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

Foods Linked to ALS

Foods Linked to ALS.jpeg

As explored in my video ALS (Lou Gehrig's Disease): Fishing for Answers, there may be a link in the consumption of the neurotoxin BMAA, produced by algae blooms, and increased risk of ALS. It now appears that BMAA could be found in high concentrations in aquatic animals in many areas of the world.

This could explain ALS clustering around lakes in New Hampshire--up to 25 times the expected rate of ALS with some families eating fish several times a week. Or in Wisconsin, where the most significant ALS risk factor was the past consumption of fish out of Lake Michigan. Or clustering in Finland's Lakeland district, or seafood eaters in France, or around the Baltic sea, building up particularly in fish, mussels and oysters.

When I think of algae blooms I think of the Chesapeake bay near where I live, that gets choked off thanks in part to the poultry industry pollution. And indeed there was a recent report linking BMAA exposure to ALS in Maryland. The ALS victims, all of whom ate Chesapeake Bay blue crabs every week, lived within a half mile of each other, which raised some eyebrows at the Hopkins ALS center. And so researchers tested a few crabs, and two out of three tested positive for BMAA, indicating that the neurotoxin is present in the aquatic food chain of the Chesapeake Bay and is a potential route for human exposure.

To bring the story full circle, things in Guam, where the link between BMAA consumption and ALS was first discovered, are looking up. The ALS epidemic there may have been triggered by their acquisition of guns. Now though, the epidemic appears to be over thanks to near-extinction of the fruit bats they were eating due to over-hunting. But while the rates decline in Guam, neurodegenerative diseases like ALS around the rest of the world are on the rise.

It's plausible that humans have been exposed to some level of BMAA throughout their evolutionary history, but the increase in algae blooms as a result of human activities is probably increasing this exposure. There is a general consensus that harmful algal blooms are increasing worldwide thanks in part to industrialized agriculture (as shown in my video Diet & Amyotrophic Lateral Sclerosis-ALS). More people means more sewage, fertilizer, and manure, which can mean more algae, which may mean more exposure to this neurotoxin, leading to a possible increased incidence of neurodegenerative diseases such as Alzheimer's, Parkinson's, and ALS.

BMAA is considered a strong contender as the cause of, or at least a major contributor to the cause of both endemic and sporadic ALS and Alzheimer's disease, and possibly conferring risk for Parkinson's diseases as well. The ramifications of this discovery are enormous.

As researchers from Australia stated, "With substantial and ever growing evidence that BMAA does play a role in the onset and progression of neurodegenerative diseases, the most important question is, what mode of activity does BMAA exert?" Huh? That's not the most important question we should be asking. The most important question is "How can we reduce our risk?"

We know that the presence of BMAA in aquatic food chains could be a significant human health hazard. There may even be a synergistic toxicity between mercury and BMAA, making certain fish even riskier. Until more is known about the possible link of BMAA to Alzheimer's and ALS, it may be prudent to limit exposure of BMAA in the human diet.

For other neurotoxins found in the food supply, see Amnesic Seafood Poisoning, Essential Tremor and Diet, Ciguatera Poisoning & Chronic Fatigue Syndrome.

Other toxic substances can also build up in the aquatic food chain, for example:

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: Peter Miller / Flickr. This image has been modified.

Original Link

Foods Linked to ALS

Foods Linked to ALS.jpeg

As explored in my video ALS (Lou Gehrig's Disease): Fishing for Answers, there may be a link in the consumption of the neurotoxin BMAA, produced by algae blooms, and increased risk of ALS. It now appears that BMAA could be found in high concentrations in aquatic animals in many areas of the world.

This could explain ALS clustering around lakes in New Hampshire--up to 25 times the expected rate of ALS with some families eating fish several times a week. Or in Wisconsin, where the most significant ALS risk factor was the past consumption of fish out of Lake Michigan. Or clustering in Finland's Lakeland district, or seafood eaters in France, or around the Baltic sea, building up particularly in fish, mussels and oysters.

When I think of algae blooms I think of the Chesapeake bay near where I live, that gets choked off thanks in part to the poultry industry pollution. And indeed there was a recent report linking BMAA exposure to ALS in Maryland. The ALS victims, all of whom ate Chesapeake Bay blue crabs every week, lived within a half mile of each other, which raised some eyebrows at the Hopkins ALS center. And so researchers tested a few crabs, and two out of three tested positive for BMAA, indicating that the neurotoxin is present in the aquatic food chain of the Chesapeake Bay and is a potential route for human exposure.

To bring the story full circle, things in Guam, where the link between BMAA consumption and ALS was first discovered, are looking up. The ALS epidemic there may have been triggered by their acquisition of guns. Now though, the epidemic appears to be over thanks to near-extinction of the fruit bats they were eating due to over-hunting. But while the rates decline in Guam, neurodegenerative diseases like ALS around the rest of the world are on the rise.

It's plausible that humans have been exposed to some level of BMAA throughout their evolutionary history, but the increase in algae blooms as a result of human activities is probably increasing this exposure. There is a general consensus that harmful algal blooms are increasing worldwide thanks in part to industrialized agriculture (as shown in my video Diet & Amyotrophic Lateral Sclerosis-ALS). More people means more sewage, fertilizer, and manure, which can mean more algae, which may mean more exposure to this neurotoxin, leading to a possible increased incidence of neurodegenerative diseases such as Alzheimer's, Parkinson's, and ALS.

BMAA is considered a strong contender as the cause of, or at least a major contributor to the cause of both endemic and sporadic ALS and Alzheimer's disease, and possibly conferring risk for Parkinson's diseases as well. The ramifications of this discovery are enormous.

As researchers from Australia stated, "With substantial and ever growing evidence that BMAA does play a role in the onset and progression of neurodegenerative diseases, the most important question is, what mode of activity does BMAA exert?" Huh? That's not the most important question we should be asking. The most important question is "How can we reduce our risk?"

We know that the presence of BMAA in aquatic food chains could be a significant human health hazard. There may even be a synergistic toxicity between mercury and BMAA, making certain fish even riskier. Until more is known about the possible link of BMAA to Alzheimer's and ALS, it may be prudent to limit exposure of BMAA in the human diet.

For other neurotoxins found in the food supply, see Amnesic Seafood Poisoning, Essential Tremor and Diet, Ciguatera Poisoning & Chronic Fatigue Syndrome.

Other toxic substances can also build up in the aquatic food chain, for example:

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: Peter Miller / 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

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

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: lightwise © 123RF.com. This image has been modified.

Original Link

Reducing Glycotoxin Intake to Help Reduce Brain Loss

Reducing Glycotoxin Intake to Prevent Alzheimer's.jpg

Each of us has about six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histones and by doing so, silence whatever genes were in that stretch of DNA, hence their name SIRtuins, which stands for silencing information regulator.

Although they were discovered only about a decade ago, the study of sirtuins "has become one of the most promising areas of biomedicine," since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer's disease, as shown in Reducing Glycotoxin Intake to Prevent Alzheimer's.

Autopsies of Alzheimer's victims reveal that loss of sirtuin activity is closely associated with the accumulation of the plaques and tangles in the brain that are characteristic of Alzheimer's disease. Sirtuin appears to activate pathways that steer the brain away from the formation of plaque and tangle proteins. "Because a decrease in sirtuin activity can clearly have deleterious effects" on nerve health, researchers are trying to come up with drugs to increase sirtuin activity, but why not just prevent its suppression in the first place?

Glycotoxins in our food suppress sirtuin activity, also known as advanced glycation end products, or AGE's. Our modern diet includes excessive AGE's, which can be neurotoxic. High levels in the blood may predict cognitive decline over time. If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.

As we age, our brain literally shrinks. In our 60's and 70's, we lose an average of five cubic centimeters of total brain tissue volume every year, but some people lose more than others. Brain atrophy may be reduced in very healthy individuals, and a few people don't lose any brain at all. Normally we lose about 2% of brain volume every year, but that's just the average. Although the average brain loss for folks in their 70's and 80's was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.

Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one's consumption of these compounds may end up having significant public health benefits. Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGE's may offer a new strategy to combat the epidemic of Alzheimer's.

Some glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating, particularly foods high in fat and protein cooked at high temperatures. In my video, Avoiding a Sugary Grave, I listed the 15 foods most contaminated with glycotoxins; mostly chicken, but also pork, beef, and fish, which may help explain why those that eat the most meat may have triple the risk of getting dementia compared to long-time vegetarians. Note there are some relatively high fat and protein plant foods such as nuts and soy products, so I no longer recommend toasting nuts and would steer clear from roasted tofu.

I've covered advanced glycation end-products in Glycotoxins, Bacon, Eggs, and Gestational Diabetes During Pregnancy, and Why is Meat a Risk Factor for Diabetes?.

More on slowing brain aging in How to Slow Brain Aging By Two Years.

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: lightwise © 123RF.com. This image has been modified.

Original Link