lundi 28 mai 2018
samedi 26 mai 2018
Evol Mismatch and diseases
Present Dysnutrition could be spelt mismatch of food supply and food behaviour with our evolutionary past. Our conditions of life our ecological niche are every day farther from our genomic foundation, it is a tech-driven process but it could be modified.
We have to slow this stretching and to maintain a quality food supply.
https://www.psychologytoday.com/intl/blog/naturally-selected/201804/evolutionary-mismatch
We have to slow this stretching and to maintain a quality food supply.
https://www.psychologytoday.com/intl/blog/naturally-selected/201804/evolutionary-mismatch
1. Li, N. P., van Vugt, M., & Colarelli, S. M. (2017). The Evolutionary Mismatch Hypothesis: Implications for Psychological Science. Current Directions in Psychological Science, 0963721417731378.
2. Giphart, R., & Van Vugt, M. (2018). Mismatch: How our stone age brains deceive us every day and what we can do about it. London: Robinson.
3. Hahn-Holbrook, J., & Haselton, M. (2014). Is postpartum depression a disease of modern civilization? Current directions in psychological science, 23(6), 395-400.
4. This View of Business: How Evolutionary Thinking Can transform the workplace. Special issue with collections from scholars and practitioners on the nexus of evolutionary and organizational sciences.
5. Van Vugt, M., & Ahuja, A. (2011). Naturally selected: The evolutionary science of leadership. New York: HarperBusiness.
6. Van Vugt, M., & Ronay, R. (2013). The evolutionary psychology of leadership: Theory, review, and roadmap. Organizational Psychology Review, 2041386613493635.
jeudi 24 mai 2018
mercredi 23 mai 2018
Sunny photons and your health
You need photons from the sun
https://grassrootshealth.net/document/sunny-hippocrates-presents-sun-wisdom/
https://grassrootshealth.net/document/sunny-hippocrates-presents-sun-wisdom/
mardi 22 mai 2018
Organic pork sausages and sugars
 |
| Lactose, dextrose, sugar and potassium nitrate, a fair contract would have been to mention the quantities Lactose, dextrose, sucre et nitrate de potassium, un contrat équitable aurait été de mentionner les quantités |
 |
| Is it mandatory to add glucose, lactose and saccharose in order to stimulate the growth of some bacterias? |
Hibiscus Juice
Read more at https://www.thestar.com.my/news/community/2007/06/05/family-goes-green-for-planet-earth/#5HwL97e66WK5wIbg.99
vendredi 18 mai 2018
Ketogenic diet is anti-inflammatory
http://www.mdpi.com/2076-3921/7/5/63/htm
More, in this paper the biochemical advantages of ketones as substrate for mitochondrial integrity are exposed
More, in this paper the biochemical advantages of ketones as substrate for mitochondrial integrity are exposed
mercredi 16 mai 2018
Palmitic acid and CVD
We should question the papers where sat fats are associated with CVD
This paper (http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0193533) is important as it challenges the over repeated "truth" that sat fats causes atheroma. I would like to address some aspects of the literature you quoted in your paper on palmitic acid. In the paper of Kabagambe, (https://academic.oup.com/jn/article/135/11/2674/4669885) it is stated that Soybean oil with 22% TF is less atherogenic than PO with 1,5% TF. So a very TF loaded oil could give less IHD to patients (table3)? That is very unlikely because TF is constantly associated with a higher IHD rate in populations that consumed them and TF is associated with an RR of CHD far more higher than any of individual sat fatty acids or all sat fats taken together. More, TF are not only associated with IHD with an increased RR proportional to consumption but they fulfilled several criteria of causality. So this paper is not reliable. But there is in my view another problem. Kabagambe reported very conflicting results in the publications you quoted. And their conclusion is erroneous because, in the multivariate model, which took in account all the differences in the two populations at the start of the study, there is no difference between PO and other oils: 1.23 (0.99–1.52). In a previous paper of the same team that you also quoted (https://www.nature.com/articles/1601709#t3), there are higher Risk Ratios of CVD with sat fats. This is less than probable and access to the raw data should be interesting, but another finding is questionable: "Consumption of cheese, a major source of lauric and myristic acid, was associated with a three-fold increase in the risk of MI ". Prospective studies (https://www.bmj.com/content/349/bmj.g6015) and epidemiological studies which showed the very low prevalence of CHD in Switzerland and France have refuted this finding. Indeed, it is very disappointing that other potential causal factors than fat, which are present in milk shouldn't have been discussed to explain a higher CVD risk (https://www.bmj.com/content/349/bmj.g6015/rr/804415). So as for other papers on the subject, the so-called atherogenicity of sat fats does not resist a very precise analysis of data and is contradicted by unpicked observational studies especially if we keep in mind that the two European countries where the consumption of sat fats is the highest (id est Switzerland and France) have the lowest prevalence of CHD; a fact that A Keys was perhaps aware of but which didn't appear in the seven countries study.
Nous devrions remettre en cause les publications où les graisses saturées sont associées aux MCV
Cet article (http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0193533) est important car il remet en question la "vérité" répétée que les graisses saturées causent l'athérome. J'aimerais aborder certains aspects de la documentation que vous avez citée dans votre document sur l'acide palmitique. Dans le papier de Kabagambe, (https://academic.oup.com/jn/article/135/11/2674/4669885) il est indiqué que l'huile de soja avec 22% TF est moins athérogène que PO avec 1,5% TF . Donc, une huile très chargée en TF pourrait donner moins d'IHD aux patients (tableau 3)? Cela est très improbable parce que TF est constamment associé à un taux plus élevé de DHI dans les populations qui les ont consommés et TF est associé à un RR de CHD beaucoup plus élevé que n'importe quel acide gras saturé ou tous les acides gras saturés pris ensemble. De plus, les TF ne sont pas seulement associés à l'IHD avec un RR accru proportionnel à la consommation, mais ils remplissent plusieurs critères de causalité. Donc, ce document n'est pas fiable. Mais il y a selon moi un autre problème. Kabagambe a rapporté des résultats très contradictoires dans les publications que vous avez citées. Et leur conclusion est erronée parce que, dans le modèle multivarié, qui a pris en compte toutes les différences dans les deux populations au début de l'étude, il n'y a pas de différence entre les OP et les autres huiles: 1,23 (0,99-1,52). Dans un article précédent de la même équipe que vous avez également cité (https://www.nature.com/articles/1601709#t3), il existe des ratios de risque plus élevés de CVD avec les graisses saturées. Ceci est moins que probable et l'accès aux données brutes devrait être intéressant, mais une autre conclusion est discutable: «La consommation de fromage, une source majeure d'acide laurique et myristique, était associée à une triple augmentation du risque d'IM». Des études prospectives (https://www.bmj.com/content/349/bmj.g6015) et des études épidémiologiques qui ont montré la très faible prévalence de la coronaropathie en Suisse et en France ont réfuté cette constatation. En effet, il est très décevant que d'autres facteurs de causalité potentiels que la graisse, qui sont présents dans le lait, n'aient pas dû être discutés pour expliquer un risque de MCV plus élevé (https://www.bmj.com/content/349/bmj.g6015/ rr / 804415). Comme pour les autres articles sur le sujet, l'athérogénicité des graisses saturées ne résiste pas à une analyse très précise des données et est contredite par des études observationnelles non sélectionnées, surtout si l'on garde à l'esprit que les deux pays européens où la consommation de graisses saturées est la plus élevée (id est la Suisse et la France) ont la plus faible prévalence de maladies coronariennes; un fait dont A Keys était peut-être conscient mais qui n'apparaissait pas dans l'étude des sept pays.
Beaucoup de contre-vérités sur le « cholestérol »: pas une seule fois le mot particules lipidiques!
http://www.rtl.fr/actu/debats-societe/cholesterol-quelle-alimentation-adopter-7793254704
Stupidité anti-scientifique absolue. Le cholestérol ALIMENTAIRE n’a rien à voir avec le cholestérol SANGUIN. Donc il est inutile de s'intéresser aux aliments « pauvres » en cholestérol. A partir de là tout est faux dans ces recommandations culinaires!
Stupidité anti-scientifique absolue. Le cholestérol ALIMENTAIRE n’a rien à voir avec le cholestérol SANGUIN. Donc il est inutile de s'intéresser aux aliments « pauvres » en cholestérol. A partir de là tout est faux dans ces recommandations culinaires!
Décryptage Nutella: un publireportage du Figaro sans avertissement
http://sante.lefigaro.fr/actualite/2016/02/04/24573-nutella-bete-noire-dietetique
Le seul sujet concernant le Nutella n’a rien à voir avec le gras et l’huile de palme.
Quand on absorbe un aliment transformé qui est à 56-57 % de sucre il faut s’assurer qu’on est pas insulino-résistant. Et ce n’est pas une condition rare! Obésité centrale, glycémie à jeun élevée et voilà l’insuliorésistance démasquée.
Le reste n’a aucune importance du point de vue nutritionnel et métabolique dans la composition du Nutella. C’est pourquoi le publireportage se focalise sur le reste...
Le seul sujet concernant le Nutella n’a rien à voir avec le gras et l’huile de palme.
Quand on absorbe un aliment transformé qui est à 56-57 % de sucre il faut s’assurer qu’on est pas insulino-résistant. Et ce n’est pas une condition rare! Obésité centrale, glycémie à jeun élevée et voilà l’insuliorésistance démasquée.
Le reste n’a aucune importance du point de vue nutritionnel et métabolique dans la composition du Nutella. C’est pourquoi le publireportage se focalise sur le reste...
dimanche 6 mai 2018
Traffic lights for diet: a system badly parametered
 |
| Looking at this picture is sufficient to explain why this system will not improve food behaviour: low-fat foods fueled the obesity epidemic (DOI 10.1038/s41574-018-0002-8) |
Reduce the eating behaviour in three colours and in addition to perpetuate past mistakes, it had to be done! Our kids and adolescents derve better. #Smartbehaviour #trafficlightsforoldcars
Let them drink full-fat milk and full-fat cheeses! You probably have seen that fish and seafood are not on the table of regulators...
It is a bet lost in advance of wanting to guide the behaviour of food with three colours. There are other, smarter ways.
Réduire le comportement alimentaire à trois couleurs et en plus perpétuer les erreurs passées, il fallait le faire! Nos enfants et adolescents méritent mieux. #Smartbehaviour#trafficlightsforoldcars
More on statins: your baseline LDL cholesterol does matter dramatically
https://jamanetwork.com/journals/jama/article-abstract/2678614?redirect=true
This very interesting meta-analysis should engage researchers to reconsider the design of future trials with lipid-lowering drugs including PCSK9 i.
Patients with low LDL cholesterol at baseline don't benefit from statins. This si not completely new but this is nicely showed by this work.
The lack of efficacy of statins for stroke is more disturbing. It means that we need the raw data of SPARCL to verify this trial.
1/ Should we reconsider prescriptions of statins according to the baseline level of LDL cholesterol?
Lin disaggrees
https://www.practiceupdate.com/c/66963/67/17/?elsca1=emc_enews_weekinreview&elsca2=email&elsca3=practiceupdate_cdd&elsca4=cdd&elsca5=newsletter&rid=MzMwNjc5MDUwNzk4S0&lid=10332481
2/ This meta-analysis of 34 trials was conducted to evaluate the effect of baseline LDL-C levels on mortality following the use of LDL-C–lowering drugs. All-cause mortality was 7.08% in those treated with more intensive therapy vs 7.70% in those who received less intensive therapy, but this varied according to baseline LDL-C levels. It is a true dilemma.
3/ The reduction in all-cause mortality was greater with a higher baseline LDL-C level but only with a baseline LDL-C ≥100 mg/dL. Similarly, cardiovascular mortality was lower in those receiving intensive therapy than those treated with less intensive therapy, and, again, the greater benefit obtained at higher baseline LDL-C levels was only seen for patients with a baseline LDL-C ≥100 mg/dL. The greatest mortality reductions were seen among people with a baseline LDL-C level ≥160 mg/dL.
1/ Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344(8934):1383-1389. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(94)90566-5/abstract
2/ LaRosa JC1, Grundy SM, Waters DD, et al; Treating to New Targets (TNT) Investigators. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-1435. http://www.nejm.org/doi/10.1056/NEJMoa050461
3/ SPARCL https://www.nejm.org/doi/full/10.1056/NEJMoa061894
 |
| Surprisingly no advantage for Stroke |
This very interesting meta-analysis should engage researchers to reconsider the design of future trials with lipid-lowering drugs including PCSK9 i.
Patients with low LDL cholesterol at baseline don't benefit from statins. This si not completely new but this is nicely showed by this work.
The lack of efficacy of statins for stroke is more disturbing. It means that we need the raw data of SPARCL to verify this trial.
1/ Should we reconsider prescriptions of statins according to the baseline level of LDL cholesterol?
Lin disaggrees
https://www.practiceupdate.com/c/66963/67/17/?elsca1=emc_enews_weekinreview&elsca2=email&elsca3=practiceupdate_cdd&elsca4=cdd&elsca5=newsletter&rid=MzMwNjc5MDUwNzk4S0&lid=10332481
2/ This meta-analysis of 34 trials was conducted to evaluate the effect of baseline LDL-C levels on mortality following the use of LDL-C–lowering drugs. All-cause mortality was 7.08% in those treated with more intensive therapy vs 7.70% in those who received less intensive therapy, but this varied according to baseline LDL-C levels. It is a true dilemma.
3/ The reduction in all-cause mortality was greater with a higher baseline LDL-C level but only with a baseline LDL-C ≥100 mg/dL. Similarly, cardiovascular mortality was lower in those receiving intensive therapy than those treated with less intensive therapy, and, again, the greater benefit obtained at higher baseline LDL-C levels was only seen for patients with a baseline LDL-C ≥100 mg/dL. The greatest mortality reductions were seen among people with a baseline LDL-C level ≥160 mg/dL.
4/ As LDL cholesterol is calculated and doesn't figure the reality of LDL particles one can take some distance with the statin dogma.
However there as some biases:
1/ "Interestingly, the older studies, such as 4S, enrolled patients with very high LDL-C because none of the participants was on any treatment. These were also the statin vs true placebo trials. So, maybe the benefit that we are seeing in patients with a high baseline LDL-C is based on this phenomenon. However, over time, we treated to lower and lower levels of LDL-C, and hence the newer trials enrolled patients with lower baseline LDL-C because those with higher LDL-C levels needed to be treated already, and therefore had lower LDL-C at baseline. Also, as statins became standard of care, the newer trials had to test statins against statins as opposed to a true placebo. Therefore, these newer studies would have a harder time showing benefits relative to death, in contrast to the older trials, which studied statins against placebo." Good point.
2/ "The final concern with this article is that the primary and secondary prevention studies were mixed together. The two groups would have very different death rates, and hence some effort should have been made to separate them."
2/ "The final concern with this article is that the primary and secondary prevention studies were mixed together. The two groups would have very different death rates, and hence some effort should have been made to separate them."
So keeping in mind that the higher the LDL at baseline the more benefit the patient will obtain with statins is fair.
Treating patients without symptoms and moderate elevation of LDL cholesterol is not evidence-based.
References
Treating patients without symptoms and moderate elevation of LDL cholesterol is not evidence-based.
1/ Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344(8934):1383-1389. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(94)90566-5/abstract
2/ LaRosa JC1, Grundy SM, Waters DD, et al; Treating to New Targets (TNT) Investigators. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-1435. http://www.nejm.org/doi/10.1056/NEJMoa050461
3/ SPARCL https://www.nejm.org/doi/full/10.1056/NEJMoa061894
samedi 5 mai 2018
Hypertension and salt (sodium chloride)
 |
| One has to keep in mind that the no salt diet is not a general recommendation but must be tailored to every individual |
https://www.ncbi.nlm.nih.gov/pubmed/28202621
 |
| Low plasma K+ decreases Na+ excretion and diuresis |
http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD004022.pub4/full
mercredi 2 mai 2018
Coronary grafting
 |
| If you need a CABG you need a mammary artery or a radial one... |
https://www.nejm.org/doi/pdf/10.1056/NEJMoa1716026
Inscription à :
Articles (Atom)
Articles
