Dickson D. Despommier on How Parasites Can Prevent Disease
In following excerpt from People, Parasites, and Plowshares: Learning from Our Body’s Most Terrifying Invaders, Dickson D. Despommier examines how some parasites might reduce the chance to suffer from other diseases:
Trichuris suis, the pig version of whipworm, has also been tried with some success in treating patients suffering from Crohn’s disease. This approach was predicated on the unusual finding that almost no one suffers from that disease anywhere throughout sub-Saharan Africa, whereas their parasite-free relatives, now living for several generations in the United States, have rates of this disorder similar for those people who have no genealogical connection to Africa. Thus a hypothesis arose suggesting that the true targets of that disabling immune disorder were our old nemesis, the intestinal worms. Proof of concept was difficult to obtain, as most institutional review boards at every research-oriented medical school remained understandably skeptical regarding the risks and benefits of such an approach and predictably denied numerous researchers’ requests to be the first to conduct such a study. Finally, enough data accumulated from the epidemiology literature to warrant a full-scale test of the hypothesis, and like so many other far-out ideas, this one struck pay dirt. The following is an abstract of a peer-reviewed and published set of studies produced by two gastroenterologists who championed this approach. They based their conclusions not only on epidemiological evidence but also on solid laboratory experimental results using mice and their worm infections to modify diseases such as type 1 diabetes, colitis, and asthma.
There is an epidemic of immune-mediated disease in highly-developed industrialized countries. Such diseases, like in. ammatory bowel disease, multiple sclerosis and asthma increase in prevalence as populations adopt modern hygienic practices. These practices prevent exposure to parasitic worms (helminths). Epidemiologic studies suggest that people who carry helminths have less immune-mediated disease. Mice colonized with helminths are protected from disease in models of colitis, encephalitis, Type 1 diabetes and asthma. Clinical trials show that exposure to helminths reduces disease activity in patients with ulcerative colitis or Crohn’s disease. This chapter reviews some of the work showing that colonization with helminths alters immune responses, against dysregulated in. ammation. These helminth-host immune interactions have potentially important implications for the treatment of immune-mediated diseases. (D. E. Elliot and J. V. Weinstock, “Helminthic Therapy: Using Worms to Treat Immune-Mediated Disease,” Advances in Experimental Medicine and Biology 666 (2009): 157–66)
If we could identify the worm components that the immune system targets, a treatment strategy could be developed that does not require the use of live worms. It should be pointed out that eventually all of those receiving therapeutic doses of worms rejected their infections and were therefore immune to reinfection, thereby terminating the therapy. This unfortunately allowed their original allergic conditions to relapse. Using a worm product (i.e., a nonliving component) to do the same job would allow for a longer treatment period, even if a mild form of immunosuppression was also needed to keep the patient from neutralizing the parasite molecule.
Hookworms have been tried in hopes of modifying other immune disorders, such as celiac disease, an allergy that many people develop to wheat gluten protein, and type 1 diabetes. In this case, however, the infection had no measurable effect on the status of the allergy when the infected patients were given a challenge of wheat glutin. The jury is still out on the efficaciousness of hookworm infection in alleviating the ravages of type 1 diabetes.