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

Gluten Sensitivity Put to the Test

NF-Feb18 Is Gluten Sensitivity Real?.jpeg

In 1980, researchers in England reported a series of women with no evidence of celiac disease (the autoimmune disorder associated with gluten intolerance), who nevertheless resolved their chronic diarrhea on a gluten-free diet. The medical profession was skeptical at the time that non-celiac gluten sensitivity existed, and even 30 years later, such patients were commonly referred to psychiatrists. Psychological testing of such patients, however, found no evidence that they were suffering from any kind of psychosomatic hysteria.

The medical profession has a history of dismissing diseases as all in people's heads--post-traumatic stress disorder, ulcerative colitis, migraines, ulcers, asthma, Parkinson's disease, and multiple sclerosis. Despite resistance from the prevailing medical community at the time, these health problems have subsequently been confirmed to be credible physiologically-based disorders rather than psychologically-based confabulations.

On the flipside, the internet is rife with unsubstantiated claims about gluten free diets, which has spilled over into the popular press to make gluten the diet villain du jour, with claims like "17 million Americans are gluten sensitive." However, it must be remembered that the gluten-free food industry is a big business. When literally billions are at stake, it's hard to trust anybody. As always, it's best to stick to the science.

What sort of evidence do we have for the existence of a condition presumed to be so widespread? Not much. The evidence base for such claims has been unfortunately very thin because we haven't had randomized controlled trials demonstrating that the entity even exists. The gold-standard for confirming non-celiac gluten sensitivity requires a gluten-free diet, followed by a double-blind, randomized, placebo-controlled food challenge. For example, give people a muffin and don't tell them if it's gluten-free or gluten-filled--to control for placebo effects--and see what happens. The reason this is necessary is because when you actually do this, a number of quote-unquote "gluten-sensitive" patients don't react at all to disguised gluten and instead react to the gluten-free placebo.

We never had that level of evidence until 2011, when a double-blind, randomized placebo-controlled trial was published, which tested to see if patients complaining of irritable bowel symptoms who claimed they felt better on a gluten free diet--despite not having celiac disease--actually could tell if they were given gluten containing bread and muffins or gluten-free bread and muffins.

Subjects started out gluten-free and symptom-free for two weeks and then were challenged with the bread and muffins. In my video, Is Gluten Sensitivity Real?, you can see what happened to the 15 patients who got the placebo, meaning they started out on a gluten-free diet and continued on a gluten-free diet. They got worse. Just the thought that they may be eating something that was bad for them made them feel crampy and bloated. This is what's called the nocebo effect. The placebo effect is when you give someone something useless and they feel better; the nocebo effect is when you give someone something harmless and they feel worse. On the other hand, the small group that got the actual gluten, felt even worse still. The researchers concluded that non-celiac gluten intolerance may therefore indeed exist.

It was a small study, though, and even though the researchers claimed the gluten-free bread and muffins were indistinguishable, maybe at some level the patients could tell which was which. So in 2012, researchers in Italy took 920 patients that had been diagnosed with non-celiac gluten sensitivity and put them to the test with a double-blinded wheat challenge by giving them capsules filled with wheat flour or filled with placebo powder. More than two-thirds failed the test, such as getting worse on the placebo or better on the wheat. But of those that passed, there was a clear benefit to staying on the wheat-free diet. The researchers concluded that their findings confirmed the existence of a non-celiac wheat sensitivity. Note I said "wheat sensitivity," not "gluten sensitivity."

Gluten itself may not be causing gut symptoms at all. Most people with wheat sensitivity have a variety of other food sensitivities. Two thirds are sensitive to cow's milk protein, and many are sensitive to eggs. If we put people on a diet low in common triggers of irritable bowel symptoms, and then challenge them with gluten, there's no effect. We find the same increase in symptoms with high gluten, low gluten, or no gluten diets, calling into question the very existence of non-celiac gluten sensitivity.

Interestingly, despite being informed that avoiding gluten didn't seem to do a thing for their gut symptoms, many participants opted to continue following a gluten-free diet as they subjectively described "feeling better." So researchers wondered if avoiding gluten might improve the mood of those with wheat sensitivity. Indeed, short-term exposure to gluten appeared to induce feelings of depression in these patients. Whether non-celiac gluten sensitivity is a disease of the mind or the gut, it is no longer a condition that can be dismissed.


More than 10,000 articles have been published on gluten in medical journals--intimidating even for me! Combined with the multi-billion dollar financial interests on both sides, it makes for a difficult task. But I think I did it! This is the first of a 3-part series summarizing the best available science on gluten. Also check out: Gluten-Free Diets: Separating the Wheat from the Chat and How to Diagnose Gluten Intolerance.

Why this apparent increase in food sensitivities in recent decades? It could be because of pollutant exposure (see Alkylphenol Endocrine Disruptors and Allergies and Dietary Sources of Alkylphenol Endocrine Disruptors).

What can we do about preventing so-called atopic diseases (like allergies, asthma, and eczema)? See my videos Preventing Allergies in Adulthood and Preventing Allergies in Childhood. The weirdest example of an emerging food sensitivity may be the tick-bite related meat allergy story I review in Alpha Gal and the Lone Star Tick and Tick Bites, Meat Allergies, and Chronic Urticaria.

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 Uprooting the Leading Causes of Death, More Than an Apple a Day, From Table to Able, and Food as Medicine.

Image Credit: Guillaume Paumier / Flickr

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How to Treat Multiple Sclerosis With Diet

NF-July17 Treating Multiple Sclerosis with Diet.jpg

Multiple sclerosis is an unpredictable and frightening degenerative autoimmune inflammatory disease of the central nervous system in which our body attacks our own nerves. It often strikes in the prime of life and can cause symptoms in the brain, such as cognitive impairment; in the eye, such as painful loss of vision; as well as tremors, weakness, loss of bladder control, pain, and fatigue.

The most frequently prescribed drug for multiple sclerosis is interferon beta, which can make one feel lousy and cost $30,000 a year. But hey, it might be worthwhile--if it actually worked. We learned recently that it doesn't seem to prevent or delay long-term disability. That leaves chemo drugs like mitoxantrone that causes irreversible heart damage in one out of every eight people who go on the drug and causes cancer (leukemia) in nearly 1% of people who take it. But MS is no walk in the park either.

If only there was a cheap, simple, safe, side-effect free solution that also just so happened to be the most effective treatment for MS ever prescribed...

Dr. Roy Swank, who we lost recently at age 99, was a distinguished neurologist whose research culminated in over 170 scientific papers. In the video, Treating Multiple Sclerosis with the Swank MS Diet, I highlight a few.

As far back as 1950, we knew there were areas in the world that had a lot of MS--North America, Europe--and other places--Africa and Asia--that hardly had any. And migration studies show that those who move from a high risk area to a low risk area significantly drop their risk, and vice versa. So it seems less genetic and more lifestyle.

Dr. Swank had an idea. As he recounts in an interview with Dr. John McDougall at the ripe young age of 84, "it seemed possible to me that this could be a matter of food, because the further north you go the less vegetarian a life is led and the more people are carnivores, you might say--they spend a lot more time eating meat."

After looking at the multiple sclerosis data from World War II in occupied countries where meat and dairy were rationed, along with his famous study in '52 that found that the frequency of MS related directly to the amount of saturated animal fat consumed daily in different areas of Norway, he concluded that it might be the animal fat that was causing the increased risk. He decided to put it to the test by restricting people's intake of saturated animal fat, most commonly coming from dairy and chicken in the U.S. (See Trans Fat, Saturated Fat, and Cholesterol: Tolerable Upper Intake of Zero).

In Treating Multiple Sclerosis with the Swank MS Diet, you can see data on his first 47 patients before cutting out about 90% of the saturated fat from their diet and after, showing a decrease in both the frequency and severity of MS attacks. Normally, we're lucky if we can get people to stick to a diet for six months, and so that's why most dietary trials last a year at the most. The first study he published reported results from the first three and a half years.

Then came the five and a half year follow-up in which he added about another 100 patients. Then the seven year follow-up, published in the Annals of Internal Medicine. Then the 20 year follow-up, and then the 34 year follow-up.

How did his patients do? If we can get to people early in their disease, when they're only mildly disabled, and restrict their saturated fat intake, Dr. Swank showed he could stop their disease in 95% of cases--no further disability 34 years later. But if they started slacking on their diet--even years in, their disease could become reactivated. They felt so great that some felt that they could cheat a little bit, since they had their disease so well under control. But eating just eight grams of saturated fat more a day was accompanied by a striking increase in disability and a near tripling of their death rate.

How about a 50 year follow-up! They were able to track down 15 of the original patients that stuck to the diet, now in their 70s and 80s, with multiple sclerosis for over 50 years, and 13 out of 15 were walking around normal in all respects. Conclusion: "This study indicated that, in all probability, MS is caused largely by consumption of saturated animal fat."

Dr. Swank thought it was the sludging of the blood caused by even a single meal of saturated fats that can clog tiny capillaries that feed our nervous system. Diets rich in saturated fat and cholesterol can thicken the blood and make our red cells sticky. A single meal of sausage and eggs can stick our blood cells together like rolls of quarters. And that kind of hyperaggregation can lead to a reduction of blood flow and oxygenation of our tissues. What's in sausage and eggs that may cause so much inflammation? See my video series on endotoxins described in my blog How Does Meat Cause Inflammation?

If we put someone's blood through a machine that sucks out about 90% of the cholesterol in their blood, we can demonstrate an immediate improvement in microcirculation in the heart muscle. But what about the brain?

The eyes are the windows... to our brain. We can visualize--in real-time--changes in blood vessel function in the retina at the back of the eye, which gives us a sense of what's happening further back in the brain. And if we lower the cholesterol level in the blood, we can immediately get a significant improvement in vasodilation--the little veins open wider and let the blood flow.

So yes, it could be the animal fat leading to clogging of our capillaries, but now we know animal fats can have all sorts of other deleterious effects such as inflammation, so who knows what the actual mechanism may be by which cutting animal fat can cut MS progression. Regardless, patients with MS that follow a diet with no more than 10 or 15 grams of saturated fat can expect to survive and thrive to a ripe old age. Of course, cutting out saturated fat completely might be better, given that heart disease is our number one killer.

The bottom line is that the results Dr. Swank published remain "the most effective treatment of multiple sclerosis ever reported in the peer reviewed medical literature." In patients with early stage MS, 95% were without progression of their disease 34 years later after adopting his low saturated fat dietary program. Even patients with initially advanced disease showed significant benefit. To date, no medication or invasive procedure has ever even come close, to demonstrating such success.

Doesn't cost $30,000 dollars; doesn't give you leukemia--and works. Better!

This all begs one big obvious question: If Dr. Swanks results are "so stunningly impressive, why haven't other physicians, neurologists, and centers adopted this method of treatment?" One reason may be that MRI machines weren't invented until the 1970s, decades after Dr. Swank's study began. MRIs are how we track the progress of MS today. We don't have to rely on patients' subjective reports or doctor's clinical judgments, we can see the disease get better or worse right there in black and white.

It's like in the 1970s when Nathan Pritikin appeared to reverse heart disease by the thousands but no one took him seriously until angiography was invented and the likes of Ornish and Esselstyn (see Our Number One Killer Can Be Stopped) could hold up angiographic images, proving conclusively that a plant-based diet could help literally open up arteries.

So what we need is someone to repeat Swank's experiment today with MRI scans every step of the way. And I'm happy to report that exact experiment was just completed by Dr. John McDougall. Dr. Swank was one of Dr. McDougall's heroes, and Dr. McDougall is one of mine. Study enrollment was completed last year and we should have the full results soon.

I touched on this in my live 2013 year-in-review lecture More Than an Apple a Day, but I'm excited to be able to take a deeper dive into this extraordinary story.

Those interested in supporting Dr. McDougall's landmark study (headed by Dr. Dennis Bourdette, M.D. and under the supervision of Dr. Vijayshree Yadav) can donate to his nonprofit McDougall Research & Education Foundation (you can also donate to NutritionFacts.org to help keep us bringing you similarly underreported yet life-saving science).

-Michael Greger, M.D.

PS: If you haven't yet, you can subscribe to my free videos here and watch my live 2012 year-in-review presentation Uprooting the Leading Causes of Death.

Image Credit: Theen Moy / Flickr

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