We were just saying how researchers have determined that the little bugs inside us have global implications, including the obesity epidemic. Human adenoviruses can evade our body’s immune response, and just hang on forever, sapping our physical resources and convincing us that life is not worth living.
Scientifically they are known as HAdV, and the tiny pests come in more than a hundred varieties or serotypes, of which at least 67 cause disease in humans. They have been sorted into groups A through F, of which groups A, C, and D contain serotypes linked to obesity.
A particularly ornery specimen, known as E4orf1-D36, has a dire potential in humans. It “activates adipogenesis and metabolic glucose and lipid regulation, potentially contributing to obesity-related disorders.” Very recent research has led to suspicion that the bug might be able to regulate the immune responses of its host, and if so, that would be a very big deal:
Modulating E4orf1-mediated adipogenesis, metabolic pathway activation or pro-survival functions in model systems could be a powerful tool for identifying potential therapeutic targets for obesity-associated diseases.
In laboratory glassware, a similar substance is now viewed suspiciously:
Meta-analyses support the association or risk between HAdV-D36 infection and the development of obesity but seems to be more linked to the accumulation of subcutaneous fat rather than visceral fat.
Another member of the gang, known as MCP-1, “plays a role in adipogenesis and recruiting monocytes and macrophages into adipose tissue, potentially contributing to insulin resistance and obesity development.”
The usual suspects
There is a very great temptation to blame the designers of roads, public spaces, and neighborhoods for the ever-growing obesity of humans all over the globe. But some skeptics scoff at that theory, and it is no wonder. Presently, the fattest people in the world inhabit geography where modern infrastructure has infiltrated the least — Samoa, Cook Islands, Niue, and the like.
However, it is possible in this case to suspect the other half of the “big two.” This would be the distribution process, such as importing to remote locales only the worst kinds of food.
The impulse to blame the built environment is understandable, and so is suspicion toward the wiles of advertisers and the complicity of manufacturers who dump all kinds of exotic chemicals into food. After all, we do need targets on which to cast the blame. Because if it’s the fault of the people themselves — if they are messing up, living incorrectly, and willfully persisting in being overweight — then we return to Square One.
It is so easy to slide back into the judgmental, punitive version of theorizing about obesity’s origins. The compulsion is strong, to specifically and definitively blame every obese person, and condemn them all as lazy, irresponsible individuals who care nothing for themselves or others.
Bring on the blame
When other factors can be credibly discounted, then it all comes back to an individual eating too much, too often. And if it is all the individual’s fault, then each overweight person is responsible for holding back human progress, as well as for costing society tons of money.
It is all too easy to conclude that every bit of ridicule and fat-shaming is well-deserved. Maybe “those people” ought to be refused airplane seats. Maybe they really don’t deserve to fly. In fact, they ought to be fat-shamed more often, because then they might quit their antisocial ways, slim down, and give the rest of us a break.
And that is just the start. Unfortunately, blame goes on from there and leads to all kinds of unacceptable thinking which, even if it were technically correct in every aspect, any attempt to turn it into public policy would be unthinkable. Aside from being morally reprehensible, it would be ineffective, which we already know from previous implementations.
Going back to “Ten putative contributors to the obesity epidemic,” we recall how its authors are suspicious of simplistic explanations like blaming the “built environment” or the way food is sold. They say,
Our point is merely that we do not have conclusive evidence that the big two or their individual elements are the preeminent contributors to the obesity. Despite the lack of solid evidence that clearly demonstrates the “culprits” are chiefly responsible for the obesity epidemic, researchers are quick to blame them even in the public eye… Such confidence in one “culprit” is then often contradicted by public health proponent advancing their favored target for intervention.
Your responses and feedback are welcome!
Source: “Perspective on Adenoviruses: Epidemiology, Pathogenicity, and Gene Therapy,” NIH.gov, August 2019
Source: “E4orf1: The triple agent of adenovirus…,” ScienceDirect.com, June 2024
Source: “Ten putative contributors to the obesity epidemic,” ncbi.nlm.nih.gov, November 2009
Image by Dr. Yale Rosen Atlas of Pulmonary Pathology/CC BY-SA 2.0 DEED
FAQs and Media Requests: 
