How Bariatric Surgery Reverses Diabetes

“Roux-en-Y gastric bypass surgery (RYGB) is one of the most successful treatment strategies for diabetes accompanying morbid obesity. Long-term diabetes remission rates of 83% have been reported.” These findings have led to the suggestion that the surgery improves diabetes by somehow altering digestive hormones, but this interpretation ignores the fact that patients are placed on a severely limited diet for a week or two after the operation just to recover from the major surgery. Severe caloric restriction alone can improve diabetes. So, is it the diet or the surgery?

To answer that question, researchers put diabetics on the exact same diet as one would eat post-RYGB surgery, with or without the actual surgery. As I discuss in Reversing Diabetes with Surgery, the researchers found that their diabetes improved rapidly on the surgery diet before they had the surgery. In fact, the improvement in blood sugar control was better on the diet alone than after the surgery.

Blood sugar control improved more in the absence of surgery.

This suggests that the whole surgical-diabetes-reversal is not due to the surgery at all, but rather because of the diet people have to go on in the hospital during recovery. So, the clinical implication is that nonsurgical interventions have just as much potential to resolve diabetes as major surgery does.

If you’re familiar with my video Diabetes as a Disease of Fat Toxicity, you’ll understand what is occurring. Namely, “[t]ype 2 diabetes can be understood as a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat”—that is, too much fat in the cells of the liver, pancreas, and muscles. Within seven days of eating about 600 calories a day by either dietary intervention or bariatric surgery, fasting glucose levels (blood sugar levels) can normalize, thanks to a fall in liver fat. If you look at CT scans, you can actually see a 35 percent reduction in liver volume as all the fat is cleared out. Then, the body starts pulling fat out of the pancreas. When the cause of diabetes goes away, the diabetes goes away.

The insulin-producing beta cells of the pancreas “had woken up!… Clearly, the [beta] cells are not permanently damaged in Type 2 diabetes, but are merely metabolically inhibited.” Studies show a reversal of diabetes up to 28 years after diagnosis.

So, diabetics enough to starve themselves can regain normal health. This information should be available to all people with type 2 diabetes, even though it is unlikely many will be motivated enough to escape from the disease. It’s not easy to not eat. Diabetics should know that if they don’t reverse their diabetes, their future health is in jeopardy, although the serious consequences must be balanced against the difficulties and privations associated with starvation diets. “For many people, this may prove too high a price to pay,” as it’s hard to voluntarily restrict food intake that much.

In that case, how about involuntary food restriction? That’s what stomach stapling surgery is. When you essentially remove someone’s stomach, they’re forced into compulsory food restriction.

Of course, major surgery carries major risks—during the operation and afterwards. There can be bleeding, leakage, infections, erosions, herniation, and severe nutritional deficiencies. Surgery or starvation? There has got to be a better way. And there is!

Instead of changing the quantity of food eaten, whether voluntarily or involuntarily, is it possible to reverse diabetes by changing the quality of the food? Watch my videos Reversing Diabetes with Food and Diabetes Reversal: Is It the Calories or the Food? to get the complete picture.


For the lowdown on saturated fat, check out Lipotoxicity: How Saturated Fat Raises Blood Sugar.

Interested in taking a deeper dive into underlying causes of type 2 diabetes? You may be interested in these:

And, for an overview, see 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:

How to Treat the Root Cause of Diabetes

After about age 20, we may have all the insulin-producing beta cells we’re ever going to get. So if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells.

You can kill pancreatic cells right in a petri dish. If you expose the insulin-producing beta cells in our pancreas to fat, they suck it up and then start dying off. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death. A chronic increase in blood fat levels can be harmful to our pancreas.

It’s not just any fat; it’s saturated fat. As you can see in my video, What Causes Diabetes?, predominant fat in olives, nuts, and avocados gives a tiny bump in death protein 5, but saturated fat really elevates this contributor to beta cell death. Therefore, saturated fats are harmful to beta cells. Cholesterol is, too. The uptake of bad cholesterol (LDL) can cause beta cell death as a result of free radical formation.

Diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood (non-esterified fatty acids, or NEFAs) may also cause beta cell death and may thus contribute to the progressive beta cell loss we see in type 2 diabetes. These findings aren’t just based on test tube studies. When researchers have infused fat directly into people’s bloodstreams, they can show it directly impairing pancreatic beta cell function. The same occurs when we ingest it.

Type 2 diabetes is characterized by “defects in both insulin secretion and insulin action,” and saturated fat appears to impair both. Researchers showed saturated fat ingestion reduces insulin sensitivity within hours. The subjects were non-diabetics, so their pancreases should have been able to boost insulin secretion to match the drop in sensitivity. But no, “insulin secretion failed to compensate for insulin resistance in subjects who ingested [the saturated fat].” This implies saturated fat impaired beta cell function as well, again just within hours after going into our mouth. “[I]ncreased consumption of [saturated fats] has a powerful short- and long-term effect on insulin action,” contributing to the dysfunction and death of pancreatic beta cells in diabetes.

Saturated fat isn’t just toxic to the pancreas. The fats found predominantly in meat and dairy—chicken and cheese are the two main sources in the American diet—are considered nearly “universally toxic.” In contrast, the fats found in olives, nuts, and avocados are not. Saturated fat has been found to be particularly toxic to liver cells, contributing to the formation of fatty liver disease. If you expose human liver cells to plant fat, though, nothing happens. If you expose our liver cells to animal fat, a third of them die. This may explain why higher intake of saturated fat and cholesterol are associated with non-alcoholic fatty liver disease.

By cutting down on saturated fat consumption, we may be able to help interrupt these processes. Decreasing saturated fat intake can help bring down the need for all that excess insulin. So either being fat or eating saturated fat can both cause excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. It’s not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have in making us fat, “may contribute to the development of insulin resistance and its clinical consequences.” After controlling for weight, alcohol, smoking, exercise, and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood.

So what causes diabetes? The consumption of too many calories rich in saturated fats. Just like everyone who smokes doesn’t develop lung cancer, everyone who eats a lot of saturated fat doesn’t develop diabetes—there is a genetic component. But just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats are currently considered the cause of type 2 diabetes.

I have a lot of videos on diabetes, including:

Preventing the disease:

And treating it:

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:

How Exactly Does Type 2 Diabetes Develop?

How Exactly Does Type 2 Diabetes Develop

Insulin resistance is the cause of both prediabetes and type 2 diabetes. Ok, 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: