Last month, I blogged about a bacterium--Helicobacter pylori--which can cause a range of stomach problems, but whose eradication in the industrialized world may be contributing to increased asthma rates. Its loss may also be linked to an increase in some other problems, such as acid-reflux disease.
Dr Blaser has discovered, for example, that H. pylori helps to regulate stomach-acid levels in a way that is usually helpful to both itself and its host. If the human side of the loop gets too strong, and the stomach becomes too acid, the bug may produce a substance called cag. The intended effect of this, Dr Blaser thinks, is to say “turn down the acid level”. However, cag also has a side-effect. It is toxic to the stomach lining, and it is this toxicity that provokes the ulcers and cancers for which H. pylori is notorious.
The obvious medical temptation—and, indeed, what has happened in practice—is to annihilate the bacterium with antibiotics. That works as an anti-ulcer treatment, but when H. pylorigoes its homeostatic effect goes with it, allowing the strength of the stomach acid to rise chronically. This acid has a tendency to spill out of the top of the stomach and into the oesophagus. That has unpleasant consequences. In fact the recent drop in H. pyloriinfections has almost exactly matched the rise in gastroesophageal reflux disease (which feels like bad heartburn). Over time, the damage the excess acid does to the walls of the oesophagus may cause cancer.
And long-term usage of acid reflux drugs may be connected to increased problems with osteoporosis.
Man and H. pylori have evolved together for at least 60,000 years. Maybe it's not just the bacterium that needs us.
...even the link between H. pylori and gastric cancer and ulcers is complicated. Just having the bacterium does not automatically mean you will get an ulcer. In the past, most people were infected with H. pylori from their childhoods until they died. Ulcers, however, generally emerge when a patient is in his 30s or 40s. In addition, they are three times more common in men than in women. H. pylori-infection rates, however, are the same in both sexes.
H. pylori also has an effect on two of the hormones that control appetite—ghrelin, which makes you feel hungry, and leptin, which does the opposite. People without H. pylori produce more ghrelin than those with. Though the connection has not been established for sure, Dr Blaser suspects the bacterium’s disappearance could thus be contributing to the epidemic of obesity that is sweeping the rich world.
Contributing...could be. But there's no doubt that too much inactivity and eating are major reasons for people getting fatter. There's also lack of sleep, which drives many people to eat for the energy boost. Et cetera. Excuses are easier than taking responsibility.
What all this suggests is that rather than trying to eradicate H. pylori, a better strategy would be to manage its relationship with humanity in a more sophisticated way. Some people are, genetically, more susceptible to ulcers and gastric cancer than others. For these unfortunates eradication may be the best option. However, if your genes predispose you to asthma or obesity, eradication may be unwise.
Moreover, people are not born with H. pylori in their stomachs. Rather, they get infected when they are young. That means a parent or doctor could choose which strain of the bacterium a child ends up carrying, rather than leaving the matter to chance. H. pylori is genetically variable (not all strains, for example, make cag). Dr Blaser envisages a future in which doctors run routine checks on babies’ genes to find out their susceptibilities, and then colonise those babies’ stomachs with the strain or strains that are best for them. If that happens, H. pylori can come off the endangered species list for good.
That's a joke--H. pylori is not on the endangered species list. Heck smallpox is (thankfully) only found in a few labs, yet it's not considered endangered. Eradication reduces biodiversity, which isn't always a bad thing...though it seems to be with H. pylori.
Comments