Santé & nutrition, que manger ?

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by Jeff Cyr

Many of you have become aware of the work of Dr. Joseph Kraft. Dr. Kraft over a period of 25 years studied glucose metabolism and blood insulin levels at St. Joseph Hospital in Chicago Illinois. Dr. Kraft performed 14,384 oral glucose tolerance tests (OGTT) with insulin assays and eventually wrote a book about this titled * Diabetes Epidemic And You*....…/dp/1425168094/ref=sr_1_1_twi_pap_2…......

Dr. Kraft studied how insulin responded to a certain load of glucose (carbohydrate). Dr. Kraft used an oral glucose solution of 75-100 grams which is equivalent to 75-100 non-fibre grams of fast acting carbohydrate, like carbs found in bread.

I won`t go into all the details of Dr. Kraft`s book. Basically Kraft wanted to find out how much insulin the pancreas would have to release to process the glucose (carbohydrate) load of 75-100 grams.

Kraft found out that a normal insulin response from the pancreas was a release of 40-50 units of insulin needed to handle this glucose (carbohydrate) load of 75-100 grams. Also a normal response would be that these test subjects had their insulin levels quickly return to their normal fasting insulin levels of 3-10 units within 3 hours. Kraft identified these test subjects as Pattern 1 normal response. These people also had their blood sugar very quickly return to their normal range.

Before I continue I need to make 1 very important point. Some people can eat a high carbohydrate diet for most of their lives and they will be fine as long as they remain insulin sensitive. If your cells hear the proper signal from insulin, glucose (carbohydrate) will very easily enter the cells and be used as energy, you maintain your metabolic flexibility. I would also add that as long as they remain Leptin sensitive also....In every case of T2D we have leptin and insulin resistance...In every case of T2D we also have very high levels of the 3 hormones Leptin, glucagon and insulin....Hyperleptinemia , Hyperglucagonemia , Hyperinsulinemia.......

Dr. Kraft also identified a Pattern 4 response in his test subjects. These Pattern 4 had fasting insulin levels of 50-60 units. Once these people drank the 100 gram load of glucose their insulin levels rose to 180 units of insulin within 1 hour of ingesting the glucose load. Their insulin levels remained very elevated for hours and only returned to their fasting levels of 60 units in 5 hours.

One very important point you have to keep in mind is that these folk had *Normal* fasting blood glucose and normal postprandial BG levels.
You have 3 phases of insulin release.

1-1st phase insulin release= In between meals your pancreas makes and stores insulin in the form of granules so when you eat your next meal the pancreas is ready to quickly release whatever amount of insulin is needed to handle the glucose (carbohydrate) load.

High blood sugar is very toxic to the cells and to the blood itself.

The human body will do whatever is necessary in the moment to protect itself, you eat a high carbohydrate meal and the pancreas will release whatever amount of insulin is needed to process the carbohydrate load.

As long as you maintain proper B cell function in the pancreas, your pancreas will be able to release enough insulin to process the said load of carbohydrate.
This 1st phase, quick and large release of insulin is lost in most T2 diabetics.

2-2nd phase insulin release. If after 30-40 minutes your blood glucose does not start to lower fast enough your pancreas hurries itself and starts to produce more insulin to try and lower your blood glucose to the normal range.

3-Basal insulin release= during periods of no food intake in-between meals your pancreas release small pulsating squirts of insulin to maintain glucose homeostasis (70-110). Your pancreas also releases a basal release of glucagon (alpha cells). Insulin and glucagon are the 2 hormones in charge of maintaining your glucose homeostasis.

OK thats enough about Dr. Kraft now I need to tell you about the important part of my post, My title of * 1 slice of toast*

Dr. Ron Rosedale many years ago while he was still in private practice would preform these Dr. Kraft style tests in his office. Rosedale had parents that would take their young children to him because they wanted to know why their kids were becoming obese. What these parents didn`t understand was that they were all basically eating the same SAD high carb diet. These kids were the age of 10-12 years old.

Rosedale would measure fasting blood sugar (FBG) and fasting insulin in these kids, all normal. Dr. Rosedale did not use the same oral glucose solution of 100 grams like Kraft did, Rosedale was smarter then that. Rosedale gave these kids *1 slice of Toast*. 1 slice of bread averages 25 grams of non-fiber fast acting carbo, *Rocket Fuel*.

Within 30-45 minutes of ingesting this slice of toast these kids insulin levels very quickly rose into the hundreds and remained elevated for quite some time. Keep in mind that these young children had most of their beta-cells in the pancreas still functional and had a *Very Large and Quick* 1st phase insulin release.

Rosedale in his writings says that in SOME of these kids it only took 2 crackers to have the same effect as that 1 slice of toast on insulin levels.

Yep, I believe that Rosedale was on to something back then, he certainly answered the parents question as to , *Why is my child Obese*

Please keep in mind that if you are this 10 year old kid (I was) you are diabetic, just undiagnosed. You have many years of high insulin (hyperinsulinemia) *Before* you start to have high blood sugar (Hyperglycemia).

You also have many years of hyperleptinemia , and hyperglucagonemia ......
Once you`re diagnosed as a T2 Diabetic with high fasting blood glucose levels, you have gone through many years of very high insulin levels circulating in your circulatory system.

You have many miles of blood vessels, veins and arteries in your circulatory system, 60,000 miles of blood vessels in the human body.

MOST doctors don`t understand this very simple fact, if you`re insulin resistant your pancreas will release large amounts of insulin when you consume a high carbohydrate meal.

The human body is designed to maintain very narrow ranges of its blood glucose levels, glucose homeostasis, 70-110 mg/dl.
High blood sugar is very toxic to all your cells and also very toxic to the blood itself.

You only need ~5~ grams of carbohydrate dissolved in your blood volume of 5 liters of blood to have a blood glucose of 100 mg/dl, 5.5MMOL…
5 liters of blood= 1000 teaspoons of blood.
5 grams of carbohydrate=1 teaspoon of glucose.
This is a ratio of 1000-1.

You only have very few glucose dependent tissues in the human body. These are found in the brain(100% if not keto-adapted), the red blood cells, the renal medulla of the kidneys, gonads and retinas, everything else in the human body runs on fat, fatty acids and ketones.

The human brain uses 23% of your total resting energy expenditure, approximately 120-150 grams of carbohydrate, just for the brain.

Once the brain is keto-adapted it runs on a combination of glucose and ketones.

This reduces your need for carbohydrate, dramatically.

Once you`re keto-adapted your minimal glucose needs are very easily meet by the process of gluconeogenesis.

Gluconeogenesis is the process when your liver takes protein amino acids and by-products of fat metabolism and makes new glucose.

Gluconeogenesis is a very slow and demand driven process, your blood glucose levels remain steady, no more blood glucose highs and lows from a high carbohydrate diet.

Blood glucose and insulin are normalized, no more hunger, no more erratic behavior.

You are no longer a slave to carbohydrate.

PS- I would like to thank Dr. Jeffry Gerber, Dr. Ted Naiman, and Ivor Cummins with their heroic efforts in the last few years with bringing the work of Dr. Kraft to the public.



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Pour continuer un peu sur les salades sauvages, on commence à récolter le pourpier dans le sud, et il y en aura en abondance j'usqu'aux gelées. 

On le trouve sur des sols arrosés et non glyphosphatés.

Le pourpier est réputé protecteur pour les tubes digestifs car c'est une plante mucilagineuse.



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Même si on n'est pas personnellement touché, quelles explications passionnantes



by Jeff Cyr

T2 diabetes is a very complex disease. T2D takes many years to become, “Full Blown” T2 diabetes.

All “Excess Energy” is stored as triglycerides (fat) primarily in your subcutaneous adipocytes (fat cells). By “Excess Energy”, I mean “Excess Food” consumption.

You sit down and eat a meal, fed state. The release and production of insulin is up regulated, the release of insulins opposing hormone, glucagon is down regulated.

Insulin is a storage hormone, it stores fat, carbohydrate and amino acids. In a “Normal healthy” metabolic person, insulin very quickly does its job.

Under these circumstances, normal healthy metabolism, minimal insulin is needed, blood glucose never raises much higher than 130-140 mg/dl, no matter how much junk processed carbohydrate you feed into the system. A few hours later blood glucose drops back down to normal ranges. Insulin, glucagon, and leptin also quickly return to “Normal” fasting levels.

When you eat a meal, once the food enters into the stomach and intestines you have incretin hormones that are up regulated in the K cells, and the L cells in the gastrointestinal areas.

The incretin hormones are a group of hormones produced by the gastrointestinal (Gut) system that enhance insulin secretion from the pancreatic beta cells, GLP-1 also suppresses the release of glucagon from the pancreatic islets. GLP-1 also increases beta cell mass in the pancreas.

The two main incretin gut hormones are GLP-1 and GIP.

1- GLP-1.......Glucagon-Like-Peptide-1
2- GIP............Glucose-Dependent-insulintropic-peptide

The combined incretin responses accounts for 50-70% of total postprandial insulin production from the pancreatic beta cells, this is very important, it gives the system the proper insulin to glucagon ratio so insulin can do its job.

T2 diabetics have an impaired GIP response. Some T2 diabetics also have an impaired GLP-1 response, all T2 diabetics have much less GLP-1 that remains intact once it reaches the pancreas.

Side note: (GLP-1 also expresses itself via the vagus nerve and the brainstem in the appetite control centers in the hypothalamus region in the brain. GLP-1, along with CCK, PYY, Leptin and other hormones communicate with the appetite control centers in the brain. A T2 diabetic will have much less GLP-1 remain “Intact” in the hypothalamus. T2 diabetics are all very leptin resistant. They have very high circulating levels of leptin, their cells do not properly hear the signal from leptin.)

GLP-1 is also extremely important because not only does it increase insulin production from the pancreatic beta cells, it also reduces glucagon production from the pancreatic alpha cells. Why is glucagon suppression important?

The proper suppression of glucagon from the pancreatic alpha cells allows for the proper Insulin to glucagon ratio (I/G ratio).

1-When a normal metabolically healthy person eats a meal with some carbohydrate, the ratio of insulin to glucagon that is released from the pancreas is approximately 7-1 in the favor of insulin. At this ratio Insulin can properly turn off glycogenolysis (the release of glucose) from the liver, and also turns off gluconeogenesis (the production of new glucose) in the fed state.

2-In a normal metabolically healthy person 1 micro unit of insulin in the pancreas suppresses the release of glucagon from the pancreatic alpha cells by 3 picograms.

3-In a T2 diabetic 1 micro unit of insulin release in the pancreas only suppresses the release of glucagon from the pancreatic alpha cells by 0.02 picograms.

4- In the T2 diabetic, when they eat the same meal with some carbohydrate the ratio of insulin to glucagon that is released from the pancreas is at a ratio of 0.4-1.......In the favor of glucagon.

5- With this ratio of insulin to glucagon, insulin is incapable of turning off glycogenolysis and gluconeogenesis. The T2 diabetic is left with run away blood sugars.

Before I go any further let me mention a few things as far as the suppression of glucagon in the pancreatic islets.

1-By the time most T2 diabetics are diagnosed they have hyperglycemia and high fasting blood glucose. They also have very high levels of glucagon, insulin, and leptin.

2-At this late stage the liver and pancreas have filled with ectopic fat inside both organs. You also have deep visceral fat surrounding these internal organs. The visceral fat surrounding the liver and pancreas interferes with proper cell communication between the two organs.

3- At this late stage of diabetes you have the up regulation of liver lipogenesis, de novo lipogenesis. The production of liver made fat.

4- This dramatic increase of liver made fat increases the synthesis of Palmitoyl-COA

5- This increase in the synthesis of Palmitoyl-COA activates the enzyme Serine-Palmitoyl Transferase.

6- This enzyme, Serine-Palmitoyl Transferase condenses the Palmitoyl-COA and Serine which produces excess ceramide .

7- The excess build up of fat in the pancreas causes this excess ceramide to accumulate inside the tissues of the pancreas.

8- This excess ceramide in the pancreas leads to what is known as beta-cell Lipo-apotosis, total beta cell death.

9- This excess production of ceramide also causes increased insulin resistance directly in the alpha cells in the pancreas, it also increases insulin resistance in all other tissues/cells.

A T2 diabetic also has other problems with the proper suppression of glucagon in the pancreatic islets. Every beta cell in the pancreas is juxtaposed to an alpha cell, meaning that every beta cell in the pancreas is in direct contact with an alpha cell.

1-Leptin and somatostatin are very powerful suppressers of glucagon in the pancreatic islets.

2- Somatostatin in produced by the delta cells in the pancreas, it suppresses both insulin and glucagon.

3- Leptin suppresses the release of glucagon in the pancreatic islets. MOST T2 diabetics are very leptin resistant. Leptin is incapable of helping with the suppression of glucagon in the pancreatic islets, insulin is left alone to try and do the job.

4-Once the T2 diabetic starts producing excess ceramide from the lipids (fats) in the pancreas, now we have a serious situation. The alpha cells in the pancreas become very insulin resistant.

In the later stages of T2 diabetes, you will have the hyper secretion of glucagon from the pancreatic islets.

You are left with constant elevated insulin and glucagon levels, also elevated leptin.

At this late stage of T2 diabetes, the improper ratio of insulin to glucagon is made in the pancreas, prior to eating a meal.

After the T2 diabetic eats a meal, we now have the problem of the incretin hormones, GLP-1 and GIP, not capable of properly doing their jobs. We are left with the improper ratio of insulin to glucagon after the meal enters into the stomach, and small intestines.

T2 diabetes is not a simple disease, it can be very complex.

We need to gather as much information as we possibly can.

With the proper information, the T2 diabetic can start to attempt, to try and turn things around.

My main objective with my writings on FaceBook, is to try and provide the most accurate information that I possibly can.

I learned about all this stuff, very late in life.

I had many, many years of very elevated blood glucose levels.

Also many, many years of very elevated insulin, glucagon, and leptin levels, lots of damage was done.

I have fixed some of the damage, I was one of the lucky ones.

Please, to those of you that read this, ask your doctor for a few simple blood labs that would give you great insight into your metabolic health.

1-Fasting blood glucose, along with fasting insulin. You need to know how much insulin is needed, for the said blood glucose level.

2- With both these numbers you can then determine your HOMA-IR score.

3- HOMA-IR = your fasting blood glucose x your fasting insulin.. divided by 405...Example....fasting blood glucose of 100..Fasting insulin level of 5.. 100 x 5 = 500.

4- Take this number of 500, and divide it by 405. 500 2797.png 405 = 1.23.. This is a good number. 1.75 and below is an indicator of good insulin sensitivity.

5- One more example. Take a fasting blood glucose of 100...Take a fasting insulin level of 10. 100 x 10 = 1000...1000 2797.png 405 = 2.47... This number of 2.47 is an indicator of insulin resistance. SOME folks will have fasting insulin levels of 20 units of insulin, 40 units, 50 units, 70 units, 90 units. So this is very important. My fasting insulin levels today are 3.

6- Measure your fasting blood triglycerides. Doctors and most labs use a reference of fasting trigs of 150 or less. This number of 150 is too high. Your fasting triglycerides should be at the minimal of 100 of less, 60 or less is even better. My fasting triglycerides on a SAD american diet were 250 mg/dl, today they are 31 mg/dl.

7- Your triglyceride to HDL ratio. Take your fasting triglycerides and divide by your HDL cholesterol.

8- Example: Fasting triglycerides of 250..HDL cholesterol of 29...These were my numbers prior to KETO. 2502797.png29 = 8.62.... This TRIG/HDL ratio is very bad. It tells us that insulin levels are very high, lots of inflammation going on, a walking time bomb. My fasting trigs today are 31, my HDL is 80, I have had my HDL as high as 105 in the past.

9- Take fasting triglycerides of 31 and divide 31 by my HDL number of 80...312797.png80 = .39.. This is a very good number, it tells us that insulin levels are low, and it tells us that we have very good cardiac health. A TRIG/HDL ratio of 2.0 and lower is consider good. A TRIG/HDL ratio of 1.0 and lower is considered optimal.

I hope this helps. We need to give proper information to all the T2 diabetics that are “Undiagnosed”.

There are MANY “Undiagnosed” T2 diabetics, walking around planet earth.



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Le 25/04/2017 à 22:49, NoName a dit :

Maintenant pareil mais tu virés le pain 


Ca fait presque deux mois que j'ai viré le pain du petit dej (et féculents des autres repas), remplacé par oeuf/jambon/fromage tous les matins. Bah c'est probablement pas qu'un effet placebo courte durée, mais j'ai une patate énergie toute la journée, qui surprend mes collègues, et moi-même par la même occasion. Aussi bien physiquement que mentalement d'ailleurs, parce que niveau concentration, c'est la même. Y a des soirs, je rentre du taff, je suis évidemment rincé, mais ce n'est plus la même lourdeur dans le corps. Pareil pour la nuit, ça fait bientôt deux ans que j'étais à tendance insomniaque, ben ça c'est terminé aussi. 

Tout ceci n'est évidemment pas lié qu'à la suppression progressive des carbs, il n'empêche que la différence, je la ressens. les lourdeurs, les sensations de faim, j'ai presque oublié ce que c'était. Oui parce que bon, ça m'arrive de bouffer un bon gros burger bien dégueulasse avec les frites qui vont avec, je le paye direct ahah.


L'autre point que j'ai remarqué, c'est la puissance addictive du sucre. Bon, je le savais déjà, je pouvais défoncer un paquet de Haribo en 5 minutes chrono, gros bonbons addict'. Là, du fait de moins en prendre, dès que je vais aller sur quelque chose riche en carbs, je ressens direct la petite voix intérieure "allez, vaz-y, reprends en, t'as vu comme c'est bon, allez fonce". C'est assez violent ;)

Bref, j'attends de voir sur la durée ce qu'il va en être, mais pour le moment, le petit dej est un bon moment de plaisir.


Le 18/05/2017 à 13:25, poney a dit :

Tu es le même Restless qui a une collec' longue comme un bras sur Discogs ?


Pour les boissons type "iso", je n'en use pas, mais quand je cours en visant un peu (un peu hein) la perf', je me concocte une boisson avec de l'eau, du jus de baie, du magnesium et du sel.


La mienne est longue aussi, mais non, ce n'est pas moi. Qu'est-ce qu'il a de beau dans la sienne ? (j'ai vu qu'ils étaient plusieurs avec ce pseudo)


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