Evolutionary adaptations developed to protect the Vikings from an infestation of parasitic worms may have resulted in certain genetic traits that increase vulnerability to certain lung diseases. During ancient times, the side-effects of this adaptation were probably harmless, although as people later began smoking and living longer, the removal of certain anti-inflammatory mechanisms appears to increase carriers’ susceptibility to pulmonary complications, like emphysema.
Emphysema occurs when air sacks in the lungs, called alveoli, become damaged, causing them to merge into one large air chamber as opposed to many small ones. This reduces the surface area of the lungs, which subsequently become less efficient.
Alveoli can become damaged by certain enzymes called proteases, which are secreted by cells involved in inflammation, one of the body’s key immune processes. To keep these enzymes under control, a protein called alpha-1 antitrypsin (A1AT) acts as a protease inhibitor, and is therefore vital in ensuring the lungs remain protected.
People who suffer from A1AT deficiency are therefore more prone to developing lung diseases, particularly if they smoke, since this increases inflammation and therefore sparks the release of more proteases. A1AT deficiency is caused by a particular heritable genetic mutation, which results in the creation of an altered form of the protein.
Archaeological studies of Viking latrines have found evidence of massive infestations of parasitic worms, while genetic analyses of fecal matter obtained during these excavations reveal that a particular mutation of the A1AT gene was prevalent among the population. A new study in the journal Scientific Reports has now put two and two together, suggesting that this mutation may have protected the Vikings from these parasites.
Using blood plasma from donors carrying both the regular and mutated form of the A1AT gene, the researchers sought to determine how levels of antibodies were affected when these worms were present. Conducting their experiments in a laboratory setting, they found that certain compounds released by the parasites destroyed an antibody called immunoglobulin E (IgE) in the plasma of non-mutant donors, but not in that of mutant donors.
This suggests that the mutated variant of A1AT protects IgE from these damaging compounds, which likely helps the body to fight the parasites since the role of IgE is to bind receptor sites on the surface of certain immune cells, activating a response against invading pathogens. By providing such protection, the mutated A1AT ensures that the IgE is able to fulfill its function and initiate the body’s natural defenses.
However, an offshoot of this is that these variants lose some of their protease-inhibiting power, making the tissue of the lungs more susceptible to damage. This would appear to explain the high rates of A1AT deficiency – and corresponding prevalence of emphysema – among present-day Scandinavians.
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