As if they didn’t have enough to worry about, people with coronary artery disease — the industrialized world’s number-one killer — are more vulnerable to getting shingles, an excruciatingly painful skin rash, than people without it are. But why this connection should exist has been a mystery until now.
Shingles, whose incidence increases exponentially after age 50, is caused by the reactivation of a the long-dormant chickenpox virus that infected most all people now over 35 years old in childhood. (The advent of a chickenpox vaccine in 1984 has radically reduced rates of infection in younger people who’ve been vaccinated.)
Even after our immune system defeats the active infection when we’re young, the virus lives on inside our nerve ganglia. In older or immune-compromised people, the long-dormant virus can reactivate, crawl along the nerve fiber and emerge at nerve endings as a painful skin rash that’s exceedingly difficult to treat.
In another study I wrote about in early 2016, a team led by Stanford immunologist Connie Weyand, MD, discovered that in coronary artery patients, a kind of immune cell whose job description includes repairing damaged tissue — for example, the tiny tears and scars that accumulate in blood vessels due to, say, high blood pressure — is actually worsening the damage by rendering arterial plaque brittle and prone to breaking up, forming clots, and cutting off the blood supply to the heart.
That 2016 study showed that this wayward immune-cell type, known as a macrophage, is predisposed to go haywire because it’s got a sweet tooth: Coronary artery disease patients’ macrophages tend to suck up far more glucose from the blood stream than they should. Anyone who’s ever raised little children probably knows what that means: These glucose-guzzling macrophages are in a constant state of excitement. Their revved-up sugar metabolism generates tons of dangerous free radicals, leading to the production and secretion of inflammatory substances that promote arterial plaque buildup and breakup.
In the new study, Weyand and her colleagues revealed that those same sugar-crazed macrophages — and not just the ones sitting in our arteries exacerbating plaque, but throughout the circulatory system — are doing another wrong thing: They’re actively shutting down our immune system’s ability to mount a response to infectious pathogens, including latent ones such as the chickenpox virus that lurks within most of us, waiting for its chance to explode on our skin.
Weyand, her immunologist collaborator/husband Jorg Goronzy, MD, (who’s a shingles expert) and others have been compiling increasingly convincing evidence that the ills of old age don’t occur independently of one another but are, instead, different faces of a many-headed hydra called inflammaging: our immune system’s diminishing ability, as we get older, to protect us against infections and cancer or respond to vaccinations, combined with — paradoxically — its increasing tendency to wallow in a state of vague, nonspecific irritability like a snarling watchdog with a hairspring-trigger.
Previously: The biggest killer of them all: Inflammaging, And one for the road: Why a single shot may not (always) be enough to stave off shingles and Glucose-guzzling immune cells may cook up coronary artery disease, Stanford study finds
Photo by Adam Engelhart