Does Rye Bread Protect Against Cancer?

Sept 14 Rye Bread copy.jpeg

Previously, I've explored the beneficial effects of flaxseeds on prostate cancer (Flaxseeds vs. Prostate Cancer), as well as breast cancer prevention and survival (Flaxseeds & Breast Cancer Prevention and Breast Cancer Survival & Lignan Intake). The cancer-fighting effect of flaxseeds is thought to be because of the lignans, which are cancer-fighting plant compounds found in red wine, whole grains, greens (cruciferous vegetables), and especially sesame seeds and flaxseeds, the most concentrated source on Earth. But this is based on per unit weight. People eat a lot more grains than seeds. Of the grains people eat, the highest concentration of lignans is found in rye. So, can rye intake decrease the risk of cancer? Theoretically yes, but unlike flaxseeds, it's never been directly put to the test... until now.

In my video Does Rye Bread Protect Against Cancer?, I discuss the evidence that does exist. If you measure the levels of lignans in the bloodstream of women living in a region where they eat lots of rye, the odds of breast cancer in women with the highest levels do seem to be just half that of women with the lowest levels. But lignans are also found in tea and berries, so we couldn't be sure where the protection is coming from. To get around this, researchers decided to measure alkylresorcinol metabolites, a class of phytonutrients relatively unique to whole grains.

Researchers collected urine from women with breast cancer and women without, and the women with breast cancer had significantly lower levels compared to those without. This suggests that women at risk for breast cancer consume significantly lower amounts of whole grains like rye. But if we follow older women in their 50s through 60s, the intake of whole grain products was not associated with risk of breast cancer. A similar result was found in older men for prostate cancer. Is it just too late at that point?

We know from data on dairy that diet in our early life may be important in the development of prostate cancer, particularly around puberty when the prostate grows and matures. If you look at what men were drinking in adolescence, daily milk consumption appeared to triple their risk of advanced prostate cancer later in life. (Learn more about milk and prostate cancer in my video Prostate Cancer and Organic Milk vs. Almond Milk.) So, researchers looked at daily rye bread consumption during adolescence.

Those who consumed rye bread daily as kids did appear to only have half the odds of advanced prostate cancer. This is consistent with immigrant studies suggesting that the first two decades of life may be most important for setting the pattern for cancer development in later life. These findings are certainly important for how we should feed our kids, but if we're already middle-aged, is it too late to change course? To answer this question, researchers in Sweden put it to the test.

Researchers took men with prostate cancer and split them into two groups. One group got lots of rye bread, while the other got lots of high-fiber, but low-lignan, wheat bread. There's been some indirect evidence that rye may be active against prostate cancer--like lower cancer rates in regions with high rye consumption--but it had never been directly investigated... until this study. Biopsies were taken from the subjects' tumors before and after three weeks of bread eating, and the number of cancer cells that were dying off were counted. Though there was no change in the cancer cell clearance of the control bread group, there was a 180% increase in the number of cancer cells being killed off in the rye group. A follow-up study lasting 6 weeks found a 14% decrease in PSA levels, a cancer marker suggesting a shrinkage of the tumor.

The researchers note they used very high rye bread intakes, and it remains to be tested if more normal intake levels would have effects that are of clinical importance. As a sadly typical American, my lack of intimate familiarity of the metric system did not flag the "485 grams" of rye bread a day as far out of the ordinary, but that translates to 15 slices! Rather than eating a loaf a day, the same amount of lignans can be found in a single teaspoon of ground flaxseeds.


I've created several videos on flaxseeds for both breast cancer prevention and treatment, including Flaxseeds & Breast Cancer Prevention, Breast Cancer Survival and Lignan Intake, Flaxseeds & Breast Cancer Survival Epidemiological Evidence, and Flaxseeds & Breast Cancer Survival: Clinical Evidence.

What's more, flaxseeds may help with cyclical breast pain (Flaxseeds for Breast Pain), prostate cancer (Flaxseed vs. Prostate Cancer), diabetes (Flaxseeds vs. Diabetes), and hypertension (Flaxseeds for Hypertension).

And if you're wondering Which Are Better: Chia Seeds or Flaxseeds?, get the answer in the video!

The wonders of whole grains are also discussed in Whole Grains May Work as Well as Drugs, Can Oatmeal Reverse Heart Disease?, and Can Oatmeal Help Fatty Liver 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:

Original Link

Does Rye Bread Protect Against Cancer?

Sept 14 Rye Bread copy.jpeg

Previously, I've explored the beneficial effects of flaxseeds on prostate cancer (Flaxseeds vs. Prostate Cancer), as well as breast cancer prevention and survival (Flaxseeds & Breast Cancer Prevention and Breast Cancer Survival & Lignan Intake). The cancer-fighting effect of flaxseeds is thought to be because of the lignans, which are cancer-fighting plant compounds found in red wine, whole grains, greens (cruciferous vegetables), and especially sesame seeds and flaxseeds, the most concentrated source on Earth. But this is based on per unit weight. People eat a lot more grains than seeds. Of the grains people eat, the highest concentration of lignans is found in rye. So, can rye intake decrease the risk of cancer? Theoretically yes, but unlike flaxseeds, it's never been directly put to the test... until now.

In my video Does Rye Bread Protect Against Cancer?, I discuss the evidence that does exist. If you measure the levels of lignans in the bloodstream of women living in a region where they eat lots of rye, the odds of breast cancer in women with the highest levels do seem to be just half that of women with the lowest levels. But lignans are also found in tea and berries, so we couldn't be sure where the protection is coming from. To get around this, researchers decided to measure alkylresorcinol metabolites, a class of phytonutrients relatively unique to whole grains.

Researchers collected urine from women with breast cancer and women without, and the women with breast cancer had significantly lower levels compared to those without. This suggests that women at risk for breast cancer consume significantly lower amounts of whole grains like rye. But if we follow older women in their 50s through 60s, the intake of whole grain products was not associated with risk of breast cancer. A similar result was found in older men for prostate cancer. Is it just too late at that point?

We know from data on dairy that diet in our early life may be important in the development of prostate cancer, particularly around puberty when the prostate grows and matures. If you look at what men were drinking in adolescence, daily milk consumption appeared to triple their risk of advanced prostate cancer later in life. (Learn more about milk and prostate cancer in my video Prostate Cancer and Organic Milk vs. Almond Milk.) So, researchers looked at daily rye bread consumption during adolescence.

Those who consumed rye bread daily as kids did appear to only have half the odds of advanced prostate cancer. This is consistent with immigrant studies suggesting that the first two decades of life may be most important for setting the pattern for cancer development in later life. These findings are certainly important for how we should feed our kids, but if we're already middle-aged, is it too late to change course? To answer this question, researchers in Sweden put it to the test.

Researchers took men with prostate cancer and split them into two groups. One group got lots of rye bread, while the other got lots of high-fiber, but low-lignan, wheat bread. There's been some indirect evidence that rye may be active against prostate cancer--like lower cancer rates in regions with high rye consumption--but it had never been directly investigated... until this study. Biopsies were taken from the subjects' tumors before and after three weeks of bread eating, and the number of cancer cells that were dying off were counted. Though there was no change in the cancer cell clearance of the control bread group, there was a 180% increase in the number of cancer cells being killed off in the rye group. A follow-up study lasting 6 weeks found a 14% decrease in PSA levels, a cancer marker suggesting a shrinkage of the tumor.

The researchers note they used very high rye bread intakes, and it remains to be tested if more normal intake levels would have effects that are of clinical importance. As a sadly typical American, my lack of intimate familiarity of the metric system did not flag the "485 grams" of rye bread a day as far out of the ordinary, but that translates to 15 slices! Rather than eating a loaf a day, the same amount of lignans can be found in a single teaspoon of ground flaxseeds.


I've created several videos on flaxseeds for both breast cancer prevention and treatment, including Flaxseeds & Breast Cancer Prevention, Breast Cancer Survival and Lignan Intake, Flaxseeds & Breast Cancer Survival Epidemiological Evidence, and Flaxseeds & Breast Cancer Survival: Clinical Evidence.

What's more, flaxseeds may help with cyclical breast pain (Flaxseeds for Breast Pain), prostate cancer (Flaxseed vs. Prostate Cancer), diabetes (Flaxseeds vs. Diabetes), and hypertension (Flaxseeds for Hypertension).

And if you're wondering Which Are Better: Chia Seeds or Flaxseeds?, get the answer in the video!

The wonders of whole grains are also discussed in Whole Grains May Work as Well as Drugs, Can Oatmeal Reverse Heart Disease?, and Can Oatmeal Help Fatty Liver 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:

Original Link

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

How to Design a Misleading Study to Show Diet Doesn’t Work

How to Design a Misleading Study to Show Diet Doesn't Work.jpeg

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

There's more great information in my video Diverticulosis: When Our Most Common Gut Disorder Hardly Existed.

This reminds me of an ancient video I did: Flawed Study Interpretation.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

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: Yoshihide Nomura / Flickr. This image has been modified.

Original Link

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease.jpeg

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

What, then, do we make of a new study concluding that a low-fiber diet was not associated with diverticulosis. I cover that in my video Does Fiber Really Prevent Diverticulosis?

For more on bowel health, see:

What if your doctor says you shouldn't eat healthy foods like nuts and popcorn because of your diverticulosis? Share with them my Diverticulosis & Nuts video.

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: Sean T Evans / Flickr. This image has been modified.

Original Link

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease

9 out of 10 That Die From it Never Knew They Even Had This Preventable Disease.jpeg

Diverticula are out-pouchings of our intestine. Doctors like using a tire analogy: high pressures within the gut can force the intestines to balloon out through weak spots in the intestinal wall like an inner tube poking out through a worn tire tread. You can see what they actually look like in my video, Diverticulosis: When Our Most Common Gut Disorder Hardly Existed. These pockets can become inflamed and infected, and, to carry the tire analogy further, can blow out and spill fecal matter into the abdomen, and lead to death. Symptoms can range from no symptoms at all, to a little cramping and bloating, to "incapacitating pain that is a medical emergency." Nine out of ten people who die from the disease never even knew they had it.

The good news is there may be a way to prevent the disease. Diverticular disease is the most common intestinal disorder, affecting up to 70% of people by age 60. If it's that common, though, is it just an inevitable consequence of aging? No, it's a new disease. In 1907, 25 cases had been reported in the medical literature. Not cases in 25% of people, but 25 cases period. And diverticular disease is kind of hard to miss on autopsy. A hundred years ago, in 1916, it didn't even merit mention in medical and surgical textbooks. The mystery wasn't solved until 1971.

How did a disease that was almost unknown become the most common affliction of the colon in the Western world within one lifespan? Surgeons Painter and Burkitt suggested diverticulosis was a deficiency disease--i.e., a disease caused by a deficiency of fiber. In the late 1800s, roller milling was introduced, further removing fiber from grain, and we started to fill up on other fiber-deficient foods like meat and sugar. A few decades of this and diverticulosis was rampant.

This is what Painter and Burkitt thought was going on: Just as it would be easy to squeeze a lump of butter through a bicycle tube, it's easy to move large, soft, and moist intestinal contents through the gut. In contrast, try squeezing through a lump of tar. When we eat fiber-deficient diets, our feces can become small and firm, and our intestines have to really squeeze down hard to move them along. This buildup of pressure may force out those bulges. Eventually, a low-fiber diet can sometimes lead to the colon literally rupturing itself.

If this theory is true, then populations eating high­-fiber diets would have low rates of diverticulosis. That's exactly what's been found. More than 50% of African Americans in their 50s were found to have diverticulosis, compared to less than 1% in African Africans eating traditional plant-based diets. By less than 1%, we're talking zero out of a series of 2,000 autopsies in South Africa and two out of 4,000 in Uganda. That's about one thousand times lower prevalence.

What, then, do we make of a new study concluding that a low-fiber diet was not associated with diverticulosis. I cover that in my video Does Fiber Really Prevent Diverticulosis?

For more on bowel health, see:

What if your doctor says you shouldn't eat healthy foods like nuts and popcorn because of your diverticulosis? Share with them my Diverticulosis & Nuts video.

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: Sean T Evans / Flickr. This image has been modified.

Original Link

The 3 Vitamins that Prevent Brain Loss

The 3 Vitamins that Prevent Brain Loss.jpeg

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

This is very similar to the findings in my video Vitamin B12 Necessary for Arterial Health.

For more details on ensuring a regular reliable source of vitamin B12:

There are more benefits to lowering your methionine intake. Check out Methionine Restriction as a Life Extension Strategy and Starving Cancer with Methionine Restriction.

For more on brain health in general, see 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:

Image Credit: Thomas Hawk / Flickr. This image has been modified.

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The 3 Vitamins that Prevent Brain Loss

The 3 Vitamins that Prevent Brain Loss.jpeg

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

This is very similar to the findings in my video Vitamin B12 Necessary for Arterial Health.

For more details on ensuring a regular reliable source of vitamin B12:

There are more benefits to lowering your methionine intake. Check out Methionine Restriction as a Life Extension Strategy and Starving Cancer with Methionine Restriction.

For more on brain health in general, see 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:

Image Credit: Thomas Hawk / Flickr. This image has been modified.

Original Link

Optimal Bowel Movement Position

Optimal Bowel Movement Position.jpeg

Compared to rural African populations eating traditional plant-based diets, white South Africans and black and white Americans have more than 50 times more heart disease, 10 times more colon cancer, more than 50 times more gallstones and appendicitis, and more than 25 times the rates of "pressure diseases"--diverticulitis, hemorrhoids, varicose veins, and hiatal hernia.

As I discussed in my Should You Sit, Squat, or Lean During a Bowel Movement?, bowel movements should be effortless. When we have to strain at stool, the pressure may balloon out-pouchings from our colon, causing diverticulosis; inflate hemorrhoids around the anus; cause the valves in the veins of our legs to fail, causing varicose veins; and even force part of the stomach up through the diaphragm into our chest cavity, causing a hiatal hernia (as I covered previously). When this was first proposed by Dr. Denis Burkitt, he blamed these conditions on the straining caused by a lack of fiber in the diet. He did, however, acknowledge there were alternative explanations. For example, in rural Africa, they used a traditional squatting position when they defecated, which may have taken off some of the pressure.

For hundreds of thousands of years, everyone used the squatting position, which may help by straightening the "anorectal angle." There's actually a kink at almost a 90-degree angle right at the end of the rectum that helps keep us from pooping our pants when we're just out walking around. That angle only slightly straightens out in a common sitting posture on the toilet. Maximal straightening out of this angle occurs in a squatting posture, potentially permitting smoother defecation. (I remember sitting in geometry class wondering when I'd ever use the stuff I was learning. Little did I know I would one day be calculating anorectal angles with it! Stay in school, kids :)

How did they figure this out? Researchers filled latex tubes with a radiopaque fluid, stuck them up some volunteers, and took X-rays with the hips flexed at various angles. They concluded that flexing the knees towards the chest like one does when squatting may straighten that angle and reduce the amount of pressure needed to empty the rectum. This idea wasn't directly put to the test until 2002, when researchers used defecography (which are X-rays taken while the person is defecating) on subjects in sitting and squatting positions. Indeed, squatting increased the anorectal angle from around 90 degrees all the way up to about 140.

So should we all get one of those little stools for our stools, like the Squatty Potty that you put in front of your toilet to step on? No, they don't seem to work. Researchers tried adding a footstool to decrease sitting height, but it didn't seem to significantly affect the time it took to empty one's bowels or decrease the difficulty of defecating. They tried even higher footstools, but people complained of extreme discomfort using them. Nothing seemed to compare with actual squatting, which may give the maximum advantage. However, in developed nations, it may not be convenient. But, we can achieve a similar effect by leaning forward as we sit, with our hands on or near the floor. The researchers advise all sufferers from constipation to adopt this forward-leaning position when defecating, as the weight of our torso pressing against the thighs may put an extra squeeze on our colons.

Instead of finding ways to add more pressure, why not get to the root of the problem? "The fundamental cause of straining is the effort required to pass unnaturally firm stools." By manipulating the anorectal angle through squatting or leaning, we can more easily pass unnaturally firm stools. But why not just treat the cause and eat enough fiber-containing whole plant foods to create stools so large and soft that you could pass them effortlessly at any angle?

Famed cardiologist Dr. Joel Kahn once said that you know you know you're eating a plant-based diet when "you take longer to pee than to poop."

In all seriousness, even squatting does not significantly decrease the pressure gradient that may cause a hiatal hernia. It does not prevent the pressure transmission down into the legs that may cause varicose veins. And this is not just a cosmetic issue. Protracted straining can cause heart rhythm disturbances and reduction in blood flow to the heart and brain, resulting in defecation-related fainting and death. Just 15 seconds of straining can temporarily cut blood flow to the brain by 21% and blood flow to the heart by nearly one-half, thereby providing a mechanism for the well-known "bed pan death" syndrome. If you think you have to strain a lot while sitting, try having a bowel movement on your back. Bearing down for just a few seconds can send our blood pressure up to nearly 170 over 110, which may help account for the notorious frequency of sudden and unexpected deaths of patients while using bed pans in hospitals. Hopefully, if we eat healthy enough, we won't end up in the hospital to begin with.

Wondering How Many Bowel Movements Should You Have Every Day? Watch the video to find out!

The "forcing part of your stomach up through the diaphragm into our chest cavity" phenomenon is covered in my video Diet and Hiatal Hernia. The "ballooning of out-pouchings from our colon" is called diverticulosis. There's a video I did about 6 years ago (Diverticulosis & Nuts), but I have some new and improved ones available: Diverticulosis: When Our Most Common Gut Disorder Hardly Existed and Does Fiber Really Prevent Diverticulosis?

More on that extraordinary African data here:

So excited to be able to slip in a plug for Dr. Kahn's work. His brand of "interpreventional cardiology" can be found at www.drjoelkahn.com.

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