Until recently, and even in common accounts today, bodily and mental ills were viewed as separate afflictions. Although hysteria and currents of magnetic fluids provided physical hypotheses for some mental disorders, the psychoses that most distorted reality were interpreted as outcomes of warring forces of the psyche, employing energies and entities—libido, cathexis, superego—that could not be observed or measured, while diseases of the body, attributed to miasmas in the air for centuries, came to be seen as results of germs.
The biopsychosocial model of disease helped to replace body-mind dualism with a unified account of each individual’s struggle to preserve their lives. It was less successful in dealing with disorders as global catastrophes, however. Epidemics and pandemics call for a new battery of concepts that have eluded public education: the difference between antibiotics and vaccines, the ecological fallacy, zoonotic diseases, and syndemics, or the synergistic interactions among epidemics.
One of the past century’s buzzwords, stress, is accepted today as a pathway for infections to attack the mind, without much public awareness of what this may involve. The ability of pandemics to present both physical and mental dangers because of stress, as COVID-19 does with obesity, takes more than a newspaper headline or TV chyron to explain. However, it bears looking into as a psychological phenomenon.
BIO: Any infectious disease starts with an infection—by bacteria, viruses, parasites, or fungi. The body normally fights such infections with the immune system, which has been overwhelmed by the unfamiliar coronavirus that causes COVID-19.
When we’re sick, we may feel pretty bad. Along with weakness and having to avoid others, the disease becomes stressful. The stress not only makes you sicker, but you become vulnerable to other disorders, like obesity.
Stress makes us eat more partly because one of the stress hormones, cortisol, turns us in that direction if the stress persists. (Not saying that acute stress makes us long for pizza. Comfort foods are iffy, since they address social needs more than appetite and spring from negative affect, whereas stress can be associated with positive or negative experiences.)
COVID-19 evokes stress, which can increase body fat to the point of obesity. Fat is not a villain but a needed part of the body, though we may not like it. The brain has a high fat content and needs fat, in the form of myelin, a fatty sheath for many axons. However, an obese body cannot be a healthy body, so the widespread prevalence of obesity has been deemed an epidemic.
Evolution gave us our bodies, but today heredity and our environment both govern obesity. You can get the big picture in this excellent review from the New England Journal of Medicine. The genetic factor is so strong that we can only manage to lose about 10 percent of our weight. Even less than that can help our health, but the environment may interfere.
The genes that affect obesity evolved from mutations a long time ago, but our culture also makes us want to overeat. As a result, though we have the same genes as our parents and grandparents, we tend to be heavier than they were, and it’s not just because they did manual labor and we sit in air-conditioned offices.
PSYCHO: Obesity has biological, psychological, and cultural origins. It interacts with COVID-19 in a number of ways. In the U.S., the interaction is greatest in the southern states. A common source of interaction is stress.
Stress is connected to obesity in a variety of ways. Cortisol causes sugar to be released into the bloodstream for quick energy, but that mechanism for fighting or fleeing an angry bear evolved before the social complexity of civilization arose to afflict us with stress-inducing decisions that do not benefit from fight-or-flight impulsiveness. (Emotions unquestionably influence decision-making and might be mistaken for a sugar buzz, but that is not an effect of cortisol.)
For all of us enmeshed in the complexities of the modern world, Tomiyama has illustrated links between stress and excessive eating in cognitive executive function, impaired behavioral self-regulation, decreased physical activity, and sleep deprivation, as well as in physiological responses that may have preceded the behavioral changes in evolution, including the effects of cortisol, potentiation of reward processing in the brain, changes in gut bacteria, as well as hormonal (leptin and ghrelin) and neuropeptide (neuropeptide Y) responses.
But as the author explains, these are not independent means of channeling stress. There are a number of feedback loops, and obesity, measured as BMI, does not signal its causation.
The largest feedback loop in the connection between stress and obesity is the action of obesity in increasing stress, from sources such as the stigma attached to obesity and health anxiety aroused by sleep apnea and cardiovascular problems associated with obesity.
Controlling stress offers opportunities to reduce obesity. When obesity evolved, though, stress often arose from crises that may differ from those we face today, particularly in psychosocial relationships. The multiplicity of causes and effects may seem beyond comprehension, yet a global pandemic with a single cause, a known viral infection, provides an example of how epidemics can interact, a deadly respiratory disease with the global and mostly behavioral epidemic of obesity, an interaction labeled a syndemic, in which COVID-19 stresses humans around the world to cause obesity, while obesity makes the vulnerability, danger and treatment for COVID-19 more difficult.
Interaction is sometimes misunderstood, as decades of fruitless debate over the nature-nurture question has demonstrated, ending in concessions that nature and nurture do not compete for the control of behavior but interact from the moment of conception, so that what emerges could not have been predicted from either genes or the environment alone.
Similarly, COVID-19 and obesity, pandemic within pandemic, hurt the population more than either pandemic could alone or serially.
Calling COVID-19 and obesity interactive does not mean merely that they are additive like coats of paint, disease upon disorder, but that each influences the effects of the other in many kinds of feedback loops. We are familiar with interactions between drugs and food (or other drugs), whereby effects appear that neither a drug in question or a food would have caused on their own.
The risk of contracting COVID-19 or obesity, or both together, is definable from population studies, but we evaluate risk individually by scariness, not statistics, and experts are not always good teachers. To escape death or obesity that may accompany the recent coronavirus, many people have eschewed masks, social distancing, lockdowns and even vaccinations—with scant regard for their neighbors—in favor of an older escape: running to nature. Those who can afford it have abandoned the cities in favor of more isolated and healthy-looking surroundings. Even those of modest means have found refuge in nearby hideaways, whose denizens might not be infected. Our fearful migrations proceed in opposite directions, southward to escape epidemics of disease and obesity, northward to escape epidemics of crime.
SOCIAL: As a population, we have been here before, and recently, in confronting the interacting threats of climate change. We are still trying to find ways to move past denial, relying more on emotions than on reason.
The outcome we need to pursue is not merely to return to homeostatic balance but to confront the allostatic load that pandemics present. Allostatic load, or the strain of making frequent bodily adjustments to pending environmental changes, is a consequence of chronic stress. Allostasis is normally an adaptive, active, anticipatory process, unlike the better known but reactive and relatively passive homeostasis.
Understanding the syndemic of COVID-19 and obesity may be easier, because it is so personal, than other interacting stressors. Understanding syndemics is worthwhile because syndemics are becoming recognized more frequently and the conclusions from studying one of them can be applied to others. This will be especially desirable when, as now, physical threats interact with seemingly very different psychosocial attacks, making new concepts helpful. We already have the example of ants who, when attacked by a fungus, quickly formed a protective shield to protect the colony’s queen. Unfortunately, Americans recently applied such protection to a leader who used his recovery to increase the exposure of the population to infection and, perhaps eventually, to obesity.