Amyotrophic Lateral Sclerosis- Cyanobacteria algal blooms and dietary BMAA exposure

Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig’s Disease) is one of the worst diseases you can have. Currently, there is no cure for it or any treatment.

Synthetic fertilizers create many problems. Fertilizers leach into streams, rivers, and lakes and disrupt the balance of aquatic ecosystems. This is creating an excess of nutrients, including nitrogen and phosphorus, in the water. This is food for the sea plants as much as it is food for land-grown crops. An abundance of nutrients created by runoff leads to excessive algal blooms. Excessive algal blooms then deplete the water of oxygen creating oceanic dead zones. Then when these algae start to decompose water quality problems emerge and the result is dead fish and other aquatic organisms. This process is called eutrophication.

One of the most significant dead zones worldwide can be found in the Gulf of Mexico, beginning at the Mississippi River delta.

This one thing should be enough reason to stop eating anything from the entire ocean at present time.

Just this form of imbalance in nature in the form of algae bloom can kill you. I am not kidding. What you do not understand is that these algae are not just some see vegetables that overgrow in seawater from fertilizers runoff and then die off. Some of them or let’s say most of them are fine and safe and won’t do long-term damage except the dead zones, but some of them are not safe because they create and excrete some of the most potent neurotoxins known to man.

When they start to overgrow because of all of the nitrogen runoff from the land they bloom and excrete enormous amounts of these neurotoxins into the water. These toxins that are chemically stable do not degrade but start to bioaccumulate like anything else. These toxins do damage to any exposure. If the exposure level is low, they will just worsen overall brain degradation and contribute to brain shrinkage with aging but if the toxins accumulate over the acceptable threshold Amyotrophic Lateral Sclerosis (ALS, Lou Gehrig’s Disease) will appear.

Stephen Hawking is an example of this. Hawking had a form of amyotrophic lateral sclerosis (ALS). Amyotrophic lateral sclerosis (ALS) is known commonly as Lou Gehrig’s disease. Amyotrophic lateral sclerosis (ALS) is a motor neuron degradation disease that in time completely paralyzes the patient eventually leading to respiratory failure. It just attacks motor neurons, so the patient’s mental capabilities remain intact, and in most cases, death comes after three years when they can no longer breathe on their own. There is no cure for it. Amyotrophic lateral sclerosis (ALS) strikes previously healthy people seemingly at random. Amyotrophic lateral sclerosis (ALS) is a progressive disease. That means that it can only go worse over time and usually kills in 2-5 years after the first signs of disease. About 10% of people with ALS survive at least ten years. Stephen Hawking was the longest-living individual in history with amyotrophic Lateral Sclerosis (ALS, Lou Gehrig’s Disease).

When the ice bucket challenge went viral, many people heard about this disease, and it became a form of social media awareness campaign that turned into a national phenomenon. Now it is nice to be there for people in need, but that will just pump our own image of self-worth. It would not help to prevent or lower the rate of the disease. Real awareness is something completely different. If people wanted to make a difference and raise awareness, they should do green algae water bucket challenge instead of an ice bucket one. Amyotrophic lateral sclerosis (ALS) is more common than recognized. We have 1 in 400 risks of getting it, and that is at a similar rate level of multiple sclerosis. Let us do some real awareness.

In 1944 U.S. forces had recaptured Guam from the Japanese. Initially, the United States occupied Guam from the Chamorro people on June 21, 1898. And currently, it is under the territory of the U.S. It is a small island in the middle of the Pacific Ocean with a big military base. After the war a navy neurologist noticed that local Chamorro people have a high rate of the very deadly form of the strange neurodegenerative disease with symptoms of dementia, shaking, paralysis, and death. In some settlements in Guam 1 in 3 people died. The illness was named amyotrophic lateral sclerosis-parkinsonism/dementia complex (ALS-PDC), known locally as lytico-bodig. They did not know what it is so they just described it as amyotrophy (atrophy of the muscles), lateral (from Latin lateralis, meaning to the side) and sclerosis (Greek σκληρός hard) is the stiffening of a structure. The rate of ALS in Guam was 50–100 times the incidence of ALS worldwide. After the systematic exclusion and statistical analysis, it was found that specific seeds of the cycad Cycas micronesica tree in the diet of the local population were the main trigger of the disease. Biochemical analysis associated neurotoxic non-protein amino acid, beta-methylamino-L-alanine (BMAA), as a primary cause of the illness.

Cycad trees were suspected because of the use of seed flour in cooking coupled with reposts of livestock ataxia after eating from it. And indeed BMAA neurotoxin was found in it. The discovery was just a part of research on the disease known as lathyrism. Lathyrism is mostly present in India, China, and the Middle East. It has very similar symptoms like progressive paralysis of the legs. Studies later linked lathyrism to the consumption of certain species of legumes that contained the compound ß-N-oxalylamino-L-alanine (BOAA). The lathyrism was the reason why the researchers tested cycad seeds for BOAA first. When the seed showed no concentrations of BOAA very similar substance had been found with a methyl group instead of an oxalyl group—BMAA. So it is chemically very similar to a neurotoxin that just has a methyl group instead. Subsequent studies on rats and monkeys showed the same result in both cases. BMAA is toxic to neurons. However, there was one big difference. Dietary exposure caused immediate symptoms in rats whereas ALS-PDC developed years or even decades after the initial exposure. One other problem was the dose.

In the 1980s neurotoxicologist, Peter Spencer did a study and reported the results of paralysis in macaques fed BMAA. However, again the dose used was much higher than the dose that people suffering from amyotrophic lateral sclerosis (ALS) were exposed to by cycad flour. People had to eat kilograms of it to ingest a comparable dose. Analysis of BMAA concentrations in cycad seeds by various research groups has highlighted that the toxin was present in the seed at low concentrations. Subsequent investigations confirmed that most of the neurotoxins, around 85 percent were removed from cycad flour during processing. There was a calculation that people would have to eat thousands of kilograms of the stuff every day to get to toxic levels of exposure. In the end, the entire theory was abandoned.

Then in the late 1990s, famed neurologist Oliver Sacks (the one who wrote Awakenings which was adapted into an Academy Award-nominated film in 1990, starring Robin Williams and Robert De Niro) and his colleague Alan Cox made some discoveries and resurrected the BMAA theory. The local Chamorro people by now with knowledge from the research that had been done started to use some tactics as a precaution. They made tortillas from cycad seed flour. However, before they use the seeds, they washed them repeatedly to remove toxins and then gave the water to the chickens to drink. If their chickens remained alive after drinking the wash water, the people deemed the seeds safe to grind and eat. However, they also ate other wild animals that they hunted and some of them also feed on cycad seeds as well. For example, for fruit bats and feral pigs, the common food was cycad seeds. Oliver Sacks got the idea that it is not the seed that is problematic but the animals that people consume because it is just another case of biomagnification.

One of the typical local meals was Mariana flying foxes simmered in coconut cream and eaten whole with skin, bones, brains, and everything. Sacks and Cox in 2002 theorized that these animals that feed on the seeds in time create a neurotoxic reservoir of BMAA in their brain tissues. Because their brains were also eaten on a regular basis by the Chamorros, chronic dietary exposure had created the reservoir of BMAA in their own brain leading after a lag time, to a neuronal meltdown and development of amyotrophic lateral sclerosis (ALS). The consumption of Guamanian flying foxes which fed on the cycads was core to the Chamorro tradition. Also, statistical correlation showed that the decline of the flying fox population due to excessive hunting correlated with the drop in the number of cases of ALS/PDC presented in Guam. Cox analyzed the skin of preserved museum flying fox specimens (collected five decades previously) and found BMAA concentrations to be extremely high.

The lag time is one of the things that made these diseases hard to track. With leg time people tend to expose themself to the toxin completely without noticing anything wrong and when the pool of this toxin accumulates and the disease shows the first symptoms, it is already too late. The final closure of the topic was autopsies on the brains of Chamorros that died from ALS/PDC that found high levels of BMAA (1). 13 Canadian subjects had no detectable levels of BMAA. They were just individuals who died of causes unrelated to neurodegeneration. However, when BMAA was measured, it was also found in the brains of all of the Canadian patients with Alzheimer’s disease. However, wait just a second. These people were in Canada not in Guam. They did not eat flying foxes or Cycat tree seeds. 

The real story here is that BMAA neurotoxin was not produced by the tree either. It was produced by Nostoc cyanobacteria, root symbionts of the cycad trees. Bacteria that live in the roots of the tree made the toxin. When the toxin gets absorbed by the roots it will be passed to the seeds, then to the bats that feed on them and then to the people.

The implication of this scientific discovery is terrifying. If cyanobacteria produce these neurotoxins, it will have massive ramifications for public health on a global scale. Cyanobacteria are ubiquitous and can be found in almost every aquatic or terrestrial habitat. They are literary everywhere from damp soil, freshwater, oceans, hot springs, bare rock and soil, rocks in the desert, and even Antarctic rocks. The name cyanobacteria come from the color of the bacteria (Greek: κυανός. Kyanós meaning blue). You know these bacteria as blue-green algae, that bloom from fertilizer runoff.

Cox found the presence of BMAA in most of the variety of cyanobacterial strains tested from all over the globe. It is not just the Guam Nostoc strain, it is every strain of this blue-green algae or to be precise 95% of all strains produce BMAA. Because of enormous algae blooms the level of BMAA today needs to be measured and studied. There were studies that measured the levels of BMAA in some of the higher trophic organisms. High concentrations were detected in various species of fish, mussels, oysters, and plankton thus indicating that the global human population is at high risk of bioaccumulation of this neurotoxic compound through the food chain everywhere in the world.

To this day there is no scientific consensus that BMAA exposure through the consumption of contaminated food could play a causal role in various neurodegenerative pathological conditions. In some studies, depending on the methods they did not find BMAA in Alzheimer’s brain tissue in others they do. Measured levels of BMAA in the brain might not mean causality; proximity is not causality. Some of the most compelling evidence was presented at the International ALS/Motor Neuron Disease (MND) Symposium in 2011. There was a research that showed that BMAA is not found in the brain tissue in higher concentrations because it will get incorporated directly into the nerve cell itself. It was shown that BMAA gets incorporated into nerve cell proteins causing the protein misfolding and ultimately cell death. Dunlop and Rodgers reported that the tRNA synthetase enzyme for the amino acid serine mistakenly picks up BMAA thinking that it is serene and then incorporates it into proteins in vitro. This substance is nothing less than pure mutagen. Consequent autofluorescence indicated that the proteins misfolded, and the cells died. What we can say for sure is that BMAA might not cause Alzheimer’s or Parkinson’s disease just by itself, but it does worsen the condition, and it does cause amyotrophic lateral sclerosis (ALS). Now to fully understand the story of BMAA since many people around the world may be exposed to it we might also ask the question why did some individuals get neurodegenerative effects from it, and some others did not?

Cox suspected that vulnerability may reflect a gene-environment interaction. If this single environmental toxin plays a role in different diseases such as Parkinson’s disease, ALS, Alzheimer’s disease, and maybe some other diseases as well, this could represent a gene-environment interaction based on individual genetic resilience. However, no one has yet investigated a genetic basis for BMAA vulnerability. It is the same story all over again. Humans did get exposed to this naturally occurring toxin during normal evolution. What is making this disease increase in prevalence is algae blooms caused by unnatural high levels of nutrient runoff from fertilizer fields, animal waste, sewage, and soil erosion in water that eventually raise the levels of blue-green algae to unnaturally high levels. Some people have better genetics dealing with this some might be sensitive. Also, it depends on how much seafood you eat. The cause of this disease is not hereditary. It is a maladaptation to our current environment. This toxin was found in freshwater fish, saltwater fish, and shellfish. Some of the fish have levels of BMAA comparable to those found in fruit bats in Guam. I cannot give estimates here because BMAA concentration varies from the place of sampling. Some species of crab, for example, might be high or low on the toxicity level depending are their algae bloom in the water or not. The more bloom, the more toxin. However, toxins spread everywhere eventually. This could explain the ALS clustering in populations who live around lakes for example. A number of ALS cases have been diagnosed among residents of Enfield, New Hampshire, a town encompassing a lake with a history of cyanobacteria and algal blooms. There were six cases of ALS diagnosed from 1975 to 1983 in long-term residents of Two Rivers, a small Wisconsin community. The probability that this occurred due to chance was less than 0.05%.

Cyanobacteria species depending on the type have the ability to produce a different array of metabolites, not just BMAA that are also neurotoxins, hepatotoxins, or dermatoxins. BMAA does not have to kill us to be bad. It can cause neurologic damage and increase the overall toxic load on our bodies and have synergistic effects with mercury and lead and all other neurotoxins to enhance cognitive decline.

In the end, it might not be the only thing that can trigger amyotrophic lateral sclerosis (ALS). BOAA triggers lathyrism for example. It is the same type of neuron death as in amyotrophic lateral sclerosis (ALS). American veterans have more instances of amyotrophic lateral sclerosis (ALS) for an unknown reason. The situation in Guam in the last decade or so is promising. Their levels of amyotrophic lateral sclerosis (ALS) are significantly lower than in the past, but now they know what the root cause of this neurologic disease epidemic they had to face was. And without the island of Guam, the rest of the world will still eat seafood thinking that it is health-promoting and safe. The problem with nature is that it is hard to science every molecule that exists. There are thousands of natural pollutants like BMAA in nature. Some of them can even be sexually transmitted like ciguatera toxin that again is produced by algae and built up in the food chain, and again it is thermally and chemically stable. It causes nightmares literally with pain and fatigue and a burning cold sensation. The reversal of temperature sensation, hot feels like cold, and cold feels like hot. It can last for years and in low doses just causes fatigue. The story of a romantic dinner with red snapper in a Greek marinade with wine. Dream tropical paradise vacation turning into cold, painful sex with nightmares. Some of the chronic fatigue syndromes cases are actually ciguatera fish poisoning. In some people, it can cause recurring symptoms during periods of stress, weight loss, exercise, or excessive alcohol use even after 25 years of initial exposure.

Because of all of the pollution, most fish today have infections both from bacteria and parasites. Never eat raw anything from the water ever in your entire life. Forget about sushi. Shifts in the balance of nature have consequences. Everything that is unnatural, and when I say that, I mean everything that our hominin ancestors did not do, or have been exposed to is disease-promoting with the potential for exposure to an unknown amount of unidentified toxins. If there were clean and pristine oceans eating predatory fish is still a bad idea, and eating a lot of fish is unnatural. Fish is inflammation-promoting meat even without all of the pollution.

References:

Passages selected from a book: Pokimica, Milos. Go Vegan? Review of Science Part 2. Kindle ed., Amazon, 2018.

1. Murch, Susan J et al. “A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam.” Proceedings of the National Academy of Sciences of the United States of America vol. 101,33 (2004): 12228-31. doi:10.1073/pnas.0404926101
2. Bradley, Walter G, and Deborah C Mash. “Beyond Guam: the cyanobacteria/BMAA hypothesis of the cause of ALS and other neurodegenerative diseases.” Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases vol. 10 Suppl 2 (2009): 7-20. doi:10.3109/17482960903286009
3. Chiu, Alexander S et al. “Does α-amino-β-methylaminopropionic acid (BMAA) play a role in neurodegeneration?.” International journal of environmental research and public health vol. 8,9 (2011): 3728-46. doi:10.3390/ijerph8093728
4. Brand, Larry E et al. “Cyanobacterial Blooms and the Occurrence of the neurotoxin beta-N-methylamino-L-alanine (BMAA) in South Florida Aquatic Food Webs.” Harmful algae vol. 9,6 (2010): 620-635. doi:10.1016/j.hal.2010.05.002