I have a piece in the NYT Mag on the community of people who self-treat with parasites. They operate almost entirely outside of any regulatory or medical oversight. This is a story about desperate people trying to cure themselves with an unproven therapy. It’s not a story about whether the therapy works. We don’t know if it does. And in fact, there’s good evidence, in the form of double-blinded placebo-controlled studies on the pig whipworm that failed to show any benefit, that this approach and the organism trichuris suis does NOT work. More on this in a bit.
For now, I hope readers — and particularly scientists and medical professionals — consider the following. This is happening. It ain’t gonna stop. The phenomenon will continue. So it would be nice if somehow the people doing this could be monitored either by their doctors or, not mutually exclusive, by scientists. And it would be really nice if the people who responded — the success stories like Vik and Amy — could be studied. That way, new insights could be captured in the scientific literature, as they were in Vik’s case.
I know that’s hard to do with medical ethics and such, but again as Vik’s case study indicates, it’s not impossible. And as his case also shows, you can learn a lot even from singleton case studies. So, to reiterate, it would be great to figure out a way for these people to be studied both for the benefit of science, and for their own safety and wellbeing.
ABOUT THE THEORY
At this point, probably dozens of rodents studies suggest that parasite infections can prevent immune-mediated disease. But here’s what’s usually overlooked in these studies: Scientists tend to infect the animals with parasites and THEN induce the disease they want to study — colitis, say. The parasites can prevent the emergence of the disease in this type of scenario. But that’s a very different proposition than sending an already existent disease into remission with parasites. I don’t know why this all-important fact is almost always overlooked. The animal studies usually don’t show a curing of disease. They show prevention of disease. It’s not the same thing.
And this is true of the greater theory as well. It predicts that people who are naturally infected with parasites will probably develop autoimmune, allergic and inflammatory diseases less often than those who aren’t. That’s pretty well supported by epidemiological studies. But curing already established diseases is another matter entirely. There’s no good evidence on that front. Not yet.
For those who might consider self infecting willy-nilly, know that you may make your disease worse. Here’s a good paper on that possibility. Why? Because there’s variety within these disease entities — within what we call Crohn’s or colitis. My inflammatory bowel disease may not be the same as yours. And indeed, in certain animal models, parasite infections worsen the condition rather than fix it.
WHAT HAPPENED WITH THE PIG WHIPWORM?
Now, about Joel Weinstock’s pig whipworm. I mention his objections to how the Coronado Biosciences trial was run in the article. An additional objection raised by Detlev Goj, the MD who developed the process for producing whipworm eggs for human consumption (grown in hyperclean, miniature Danish pigs) is that Coronado changed the formula of the buffering solution for the whipworm eggs just before the trials. That’s the liquid used to store the ova.
Coronado’s scientists allegedly raised the Ph, making the solution less acidic. Goj thinks this weakened the organism. Coronado counters that they had quality control — that the eggs were tested for viability. But Goj thinks that weak eggs could still pass a viability test, but no longer hatch well in people — that the altered buffer solution could weaken them. That’s because the viability tests occur in pigs—their native host–where they presumably hatch easily even if weakened. But they’re actually meant to work in people.
It’s hard to know what to think about any of this, honestly. I tend to suspect that the most obvious answer — that the agent doesn’t work — is the most likely. But who knows. I have spoken to people who claimed the pig whipworm did wonders for them. Is that all placebo? Perhaps.
The broader point, though, is that if parasites really do cure disease, it shouldn’t be so darn difficult to prove it scientifically. And the only semi-robust evidence that parasites can cure disease are Joel Weinstock’s original 2005 studies, which were quite small.
Of course, different organisms engage with their hosts in different ways. Alex Loukas suspects that the pig whipworm, which is adapted to pigs, doesn’t have the ability to really modulate the human immune system. He thinks it was doomed from the start. Yet he firmly believes in this approach — but with human hookworm. And he has that tiny uncontrolled experiment on celiac volunteers showing benefit.
P’NG LOKE’S WORK
Here’s one of P’ng Loke’s studies showing that parasites could correct microbial dysbiosis in macaques. This is in contrast to what I was saying earlier about there being little evidence showing parasites could cure already-established disease. In this case, parasites caused monkey colitis to remit. It did so in part by correcting the microbiome, causing a rebound of anti-inflammatory bacteria. Those monkeys have spontaneous colitis, by the way, a huge problem in captive macaque colonies everywhere. And that’s Vik’s whipworm. It’s human-adapted. Ultimately it didn’t survive in these monkeys. There’s some talk about treating them with a parasite adapted to monkeys. We’ll see.
Here’s P’ng Loke’s study on deworming naturally parasite-infested Malay villagers and seeing a decline in those antiinflammatory bacteria. One important takeaway from this study relates to gene-helminth-microbiome interactions. There’s a variant of a microbial sensor gene called NOD2 that increases the risk of Crohn’s. Loke showed that mice with that variant tended to have a lower abundance of anti inflammatory bacteria thought to prevent Crohn’s. Meaning that the gene seemed to increase the risk of disease by unfavorably shaping the microbiome.
But he’s also discovered that having a helminth present essentially cancels out the corrupting influence of the NOD2 gene. It causes those anti inflammatory bacteria to rebound despite the gene. One implication is that people with the NOD2 gene may not have the same liability toward Crohn’s when helminths are also present. Of course, parasites used to be present in our guts basically all the time. So it’s their absence that may have unleashed our own genetic tendencies toward autoimmunity.
And another thing: The study suggests that perhaps it’s those people with certain gene variants that cause dysbiosis, like the NOD2 variant, that will respond to helminth therapy. Other people with different underlying disease pathways may not.