How Exactly Does Type 2 Diabetes Develop?

How Exactly Does Type 2 Diabetes Develop.jpeg

Insulin resistance is the cause of both prediabetes and type 2 diabetes. OkK, so what is the cause of insulin resistance? Insulin resistance is now accepted to be closely associated with the accumulation of fat within our muscle cells. This fat toxicity inside of our muscles is a major factor in the cause of insulin resistance and type 2 diabetes, as it interferes with the action of insulin. I've explored how fat makes our muscles insulin resistant (see What Causes Insulin Resistance?), how that fat can come from the fat we eat or the fat we wear (see The Spillover Effect Links Obesity to Diabetes), and how not all fats are the same (see Lipotoxicity: How Saturated Fat Raises Blood Sugar). It's the type of fat found predominantly in animal fats, relative to plant fats, that appears to be especially deleterious with respect to fat-induced insulin insensitivity. But this insulin resistance in our muscles starts years before diabetes is diagnosed.

In my video, Diabetes as a Disease of Fat Toxicity, you can see that insulin resistance starts over a decade before diabetes is actually diagnosed, as blood sugar levels slowly start creeping up. And then, all of the sudden, the pancreas conks out, and blood sugars skyrocket. What could underlie this relatively rapid failure of insulin secretion?

At first, the pancreas pumps out more and more insulin, trying to overcome the fat-induced insulin resistance in the muscles, and high insulin levels can lead to the accumulation of fat in the liver, called fatty liver disease. Before diagnosis of type 2 diabetes, there is a long silent scream from the liver. As fat builds up in our liver, it also becomes resistant to insulin.

Normally, the liver is constantly producing blood sugar to keep our brain alive between meals. As soon as we eat breakfast, though, the insulin released to deal with the meal normally turns off liver glucose production, which makes sense since we don't need it anymore. But when our liver is filled with fat, it becomes insulin resistant like our muscles, and doesn't respond to the breakfast signal; it keeps pumping out blood sugar all day long on top of whatever we eat. Then the pancreas pumps out even more insulin to deal with the high sugars, and our liver gets fatter and fatter. That's one of the twin vicious cycles of diabetes. Fatty muscles, in the context of too many calories, leads to a fatty liver, which leads to an even fattier liver. This is all still before we have diabetes.

Fatty liver can be deadly. The liver starts trying to offload the fat by dumping it back into the bloodstream in the form of something called VLDL, and that starts building up in the cells in the pancreas that produce the insulin in the first place. Now we know how diabetes develops: fatty muscles lead to a fatty liver, which leads to a fatty pancreas. It is now clear that type 2 diabetes is a condition of excess fat inside our organs, whether we're obese or not.

The only thing that was keeping us from diabetes-unchecked skyrocketing blood sugars-is that the pancreas was working overtime pumping out extra insulin to overcome insulin resistance. But as the so-called islet or Beta cells in the pancreas are killed off by the fatty buildup, insulin production starts to fail, and we're left with the worst of both worlds: insulin resistance combined with a failing pancreas. Unable to then overcome the resistance, blood sugar levels go up and up, and boom: type 2 diabetes.

This has implications for cancer as well. Obesity leads to insulin resistance and our blood sugars start to go up, so our pancreas starts pumping out more insulin to try to force more sugar into our muscles, and eventually the fat spills over into the pancreas, killing off the insulin-producing cells. Then we develop diabetes, in which case we may have to start injecting insulin at high levels to overcome the insulin-resistance, and these high insulin levels promote cancer. That's one of the reasons we think obese women get more breast cancer. It all traces back to fat getting into our muscle cells, causing insulin resistance: fat from our stomach (obesity) or fat going into our stomach (saturated fats in our diet).

Now it should make sense why the American Diabetes Association recommends reduced intake of dietary fat as a strategy for reducing the risk for developing diabetes.


The reason I'm going into all this detail is that I'm hoping to empower both those suffering from the disease and those treating sufferers so as to better understand dietary interventions to prevent and treat the epidemic.

Here are some videos on prevention:

And here are some on treatment:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Nephron. This image has been modified.

Original Link

How Exactly Does Type 2 Diabetes Develop?

How Exactly Does Type 2 Diabetes Develop.jpeg

Insulin resistance is the cause of both prediabetes and type 2 diabetes. OkK, so what is the cause of insulin resistance? Insulin resistance is now accepted to be closely associated with the accumulation of fat within our muscle cells. This fat toxicity inside of our muscles is a major factor in the cause of insulin resistance and type 2 diabetes, as it interferes with the action of insulin. I've explored how fat makes our muscles insulin resistant (see What Causes Insulin Resistance?), how that fat can come from the fat we eat or the fat we wear (see The Spillover Effect Links Obesity to Diabetes), and how not all fats are the same (see Lipotoxicity: How Saturated Fat Raises Blood Sugar). It's the type of fat found predominantly in animal fats, relative to plant fats, that appears to be especially deleterious with respect to fat-induced insulin insensitivity. But this insulin resistance in our muscles starts years before diabetes is diagnosed.

In my video, Diabetes as a Disease of Fat Toxicity, you can see that insulin resistance starts over a decade before diabetes is actually diagnosed, as blood sugar levels slowly start creeping up. And then, all of the sudden, the pancreas conks out, and blood sugars skyrocket. What could underlie this relatively rapid failure of insulin secretion?

At first, the pancreas pumps out more and more insulin, trying to overcome the fat-induced insulin resistance in the muscles, and high insulin levels can lead to the accumulation of fat in the liver, called fatty liver disease. Before diagnosis of type 2 diabetes, there is a long silent scream from the liver. As fat builds up in our liver, it also becomes resistant to insulin.

Normally, the liver is constantly producing blood sugar to keep our brain alive between meals. As soon as we eat breakfast, though, the insulin released to deal with the meal normally turns off liver glucose production, which makes sense since we don't need it anymore. But when our liver is filled with fat, it becomes insulin resistant like our muscles, and doesn't respond to the breakfast signal; it keeps pumping out blood sugar all day long on top of whatever we eat. Then the pancreas pumps out even more insulin to deal with the high sugars, and our liver gets fatter and fatter. That's one of the twin vicious cycles of diabetes. Fatty muscles, in the context of too many calories, leads to a fatty liver, which leads to an even fattier liver. This is all still before we have diabetes.

Fatty liver can be deadly. The liver starts trying to offload the fat by dumping it back into the bloodstream in the form of something called VLDL, and that starts building up in the cells in the pancreas that produce the insulin in the first place. Now we know how diabetes develops: fatty muscles lead to a fatty liver, which leads to a fatty pancreas. It is now clear that type 2 diabetes is a condition of excess fat inside our organs, whether we're obese or not.

The only thing that was keeping us from diabetes-unchecked skyrocketing blood sugars-is that the pancreas was working overtime pumping out extra insulin to overcome insulin resistance. But as the so-called islet or Beta cells in the pancreas are killed off by the fatty buildup, insulin production starts to fail, and we're left with the worst of both worlds: insulin resistance combined with a failing pancreas. Unable to then overcome the resistance, blood sugar levels go up and up, and boom: type 2 diabetes.

This has implications for cancer as well. Obesity leads to insulin resistance and our blood sugars start to go up, so our pancreas starts pumping out more insulin to try to force more sugar into our muscles, and eventually the fat spills over into the pancreas, killing off the insulin-producing cells. Then we develop diabetes, in which case we may have to start injecting insulin at high levels to overcome the insulin-resistance, and these high insulin levels promote cancer. That's one of the reasons we think obese women get more breast cancer. It all traces back to fat getting into our muscle cells, causing insulin resistance: fat from our stomach (obesity) or fat going into our stomach (saturated fats in our diet).

Now it should make sense why the American Diabetes Association recommends reduced intake of dietary fat as a strategy for reducing the risk for developing diabetes.


The reason I'm going into all this detail is that I'm hoping to empower both those suffering from the disease and those treating sufferers so as to better understand dietary interventions to prevent and treat the epidemic.

Here are some videos on prevention:

And here are some on treatment:

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Nephron. This image has been modified.

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

What Not to Add to White Rice, Potatoes, or Pasta

What Not to Add to White Rice, Potatoes, or Pasta.jpeg

Rice currently feeds almost half the human population, making it the single most important staple food in the world, but a meta-analysis of seven cohort studies following 350,000 people for up to 20 years found that higher consumption of white rice was associated with a significantly increased risk of type 2 diabetes, especially in Asian populations. They estimated each serving per day of white rice was associated with an 11% increase in risk of diabetes. This could explain why China has almost the same diabetes rates as we do.

Diabetes rates in China are at about 10%; we're at about 11%, despite seven times less obesity in China. Japan has eight times less obesity than we do, yet may have a higher incidence of newly diagnosed diabetes cases than we do--nine per a thousand compared to our eight. They're skinnier and still may have more diabetes. Maybe it's because of all the white rice they eat.

Eating whole fruit is associated with lower risk of diabetes, whereas eating fruit processed into juice may not just be neutral, but actually increases diabetes risk. In the same way, eating whole grains, like whole wheat bread or brown rice is associated with lower risk of diabetes, whereas eating white rice, a processed grain, may not just be neutral, but actually increase diabetes risk.

White rice consumption does not appear to be associated with increased risk of heart attack or stroke, though, which is a relief after an earlier study in China suggested a connection with stroke. But do we want to eat a food that's just neutral regarding some of our leading causes of death, when we can eat whole foods that are associated with lower risk of diabetes, heart attack, stroke, and weight gain?

If the modern diabetes epidemic in China and Japan has been linked to white rice consumption, how can we reconcile that with low diabetes rates just a few decades ago when they ate even more rice? If you look at the Cornell-Oxford-China Project, rural plant-based diets centered around rice were associated with relatively low risk of the so-called diseases of affluence, which includes diabetes. Maybe Asians just genetically don't get the same blood sugar spike when they eat white rice? This is not the case; if anything people of Chinese ethnicity get higher blood sugar spikes.

The rise in these diseases of affluence in China over the last half century has been blamed in part on the tripling of the consumption of animal source foods. The upsurge in diabetes has been most dramatic, and it's mostly just happened over the last decade. That crazy 9.7% diabetes prevalence figure that rivals ours is new--they appeared to have one of the lowest diabetes rates in the world in the year 2000.

So what happened to their diets in the last 20 years or so? Oil consumption went up 20%, pork consumption went up 40%, and rice consumption dropped about 30%. As diabetes rates were skyrocketing, rice consumption was going down, so maybe it's the animal products and junk food that are the problem. Yes, brown rice is better than white rice, but to stop the mounting Asian epidemic, maybe we should focus on removing the cause--the toxic Western diet. That would be consistent with data showing animal protein and fat consumption associated with increased diabetes risk.

But that doesn't explain why the biggest recent studies in Japan and China associate white rice intake with diabetes. One possibility is that animal protein is making the rice worse. If you feed people mashed white potatoes, a high glycemic food like white rice, you can see in my video If White Rice is Linked to Diabetes, What About China? the level of insulin your pancreas has to pump out to keep your blood sugars in check. But what if you added some tuna fish? Tuna doesn't have any carbs, sugar, or starch so it shouldn't make a difference. Or maybe it would even lower the mashed potato spike by lowering the glycemic load of the whole meal? Instead you get twice the insulin spike. This also happens with white flour spaghetti versus white flour spaghetti with meat. The addition of animal protein makes the pancreas work twice as hard.

You can do it with straight sugar water too. If you do a glucose challenge test to test for diabetes, where you drink a certain amount of sugar and add some meat, you get a much bigger spike than without meat. And the more meat you add, the worse it gets. Just adding a little meat to carbs doesn't seem to do much, but once you get up to around a third of a chicken breast's worth, you can elicit a significantly increased surge of insulin. This may help explain why those eating plant-based have such low diabetes rates, because animal protein can markedly potentiate the insulin secretion triggered by carbohydrate ingestion.

The protein exacerbation of the effect of refined carbs could help explain the remarkable results achieved by Dr. Kempner with a don't-try-this-at-home diet composed of mostly white rice and sugar. See my video, Kempner Rice Diet: Whipping Us Into Shape.

Refined grains may also not be good for our blood pressure (see Whole Grains May Work As Well As Drugs).

What should we be eating to best decrease our risk of diabetes? See:

And check out my summary video, How Not to Die from Diabetes.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

Lipotoxicity: How Saturated Fat Raises Blood Sugar

NF-Nov24 Lipotoxicity How Saturated Fat Raises Blood Sugar copy.jpg

The reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance may be because saturated fats appear to impair blood sugar control the most.

The association between fat and insulin resistance is now widely accepted. Insulin resistance is due to so-called ectopic fat accumulation, the buildup of fat in places it's not supposed to be, like within our muscle cells. But not all fats affect the muscles the same. The type of fat, saturated vs. unsaturated, is critical. Saturated fats like palmitate, found mostly in meat, dairy and eggs, cause insulin resistance, but oleate, found mostly in nuts, olives and avocados may actually improve insulin sensitivity.

What makes saturated fat bad? Saturated fat causes more toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals and inflammation, establishing a vicious cycle of events in which saturated fat induces free radicals, causes dysfunction in the little power plants within our muscle cells (mitochondria), which then causes an increase in free radical production and an impairment of insulin signaling. I explain this in my video Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation from saturated fat has been demonstrated to raise insulin resistance through free radical production. Saturated fat also has been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacyl-glycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance.

While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create those toxic breakdown products like ceramide that causes lipotoxicity. Lipo- meaning fat, as in liposuction. This fat toxicity in our muscles is a well-known concept in the explanation of trigger for insulin resistance.

I've talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer and heart disease, but they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources while trans fats originate in meat and milk in addition to partially hydrogenated and refined vegetable oils.

That's why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. In a study done by Swedish researchers, insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.

We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst, but they don't just lead to inhibition of insulin signaling, the activation of inflammatory pathways and the increase in free radicals, they also cause an alteration in gene expression. This can lead to a suppression of key mitochondrial enzymes like carnitine palmitoyltransferase, which finally solves the mystery of why those eating vegetarian have a 60 percent higher expression of that fat burning enzyme. They're eating less saturated fat.

So do those eating plant-based diets have less fat clogging their muscles and less insulin resistance too? There hasn't been any data available regarding the insulin sensitivity or inside muscle cell fat of those eating vegan or vegetarian... until now. Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Those eating plant-based diets have the unfair advantage of being much slimmer, so they found omnivores who were as skinny as vegans to see if plant-based diets had a direct benefit, as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.

They found significantly less fat trapped in the muscle cells of vegans compared to omnivores at the same body weight, better insulin sensitivity, better blood sugar levels, better insulin levels and, excitingly, significantly improved beta-cell function (the cells in the pancreas that make the insulin). They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that plant-based diets are beta-cell protective as well, helping also to prevent our seventh leading cause of death, diabetes.

This is the third of a three-part series, starting with What Causes Insulin Resistance? and The Spillover Effect Links Obesity to Diabetes.

Even if saturated fat weren't associated with heart disease, its effects on pancreatic function and insulin resistance in the muscles would be enough to warrant avoiding it. Despite popular press accounts, saturated fat intake remains the primary modifiable determinant of LDL cholesterol, the #1 risk factor for our #1 killer-heart disease. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

How low should we shoot for in terms of saturated fat intake? As low as possible, according to the U.S. National Academies of Science Institute of Medicine: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Andrew Malone / Flickr

Original Link

Lipotoxicity: How Saturated Fat Raises Blood Sugar

NF-Nov24 Lipotoxicity How Saturated Fat Raises Blood Sugar copy.jpg

The reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance may be because saturated fats appear to impair blood sugar control the most.

The association between fat and insulin resistance is now widely accepted. Insulin resistance is due to so-called ectopic fat accumulation, the buildup of fat in places it's not supposed to be, like within our muscle cells. But not all fats affect the muscles the same. The type of fat, saturated vs. unsaturated, is critical. Saturated fats like palmitate, found mostly in meat, dairy and eggs, cause insulin resistance, but oleate, found mostly in nuts, olives and avocados may actually improve insulin sensitivity.

What makes saturated fat bad? Saturated fat causes more toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals and inflammation, establishing a vicious cycle of events in which saturated fat induces free radicals, causes dysfunction in the little power plants within our muscle cells (mitochondria), which then causes an increase in free radical production and an impairment of insulin signaling. I explain this in my video Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation from saturated fat has been demonstrated to raise insulin resistance through free radical production. Saturated fat also has been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacyl-glycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance.

While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create those toxic breakdown products like ceramide that causes lipotoxicity. Lipo- meaning fat, as in liposuction. This fat toxicity in our muscles is a well-known concept in the explanation of trigger for insulin resistance.

I've talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer and heart disease, but they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources while trans fats originate in meat and milk in addition to partially hydrogenated and refined vegetable oils.

That's why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. In a study done by Swedish researchers, insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.

We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst, but they don't just lead to inhibition of insulin signaling, the activation of inflammatory pathways and the increase in free radicals, they also cause an alteration in gene expression. This can lead to a suppression of key mitochondrial enzymes like carnitine palmitoyltransferase, which finally solves the mystery of why those eating vegetarian have a 60 percent higher expression of that fat burning enzyme. They're eating less saturated fat.

So do those eating plant-based diets have less fat clogging their muscles and less insulin resistance too? There hasn't been any data available regarding the insulin sensitivity or inside muscle cell fat of those eating vegan or vegetarian... until now. Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Those eating plant-based diets have the unfair advantage of being much slimmer, so they found omnivores who were as skinny as vegans to see if plant-based diets had a direct benefit, as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.

They found significantly less fat trapped in the muscle cells of vegans compared to omnivores at the same body weight, better insulin sensitivity, better blood sugar levels, better insulin levels and, excitingly, significantly improved beta-cell function (the cells in the pancreas that make the insulin). They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that plant-based diets are beta-cell protective as well, helping also to prevent our seventh leading cause of death, diabetes.

This is the third of a three-part series, starting with What Causes Insulin Resistance? and The Spillover Effect Links Obesity to Diabetes.

Even if saturated fat weren't associated with heart disease, its effects on pancreatic function and insulin resistance in the muscles would be enough to warrant avoiding it. Despite popular press accounts, saturated fat intake remains the primary modifiable determinant of LDL cholesterol, the #1 risk factor for our #1 killer-heart disease. See The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

How low should we shoot for in terms of saturated fat intake? As low as possible, according to the U.S. National Academies of Science Institute of Medicine: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Andrew Malone / Flickr

Original Link

Fat is the Cause of Type 2 Diabetes

NF-Nov17 What Causes Insulin Resistance copy.jpg

Studies dating back nearly a century noted a striking finding: If you take young, healthy people and split them up into two groups--half on a fat-rich diet and half on a carbohydrate-rich diet--we find that within just two days, glucose intolerance skyrockets in the fat group. The group that had been shoveling fat in ended up with twice the blood sugar. As the amount of fat in the diet goes up, so does one's blood sugar. Why would eating fat lead to higher blood sugar levels? It would take scientists nearly seven decades to unravel this mystery, but it would end up holding the key to our current understanding of the cause of type 2 diabetes.

The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract, it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.

Blood sugar, though, is like a vampire. It needs an invitation to come into our cells. That invitation is insulin. Insulin is the key that unlocks the door that lets glucose in the blood enter muscle cells. When insulin attaches to the insulin receptor on the cell, it activates an enzyme, which activates another enzyme, which activates two more enzymes, which finally activates glucose transport (as diagrammed in my video What Causes Insulin Resistance?).

What if there was no insulin? Blood sugar would be stuck in the bloodstream banging on the door to our muscles, unable to get inside. With nowhere to go, sugar levels in the blood would rise and rise. That's what happens in type 1 diabetes: the cells in the pancreas that make insulin get destroyed, and without insulin, sugar in the blood can't get out of the blood into the muscles, and so blood sugar rises. But there's a second way we could end up with high blood sugar.

What if there's enough insulin, but the insulin doesn't work? The key is there, but something's gummed up the lock. This is insulin resistance. Our muscle cells become resistant to the effect of insulin. What's gumming up the locks on our muscle cells? What's preventing insulin from letting glucose in? Tiny droplets of fat inside our muscle cells, so-called intramyocellular lipid.

Fat in the bloodstream can build up inside the muscle cell, creating toxic fatty breakdown products and free radicals that block the insulin signaling process. No matter how much insulin we have in our blood, it's not able to sufficiently open the glucose gates and blood sugar levels build up in the blood. And this can happen within three hours. One hit of fat can start causing insulin resistance, inhibiting blood sugar uptake after just 160 minutes.

This mechanism by which fat induces insulin resistance wasn't known until fancy MRI techniques were developed to see what was happening inside people's muscles as fat was infused into their bloodstream. That's how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.

We can also do the opposite experiment. Lower the level of fat in people's blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn't work very well. Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better--a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.

The effect is really dramatic--check out at least the end of my video What Causes Insulin Resistance? to see what happens as dietary fat intake drops.

The most concerning downside of low-carb diets, though, is heart health: Low Carb Diets and Coronary Blood Flow

This is the first of a 3-part series on the cause of type 2 diabetes, so as to better understand dietary interventions to prevent and treat the epidemic. In The Spillover Effect Links Obesity to Diabetes, I talk about how that fat can come either from our diet or excess fat stores, and then in Lipotoxicity: How Saturated Fat Raises Blood Sugar, I show how not all fats are equally to blame.

Here are some of my recent diabetes videos:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: [Gema Ibarra] © 123RF.com

Original Link

Fat is the Cause of Type 2 Diabetes

NF-Nov17 What Causes Insulin Resistance copy.jpg

Studies dating back nearly a century noted a striking finding: If you take young, healthy people and split them up into two groups--half on a fat-rich diet and half on a carbohydrate-rich diet--we find that within just two days, glucose intolerance skyrockets in the fat group. The group that had been shoveling fat in ended up with twice the blood sugar. As the amount of fat in the diet goes up, so does one's blood sugar. Why would eating fat lead to higher blood sugar levels? It would take scientists nearly seven decades to unravel this mystery, but it would end up holding the key to our current understanding of the cause of type 2 diabetes.

The reason athletes carb-load before a race is to build up the fuel supply within their muscles. We break down the starch into glucose in our digestive tract, it circulates as blood glucose (blood sugar) and is taken up by our muscles to be stored and burnt for energy.

Blood sugar, though, is like a vampire. It needs an invitation to come into our cells. That invitation is insulin. Insulin is the key that unlocks the door that lets glucose in the blood enter muscle cells. When insulin attaches to the insulin receptor on the cell, it activates an enzyme, which activates another enzyme, which activates two more enzymes, which finally activates glucose transport (as diagrammed in my video What Causes Insulin Resistance?).

What if there was no insulin? Blood sugar would be stuck in the bloodstream banging on the door to our muscles, unable to get inside. With nowhere to go, sugar levels in the blood would rise and rise. That's what happens in type 1 diabetes: the cells in the pancreas that make insulin get destroyed, and without insulin, sugar in the blood can't get out of the blood into the muscles, and so blood sugar rises. But there's a second way we could end up with high blood sugar.

What if there's enough insulin, but the insulin doesn't work? The key is there, but something's gummed up the lock. This is insulin resistance. Our muscle cells become resistant to the effect of insulin. What's gumming up the locks on our muscle cells? What's preventing insulin from letting glucose in? Tiny droplets of fat inside our muscle cells, so-called intramyocellular lipid.

Fat in the bloodstream can build up inside the muscle cell, creating toxic fatty breakdown products and free radicals that block the insulin signaling process. No matter how much insulin we have in our blood, it's not able to sufficiently open the glucose gates and blood sugar levels build up in the blood. And this can happen within three hours. One hit of fat can start causing insulin resistance, inhibiting blood sugar uptake after just 160 minutes.

This mechanism by which fat induces insulin resistance wasn't known until fancy MRI techniques were developed to see what was happening inside people's muscles as fat was infused into their bloodstream. That's how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.

We can also do the opposite experiment. Lower the level of fat in people's blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn't work very well. Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better--a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.

The effect is really dramatic--check out at least the end of my video What Causes Insulin Resistance? to see what happens as dietary fat intake drops.

The most concerning downside of low-carb diets, though, is heart health: Low Carb Diets and Coronary Blood Flow

This is the first of a 3-part series on the cause of type 2 diabetes, so as to better understand dietary interventions to prevent and treat the epidemic. In The Spillover Effect Links Obesity to Diabetes, I talk about how that fat can come either from our diet or excess fat stores, and then in Lipotoxicity: How Saturated Fat Raises Blood Sugar, I show how not all fats are equally to blame.

Here are some of my recent diabetes videos:

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: [Gema Ibarra] © 123RF.com

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Why Would Eating Fish Increase Diabetes Risk?

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In the past two years, six separate meta-analyses have been published on the relationship between fish consumption and type 2 diabetes. The whole point of a meta-analysis is to compile the best studies done to date and see what the overall balance of evidence shows. The fact that there are six different ones published recently highlights how open the question remains. One thread of consistency, though, was that fish consumers in the United States tended to be at greater risk for diabetes.

If we include Europe, then fish eaters appeared to have a 38% increased risk of diabetes. On a per serving basis, that comes out to be about a 5% increase in risk for every serving of fish one has per week. To put that into perspective, a serving of red meat per day is associated with 19% increase in risk. Just one serving per day of fish would be equivalent to a 35% increase in risk. But why might fish be worse than red meat?

Fish intake may increase type 2 diabetes risk by increasing blood sugar levels, as a review of the evidence commissioned by the U.S. government found. The review found that blood sugars increase in diabetics given fish oil. Another possible cause is that omega 3's appear to cause oxidative stress. A recent study, highlighted in my video, Fish and Diabetes, found that the insulin producing cells in the pancreas don't appear to work as well in people who eat two or more servings of fish a week. Or it may not be related to omega 3's at all but rather the environmental contaminants that build up in fish.

It all started with Agent Orange. We sprayed 20 million gallons of the stuff on Vietnam, and some of it was contaminated with trace amounts of dioxins. Though the Red Cross estimates that a million Vietnamese were adversely affected, what about all the servicemen who were exposed spraying it across the countryside? Reports started showing up that veterans exposed to Agent Orange appeared to have higher diabetes rates than unexposed veterans, a link that's now officially recognized.

These so-called "persistent organic pollutants" are mainly man-made industrial chemicals and are among the most hazardous compounds ever synthesized. They include dioxins, PCBs, and certain chlorine-containing pesticides, all of which are highly resistant to breakdown in the environment.

Initially condemned for their deleterious effect on reproductive function and their ability to cause cancer, there is now a growing body of evidence showing that exposure to these pollutants leads to metabolic diseases such as diabetes. This is a breakthrough that "should require our greatest attention."

For more on the role industrial pollutants may play in our diabetes epidemic, see Diabetes and Dioxins and Pollutants in Salmon and Our Own Fat.

More on the changing views surrounding fish oil supplements in Is Fish Oil Just Snake Oil?

Other foods associated with diabetes risk include processed meat and eggs. See Bacon, Eggs, and Gestational Diabetes During Pregnancy and Eggs and Diabetes, while Indian gooseberries and flaxseeds may help (Amla Versus Diabetes and Flaxseed vs. Diabetes).

Other videos on how polluted our oceans now are include:

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Image Credit: Gideon / Flickr

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How Phytates Fight Cancer Cells

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Phytate is a compound found in beans, grains, nuts and seeds. The average daily intake of phytate in vegetarian diets is about twice that of those eating mixed diets of plant and animal foods, which may help explain their low cancer rates. Aside from helping to prevent cancer, dietary phytate has been reported to help prevent kidney stone formation, protect against diabetes mellitus, dental cavities, and heart disease.

Do all these potentially beneficial effects sound too good to be true? Are there other examples of compounds made by plants that can have benefits across multiple diseases? Why yes! Aspirin, for example, which is found throughout the plant kingdom may also account for a variety of plant-based benefits (See Aspirin Levels in Plant Foods).

But of all the things phytates can do, the anticancer activity of phytate (also known as phytic acid, IP6, or inositol hexaphosphate), is considered one of its most important beneficial activities. Dietary phytates are quickly absorbed from the gastrointestinal tract and rapidly taken up by cancer cells throughout the body, and have been shown to inhibit the growth of all tested cancerous cell lines in vitro. Phytates have been shown to inhibit the growth of human leukemia cells, colon cancer cells, both estrogen receptor-positive and negative breast cancer cells, voicebox cancer, cervical cancer, prostate cancer, liver tumors, pancreatic, melanoma, and muscle cancers. All at the same time not affecting normal cells. That's the most important expectation of a good anticancer agent: the ability to only affect cancerous cells and to leave normal cells alone.

In my video, Phytates for Rehabilitating Cancer Cells, you can see how leukemia cells taken from cancer patients are killed by phytates, whereas normal bone marrow cells, are spared. This may explain why bean extracts kill off colon cancer cells in vitro, but leave normal colon cells alone.

What are the mechanisms of action by which phytates battle cancer? In other words, how do phytates fight? How don't they fight? Phytate targets cancer through multiple pathways, a combination of antioxidant, anti-inflammatory, immune-enhancing activities, detox, differentiation, and anti-angiogenesis. In other words, phytate appears to affect all the principal pathways of malignancy.

The antioxidative property is one of the most impressive characteristics of phytate. In fact that's why the meat industry adds phytates to meat to prevent the fat oxidation that begins at the moment of slaughter. Phytates can also act on our immune functions by augmenting natural killer cell activity, the cells in our body that hunt down and dispose of cancer cells, as well as neutrophils, which help form our first line of defense. And then phytates starve tumors as more of a last line of defense. Not only can phytates block the formation of new blood vessels that may be feeding tumors, but disrupt pre-formed capillary tubes, indicating that phytates may not just help blockade tumors, but actively cut off existing supply lines.

What's really remarkable about phytate, though, is that unlike most other anti-cancer agents, it not only causes a reduction in cancer cell growth but also enhances differentiation, meaning it causes cancer cells to stop acting like cancer cells and go back to acting like normal cells. You can see this with colon cancer cells for example. In the presence of phytates, human colon cancer cells mature to structurally and behaviorally resemble normal cells. And this has been demonstrated in leukemia cells, prostate cancer, breast cancer, and muscle cancer cells as well.

For more on the cancer and phytate connection, check out Phytates for the Prevention of Cancer and Phytates for the Treatment of Cancer.

This video reminds me of my video on the spice, turmeric, Turmeric Curcumin Reprogramming Cancer Cell Death.

What else can we eat to improve the cancer-fighting front of our immune system? See Boosting Natural Killer Cell Activity.

More on the concept of starving tumors of their blood supply in Anti-Angiogenesis: Cutting Off Tumor Supply Lines.

Is there clinical evidence of plants actually reversing cancer progression? You won't believe your eyes:

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day, and From Table to Able.

Image Credit: Avi / Flickr

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