Diet and Hiatal Hernia

Diet and Hiatal Hernia.jpeg

In terms of preventing acid reflux heartburn, high-fat meals cause dramatically more acid exposure in the esophagus in the hours after a meal. I talked about this in Diet and GERD Acid Reflux Heartburn. High fiber intake decreases the risk, but why? One typically thinks of fiber as helping out much lower in the digestive tract.

A systematic review and meta-analysis published in 2013 found a highly significant protective association between esophageal adenocarcinoma and dietary fiber intake, suggesting that individuals with the highest fiber intakes have an approximately 30% lower risk of cancer. This could be because of the phytates in high-fiber foods slowing cancer growth, fiber's anti-inflammatory effects, or even fiber removing carcinogens. But those are all generic anti-cancer effects of whole plant foods. Specific to this type of acid irritation-induced esophageal cancer, fiber may reduce the risk of reflux in the first place. But how?

As you can see in my video, Diet and Hiatal Hernia, hiatus hernia occurs when part of the stomach is pushed up through the diaphragm into the chest cavity, which makes it easy for acid to reflux into the esophagus and throat. Hiatus hernia affects more than 1 in 5 American adults. In contrast, in rural African communities eating their traditional plant-based diets, the risk wasn't 1 in 5; it was closer to 1 in 1,000--almost unheard of. Hiatus hernia is almost peculiar to those who consume western-type diets. Why are plant-based populations protected? Perhaps because they pass such large, soft stools, three or four times the volume as Westerners.

What does the size and consistency of one's bowel movement have to do with hiatal hernia? A simple model may be helpful in illustrating the mechanism that produces upward herniation of the stomach through the hole (called the esophageal hiatus) in the diaphragm, which separates the abdomen from the chest. If a ball with a hole in its wall is filled with water and then squeezed, the water is pushed out through the hole. If we liken the abdominal cavity to the ball, the esophageal hiatus in the diaphragm corresponds with the hole in the ball. Abdominal straining during movement of firm feces corresponds to squeezing the ball and may result in the gradual expulsion of the upper end of the stomach from the abdominal cavity up into the chest. It's like when we squeeze a stress ball. Straining at stool raises pressures inside our abdominal cavity more than almost any other factor.

In effect, straining at stool puts the squeeze on our abdomen and may herniate part of our stomach up. "Consistent with this concept is the observation that in Africans the lower esophageal sphincter is entirely subdiaphragmatic, whereas it usually straddles the diaphragm in Westerners and is above the diaphragm in the presence of hiatus hernia."

This same abdominal pressure from straining may cause a number of other problems, too. Straining can cause herniations in the wall of the colon itself, known as diverticulosis. That same pressure can backup blood flow in the veins around the anus, causing hemorrhoids, and also push blood flow back into the legs, resulting in varicose veins.

Hiatal hernia is not the only condition that high-fiber diets may protect against. See:

I also have a load of other bowel movement 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:

Image Credit: Sally Plank. This image has been modified.

Original Link

Diet and Hiatal Hernia

Diet and Hiatal Hernia.jpeg

In terms of preventing acid reflux heartburn, high-fat meals cause dramatically more acid exposure in the esophagus in the hours after a meal. I talked about this in Diet and GERD Acid Reflux Heartburn. High fiber intake decreases the risk, but why? One typically thinks of fiber as helping out much lower in the digestive tract.

A systematic review and meta-analysis published in 2013 found a highly significant protective association between esophageal adenocarcinoma and dietary fiber intake, suggesting that individuals with the highest fiber intakes have an approximately 30% lower risk of cancer. This could be because of the phytates in high-fiber foods slowing cancer growth, fiber's anti-inflammatory effects, or even fiber removing carcinogens. But those are all generic anti-cancer effects of whole plant foods. Specific to this type of acid irritation-induced esophageal cancer, fiber may reduce the risk of reflux in the first place. But how?

As you can see in my video, Diet and Hiatal Hernia, hiatus hernia occurs when part of the stomach is pushed up through the diaphragm into the chest cavity, which makes it easy for acid to reflux into the esophagus and throat. Hiatus hernia affects more than 1 in 5 American adults. In contrast, in rural African communities eating their traditional plant-based diets, the risk wasn't 1 in 5; it was closer to 1 in 1,000--almost unheard of. Hiatus hernia is almost peculiar to those who consume western-type diets. Why are plant-based populations protected? Perhaps because they pass such large, soft stools, three or four times the volume as Westerners.

What does the size and consistency of one's bowel movement have to do with hiatal hernia? A simple model may be helpful in illustrating the mechanism that produces upward herniation of the stomach through the hole (called the esophageal hiatus) in the diaphragm, which separates the abdomen from the chest. If a ball with a hole in its wall is filled with water and then squeezed, the water is pushed out through the hole. If we liken the abdominal cavity to the ball, the esophageal hiatus in the diaphragm corresponds with the hole in the ball. Abdominal straining during movement of firm feces corresponds to squeezing the ball and may result in the gradual expulsion of the upper end of the stomach from the abdominal cavity up into the chest. It's like when we squeeze a stress ball. Straining at stool raises pressures inside our abdominal cavity more than almost any other factor.

In effect, straining at stool puts the squeeze on our abdomen and may herniate part of our stomach up. "Consistent with this concept is the observation that in Africans the lower esophageal sphincter is entirely subdiaphragmatic, whereas it usually straddles the diaphragm in Westerners and is above the diaphragm in the presence of hiatus hernia."

This same abdominal pressure from straining may cause a number of other problems, too. Straining can cause herniations in the wall of the colon itself, known as diverticulosis. That same pressure can backup blood flow in the veins around the anus, causing hemorrhoids, and also push blood flow back into the legs, resulting in varicose veins.

Hiatal hernia is not the only condition that high-fiber diets may protect against. See:

I also have a load of other bowel movement 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:

Image Credit: Sally Plank. This image has been modified.

Original Link

Solving a Colon Cancer Mystery

Solving-a-Colon-Cancer-Mystery.jpeg

Colorectal cancer is the second leading cause of cancer death in the United States, after lung cancer. The rates of lung cancer around the world vary by a factor of 10. If there was nothing we could do to prevent lung cancer--if it just happened at random--we'd assume that the rates everywhere would be about the same. But since there's such a huge variation in rates, it seems like there's probably some external cause. Indeed, we now know smoking is responsible for 90% of lung cancer cases. If we don't want to die of the number-one cancer killer, we can throw 90% of our risk out the window just by not smoking.

There's an even bigger variation around the world for colon cancer. As discussed in Solving a Colon Cancer Mystery, it appears colon cancer doesn't just happen, something makes it happen. If our lungs can get filled with carcinogens from smoke, maybe our colons are getting filled with carcinogens from food. Researchers from the University of Pittsburgh and the University of Limpopo sought to answer the question, "Why do African Americans get more colon cancer than native Africans?" Why study Africans? Because colon cancer is extremely rare in native African populations, more than 50 times lower than rates of Americans, white or black.

It's the fiber, right? The first to describe the low rates of colon cancer in native Africans, Dr. Denis Burkitt ascribed it to their staple diet traditionally high in whole grains and, consequently, high in fiber content. We seem to get a 10% reduction in risk for every 10 grams of fiber we eat a day. If it's a 1% drop for each gram, and native Africans are eating upwards of 100 grams a day, it could explain why colon cancer is so rare in sub-Saharan Africa.

Wait a second. The modern African diet is highly processed and low in fiber, yet there has been no dramatic increase in colon cancer incidence. Their diet today has such a low fiber content because most populations now depend on commercially produced refined cornmeal. We're not just talking low fiber intake, we're talking United States of America low, down around half the recommended daily allowance. Yet colon disease in Africa is still about 50 times less common than in the United States.

Maybe it's because native Africans are thinner and exercise more? No, they're not, and no, they don't. If anything, their physical activity levels may now be even lower than Americans'. So if they're sedentary like us and eating mostly refined carbs, few whole plant foods, and little fiber like us, why do they have 50 times less colon cancer than we do? There is one difference. The diet of both African Americans and Caucasian Americans is rich in meat, whereas the native Africans' diet is so low in meat and saturated fat they have total cholesterol levels averaging 139 mg/dL, compared to over 200 mg/dL in the United States.

They may not get a lot of fiber anymore, but they continue to minimize meat and animal fat consumption, which supports other evidence indicating the most powerful determinants of colon cancer risk may be meat and animal fat intake levels. So why do Americans get more colon cancer than Africans? Maybe the rarity of colon cancer in Africans is not the fiber, but their low animal product consumption.

Although opinions diverge as to whether cholesterol, animal fat, or animal protein is most responsible for the increased colon cancer risk, given that all three have been proven to have carcinogenic properties, it may not really matter which component is worse, as a diet laden in one is usually laden in the others.

I've previously suggested phytates may play a critical role as well (Phytates for the Prevention of Cancer). Resistant starch may be another player. Since native Africans cool down their corn porridge, some of the starch can crystallize and effectively turn into fiber. (This is the same reason pasta salad and potato salad better feed our gut bacteria than starchy dishes served hot.) I touch on it briefly in Bowel Wars: Hydrogen Sulfide vs. Butyrate. Resistant starch may also help explain Beans and the Second Meal Effect. And for even more, see Resistant Starch & Colon Cancer and Getting Starch to Take the Path of Most Resistance.

Fiber may just be a marker for healthier eating since it's only found concentrated in unprocessed plant foods. So the apparent protection afforded by high fiber diets may derive from whole food plant-based nutrition rather than the fiber itself (so fiber supplements would not be expected to provide the same protection). Here are some videos that found protective associations with higher fiber diets:

What might be in animal products that can raise cancer risk? Here's a smattering:

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: Department of Foreign Affairs and Trade / Flickr. This image has been modified.

Original Link

Solving a Colon Cancer Mystery

Solving-a-Colon-Cancer-Mystery.jpeg

Colorectal cancer is the second leading cause of cancer death in the United States, after lung cancer. The rates of lung cancer around the world vary by a factor of 10. If there was nothing we could do to prevent lung cancer--if it just happened at random--we'd assume that the rates everywhere would be about the same. But since there's such a huge variation in rates, it seems like there's probably some external cause. Indeed, we now know smoking is responsible for 90% of lung cancer cases. If we don't want to die of the number-one cancer killer, we can throw 90% of our risk out the window just by not smoking.

There's an even bigger variation around the world for colon cancer. As discussed in Solving a Colon Cancer Mystery, it appears colon cancer doesn't just happen, something makes it happen. If our lungs can get filled with carcinogens from smoke, maybe our colons are getting filled with carcinogens from food. Researchers from the University of Pittsburgh and the University of Limpopo sought to answer the question, "Why do African Americans get more colon cancer than native Africans?" Why study Africans? Because colon cancer is extremely rare in native African populations, more than 50 times lower than rates of Americans, white or black.

It's the fiber, right? The first to describe the low rates of colon cancer in native Africans, Dr. Denis Burkitt ascribed it to their staple diet traditionally high in whole grains and, consequently, high in fiber content. We seem to get a 10% reduction in risk for every 10 grams of fiber we eat a day. If it's a 1% drop for each gram, and native Africans are eating upwards of 100 grams a day, it could explain why colon cancer is so rare in sub-Saharan Africa.

Wait a second. The modern African diet is highly processed and low in fiber, yet there has been no dramatic increase in colon cancer incidence. Their diet today has such a low fiber content because most populations now depend on commercially produced refined cornmeal. We're not just talking low fiber intake, we're talking United States of America low, down around half the recommended daily allowance. Yet colon disease in Africa is still about 50 times less common than in the United States.

Maybe it's because native Africans are thinner and exercise more? No, they're not, and no, they don't. If anything, their physical activity levels may now be even lower than Americans'. So if they're sedentary like us and eating mostly refined carbs, few whole plant foods, and little fiber like us, why do they have 50 times less colon cancer than we do? There is one difference. The diet of both African Americans and Caucasian Americans is rich in meat, whereas the native Africans' diet is so low in meat and saturated fat they have total cholesterol levels averaging 139 mg/dL, compared to over 200 mg/dL in the United States.

They may not get a lot of fiber anymore, but they continue to minimize meat and animal fat consumption, which supports other evidence indicating the most powerful determinants of colon cancer risk may be meat and animal fat intake levels. So why do Americans get more colon cancer than Africans? Maybe the rarity of colon cancer in Africans is not the fiber, but their low animal product consumption.

Although opinions diverge as to whether cholesterol, animal fat, or animal protein is most responsible for the increased colon cancer risk, given that all three have been proven to have carcinogenic properties, it may not really matter which component is worse, as a diet laden in one is usually laden in the others.

I've previously suggested phytates may play a critical role as well (Phytates for the Prevention of Cancer). Resistant starch may be another player. Since native Africans cool down their corn porridge, some of the starch can crystallize and effectively turn into fiber. (This is the same reason pasta salad and potato salad better feed our gut bacteria than starchy dishes served hot.) I touch on it briefly in Bowel Wars: Hydrogen Sulfide vs. Butyrate. Resistant starch may also help explain Beans and the Second Meal Effect. And for even more, see Resistant Starch & Colon Cancer and Getting Starch to Take the Path of Most Resistance.

Fiber may just be a marker for healthier eating since it's only found concentrated in unprocessed plant foods. So the apparent protection afforded by high fiber diets may derive from whole food plant-based nutrition rather than the fiber itself (so fiber supplements would not be expected to provide the same protection). Here are some videos that found protective associations with higher fiber diets:

What might be in animal products that can raise cancer risk? Here's a smattering:

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: Department of Foreign Affairs and Trade / Flickr. This image has been modified.

Original Link

What Animal Protein Does in Your Colon

What Animal Protein Does in Your Colon.jpeg

There's a take-off of the industry slogan, "Beef: It's What's For Dinner" - "Beef: It's What's Rotting in Your Colon." I saw this on a shirt once with some friends and I was such the party pooper--no pun intended--explaining to everyone that meat is fully digested in the small intestine, and never makes it down into the colon. It's no fun hanging out with biology geeks.

But I was wrong!

It's been estimated that with a typical Western diet, up to 12 grams of protein can escape digestion, and when it reaches the colon, it can be turned into toxic substances like ammonia. This degradation of undigested protein in the colon is called putrefaction, so a little meat can actually end up putrefying in our colon. The problem is that some of the by-products of this putrefaction process can be toxic.

It's generally accepted that carbohydrate fermentation--the fiber and resistant starches that reach our colon--results in beneficial effects because of the generation of short-chain fatty acids like butyrate, whereas protein fermentation is considered detrimental. Protein fermentation mainly occurs in the lower end of colon and results in the production of potentially toxic metabolites. That may be why colorectal cancer and ulcerative colitis tends to happen lower down--because that's where the protein is putrefying.

Probably the simplest strategy to reduce the potential harm of protein fermentation is to reduce dietary protein intake. But the accumulation of these toxic byproducts of protein metabolism may be attenuated by the fermentation of undigested plant matter. In my video, Bowel Wars: Hydrogen Sulfide vs. Butyrate, you can see a study out of Australia showed that if you give people foods containing resistant starch you can block the accumulation of potentially harmful byproducts of protein metabolism. Resistant starch is resistant to small intestine digestion and so it makes it down to our colon where it can feed our good bacteria. Resistant starch is found in cooked beans, split peas, chickpeas, lentils, raw oatmeal, and cooled cooked pasta (like macaroni salad). Apparently, the more starch that ends up in the colon, the less ammonia that is produced.

Of course, there's protein in plants too. The difference is that animal proteins tend to have more sulfur-containing amino acids like methionine, which can be turned into hydrogen sulfide in our colon. Hydrogen sulfide is the rotten egg gas that may play a role in the development of the inflammatory bowel disease, ulcerative colitis (see Preventing Ulcerative Colitis with Diet).

The toxic effects of hydrogen sulfide appear to be a result of blocking the ability of the cells lining our colon from utilizing butyrate, which is what our good bacteria make from the fiber and resistant starch we eat. It's like this constant battle in our colon between the bad metabolites of protein, hydrogen sulfide, and the good metabolites of carbohydrates, butyrate. Using human colon samples, researchers were able to show that the adverse effects of sulfide could be reversed by butyrate. So we can either cut down on meat, eat more plants, or both.

There are two ways hydrogen sulfide can be produced, though. It's mainly present in our large intestine as a result of the breakdown of sulfur-containing proteins, but the rotten egg gas can also be generated from inorganic sulfur preservatives like sulfites and sulfur dioxide.

Sulfur dioxide is used as a preservative in dried fruit, and sulfites are added to wines. We can avoid sulfur additives by reading labels or by just choosing organic, since they're forbidden from organic fruits and beverages by law.

More than 35 years ago, studies started implicating sulfur dioxide preservatives in the exacerbation of asthma. This so-called "sulfite-sensitivity" seems to affect only about 1 in 2,000 people, so I recommended those with asthma avoid it, but otherwise I considered the preservative harmless. I am now not so sure, and advise people to avoid it when possible.

Cabbage family vegetables naturally have some sulfur compounds, but thankfully, after following more than a hundred thousand women for over 25 years, researchers concluded cruciferous vegetables were not associated with elevated colitis risk.

Because of animal protein and processed food intake, the standard American diet may contain five or six times more sulfur than a diet centered around unprocessed plant foods. This may help explain the rarity of inflammatory bowel disease among those eating traditional whole food, plant-based diets.

How could companies just add things like sulfur dioxide to foods without adequate safety testing? See Who Determines if Food Additives are Safe? For other additives that may be a problem, see Titanium Dioxide & Inflammatory Bowel Disease and Is Carrageenan Safe?

More on this epic fermentation battle in our gut in Stool pH and Colon Cancer.

Does the sulfur-containing amino acid methionine sound familiar? You may remember it from such hits as Starving Cancer with Methionine Restriction and Methionine Restriction as a Life Extension Strategy.

These short-chain fatty acids released by our good bacteria when we eat fiber and resistant starches are what may be behind the second meal effect: Beans and the Second Meal Effect.

I mentioned ulcerative colitis. What about the other inflammatory bowel disease Crohn's? See Preventing Crohn's Disease With Diet and Dietary Treatment of Crohn's Disease.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

What Animal Protein Does in Your Colon

What Animal Protein Does in Your Colon.jpeg

There's a take-off of the industry slogan, "Beef: It's What's For Dinner" - "Beef: It's What's Rotting in Your Colon." I saw this on a shirt once with some friends and I was such the party pooper--no pun intended--explaining to everyone that meat is fully digested in the small intestine, and never makes it down into the colon. It's no fun hanging out with biology geeks.

But I was wrong!

It's been estimated that with a typical Western diet, up to 12 grams of protein can escape digestion, and when it reaches the colon, it can be turned into toxic substances like ammonia. This degradation of undigested protein in the colon is called putrefaction, so a little meat can actually end up putrefying in our colon. The problem is that some of the by-products of this putrefaction process can be toxic.

It's generally accepted that carbohydrate fermentation--the fiber and resistant starches that reach our colon--results in beneficial effects because of the generation of short-chain fatty acids like butyrate, whereas protein fermentation is considered detrimental. Protein fermentation mainly occurs in the lower end of colon and results in the production of potentially toxic metabolites. That may be why colorectal cancer and ulcerative colitis tends to happen lower down--because that's where the protein is putrefying.

Probably the simplest strategy to reduce the potential harm of protein fermentation is to reduce dietary protein intake. But the accumulation of these toxic byproducts of protein metabolism may be attenuated by the fermentation of undigested plant matter. In my video, Bowel Wars: Hydrogen Sulfide vs. Butyrate, you can see a study out of Australia showed that if you give people foods containing resistant starch you can block the accumulation of potentially harmful byproducts of protein metabolism. Resistant starch is resistant to small intestine digestion and so it makes it down to our colon where it can feed our good bacteria. Resistant starch is found in cooked beans, split peas, chickpeas, lentils, raw oatmeal, and cooled cooked pasta (like macaroni salad). Apparently, the more starch that ends up in the colon, the less ammonia that is produced.

Of course, there's protein in plants too. The difference is that animal proteins tend to have more sulfur-containing amino acids like methionine, which can be turned into hydrogen sulfide in our colon. Hydrogen sulfide is the rotten egg gas that may play a role in the development of the inflammatory bowel disease, ulcerative colitis (see Preventing Ulcerative Colitis with Diet).

The toxic effects of hydrogen sulfide appear to be a result of blocking the ability of the cells lining our colon from utilizing butyrate, which is what our good bacteria make from the fiber and resistant starch we eat. It's like this constant battle in our colon between the bad metabolites of protein, hydrogen sulfide, and the good metabolites of carbohydrates, butyrate. Using human colon samples, researchers were able to show that the adverse effects of sulfide could be reversed by butyrate. So we can either cut down on meat, eat more plants, or both.

There are two ways hydrogen sulfide can be produced, though. It's mainly present in our large intestine as a result of the breakdown of sulfur-containing proteins, but the rotten egg gas can also be generated from inorganic sulfur preservatives like sulfites and sulfur dioxide.

Sulfur dioxide is used as a preservative in dried fruit, and sulfites are added to wines. We can avoid sulfur additives by reading labels or by just choosing organic, since they're forbidden from organic fruits and beverages by law.

More than 35 years ago, studies started implicating sulfur dioxide preservatives in the exacerbation of asthma. This so-called "sulfite-sensitivity" seems to affect only about 1 in 2,000 people, so I recommended those with asthma avoid it, but otherwise I considered the preservative harmless. I am now not so sure, and advise people to avoid it when possible.

Cabbage family vegetables naturally have some sulfur compounds, but thankfully, after following more than a hundred thousand women for over 25 years, researchers concluded cruciferous vegetables were not associated with elevated colitis risk.

Because of animal protein and processed food intake, the standard American diet may contain five or six times more sulfur than a diet centered around unprocessed plant foods. This may help explain the rarity of inflammatory bowel disease among those eating traditional whole food, plant-based diets.

How could companies just add things like sulfur dioxide to foods without adequate safety testing? See Who Determines if Food Additives are Safe? For other additives that may be a problem, see Titanium Dioxide & Inflammatory Bowel Disease and Is Carrageenan Safe?

More on this epic fermentation battle in our gut in Stool pH and Colon Cancer.

Does the sulfur-containing amino acid methionine sound familiar? You may remember it from such hits as Starving Cancer with Methionine Restriction and Methionine Restriction as a Life Extension Strategy.

These short-chain fatty acids released by our good bacteria when we eat fiber and resistant starches are what may be behind the second meal effect: Beans and the Second Meal Effect.

I mentioned ulcerative colitis. What about the other inflammatory bowel disease Crohn's? See Preventing Crohn's Disease With Diet and Dietary Treatment of Crohn's Disease.

In health,

Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Image Credit: Sally Plank / Flickr. This image has been modified.

Original Link

Clostridium difficile in the Food Supply

Clostridium difficile in the Food Supply.jpeg

Clostridium difficile is one of our most urgent bacterial threats, sickening a quarter million Americans every year, and killing thousands at the cost of a billion dollars a year. And it's on the rise.

As shown in C. difficile Superbugs in Meat, uncomplicated cases have been traditionally managed with powerful antibiotics, but recent reports suggest that hypervirulent strains are increasingly resistant to medical management. There's been a rise in the percentage of cases that end up under the knife, which could be a marker of the emergence of these hypervirulent strains. Surgeons may need to remove our colon entirely to save our lives, although the surgery is so risky that the operation alone may kill us half the time.

Historically, most cases appeared in hospitals, but a landmark study published in the New England Journal of Medicine found that only about a third of cases could be linked to contact with an infected patient.

Another potential source is our food supply.

In the US, the frequency of contamination of retail chicken with these superbugs has been documented to be up to one in six packages off of store shelves. Pig-derived C. diff, however, have garnered the greatest attention from public health personnel, because the same human strain that's increasingly emerging in the community outside of hospitals is the major strain among pigs.

Since the turn of the century, C. diff is increasingly being reported as a major cause of intestinal infections in piglets. C. diff is now one of the most common causes of intestinal infections in baby piglets in the US. Particular attention has been paid to pigs because of high rates of C. diff shedding into their waste, which can lead to the contamination of retail pork. The U.S. has the highest levels of C. diff meat contamination tested so far anywhere in the world.

Carcass contamination by gut contents at slaughter probably contributes most to the presence of C. diff in meat and meat products. But why is the situation so much worst in the US? Slaughter techniques differ from country-to-country, with those in the United States evidently being more of the "quick and dirty" variety.

Colonization or contamination of pigs by superbugs such as C. difficile and MRSA at the farm production level may be more important than at the slaughterhouse level, though. One of the reasons sows and their piglets may have such high rates of C. diff is because of cross-contamination of feces in the farrowing crate, which are narrow metal cages that mother pigs are kept in while their piglets are nursing.

Can't you just follow food safety guidelines and cook the meat through? Unfortunately, current food safety guidelines are ineffective against C. difficile. To date, most food safety guidelines recommend cooking to an internal temperature as low as 63o C-the official USDA recommendation for pork-but recent studies show that C. diff spores can survive extended heating at 71o. Therefore, the guidelines should be raised to take this potentially killer infection into account.

One of the problems is that sources of C. diff food contamination might include not only fecal contamination on the surface of the meat, but transfer of spores from the gut into the actual muscles of the animal, inside the meat. Clostridia bacteria like C. diff comprise one of the main groups of bacteria involved in natural carcass degradation, and so by colonizing muscle tissue before death, C. diff can not only transmit to new hosts that eat the muscles, like us, but give them a head start on carcass break-down.

Never heard of C. diff? That's the Toxic Megacolon Superbug I've talked about before.

Another foodborne illness tied to pork industry practices is yersiniosis. See Yersinia in Pork.

MRSA (Methicillin-resistant Staph aureus) is another so-called superbug in the meat supply:

More on the scourge of antibiotic resistance and what can be done about it:

How is it even legal to sell foods with such pathogens? See Salmonella in Chicken & Turkey: Deadly But Not Illegal and Chicken Salmonella Thanks to Meat Industry Lawsuit.

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: USDA / Flickr. This image has been modified.

Original Link

Clostridium difficile in the Food Supply

Clostridium difficile in the Food Supply.jpeg

Clostridium difficile is one of our most urgent bacterial threats, sickening a quarter million Americans every year, and killing thousands at the cost of a billion dollars a year. And it's on the rise.

As shown in C. difficile Superbugs in Meat, uncomplicated cases have been traditionally managed with powerful antibiotics, but recent reports suggest that hypervirulent strains are increasingly resistant to medical management. There's been a rise in the percentage of cases that end up under the knife, which could be a marker of the emergence of these hypervirulent strains. Surgeons may need to remove our colon entirely to save our lives, although the surgery is so risky that the operation alone may kill us half the time.

Historically, most cases appeared in hospitals, but a landmark study published in the New England Journal of Medicine found that only about a third of cases could be linked to contact with an infected patient.

Another potential source is our food supply.

In the US, the frequency of contamination of retail chicken with these superbugs has been documented to be up to one in six packages off of store shelves. Pig-derived C. diff, however, have garnered the greatest attention from public health personnel, because the same human strain that's increasingly emerging in the community outside of hospitals is the major strain among pigs.

Since the turn of the century, C. diff is increasingly being reported as a major cause of intestinal infections in piglets. C. diff is now one of the most common causes of intestinal infections in baby piglets in the US. Particular attention has been paid to pigs because of high rates of C. diff shedding into their waste, which can lead to the contamination of retail pork. The U.S. has the highest levels of C. diff meat contamination tested so far anywhere in the world.

Carcass contamination by gut contents at slaughter probably contributes most to the presence of C. diff in meat and meat products. But why is the situation so much worst in the US? Slaughter techniques differ from country-to-country, with those in the United States evidently being more of the "quick and dirty" variety.

Colonization or contamination of pigs by superbugs such as C. difficile and MRSA at the farm production level may be more important than at the slaughterhouse level, though. One of the reasons sows and their piglets may have such high rates of C. diff is because of cross-contamination of feces in the farrowing crate, which are narrow metal cages that mother pigs are kept in while their piglets are nursing.

Can't you just follow food safety guidelines and cook the meat through? Unfortunately, current food safety guidelines are ineffective against C. difficile. To date, most food safety guidelines recommend cooking to an internal temperature as low as 63o C-the official USDA recommendation for pork-but recent studies show that C. diff spores can survive extended heating at 71o. Therefore, the guidelines should be raised to take this potentially killer infection into account.

One of the problems is that sources of C. diff food contamination might include not only fecal contamination on the surface of the meat, but transfer of spores from the gut into the actual muscles of the animal, inside the meat. Clostridia bacteria like C. diff comprise one of the main groups of bacteria involved in natural carcass degradation, and so by colonizing muscle tissue before death, C. diff can not only transmit to new hosts that eat the muscles, like us, but give them a head start on carcass break-down.

Never heard of C. diff? That's the Toxic Megacolon Superbug I've talked about before.

Another foodborne illness tied to pork industry practices is yersiniosis. See Yersinia in Pork.

MRSA (Methicillin-resistant Staph aureus) is another so-called superbug in the meat supply:

More on the scourge of antibiotic resistance and what can be done about it:

How is it even legal to sell foods with such pathogens? See Salmonella in Chicken & Turkey: Deadly But Not Illegal and Chicken Salmonella Thanks to Meat Industry Lawsuit.

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: USDA / Flickr. This image has been modified.

Original Link

Striving for Alkaline Pee and Acidic Poo

Stool pH and Colon Cancer.jpg

More than 30 years ago, an idea was put forward that high colonic pH promoted colorectal cancer. A high colonic pH may promote the creation of carcinogens from bile acids, a process that is inhibited once you get below a pH of about 6.5. This is supported by data which shows those at higher risk for colon cancer may have a higher stool pH, and those at lower risk have a low pH. There was a dramatic difference between the two groups, with most of the high risk group over pH 8, and most of the low risk group under pH 6 (see Stool pH and Colon Cancer).

This may help explain the 50-fold lower rates of colon cancer in Africa compared to America. The bacteria we have in our gut depends on what we eat. If we eat lots of fiber, then we preferentially feed the fiber eating bacteria, which give us back all sorts of health promoting substances like short-chain fatty acids that have anti-inflammatory and anti-cancer properties. More of these organic acids were found in the stools of native Africans than African Americans. More acids, so lower pH. Whereas putrefactive bacteria, eating animal protein, are able to increase stool pH by producing alkaline metabolites like ammonia.

The pH of the stools of white versus black children in Africa was compared. Children were chosen because you can more readily sample their stools, particularly the rural black schoolchildren who were eating such high fiber diets--whole grains, legumes, nuts, vegetables, fruits, and wild greens--that 90% of them could produce a stool on demand. Stuffed from head to tail with plants, they could give you a stool sample at any time, just as easy as getting a urine sample. It was hard to even get access to the white kids, though, who were reluctant to participate in such investigations, even though they were given waxed cartons fitted with lids while all the black kids got was a plate and a square of paper towel.

The researchers found significantly lower fecal pH in those eating the traditional, rural plant-based diets compared to those eating the traditional Western diet, who were eating far fewer whole plant foods than the black children. But, remove some of those whole plant foods, like switch their corn for white bread for just a few days and their stool pH goes up, and add whole plant foods like an extra five to seven servings of fruit every day, and their stool pH goes down even further and gets more acidic. It makes sense because when you ferment fruits, veggies, and grains, they turn sour, like vinegar, sauerkraut, or sourdough, because good bacteria like lactobacillus produce organic acids like lactic acid. Those who eat a lot of plants have more of those good bugs. So, using the purple cabbage test highlighted in my video, Testing Your Diet with Pee & Purple Cabbage, we want blue pee, but pink poo.

If you compare the fecal samples of those eating vegetarian or vegan to those eating standard diets, plant-based diets appear to shift the makeup of the bacteria in our gut, resulting in a significantly lower stool pH, and the more plant-based, the lower the pH dropped. It's like a positive feedback loop: fiber-eating bacteria produce the acids to create the pH at which fiber-eating bacteria thrive while suppressing the group of less beneficial bugs.

It might taken even as little as two weeks to bring stool pH down on a plant-based diet. In a study published in the British Journal of Cancer, a dozen volunteers carefully selected for their trustworthiness and randomized to sequentially go on regular, vegetarian, or vegan diets and two weeks in, a significant drop in fecal pH was achieved eating completely plant-based.

But there are differing qualities of plant-based diets. For example, the two groups followed in the study I mentioned earlier had dramatically different stool pH, yet both groups were vegetarian. The high risk group was eating mostly refined grains, very little fiber, whereas the low risk group was eating whole grains and beans, packed with fiber for our fiber-friendly flora to munch on.

Just as a "reduction of high serum cholesterol contributes to the avoidance of coronary heart disease," a fall in the fecal pH value may contribute to the avoidance of bowel cancer and through the same means, eating more whole plant foods.

More on colon cancer prevention in:

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: Kitti Sukhonthanit © 123RF.com. This image has been modified.

Original Link

Striving for Alkaline Pee and Acidic Poo

Stool pH and Colon Cancer.jpg

More than 30 years ago, an idea was put forward that high colonic pH promoted colorectal cancer. A high colonic pH may promote the creation of carcinogens from bile acids, a process that is inhibited once you get below a pH of about 6.5. This is supported by data which shows those at higher risk for colon cancer may have a higher stool pH, and those at lower risk have a low pH. There was a dramatic difference between the two groups, with most of the high risk group over pH 8, and most of the low risk group under pH 6 (see Stool pH and Colon Cancer).

This may help explain the 50-fold lower rates of colon cancer in Africa compared to America. The bacteria we have in our gut depends on what we eat. If we eat lots of fiber, then we preferentially feed the fiber eating bacteria, which give us back all sorts of health promoting substances like short-chain fatty acids that have anti-inflammatory and anti-cancer properties. More of these organic acids were found in the stools of native Africans than African Americans. More acids, so lower pH. Whereas putrefactive bacteria, eating animal protein, are able to increase stool pH by producing alkaline metabolites like ammonia.

The pH of the stools of white versus black children in Africa was compared. Children were chosen because you can more readily sample their stools, particularly the rural black schoolchildren who were eating such high fiber diets--whole grains, legumes, nuts, vegetables, fruits, and wild greens--that 90% of them could produce a stool on demand. Stuffed from head to tail with plants, they could give you a stool sample at any time, just as easy as getting a urine sample. It was hard to even get access to the white kids, though, who were reluctant to participate in such investigations, even though they were given waxed cartons fitted with lids while all the black kids got was a plate and a square of paper towel.

The researchers found significantly lower fecal pH in those eating the traditional, rural plant-based diets compared to those eating the traditional Western diet, who were eating far fewer whole plant foods than the black children. But, remove some of those whole plant foods, like switch their corn for white bread for just a few days and their stool pH goes up, and add whole plant foods like an extra five to seven servings of fruit every day, and their stool pH goes down even further and gets more acidic. It makes sense because when you ferment fruits, veggies, and grains, they turn sour, like vinegar, sauerkraut, or sourdough, because good bacteria like lactobacillus produce organic acids like lactic acid. Those who eat a lot of plants have more of those good bugs. So, using the purple cabbage test highlighted in my video, Testing Your Diet with Pee & Purple Cabbage, we want blue pee, but pink poo.

If you compare the fecal samples of those eating vegetarian or vegan to those eating standard diets, plant-based diets appear to shift the makeup of the bacteria in our gut, resulting in a significantly lower stool pH, and the more plant-based, the lower the pH dropped. It's like a positive feedback loop: fiber-eating bacteria produce the acids to create the pH at which fiber-eating bacteria thrive while suppressing the group of less beneficial bugs.

It might taken even as little as two weeks to bring stool pH down on a plant-based diet. In a study published in the British Journal of Cancer, a dozen volunteers carefully selected for their trustworthiness and randomized to sequentially go on regular, vegetarian, or vegan diets and two weeks in, a significant drop in fecal pH was achieved eating completely plant-based.

But there are differing qualities of plant-based diets. For example, the two groups followed in the study I mentioned earlier had dramatically different stool pH, yet both groups were vegetarian. The high risk group was eating mostly refined grains, very little fiber, whereas the low risk group was eating whole grains and beans, packed with fiber for our fiber-friendly flora to munch on.

Just as a "reduction of high serum cholesterol contributes to the avoidance of coronary heart disease," a fall in the fecal pH value may contribute to the avoidance of bowel cancer and through the same means, eating more whole plant foods.

More on colon cancer prevention in:

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: Kitti Sukhonthanit © 123RF.com. This image has been modified.

Original Link