Mammalian-meat allergy differs from most other food allergies in several important ways. One is the delayed reaction; it’s not uncommon for sufferers to wake up in the middle of the night, hours after a steak dinner, covered with hives and struggling to breathe. By contrast, those with food allergies to peanuts usually develop symptoms within minutes after ingesting the offending food. And whereas in most cases of allergy, the immune system pursues a protein, meat allergy is set off by a sugar.
Another unusual aspect of meat allergy is that it can emerge after a lifetime spent eating meat without problems. In other food allergies, scientists think that children’s immune systems may never learn to tolerate the food in the first place. But in meat allergy, the tick seems to break an already established tolerance, causing the immune system to attack what it previously ignored. One way to understand how the parasite pulls this off is to consider its bite as a kind of inadvertent vaccine.
As it happens, an immune response to alpha-gal is also what drives, in part, the rejection of tissue transplanted from animals to people. Scientists have developed genetically modified pigs meant to supply parts that can be grafted onto human bodies without eliciting an anti-alpha-gal immune reaction. Now, as awareness of the meat allergy spreads, there has been talk of using such alpha-gal-free pigs for food — pork chops your doctor can prescribe if you find yourself allergic to meat.
Moises Velasquez-Manoff
Fascinating article about a condition I had never heard of before: meat allergy (specifically red meat, as bird and fish meat do not contain the specific sugar molecule triggering this allergic response). As with many current issues, a closer investigation uncovers links to other areas, from our changing life styles and ecological imbalances that lead to higher numbers of ticks, to our evolutionary past. SF author Peter Watts also wrote about this strange reaction on his blog, lamenting that he missed the opportunity to mention it in Blindsight as the reason for his vampires turning to cannibalism.
One explanation for the disappearance of alpha-gal is that it was driven by some catastrophe, a deadly infection that afflicted Old World primates, perhaps, and as a result maybe these distant relatives of ours stopped being able to produce the sugar because doing so conferred an evolutionary advantage. The mutation that eliminated alpha-gal could have improved a primate’s ability to fight off an infection by enabling its immune system to more easily distinguish between its own body and some pathogen with alpha-gal.
What could this pathogen have been? In the late 2000s, Miguel Soares, a scientist at the Instituto Gulbenkian de Ciência in Oeiras, Portugal, began to suspect the plasmodium parasite that causes malaria. Because the protozoan is so deadly and has historically been so widespread in warmer climes, geneticists often say that malaria has been the single greatest force shaping the human genome in our recent evolutionary history. The parasite remains a leading cause of death in the developing world. And it’s coated in alpha-gal.
Soares and his colleagues investigated a rural Malian population that was naturally exposed to malaria. As it happens, humans produce some antibodies to alpha-gal all the time. They’re not allergic antibodies like those responsible for Lee Niegelsky’s anaphylactic experience, but antimicrobial ones that give rise to a different, less drastic immune response. Between 1 and 5 percent of all the antibodies circulating in any person, a remarkably large quantity, are directed at alpha-gal, Soares estimates.
Model of delayed anaphylaxis to red meat
The α-Gal syndrome and the ‘glycolipid hypothesis’. Epitopes containing α-Gal are consumed as glycoproteins and glycolipids in mammalian products. Neutral glycosphingolipids account for most of the α-Gal-bearing lipids. The mechanism and efficiency of transit through the epithelial barrier is unclear and may involve passive or active processes. Glycolipids are packaged into chylomicron lipoprotein particles, although incorporation into HDL within the intestine is also possible. These lipoprotein particles transit via the lacteals into the thoracic duct before entering the systemic circulation at the left subclavian vein. Lipids can only filter into interstitial tissue after passing to the relatively smaller LDL or HDL particles. Peak levels of lipids emerge from the thoracic duct ~4 hours post-prandial.
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