Meat and your health

https://sustainabledish.com/20-ways-eat-lancets-global-diet-is-wrongfully-vilifying-meat/?fbclid=IwAR1do9DRQVogOC-atvH4xRVO2DF3EHl4pyPOtM6kXOC4Ars7fZqM5JcDrkM

Milk and pesticides

https://eu.usatoday.com/story/money/2019/06/26/study-finds-organic-milk-cleaner-than-conventional-dairy/1482508001/

Inflammation in arteries

What is triggering inflammation in arteries?
I ask myself the same question since I read the seminal paper of Ross.
1/ in my practice I observed that heavy smokers do have the more extensive and accelerated forms of atheroma. They also present this kind of low grade systemic inflammatory state with a moderate increase of CRP and other inflammatory proteins, fibrinogen and prothrombotic imbalance of platelet activity and coagulation.
2/ but atheroma occur also in non-smokers I agree. Who are those patients? First the diabetic patients and patients with insulin resistance. Interestingly in the two papers, I sent to our group, excessive glycolysis in immune cells ( either because of dietary prédominance of carbs and/or because of genomics ) could contribute locally to an inflammatory metabolic state which builds plaques in areas of shear stress, or of damage to the glycocalyx or of retention of LDL or chylomicrons.
3/ atheroma is not a mandatory ageing process of arteries. I operated on nonagenarian patients for cardiac emboli with normal femoral, iliac or more distal arteries.


Obviously, there are initial damages of the arterial wall, to the glycocalyx and to endothelial cells by flow disturbances ( hypertension), smoke products, hyperglycemia and possible infections (bacteria in the blood).

Those damages occur only in arteries because flow conditions in veins do not damage the glycocalyx nor the endothelial cells despite the circulation of the same chemical molecules or biological weapons.

Those damages occur in transfer arteries and not on branches which penetrate deeply in organs. One possible explanation is the fact that in those arteries no lipid particles are supposed to cross to tissues. So they are stagnating in the wall after entering it, because of the damages to glycocalyx and endothelial cells.

Those damages allow LDL particles to enter the arterial wall at those sites where the endothelial barrier is the more damaged. Plaque formation is the following step because retention and inflammation drive immune cells to try to solve the problem by scavenging and destroy those LDL particles either native or modified by ROS in the subendothelial space or in the media of the artery.
Further steps are well known.

Two final remarks:
-only LC W3 PUFA and a potent anti-inflammatory drug have shown a significant risk reduction of cardiac deaths in clinical trials
-if glycolysis is so important in immune cells involved locally in plaque building, a drastic reduction of carbs should be a potent anti-inflammatory tool even in secondary prevention...

This puzzle is far from complete but it seems to me better shaping the reality.

Number of LDL particles
https://www.biorxiv.org/content/10.1101/691089v1?fbclid=IwAR3ruGfvYNffBiPKfC0cLX6Tv7H3BdcvYbbepyBuDn_lhto2WUsRbL4sfuY

Those with insulin resistance have smaller particles.

Why?

Because of cholesteryl ester transfer protein (CETP) and the transferring CE and triglycerides between the lipoproteins. LDLs become smaller, HDLs become smaller and go out through the kidneys, and you have similar levels of serum cholesterol but more particles. The size may have some influence but it’s possible larger can have their own issues because of aggregation and possibly more readily retained.

More particles increases the likelihood of modification happening. It is also a sign, as we have discussed, that the particles are hanging around longer in serum, depleting their antioxidant potential, which increases the likelihood of modification.
it will correlate with that, yes, as will the total-to-HDL-C ratio, the particle size, and the ApoB, but it is not deterministic of it. Particles getting into the subendothelial space is necessary but not sufficient for them to be atherogenic. Residence time within the subendothelial space is strongly influenced by the proteglycan matrix, the vulnerability to oxidation is strongly influenced by particle composition including antioxidant load, and how oxidizing an environment the subendothelial space is is strongly influenced by inflammation and other factors in the endothelial cells. More non-atherogenic particles in non-atherogenic conditions isn't going to increase the atherogenicity.

A Mendelian randomization tries to look at causality, doesn't it? Rather than biomarkers?

No excuse Doc to ignore nutrition and diet

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2737323?guestAccessKey=f3b2d083-487f-42ea-a19b-c891a328eb24&utm_content=weekly_highlights&utm_term=070619&utm_source=silverchair&utm_campaign=jama_network&cmp=1&utm_medium=email

Fixed costs (mainly social and taxes) are ruining our breeders not concurrence

The big lie: France does have the highest fixed costs, so it is not concurrence which ruins our farmers!

https://www.lesechos.fr/industrie-services/conso-distribution/agroalimentaire-la-france-perd-la-main-en-europe-1035838

« Proprement hallucinant ! Souvenez vous de vos cours de lycée : qu'est ce qui caractérise un pays du tiers-monde ? Il exporte des matières premières (faible valeur-ajoutée) et importe des produits transformés ou manufacturés (forte valeur-ajoutée). Qu'apprend-on dans cet article : la France exporte son blé et importe des céréales du petit-déjeuner et elle exporte ses vaches pour importer des steaks. On y est ! Comment en est-on arrivé là : en saccageant le capitalisme familial dont les ETI font par exemple la grandeur économique de l'Allemagne mais aussi à cause du poids des charges et de la rigidité du droit du travail. Il faut libérer la France de ces carcans en appliquant la seule politique qui n'a jamais été appliquée en France alors que nous en sommes les inventeurs : le libéralisme. »

Ce commentaire illustre bien que la  dépenses publique astronomique de la France et en particulier sa dépense sociale à 759,1 milliards d’euros est le stade ultime avant le communisme.

Dans le graphique du haut on saisit très bien la médiocrité de la classe politique alors que n'importe lequel des épiciers de supérette aurait agi avant de se noyer.

Does grass-fed beef have any heart-health benefits that other types of beef don't?

Does grass-fed beef have any heart-health benefits that other types of beef don't?

Answer From Francisco Lopez-Jimenez, M.D.

Possibly. The difference in the diets of the cattle changes the nutrients and fats you get from eating the different types of beef. Grass-fed beef generally comes from cattle that eat only grass and other foraged foods throughout their lives.

Often, conventional beef cattle eat a diet that includes grains, such as corn, at some point. When compared with other types of beef, grass-fed beef may have some heart-health benefits. Grass-fed beef may have:

• Less total fat
• More heart-healthy omega-3 fatty acids
• More conjugated linoleic acid, a type of fat that's thought to reduce heart disease and cancer risks
• More antioxidant vitamins, such as vitamin E

Lean beef that's 10 percent fat or less — whether it's grass-fed beef or another type of beef — can be part of a heart-healthy diet. Although many people think grass-fed beef tastes better, it's generally more expensive and there is limited long-term research to definitively prove that grass-fed beef is better for you. Talk to your doctor or dietitian if you're thinking about adding more lean beef, including grass-fed beef, into your diet.

Sugar beverages

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2733424?resultClick=3&fbclid=IwAR19t0DhXoIceRxSEi5WLULKCGjh27-bKp40LcXvd7O5ntvYcmZeRrMFk1c