White Meat May Be as Cholesterol-Raising as Red

White Meat May Be as Cholesterol-Raising as Red.jpeg

In light of recommendations for heart healthy eating from national professional organizations encouraging Americans to limit their intake of meat, the beef industry commissioned and co-wrote a review of randomized controlled trials comparing the effects of beef versus chicken and fish on cholesterol levels published over the last 60 years. They found that the impact of beef consumption on the cholesterol profile of humans is similar to that of fish and/or poultry--meaning that switching from red meat to white meat likely wouldn't make any difference. And that's really no surprise, given how fat we've genetically manipulated chickens to be these days, up to ten times more fat than they had a century ago (see Does Eating Obesity Cause Obesity?).

There are a number of cuts of beef that have less cholesterol-raising saturated fat than chicken (see BOLD Indeed: Beef Lowers Cholesterol?), so it's not so surprising that white meat was found to be no better than red, but the beef industry researchers conclusion was that "therefore you can eat beef as part of a balanced diet to manage your cholesterol."

Think of the Coke versus Pepsi analogy. Coke has less sugar than Pepsi: 15 spoonfuls of sugar per bottle instead of 16. If studies on blood sugar found no difference between drinking Coke versus Pepsi, you wouldn't conclude that "Pepsi may be considered when recommending diets for the management of blood sugars," you'd say they're both equally as bad so we should ideally consume neither.

That's a standard drug industry trick. You don't compare your fancy new drug to the best out there, but to some miserable drug to make yours look better. Note they didn't compare beef to plant proteins, like in this study published in the American Journal of Clinical Nutrition. As I started reading it, though, I was surprised that they found no benefit of switching to a plant protein diet either. What were they eating? You can see the comparison in Switching from Beef to Chicken & Fish May Not Lower Cholesterol.

For breakfast, the plant group got a kidney bean and tomato casserole and a salad, instead of a burger. And for dinner, instead of another burger, the plant protein group just got some boring vegetables. So why was the cholesterol of the plant group as bad as the animal group? They had the plant protein group eating three tablespoons of beef tallow every day--three tablespoons of straight beef fat!

This was part of a series of studies that tried to figure out what was so cholesterol-raising about meat--was it the animal protein or was it the animal fat? So, researchers created fake meat products made to have the same amount of saturated fat and cholesterol by adding extracted animal fats and cholesterol. Who could they get to make such strange concoctions? The Ralston Purina dog food company.

But what's crazy is that even when keeping the saturated animal fat and cholesterol the same (by adding meat fats to the veggie burgers and making the plant group swallow cholesterol pills to equal it out), sometimes they still saw a cholesterol lowering advantage in the plant protein group.

If you switch people from meat to tofu, their cholesterol goes down, but what if you switch them from meat to tofu plus lard? Then their cholesterol may stay the same, though tofu and lard may indeed actually be better than meat, since it may result in less oxidized cholesterol. More on the role of oxidized cholesterol can be found in my videos Does Cholesterol Size Matter? and Arterial Acne.

Just swapping plant protein for animal protein may have advantages, but if you really want to maximize the power of diet to lower cholesterol, you may have to move entirely toward plants. The standard dietary advice to cut down on fatty meat, dairy, and eggs may lower cholesterol 5-10%, but flexitarian or vegetarian diets may drop our levels 10 to 15%, vegan diets 15 to 25%, and healthier vegan diets can cut up to 35%, as seen in this study out of Canada showing a whopping 61 point drop in LDL cholesterol within a matter of weeks.


You thought chicken was a low-fat food? It used to be a century ago, but not anymore. It may even be one of the reasons we're getting fatter as well: Chicken Big: Poultry and Obesity and Infectobesity: Adenovirus 36 and Childhood Obesity.

Isn't protein just protein? How does our body know if it's coming from a plant or an animal? How could it have different effects on cardiovascular risk? See Protein and Heart Disease, another reason why Plant Protein [is] Preferable.

Lowering cholesterol in your blood is as simple as reducing one's intake of three things: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

What about those news stories on the "vindication" of saturated fat? See the sneaky science in The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

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: CDC/Debora Cartagena via Freestockphotos.biz. This image has been modified.

Original Link

White Meat May Be as Cholesterol-Raising as Red

White Meat May Be as Cholesterol-Raising as Red.jpeg

In light of recommendations for heart healthy eating from national professional organizations encouraging Americans to limit their intake of meat, the beef industry commissioned and co-wrote a review of randomized controlled trials comparing the effects of beef versus chicken and fish on cholesterol levels published over the last 60 years. They found that the impact of beef consumption on the cholesterol profile of humans is similar to that of fish and/or poultry--meaning that switching from red meat to white meat likely wouldn't make any difference. And that's really no surprise, given how fat we've genetically manipulated chickens to be these days, up to ten times more fat than they had a century ago (see Does Eating Obesity Cause Obesity?).

There are a number of cuts of beef that have less cholesterol-raising saturated fat than chicken (see BOLD Indeed: Beef Lowers Cholesterol?), so it's not so surprising that white meat was found to be no better than red, but the beef industry researchers conclusion was that "therefore you can eat beef as part of a balanced diet to manage your cholesterol."

Think of the Coke versus Pepsi analogy. Coke has less sugar than Pepsi: 15 spoonfuls of sugar per bottle instead of 16. If studies on blood sugar found no difference between drinking Coke versus Pepsi, you wouldn't conclude that "Pepsi may be considered when recommending diets for the management of blood sugars," you'd say they're both equally as bad so we should ideally consume neither.

That's a standard drug industry trick. You don't compare your fancy new drug to the best out there, but to some miserable drug to make yours look better. Note they didn't compare beef to plant proteins, like in this study published in the American Journal of Clinical Nutrition. As I started reading it, though, I was surprised that they found no benefit of switching to a plant protein diet either. What were they eating? You can see the comparison in Switching from Beef to Chicken & Fish May Not Lower Cholesterol.

For breakfast, the plant group got a kidney bean and tomato casserole and a salad, instead of a burger. And for dinner, instead of another burger, the plant protein group just got some boring vegetables. So why was the cholesterol of the plant group as bad as the animal group? They had the plant protein group eating three tablespoons of beef tallow every day--three tablespoons of straight beef fat!

This was part of a series of studies that tried to figure out what was so cholesterol-raising about meat--was it the animal protein or was it the animal fat? So, researchers created fake meat products made to have the same amount of saturated fat and cholesterol by adding extracted animal fats and cholesterol. Who could they get to make such strange concoctions? The Ralston Purina dog food company.

But what's crazy is that even when keeping the saturated animal fat and cholesterol the same (by adding meat fats to the veggie burgers and making the plant group swallow cholesterol pills to equal it out), sometimes they still saw a cholesterol lowering advantage in the plant protein group.

If you switch people from meat to tofu, their cholesterol goes down, but what if you switch them from meat to tofu plus lard? Then their cholesterol may stay the same, though tofu and lard may indeed actually be better than meat, since it may result in less oxidized cholesterol. More on the role of oxidized cholesterol can be found in my videos Does Cholesterol Size Matter? and Arterial Acne.

Just swapping plant protein for animal protein may have advantages, but if you really want to maximize the power of diet to lower cholesterol, you may have to move entirely toward plants. The standard dietary advice to cut down on fatty meat, dairy, and eggs may lower cholesterol 5-10%, but flexitarian or vegetarian diets may drop our levels 10 to 15%, vegan diets 15 to 25%, and healthier vegan diets can cut up to 35%, as seen in this study out of Canada showing a whopping 61 point drop in LDL cholesterol within a matter of weeks.


You thought chicken was a low-fat food? It used to be a century ago, but not anymore. It may even be one of the reasons we're getting fatter as well: Chicken Big: Poultry and Obesity and Infectobesity: Adenovirus 36 and Childhood Obesity.

Isn't protein just protein? How does our body know if it's coming from a plant or an animal? How could it have different effects on cardiovascular risk? See Protein and Heart Disease, another reason why Plant Protein [is] Preferable.

Lowering cholesterol in your blood is as simple as reducing one's intake of three things: Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero.

What about those news stories on the "vindication" of saturated fat? See the sneaky science in The Saturated Fat Studies: Buttering Up the Public and The Saturated Fat Studies: Set Up to Fail.

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: CDC/Debora Cartagena via Freestockphotos.biz. This image has been modified.

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Virus in Chicken Could Be Linked to Obesity

NF-May31 Infectobesity Adenovirus 36 and Childhood Obesity.jpeg

Recently, there has been research examining the connection between poultry consumption and weight gain. One study out of the Netherlands examining about 4,000 people, correlated chicken consumption with weight gain. Another study followed 89,000 people in four other countries and found that animal protein intake was associated with long-term weight gain, and poultry was the worst, with 40 percent more weight gain than red meat or processed meat.

What makes poultry so bad? Yes, chickens are fatty these days because of the way we've genetically manipulated them--up to ten times more fat and calories than they used to have--but one bizarre theory postulated that it might be due to an obesity-causing chicken virus. In one study, one in five obese humans tested positive to the chicken virus SMAM-1, with those exposed to the chicken virus averaging 33 pounds heavier than those testing negative.

SMAM-1 was the first chicken virus to be associated with human obesity, but not the last. The original obesity-causing chicken virus SMAM-1 was able to effectively transmit obesity from one chicken to another when caged together, similar to a human adenovirus Ad-36, a human obesity-associated virus first associated with obesity in chickens and mice. Ad-36 spreads quickly from one chicken to another via nasal, oral or fecal excretion and contamination, causing obesity in each chicken. This of course raises serious concerns about Ad-36-induced adiposity in humans.

The easiest way to test this hypothesis is to experimentally infect humans with the virus. However, ethical reasons preclude experimental infection of humans, and so the evidence will have to remain indirect. In the absence of direct experimental data, we must rely on population studies, similar to how researchers nailed smoking and lung cancer. About 15 percent of Americans are already infected with Ad-36, so we can follow them and see what happens. That's exactly what a research team out of Taiwan did (highlighted in my video Infectobesity: Adenovirus 36 and Childhood Obesity). They followed 1,400 Hispanic men and women for a decade and found that not only were those exposed to the virus fatter than those who were not, but also over the ten years, those with a history of infection had a greater percentage of body fat over time.

Most studies done to date on adults have found a connection between exposure to Ad-36 and obesity, and all studies done so far on childhood obesity show an increase in prevalence of infection in obese children compared to non-obese children. We're now up to more than a thousand children studied with similar findings. Obese children who tested positive for the virus weighed 35 pounds more than children who tested negative.

The virus appears to both increase the number of fat cells by mobilizing precursor stem cells and increase the accumulation of fat within the cells. If we take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about five times the rate in people who came to the liposuction clinic already infected. Fat taken from non-infected people that was then exposed to the virus start sucking up fat at a faster rate, potentially inducing obesity without increasing food intake.

Just as Ad-36 can be transmitted horizontally from one infected chicken to another in the same cage, subsequently causing obesity in each chicken, this same virus is also easily transmitted among humans, raising the question as to whether at least some cases of childhood obesity can be considered an infectious disease. Researchers publishing in the International Journal of Pediatric Obesity speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.

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: Glasseyes view / Flickr

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Treating Pancreatic Cancer with Turmeric Curcumin

NF-May26 Turmeric Curcumin and Pancreatic Cancer.jpeg

Pancreatic cancer is among the most aggressive forms of human cancer, characterized by a very high mortality rate. It represents the fourth leading cause of cancer death in United States, killing 32,000 people annually. With a five-year survival rate of only three percent and a median survival rate of less than six months, pancreatic cancer carries one of the poorest prognoses. The diagnosis of pancreatic cancer is one of the worst things a doctor ever has to tell a patient. The only FDA-approved therapies for it, Gemcitabine and Erlotinib, produce objective responses in less than ten percent of patients, while causing severe side-effects in the majority. There is a desperate need for new options.

Clinical research to test new treatments is split into phases. Phase I trials are just to make sure the treatment is safe, to see how much you can give before it becomes toxic. Curcumin, the natural yellow pigment in the spice turmeric has passed a number of those. In fact, there was so little toxicity, the dosing appeared limited only by the number of pills patients were willing to swallow.

Phase II trials are conducted to see if the drug actually has an effect. Curcumin did, in 2 of the 21 patients that were evaluated. One patient had a 73 percent tumor reduction, but the effect was short-lived. One lesion remained small, but a curcumin-resistant tumor clone emerged. The other patient, who had a stable disease for over 18 months, showed slow improvement over a year. The only time that patient's cancer markers bumped up was during a brief three-week stint where the curcumin was stopped.

So curcumin does seem to help some patients with pancreatic cancer, and most importantly, there appears to be little downside. No curcumin-related toxic effects were observed in up to doses of eight grams per day. What happens after eight grams? We don't know because no one was willing to take that many pills. The patients were willing to go on one of the nastiest chemotherapy regimens on the planet, but didn't want to be inconvenienced with swallowing a lot of capsules.

The only surefire way to beat pancreatic cancer is to prevent it in the first place. In 2010 I profiled a study conducted by the National Institutes of Health, the largest such study in history, which found that dietary fat of animal origin was associated with increased pancreatic cancer risk.

Which animal fat is the worst? The second largest study (highlighted in my video: Turmeric Curcumin and Pancreatic Cancer) has since chimed in to help answer that question. Researchers found that poultry was the worst, with 72 percent increased risk of pancreatic cancer associated with every 50 grams of daily poultry consumption. Fifty grams is just about a quarter of a chicken breast. The reason white meat came out worse than red may be because of the cooked meat carcinogens in chicken, the heterocyclic amines that build up in grilled and baked chicken. These mutagenic chemicals have been associated with a doubling of pancreatic cancer risk (See Estrogenic Cooked Meat Carcinogens).

Meat has been associated with significantly increased risk, whereas fake meat is associated with significantly less risk. Those who eat plant-based meats like veggie burgers or veggie dogs three or more times a week had less than half the risk of fatal pancreatic cancer. Legumes and dried fruit appear to be similarly protective.

My grandfather died of pancreatic cancer. By the time the first symptom arose, a dull ache in his gut, it was too late. That's why we need to work on preventing it.

I previously touched on pancreatic cancer prevention in Poultry Exposure Tied to Liver and Pancreatic Cancer and attempts at pancreatic cancer treatment in Gerson Therapy for Cancer and Gerson-style Therapy vs. Chemotherapy.

For more on the heterocyclic amine cooked meat carcinogens:

I've done a bunch of videos on turmeric and various cancers:

And more on this amazing spice (and more to come):

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: Sara Marlowe / Flickr

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Might Turmeric Help Prevent Alzheimer’s?

NF-Apr12 Preventing Alzheimer's with Turmeric.jpeg

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

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Hives from Tick Bite-Induced Meat Allergies

NF-Aug27 Tick Bites, Meat Allergies, and Chronic Urticaria.jpg

In a previous video Alpha Gal and the Lone Star Tick, I started talking about a tick bite-induced meat allergy, called Alpha-Gal, that is unlike any other food allergy we know. The most interesting feature of the reactions may be that first symptoms can occur hours after eating meat. Normally, an allergic reaction to a bee sting, for example, happens within minutes. With this meat allergy, we could have a piece of bacon for breakfast and our throat wouldn't start closing off until the afternoon. Because the cause and effect are temporarily separated, we often blame other factors, such as what we ate for lunch, or we just call it "spontaneous" or "idiopathic" anaphylaxis, which is just doctor-speak for "we have no idea what the cause is."

The delay likely occurs because the alpha-gal is probably absorbed along with the fat in meat, given that the allergic reaction occurring four to five hours after meat ingestion corresponds to the peak absorption time of fatty acids from the intestinal tract.

What makes the allergy even more difficult to diagnose is that the majority of victims experience only occasional overt reactions, despite regular meat consumption. Fattier meats, like pork rinds, may provoke episodes more consistently and severely, but still don't trigger a reaction every time.

Tick bite-induced meat allergy is on the rise. Ten years ago we didn't even know this thing existed, but now in tick-ridden states as many as 20% of the population have these anti-meat allergic antibodies (See Tick Bites, Meat Allergies, and Chronic Urticaria). And more and more people are coming in affected, though probably no more than 10% who test positive go on to experience hives or serious allergic reaction to meat.

We're also seeing it more and more in kids. Researchers in Virginia have found that it is not uncommon, though identification of the allergy may not be straightforward. Unlike in adults, who frequently present with systemic reactions, the majority of children with this syndrome present with just skin manifestations, such as hives. However, this doesn't mean it's not serious. In fact, nearly half the kids ended up in the ER, and about 1 in 12 needed to be hospitalized.

Up to a quarter of the population breaks out in hives at some time in their lives, but some children can be affected for weeks or months. It can be triggered by infections, foods, drugs, parasites, or be autoimmune, but in a large subset of cases we don't know what the trigger is, and so, call it chronic "idiopathic" urticaria. It's a common thing pediatricians see. The only cure is avoiding and eliminating whatever is triggering it, but in three quarters of cases we have no clue.

We now know that many children who had been diagnosed with mysterious hives or allergic reactions and may have been specifically told that the reactions were not a result of a food allergy, may have actually been suffering from anti-gal meat allergies. The serious nature of the reactions and the rising frequency of allergic swelling and hives across all age groups underscore the importance of identifying what's going on, and physicians should keep this new diagnosis in mind.

Allergies to meat might be more common than previously thought, as much as 2% of the population (which would mean millions of people). But to put this in context, Americans are much more likely to suffer an anaphylactic reaction due to seafood, tick bite or not, no matter where they live. A national survey of emergency rooms found shellfish was by far the most frequently implicated food, and unlike many other allergies, kids don't tend to outgrow fish and shellfish allergies.

Some fish allergies are actually allergies not to the fish, but to worms in the fish, like anisakis, which are found particularly in cod, anchovies, and squid. Exposure to these parasites in fish, living or dead, is a widespread problem. In fact, we can even have an allergic reaction to the parasitic fish worm when we eat chickens that were fed on fishmeal. This is one of the ways someone who's allergic to fish could get triggered by chicken.

Because of these worms, researchers recommend that people stop eating seafood and sushi altogether, because besides inducing allergenic reactions, the worms may cause a leaky gut syndrome, which often is unrecognized and can predispose someone to other, more important pathologies than just being itchy all over.

I previously covered anisakis in Allergenic Fish Worms and other allergenic parasite reactions in Chronic Headaches and Pork Tapeworms.

The worms might not the only thing increasing allergies in fish. See:

I also did a 4-part series on allergies in general if anyone's interested:

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: Meredith P. / Flickr

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Why Would Eating Fish Increase Diabetes Risk?

NF-Jul23 Fish and Diabetes.jpg

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

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

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

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

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

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

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

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

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

Other videos on how polluted our oceans now are include:

-Michael Greger, M.D.

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

Image Credit: Gideon / Flickr

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Colon Cancer Prevention: Is it the Fiber or the Phytates?

NF - May21 Phytates for the Prevention of Cancer.jpg

Dietary factors are considered the most important environmental risk factors for cancer. Within recent years, a large number of naturally occurring health-enhancing substances of plant origin known as phytonutrients have been recognized to have beneficial effects on certain cancers. Beans, chickpeas, split peas and lentils are packed with all sorts of wonderful nutrients, but the reason they may protect against several degenerative diseases may be due to non-nutritive compounds, or even so-called "antinutrient" compounds like phytates.

Phytates have a somewhat negative reputation for binding to certain minerals (like iron, zinc and manganese) and slowing their absorption. But they have also been found to offer anti-inflammatory health benefits. "The reputation of phytate has had a roller coaster ride ever since its discovery; it has undergone alternate eminence and infamy." (I previously explored the surprising new science about phytates in my video Phytates for the Prevention of Osteoporosis). Could they play a potential role in preventing colon cancer?

In the U.S., colon cancer is the second leading cause of cancer death, but some parts of the world have had just a tiny fraction of our rates, with the highest rates reported in Connecticut, and the lowest in Kampala, Uganda. The famous surgeon Denis Burkitt spent 24 years in Uganda and most of the hospitals he contacted there had never seen a case of colon cancer. Noting they live off diets centered on whole plant foods, he figured that maybe it was the fiber that was so protective.

Some studies have called that interpretation into question. Danes appear to have more colon cancer than Finns, yet Danes consume almost twice the dietary fiber. What else, then, could explain the low cancer rates among plant-based populations? Well, fiber isn't the only thing found in whole plant foods, but missing from processed and animal foods. Maybe it's the phytate.

Dietary phytate, rather than fiber per se, may be the most important variable governing the frequency of colon cancer, as phytate is known to be a powerful inhibitor of the iron-mediated production of hydroxyl radicals, a particularly dangerous type of free radical. So the standard American diet may be a double whammy, the heme iron in muscle meat plus the lack of phytate in refined plant foods to extinguish the iron radicals.

This may account for what researchers found in the Adventist study, highlighted in my video, Phytates for the Prevention of Cancer. They found excess risk of cancer for higher intakes of both red meat and white meat, suggesting all meats contribute to colon cancer formation -- about twice the risk for red meat eaters, and three times the risk for those eating chicken and fish.

Those who eat meat could reduce their risk in two ways: by cutting down on meat or by eating more beans, an excellent source of phytates.

So it's not just how much meat we eat, but our meat to vegetables ratio. Between the two extremes (high-vegetable and low-meat diets versus high-meat and low-vegetable diets) a risk ratio of about eight appears to exist, sufficient to explain a substantial part of the international variation in the incidence of colorectal cancer. Those with the worst of both worlds, high meat and low vegetable, were at eight times the risk.

More on colon cancer in Stool Size Matters.

Here are a few of my latest videos on the latest wonders of the musical fruit:

What about that music, though? See my blog Beans and Gas: Clearing the air.

What about soybeans and cancer? See Breast Cancer Survival and Soy and BRCA Breast Cancer Genes and Soy.

Other ways to mediate the effects of meat intake can be found in my video Reducing Cancer Risk in Meateaters.

For more about how phytates may play a role in both cancer prevention and treatment see Phytates for Rehabilitating Cancer Cells and Phytates for the Treatment of Cancer.

-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: Ton Rulkens / Flickr

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How Long to Avoid Fish Before Conception?

NF-Dec25 How Long to Detox from Fish Before Pregnancy?.jpg

Mothers' increased consumption of fish before and during pregnancy leads to increased exposure to both mercury and the long-chain omega 3 DHA. Mercury may negatively affect brain development in one's unborn baby, whereas DHA may stimulate brain development. However, the negative effect of mercury appears to outweigh the beneficial effect of DHA for most species of fish (see Mercury vs. Omega-3s for Brain Development).

Unfortunately, women of childbearing age appear less aware and knowledgeable about this problem than other women, despite FDA and EPA campaigns to inform every OB/GYN and pediatrician in the country about the potential risks of mercury in fish.

Since mercury sticks around in the body, women may want to avoid fish with high levels of mercury for a year before they get pregnant, not just during pregnancy. The rationale for avoiding fish for a year before pregnancy is because the half-life of mercury in the body is estimated to be about two months. In a study I profile in my video How Long to Detox from Fish Before Pregnancy a group of researchers fed subjects two servings a week of tuna and other high mercury fish to push their mercury levels up, and then stopped the fish. Slowly but surely their levels came back down (see the video for the graph). I know a lot of moms are concerned about exposing their children to mercury containing vaccines, but if they eat even just a serving a week of fish during pregnancy, the latest data shows that their infants end up with substantially more mercury in their bodies than if they were injected with up to six mercury-containing vaccines.

Given the two-month half-life of mercury, within a year of stopping fish consumption our bodies can detox nearly 99% of the mercury. Unfortunately the other industrial pollutants in fish can take longer for our body to get rid of. Certain dioxins, PCBs, and DDT metabolites found in fish have a half-life as long as ten years. So getting that same 99% drop could take 120 years, which is a long time to delay one's first child.

The fact that we can still find DDT in umbilical cord blood decades after the pesticide was banned speaks to the persistence of some pollutants. There's a shortcut for moms, but it's The Wrong Way to Detox.

What effects do these other pollutants have? Well, high concentrations of industrial contaminants are associated with 38 times the odds of diabetes--that's as strong as the relationship between smoking and lung cancer! Isn't diabetes mostly associated with obesity though? Well, these pollutants are fat-soluble, so "as people get fatter the retention and toxicity of persistent organic pollutants related to the risk of diabetes may increase." This suggests the shocking possibility that obesity "may only be a vehicle" for such chemicals.

Now the pollutants could just be a marker for animal product consumption, which may be why there's such higher diabetes risk, since more than 90% of the persistent organic pollutants comes from animal foods. And indeed, in the U.S. every additional serving of fish a week is associated with a 5% increased risk of diabetes, which makes fish consumption about 80% worse than red meat. PCBs are found most concentrated in fish and eggs (Food Sources of PCB Chemical Pollutants), which may be why there are lower levels of Industrial Pollutants in Vegans. This may also help explain the remarkable findings in Eggs and Diabetes.

More on the risks of mercury can be found in these videos:

-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: Tatiana Vdb / Flickr

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Why the Egg-Cancer Link?

NF-Aug21 Why the Egg Cancer-link?.jpg

Two million men in the U.S. are living with prostate cancer -- but that's better than dying from prostate cancer. Catch it when it's localized and the five-year survival is practically guaranteed, but once it really starts spreading, chances drop to one in three. "Thus, identification of modifiable factors that affect the progression of prostate cancer is something that deserves study," noted Dr. Erin Richard and colleagues at Harvard. So, they took more than a thousand men with early stage prostate cancer and followed them for a couple years to see if there was anything in their diet associated with a resurgence of the cancer, such as spreading to the bone.

Compared to men who hardly ate any eggs, men who ate even less than a single egg a day had a significant 2-fold increased risk of prostate cancer progression. The only thing worse was poultry consumption, with up to four times the risk of progression among high-risk men. They think it might be the cooked meat carcinogens that for some reason build up more in chicken and turkey muscle than in other meats. For more on these so-called heterocyclic amines, see my videos: Heterocyclic Amines in Eggs, Cheese, and Creatine?, Estrogenic Cooked Meat Carcinogens, and PhIP: The Three Strikes Breast Carcinogen.

But what about the eggs? Why would less than once-a-day egg consumption double the risk of cancer progression? "A plausible mechanism that may explain the association between eggs and prostate cancer progression is high dietary choline," the researchers suggested. Egg consumption is a determinant of how much choline you have in your blood, and higher blood choline has been associated with a greater risk of getting prostate cancer in the first place. So the choline in eggs may both increase one's risk of getting it and having it spread.

Studies have associated choline consumption not just with getting cancer and spreading cancer, but also with significantly increased risk of dying from it. Those who ate the most had a 70% increased risk of lethal prostate cancer. Another recent study found that men who consumed two and a half or more eggs per week -- that's just like one egg every three days -- had an 81 percent increased risk of lethal prostate cancer.

Maybe that's why meat, milk, and eggs have all been associated with advanced prostate cancer--because of the choline. Choline is so concentrated in cancer cells that doctors can follow choline uptake to track the spread of cancer throughout the body. But why may dietary choline increase the risk of lethal prostate cancer? Dietary choline is converted in the gut to trimethylamine (see my video Carnitine, Choline, Cancer and Cholesterol: The TMAO Connection), so the Harvard researchers speculated that the TMAO from the high dietary choline intake may increase inflammation, which may promote progression of prostate cancer to a lethal disease.

In one of my videos, Eggs and Choline: Something Fishy, I talked about what trimethylamine might do to one's body odor.

In the New England Journal of Medicine, the same Cleveland Clinic research team that did the famous study on carnitine repeated the study, but instead of feeding people a steak, they fed people some hard-boiled eggs. Just as they suspected, a similar spike in that toxic TMAO. So it's not just red meat. And the link between TMAO levels in the blood and strokes, heart attacks, and death was seen even in low-risk groups like those with low-risk cholesterol levels. Thus, because of the choline, eating eggs may increase our risk regardless of what our cholesterol is.

It's ironic that the choline content of eggs is something the egg industry actually boasts about. And the industry is aware of the cancer data. Through the Freedom of Information Act, I was able to get my hands on an email (which you can view in my video, Eggs, Choline, and Cancer) from the executive director of the industry's Egg Nutrition Center to an American Egg Board executive talking about how choline may be a culprit in promoting cancer progression. "Certainly worth keeping in mind," he said, "as we continue to promote choline as another good reason to consume eggs."

With regard to the prevention of prostate cancer progression, chicken and eggs may be the worst foods to eat, but what might be the best? See my video Prostate Cancer Survival: The A/V Ratio.

To prevent prostate cancer in the first place, see videos such as:

What about reversing cancer progression? See Dr. Ornish's work Cancer Reversal Through Diet?, followed up by the Pritikin Foundation: Ex Vivo Cancer Proliferation Bioassay. Flax may help as well (Flaxseed vs. Prostate Cancer).

-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: Christopher Craig / Flickr

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