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

GMO Soy and Breast Cancer

July12.jpg

In response to concerns raised about the toxicity of Monsanto's roundup pesticide, which ends up in GMO foods (See Is Monsanto's Roundup Pesticide Glyphosate Safe?), Monsanto's scientists countered that these in vitro experiments used physiological irrelevant concentrations, meaning dripping roundup on cells in a petri dish at levels far above what would be realistically found in the human body.

Sure, it's probably not a good idea to mix up your alcohol with your roundup and chug the stuff, or try to commit suicide by drinking or injecting it. And there are rare cases of Parkinson's reported after getting directly sprayed with it, or working for years in a pesticide production plant, but that's not your typical consumer exposure.

As shown in my video GMO Soy and Breast Cancer, some of the researchers responded to the accusation claiming they used the kinds of concentrations that are used out in the fields. Therefore every little droplet we spray worldwide is above the threshold concentration they found to cause adverse effects. Monsanto's folks responded saying, "Yes, that's the concentration we spray, but that's not the concentration that human cells are bathing in. Once it gets into drinking water or food, it's highly diluted." And, they're quick to point out, if we look at people with the greatest exposure--pesticide workers--the vast majority of studies show no link between the use of Roundup and cancer or non-cancer diseases. There are a few suggestive findings suggesting a link with non-Hodgkin's lymphoma. One study of pesticide applicators suggested an association with multiple myeloma, and one study of the children of pesticide applicators found a tentative association with ADHD, but again these are folks experiencing a much greater exposure level than the general population that may just get a few parts per million in their food. But there had never been any studies done on the tiny levels found circulating in people's bodies, until now.

In a study out of Thailand, the maximum residue levels were set at parts per million (the concentrations found within human bodies is measured in parts per billion). The study found glyphosate can activate estrogen receptors at a few parts per trillion, increasing the growth of estrogen receptor positive human breast cancer cells in a petri dish. These results indicate "that truly relevant concentrations of the pesticide found on GMO soybeans possesses estrogenic activity."

But consumption of soy is associated with lower breast cancer risk (See BRCA Breast Cancer Genes and Soy), and improved breast cancer survival (See Breast Cancer Survival and Soy).

That may be because most GMO soy in the U.S. is fed to chickens, pigs, and cows as livestock feed, whereas most of the major soy food manufacturers use non-GMO soy. Or it could be because the benefits of eating any kind of soy may far outweigh the risks, but why accept any risk at all when we can choose organic soy products, which by law exclude GMOs.

The bottom-line is that there is no direct human data suggesting harm from eating GMOs, though in fairness such studies haven't been done, which is exactly the point that critics counter. This is why we need mandatory labeling on GMO products so that public health researchers can track whether GMOs are having any adverse effects.

It is important to put the GMO issue in perspective though. As I've shown (See Lifestyle Medicine: Treating the Causes of Disease), there are dietary and lifestyle changes we can make that could eliminate most heart disease, strokes, diabetes, and cancer. Millions of lives could be saved. A healthy enough diet can even reverse our number one killer, heart disease. So, I'm sympathetic to the biotech industry's exasperation about GMO concerns when we still have people dropping dead from everything else they're eating. As one review concluded "consumption of genetically modified food entails risk of undesirable effects... similar to the consumption of traditional food." In other words, buying the non-GMO Twinkie isn't doing our body much of a favor.

For more on the public health implications of genetically engineered crops in our food supply, check out the these 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 Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image: Nesbitt_Photo / Flickr

Original Link

Preventing Breast Cancer with Flax Seeds

NF-May24 Can Flax Seeds Help Prevent Breast Cancer?.jpeg

I've previously discussed the role of dietary lignans in the reduction of breast cancer risk and improvement in breast cancer survival, based on studies that showed that women with breast cancer who ate the most lignans appeared to live longer (Flaxseeds & Breast Cancer Survival: Epidemiological Evidence and Flaxseeds & Breast Cancer Survival: Clinical Evidence). However, lignans are found throughout the plant kingdom--in seeds, whole grains, vegetables, fruits, berries--so how do we know lignans aren't merely a marker for the intake of unrefined plant foods? For example, those who eat lots of plants--vegetarians--have about eight times the lignan intake than omnivores.

In a petri dish, lignans have been shown to both have direct anticancer growth activity against human breast cancer cells and to prevent cancer cell migration. But it wasn't until 2005 that it was put to the test in people. Researchers from the University of Toronto conducted a randomized double-blind placebo-controlled clinical trial (as seen in my video, Can Flax Seeds Help Prevent Breast Cancer?) of flaxseeds, the world's most concentrated source of lignans in breast cancer patients. The researchers found that flax appears to have the potential to reduce human breast tumor growth in just a matter of weeks. Therefore, I started recommending ground flax seeds to breast cancer patients.

Can lignans also help prevent breast cancer in the first place? High lignan intake is associated with reduced breast cancer risk, but again lignan intake may just be saying an indicator of high plant food intake in general. So researchers from the University of Kansas gave women at high risk for breast cancer a teaspoon of ground flaxseeds a day for a year, and found on average a drop in precancerous changes in the breast.

What about women who regularly eat flax seeds? Outside of an experimental setting, there just weren't a lot of women eating flax seeds regularly to study--until now. Matching 3,000 women with breast cancer to 3,000 women without, a study published in Cancer Causes and Control found that consumption of flaxseed (and of flax bread) was associated with a 20-30 percent reduction in breast cancer risk. The researchers note that, as flaxseeds are packed with lignans, only a small daily serving of flaxseed is required to attain the level of lignan intake associated with a reduction in breast cancer risk. Researchers concluded: "As it appears that most women do not consume flaxseed and that small amounts may be associated with reduced breast cancer risk, interventions to increase the prevalence of flaxseed consumption might be considered."

The latest review summarizes the association between flax and decreased risk of breast cancer, better mental health, and lower mortality among breast cancer patients. The only other study of flax and brain health I'm aware of was an exploration of 100 commonly used drugs and supplements on cognition in older adults, which found that flax is one of the few things that appears to help.

How else may flaxseeds aid in preventing and treating breast cancer? There's an inflammatory molecule called interleukin-1, which may help tumors feed, grow, and invade. Our bodies therefore produce an interkeukin-1 receptor antagonist, binding to the IL-1 receptor and blocking the action of IL-1. The activity of this protective inhibitor can be boosted with the drug tamoxifen--or by eating flax seed. In premenopausal women, the proinflammatory profile of interleukin-1 can be counteracted by a dietary addition of a few spoonfuls of ground flax. One month of flax may be able to increase the anti-inflammatory inhibitor levels by over 50 percent, better even than the drug.

Yes, having one's ovaries removed may reduce breast cancer risk as much as 60 percent, but at the cost of severe side-effects. The drug tamoxifen may reduce the incidence of breast cancer by more than 40 percent, but may induce other severe side effects such as uterine cancer and blood clots. That's why less toxic (even safe!) breast cancer preventive strategies such as dietary modifications need to be developed. These lignan phytoestrogens in flaxseeds may be one successful route given the data showing reduced breast cancer risk and improved overall survival.

Lignans are not a magic bullet to prevent breast cancer--we can't just sprinkle some flax on your bacon cheeseburger--but as a part of a healthy diet and life-style, they might help to reduce breast cancer risk in the general population.

Flaxseeds may also help fight hormone-mediated cancers in men. See Flaxseed vs. Prostate Cancer and Was It the Flaxseed, Fat Restriction, or Both?

What else can these puppies do? See:

I have another 100+ videos on breast cancer if you want to become an expert and help take care of yourself and/or the women in your life. Here's a few recent ones to get you started:

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: Alisha Vargas / Flickr

Original Link

When Charities Collaborate With the Food Industry

NF-Mar29 Collaboration with the New Vectors of Disease.jpeg

When the history of the world's attempt to address obesity is written, one researcher writes, "the greatest failure may be collaboration with and appeasement of the food industry." For instance, Yum! Brands, who owns Kentucky Fried Chicken, linked up with a leading U.S. breast cancer charity, to sell pink buckets of fried chicken.

Save the Children, an organization aiming to positively change the lives of children, was initially a staunch supporter of soda taxes. Recently, however, the organization withdrew its support, saying that support of the soda taxes did not fit the way Save the Children works. Perhaps it is only a coincidence that it was seeking a grant from Coca-Cola and had accepted a $5 million grant from Pepsi.

Through these partnerships, the food industry seeks to emphasize that inactivity -- not the promotion and consumption of its calorie-rich products -- is the prime cause of obesity. But studies showing that obesity is rising even in areas where people are exercising more are most likely explained by the fact that the rate of physical activity levels are being outstripped by our eating activity levels. We can outrun our mouths.

As stated by researcher, Bruce Neal, from the University of Sydney (highlighted in my video, Collaboration with the New Vectors of Disease), "The message is plain - the primary driver of the obesity epidemic in the United States is now the food supply, and interventions targeting physical activity are not going to resolve it. So, while physical activity is good regardless, it will not address most of the burden of ill health caused by obesity. That is going to require a new focus on the root cause of the problem--the American diet."

This researcher adds, "At the heart of the 'energy in' side of the obesity problem is the food and beverage industry. Put simply, the enormous commercial success enjoyed by the food industry is now causing what promises to be one of the greatest public health disasters of our time. As fast as we rid the world of the microbial causes of pestilence and famine, they are replaced by new vectors of disease in the form of trans-national food corporations that market salt, fat, sugar, and calories in unprecedented quantities. So policy makers should work on pricing strategies that subsidize the cost of healthier foods."

First, we need to shift relative prices to make it more expensive to consume animal products compared to fruit, vegetables and beans. Second, we need to increase demand for plant foods, which is not as easy given the hundreds of billions of dollars in annual subsidies - our tax payer dollars going to make animal products artificially cheap.

Dr. Bruce Neal then concludes, "The food industry will rail against the 'nanny state' and fight tooth and nail for its right to market a range of options to responsible individuals able to make choices for themselves-it's the American way. For context though, these arguments are no different to those used by the tobacco industry, which also markets habituating unhealthy products in pursuit of profit. In the case of tobacco, the American people have agreed that controls must be applied to limit the harms caused. Poor diet is now responsible for an even greater burden of disease than tobacco, and food companies must be controlled in the same way if the harms are to be reduced. As unpalatable as this may be, the food industry would do well to strengthen their public health conscience, given that consumers are always going to need their goods, something that cannot be said for the tobacco industry." You hear that a lot in public health circles, how we have to work with the companies, because unlike tobacco, we have to eat. But just like yes, we need to breath, but we don't need to breathe smoke, yes we need to eat, but we don't need to eat junk.

Is it our physical activity or eating activity? See Diet vs. Exercise for Weight Loss and How Much Exercise to Sustain Weight Loss?

I touched on the pink buckets of KFC in my video Breast Cancer Survival, Butterfat, and Chicken.

For more on the idea of subsidizing healthy foods or at least stopping tax money to supporting junk, check out my video Taxpayer Subsidies for Unhealthy Foods.

It's sad when non-profits collaborate with companies that contribute to suffering, but seems particularly egregious when the Registered Dietitian group does it. See Academy of Nutrition and Dietetics Conflicts of Interest.

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, and From Table to Able.

Image Credit: Rafael Edwards / Flickr

Original Link

How to Cook Broccoli

NF-Feb9 Second Strategy to Cooking Broccoli.jpeg

When I used to teach medical students at Tufts, I gave a lecture about this amazing new therapeutic called "iloccor-B." I'd talk about all the new science, all the things it could do, its excellent safety profile. Just as they were all scrambling to buy stock in the company and prescribe it to all their patients, I'd do the big reveal. Apologizing for my "dyslexia," I would admit that I'd got it backwards. All this time I had been talking about broccoli.

The main active ingredient in broccoli is thought to be sulforaphane, which may protect our brains, protect our eyesight, protect our bodies against free radicals, boost our detoxification enzymes, and help prevent and treat cancer.

In my videos The Best Detox and Sometimes the Enzyme Myth is the Truth, I talked about how the formation of sulforaphane is like a chemical flare reaction, requiring the mixing of a precursor compound with an enzyme, which is destroyed by cooking. This may explain why we get dramatic suppression of cancer cell growth from raw broccoli, cauliflower and Brussels sprouts, but hardly anything from boiled, microwaved or steamed (except for microwaved broccoli, which actually retains some cancer fighting abilities). But who wants to eat raw Brussels sprouts?

There is a strategy to get the benefits of raw in cooked form. In raw broccoli, the sulforaphane precursor, called glucoraphanin, mixes with the enzyme (myrosinase) when you chew or chop it. If given enough time--such as when sitting in your upper stomach waiting to get digested--sulforaphane is born. The precursor and sulforaphane are resistant to heat and therefore cooking, but the enzyme is destroyed. No enzyme = no sulforaphane.

That's why I described the "hack and hold" technique--if we chop the broccoli, Brussels sprouts, kale, collards, or cauliflower first and then wait 40 minutes, we can cook them all we want. The sulforaphane is already made; the enzyme has already done its job, so we don't need it anymore.

When most people make broccoli soup, for example, they're doing it wrong. Most people cook the broccoli first, then blend it. We now know it should be done the exact opposite way. Blend it first, wait, and then cook it.

What if we're using frozen broccoli, though? In my video, Second Strategy to Cooking Broccoli, you can see the amount of sulforaphane in someone's body after they eat broccoli soup made from fresh broccoli versus from frozen broccoli. The difference is dramatic. Commercially produced frozen broccoli lacks the ability to form sulforaphane because vegetables are blanched (flash-cooked) before they're frozen for the very purpose of deactivating enzymes. This prolongs shelf life in the frozen foods section, but the myrosinase is dead by the time you take it out of your freezer. It doesn't matter how much you chop it, or how long you wait, no sulforaphane is going to be made. This may be why fresh kale suppresses cancer cell growth up to ten times more than frozen.

The frozen broccoli is still packed with the precursor--remember that's heat resistant--and we could get lots of sulforaphane out of the frozen broccoli by adding some outside enzyme. Where do we get myrosinase enzyme from? Researchers just buy theirs from a chemical company. But we can just walk into any grocery store.

All cruciferous vegetables have this myrosinase. Mustard greens, a cruciferous vegetable, grow out of little mustard seeds, which we can buy ground up in the spice aisle as mustard powder. If we sprinkled some mustard powder on our cooked frozen broccoli, would it start churning out sulforaphane? We didn't know...until now.

Boiling broccoli prevents the formation of any significant levels of sulforaphane due to inactivation of the enzyme. However, researchers from the University of Reading found that the addition of powdered mustard seeds to the heat processed broccoli significantly increased the formation of sulforaphane. In the video I mentioned earlier, Second Strategy to Cooking Broccoli, you can see the amount of sulforaphane in boiled broccoli versus the amount after half a teaspoon or a teaspoon of mustard powder is added. Both a half teaspoon and a full teaspoon increase sulforaphane by the same amount, suggesting that we could use even use less mustard powder for the same effect. Therefore, although domestic cooking leads to the deactivation of myrosinase and stops sulforaphane formation, the addition of powdered mustard seeds to cooked cabbage-family vegetables provides a natural source of the enzyme such that it's practically like eating them raw.

So, if we forget to chop our greens in the morning for the day, or are using frozen, we can just sprinkle some mustard powder on top at the dinner table and we're all set. Daikon radish, horseradish, or wasabi--all cruciferous vegetables packed with the enzyme--work as well. Just a quarter teaspoon of Daikon radish root for seven cups of broccoli worked--just a tiny pinch can do it. Or you can add a small amount of fresh greens to your cooked greens, because the fresh greens have myrosinase enzyme that can go to work on the cooked greens.

I love kitchen chemistry--it totally revolutionized my daily greens prep. One of the first things I used to do in the morning is chop my greens for the day, so when lunch and supper rolls around they'd be good to go. But now with the mustard powder plan, I don't have to pre-chop.

This helps explain the results I presented in Raw Broccoli and Bladder Cancer Survival.

OK, but what's so great about this sulforaphane stuff? For a taste, see:

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: Jessica Spengler / Flickr

Original Link

Bile Acids and Breast Cancer

NF-Jan19 Breast Cancer and Constipation.jpg

Why do constipated women appear to be at higher risk for breast cancer? The results of a 1989 study out of the American Journal of Public Health suggested a slight increased risk of breast cancer for both decreased frequency of bowel movements and firm stool consistency. Women who had three or more bowel movements a day appeared to cut their risk of breast cancer in half. This could be because constipation means a greater contact time between our waste and our intestinal wall, which may increase the formation and absorption of fecal mutagens--substances that cause DNA mutations and cancer--into our circulation, eventually ending up in breast tissue.

The concept that more frequent bowl movements decrease breast cancer risk dates back more than a century, where severe constipation, so-called "chronic intestinal stasis," was sometimes dealt with surgically. Figuring that the colon was an inessential part of the human anatomy, why not cure constipation by just cutting it out? After the surgery, they noticed that potentially precancerous changes in the breasts of constipated women seemed to disappear.

It would take another 70 years before researchers followed up on the clues by those distinguished surgeons who claimed breast pathology cleared when constipation was corrected. A 1981 study published in The Lancet investigated the relation between potentially precancerous changes in the breast and the frequency of bowl movements in nearly 1,500 women (See Breast Cancer and Constipation). The researchers found that the risk of precancerous changes was four times greater in women reporting two or fewer bowel movements a week compared to more than once daily.

We know that even the non-lactating breast actively takes up chemical substances from the blood. We also know that there are mutagens in feces. It is not unreasonable to suggest that potentially toxic substances derived from the colon have damaging or even carcinogenic effects upon the lining of the breast. Toxic substances like bile acids. Bile acids were first shown to promote tumors in mice in 1940, but subsequent experiments on rats led to the mistaken belief that bile acids just promoted existing cancers and couldn't initiate tumors themselves. However, there is a fundamental difference between the rodent models and human cancer. Rats only live a few years while humans can live dozens, so the opportunity for cancer causing mutations may be at least 30 times greater in humans. We now have at least 15 studies that show that bile acids can damage DNA, strongly suggesting they can initiate new cancers as well.

Bile acids are formed as a way of getting rid of excess cholesterol. Our liver dumps bile acids into the intestine for disposal, assuming our intestines will be packed with fiber to trap it and flush it out of the body. But if we haven't been eating enough fiber-rich whole plant foods, bile acids can be reabsorbed back into the body and build up in the breast.

Carcinogenic bile acids are found concentrated in the fluid of breast cysts at up to a hundred times the level found in the bloodstream. By radioactively tagging bile acids, researchers were able to show that intestinal bile acids rapidly gain access to the breast, where they can exert an estrogen-like cancer-promoting effect on breast tumor cells. This would explain why we see 50% higher bile acid levels in the bloodstream of newly diagnosed breast cancer victims. These findings support the concept of a relationship between intestinally-derived bile acids and risk of breast cancer. So how can we facilitate the removal of bile acids from our body?

Slowed colonic transit can increase bile acid levels. Therefore, to decrease absorption of bile acids, we can speed up the so-called "oro-anal transit time," the speed at which food goes from mouth to toilet, by eating lots of fiber. A diet packed with plants greatly increases bile acid excretion.

Fiber can bind up and remove other toxic elements like lead and mercury as well as cholesterol and bile acids. But plants can bind bile acids even independent of fiber. Vegan diets bind significantly more bile acid than lacto-ovo or non-vegetarian diets even at the same fiber intake, which could explain why individuals eating vegetarian might excrete less mutagenic feces in the first place.

I touched on this in my live presentation From Table to Able: Combating Disabling Diseases with Food, but what I didn't get to discuss is the relative bile acid binding abilities of different foods. I cover that in my video Which Vegetable Binds Bile Best?

What intestinal transit time should we be shooting for? See Food Mass Transit. That may be why Stool Size Matters. Also, How Many Bowel Movements Should You Have Every Day? We can improve speed and size by Bulking Up on Antioxidants and eating lots of whole plant foods (Prunes vs. Metamucil vs. Vegan Diet).

Fiber may also help women remove excess estrogen from their body. See my video Fiber vs. Breast Cancer. For more on the wonders of fiber, see Dr. Burkitt's F-Word Diet.

For more of my latest videos on breast cancer prevention and survival, see:

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, and Food as Medicine.

Image Credit: Photocapy / Flickr

Original Link

How a Tick Bite Can Lead to Food Allergies

NF-Aug25 Alpha Gal and the Lone Star Tick.jpg

In the beginning, Aristotle defined two forms of life on planet Earth: plants and animals. Two thousand years later, the light microscope was invented and we discovered tiny, single-celled organisms like amoebas. Then, the electron microscope was invented and we discovered bacteria. Finally, in 1969, biologists recognized fungi as a separate category, and we've had at least five kingdoms of life ever since.

In my video, Higher Quality May Mean Higher Risk, I talk about the potential downsides of consuming proteins from within our own kingdom, such as the impact our fellow animal proteins can have on boosting our liver's production of a cancer-promoting hormone called IGF-1.

In Eating Outside Our Kingdom, I talked about other potential advantages of preferably dipping into the plant and mushroom kingdoms for dinner, not only from a food safety perspective (we're more likely to get infected by animal pathogens than Dutch Elm Disease), but because of the potential for cross-reactivity between animal and human proteins. Our immune system is more likely to get confused between a chicken leg and our own legs than it is with a banana, so there may be less potential to trigger an autoimmune reaction, like degenerative brain diseases or inflammatory arthritis (See Diet & Rheumatoid Arthritis). In attacking some foreign animal meat protein, some of our own similarly composed tissues may get caught in the crossfire.

It's not just proteins. If you remember the Neu5Gc story (see Inflammatory Meat Molecule Neu5GC), sialic acid in other animals may cause inflammation in our arteries (see Nonhuman Molecules Lining Our Arteries) and help breast tumors and other human cancers to grow (see How Tumors Use Meat to Grow: Xeno-Autoantibodies). Now a new twist has been added to the story.

The reason Neu5Gc triggers inflammation is because humans lost the ability to make it two million years ago, and so when our body is exposed to it through animal products, it's treated as a foreign molecule, causing inflammation. But there's also another oligosaccharide called alpha-gal that humans, chimps, and apes lost the ability to make 20 million years ago, but is still made by a variety of animals, including many animals we eat.

Anti-gal antibodies may be involved in a number of detrimental processes that may result in allergic, autoimmune, and autoimmune-like diseases, such as auto-immune thyroid disorders. We see higher levels of anti-gal antibodies in Crohn's disease victims. These antibodies even react against about half of human breast tumors, and we can find them in atherosclerotic plaques in people's necks. However, those are all mostly speculative risks. We do know that alpha-gal is a major obstacle to transplanting pig organs into people, like kidneys, because our bodies reject alpha-gal as foreign. In fact, alpha-gal is thought to be the major target for human anti-pig antibodies.

It's interesting that if we look at those that abstain from pork for whatever reason, they have fewer swine-specific immune cells in their bloodstream. Researchers speculate that oral intake of pork could ferry swine molecules into the bloodstream via gut-infiltrating lymphocytes to prime the immune response. So we can have an allergic reaction to eating pig kidneys too, but such severe meat allergies were considered rare, until an unusual report surfaced. First described in 2009, the report included details on 24 cases of meat allergies triggered by tick bites.

Within a year, it was obvious that the cases should be counted in hundreds rather than dozens. By 2012, there were thousands of cases across a large area of the southern and eastern U.S., and new cases are now popping up in several countries around the world.

The culprit, the lone star tick, so-called because females have a white spot on their back, are famous for causing Masters' disease, a disease similar to Lyme syndrome, also known as STARI (southern tick associated rash illness). But thanks to the lone star tick steadily expanding its range (even as far as Long Island, NY), it's not necessarily just so Southern any more.

What is the relevance of tick bites to the production of allergy-causing anti-meat antibodies to alpha-gal? Good question. What we know is that if you get bitten by one of these ticks, you can develop an allergy to meat (See Alpha Gal and the Lone Star Tick). This appears to be the first example of a response to an external parasite giving rise to an important form of food allergy. We don't know the exact mechanism, but it may be because there's something in the tick saliva that's cross-reacting with alpha-gal, or because the tick is injecting you with animal allergens from its last meal.

What role may these tick-bite induced allergies play in the development of chronic hives and other allergic skin reactions in children? See Tick Bites, Meat Allergies, and Chronic Urticaria.

Here's some videos unearthing the IGF-1 story:

Neu5Gc is what opened up this whole can of worms:

I wonder if alpha gal is playing a role in the improvements in arthritis and Crohn's on plant-based diets: Dietary Treatment of Crohn's Disease and Diet & Rheumatoid Arthritis.

In health,
Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my videos for free by clicking here and watch my full 2012 - 2015 presentations Uprooting the Leading Causes of Death, More than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: USGS Bee Inventory and Monitoring Lab / Flickr

Original Link

Breast Cancer Cells Feed on Cholesterol

NF-Jul14 Cholesterol Feeds Breast Cancer Cells.jpg

One in eight American women will be diagnosed with breast cancer in her lifetime. There are a number of compounds in plant foods that may protect against breast cancer by a variety of mechanisms. I've talked about the benefits of broccoli, flaxseeds, and soy foods before (See Breast Cancer Survival Vegetable, Flaxseeds & Breast Cancer Prevention, and Breast Cancer Survival and Soy) but a recent German study reported something new. The researchers found that sunflower and pumpkin seeds were associated with reduced breast cancer risk. They initially chalked the association up to the lignans in the seeds (See Breast Cancer Survival and Lignan Intake), but their lignan lead didn't pan out. Maybe it's the phytosterols found concentrated in seeds? (See Optimal Phytosterol Source).

There is evidence that phytosterols may be anticancer nutrients and play a role in reducing breast cancer risk. I thought phytosterols just lowered cholesterol? (See How Phytosterols Lower Cholesterol) What does cancer have to do with cholesterol?

Increasing evidence demonstrates the role that cholesterol may play in the development and progression of breast cancer. Cancer feeds on cholesterol. Transformed cells take up LDL, so-called "bad" cholesterol, and it's capable of stimulating the growth of human breast cancer cells in a petri dish.

The ability to accumulate fat and cholesterol may enable cancer cells to take advantage of people eating high fat and high cholesterol diets and at least partially explain the benefit of a low-fat diet on lowering human breast cancer recurrence. Although the data has been mixed, the largest study to date (highlighted in my video, Cholesterol Feeds Breast Cancer Cells) found a 17% increased breast cancer risk in women who had a total cholesterol over 240 compared to women whose cholesterol was under 160. However, the researchers could not rule out that there may be something else in cholesterol-raising foods that's increasing breast cancer risk.

Tumors suck up so much cholesterol that LDL has been considered a vehicle for delivering antitumor drugs to cancer cells. Since cancer feeds on cholesterol, maybe we could stuff some chemo into it like a Trojan horse poison pill?

The uptake of LDL into tumors may be why people's cholesterol levels drop low after they get cancer--the tumor is eating it up. In fact, patient survival may be lowest when cholesterol uptake is highest. "High LDL receptor content in breast cancer tissue seems to indicate a poor prognosis, [suggesting] that breast tumors rich in LDL receptors may grow rapidly [in the body]." We've known about this for decades. You can tell that wass an old study because, when it was published in the '80s, only 1 in 11 American women got breast cancer.

If cholesterol increases breast cancer risk, what about the use of cholesterol-lowering drugs? See Statin Cholesterol Drugs and Invasive Breast Cancer.

More videos on broccoli and soy's protective effects against breast cancer:

Some I didn't mention 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: Andrew Bennett / Flickr

Original Link

Phytates in Beans: Anti-Nutrient or Anti-Cancer?

NF-May28 Phytates for the Treatment of Cancer.jpg

In my videos, Phytates in the Prevention of Cancer and Phytates for Rehabilitating Cancer Cells, I described how phytates in beans may be the reason why legumes are so successful in preventing cancer and re-educating cancer cells. What about phytates for the treatment of cancer?

Colorectal cancer is the second leading cause of cancer death in the United States. It arises from "adenomatous polyps," meaning that colon cancer starts out as a benign little bump called a polyp and then grows into cancer that can eventually spread to other organs and kill. So the National Cancer Institute funded the Polyp Prevention Trial, highlighted in my video, Phytates for the Treatment of Cancer, to determine the effects of a high-fiber, high fruit and vegetable, low-fat diet.

Researchers found no significant associations between polyp formation and overall change in fruit and vegetable consumption. However, those with the greatest increase in bean intake only had about a third of the odds of advanced polyps popping up. It could have been the fiber in the beans, but there's lots of fiber in fruits and vegetables, too. So it may have been the phytate.

If the tumors develop from polyps, they still need to spread. Tumor growth, invasion, and metastasis are multistep processes that include cell proliferation, digestion through the surrounding tissue, and migration through barrier membranes to reach the bloodstream so the tumor can establish new proliferating colonies of cancer cells. A critical event in tumor cell invasion is the first step: the tunneling through the surrounding matrix. To do this, the cancer cells use a set of enzymes called matrix metalloproteinases. This is where phytates might come in. We've known that phytates inhibit cancer cell migration in vitro, and now perhaps we know why. Phytates help block the ability of cancer cells to produce the tumor invasion enzyme in the first place (at least for human colon and breast cancer cells).

So what happens if you give phytates to breast cancer patients? Although a few case studies where phytates were given in combination with chemotherapy clearly showed encouraging data, organized, controlled, randomized clinical studies were never done--until now. Fourteen women with invasive breast cancer were divided randomly into two groups. One group got extra phytates; the other got placebo. At the end of six months, the phytate group had a better quality of life, significantly more functionality, fewer symptoms from the chemo, and did not get the drop in immune cells and platelets chemo patients normally experience.

What are the potential side effects of phytates? Less heart disease, less diabetes, and fewer kidney stones.

Because cancer development is such an extended process--it can take decades to grow--we need cancer preventive agents that we can take long-term. Phytates, which naturally occur in beans, grains, nuts, and seeds, seem to fit the bill.

In the past, there were concerns that the intake of foods high in phytates might reduce the bioavailability of dietary minerals, but recent studies demonstrate that this co-called "anti-nutrient" effect can be manifested only when large quantities of phytates are consumed in combination with a nutrient poor diet. For example, there used to be a concern that phytate consumption might lead to calcium deficiency, which then led to weakened bones, but researchers discovered that the opposite was true, that phytates actually protect against osteoporosis (See Phytates for the Prevention of Osteoporosis). In essence, phytates have many characteristics of a vitamin, contrary to the established and, unfortunately, still existing dogma among nutritionists regarding its 'anti-nutrient' role.

As one paper in the International Journal of Food Science & Technology suggests:

"Given the numerous health benefits, phytates participation in important intracellular biochemical pathways, normal physiological presence in our cells, tissues, plasma, urine, etc., the levels of which fluctuate with intake, epidemiological correlates of phytate deficiency with disease and reversal of those conditions by adequate intake, and safety - all strongly suggest for phytates inclusion as an essential nutrient, perhaps a vitamin."

The paper concludes that inclusion of phytates in our diet for prevention and therapy of various ailments, cancer in particular, is warranted.

More on preventing tumor invasion and metastasis in:

Other foods that can help stop the progression of precancerous lesions (like the adenomatous polyps) are profiled in Strawberries versus Esophageal Cancer and Black Raspberries versus Oral Cancer.

There's a substance in mushrooms that's also another "essential" nutrient candidate. See Ergothioneine: A New Vitamin?

-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: The Ewan / Flickr

Original Link