چاقی مفرط و دیابت

دوره: چیزهایی که آموخته ام / درس 38

چیزهایی که آموخته ام

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Obesity & Diabetes Explained

In my last video, I talked about how despite what some authorities may say, Type 2 diabetes does not have to be a chronic and progressive condition as clearly evidenced by the fact that Doctors like Jason Fung, David Unwin, Sarah Hallberg, and Ted Naiman just to name a few have been reversing people’s diabetes with fasting or a low carb or ketogenic diet.

While some people might be suspicious of a new fad diet supposedly reversing diabetes, low carb isn’t actually new at all, nor is the concept of using it to reverse diabetes. Dr. Richard Thomas Williamson wrote in his 1898 book “Diabetes Mellitus and Its Treatment” : that “Potatoes should be excluded from the diet first, then bread, and gradually all carbohydrates should be cut off.”

In 1797 military surgeon John Rollo released a book that described how he treated diabetes with a carbohydrate restricted meat diet. Referring to this, Dr. Williamson wrote “Ever since Rollo published his book on diabetes in 1797, and pointed out the value of restriction of the carbohydrates in the food, it has been acknowledged that of all forms and methods of treatment this dietetic one is the most important.”

Interestingly, the concept of “grain avoidance” or bìgǔ, (also known as BIGU) has been around for more than 2000 years, going back to the Han dynasty. Someone named Wáng xuán hé wrote in around the year 680AD that “before the times of farming, ancient people did not eat grain, so they were long lived.”

Not that this is a medical paper of course, but it’s interesting that people were specifically avoiding grain more than a millenium ago. Eastern Jin Dynasty scholar Ge Hong claimed that there was not one fat person among those practicing bìgǔ for spiritual reasons.

Before I get into discussing recent concerns about low carb diets, we need to look in more depth at how carbohydrate is a factor in the development of diabetes. Based on the work of Dr. Ted Naiman, Dr. Jason Fung and Ivor Cummins, the path to developing diabetes looks something like this: -First, something is filling up your fat cells, making you fat.

-More specifically, something isn’t just filling your fat cells up with fat, it’s pinning that fat there and preventing it from being pulled out of the fat cell to be burned up for energy. -As we discussed last time, this thing filling up your fat cells is insulin.

Insulin is an anabolic hormone that has many functions, but one is that it acts as your “fat storage” hormone and by inhibiting three important enzymes, it prevents you from burning fat. -Simply put, the more insulin you have floating around, the harder it is to empty your fat cells and the fat builds up.

“And the big question is why did you fill up your adipocytes. Why are they all full? Is it because humans shouldn’t eat fat? No. You filled up your fat cells, because you suck at burning fat because you eat too much glucose… you’re eating carbs and glucose, you’re not burning fat, it accumulates, you fill up your adipose.”

-What Dr. Ted Naiman said here is easy to follow because glucose which comes from carbohydrates raises insulin more than protein and much more than dietary fat. However, in this presentation, Dr. Naiman talks about another phenomenon usually called the Randle cycle.

This is where independent of the action of insulin, glucose prevents the burning of fat all by itself. And it makes sense that you’d want to preferentially burn glucose over fat because you need to be able to quickly sort out incoming glucose first since there’s not many places to put it.

Depending on the person you can store a couple hundred grams of glucose across your muscles and liver as glycogen, but if you don’t empty your glycogen by from the liver by not eating carbohydrate long enough and you don’t empty muscle glycogen by doing enough exercise, that tank of glycogen will fill up.

At this point there’s nowhere to put incoming carbohydrate, so insulin has to turn it into fat via a process called de novo lipogenesis so it can be stored in the only place available: your fat cells. Dr. Naiman presents a model for how this works “But as you add carbohydrates and raise glucose, you literally have to switch your metabolism over and burn more glucose just to get rid of it.

In fact if you eat enough carbohydrates and glucose, you literally have to convert it to fat via de novo lipogenesis. Only when carbohydrates and glucose are absent can you switch your fuel mixture over and burn fat again.” This highlights how dietary fat can also be very fattening, if you eat it with a enough carbohydrate because the carbohydrate will prevent you from burning that fat and the insulin release will hold the fat in storage.

So, to put this together: if you eattoo much low fiber carbohydrate too frequently, it will interfere with your ability to burn fat and fat will accumulate. As your fat cells get more and more filled with fat, you’ll need more insulin to hold that fat in place, making your fasting insulin very high - kind of like needing more force to cram more stuff in your suitcase.

And these higher levels of insulin worsen the whole cycle making you more resistant to insulin, meaning glucose is harder to process because there’s basically nowhere to put that glucose - you can only make energy from glucose at a certain rate, and your glycogen stores were filled up a long time ago, so the glucose needs to be turned into fat for storage, but your fat cells are already filled up.

So at this point, where do you put the incoming glucose and fat?? Unfortunately it just overflows into the abdominal cavity, the liver, the muscle and the pancreas. The pancreas seems to be the last place that the fat accumulates, and when the pancreas is stuffed with fat, the beta cells stop functioning properly.

Whereas your beta cells were initially pumping out a ton of insulin to make everything I just mentioned happen, now that the beta cells have become dysfunctional, they stop properly producing insulin, then your insulin levels drop drastically meaning glucose can’t be dealt with, so you get diabetic level blood sugar and then you’re prescribed insulin injections to keep the blood sugar down but that makes it even harder to empty the fat cells, so the situation gets worse and worse .

Keep in mind that as Ivor Cummins points out in this talk, there are other unhealthy lifestyle factors that can worsen this insulin resistance and worsen this whole situation - things like insufficient sleep, smoking, and poor omega-3 to omega-6 ratio.

Maybe the worst is fructose, a component of table sugar that directly worsens insulin resistance in the liver. “Soda and other sugary drinks are the only individual food that’s actually directly linked to obesity.

Everyone seems to think a day without orange juice is like a day without sunshine. Juice is just like soda. There is no difference. When you take fruit and you squeeze it, you throw the fiber in the garbage, that was the good part of the fruit.”

So depending on the person, they might be fine and insulin sensitive eating spaghetti carbonara twice a day for many years if they’re not drinking too much fruit juice or sugar sweetened sodas and have these other factors in order.

Before we move on let me present two pieces of evidence for the overflow phenomenon. Going back to Dr. Ted Naiman’s talk, he gives an excellent example of overstuffed fat causing insulin resistance: People with lipodystrophy.

this is a disorder where you have hardly any subcutaneous fat - So these people barely have any space to safely store any fat. So where does new fat go? “But The visceral fat is completely maxed out, and almost everyone with lipodystrophy has horrible insulin resistance and horrible brittle diabetes” This could explain the peculiar situation in Japan, where despite having a very low obesity rate of about 3.7%, their rate of diabetes is 7.6%, only 2% lower than America’s 9.4% , but America’s obesity rate is about 30%.

The people of Japan and other asian countries’ difficulty getting fat could ironically be making them more susceptible to diabetes and insulin resistance because they have less safe storage space for fat.

So what happens if you give an insulin resistant person a new place to store fat ? There was a study that tried just that. They got some lipodystrophic mice with diabetes. Then Surgically implanted some fat tissue under the mouse’s skin, and connected it to their blood supply and then, having a new place to put fat cleared up the road block and magically cured insulin resistance in these mice.

So, given all this, fixing these other factors Ivor Cummins talked about and by fasting or going on a low carbohydrate diet so you get the insulin down and the fat burning up would make the most sense as a line of treatment. But, You surely saw articles about that study showing that low carb diets are bad for longevity.

Though, as Nina Teicholz points out, this study was based on a simple fill in the dot questionnaire, similar to this one, which queried the participants on on only 66 foods. What if you don’t happen to eat these particular vegetables? The data gets left out. What if you eat a bunch of pizza and energy drinks, it’s not on the list so that data is left out too.

As Teicholz explains: “Further, the ARIC participants’ eating habits were tracked only twice, from 1987-89 and 1993-95. After 1995 the study’s participants were assumed to have continued eating the same diet for the next 15 years.” Finally, Diet questionnaires are inherently unreliable since most people aren’t tracking precisely what they ate in what amount.

Especially in this case, you can’t hope to be precise with this kind of questionnaire. Can you remember how many times per month you ate bananas, broccoli and chicken over the past year?? On the other hand, this study, published last year in the same journal found the exact opposite result.

The study concluded that “High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, … whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Next, you may have heard that top US cardiologist Kim Williams was saying just last month that “No one should be doing the ketogenic diet.” His argument is based on a 2013 systematic review of 17 studies that found low-carbohydrate diets to be associated with an increased risk of heart disease and death.

So, I went ahead and took a look at these 17 studies which by the way are based on questionnaires. First of all, let me point out that none of these studies even mentioned a ketogenic diet. One study specifically said “Our results do not support a clear, general association between LCHP score and mortality.”

And four studies actually showed better health outcomes with carbohydrate reduction, particularly high glycemic carbohydrates which would be the ones that raise insulin the most. Maybe most importantly, several of these studies did not state the specific carb intakes so for those we have no idea if people are eating an actual low carb diet or just eating “less carb than most people.”

This is very important, because many of the benefits of low carb and keto arise only when you sufficiently restrict carbohydrate and get your insulin low enough. The ten studies that did clearly state carb intake showed that the diets were not actually low carb or keto at all.

Low carb typically allows a maximum of 60g of carbohydrate or around 10% of your daily calories from carbs, and the ketogenic diet only allows 5% of your calories from carbs. Two studies only went as low as 25% of calories from carbs and the remaining seven six didn’t even get below 30% - this a three times higher carb intake than what is actually considered “low carb,” and 6 times higher than ketogenic diet.

So this data being used to criticize ketogenic diets is not actually data on ketogenic diets or even low carb diets. On the other hand we have a study looking at 83 obese people on a proper ketogenic diet for 24 weeks.

By the way, the diet was administered to the patients, data was not based on questionnaires. It concluded: “The present study shows the beneficial effects of a long-term ketogenic diet. It significantly reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol.

Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients.” And there’s plenty more studies that showcase the beneficial effects of a ketogenic diet - I’ve put links to a couple dozen of them in the description. So as we’ve seen, based on how diabetes develops, a low carb or ketogenic diet would be the most logical approach to treating it, yet people are constantly advised against it.

Another approach this video unfortunately didn’t get to touch on is fasting- this is another excellent way to lower insulin, increase fat burning and restore insulin sensitivity. This is mentioned in Jason Fung’s book the diabetes code.

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