lundi 29 février 2016
What is the real cost of food?
"Cheap food is an illusion. There is no such thing as cheap food. The real cost of the food is paid somewhere. And if it isn't paid at the cash register, it's charged to the environment or to the public purse in the form of subsidies. And it's charged to your health."~Michael Pollan
dimanche 28 février 2016
samedi 27 février 2016
vendredi 26 février 2016
jeudi 25 février 2016
Labelling scandal: in EU saturated fats are mandatory on labels but not industrial trans fats
http://www.ncbi.nlm.nih.gov/pubmed/18468872
http://journals.cambridge.org/download.php?file=%2FNRR%2FNRR24_01%2FS0954422411000011a.pdf&code=56a9ee4438d93f1d5e74d9e8bd98cb77
We should do more about this issue.
Saturated fats are neutral, they were incriminated in the past on an erroneous base. Industrial trans fats are deleterious for CVD, D2 and cancer. Why the EU did not ignore those scientific facts? Because of the pressure of the agro-food industry and the dairy industry. But we know now that only industrial trans fats (ITF) are deleterious.
So the EU bureaucrats should take one decision on this issue in order to protect public health as ITF are not GRAS: requiring labelling of ITF for all foods in the EU.
http://journals.cambridge.org/download.php?file=%2FNRR%2FNRR24_01%2FS0954422411000011a.pdf&code=56a9ee4438d93f1d5e74d9e8bd98cb77
We should do more about this issue.
Saturated fats are neutral, they were incriminated in the past on an erroneous base. Industrial trans fats are deleterious for CVD, D2 and cancer. Why the EU did not ignore those scientific facts? Because of the pressure of the agro-food industry and the dairy industry. But we know now that only industrial trans fats (ITF) are deleterious.
So the EU bureaucrats should take one decision on this issue in order to protect public health as ITF are not GRAS: requiring labelling of ITF for all foods in the EU.
mercredi 24 février 2016
mardi 23 février 2016
samedi 20 février 2016
Arsenic does not increase your CVD risk unless you smoke or have been a heavy smoker
http://www.sciencedirect.com/science/article/pii/S0041008X1530003X
This study is indeed very interesting egos the authors did statistics to separate the effect on arsenic and smoking on your CVD risk.
Arsenic measured in your toe nail is not it not correlated to your CVD risk.
If your are a smoker or if you stopped smoking after eight long-term use of tobacco then arsenic increases from 50 to 70 percent your risk of cardiovascular disease.
These results are consistent with evidence from more highly exposed populations suggesting a synergistic relationship between arsenic exposure and smoking on health outcomes and support a role for lower-level arsenic exposure in ischemic heart disease mortality.
This study is indeed very interesting egos the authors did statistics to separate the effect on arsenic and smoking on your CVD risk.
Arsenic measured in your toe nail is not it not correlated to your CVD risk.
If your are a smoker or if you stopped smoking after eight long-term use of tobacco then arsenic increases from 50 to 70 percent your risk of cardiovascular disease.
These results are consistent with evidence from more highly exposed populations suggesting a synergistic relationship between arsenic exposure and smoking on health outcomes and support a role for lower-level arsenic exposure in ischemic heart disease mortality.
jeudi 18 février 2016
mercredi 17 février 2016
mardi 16 février 2016
lundi 15 février 2016
dimanche 14 février 2016
Sugar collapses your testosterone blood level
Is it possible that testosterone decline was rooted in the overwhelming wave of dietary sugar?
http://www.jci.org/articles/view/32249/figure/1
http://www.jci.org/articles/view/32249/figure/1
Effect of Glycaemic index of the diet on salivary cortisol and testosterone levels in females
Emad Al-Dujaili & Sophie Ashmore
There has been great interest in the effect of Glycaemic index (GI) of food on weight reduction, obesity, metabolic syndrome and general well being in women. The majority of research into GI was focussed towards improving blood glucose control in diabetes. Also, favourable changes in blood lipids and some beneficial effect in cancers have been reported. The aim of this pilot study is to investigate the impact of ingesting food with varying GI on salivary cortisol and testosterone levels.
A cross-over design was adopted and 8 healthy female subjects volunteered for the study (20–23 years old). The project has received ethical approval by QMUC ethical committee. A diet is said to be of low GI if it has a GI of less than 55, medium GI if it has a GI of 56–69, and a high GI if it is 70 or greater. All subjects consumed a low GI or high GI diet for three days each, with a washout period separating the two. Saliva samples at baseline, after the low GI diet, washout period and high GI diet were collected at 4 different times during the day. Salivary cortisol and testosterone concentrations were measured by ELISA methods.
GI was significantly different between the low and high GI diets. No significant difference in cortisol concentration was found on either diet. Significantly more testosterone was produced on the low GI diet compared to basal values (related t-test P=0.05) (see Table below). It was found that lower calories were consumed on the low GI diet compared to the high GI diet and the subject’s normal diet was very similar to the high GI diet.
| Steroid | Basal | Low GI | Washout | High GI | Unit |
| Cortisol | 8.834 | 11.18 | 9.54 | 9.19 | ng/mL |
| Testosterone | 83.71 | 123.2 | 111.14 | 101.15 | pg/mL |
In conclusion, it appears that GI of the diet consumed by females influences a variety of parameters and that a low GI diet might increase salivary testosterone concentrations.
jeudi 11 février 2016
Scientific quality
http://m.ajcn.nutrition.org/content/early/2016/02/10/ajcn.115.112771.abstract?papetoc
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0144980
http://ajcn.nutrition.org/content/102/5/991.abstract
http://ajcn.nutrition.org/content/102/5/991.abstract
mercredi 10 février 2016
Meta-analysis on palm oil
http://www.straitstimes.com/asia/palm-oil-producers-angry-over-nus-finding-on-cholesterol-link?utm_campaign=Echobox&utm_medium=Social&utm_source=Facebook#xtor=CS1-10
Palm Oil Consumption Increases LDL Cholesterol Compared with Vegetable Oils Low in Saturated Fat in a Meta-Analysis of Clinical Trials1,2,3
Ye Sun4,7,
Nithya Neelakantan4,
Yi Wu4,
Rashmi Lote-Oke4,
An Pan4, and
Rob M van Dam4–7*
+Author Affiliations
4Saw Swee Hock School of Public Health and
5Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore;
6Department of Nutrition, Harvard School of Public Health, Boston, MA; and
7NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore
Palm Oil Consumption Increases LDL Cholesterol Compared with Vegetable Oils Low in Saturated Fat in a Meta-Analysis of Clinical Trials1,2,3
Ye Sun4,7,
Nithya Neelakantan4,
Yi Wu4,
Rashmi Lote-Oke4,
An Pan4, and
Rob M van Dam4–7*
+Author Affiliations
4Saw Swee Hock School of Public Health and
5Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore;
6Department of Nutrition, Harvard School of Public Health, Boston, MA; and
7NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore
This meta-analysis is helpful.
First and overall it deals with lipid profile as a risk factor of atheroma. It is not an epidemiologic study or a meta-analysis of epidemiological studies about CVD and PO consumption. Epidemiologic study of saturated fat consumption and CVD especially CVD mortality of myocardial infarction and stroke did not show any significant correlation.
If we study lipid profile this meta-analysis is helpful.
Saturated fats and especially palmitic acid increase LDL cholesterol and moderately HDL cholesterol.
If you consume a lot of palm oil especially refined you should mix with olive oil or another oil less rich in palmitic and/or other saturated fatty acids.
First and overall it deals with lipid profile as a risk factor of atheroma. It is not an epidemiologic study or a meta-analysis of epidemiological studies about CVD and PO consumption. Epidemiologic study of saturated fat consumption and CVD especially CVD mortality of myocardial infarction and stroke did not show any significant correlation.
If we study lipid profile this meta-analysis is helpful.
Saturated fats and especially palmitic acid increase LDL cholesterol and moderately HDL cholesterol.
If you consume a lot of palm oil especially refined you should mix with olive oil or another oil less rich in palmitic and/or other saturated fatty acids.
If your consumption is low you can enjoy the taste and texture of cooking with palm oil especially red palm oil.
You should another time be advised to avoid trans fats which are easily replaced by palm or coconut oils.
http://www.italiaatavola.net/alimenti/tendenze-e-mercato/2015/12/15/olio-palma-grasso-naturale-preso-ostaggio-falsa-credenza/42414
You should another time be advised to avoid trans fats which are easily replaced by palm or coconut oils.
http://www.italiaatavola.net/alimenti/tendenze-e-mercato/2015/12/15/olio-palma-grasso-naturale-preso-ostaggio-falsa-credenza/42414
mardi 9 février 2016
Misconception about D2 and insulin resistance
Sugar is provoking a lot of deleterious effects on cell components when out of the normal range in the blood. The body goes to different and even extraordinary measures to keep it in normal range. When you take in a huge amount, say from a banana, with waffle and syrup, the body suffers a metabolic emergency, trying to dispose of the toxic stuff.
Insulin is secreted in large quantities to deal with a high carbohydrate intake after sugar digested and glucose released. Insulin activates very potent mechanisms to recent sugar toxicity. It pushes fat out of the way by stopping lipolysis, and pushes glucose to the front of the queue to be burned.
The body is not burning glucose because it likes glucose as a fuel. It is burning glucose until blood glucose level is non toxic i.e. under 1g/l. In the liver insulin signals to cells to take excess glucose in the blood and turn it into fat it is neolipidogenesis. In the adipose tissue, insulin pushes fat into the fat cells and won’t let it out as NEFA or FFA (http://m.diabetes.diabetesjournals.org/content/60/10/2441.full)
All of this is done to keep blood sugar in the normal range by disposing of excess glucose.
1/ this state is continuous over day and night if you eat continuously in excess mainly sugars
2/ this continuous insulin secretion leads after time to insulin resistance which is an adapted reaction of cells all over the body to insulin excess
3/ in order to maintain glucose level in the blood more insulin is needed but production could be impaired by cell loss in the pancreas.
4/ fructose either free or from saccharose leads to less insulin secretion but increases visceral and liver fat.
This is metabolic syndrome and D2 genesis !
dimanche 7 février 2016
samedi 6 février 2016
vendredi 5 février 2016
jeudi 4 février 2016
mercredi 3 février 2016
mardi 2 février 2016
D2: insulin resistance disease is an adaptation
http://www.cardiab.com/content/15/1/17
http://www.ncbi.nlm.nih.gov/m/pubmed/25713189/
As a matter of fact insulin resistance is a very potent biomarker of cardiovascular diseases in a healthy population
Yip J, Facchini FS, Reaven GM 1998 Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. J Clin Endocrinol Metab 83:2773–2776 [Abstract][Medline]
http://press.endocrine.org/doi/10.1210/jcem.86.8.7763?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&
As a matter of fact insulin resistance is a very potent biomarker of cardiovascular diseases in a healthy population
Yip J, Facchini FS, Reaven GM 1998 Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. J Clin Endocrinol Metab 83:2773–2776 [Abstract][Medline]
http://press.endocrine.org/doi/10.1210/jcem.86.8.7763?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&
lundi 1 février 2016
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