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

How Much Added Sugar is Too Much?

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In 1776, at the time of the American Revolution, Americans consumed about four pounds of sugar per person each year. By 1850, this had risen to 20 pounds, and by 1994 to 120 pounds. Now we're closer to 160 (See How Much Added Sugar is Too Much?). Half of table sugar is fructose, taking up about 10 percent of our diet. This is not from eating apples, but rather the fact that we're each guzzling the equivalent of 16-ounce soft drink every day; that's about 50 gallons a year.

Even researchers paid by the likes of the Dr. Pepper Snapple Group and The Coca Cola Company acknowledge that sugar is empty calories, containing "no essential micronutrients, and therefore if we're trying to reduce calorie intake, reducing sugar consumption is obviously the place to start." Concern has been raised, though, that sugar calories may be worst than just empty.

A growing body of scientific evidence suggests that "the fructose added to foods and beverages in the form of table sugar and high fructose corn syrup in large enough amounts can trigger processes that lead to liver toxicity and other chronic diseases."

Fructose hones in like a laser beam on the liver, and like alcohol, fructose can increase the fat in the liver. The increase in non-alcoholic fatty liver disease is one of the most remarkable medical developments over the past three decades--the emergence of fatty liver inflammation as a public health problem here and around the globe.

These may not be messages that the sugar industry or beverage makers want to hear. In response, the director-general of the industry front group, the World Sugar Research Organization, replied, "Overconsumption of anything is harmful, including water and air." Yes, he compared the overconsumption of sugar to breathing too much.

Under American Heart Association's new sugar guidelines, most American women should consume no more than 100 calories per day from added sugars, and most American men should eat or drink no more than 150. That means one can of soda could take us over the top for the day. The new draft guidelines from the World Health Organization suggests we could benefit from restricting added sugars to under 5 percent of calories. That's about six spoonfuls of added sugar. I don't know why they don't just recommend zero as optimal, but you can get a sense of how radical their proposal is given that we consume an average of 12-18 spoonfuls a day right now.

This underscores why a whole foods, plant-based diet is preferable to a plant-based diet that includes processed junk.

I've touched on the harm of refined sugars before in:

For healthful alternatives in baking, see The Healthiest Sweetener, and for beverages, Erythritol May Be a Sweet Antioxidant.

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 Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Adam Engelhart / Flickr

Original Link

Coffee for Hepatitis C

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Decades ago, researchers in Norway came upon an unexpected finding. Alcohol consumption was associated with liver inflammation (no surprise), but a protective association was found for coffee consumption. These findings were replicated in the U.S. and around the world. Those at risk for liver disease--who drank a lot of alcohol or were overweight--appeared to cut their risk in half if they drank more than two cups of coffee a day.

Liver cancer is one of the most feared complications of liver inflammation. Hepatocellular carcinoma is the third leading cause of cancer death, and the incidence has been rapidly rising in the United States and Europe, largely driven by the burden of hepatitis C infection and fatty liver disease. Putting together all the best studies done to date, those drinking the most coffee had half the risk of liver cancer compared to those that drank the least. Since the meta-analysis was published, a new study found that male smokers may be able to cut their risk of liver cancer more than 90% by drinking four or more cups of coffee a day. (Of course, they could also stop smoking!). It's similar to heavy drinkers of alcohol: drinking more coffee may decrease liver inflammation, but not as much as drinking less alcohol.

Liver cancers are among the most avoidable cancers, through hepatitis B vaccination, control of hepatitis C transmission, and reduction of alcohol drinking. These three measures could, in principle, wipe out 90% of liver cancers worldwide. It remains unclear whether coffee drinking has an additional role on top of that, but in any case such a role would be limited compared to preventing liver damage in the first place. But what if you already have hepatitis C or are among the 30% of Americans with non-alcoholic fatty liver disease due to obesity, which may quadruple one's risk of dying from liver cancer? Coffee seems to help with hepatitis C, reducing liver damage, disease activity, and mortality. It was only the lack of randomized, interventional studies on the topic that prevented us from concluding that coffee has a protective effect.

But in 2013 we got such a study, a randomized controlled trial on the effects of coffee consumption in chronic hepatitis C (highlighted in my video, Preventing Liver Cancer with Coffee). Forty patients with chronic hepatitis C were randomized into two groups: the first consumed four cups of coffee/day for 30 days, while the second remained coffee "abstinent." Then the groups switched for the second month. Two months is too soon to detect changes in cancer rates, but the researchers were able to demonstrate that coffee consumption reduces oxidative DNA damage, increases the death of virus infected cells, stabilizes chromosomes, and reduces fibrosis, all of which could explain the role coffee appears to play in reducing the risk of disease progression and of evolution to cancer.

Is it time to write a prescription for coffee for those at risk for liver disease? Some say no: "[A]lthough the results are promising, additional work is needed to identify which specific component of coffee is the contributing factor in reducing liver disease and related mortality." There are, after all, more than 1000 compounds that could be responsible for its beneficial effects. But that's such a pharmacological worldview. Why do we have to know exactly what it is in the coffee bean before we can start using them to help people? Yes, more studies are needed, but in the interim; moderate, daily, unsweetened coffee ingestion is a reasonable adjunct to therapy for people at high risk such as those with fatty liver disease.

Daily consumption of caffeinated beverages can lead to physical dependence. Caffeine withdrawal symptoms can include days of headache, fatigue, difficulty with concentration, and mood disturbances. But this dependence could be a good thing: "The tendency for coffee to promote habitual consumption may ultimately be advantageous if its myriad potential health benefits are confirmed."

More on coffee in:

Broccoli can boost the liver's detoxifying enzymes (Prolonged Liver Function Enhancement from Broccoli) but one can overdo it (Liver Toxicity Due to Broccoli Juice?).

What other foods might reduce DNA damage? See:

-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, From Table to Able, and Food as Medicine.

Image Credit: Matthew Wicks / Flickr

Original Link