In this video, the presenter explores some recent research on insulin resistance, high blood sugar, and diabetes. While sugar has always been the main focus when it comes to these conditions, the presenter argues that trans fats might play a significant role as well. The research discussed includes studies conducted on rodents and monkeys, showing that a high trans fat diet led to increased blood sugar levels and fatty liver issues. The presenter suggests that addressing both sugar and trans fats is necessary in tackling insulin resistance. Methods such as intermittent fasting, reducing sugar and fat intake, and exercising are proposed as ways to combat visceral fat and improve insulin function.
Key Insights:
- New research suggests that sugar may not be the sole culprit in insulin resistance, high blood sugar, and diabetes.
- A rodent model study found that a high trans fat diet, despite having the same carbohydrate intake as a high sugar diet, led to a 44% increase in blood sugar levels.
- A six-year study on monkeys showed that a diet high in trans fats resulted in more weight gain, abdominal fat, and fatty liver issues compared to a diet high in monounsaturated fats.
- The monkeys consuming trans fats also had increased inflammation and higher insulin levels, despite no changes in carbohydrate intake.
- This suggests that trans fats may play a significant role in insulin resistance, in addition to sugar consumption.
- Addressing both sugar and trans fat intake is crucial in reducing insulin resistance and related health problems.
- Strategies to deal with fatty liver and visceral fat include reducing sugar and fat intake, intermittent fasting, exercise, and lower carb diets.
Transcript
Have we possibly been jumping to conclusions a little bit when it comes down to insulin resistance, high blood sugar, and diabetes? Like, I know we always point our fingers at sugar, and that’s important because sugar is problematic here. But are we missing something that’s really, really important? So let’s break down what some of the newer research suggests. And full disclaimer, we have to look at some monkey data, we even have to look at rodent model data. And I understand that’s not humans, but we also have to look at good data when we see it to understand what might be going on and then sort of cross-reference with human model data that we already have as well. So let’s dive in.
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The first thing I want to look at is a study that was published in Frontiers in Immunology. This was pretty interesting because it was a rodent model study. But what they did is they had rodents consume a high-sugar and high-fat diet, or a high-sugar and high trans fat diet, same amount of macronutrients, same amount of calories. Now, of course, there was a control diet as well. What they did is for 12 weeks, they monitored them with real-time PCR testing. Now, this is what’s cool, and this is where you’ve gotta be real. It’s like, you can’t do 12 weeks real-time PCR testing in a human. So, I understand it’s not apples to apples, but it’s still fascinating. So, what they found when they were monitoring in real time is that there was a 22% and a 44% increase in blood sugar in the trans fat group, even though carbohydrate intake was the same between the groups. Whoa! What’s happening here?
Well, we have to turn to some other data, and we look at this other data that was done in monkeys, and this is fascinating. This particular study was published in the journal Obesity, and it was a six-year-long study where they fully detailed out and they monitored these monkeys for six years. Now, one group had a higher monounsaturated fat diet, and the other group had equal calories, equal carbs, equal fat, except the fat was trans fats, just like these monkeys were swinging through Taco Bell or something every day. Okay, well, what they found was at the end of six years, and they really analyzed this, the monkeys that had the trans fats had significantly more weight gain. But they also had significantly more abdominal fat, specifically. Now, that could be subcutaneous fat, could be visceral fat, yada yada. But when you break it down more, I thought, „Wait a minute, these monkeys had major, major fatty liver issues, whereas the other monkeys did not.“ So, they added something that was very unnatural, trans fats, some kind of hydrogenated thing, and their livers became fatty. Well, liver fat and visceral fat are very, very similar, as a matter of fact. Some people will even say that like visceral fat is just a proxy for liver fat. So, they also saw huge increases in inflammation. Okay? And then, they also saw there was an increase in the expression, the gene expression, of something called CD36, which is a fatty acid transporter which, in certain contexts, can be good. But in this particular context, it is a transporter that would be transporting fat into the liver, increasing non-alcoholic hepatic steatosis, non-alcoholic fatty liver.
What does this mean when it comes down to blood sugar? I mean, we’re seeing obviously some issues here, where they saw a 75% increase in hyperinsulinemia in the monkeys that had the trans fats. They’re high levels of insulin. What the heck is going on? They’re not even changing their carbs. So here we are saying it’s all sugar, it’s all sugar all the time, which I get it. But have we ever thought that maybe it’s a two-part equation? We have trans fats coming in that are clearly impacting our insulin and impacting our sugar. But at the same time, we’re also definitely not slowing down on our sugar intake anytime soon. So we have this double whammy effect. Now, I don’t think that we should not be addressing sugar, but I do think that we should certainly be addressing trans fats a lot more because we’re not seeing many people talking about it because it’s just not that fun or sexy to talk about. But it’s one of the most real things right in our face.
Now, you know what happens when you have liver fat, when you have visceral fat? It changes how the liver can produce insulin. It changes not only insulin receptor sensitivity, so insulin can’t dock properly, but it literally makes the beta cells not produce insulin as well. I think we easily forget that insulin resistance is more so caused by the pancreas being dysfunctional than it is by the sugar, that is almost a casualty of the pancreas not being able to function properly. And then, when we add more sugar in with an inability to deal with it, we run into a monstrous problem. Can too much sugar cause insulin resistance? Based upon the data, I absolutely think so. Does trans fats potentially cause insulin resistance based on the data? I absolutely think so. So, together, we have a serious problem.
What do you do about it? You deal with the fatty liver first. You deal with the visceral fat first. And how do you deal with that? Well, one argument would say you reduce sugar. Another argument would say you reduce fats. I say you reduce both. I say you take breaks from food. I say you try intermittent fasting and just cut it out altogether for a little bit because the data is pretty strong that aggressive caloric restriction, intermittent fasting, exercise, fasted exercise, and not-infested exercise, all of it, however you want to fight, is all a major reducer of visceral fat. Reducing sugary beverages reduces visceral fat. Exercising reduces visceral fat. Intermittent fasting, 24-hour fasting, lower carb diets reduce visceral fat. All of them reduce that. And if we focus on that first, everything else will come, follow suit. So as always, keep it locked to my channel. I’ll see you tomorrow.
