Santé & nutrition, que manger ?

[Noob]

4 minutes ago, Mathieu_D said:

Alors oui il faut colorer à la cocotte. (j'ai fait avant mais j'ai vu que certains conseillent après)

A moins de faire sous vide je ferais pas après. Le temps de montée en température de la viande doit être limite question sécurité si tu saisis pas avant.

[ttoinou]

Intéressant ! Je testerais. Les dernières fois jme suis fait de l'agneau 6h à ~160 °C ça devient super tendre et fait une petite sauce

[Mathieu_D]

Ha oui je fais des épaules d'agneau 3h à 140°C des fois. C'est très bon.

[Nick de Cusa]

11 petits coeurs pour ce message somme toute libertarien

 

 

[RaHaN]

il y a 27 minutes, Nick de Cusa a dit :

11 petits coeurs pour ce message somme toute libertarien

Dont Unwin.

 

 

 

[RaHaN]

Bon, les low carber. Je suis en bad.

J'ai passé un entretien pour une nouvelle structure, où c'est l'infirmier qui confectionne les repas, de A à Z.

Je vais devoir commander des pâtes, du riz, des patates, du pain. Je vais avoir l'impression d'empoisonner les gosses.

Dans le projet, les pros doivent aussi manger avec eux, la même chose. L'occasion de jeûner.

 

L'autre versant, c'est que ça va être un bon moyen de faire connaitre le low carb.

Faut pas que je rêve, y aura pas de journée carnivore. Mais bon !  

[Eltourist]

Miam !

[Boz]

Bon courage, vas-y en douceur ! C'est quoi comme structure ?

[Hank Rearden]

Il y a 10 heures, Restless a dit :

Dont Unwin.

 

 

 

 

Moralité : mangez des carottes et buvez un petit peu d'alcool. 

[Nick de Cusa]

On 12/17/2018 at 9:29 PM, Restless said:

Bon, les low carber. Je suis en bad.

J'ai passé un entretien pour une nouvelle structure, où c'est l'infirmier qui confectionne les repas, de A à Z.

Je vais devoir commander des pâtes, du riz, des patates, du pain. Je vais avoir l'impression d'empoisonner les gosses.

Dans le projet, les pros doivent aussi manger avec eux, la même chose. L'occasion de jeûner.

 

L'autre versant, c'est que ça va être un bon moyen de faire connaitre le low carb.

Faut pas que je rêve, y aura pas de journée carnivore. Mais bon !  

Tu es infirmier ? À mes yeux c'est une vraie noble profession

[Nick de Cusa]

Jeff Cyr (le meilleur en vulgarisation sur le sujet ?) a fait un résumé de synthèse sur qui chope le diabète type 2, comment et pourquoi)

 

 

[ttoinou]

il y a 10 minutes, Nick de Cusa a dit :

Jeff Cyr (le meilleur en vulgarisation sur le sujet ?) a fait un résumé de synthèse sur qui chope le diabète type 2, comment et pourquoi)

 

 

 

Révélation

WHY DO SOME DEVELOP T2 DIABETES
By Jeff Cyr

Why do some folks go on to develop T2 diabetes? Why do some develop T2 diabetes, and others do not? Why do some folks remain very insulin sensitive, are able to eat a carb centric diet for most of their lives, and remain healthy. I am going to give it my best effort to try and make folks understand why, understand why some go on to develop T2D. I will try my best to provide proper references when needed. I am not going to talk about the microbiome, blue light, environmental factors, etc. I am going to try and explain how you become insulin resistant, which cases insulin levels to rise, eventually leading to constant high levels of blood insulin, Hyperinsulinemia.

What really causes you to become insulin resistant, it is not carbohydrate, not carbohydrate by itself. It starts with the constant over-nutrition from hyperpalatable foods. Foods that are mainly combined with carbs and fats, processed foods that line our grocery shelves. Folks usually don't just eat meat and vegetables anymore. Folks are much more sedentary today, lots of folks have office jobs, I am sitting down typing this post. You become carbohydrate intolerant, once you've lost most of your beta-cell mass, once you're finally diagnosed as a T2 diabetic. By the time MOST T2 diabetics are diagnosed, they've lost approximately 50% of their beta-cell mass, they also have very impaired function of the gut incretin hormones, GIP, and GLP-1.

A persons Fat Mass, the type of fat mass will determine their metabolic health. Also, The hormones Adiponectin, Leptin, and the excess toxic Ceramides I will try and explain.

1-We all have our own personal fat threshold (PFT), the amount of fat mass, amount of fat pads, that we can safely make in our subcutaneous adipose tissue (SAT). Our SAT, usually stores 80-85% of our excess energy in the form of triglycerides. When we eat food, we need a place to safely store the excess energy from food. We use this stored energy during times of no food, times in-between meals, and while we sleep at night. Subcutaneous adipose tissue is a protective mechanism, it protects us from T2 diabetes, fatty liver. Our internal organs like the liver and pancreas are designed to have very minimal fat, maybe 3% fat by weight of the organ.

2- Human beings have visceral adipose tissue (VAT). Normally, you have approximately 10-15% of your fat mass as visceral adipose tissue. Visceral fat is stored deep below the stomach wall (intra-abdominal fat), packed in between your internal organs. The liver, pancreas, intestines, kidneys, etc. It is normal to have SOME visceral fat. The problems begin once we start to have spill over from the SAT, that ends up as more visceral fat, this also leads to ectopic fat deposited directly inside internal organs like the liver, pancreas, intestines, kidneys. This is the start of fatty liver, fatty pancreas, T2 diabetes, utter chaos, mass destruction, total metabolic dysregulation.

3-Subcutaneous adipose tissue grows by two mechanisms: Hyperplasia (increase in cell NUMBER), Hypertrophy (increase in cell SIZE). Folks that have subcutaneous adipose tissue that grows by hypertrophy are genetically predisposed to developing T2 diabetes. Their adipocytes (fat cells) grow in cell size, cell diameter. During times of over-nutrition, over-feeding, these adipocytes grow in cell size, they will reach a point that they will become too large in diameter.They will become very insulin resistant, very inflamed. Basal insulin levels will need to rise, to try and regulate the proper release of fatty acids from these over-stuffed adipocytes. Post-prandial (after you eat) levels of insulin will need to rise also. You start to become hyperinsulinemic, blood triglycerides start to rise. If you continue over-feeding, your adipocytes in your adipose tissue will reach a point that they will no longer be able to accept any more excess energy from food. At this point the excess energy from food will be diverted directly to visceral and ectopic stores. As soon as adipose tissue becomes dysfunctional, liver takes the first hit, liver starts to fill with fat.

✅"Genetic predisposition for type 2 diabetes is associated with impaired insulin sensitivity, adipocyte hypertrophy and other markers of adipose tissue dysfunction. A dysregulated subcutaneous adipose tissue may be a major susceptibility factor for later development of type 2 diabetes."
https://journals.plos.org/plosone/article…#

4-We need proper adiponectin levels for adipose tissue to grow in cell number(hyperplasia). Folks that have adipose tissue that grows in cell size(hypertrophy) will lose their ability to properly make adiponectin, this will lead to the over production of toxic Ceramides. I will explain this later. Once these adipocytes become too large in diameter, this changes the ratio of release of adiponectin and leptin from your adipocytes. Adiponectin levels fall dramatically, the secretion of leptin is up regulated, along with many other pro-inflammatory markers

5-These large, sick, and very inflamed adipocytes start releasing very inflammatory markers along with the Free fatty acids and glycerol. Some of these inflammatory markers are IL-1,IL-6, IL-18, leptin. Yes, leptin is very pro inflammatory. Your adipose tissue secretes many hormones. Three very critical hormones that are released are adipocentin, leptin, and ASP. ASP is involved in clearance of triglycerides.
You always want a higher adipocentin to leptin ratio of release from your adipose tissue. Adipocentin is a protective, anti infamatory hormone that is involved in many functions.

6-Adipose tissue (body fat) is composed of adipocytes. Adipose tissue also contains the cells to make more adipocytes, known as pre-adipocytes.

7-Folks that are Metabolically Healthy will have many small adipocytes(Hyperplasia). These folks will also have plenty of pre-adipocytes, ready to multiply as needed. This is known as the process of adipogenesis..We NEED proper adiponectin to make this happen, more on adiponectin later.

✅Adipogenesis is the process of cell differentiation by which pre-adipocytes become adipocytes. Adipogenesis has been one of the most intensively studied models of cellular differentiation."
https://en.wikipedia.org/wiki/Adipogenesis… ..

8-When these(Metabolically healthy) folks eat a meal, the existing SAT adipocytes are capable of properly expanding and are capable of trapping the excess energy, fatty acid trapping, in the postprandial phase of the meal. These metabolically healthy folks adipose tissue also properly regulates the release, the proper amount of fatty acids into the circulation for use as direct energy when needed.

9-These folks will have normal blood glucose, normal insulin, glucagon, leptin, plenty of adiponectin. These folks, if they choose to, could continue Overfeeding, and as long as they would be able to properly make more fat pads, more adipocytes in the subcutaneous adipose tissue. These folks could keep on growing in fat mass, they could weigh, 300 pounds, 500, 700, 1000 pounds. These folks would still have, normal blood glucose, normal insulin, glucagon, leptin, plenty of adiponectin. These folks would have no diabetes, no fatty liver or fatty pancreas, what a wonderful world.

Now I need to explain the hormone adiponectin a bit more in detail, what it does inside the human body. Adiponectin is 1000-times more abundant inside the human body than any other hormone. Adiponectin is what determines ones level of insulin sensitivity, ones level of insulin resistance. First here is a short list of what adiponectin actually does.

✅increases fatty acid oxidation.

✅Increases our metabolic rate.

✅Adiponectin is very insulin sensitizing.

✅Adiponectin preserves pancreatic beta-cells.

✅Adiponectin promotes glucose-stimulated insulin secretion (GSIS), prevents apoptosis (cell death), and enhances the viability of pancreatic beta-cells under a variety of conditions.

✅Adiponcetin promotes insulin sensitivity, inhibits cell death, and suppresses inflammation.

✅In the liver, adiponectin lowers the rate of GNG, and lipogenesis. Increases liver insulin sensitivity.

✅In adipose tissue adiponectin increases glucose uptake and fat storage from the meal you just ate, also increases the conversion of pre-adipocytes to new adipocytes so one can safely (properly) expand the fat mass (fat Pads) during times of over-nutrition.

✅Adiponectin circulates in 1000-times higher concentrations than other hormones. Levels of adiponectin range from 3-33 ug/ml.

✅Adiponectin is insulin-sensitizing, anti-atherogenic, and anti-inflammatory. Adiponectin regulates food intake via cross talk with the appetite control centers in the brain (Hypothalamus).

✅Adiponectin controls/regulates the secretion of IL-1, IL-6, TNF-a which are all very pro-inflammatory of all cells/tissues.

✅Adiponectin is the most promising therapeutic properties amongst all adipokines in the treatment of diabetes.

✅Adiponectin controls (regulates) the amount of toxic ceramides circulating in our blood lipids.

Before I continue I will list a few reference papers about adiponectin from the Professor that discovered adiponectin in 1995, Professor Phillipp Scherer from UTSW in Dallas Texas.
https://www.cuimc.columbia.edu/…/columbia-honors-philipp-sc… .

✅"Adiponectin, a fat-derived hormone, was discovered two decades ago. It attracted considerable attention due to its involvement as a critical messenger for the crosstalk between adipose tissue and other metabolic related organs. Over the past 20 years, the metabolism community has shown tremendous interest in adiponectin, and enormous efforts have been directed to dissect the molecular mechanisms of action (Figure 1). Adiponectin targets the liver, heart, pancreatic β cells, kidney, potentially muscle, and many other cell types in various tissues. Adiponectin strongly suppresses hepatic gluconeogenesis by inhibiting genes involved in glucose production. Through its local action in key metabolic tissues, adiponectin promotes insulin sensitization and therefore improves whole body energy homeostasis. Adiponectin exerts strong protection against a number of pathological events in various cells by suppressing cell death, inhibiting inflammation, and enhancing cell survival. The identification of adiponectin receptors has greatly facilitated our efforts to delineate adiponectin functions. Solving the crystal structures of both adiponectin and its receptors has provided critical insights toward a better understanding of the molecular mechanisms, which also enables the structure-guided design of adiponectin mimetics with potentially potent effects on diabetes, atherosclerosis, and cardiovascular disease."
Full text=https://academic.oup.com/jmcb/article/8/2/93/2459553 .

✅"Adiponectin is an adipokine that is specifically and abundantly expressed in adipose tissue and directly sensitizes the body to insulin. Hypoadiponectinemia, caused by interactions of genetic factors such as SNPs in the Adiponectin gene and environmental factors causing obesity, appears to play an important causal role in insulin resistance, type 2 diabetes, and the metabolic syndrome, which are linked to obesity. The adiponectin receptors, AdipoR1 and AdipoR2, which mediate the antidiabetic metabolic actions of adiponectin, have been cloned and are downregulated in obesity-linked insulin resistance. Upregulation of adiponectin is a partial cause of the insulin-sensitizing and antidiabetic actions of thiazolidinediones. Therefore, adiponectin and adiponectin receptors represent potential versatile therapeutic targets to combat obesity-linked diseases characterized by insulin resistance. This Review describes the pathophysiology of adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome."
https://www.jci.org/articles/view/29126 .

✅"Adiponectin is a fat-derived hormone whose reduction plays central roles in obesity-linked diseases including insulin resistance/type 2 diabetes and atherosclerosis. The cloning of Adiponectin receptors AdipoR1 and AdipoR2 has stimulated adiponectin research, revealing pivotal roles for AdipoRs in pleiotropic adiponectin actions, as well as some postreceptor signaling mechanisms. Adiponectin signaling has thus become one of the major research fields in metabolism and clinical medicine. Studies on AdipoRs will further our understanding of the role of adiponectin in obesity-linked diseases and shortened life span and may guide the design of antidiabetic and antiaging drugs with AdipoR as a target"
https://www.sciencedirect.com/…/arti…/pii/S1550413113000065… ..

✅"Among these adipokines, adiponectin is one of the most potent molecules with respect to its insulin-sensitizing activity. However, unlike the vast majority of adipocyte-derived factors, the levels of adiponectin in circulation display an inverse correla- tion with adiposity. Given the established beneficial roles of adiponectin on whole body metabolism and its profound protective effects against many chronic diseases, a better understanding of the regulation of adiponectin secretion is very important. Here, we focus on the regulation of adiponectin secretion from the adipocyte as a paradigm of protein release from the secretory pathway of the adipocyte and the changes it undergoes in the context of obesity and other pathological settings. Beyond the mechanics of protein release, we will extend the discussion to other recent developments in the area of adipokines and their effects on metabolism."
https://nyaspubs.onlinelibrary.wiley.com/…/j.1749-6632.2010…

10-Now i am going to talk about the folks that have the genetic predisposition to developing T2 diabetes, folks that have subcutaneous adipose tissue (SAT) that grows by the process of hypertrophy (increase in cell SIZE). Increase in cell diameter. Some of these folks are born with lower serum levels of adiponectin, some are born with Adiponectin gene polymorphisms.
✅"Adiponectin may be used as a predictive biomarker of MetS, and shows a significant association with CVD risk factors in Chinese adolescents. Adiponectin gene polymorphisms are associated with serum adiponectin concentrations and the presence of MetS.
https://www.ncbi.nlm.nih.gov/pubmed/25074391/ .
✅"The adiponectin gene variants and haplotype contribute to the genetic risk towards the development of type 2 diabetes, obesity and hypoadiponectinemia in the south Indian population."
https://www.ncbi.nlm.nih.gov/pubmed/24055485/ .
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410438/… .

11-These folks that have a genetic predisposition to developing T2 diabetes because their adipose tissue grows in cell size. If they gain body fat, if they reach the point that their subcutaneous adipose tissue can no longer accept any excess energy from food, they've become hyperinsulinemic, they've severely down regulated the secretion of the hormone adiponectin, they've created another huge problem. A problem that will lead to much more chaos and havoc. These hyperinsulinemic and hypertrophic fat cells also force a change in the molecular weight of adiponectin. There are 3 different iso-forms of the hormone adiponectin. You have low, medium, and high molecular weight (HMW) forms of adiponectin. The HMW form of adiponectin is the most active form of the 3 different iso-forms. The high molecular weight (HMW) form makes adiponectin do what it is supposed to do, much more effectively than the low, or medium weight iso-forms.

✅"We report that the HMW form of adiponectin is prone to be reduced under hyperinsulinemic conditions. This has profound physiological implications. Hyperinsulinemia is frequently an indicator of insulin resistance. Hypoadiponectinemia is not only frequently associated with insulin resistance (16) but also may be directly causative for reduced insulin sensitivity (17). This suggests a vicious cycle during the initial stages of hyperinsulinemia, whereby high insulin levels lead to a downregulation of adiponectin levels, which in turn decreases insulin sensitivity further, prompting an even higher level of circulating insulin to maintain glucose homeostasis. Previous experiments in rodents (5) have demonstrated that the impact on HMW levels is primarily mediated through insulin and not hyperglycemia."
http://diabetes.diabetesjournals.org/content/56/8/2174.long .

✅"There is a mounting body of evidence to suggest that adiponectin is an insulin-sensitizing hormone and that the plasma level of this hormone is the best predictor of the subsequent development of type 2 diabetes among the various plasma biomarkers (34). Recently, however, it has been reported that adiponectin forms a wide range of multimers in plasma and that mutations in the adiponectin gene that inhibit the formation of HMW adiponectin are closely associated with the subsequent development of type 2 diabetes. Therefore, it was considered that HMW adiponectin value might be an attractive biomarker for the prediction of insulin resistance and metabolic syndrome. "
The high–molecular weight (HMW) form of adiponectin, an adipocyte-derived insulin-sensitizing hormone, has been reported to be the most active form of this hormone. The HMWR value has better predictive power for the prediction of insulin resistance and metabolic syndrome than plasma total adiponectin level."
http://care.diabetesjournals.org/content/29/6/1357 .

12-Once you no longer have the proper amount of the high molecular weight (HMW) form of adiponectin, adiponectin can no longer control the rate, the amount of toxic Ceramides in our circulating lipids. Ceramides are fat-derived signaling molecules, we need SOME, in excess they become very toxic. Excess ceramides in our lipids and tissues does 3 things.

✅ Excess ceramides causes extreme insulin resistance in all cells/tissues.

✅ Excess ceramides causes extreme inflammation in all cells/tissues.

✅ Ceramides control the rate of cell death (apoptosis). Excess ceramides dramatically increases the rate of cell death (apoptosis).

13- HMW adiponectin activates the 2 adiponectin receptors that are needed to turn on, needed to activate a Ceramadise activity that converts these excess toxic ceramides to the opposing fat-derived signaling molecule, sphingosine-1-phosphate (S1P).

S1P does the exact opposite of ceramides.

✅Improves insulin sensitivity in all cells/tissues.

✅Is very anti-inflammatory in all cells/tissues.

✅Slows down the rate of cell death (apoptosis).

Here are a few reference papers to back this up.

✅“The adipocyte-derived secretory factor adiponectin promotes insulin sensitivity, decreases inflammation and promotes cell survival. To date, no unifying mechanism explains how adiponectin can exert such a variety of beneficial systemic effects. Here, we show that adiponectin potently stimulates a ceramidase activity associated with its two receptors, adipoR1 and adipoR2, and enhances ceramide catabolism and formation of its anti-apoptotic metabolite – sphingosine-1-phosphate (S1P), independently of AMPK.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134999/ .

✅"Overexpression of Acid Ceramidase in the Liver Reduces Hepatic Ceramide Levels and Improves Hepatic and Adipose Insulin Sensitivity. Induction of ceramidase activity in either tissue promotes a lowering of hepatic ceramides and reduced activation of the ceramide-activated protein kinase C isoform PKCζ, though the induction of ceramidase activity in the adipocyte prompts more rapid resolution of hepatic steatosis than overexpression of the enzyme directly in the liver. Collectively, our observations suggest the existence of a rapidly acting “cross-talk” between liver and adipose tissue sphingolipids, critically regulating glucose metabolism and hepatic lipid uptake.
https://www.sciencedirect.com/…/arti…/pii/S1550413115002740… .

If you have the type of fat mass that predisposes you to developing T2 diabetes, does that mean that you will automatically get T2 diabetes, NO!

You can control the size, the diameter of your fat cells in your adipose tissue. If you control the size/diameter of your fat cells, they will secrete the proper amount of adiponectin, the proper amount of leptin.

If you eat properly, do some exercise, stay active, you can maintain the same body weight. You can have normal insulin levels. With normal insulin levels you will have the high molecular weight form of the hormone adiponectin that is needed to control basically everything I have just written about. You will control the rate and amount of the toxic ceramides, you will have proper adiponectin, the correct iso-form of adiponectin to make adiponectin work the way it was meant to work. You do not need to develop T2 diabetes. Your adipose tissue will protect you during times of normal feeding. Your adipose tissue will store the excess energy from food, protecting your internal organs from the toxic fatty acids that cause lipotoxicity and eventually glucotoxicity, and diabetes.

What if you have T2 diabetes? Can you fix this, can you recapture your proper adiponectin? You most certainly can. Here is how you do it.

1-You need to shrink the fat cell. Once you shrink the fat cell, the proper release of adiponectin and leptin return.

2-The correct ratio of the high molecular weight adiponectin returns. You are able to rid yourself of the excess toxic ceramides that were doing lots of damage.

3-This is just my personal opinion about diet for T2D, you can take it or leave it.

4-I would eat adequate protein. I would try to use leaner sources of protein at first.

5-I would eat plenty of above ground fibrous vegetables, IF you like vegetables.

6-I would only use healthy fats like extra virgin olive oil, virgin coconut oil, grass-feed butter.

7-I would use less dietary fat at first(sparingly) because you do need to lose weight. You need to shrink your fat cells.

8-Use more of your own stored body fat for direct energy

9-T2 diabetes is not a progressive disease, you can most certainly turn this around.

10-I would do daily exercise if possible. Weight/resistance training if possible. If not possible, start with walking/biking/yoga. You do what you have to do, to make this work for you!

T2 diabetes(NAFLD) have become worldwide epidemics, primed to bankrupt the health care systems of many countries.

We can all do better.

We need to do better.

Lives are at stake.

All lives matter.

Thanks to those that actually read through the entire post!

Pour ceux qui ne lancent pas les trackers facebook et qui ne peuvent pas suivre le lien

[Nick de Cusa]

à lire absolument, c'est cutting edge sur le métabolisme. Jeff est tristement en invalidité, mais purée qu'est-ce qu'il utilise bien son temps

[ttoinou]

Purée j'ai rien compris. Pas facile de se remettre à la bio, en anglais en plus

[Nick de Cusa]

ah si tu veux t'informer, de nos jours

[ttoinou]

A part ce forum je ne lis qu'en anglais. Mais là se remettre dans la biologie avec le vocabulaire technique

[NicolasB]

Merci pour ces infos. mais du coup, quel est le lien de ce forum?

[Nick de Cusa]

je ne comprends pas ta question ?

[NicolasB]

Le site de Garry Fettke : quelle est son adresse?

[Nick de Cusa]

ah, je ne sais pas, je le suis sur Twitter

[Hank Rearden]

On trouve ce site sur le net, tenu par son épouse ? Belinda Fettke

 

https://isupportgary.com

[Nick de Cusa]

tiens, mon record de petits coeurs sur ce coup là

 

 

[Boz]

C'était bien répondu, Nick !

[NoName]

Mon Dieu faut être con pour dire ça de base

 

Les Amish non plus ils connaissent pas le diabète et l'obésité, mais le fait de consommer 4000 calorie par jour joue sûrement un rôle 

[Hank Rearden]

Où nous reapprenons que nous sommes de mammifères omnivores. Le lait ( maternel ou de vache et pas de riz) pour un bébé, c'est pas trop mal.

 

https://metro.co.uk/2018/12/24/couple-fed-infant-daughter-vegan-diet-restricted-gave-rickets-8280699/amp/

[Nick de Cusa]

vraiment tout plein de bonnes choses dont l'ordre qu'applique le corps pour utiliser les différents macronutriments (merci à Ulrich Genisson pour le partage sur Facebook)

 

https://optimisingnutrition.com/2018/12/28/how-to-reverse-type-2-diabetes/

[RaHaN]

Le 17/12/2018 à 19:01, Boz a dit :

Bon courage, vas-y en douceur ! C'est quoi comme structure ?

J'ai pas été pris finalement, donc comme ça, c'est réglé. C'était une crèche.

 

Le 19/12/2018 à 04:19, Nick de Cusa a dit :

Tu es infirmier ?

Toi, tu ne lis pas mes articles, je vais me fâcher  

J'ai surtout le souhait de faire un pont entre la nutrition et la psychologie, mais n'étant ni bon pour me vendre ni l'esprit entrepreneuriale, pour le moment, c'est le désert. J'aime lire en ce moment quoi. Et m'énerver sur l'OMS.

 

----------------------------------------------------------------------------------------------------------------------------------------------------------------------

Bon. Ils sont sympas à l'OMS. Ils donnent des tips pour une alimentation saine cette année ! C'est parti !

 

Citation

 

- Mangez varié !
Des bons gros glucides pour commencer : blé, maïs, riz et les pommes de terre, avec des légumineuses comme les lentilles et les haricots, beaucoup de fruits et légumes frais!

Et aussi des aliments à grains entiers, tout pleins de fibres pour bien faire passer tout ça !

 

 

 

Citation

 

- Réduisez votre consommation de sel !

"Une trop grande quantité de sel peut faire augmenter la tension artérielle, ce qui constitue un facteur de risque majeur de maladie cardiaque ! Il faut 5 grammes de sel, soit 2,3gr de Sodium."

 

 

Citation

 

- Réduire l'utilisation de certaines graisses et huiles !

"Nous avons tous besoin d'un peu de gras dans notre alimentation, mais manger trop - surtout les mauvaises sortes - augmente les risques d'obésité, de maladies cardiaques et d'AVC.  Les gras trans produits industriellement sont les plus dangereux pour la santé."

 

Ça commence bien, et en fait non.

 

Citation

Remplacez le beurre, le saindoux et le ghee par des huiles plus saines comme les huiles de soja, de canola (colza), de maïs, de carthame et de tournesol.

Des acides gras saturés, par des huiles végétales raffinées :

- Polyinsaturés, donc plus facilement oxydables.

- Riches en oméga6, donc plus inflammatoires.

 

h16 style

 

Mais bon, c'est vrai que les saturés, c'est la cata.

 

Citation

-Limitez votre consommation de sucre
Trop de sucre n'est pas seulement mauvais pour nos dents, mais augmente le risque de prise de poids malsaine et d'obésité, ce qui peut entraîner de graves problèmes de santé chroniques.

 

C'est exact. Et on peut même aller plus loin. Pas de sucre à un effet positif sur l'épilepsie, le syndrome métabolique, l'obésité, le diabète, certains cancers, Parkinson, Alzeihmer, le syndrome dépressif, la fibromyalgie, le psoriasis, etc..

 

Le dernier point est sur l'alcool, mais je crois que je peux m'arrêter ici. 

[NoName]

c'est quoi la référence de la vidéo que tu as screené ?

[RaHaN]

il y a 3 minutes, NoName a dit :

c'est quoi la référence de la vidéo que tu as screené ?

 

[Nick de Cusa]

9 hours ago, Restless said:

...

Toi, tu ne lis pas mes articles, je vais me fâcher  

...

Ha ha ha, non, ça y est, j'ai recollé les morceaux du puzzle

 

Lis donc Grit D'angela Duckworth et Mindset de Carol S. Dweck pour trouver ton chemin pour "devenir" entrepreneur, c'est du self help qui aide, pas du "en 7 pas, ou en 9 étapes"