Sushi Worm Parasite

Sushi Worm Parasite.jpeg

There was a report recently of a woman in San Francisco suffering from gnathostomiasis. I had learned about the disease while I was in medical school, but never actually saw a case. Evidently, it's now on the rise. Clinically, the disease commonly presents as "migratory cutaneous swelling" (bumps on the skin that move around). Why? Because there's a worm under there that migrates through the tissues under the skin and causes recurring episodes of migratory swelling or creeping eruptions. The worm's head has rings of little hooks that allow it to burrow through tissue. There is no effective treatment, other than removal of the worm. Since humans are basically dead-end hosts for the larva, they can't develop into mature worms. The symptoms patients experience are due to the organism wandering throughout the body (see Migratory Skin Worms from Sushi).

In addition to burrowing under our skin, it can also crawl into our eyeballs. The 42-year-old woman is described as having a four-year history of migratory swellings on her face, then a little bleeding from the eyelid... and we know where this is going. No problem, though! We can make a little cut, stick in some forceps, locate the worm, and then just pull the sucker right out of the eyeball. If you have any pimples on your face that move around, better to have your doctor grab them before they start swimming around in your eyes.

By far the most serious manifestation is when they get into your brain. As the worm migrates along the nerves, the patient can experience excruciating pain. The condition can lead to paralysis, bleeding in the brain, and finally death. However, in non-cerebral disease, it's the worms that die, though it may take about 12 years.

How do the worms get into our brain, causing so-called neurognathostomiasis? Gnathostoma worms are highly invasive parasites. After you leave the sushi bar, the larvae can penetrate the wall of your intestine. They can then enter the brain through the base of the skull, crawling along the spinal nerves and vessels. They start out in the nerve roots, enter the spinal cord, and then can climb up into the brain. The worm isn't poisonous or anything; it's just the migration of the worm through the body that causes direct mechanical injury because of tearing of nerve tissues.

The bottom line: This diagnosis should be considered in patients who present with nonspecific little lumps and bumps, especially when there is a history of frequent consumption of raw fish.

Thankfully, most raw foodists stick to plants and thereby avoid scenarios like this: A 21-year-old woman experienced acute, severe pain in her mouth immediately after swallowing a raw squid. It seems consuming a squid with "sperm bags and an active ejaculatory apparatus" can result in the "unintended ejection of the sperm bag" and injury to the oral cavity. The researchers conclude that eating raw food, especially living organisms, can be risky. Though some living organisms (plants!) may be substantially less risky than others.

This is like my Tongue Worm in Human Eye or Cheese Mites and Maggots videos. Extremely rare, but extremely fascinating (to me at least!).

There is one parasitic infection that is much more common and a major cause of disability worldwide,though, neurocysticercosis:

I think the only other sushi videos I have are Fecal Contamination of Sushi and Allergenic Fish Worms, though the nori seaweed is good for you (Which Seaweed Is Most Protective Against Breast Cancer? and Avoiding Iodine Deficiency).

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

Original Link

Sushi Worm Parasite

Sushi Worm Parasite.jpeg

There was a report recently of a woman in San Francisco suffering from gnathostomiasis. I had learned about the disease while I was in medical school, but never actually saw a case. Evidently, it's now on the rise. Clinically, the disease commonly presents as "migratory cutaneous swelling" (bumps on the skin that move around). Why? Because there's a worm under there that migrates through the tissues under the skin and causes recurring episodes of migratory swelling or creeping eruptions. The worm's head has rings of little hooks that allow it to burrow through tissue. There is no effective treatment, other than removal of the worm. Since humans are basically dead-end hosts for the larva, they can't develop into mature worms. The symptoms patients experience are due to the organism wandering throughout the body (see Migratory Skin Worms from Sushi).

In addition to burrowing under our skin, it can also crawl into our eyeballs. The 42-year-old woman is described as having a four-year history of migratory swellings on her face, then a little bleeding from the eyelid... and we know where this is going. No problem, though! We can make a little cut, stick in some forceps, locate the worm, and then just pull the sucker right out of the eyeball. If you have any pimples on your face that move around, better to have your doctor grab them before they start swimming around in your eyes.

By far the most serious manifestation is when they get into your brain. As the worm migrates along the nerves, the patient can experience excruciating pain. The condition can lead to paralysis, bleeding in the brain, and finally death. However, in non-cerebral disease, it's the worms that die, though it may take about 12 years.

How do the worms get into our brain, causing so-called neurognathostomiasis? Gnathostoma worms are highly invasive parasites. After you leave the sushi bar, the larvae can penetrate the wall of your intestine. They can then enter the brain through the base of the skull, crawling along the spinal nerves and vessels. They start out in the nerve roots, enter the spinal cord, and then can climb up into the brain. The worm isn't poisonous or anything; it's just the migration of the worm through the body that causes direct mechanical injury because of tearing of nerve tissues.

The bottom line: This diagnosis should be considered in patients who present with nonspecific little lumps and bumps, especially when there is a history of frequent consumption of raw fish.

Thankfully, most raw foodists stick to plants and thereby avoid scenarios like this: A 21-year-old woman experienced acute, severe pain in her mouth immediately after swallowing a raw squid. It seems consuming a squid with "sperm bags and an active ejaculatory apparatus" can result in the "unintended ejection of the sperm bag" and injury to the oral cavity. The researchers conclude that eating raw food, especially living organisms, can be risky. Though some living organisms (plants!) may be substantially less risky than others.

This is like my Tongue Worm in Human Eye or Cheese Mites and Maggots videos. Extremely rare, but extremely fascinating (to me at least!).

There is one parasitic infection that is much more common and a major cause of disability worldwide,though, neurocysticercosis:

I think the only other sushi videos I have are Fecal Contamination of Sushi and Allergenic Fish Worms, though the nori seaweed is good for you (Which Seaweed Is Most Protective Against Breast Cancer? and Avoiding Iodine Deficiency).

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

Original Link

Sushi Worm Parasite

Sushi Worm Parasite.jpeg

There was a report recently of a woman in San Francisco suffering from gnathostomiasis. I had learned about the disease while I was in medical school, but never actually saw a case. Evidently, it's now on the rise. Clinically, the disease commonly presents as "migratory cutaneous swelling" (bumps on the skin that move around). Why? Because there's a worm under there that migrates through the tissues under the skin and causes recurring episodes of migratory swelling or creeping eruptions. The worm's head has rings of little hooks that allow it to burrow through tissue. There is no effective treatment, other than removal of the worm. Since humans are basically dead-end hosts for the larva, they can't develop into mature worms. The symptoms patients experience are due to the organism wandering throughout the body (see Migratory Skin Worms from Sushi).

In addition to burrowing under our skin, it can also crawl into our eyeballs. The 42-year-old woman is described as having a four-year history of migratory swellings on her face, then a little bleeding from the eyelid... and we know where this is going. No problem, though! We can make a little cut, stick in some forceps, locate the worm, and then just pull the sucker right out of the eyeball. If you have any pimples on your face that move around, better to have your doctor grab them before they start swimming around in your eyes.

By far the most serious manifestation is when they get into your brain. As the worm migrates along the nerves, the patient can experience excruciating pain. The condition can lead to paralysis, bleeding in the brain, and finally death. However, in non-cerebral disease, it's the worms that die, though it may take about 12 years.

How do the worms get into our brain, causing so-called neurognathostomiasis? Gnathostoma worms are highly invasive parasites. After you leave the sushi bar, the larvae can penetrate the wall of your intestine. They can then enter the brain through the base of the skull, crawling along the spinal nerves and vessels. They start out in the nerve roots, enter the spinal cord, and then can climb up into the brain. The worm isn't poisonous or anything; it's just the migration of the worm through the body that causes direct mechanical injury because of tearing of nerve tissues.

The bottom line: This diagnosis should be considered in patients who present with nonspecific little lumps and bumps, especially when there is a history of frequent consumption of raw fish.

Thankfully, most raw foodists stick to plants and thereby avoid scenarios like this: A 21-year-old woman experienced acute, severe pain in her mouth immediately after swallowing a raw squid. It seems consuming a squid with "sperm bags and an active ejaculatory apparatus" can result in the "unintended ejection of the sperm bag" and injury to the oral cavity. The researchers conclude that eating raw food, especially living organisms, can be risky. Though some living organisms (plants!) may be substantially less risky than others.

This is like my Tongue Worm in Human Eye or Cheese Mites and Maggots videos. Extremely rare, but extremely fascinating (to me at least!).

There is one parasitic infection that is much more common and a major cause of disability worldwide,though, neurocysticercosis:

I think the only other sushi videos I have are Fecal Contamination of Sushi and Allergenic Fish Worms, though the nori seaweed is good for you (Which Seaweed Is Most Protective Against Breast Cancer? and Avoiding Iodine Deficiency).

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

Original Link

Using a Smell Test to Diagnose Alzheimer’s Disease

Using a Smell Test to Diagnose Alzheimer's Disease.jpeg

Alzheimer's disease (AD) pathology appears to start in the part of the brain that handles smell before subsequently spreading to additional brain regions and then, ultimately, taking over much of the rest of the brain. This led some to speculate that Alzheimer's disease may begin in the nose. Perhaps there's some environmental agent that might enter the brain through some portal in the nostrils?

This is the so-called olfactory vector hypothesis. The anatomy of the nose is well suited for the transfer of things directly into the brain, since the olfactory nerves that stick out into the nose project directly into the brain, bypassing the blood-brain barrier. The nose was actually a major infection route for the polio virus. Public health officials you started cauterizing the nasal passages of schoolchildren by spraying caustic chemicals up their noses in an effort to prevent the disease.

The concern is if people breathe in some ionized metals like aluminum dust, for example, it could be transported into the brain through these olfactory nerves at a rate of about 2 millimeters an hour, which is practically 2 inches a day. Doubt has been cast on this theory, however, by a case report of a woman born with a birth defect in which she had no smell nerves yet still developed Alzheimer's-like pathology. And so, to date, all the supporting evidence is really just circumstantial. It is clear, though, that changes in the sense of smell is among the first clinical signs of Alzheimer's, occurring during the preclinical phase--that is, before there's any noticeable cognitive decline. Could we use these changes to predict or diagnose the disease?

For years, researchers have been trying to find markers of brain illness hidden in people's ability to smell using all sorts of fancy gadgets. For example, functional MRI scans can detect differences in brain activation in response to an odor. In my video, Peanut Butter Smell Test for Alzheimer's, you can see the responses to lavender. You'll see a representation of a normal brain's responses to the odor versus an Alzheimer's brain. This unequivocally demonstrates that we can pick up changes in smell function due to Alzheimer's. But do we really need a million-dollar machine?

An ingenious group of researchers at the University of Florida discovered all we may need is some peanut butter and a ruler.

Considering that the left side of the brain primarily processes what we smell through our left nostril and the right side of our brain covers the right nostril, and understanding that Alzheimer's strikes the left side more than the right, what if you performed the following experiment: Close your eyes and mouth, breathe normally through the nose, then close one nostril, and hold a foot-long ruler out from the open nostril. Once your eyes, mouth, and one nostril are closed, open a container of peanut butter at the bottom of the ruler (one foot away from your open nostril). Move the peanut butter closer by 1 centimeter upon each exhale until you can detect the odor. Then repeat the whole procedure again using your other nostril.

This is exactly what the University of Florida researchers did with their subjects. What did they find? The normal elderly control subjects in the study smelled the peanut butter as soon as it came within an average of 18 centimeters (about 7 inches) from either nostril. It was about the same, roughly 7 inches, in the right nostrils of Alzheimer's patients. But in their left nostrils, it was a mere 2 inches! The peanut butter had to be only 2 inches away before the Alzheimer's patients could detect it through their left nostrils. This happened every single time. Indeed, the researchers found that a "left nostril impairment of odor detection was present in all the patients with probable AD." There was no left-right difference in the control group; they could smell the peanut butter when it was the same distance away from both their left and right nostrils. In the Alzheimer's group, however, there was a 12-centimeter difference.

The disparity was so great that we may be able to set a cutoff value for the diagnosis of Alzheimer's. The researchers reported that "[c]ompared to patients with other causes of dementia this nostril asymmetry of odor detection...was 100% sensitive and 100% specific for probable AD," meaning no false positives and no false negatives. Compared to healthy people, it was 100% sensitive in picking up cases of probable Alzheimer's and 92% specific. What exactly does that mean? In this study, if you had Alzheimer's, there was a 100% chance of having that wide left-right discrepancy. But, if you did have that discrepancy, the chance of having Alzheimer's was only 92%. This means there were some false positives.

The reason it's only "probable" Alzheimer's is because the only way we can really confirm someone has the disease is on autopsy. The current criteria for diagnosing Alzheimer's require an extensive evaluation, combined with fancy positron emission tomography (PET) scans and spinal taps. All of these tests are expensive and hard to get, can be invasive, and can have potential complications. On top of that, they are neither highly sensitive nor specific. The left-right nostril / peanut butter odor detection test, however, was fast, simple, non-invasive, and inexpensive. They concluded that may make peanut butter an ideal instrument for the early detection of Alzheimer's disease.

Does all this sound a bit too good to be true? It may be. A University of Pennsylvania research team was unable to replicate the results. Click here to read their paper. So at this point, the data are mixed. I'll do another post once more studies are published and we have a better handle on whether it's useful or not.

Of course, it's better to prevent Alzheimer's in the first place. Check out these videos for more information.

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

Original Link

Using a Smell Test to Diagnose Alzheimer’s Disease

Using a Smell Test to Diagnose Alzheimer's Disease.jpeg

Alzheimer's disease (AD) pathology appears to start in the part of the brain that handles smell before subsequently spreading to additional brain regions and then, ultimately, taking over much of the rest of the brain. This led some to speculate that Alzheimer's disease may begin in the nose. Perhaps there's some environmental agent that might enter the brain through some portal in the nostrils?

This is the so-called olfactory vector hypothesis. The anatomy of the nose is well suited for the transfer of things directly into the brain, since the olfactory nerves that stick out into the nose project directly into the brain, bypassing the blood-brain barrier. The nose was actually a major infection route for the polio virus. Public health officials you started cauterizing the nasal passages of schoolchildren by spraying caustic chemicals up their noses in an effort to prevent the disease.

The concern is if people breathe in some ionized metals like aluminum dust, for example, it could be transported into the brain through these olfactory nerves at a rate of about 2 millimeters an hour, which is practically 2 inches a day. Doubt has been cast on this theory, however, by a case report of a woman born with a birth defect in which she had no smell nerves yet still developed Alzheimer's-like pathology. And so, to date, all the supporting evidence is really just circumstantial. It is clear, though, that changes in the sense of smell is among the first clinical signs of Alzheimer's, occurring during the preclinical phase--that is, before there's any noticeable cognitive decline. Could we use these changes to predict or diagnose the disease?

For years, researchers have been trying to find markers of brain illness hidden in people's ability to smell using all sorts of fancy gadgets. For example, functional MRI scans can detect differences in brain activation in response to an odor. In my video, Peanut Butter Smell Test for Alzheimer's, you can see the responses to lavender. You'll see a representation of a normal brain's responses to the odor versus an Alzheimer's brain. This unequivocally demonstrates that we can pick up changes in smell function due to Alzheimer's. But do we really need a million-dollar machine?

An ingenious group of researchers at the University of Florida discovered all we may need is some peanut butter and a ruler.

Considering that the left side of the brain primarily processes what we smell through our left nostril and the right side of our brain covers the right nostril, and understanding that Alzheimer's strikes the left side more than the right, what if you performed the following experiment: Close your eyes and mouth, breathe normally through the nose, then close one nostril, and hold a foot-long ruler out from the open nostril. Once your eyes, mouth, and one nostril are closed, open a container of peanut butter at the bottom of the ruler (one foot away from your open nostril). Move the peanut butter closer by 1 centimeter upon each exhale until you can detect the odor. Then repeat the whole procedure again using your other nostril.

This is exactly what the University of Florida researchers did with their subjects. What did they find? The normal elderly control subjects in the study smelled the peanut butter as soon as it came within an average of 18 centimeters (about 7 inches) from either nostril. It was about the same, roughly 7 inches, in the right nostrils of Alzheimer's patients. But in their left nostrils, it was a mere 2 inches! The peanut butter had to be only 2 inches away before the Alzheimer's patients could detect it through their left nostrils. This happened every single time. Indeed, the researchers found that a "left nostril impairment of odor detection was present in all the patients with probable AD." There was no left-right difference in the control group; they could smell the peanut butter when it was the same distance away from both their left and right nostrils. In the Alzheimer's group, however, there was a 12-centimeter difference.

The disparity was so great that we may be able to set a cutoff value for the diagnosis of Alzheimer's. The researchers reported that "[c]ompared to patients with other causes of dementia this nostril asymmetry of odor detection...was 100% sensitive and 100% specific for probable AD," meaning no false positives and no false negatives. Compared to healthy people, it was 100% sensitive in picking up cases of probable Alzheimer's and 92% specific. What exactly does that mean? In this study, if you had Alzheimer's, there was a 100% chance of having that wide left-right discrepancy. But, if you did have that discrepancy, the chance of having Alzheimer's was only 92%. This means there were some false positives.

The reason it's only "probable" Alzheimer's is because the only way we can really confirm someone has the disease is on autopsy. The current criteria for diagnosing Alzheimer's require an extensive evaluation, combined with fancy positron emission tomography (PET) scans and spinal taps. All of these tests are expensive and hard to get, can be invasive, and can have potential complications. On top of that, they are neither highly sensitive nor specific. The left-right nostril / peanut butter odor detection test, however, was fast, simple, non-invasive, and inexpensive. They concluded that may make peanut butter an ideal instrument for the early detection of Alzheimer's disease.

Does all this sound a bit too good to be true? It may be. A University of Pennsylvania research team was unable to replicate the results. Click here to read their paper. So at this point, the data are mixed. I'll do another post once more studies are published and we have a better handle on whether it's useful or not.

Of course, it's better to prevent Alzheimer's in the first place. Check out these videos for more information.

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

Original Link

The Food Safety Risk of Organic versus Conventional

The Food Safety Risk of Organic versus Conventional.jpeg

The stated principles of organic agriculture are "health, ecology, fairness, and care," but if you ask people why they buy organic, the strongest predictor is concern for their own health. People appear to spend more for organic foods for selfish reasons, rather than altruistic motives. Although organic foods may not have more nutrients per dollar (see my video Are Organic Foods More Nutritious?), consumption of organic foods may reduce exposure to pesticide residues and antibiotic-resistant bacteria.

Food safety-wise, researchers found no difference in the risk for contamination with food poisoning bacteria in general. Both organic and conventional animal products have been found to be commonly contaminated with Salmonella and Campylobacter, for example. Most chicken samples (organic and inorganic), were found to be contaminated with Campylobacter, and about a third with Salmonella, but the risk of exposure to multidrug-resistant bacteria was lower with the organic meat. They both may carry the same risk of making us sick, but food poisoning from organic meat may be easier for doctors to treat.

What about the pesticides? There is a large body of evidence on the relation between exposure to pesticides and elevated rate of chronic diseases such as different types of cancers, diabetes, neurodegenerative disorders like Parkinson's, Alzheimer's, and ALS, as well as birth defects and reproductive disorders--but these studies were largely on people who live or work around pesticides.

Take Salinas Valley California, for example, where they spray a half million pounds of the stuff. Daring to be pregnant in an agricultural community like that may impair childhood brain development, such that pregnant women with the highest levels running through their bodies (as measured in their urine) gave birth to children with an average deficit of about seven IQ points. Twenty-six out of 27 studies showed negative effects of pesticides on brain development in children. These included attention problems, developmental disorders, and short-term memory difficulties.

Even in urban areas, if you compare kids born with higher levels of a common insecticide in their umbilical cord blood, those who were exposed to higher levels are born with brain anomalies. And these were city kids, so presumably this was from residential pesticide use.

Using insecticides inside your house may also be a contributing risk factor for childhood leukemia. Pregnant farmworkers may be doubling the odds of their child getting leukemia and increase their risk of getting a brain tumor. This has lead to authorities advocating that awareness of the potentially negative health outcome for children be increased among populations occupationally exposed to pesticides, though I don't imagine most farmworkers have much of a choice.

Conventional produce may be bad for the pregnant women who pick them, but what about our own family when we eat them?

Just because we spray pesticides on our food in the fields doesn't necessarily mean it ends up in our bodies when we eat it, or at least we didn't know that until a study was published in 2006. Researchers measured the levels of two pesticides running through children's bodies by measuring specific pesticide breakdown products in their urine. In my video, Are Organic Foods Safer?, you can see the levels of pesticides flowing through the bodies of three to 11-year olds during a few days on a conventional diet. The kids then went on an organic diet for five days and then back to the conventional diet. As you can see, eating organic provides a dramatic and immediate protective effect against exposures to pesticides commonly used in agricultural production. The study was subsequently extended. It's clear by looking at the subsequent graph in the video when the kids were eating organic versus conventional. What about adults, though? We didn't know... until now.

Thirteen men and women consumed a diet of at least 80% organic or conventional food for seven days and then switched. No surprise, during the mostly organic week, pesticide exposure was significantly reduced by a nearly 90% drop.

If it can be concluded that consumption of organic foods provides protection against pesticides, does that also mean protection against disease? We don't know. The studies just haven't been done. Nevertheless, in the meantime, the consumption of organic food provides a logical precautionary approach.

For more on organic foods:

For more on the infectious disease implications of organic versus conventional, see Superbugs in Conventional vs. Organic Chicken. Organic produce may be safer too. See Norovirus Food Poisoning from Pesticides. Organic eggs may also have lower Salmonella risk, which is an egg-borne epidemic every year in the US. See my video Who Says Eggs Aren't Healthy or Safe?

More on Parkinson's and pesticides in Preventing Parkinson's Disease With Diet.

Those surprised by the California data might have missed my video California Children Are Contaminated.

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: IFPRI -IMAGES / Flickr. This image has been modified.

Original Link

The Food Safety Risk of Organic versus Conventional

The Food Safety Risk of Organic versus Conventional.jpeg

The stated principles of organic agriculture are "health, ecology, fairness, and care," but if you ask people why they buy organic, the strongest predictor is concern for their own health. People appear to spend more for organic foods for selfish reasons, rather than altruistic motives. Although organic foods may not have more nutrients per dollar (see my video Are Organic Foods More Nutritious?), consumption of organic foods may reduce exposure to pesticide residues and antibiotic-resistant bacteria.

Food safety-wise, researchers found no difference in the risk for contamination with food poisoning bacteria in general. Both organic and conventional animal products have been found to be commonly contaminated with Salmonella and Campylobacter, for example. Most chicken samples (organic and inorganic), were found to be contaminated with Campylobacter, and about a third with Salmonella, but the risk of exposure to multidrug-resistant bacteria was lower with the organic meat. They both may carry the same risk of making us sick, but food poisoning from organic meat may be easier for doctors to treat.

What about the pesticides? There is a large body of evidence on the relation between exposure to pesticides and elevated rate of chronic diseases such as different types of cancers, diabetes, neurodegenerative disorders like Parkinson's, Alzheimer's, and ALS, as well as birth defects and reproductive disorders--but these studies were largely on people who live or work around pesticides.

Take Salinas Valley California, for example, where they spray a half million pounds of the stuff. Daring to be pregnant in an agricultural community like that may impair childhood brain development, such that pregnant women with the highest levels running through their bodies (as measured in their urine) gave birth to children with an average deficit of about seven IQ points. Twenty-six out of 27 studies showed negative effects of pesticides on brain development in children. These included attention problems, developmental disorders, and short-term memory difficulties.

Even in urban areas, if you compare kids born with higher levels of a common insecticide in their umbilical cord blood, those who were exposed to higher levels are born with brain anomalies. And these were city kids, so presumably this was from residential pesticide use.

Using insecticides inside your house may also be a contributing risk factor for childhood leukemia. Pregnant farmworkers may be doubling the odds of their child getting leukemia and increase their risk of getting a brain tumor. This has lead to authorities advocating that awareness of the potentially negative health outcome for children be increased among populations occupationally exposed to pesticides, though I don't imagine most farmworkers have much of a choice.

Conventional produce may be bad for the pregnant women who pick them, but what about our own family when we eat them?

Just because we spray pesticides on our food in the fields doesn't necessarily mean it ends up in our bodies when we eat it, or at least we didn't know that until a study was published in 2006. Researchers measured the levels of two pesticides running through children's bodies by measuring specific pesticide breakdown products in their urine. In my video, Are Organic Foods Safer?, you can see the levels of pesticides flowing through the bodies of three to 11-year olds during a few days on a conventional diet. The kids then went on an organic diet for five days and then back to the conventional diet. As you can see, eating organic provides a dramatic and immediate protective effect against exposures to pesticides commonly used in agricultural production. The study was subsequently extended. It's clear by looking at the subsequent graph in the video when the kids were eating organic versus conventional. What about adults, though? We didn't know... until now.

Thirteen men and women consumed a diet of at least 80% organic or conventional food for seven days and then switched. No surprise, during the mostly organic week, pesticide exposure was significantly reduced by a nearly 90% drop.

If it can be concluded that consumption of organic foods provides protection against pesticides, does that also mean protection against disease? We don't know. The studies just haven't been done. Nevertheless, in the meantime, the consumption of organic food provides a logical precautionary approach.

For more on organic foods:

For more on the infectious disease implications of organic versus conventional, see Superbugs in Conventional vs. Organic Chicken. Organic produce may be safer too. See Norovirus Food Poisoning from Pesticides. Organic eggs may also have lower Salmonella risk, which is an egg-borne epidemic every year in the US. See my video Who Says Eggs Aren't Healthy or Safe?

More on Parkinson's and pesticides in Preventing Parkinson's Disease With Diet.

Those surprised by the California data might have missed my video California Children Are Contaminated.

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: IFPRI -IMAGES / 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.

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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

Why Is Milk Consumption Associated with More Bone Fractures?

Why Is Milk Consumption Associated with More Bone Fractures?.jpg

Milk is touted to build strong bones, but a compilation of all the best studies found no association between milk consumption and hip fracture risk, so drinking milk as an adult might not help bones, but what about in adolescence? Harvard researchers decided to put it to the test.

Studies have shown that greater milk consumption during childhood and adolescence contributes to peak bone mass, and is therefore expected to help avoid osteoporosis and bone fractures in later life. But that's not what researchers have found (as you can see in my video Is Milk Good for Our Bones?). Milk consumption during teenage years was not associated with a lower risk of hip fracture, and if anything, milk consumption was associated with a borderline increase in fracture risk in men.

It appears that the extra boost in total body bone mineral density from getting extra calcium is lost within a few years; even if you keep the calcium supplementation up. This suggests a partial explanation for the long-standing enigma that hip fracture rates are highest in populations with the greatest milk consumption. This may be an explanation for why they're not lower, but why would they be higher?

This enigma irked a Swedish research team, puzzled because studies again and again had shown a tendency of a higher risk of fracture with a higher intake of milk. Well, there is a rare birth defect called galactosemia, where babies are born without the enzymes needed to detoxify the galactose found in milk, so they end up with elevated levels of galactose in their blood, which can causes bone loss even as kids. So maybe, the Swedish researchers figured, even in normal people that can detoxify the stuff, it might not be good for the bones to be drinking it every day.

And galactose doesn't just hurt the bones. Galactose is what scientists use to cause premature aging in lab animals--it can shorten their lifespan, cause oxidative stress, inflammation, and brain degeneration--just with the equivalent of like one to two glasses of milk's worth of galactose a day. We're not rats, though. But given the high amount of galactose in milk, recommendations to increase milk intake for prevention of fractures could be a conceivable contradiction. So, the researchers decided to put it to the test, looking at milk intake and mortality as well as fracture risk to test their theory.

A hundred thousand men and women were followed for up to 20 years. Researchers found that milk-drinking women had higher rates of death, more heart disease, and significantly more cancer for each glass of milk. Three glasses a day was associated with nearly twice the risk of premature death, and they had significantly more bone and hip fractures. More milk, more fractures.

Men in a separate study also had a higher rate of death with higher milk consumption, but at least they didn't have higher fracture rates. So, the researchers found a dose dependent higher rate of both mortality and fracture in women, and a higher rate of mortality in men with milk intake, but the opposite for other dairy products like soured milk and yogurt, which would go along with the galactose theory, since bacteria can ferment away some of the lactose. To prove it though, we need a randomized controlled trial to examine the effect of milk intake on mortality and fractures. As the accompanying editorial pointed out, we better find this out soon since milk consumption is on the rise around the world.

What can we do for our bones, then? Weight-bearing exercise such as jumping, weight-lifting, and walking with a weighted vest or backpack may help, along with getting enough calcium (Alkaline Diets, Animal Protein, & Calcium Loss) and vitamin D (Resolving the Vitamin D-Bate). Eating beans (Phytates for the Prevention of Osteoporosis) and avoiding phosphate additives (Phosphate Additives in Meat Purge and Cola) may also help.

Maybe the galactose angle can help explain the findings on prostate cancer (Prostate Cancer and Organic Milk vs. Almond Milk) and Parkinson's disease (Preventing Parkinson's Disease With Diet).

Galactose is a milk sugar. There's also concern about milk proteins (see my casomorphin series) and fats (The Saturated Fat Studies: Buttering Up the Public and Trans Fat in Meat and Dairy) as well as the hormones (Dairy Estrogen and Male Fertility, Estrogen in Meat, Dairy, and Eggs and Why Do Vegan Women Have 5x Fewer Twins?).

Milk might also play a role in diabetes (Does Casein in Milk Trigger Type 1 Diabetes, Does Bovine Insulin in Milk Trigger Type 1 Diabetes?) and breast cancer (Is Bovine Leukemia in Milk Infectious?, The Role of Bovine Leukemia Virus in Breast Cancer, and Industry Response to Bovine Leukemia Virus in Breast Cancer).

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.

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