Trypanosoma cruzi is an insect-borne protozoan parasite and one of the world's most infectious diseases. It causes Chagas disease, which the Center for Disease Control and Prevention (CDC) classified as one of 5 neglected parasitic infections.
Trypanosoma cruzi is an insect-borne protozoan parasite and one of the world’s most infectious diseases. It causes Chagas disease, which the Center for Disease Control and Prevention (CDC) classified as one of 5 neglected parasitic infections.
In its acute phase, infected individuals could have fever, fatigue, body aches, headache, rashes, loss of appetite, diarrhea, and vomiting. Or, they could simply be symptomless. However, chronic infection often resulted in cardiomyopathy and intestinal complications including megaesophagus. In endemic regions (Mexico, Central, and South America), mortality and morbidity are often reported to be high..
It appeared that metabolic syndrome (METS) and Chagas disease may have evolved in a parallel way. Researchers from several prominent medical centers in New York have published a study in Diabetes Metabolism Research and Reviews indicating that METS could be an evolutionary strategy to protect against Trypanosoma cruzi.
The experts theorized that metabolic syndrome’s major benefit may be controlling widespread, potentially devastating infections that the body cannot self-cure, including tuberculosis, and American trypanosomiasis.
The research team fed mice (n=100) a high-fat diet for 8 weeks to mimic the weight gain and systemic changes found in obesity and metabolic syndrome. They infected laboratory mice with T. cruzi (Brazil strain). One hundred twenty mice consumed a regular diet, and of these 20 were also given metformin starting 20 days before infections, 40 were infected with T. cruzi, and an additional 40 were infected with T. cruzi and given metformin starting 20 days before infection.
Consuming a high fat diet protected mice from T. cruzi-induced myocardial damage, and significantly reduced post-infection mortality. Lethality was reduced from 55% to 20%.
The addition of metformin, a drug known to be a reasonable adjunct therapy in tuberculosis cases, reduced mortality to 3%. Both the high fat diet and metformin, which are known to differentially attenuate host metabolism. Both effectively reduced mortality in T. cruzi infected mice.
In humans, the metabolic syndrome appeared to not only activate immunity, but also created metabolic alterations that promote diseases later in life.
According to the study findings, during millions of years of evolution, host resources had been channeled into immune defenses starting early in life, and were used to prevent infectious diseases, especially chronic infections like tuberculosis and Chagas disease. Economically-developed countries had controlled these infections, inevitably producing longer lifespans. Meanwhile, immune system activation had fewer benefits, and residents of these countries no longer need protection from T. cruzi. The evolutionary process didn’t recognize the need to reverse METS, and the result had been an explosion of metabolic syndrome’s negative effects in later life.