It’s easy to decide that iodine deficiency plays some role in neurological diseases like ALS and Alzheimers. For over fifty years we’ve known that you’re much likelier to get one of these diseases if you spent your infancy in a region that’s deficient in iodine. Another example: exposure to the fungicide maneb dramatically increases the chances of getting a neurological disease from a toxin; maneb works by disrupting the use of iodine in animals. Our instincts shout that iodine must be involved; but we can’t say it out loud. Although iodine deficiency remains the number one cause of mental retardation in the world, we can’t prove it has a role in Alzheimer’s or ALS. No one has found a smoking gun.
A deficiency in thiamine (commonly known as Vitamin B1) is also a tempting suspect. For nearly a hundred years we’ve known that a severe B1 deficiency causes confusion, memory loss, paralysis, and death. The disease (called beri beri) includes all the symptoms of the worst neurological diseases. And the effects can be startlingly fast, first paralyzing and then killing the victim within days. Many scientists are scrambling to prove that thiamine deficiency is involved in Alzheimer’s and ALS; some are confident they’re close to a solution. But humans can store B1, we get it in our diet, much of our food is fortified with it just to make sure. How in the world would a modern American become so deficient he would develop neurological symptoms? It just doesn’t seem likely. Something’s missing.
I got to wondering about one aspect of thiamine that seems a little weird: the storage of the vitamin in our bodies. Animals, including humans, can’t manufacture thiamine, so they have to get it from their diet, or from the bacteria in their intestines. A human can store enough to last anywhere from one week to a month. After that, unless it’s replenished, they start showing symptoms. A cow stores more; beyond that, bacteria in its complicated digestive system churn the stuff out. Unlike other animals, pigs store a lot of thiamine in their muscle tissue. In one experiment, young pigs thrived for two months without any thiamine in their diet. At that point, the pigs showed no side effects so they stopped the study; we don’t really know how long a pig can survive. Pigs seem to be the champions of thiamine storage.
But goats can’t store thiamine. Luckily, the first of their four stomachs teems with bacteria that produce it. A goat might have 200 times as much thiamine in its blood as its human caretaker. As long as a goat keeps eating, the bacteria provide it with all the B1 it needs. But if a goat stops eating, or eats something that destroys thiamine (like moldy straw) or eats too much grain, it comes down with “goat polio.” Like the human B1 deficiency, beri beri, the symptoms include confusion, “star gazing,” and ultimately paralysis and death. Without thiamine, a goat can die within a day or two. That’s fast.
Thinking about this in the middle of the night, I got an idea: if something mucked up a human’s ability to store thiamine, that might cause a sudden case of beri beri including symptoms ranging from depression, confusion and memory loss to paralysis and death. I tried to find an article that explained the mechanism of thiamine storage, but couldn’t find one. What I did find was just as interesting: when people suffer from an over-active thyroid, so they have too much thyroxine in their system, they can’t store thiamine.
That’s right. In those fairly rare situations where a thyroid gland pumps out too much product, one of the results is that humans can’t store Vitamin B1.
At first this just puzzled me. People point to an iodine deficiency when they talk about a connection to neurological diseases. And iodine deficiency causes the thyroid to under produce, not over produce.
But there’s one exception to that. When people have been deficient in iodine for a long time, their thyroid works extra hard trying to compensate. It can work so hard it swells until it’s a visible lump in a person’s neck called a goiter. This is a huge problem in third world countries. The cure is simple: give the patient iodine. But that swollen thyroid gland has been training for a long time to work very hard. If you provide too much iodine right away, the thyroid acts like a revving race car whose brake is suddenly released. It will flood the body with thyroxin to the point the patient can suffer a heart attack.
Here’s the hypothesis. I don’t know that this is true, and maybe other people have thought of it. It’s just an idea:
Could something similar happen in people who have had a milder iodine deficiency for a long time? Maybe not diagnosed; the patient probably has no visible goiter. Just a thyroid that’s been working hard against the emergency brake for too long. The patient probably feels tired all the time and tends to gain weight. Then, he changes his diet. Maybe he starts eating seafood, or iodized salt. Maybe he moves to a region that isn’t deficient in iodine. For whatever reason, he now has enough iodine and his thyroid gland explodes with joyful production. Suddenly, his body has more thyroxine than it knows what to do with. He probably feels more energy than he has in years, so he doesn’t complain. What he doesn’t know, in this hypothesis, is that now his body can’t store thiamine. If he gets it in his daily diet, fine. But perhaps his new diet doesn’t include enough. Or maybe by evil coincidence, he eats something that destroys thiamine before he can absorb it. This combination of events would be rare, but possible. Within a very short time, maybe less than a week, he starts showing symptoms of a B1 deficiency. Routine blood tests wouldn’t catch this. In fact, before 2008 blood tests failed to accurately measure thiamine levels in the blood.
The original experiments that led to the discovery of B1 noticed that the damage from thiamine deficiency was reversible when caught in time. Chickens showing signs of paralysis made a full recovery when they got the vitamin on one day. A day or two later they would survive, but remain paralyzed. After a certain time, the disease was fatal. So, if this little theory is correct, patients who ultimately got some B1 might recover or not, depending on the timing. That would make it much more difficult to notice the connection. I can see why people might overlook it. By the time anyone checks for thiamine, the levels could be normal again, with the damage already done.
Consider the natives of Guam (known as Guamanians or Chamorros) in the 1940s. They came down with the symptoms of ALS at such an alarming rate that “lytico bodig” was the number one cause of death. But why? Scientists have focussed on the toxins in the cycad nuts they ate, which can cause these symptoms, but only in high concentrations. Maybe there was an additional contributing factor. Thiamine deficiency was considered the largest health problem in the South Pacific (presumably including Guam) until mid 20th century. But the lytico-bodig disease seemed to lie dormant for a long time and then strike suddenly, sometimes years after a patient had left Guam. That’s not typical of a vitamin deficiency.
When Japan occupied Guam in 1942, it commandeered the natives’ food and forced many Guamanians to work growing food for the Japanese military. The plan failed; the island couldn’t grow enough food to support all the Japanese soldiers, let alone feed the natives what was left. Chamorros were chronically hungry; many hid in the jungles for years and had to subsist on whatever they could find. Was their diet deficient in iodine? We can’t know, because the very first study of iodine on the island wasn’t begun until 2012 after scientists discovered that the islands of Fiji and Vanautu were deficient in iodine. If the results have been published, I haven’t found them.
If the plants and animals of Guam had the same low levels of iodine as Fiji, the Guamians who spent years in the jungle may have developed thyroid glands that worked very hard to compensate. When they came out of the jungle and caught some fish, they may have created a perfect storm. The seafood contained a lot of iodine, so their thyroid glands shot into overdrive. The excess thyroxine may have prevented them from storing whatever thiamine they ate. Plus, they ate the fish raw, and many fish contain thiaminase. Unless destroyed by the heat of cooking, thiaminase breaks apart thiamine molecules in the body. The final fatal puzzle piece may have been the toxin BMAA which they got from eating cycad nuts and fruit bats. By itself, the concentration of toxins may not have induced paralysis. But in combination with the sudden thiamine deficiency, maybe it was.
In 1952, the Philippines (the largest rice exporter in the region) passed a law mandating that all its rice must be fortified with thiamine. No Guamanian born after 1952 has been diagnosed with “lytico-bodig.”
Perhaps that’s not just a coincidence.