||||||||||||||||||||||||||
| Citation: European Heart Journal ( 2014 ) 35 ( Abstract Supplement ), 181 | ||||||||||||||||||||||||||||||||||||||||||||||||||
Background: Since the early 90s, a growing body of evidence has indicated that the mild to moderate consumption of wine, has a protective effect against cardiovascular diseases.
Methods: The IVV study is a first long-term, prospective, multicenter, randomized trial comparing the effects of red (RW) and white wine (WW) on atherosclerosis markers. 146 healthy subjects at mild to moderate risk of atherosclerosis have been randomized to a regular consumption of red wine (Pinot Noir) or white wine (Chardonnay-Pinot) /1 producer, 1 terroir/ for one year (women 0,2 l, men 0,3 l, 5 times a week, logbook for wine and other alcoholic beverages consumption). The primary endpoint is the level of HDL-cholesterol at one year, secondary endpoints are the levels of other markers of atherosclerosis (LDL-cholesterol, C-reactive protein) and oxidative stress (Lp-PLA2, Copeptin).
Results: The level of HDL significantly decreased at 6 months in WW group in comparison with baseline value (Table 1). We did not detect any differences in the levels of ALT, GGT or bilirubin.
Conclusion: In this prospective randomized trial we did not find between long-term mild consumption of red or white wine any clinically relevant differences in the lipid profile, CRP, fasting blood glucose, other markers of atherosclerosis i.e. Lp-PLA2 or copeptin, and liver function tests. Moreover, we were unable to confirm the hypothesis coming mostly from the retrospective studies that wine drinking is associated with elevation of HDL.
The study is registred by ISRCTN under Ref. No. 54359610.
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| Table 1. Change in endpoints at 6 and 12 months from the enrollment according to wine | ||||||||||||||||||||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||
So HDL-C does not increase after wine consumption either white or red ones. If you look at the slides only 2 times a week exercise improve the so-called markers of atheroma...
Why sugaring Iberico? Avoid this production
 |
| From the black pig fed in at least one hectare to the ham we need salt and dry air... |
 |
| Why adding all this stuff? Use pepper or piment d'Espelette like the Basks. http://tienda.covap.es/index.php?route=common/home |
Soybean oil and the role of veg oils in cvd
Soybean Oil Causes More Obesity and Diabetes Than Fructose
Soybean oil could contribute more to the development of diabetes and obesity than sugar….
Consumption of soybean oil, which is high in polyunsaturated fatty acids, has increased greatly within recent years as studies have shown that saturated fatty acids are associated with the risk of cardiovascular disease. Nutritional guidelines were created due to the results of these studies to encourage people to reduce their intake of saturated fats, commonly found in meat and dairy products, and to increase their intake of polyunsaturated fatty acids found in plant oils, such as soybean oil, a main ingredient in vegetable oil.
Researchers from the University of California Riverside conducted a study with male mice to examine the effect of both soybean oil and fructose on the development of obesity and its associated co-morbidities. The mice were fed a series of four diets containing 40% fat, similar to what Americans consume today. One of the diets included coconut oil, which contains mostly saturated fat, and another diet included soybean oil, which contains mostly polyunsaturated fat. The other two diets included fructose, commonly found in soda and processed food.
Mice on the high soybean oil diet had greater signs of metabolic syndrome such as increased weight gain, larger fat deposits, fatty liver with signs of injury, diabetes, and insulin resistance when compared to the mice on the high coconut oil diet. The mice on the fructose diet had less severe metabolic effects than the mice on the soybean oil diet. Mice on the soybean oil diet gained almost 25% more weight than the mice on the coconut oil diet and 9% more weight than the mice on the fructose diet.
The results from this study indicate that soybean oil causes more obesity and diabetes than a diet high in fructose. However, the study did not look at the impact of diet on cardiovascular disease. The researchers noted in their study that consumption of vegetable oil could be beneficial for cardiovascular health, even if it also induces obesity and diabetes.
Practice Pearls:Consumption of soybean oil, which is high in polyunsaturated fatty acids, has increased greatly within recent years as studies have shown that saturated fatty acids are associated with the risk of cardiovascular disease.Mice on the high soybean oil diet had greater signs of metabolic syndrome such as increased weight gain, larger fat deposits, fatty liver with signs of injury, diabetes, and insulin resistance when compared to the mice on the high coconut oil diet. The mice on the fructose diet had less severe metabolic effects than the mice on the soybean oil diet.The results from this study indicate that soybean oil causes more obesity and diabetes than a diet high in fructose. However, consumption of vegetable oil could be beneficial for cardiovascular health, even if it also induces obesity and diabetes.
Deol P, Evans JR, Dhahbi J, et al. "Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver." PLoS ONE. 2015;10(7).
http://www.diabetesincontrol.com/articles/diabetes-news/18371-soybean-oil-causes-more-obesity-and-diabetes-than-fructose?utm_content=buffer78e1c&utm_medium=social&utm_source=twitter.com&utm_campaign=buffer
mardi 25 août 2015
Do we skip uncontrolled trials?
- Smith MM, Sommer AJ, Starkoff BE and Devor ST. Crossfit-based high intensity power training improves maximal aerobic fitness and body composition. J Strength Cond Res doi: 10.1519/JSC.0b013e318289e59f
lundi 24 août 2015
Fast sugars and concentrated sugars or both
When you eat food it can contains either fast sugars or concentrated sugars. Fast sugars are simple or diosides which mean that two molecules of sugar are attached.
Glucose, fructose, saccharose (sucrose), lactose, are sweet. You feel the taste of sugar!
Concentrated sugars are chain of glucose.
Starch, glycogen, other polysaccharides are not sweet but their are concentrated glucose under the form of trains which each wagon is a molecule of glucose.
It is misleading to call concentrated sugars as slow sugars! They represent on the contrary a big carb load for the body metabolism.
Paradox or inappropriate use of statins?
"This survey investigates the use of statins in individuals older than 79 years by vascular disease.
There is little randomized evidence to guide the use of statins (HMG-CoA reductase inhibitors) in very elderly individuals (>79 years).1,2 Despite this, the very elderly have the highest rate of statin use in the United States.3 Given that few studies have investigated the use of statins among this population in a longitudinal manner by vascular disease, we set out to do so."
Butter not milk is protecting french people from CVD
Per capita consumption of milk and milk products in selected countries in 2011[20]
CountryMilk (liters)Cheese (kg)Butter (kg)
Ireland135.6 6.7 2.4
Finland127.0 22.5 4.1
United Kingdom105.9 10.9 3.0
Australia105.3 11.7 4.0
Sweden90.1 19.1 1.7
Canada78.4 12.3 2.5
United States75.8 15.1 2.8
Europe62.8 17.1 3.6
Brazil55.7 3.6 0.4
France55.5 26.3 7.5
Italy54.2 21.8 2.3
Germany51.8 22.9 5.9
Greece49.1 23.4 0.7
Netherlands47.5 19.4 3.3
India39.5 - 3.5
China9.1 - 0.1
CountryMilk (liters)Cheese (kg)Butter (kg)
Ireland135.6 6.7 2.4 Finland127.0 22.5 4.1 United Kingdom105.9 10.9 3.0 Australia105.3 11.7 4.0 Sweden90.1 19.1 1.7 Canada78.4 12.3 2.5 United States75.8 15.1 2.8 Europe62.8 17.1 3.6 Brazil55.7 3.6 0.4 France55.5 26.3 7.5 Italy54.2 21.8 2.3 Germany51.8 22.9 5.9 Greece49.1 23.4 0.7 Netherlands47.5 19.4 3.3 India39.5 - 3.5 China9.1 - 0.1dimanche 23 août 2015
jeudi 20 août 2015
mercredi 19 août 2015
Gov policies failed so let companies, schools, universities, administrations teach their workforce about nutrition
mardi 18 août 2015
Statins work for severe atheromatous patients who underwent CABG
 |
| Figure 2: Forrest plots of pooled treatment effect estimates of analysed clinical outcomes from all included trials (n = 54). AF: atrial fibrillation; OR: odds ratio; CI: confidence interval. |
"Importantly, the findings of the presented meta-analysis must be weighed against the clinical relevance for the individual patient. Whereas the described reductions of the length of stay on the ICU or in the hospital predominantly have more economic rather than clinical implications for the individual patient, it needs to be stressed that one death seems to be avoided in 118 patients with a statin pretreatment before surgery—a low-cost therapy that is well tolerated by most patients. Furthermore, the beneficial effect on the incidence of stroke and atrial fibrillation definitely is clinically relevant due to associated consequences for the patient in addition to the extensive additional health care costs."
"Although this work represents an updated version of the recently published meta-analysis of Liakopoulos et al. with a 3-fold increased patient population, the findings of the present review are still limited by the low number of available RCTs assessing statin effects on postoperative adverse events in patients undergoing cardiac surgery. It is noteworthy, that of all 54 included studies only 12 trials were RCTs with a negligible impact on the overall result with about 1000 patients. "
Look at this RCT
StaRT-CABG Trial; www.start-cabg.de
And
And
Sanders R, et al "Preoperative cardiovascular medication and postoperative mortality from coronary artery bypass graft surgery" Euroanaesthesia 2015; Abstract 7AP3-1.
7AP3-1
Preoperative cardiovascular medication and postoperative
mortality from coronary artery bypass graft surgery
Sanders R.1, Venkatesan S.2, Okoli G.2, Myles P. 2
1Universit y of Wisconsin, Dept of Anaesthesiology, Madison, United States,
2Universit y of Not tingham, Public Health, Nottingham, United Kingdom
Background and Goals of Study: Preoperative cardiovascular medication
can influence perioperative risk. Statins reduce perioperative risk from coronary
bypass graf t (CABG) surgery1 however the influence of other medication
including angiotensin converting enzyme inhibitors, calcium channel antagonists,
alpha2 adrenergic agonists and beta blockers is less clear2-4. Herein we
evaluated the influence of each of these medications on perioperative risk and
the long term and class protective ef fect of statins.
Materials and Methods: United Kingdom Clinical Practice Research Datalink
data from 16,192 patients aged 40 years or older that underwent CABG surgery
were obtained. Five multivariable logistic regression models, including
propensity scores and further Cox Regression analysis, were employed to
probe the robustness of the ef fect on perioperative mortality.
Results and Discussion: Exposure to statins was most prevalent (85.1% of
patients), followed by beta-blockers (72.8%), ACE inhibitors (60.5%), calcium
channel blockers (42.8%) and alpha-2 agonists (1.2%). Statins were associated
with a statistically significant protective ef fect against perioperative mortality
in all five logistic regression models with adjusted ORs (95% CI) ranging
from 0.26 (0.13 to 0.54) to 0.35 (0.18 to 0.67). Cox regression for perioperative
mortality [adjusted HR (95% CI): 0.40 (0.20 to 0.80)] and six-month mortality
[HR (95% CI): 0.63 (0.42 to 0.92)] produced similar results. Of the statins
tested, only simvastatin exerted protective ef fects (adjusted OR 0.33 (0.14 -
0.78). Consistent ef fects on perioperative mortality, for the other medications,
were not observed.
Conclusions: Statins exerted a significant protective ef fect on perioperative
mortality from CABG surgery that was not shared by the other cardiovascular
medications. Further data are needed on whether all statins exert similar effects.
[Figure 1]
References:
1. Kuhn Eur J Cardiothorac Surg. 2014;45:17-26.
2. Wijeysundera JACC 2003;41:1496-1505.
3. Yacoub Am J Kidney Dis. 2013;62:1077-1086.
4. Brinkman et al. JAMA Intern Med. 2014;174:1320-132.
lundi 17 août 2015
dimanche 16 août 2015
samedi 15 août 2015
vendredi 14 août 2015
Dietary sources of estrogen matter
Epidemiology
An estrogen-associated dietary pattern and breast cancer risk in the Swedish Mammography Cohort
Article first published online: 14 MAY 2015
DOI: 10.1002/ijc.29586
© 2015 UICC
Issue
International Journal of Cancer
Early View (Online Version of Record published before inclusion in an issue)
mercredi 12 août 2015
mardi 11 août 2015
Cholesterol and the brain: a very complex issue
http://atvb.ahajournals.org/content/24/5/806.abstract
http://cardiovascres.oxfordjournals.org/content/103/3/405.full
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| Production and interconversion of HDL particles in CNS and plasma. In brain parenchyma, ABCA1 transporter is expressed in neurons and astrocytes where it promotes the efflux of PL and UC to glia-derived apoE, thus leading to the formation of nascent lipoproteins. Moreover, discoidal apoA-I-containing HDL particles may enter the CNS via SR-BI-mediated uptake and other unknown mechanisms. Discoidal particles can further acquire PL and UC via ABCA1 and ABCG1. Maturation of discoidal particles into spherical lipoproteins likely involves the activity of LCAT, CETP, and PLTP, similar to what happens in plasma. Newly generated particles can be finally uptaken by neurons or astrocytes through the binding of apoE to LDLR family receptors. ABCA1: ATP-binding cassette transporter A1, ABCG1: ATP-binding cassette transporter G1; BBB: blood–brain barrier; CETP: cholesteryl ester transfer protein; CNS: central nervous system; EL: endothelial lipase; HL: hepatic lipase; LDLRs: LDL receptor family receptors; LCAT: lecithin:cholesterol:acyltransferase; PL: phospholipids; PLTP: phospholipid transfer protein; UC: unesterified cholesterol. |
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| Major cholesterol and apoE pathways in the CNS. Cholesterol is synthesized de novo in brain cells (neurons, astrocytes, microglial cells). Efflux of CNS cholesterol through the BBB occurs as 24(S)-hydroxycholesterol (24S-OH-C) and 27-hydroxycholesterol (27-OH-C). 24S-OH-C is produced exclusively in the CNS, 27-OH-C is produced in most organs. Unlike cholesterol, 24-S-OH-C and 27-OH-C can cross the BBB because of the hydroxylated side chains. Primarily astrocytes and microglia secrete HDL-like lipoproteins composed of cholesterol and phospholipids and apoE as the major apoprotein. ApoE is the ligand of these lipoproteins to the receptors of the LDL receptor family such as the LDL-receptor and LRP. Exchange of cholesterol and apos between CNS cells occurs via these lipoproteins. In plasma, 24S-OH-C and 27-OH-C are transported on lipoproteins such as LDL and HDL. De novo cholesterol synthesis in CNS cells can be regulated by the apoE-mediated uptake of lipoproteins via the LDL receptor family. ApoE is produced within the CNS and interacts with Aβ. The availability of cholesterol and of apoE are thought to affect amyloidogenesis and apoE (in particular the isoform apoE4) promoting the formation of amyloid fibrils from soluble Aβ in the CNS. The data for the steady state cholesterol pool have been determined from studies in healthy adults. The flux of cholesterol across the whole body is ~700 mg/day (CHOL INPUT/OUTPUT). The flux across the CNS is only 0.9% of whole body (~12 mg/day). The efflux of 24(S)-hydroxycholesterol through the BBB is limited to ~6-7 mg per day [64, 67], the daily influx of 27-hydroxycholesterol into the brain has been estimated to be ~5 mg [1]. Please note that the brain per kg organ contains 10 times more cholesterol than the rest of the body. |
How liver manage fat of different origins: dietary, de novo synthesis, release from adipose tissue
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| Overview of hepatic fatty acid metabolism in the postprandial state. Fatty acids enter a pool where they may be partitioned into oxidation (1) or esterification (2) pathways. There are TG storage and secretory pools. Fatty acids liberated from the hydrolysis of TG in the secretory TG pool, or TG particles, may then be partitioned to a storage TG pool (3). TG in the secretory pool is utilised for very low-density lipoprotein (VLDL) production (4) which enters systemic circulation. It remains unclear if fatty acids liberated from the TG pools enter oxidation pathways (dotted line, (5)). Abbreviations: TG, triglyceride; VLDL, very low-density lipoprotein; DNL, de novo lipogenesis; FA, fatty acid; NEFA, non-esterified fatty acids; ApoB, apolipoprotein B; 3OHB, 3-hydroxybutyrate; ER, endoplasmic reticulum. |
For instance if you have big fat stores, if you eat lot of sugars and no fat, your liver will synthetize VLDL... Despite your fat intake is very low.
Second example if you are on a low carb diet, if your BMI and W/H ratio are normal your liver has less sources of de novo lipogenesis, less free fatty acids released by fat stores and will only rely on your fat intake to synthesize VLDL.
Second example if you are on a low carb diet, if your BMI and W/H ratio are normal your liver has less sources of de novo lipogenesis, less free fatty acids released by fat stores and will only rely on your fat intake to synthesize VLDL.
"Determining the contribution of specific fatty acid sources (Figure 1) can be achieved with the use of stable-isotope tracers. Using a multi-tracer approach Donnelly et al. [48] determined the contribution of specific sources of fatty acid to liver and VLDL-TG in NAFLD patients (n = 8). After five days of labeling, they reported there was no difference in the contribution of fatty acids originating from systemic NEFA, DNL or diet to liver and VLDL-TG [48]. On the basis of this observation, the authors suggested that VLDL-TG may be used as a surrogate marker of the liver TG/fatty acid pool [48]. Dietary fatty acids have been reported to contribute 2%–28% of VLDL-TG [48,49,50,51]. Fatty acids originating from systemic NEFA contribute 45%–75% and from hepatic DNL fatty acids contribute 13%–37% to VLDL-TG [48,49,50,51]. The wide-range in findings may be explained by differences in the length of the postprandial phase, the type of test meal fed and hepatic uptake, and/or alterations in the turnover time of the hepatic TG pool, which may be influenced by size of the pool."
Some insights in the different sources of hepatic synthesis of VLDL.
And this remark:
"These data demonstrate that the most important contributing factor to whether liver fat accumulation occurs is the amount of total energy consumed, rather than the composition of the diet. Notably, liver fat decreases more rapidly when a hypo-caloric diet devoid of carbohydrate is consumed, compared to calorie restriction alone [62,64]."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4245577/
And this remark:
"These data demonstrate that the most important contributing factor to whether liver fat accumulation occurs is the amount of total energy consumed, rather than the composition of the diet. Notably, liver fat decreases more rapidly when a hypo-caloric diet devoid of carbohydrate is consumed, compared to calorie restriction alone [62,64]."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4245577/
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