Hookworms reduce auto immune diseases?

The idea is that they release an inhibitor substance to reduce the body’s tendency to reject the hookworms.

And the hope is that it might be an inhibitor that reduces autoimmune disorders that are sometimes devastating like Celiac Sprue, Lupus, Rheumatoid Arthritis, Dermatomyositis, Scleroderma.

http://www.realclearscience.com/blog/2015/09/should_we_bring_back_hookworm_to_the_us.html

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6 responses to “Hookworms reduce auto immune diseases?

  1. How Are Hookworm Infections Treated?
    Treatment for hookworm infections aims to get rid of the parasites, improve nutrition, and treat complications from anemia. Your doctor will prescribe medications that destroy parasites, such as albendazole and mebendazole. These medications are generally taken for one to three days to treat the infection.

    Your doctor might also have you take an iron supplement if you have anemia. Your doctor will also help you recover from any nutritional deficiencies you have. If you have ascites, you will add additional protein to your diet.
    http://www.healthline.com/health/hookworm#Complications6

  2. Sort of reminds me of the old (pre-FDA) tapeworm diet. http://nuttyfacts.blogspot.com/2013/08/the-tapeworm-diet.html
    From whayt I see on the ‘net, there are still some folks willing to try it – ingesting tapeworm eggs for rapid weight loss.

  3. Aren’t correlations wonderful? In seeking correlates for the “explosion” in the incidence of autoimmune disorders (or is it simply an increased awareness?) I don’t think I would have settled on the hookworm as a likely candidate. How about tuberculosis,polio, or any other number of infectious diseases whose incidence has dramatically declined over the same period? Shouldn’t they be given a shot at reducing the rate of autoimmune disorders? I think the author is also confused about the role that the body’s immune system plays in eradicating intraluminal parasites. Parasites inside the intestinal lumen are no more “in the body” than the bacteria that populate the lumen of the colon and rapidly bring on severe disease and subsequent death should they penetrate the wall of the intestine and gain access to the abdominal cavity. Remember that the entire gastrointestinal tract is one long convoluted tube that is (potentially) open to the external environment at both ends and thus not really “in the body” in that sense.

    • Ernest, there is more than just correlations. When you look into the mechanics of the most prevalent autoimmune disorders you find that they are all IgE-mediated. What is the normal function of IgEs? Regulating worm populations and dealing with components of worm excreta that get into the bloodstream. No other function has ever been found. Now with their habitual targets missing, the IgEs are trained to our own proteins and glycans. We the citizens of civilized world have been effectively free of worms for as long as we’ve been hearing about allergies.

      Having arbitrarily decided to be rid of one of our integral organs (perhaps not the most glorious or the least troublesome one), we are now dealing with the fallout. People who have never been exposed to worms are affected more than those who have at least had them as children.

      Note, too, that it wasn’t just about us regulating worms using worm-specific subsystems that are now running amok; worms possess extreme skills in fine-tuning our immune system to their own and often to our mutual advantage.

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706953/

      This is one of a few rare cases where unexplained correlations eventually led to understanding.

      • I wonder to what extent my own experience is tied to this. My wife and I went out to a nice dinner last year, and got a Camplobacter jejuni infection for our trouble. It killed her, and triggered a CIDP autoimmune response in me that has left me wheelchair-bound. Apparently the antibodies for C. jejuni are perfectly happy to feast upon the Schwann cells wrapped around peripheral nerves instead.

        ===|==============/ Keith DeHavelle

        • Shockingly sad news, Keith. I am so sorry for you.

          There is probably no direct connection between your experience and the hookworm story, which should properly have been titled “Hookworms reduce autoimmune diseases caused by the absence of hookworms and other parasites”. There are way too many different autoimmune diseases to cover under the same title. The parasite story is (mostly) about mast cells and basophils releasing inflammatory agents and triggering expulsion or encapsulation cascades on the surface of the skin (including “inner skin” lining all our cavities — intestines, lungs, nasal cavity, and sinuses). Those events are set off by chitin-sensitive antibodies called IgE binding something, presumably an antigen. Here’s a nice diagram summarizing how things work:

          http://www.nature.com/nri/journal/v13/n5/fig_tab/nri3427_F3.html

          All antibodies, including IgE, evolve in a complex feedback loop that encourages the proliferation of antigen-binding antibodies while at the same time killing the cells that produce antibodies binding our own stuff. There is almost never a good way to sort all good stuff from all bad stuff based on surface structure. It all works by trial and error, eventually arriving at a reasonable trade-off between false positives and false negatives, but there is no guarantee that such a trade-off can be achieved. The selection mechanism is only good enough to work for most of us under the most common circumstances. The gist of the hookworm story and similar is that the IgE-mediated immunity tends to produce false positives if it has not been exposed to true antigens — arthropod or worm chitin — long enough, especially in the early stages of development.

          Now, Guillain-Barré, CIDP, and many autoimmune reactions following bacterial or viral infections (sometimes vaccinations) are caused by similarities between the antigen and surface proteins or glycans found on host cells. Turns out, there is a lot of similarity between the oligosaccharides displayed on the surface of Campylobacter and mammalian gangliosides:

          http://www.ncbi.nlm.nih.gov/pubmed/22952833.

          In all such cases, the system is unable to resolve whatever small differences there are between the true antigen and the host cell and attacks the host cell by the same mechanism it uses to deal with bacterial and viral pathogens long after the pathogens are gone: IgG- or IgM-mediated phagocytosis. In a way, that is the opposite of what happens in the hookworm story, where problems arise due to the lack of exposure. Exposure to “molecular mimicry” is precisely the kind you want to avoid.

          At this point, I hope your immunological memory is not too good. It will eventually degrade; let’s hope it does so sooner rather than later. It also depends on the amount of inflammation during the original response.

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