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

Benefits of Oatmeal for Fatty Liver Disease

Benefits of Oatmeal for Fatty Liver Disease.jpeg

If oatmeal is so powerful that it can clear up some of the ravages of chemotherapy just applied to the skin (see my video Oatmeal Lotion for Chemotherapy-Induced Rash), what might it do if we actually ate it? Oats are reported to possess varied drug-like activities like lowering blood cholesterol and blood sugar, boosting our immune system, anticancer, antioxidant, and anti-atherosclerosis activites, in addition to being a topical anti-inflammatory, and reprtedly may also be useful in controlling childhood asthma and body weight.

Whole-grain intake in general is associated with lower risk of type 2 diabetes, cardiovascular disease, and weight gain, as shown in my video Can Oatmeal Help Fatty Liver Disease?. All of the cohort studies on type 2 diabetes and heart disease show whole grain intake is associated with lower risk.

Researchers have observed the same for obesity--consistently less weight gain for those who consumed a few servings of whole grains every day. All the forward-looking population studies demonstrate that a higher intake of whole grains is associated with lower body mass index and body weight gain. However, these results do not clarify whether whole grain consumption is simply a marker of a healthier lifestyle or a factor favoring lower body weight.

For example, high whole grain consumers--those who eat whole wheat, brown rice, and oatmeal for breakfast--tend to be more physically active, smoke less, and consume more fruit, vegetables, and dietary fiber than those that instead reach for fruit loops. Statistically, one can control these factors, effectively comparing nonsmokers to nonsmokers with similar exercise and diet as most of the studies did, and they still found whole grains to be protective via a variety of mechanisms.

For example, in terms of helping with weight control, the soluble fiber of oatmeal forms a gel in the stomach, delaying stomach emptying, making one feel full for a longer period. It seems plausible that whole grain intake does indeed offer direct benefits, but only results of randomized controlled intervention studies can provide direct evidence of cause and effect. In other words, the evidence is clear that oatmeal consumers have lower rates of disease, but that's not the same as proving that if we start eating more oatmeal, our risk will drop. To know that, we need an interventional trial, ideally a blinded study where you give half the people oatmeal, and the other half fake placebo oatmeal that looks and tastes like oatmeal, to see if it actually works. And that's what we finally got--a double-blinded randomized trial of overweight and obese men and women. Almost 90% of the real oatmeal-treated subjects had reduced body weight, compared to no weight loss in the control group. They saw a slimmer waist on average, a 20 point drop in cholesterol, and an improvement in liver function.

Nonalcoholic fatty liver disease, meaning a fatty liver caused by excess food rather than excess drink, is now the most common cause of liver disease in the United States, and can lead in rare cases to cirrhosis of the liver, cancer of the liver, and death. Theoretically, whole grains could help prevent and treat fatty liver disease, but this is the first time it had been put to the test. A follow-up study in 2014 confirmed these findings of a protective role of whole grains, but refined grains was associated with increased risk. So one would not expect to get such wonderful results from wonder bread.

How can you make your oatmeal even healthier? See Antioxidants in a Pinch.

Whole Grains May Work As Well As Drugs for hypertension, but refined grain intake may linked with high blood pressure and diseases like diabetes. But If White Rice is Linked to Diabetes, What About China?.

More on keeping the liver healthy in videos like:

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

Benefits of Oatmeal for Fatty Liver Disease

Benefits of Oatmeal for Fatty Liver Disease.jpeg

If oatmeal is so powerful that it can clear up some of the ravages of chemotherapy just applied to the skin (see my video Oatmeal Lotion for Chemotherapy-Induced Rash), what might it do if we actually ate it? Oats are reported to possess varied drug-like activities like lowering blood cholesterol and blood sugar, boosting our immune system, anticancer, antioxidant, and anti-atherosclerosis activites, in addition to being a topical anti-inflammatory, and reprtedly may also be useful in controlling childhood asthma and body weight.

Whole-grain intake in general is associated with lower risk of type 2 diabetes, cardiovascular disease, and weight gain, as shown in my video Can Oatmeal Help Fatty Liver Disease?. All of the cohort studies on type 2 diabetes and heart disease show whole grain intake is associated with lower risk.

Researchers have observed the same for obesity--consistently less weight gain for those who consumed a few servings of whole grains every day. All the forward-looking population studies demonstrate that a higher intake of whole grains is associated with lower body mass index and body weight gain. However, these results do not clarify whether whole grain consumption is simply a marker of a healthier lifestyle or a factor favoring lower body weight.

For example, high whole grain consumers--those who eat whole wheat, brown rice, and oatmeal for breakfast--tend to be more physically active, smoke less, and consume more fruit, vegetables, and dietary fiber than those that instead reach for fruit loops. Statistically, one can control these factors, effectively comparing nonsmokers to nonsmokers with similar exercise and diet as most of the studies did, and they still found whole grains to be protective via a variety of mechanisms.

For example, in terms of helping with weight control, the soluble fiber of oatmeal forms a gel in the stomach, delaying stomach emptying, making one feel full for a longer period. It seems plausible that whole grain intake does indeed offer direct benefits, but only results of randomized controlled intervention studies can provide direct evidence of cause and effect. In other words, the evidence is clear that oatmeal consumers have lower rates of disease, but that's not the same as proving that if we start eating more oatmeal, our risk will drop. To know that, we need an interventional trial, ideally a blinded study where you give half the people oatmeal, and the other half fake placebo oatmeal that looks and tastes like oatmeal, to see if it actually works. And that's what we finally got--a double-blinded randomized trial of overweight and obese men and women. Almost 90% of the real oatmeal-treated subjects had reduced body weight, compared to no weight loss in the control group. They saw a slimmer waist on average, a 20 point drop in cholesterol, and an improvement in liver function.

Nonalcoholic fatty liver disease, meaning a fatty liver caused by excess food rather than excess drink, is now the most common cause of liver disease in the United States, and can lead in rare cases to cirrhosis of the liver, cancer of the liver, and death. Theoretically, whole grains could help prevent and treat fatty liver disease, but this is the first time it had been put to the test. A follow-up study in 2014 confirmed these findings of a protective role of whole grains, but refined grains was associated with increased risk. So one would not expect to get such wonderful results from wonder bread.

How can you make your oatmeal even healthier? See Antioxidants in a Pinch.

Whole Grains May Work As Well As Drugs for hypertension, but refined grain intake may linked with high blood pressure and diseases like diabetes. But If White Rice is Linked to Diabetes, What About China?.

More on keeping the liver healthy in videos like:

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 About All the Sugar in Fruit?

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If the fructose in sugar and high fructose corn syrup has been considered "alcohol without the buzz" in terms of the potential to inflict liver damage, what about the source of natural fructose, fruit?

If you compare the effects of a diet restricting fructose from both added sugars and fruit to one just restricting fructose from added sugars, the diet that kept the fruit did better. People lost more weight with the extra fruit present than if all fructose was restricted. Only industrial, not fruit fructose intake, was associated with declining liver function and high blood pressure. Fructose from added sugars was associated with hypertension; fructose from natural fruits is not.

If we have people drink a glass of water with three tablespoons of table sugar in it, which is like a can of soda, they get a big spike in blood sugar within the first hour (as you can see in my video If Fructose is Bad, What About Fruit?). Our body freaks out and releases so much insulin we actually overshoot, and by the second hour we're relatively hypoglycemic, dropping our blood sugar below where they were when we started out fasting. In response, our body dumps fat into our blood stream as if we're starving, because our blood sugars just dropped so low so suddenly.

What if you eat blended berries in addition to the sugar? They have sugars of their own in them, in fact an additional tablespoon of sugar worth, so the blood sugar spike should be worse, right?

Not only is there no additional blood sugar spike, there was no hypoglycemic dip afterwards. Blood sugar just went up and down without that overshoot and without the surge of fat into the blood.

This difference may be attributed to the semisolid consistency of the berry meals, which may have decreased the rate of stomach emptying compared with just guzzling sugar water. In addition, the soluble fiber in the berries has a gelling effect in our intestines that slows the release of sugars. To test to see if it was the fiber, researchers repeated the experiment with berry juice that had all the sugar but none of the fiber. A clear difference was observed early on in the blood sugar insulin responses. At the 15-minute mark, the blood sugar spike was significantly reduced by the berry meals, but not by the juices, but the rest of the beneficial responses were almost the same between the juice and the whole fruit, suggesting that fiber may just be part of it. It turns out there are fruit phytonutrients that inhibit the transportation of sugars through the intestinal wall into our blood stream. Phytonutrients in foods like apples and strawberries can block some of the uptake of sugars by the cells lining our intestines.

Adding berries can actually blunt the insulin spike from high glycemic foods. For example, white bread creates a big insulin spike within two hours after eating it. Eat that same white bread with some berries, though, and we're able to blunt the spike. So, even though we've effectively added more sugars in the form of berries, there's less of an insulin spike, which has a variety of potential short and long-term benefits. So if you're going to make pancakes, make sure they're blueberry pancakes.

Surprised about the juice results? Me too! More on juice:

A few videos I have on industrial sugars:

How else can we blunt the glycemic spike?

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--2013: Uprooting the Leading Causes of Death, More Than an Apple a Day, 2014: From Table to Able: Combating Disabling Diseases with Food, 2015: Food as Medicine: Preventing and Treating the Most Dreaded Diseases with Diet, and my latest, 2016: How Not To Die: The Role of Diet in Preventing, Arresting, and Reversing Our Top 15 Killers.

Original Link

Caloric Restriction vs. Plant-Based Diets

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Hundreds of thousands of deaths in the United States every year are attributed to obesity, now overtaking smoking as perhaps the main preventable cause of illness and premature death. In particular, excess body fatness is an important cause of most cancers, according to a meta-analysis of studies done to date. For some cancers, about half of the cases may be attributable to just being overweight or obese.

What's the connection, though? Why do individuals who are obese have increased cancer risk? To answer this question we must consider the biochemical consequences of obesity, like IGF-1; insulin like growth factor one is a cancer-promoting growth hormone associated with a variety of common cancers in adults, as well as children. Kids who got cancer had about four times the levels of IGF-1 circulating in their bloodstream, whereas people growing up with abnormally low levels of IGF-1 don't seem to get cancer at all.

I've talked about this cancer-proofing mutation (See Cancer-Proofing Mutation), the role animal protein intake plays in boosting IGF-1 production from our liver (Protein Intake & IGF-1 Production), which may explain plant-based protection from cancer (The Answer to the Pritikin Puzzle), and how plant-based one has to eat (How Plant-Based to Lower IGF-1?), but our liver is not the only tissue that produced IGF-1, fat cells produce IGF-1 too. That may help explain this "twenty-first century cancer epidemic caused by obesity."

So of course drug companies have come up with a variety of IGF-1 blocking chemo agents, with cute names like figitumamab, but with not-so-cute side effects "such as early fatal toxicities." So perhaps better to lower IGF-1 the natural way, by eating a plant-based diet, as vegan women and men have lower IGF-1 levels. Maybe, though, it's just because they're so skinny. The only dietary group that comes close to the recommended BMI of 21 to 23 were those eating strictly plant-based diets, so maybe it's the weight loss that did it. Maybe we can eat whatever we want as long as we're skinny.

To put that to the test, we'd have to find a group of people that eat meat, but are still as slim as vegans. And that's what researchers did - long-distance endurance runners, running an average of 48 miles a week for 21 years were as slim as vegans. If we run 50,000 miles we too can maintain a BMI of even a raw vegan. So what did they find?

If we look at blood concentrations of cancer risk factors among the groups of study subjects, we see that only the vegans had significantly lower levels of IGF-1. That makes sense given the role animal protein plays in boosting IGF-1 levels.

But the vegan group didn't just eat less animal protein, they ate fewer calories. And in rodents at least, caloric restriction alone reduces IGF-1 levels. So maybe low IGF-1 among vegans isn't due to their slim figures, but maybe the drop in IGF-1 in vegans is effectively due to their unintentional calorie restriction. So we have to compare vegans to people practicing severe calorie restriction.

To do this, the researchers recruited vegans from the St. Louis Vegetarian Society, and went to the Calorie Restriction Society to find folks practicing severe caloric restriction. What did they find?

Only the vegan group got a significant drop in IGF-1. These findings demonstrate that, unlike in rodents, long-term severe caloric restriction in humans does not reduce the level of this cancer-promoting hormone. It's not how many calories we eat, but the protein intake that may be the key determinant of circulating IGF-1 levels in humans, and so reduced protein intake may become an important component of anti-cancer and anti-aging dietary interventions.

That same data set that compared plant eaters to marathon runners was also featured in Hibiscus Tea vs. Plant-Based Diets for Hypertension and Arteries of Vegans vs. Runners.

These studies are highlighted in my video Caloric Restriction vs. Plant-based Diets.

More on the caloric consumption and longevity:

What exactly is IGF-1 and what is the relationship to animal protein consumption?:

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: Heather Hammond / Flickr

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Might Turmeric Help Prevent Alzheimer’s?

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There are plenty of anti-inflammatory drugs out there that may reduce the risk of Alzheimer's disease, but stomach, liver, and kidney toxicity precludes their widespread use. So maybe using an anti-inflammatory food like the spice, turmeric, found in curry powder, could offer the benefits without the risks? Before even considering putting it to the test, though, one might ask, "Well, do populations that eat a lot of turmeric have a lower prevalence of dementia?" And indeed, those living in rural India who do just that may actually have the lowest reported prevalence of dementia and Alzheimer's.

In rural Pennsylvania, the incidence rate of Alzheimer's disease among seniors is 19/1000. Nineteen people in a thousand over age 65 develop Alzheimer's every year in rural Pennsylvania. In rural India, using the same diagnostic criteria, that same rate is three, confirming they have among the lowest reported Alzheimer's rates in the world.

Although the lower prevalence of Alzheimer's in India is generally attributed to the turmeric consumption as a part of curry, and it is assumed that people who use turmeric regularly have a lower incidence of the disease, but let's not just assume. As highlighted in my video, Preventing Alzheimer's with Turmeric, a thousand people were tested, and those who consumed curry at least occasionally did better on simple cognitive tests than those who didn't. Those that ate curry often also had only about half the odds of showing cognitive impairment, after adjusting for a wide variety of potential confounding factors. This suggests that curry consumption may indeed be associated with better cognitive performance.

Of course it probably matters what's being curried--are we talking chicken masala, or chana masala, with chickpeas instead of chicks? It may be no coincidence that the country with among the lowest rates of Alzheimer's also has among the lowest rates of meat consumption, with a significant percentage of Indians eating meat-free and egg-free diets.

Studies have suggested for nearly 20 years now that those who eat meat--red meat or white meat--appear between two to three times more likely to become demented compared to vegetarians. And the longer one eats meat-free, the lower the associated risk of dementia, whether or not you like curry.

There's another spice that may be useful for brain health. See my video Saffron for the Treatment of Alzheimer's. What about coconut oil? See Does Coconut Oil Cure Alzheimer's? In terms of preventing cognitive decline in the first place, check out my video How to Slow Brain Aging By Two Years.

I've raised the issue of plant-based diets and dementia in Alzheimer's Disease: Grain Brain or Meathead?

For more on spices and inflammation, see Which Spices Fight Inflammation? and the follow-up, Spicing Up DNA Protection.

What about treating Alzheimer's disease with the spice turmeric? That's the topic of my video, Treating Alzheimer's with Turmeric.

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: Marcel Oosterwijk / Flickr

Original Link

Four Brazil Nuts Once a Month…

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One of the craziest studies I read all year involved feeding people a single serving of Brazil nuts to see what it would do to the cholesterol levels of healthy volunteers. They gave ten men and women a single meal containing zero, one, four, or eight Brazil nuts, and found that the ingestion of just that single serving almost immediately improved cholesterol levels. LDL, so-called "bad" cholesterol levels in the blood, was significantly lower starting just nine hours after the ingestion of nuts, and by no insignificant amount, nearly 20 points within a day. Even drugs don't work that fast. It takes statins around four days to have a significant effect.

But that's not even the crazy part.

The researchers went back and measured their cholesterol five days later, and then 30 days later. Now keep in mind they weren't eating Brazil nuts this whole time. They just had that single serving of Brazil nuts a month before and their cholesterol was still down 30 days later. It went down and stayed down, after eating just four nuts... That's nuts!

And no, the study was not funded by the Brazil nut industry.

Interestingly, four nuts actually seemed to work faster than the eight nuts to lower bad cholesterol and boost good cholesterol. These results suggest that eating just four nuts might be enough to improve the levels of LDL and HDL for up to 30 days, and maybe longer--they didn't test past 30.

Now normally, when a study comes out in the medical literature showing some too-good-to-be-true result like this you want to wait to see the results replicated before you change your clinical practice, before you recommend something to your patients, particularly when the study is done on only ten people, and especially when the findings are literally just too incredible to be believed. But when the intervention is cheap, easy, harmless and healthy--eating four Brazil nuts a month--then, in my opinion, the burden of proof is kind of reversed. I think the reasonable default position is to do it until proven otherwise.

They concluded a single serving was sufficient "without producing liver and kidney toxicity." What they're referring to is the high selenium content of Brazil nuts--so high that four eaten every day may actually bump us up against the tolerable daily limit for selenium, but not something we have to worry about if we're just eating four once a month.

I'd be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).

Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!

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: CIFOR / Flickr

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Hummus for a Healthy Heart

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I've talked previously about the anti-diabetic and anti-obesity effects of various phytonutrients in beans, but beans have protective effects on the cardiovascular system as well. As one academic review suggested, plant-specific compounds can have a remarkable impact on the health care system and may provide therapeutic health benefits, including the prevention and treatment of diseases and disorders. Plants have antioxidant effects, anti-inflammatory effects, protect our livers, lower cholesterol and blood pressure, and help prevent aging, diabetes, osteoporosis, DNA damage, heart disease and other disorders. Those without legumes in their daily diet, for example, may be at quadruple the odds of suffering high blood pressure.

Legumes such as chickpeas have been used to treat high blood pressure and diabetes for thousands of years. And they can also lower cholesterol levels. Researchers placed people in Northern India on high fat diets to raise their cholesterol levels up to that of the Western world (up around 206 mg/dL) and swapped in chickpeas for some of the grains they were eating. In five months, their cholesterol levels dropped to about 160, almost to the target of around 150. Cholesterol was reduced more than 15 percent in most of the subjects. In a randomized crossover trial, highlighted in my video, Beans, Beans, They're Good for Your Heart, two servings a day of lentils, chickpeas, beans, or split peas cut cholesterol levels so much that many participants moved below the range for which statin drugs are typically prescribed.

In the India study, although the subjects' cholesterol levels were comparable to the Western world at the start of the treatment with chickpeas, before the studym the participants were eating a low-fat diet. So low that their cholesterol levels started out at 123, well within the safe zone. Only after packing their diets with saturated fat were the researchers able to boost their cholesterol up to typical American levels, which could then be ameliorated by adding chickpeas. So it would be better if they just ate healthy in the first place. Or even better, healthy with hummus: a healthy diet with lots of legumes.


Beans dips like hummus are among my favorite go-to snacks. I like to dip snap peas and red bell pepper slices in them. I'd love to hear everyone's favorite recipe. You show me yours and I'll show you mine :)

Canned Beans or Cooked Beans? Click the link to find out!

Beans can help us live longer (Increased Lifespan from Beans), control our blood sugars (Beans and the Second Meal Effect), and help prevent and treat diabetes (Preventing Prediabetes By Eating More and Diabetics Should Take Their Pulses).

What about the purported "anti-nutrient" phytates in beans? You mean the Phytates for the Prevention of Cancer, the Phytates for Rehabilitating Cancer Cells, and the Phytates for the Treatment of Cancer? Phytate-containing foods may also help protect our bones (Phytates for the Prevention of Osteoporosis).

Why not just take cholesterol pills every day for the rest of our life? See my videos Statin Muscle Toxicity and Statin Cholesterol Drugs and Invasive Breast Cancer.

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: homami / Flickr

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Should We Take Chlorella to Boost Natural Killer Cell Activity?

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