Antioxidant- and Folate-Rich Foods for Depression

Antioxidant- and Folate-Rich Foods for Depression.jpeg

According to the Centers for Disease Control and Prevention, the rates of all of our top 10 killers have fallen or stabilized except for one, suicide. As shown in my video, Antioxidants & Depression, accumulating evidence indicates that free radicals may play important roles in the development of various neuropsychiatric disorders including major depression, a common cause of suicide.

In a study of nearly 300,000 Canadians, for example, greater fruit and vegetable consumption was associated with lower odds of depression, psychological distress, self-reported mood and anxiety disorders and poor perceived mental health. They conclude that since a healthy diet comprised of a high intake of fruits and vegetables is rich in anti-oxidants, it may consequently dampen the detrimental effects of oxidative stress on mental health.

But that study was based on asking how many fruits and veggies people ate. Maybe people were just telling the researchers what they thought they wanted to hear. What if you actually measure the levels of carotenoid phytonutrients in people's bloodstreams? The same relationship is found. Testing nearly 2000 people across the United States, researchers found that a higher total blood carotenoid level was indeed associated with a lower likelihood of elevated depressive symptoms, and there appeared to be a dose-response relationship, meaning the higher the levels, the better people felt.

Lycopene, the red pigment predominantly found in tomatoes (but also present in watermelon, pink grapefruit, guava and papaya) is the most powerful carotenoid antioxidant. In a test tube, it's about 100 times more effective at quenching free radicals than a more familiar antioxidant like vitamin E.

Do people who eat more tomatoes have less depression, then? Apparently so. A study of about a thousand older men and women found that those who ate the most tomato products had only about half the odds of depression. The researchers conclude that a tomato-rich diet may have a beneficial effect on the prevention of depressive symptoms.

Higher consumption of fruits and vegetables has been found to lead to a lower risk of developing depression, but if it's the antioxidants can't we just take an antioxidant pill? No.

Only food sources of antioxidants were protectively associated with depression. Not antioxidants from dietary supplements. Although plant foods and food-derived phytochemicals have been associated with health benefits, antioxidants from dietary supplements appear to be less beneficial and may, in fact, be detrimental to health. This may indicate that the form and delivery of the antioxidants are important. Alternatively, the observed associations may be due not to antioxidants but rather to other dietary factors, such as folate, that also occur in plant-rich diets.

In a study of thousands of middle-aged office workers, eating lots of processed food was found to be a risk factor for at least mild to moderate depression five years later, whereas a whole food pattern was found to be protective. Yes, it could be because of the high content of antioxidants in fruits and vegetables but could also be the folate in greens and beans, as some studies have suggested an increased risk of depression in folks who may not have been eating enough.

Low folate levels in the blood are associated with depression, but since most of the early studies were cross-sectional, meaning a snapshot in time, we didn't know if the low folate led to depression or the depression led to low folate. Maybe when you have the blues you don't want to eat the greens.

But since then a number of cohort studies were published, following people over time. They show that a low dietary intake of folate may indeed be a risk factor for severe depression, as much as a threefold higher risk. Note this is for dietary folate intake, not folic acid supplements; those with higher levels were actually eating healthy foods. If you give people folic acid pills they don't seem to work. This may be because folate is found in dark green leafy vegetables like spinach, whereas folic acid is the oxidized synthetic compound used in food fortification and dietary supplements because it's more shelf-stable. It may have different effects on the body as I previously explored in Can Folic Acid Be Harmful?

These kinds of findings point to the importance of antioxidant food sources rather than dietary supplements. But there was an interesting study giving people high dose vitamin C. In contrast to the placebo group, those given vitamin C experienced a decrease in depression scores and also greater FSI. What is FSI? Frequency of Sexual Intercourse.

Evidently, high dose vitamin C improves mood and intercourse frequency, but only in sexual partners that don't live with one another. In the placebo group, those not living together had sex about once a week, and those living together a little higher, once every five days, with no big change on vitamin C. But for those not living together, on vitamin C? Every other day! The differential effect for non-cohabitants suggests that the mechanism is not a peripheral one, meaning outside the brain, but a central one--some psychological change which motivates the person to venture forth to have intercourse. The mild antidepressant effect they found was unrelated to cohabitation or frequency, so it does not appear that the depression scores improved just because of the improved FSI.

For more mental health video, see:

Anything else we can do to enhance our sexual health and attractiveness? See:

In health,

Michael Greger, M.D.

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

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

Original Link

Antioxidant- and Folate-Rich Foods for Depression

Antioxidant- and Folate-Rich Foods for Depression.jpeg

According to the Centers for Disease Control and Prevention, the rates of all of our top 10 killers have fallen or stabilized except for one, suicide. As shown in my video, Antioxidants & Depression, accumulating evidence indicates that free radicals may play important roles in the development of various neuropsychiatric disorders including major depression, a common cause of suicide.

In a study of nearly 300,000 Canadians, for example, greater fruit and vegetable consumption was associated with lower odds of depression, psychological distress, self-reported mood and anxiety disorders and poor perceived mental health. They conclude that since a healthy diet comprised of a high intake of fruits and vegetables is rich in anti-oxidants, it may consequently dampen the detrimental effects of oxidative stress on mental health.

But that study was based on asking how many fruits and veggies people ate. Maybe people were just telling the researchers what they thought they wanted to hear. What if you actually measure the levels of carotenoid phytonutrients in people's bloodstreams? The same relationship is found. Testing nearly 2000 people across the United States, researchers found that a higher total blood carotenoid level was indeed associated with a lower likelihood of elevated depressive symptoms, and there appeared to be a dose-response relationship, meaning the higher the levels, the better people felt.

Lycopene, the red pigment predominantly found in tomatoes (but also present in watermelon, pink grapefruit, guava and papaya) is the most powerful carotenoid antioxidant. In a test tube, it's about 100 times more effective at quenching free radicals than a more familiar antioxidant like vitamin E.

Do people who eat more tomatoes have less depression, then? Apparently so. A study of about a thousand older men and women found that those who ate the most tomato products had only about half the odds of depression. The researchers conclude that a tomato-rich diet may have a beneficial effect on the prevention of depressive symptoms.

Higher consumption of fruits and vegetables has been found to lead to a lower risk of developing depression, but if it's the antioxidants can't we just take an antioxidant pill? No.

Only food sources of antioxidants were protectively associated with depression. Not antioxidants from dietary supplements. Although plant foods and food-derived phytochemicals have been associated with health benefits, antioxidants from dietary supplements appear to be less beneficial and may, in fact, be detrimental to health. This may indicate that the form and delivery of the antioxidants are important. Alternatively, the observed associations may be due not to antioxidants but rather to other dietary factors, such as folate, that also occur in plant-rich diets.

In a study of thousands of middle-aged office workers, eating lots of processed food was found to be a risk factor for at least mild to moderate depression five years later, whereas a whole food pattern was found to be protective. Yes, it could be because of the high content of antioxidants in fruits and vegetables but could also be the folate in greens and beans, as some studies have suggested an increased risk of depression in folks who may not have been eating enough.

Low folate levels in the blood are associated with depression, but since most of the early studies were cross-sectional, meaning a snapshot in time, we didn't know if the low folate led to depression or the depression led to low folate. Maybe when you have the blues you don't want to eat the greens.

But since then a number of cohort studies were published, following people over time. They show that a low dietary intake of folate may indeed be a risk factor for severe depression, as much as a threefold higher risk. Note this is for dietary folate intake, not folic acid supplements; those with higher levels were actually eating healthy foods. If you give people folic acid pills they don't seem to work. This may be because folate is found in dark green leafy vegetables like spinach, whereas folic acid is the oxidized synthetic compound used in food fortification and dietary supplements because it's more shelf-stable. It may have different effects on the body as I previously explored in Can Folic Acid Be Harmful?

These kinds of findings point to the importance of antioxidant food sources rather than dietary supplements. But there was an interesting study giving people high dose vitamin C. In contrast to the placebo group, those given vitamin C experienced a decrease in depression scores and also greater FSI. What is FSI? Frequency of Sexual Intercourse.

Evidently, high dose vitamin C improves mood and intercourse frequency, but only in sexual partners that don't live with one another. In the placebo group, those not living together had sex about once a week, and those living together a little higher, once every five days, with no big change on vitamin C. But for those not living together, on vitamin C? Every other day! The differential effect for non-cohabitants suggests that the mechanism is not a peripheral one, meaning outside the brain, but a central one--some psychological change which motivates the person to venture forth to have intercourse. The mild antidepressant effect they found was unrelated to cohabitation or frequency, so it does not appear that the depression scores improved just because of the improved FSI.

For more mental health video, see:

Anything else we can do to enhance our sexual health and attractiveness? See:

In health,

Michael Greger, M.D.

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

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

Original Link

What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

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: GraphicStock. This image has been modified.

Original Link

What Is the Cause of ALS?

What Is the Cause of ALS?.jpeg

Lou Gehrig's disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random. Of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.

ALS is more common than generally recognized, with an incidence rate now close to that of multiple sclerosis. What causes it? 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease!

Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating from it. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that's what was causing such high levels of ALS? But the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat a thousand kilograms a day to get a toxic dose--that's around a ton of seeds daily. So, the whole cycad theory was thrown out and the trail went cold.

But then famed neurologist Oliver Sachs and colleagues had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats (also known as flying foxes) who ate Cycad tree seeds. So maybe this is a case of biomagnification up the food chain, as about a "tons" worth of BMAA does accumulate in the flesh of flying foxes.

The final nail in the coffin was the detection of high levels of BMMA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people that died. So with the final puzzle piece apparently in place, the solution was found to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson's disease and dementia, so they called it ALS parkinsonism dementia complex. So when the researchers were choosing a comparison group control brains, they also included two cases of Alzheimer's disease. But these brains had BMAA in their brains too. And not only that, but these were Alzheimer's victims in Canada, on the opposite side of the globe. So the researchers ran more autopsies and found no BMAA in the control brains, but BMAA detected in all the Canadian Alzheimer's victims tested.

Canadians don't eat fruit bats. What was going on? Well, the neurotoxin isn't made by the bat, it's made by the trees, although Canadians don't eat cycad trees either. It turns out that cycad trees don't make the neurotoxin either; it's actually a blue-green algae that grows in the roots of the cycad trees which makes the BMAA that gets in the seeds, which gets in the bats, that finally gets into the people. And it's not just this specific type of blue-green algae, but nearly all types of blue-green algae found all over the world produce BMAA. Up until only about a decade ago we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world; from Europe to the U.S., Australia, the Middle East, and elsewhere.

If these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases including ALS worldwide. Researchers in Miami put it to the test and found BMAA in the brains of Floridians who died from sporadic Alzheimer's disease and ALS, but not in the brains of those that died of a different neurodegenerative disease called Huntington's, which we know is caused by a genetic mutation, not some neurotoxin. They found significant levels of BMAA in 49 out of 50 samples from 12 Alzheimer's patients and 13 ALS patients. The results (shown in the my video ALS: Fishing for Answers) for American Alzheimer's and ALS patients from the Atlantic southeast and from Canadian Alzheimer's patients from the Pacific Northwest suggested that exposure to BMAA was widespread. The same thing was then found in the brains of those dying from Parkinson's disease. You can apparently even pick up more BMAA in the hair of live ALS patients compared to controls.

So is BMAA present in Florida seafood? Yes, in freshwater fish and shellfish, like oysters and bass, and out in the ocean as well. Some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam.

In the U.S., fish may be the fruit bats.

Maybe the ice bucket challenge should be to not serve seafood in them. See my video Diet and Amyotrophic Lateral Sclerosis (ALS) for more.

Diet may also play a role in other neurodegenerative disorders:

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: GraphicStock. This image has been modified.

Original Link

Starch-Blocking Foods for Diabetics?

NF-Dec29 Diabetics Should Take Their Pulses.jpg

How did doctors treat diabetes before insulin? Almost a thousand medicinal plants are known antidiabetic agents, including beans, most of which have been used in traditional medicine. Of course, just because something has been used for centuries doesn't mean it's safe. Other treatments for diabetes in the past included arsenic and uranium. Thankfully many of these other remedies fell by the wayside, but scientific interest in the antidiabetic potential of beans was renewed in the past decade.

Diabetes is a global public health epidemic. Although oral hypoglycemic medications and injected insulin are the mainstay of treatment of diabetes and are effective in controlling high blood sugars, they have side effects such as weight gain, swelling, and liver disease. They also are not shown to significantly alter the progression of the disease. Thankfully, lifestyle modifications have proven to be greatly effective in the management of this disease. And if there is one thing diabetics should eat, it's legumes (beans, chickpeas, split peas, and lentils).

Increased consumption of whole grains and legumes for health-promoting diets is widely promoted by health professionals. One of the reasons is that they may decrease insulin resistance, the defining trait of type 2 diabetes. The European Association for the Study of Diabetes, the Canadian Diabetes Association and the American Diabetes Association all recommend the consumption of dietary pulses as a means of optimizing diabetes control. What are pulses? They're peas and beans that come dried, and are therefore a subset of legumes. They exclude green beans and fresh green peas, which are considered more vegetable crops, and the so-called oil seeds--soybeans and peanuts.

A review out of Canada (highlighted in my video, Diabetes Should Take Their Pulses) compiled 41 randomized controlled experimental trials, totaling more than a thousand patients, and corroborated the diabetes association nutrition guidelines recommending the consumption of pulses as a means of optimizing diabetes control. They discovered that some pulses are better than others. Some of the best results came from the studies that used chickpeas. In terms of beans, pintos and black beans may beat out kidney beans. Compared to the blood sugar spike of straight white rice, the combination of black or pinto beans with rice appeared to reduce the spike more than kidney beans and rice.

Dark red kidney beans may not be as effective because they have lower levels of indigestible starch. One of the reasons beans are so healthy is they contain compounds that partially block our starch-digesting enzyme, which allows some starch to make it down to our colon to feed our good gut bacteria. In fact, the inhibition of this starch-eating enzyme amylase, just by eating beans, approximates that of a carbohydrate-blocking drug called acarbose (sold as Precose), a popular diabetes medication. The long-term use of beans may normalize hemoglobin A1C levels (which is how you track diabetes) almost as well as the drug.

What about avoiding metabolic derangements in the first place? See my video Preventing Prediabetes By Eating More.

What else may help?

What may hurt?

-Michael Greger, M.D.

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

Image Credit: Emily Carlin / Flickr

Original Link