Obesity and Covid-19: a tale of two pandemics
Covid-19 is a having a massive impact on humanity. But why have we seemingly slept-walked our way into one of the biggest risk factors of all, an obesity pandemic?
As humans develop as a species, the challenges we face continue to change. We are increasingly moving into a world where the threats to our survival are becoming very different to those faced by other organisms, and it is possible that our intrinsic survival mechanisms have not yet caught up with the 'world of abundance' we are increasingly inhabiting.
As food acquisition becomes ever easier, mechanisms evolved by our body to drive us to consume as much as we can get may in fact risk pushing us into obesity. Obesity is a major risk factor for many diseases such as cardiovascular disease and type II diabetes, and it can negatively impact mental health.
More relevant at the moment is that obesity also dramatically increases the risk of poor outcomes with COVID-19, as outlined by the World Obesity Federation report released in March 2021. Of the 2.5 million deaths due to COVID-19 reported by the end of February 2021, a staggering 2.2 million, the report states, were in countries where more than half of the population is classified as overweight.
The COVID-19 pandemic has been a stark reminder that the health of our population is, in many ways, fragile. In July 2020, Public Health England published a report emphasising the negative impacts of an overweight or obese BMI on outcomes following COVID-19 infection. This could be explained by the increased incidence of hypertension and type II diabetes in these individuals - both major risk factors for worse COVID-19 prognosis - but the picture is likely more complicated than this. Higher BMIs may be correlated with lower levels of a hormone called adiponectin.
Lower adiponectin levels, some lines of evidence suggest, are associated with impaired lung function, possibly owing to its anti-inflammatory effects. And poor lung function can make respiratory infections much more dangerous.
Despite the risks of its excess, fat, or adipose tissue, has a diverse range of functions that should not be overlooked. It acts as an energy store that provides resources for necessary human functions, such as growth and reproduction; it also provides thermal insulation and buoyancy. So it is easy to see how human would have benefited from this over evolutiony time: maximising adipose tissue is a healthy survival strategy for coping with periods of food shortage and also can help to overcome hostile environments.
As humans began to settle and form communities, uncertain food supplies meant that having excess body fat was often regarded as a sign of wealth and prosperity in many cultures. For example, the semi-historical Chinese Budai monk is traditionally depicted with a round belly, representing abundance.
We may well also have our fat stores to thank for brain development early in life. Our brains have an extremely high energy demand, accounting for an estimated 20% of our total energy expenditure in adulthood and a staggering 60% in newborns. Particularly in stressful situations, body fat may be responsible for guaranteeing energy supply to the brain. Fat even has a role as an endocrine tissue, receiving and sending out hormonal signals involved in a host of processes ranging from appetite control to tissue repair.
But whilst fat does have its uses, just like most things in life, too much or too little can be detrimental to health, and there are many reasons why this may occur. During our evolutionary past, availability of food would have been the challenge and indeed still is in some regions. According to the State of Food Security and Nutrition in the World, nearly 690 million people went hungry in 2019. Nevertheless, another important consideration lies in the form of control of hunger and appetite.
Hunger motivates the consumption of food, while satiety gives feelings of fullness. The regulation and balance between these sensations is complex and remains an area of ongoing research. The regulation of hunger has many moving parts. When food passes through the gastrointestinal tract, the increased "stretch" it imparts is conveyed, via nerve fibres, to inhibit the "hunger centre" in our brains. A neuropeptide hunger hormone called orexin meanwhile works to promote wakefulness and the desire to eat, while hormones like cholecystokinin, released when fat-rich foods are consumed, act to suppress hunger. In contrast, as the stomach begins to shrink when food moves out of it, the hunger stimulating signal ghrelin is released.
Other signals can provoke feelings of hunger too, such as the fight-or-flight hormone adrenaline. Evolutionarily speaking, this likely reflects the increased need for energy release in situations of physical stress. But, in the modern world, these mechanisms may be contributing to problems such as stress eating. Psychological factors can also affect our short term desire to eat and motivate us to prioritise eating over exercise. In the past, these would have served as key drivers for humans to face environmental risks and adversities to obtain our next meal. But when ample calorie-rich food is only a Deliveroo ride away, these reactions are instead turning a behavioural lifebelt into a spare tyre around the average person's middle.
A key player in the long-term regulation of appetite is the hormone leptin. Leptin is produced by adipose tissue and is transported in the blood to act on a range of different organs, including the brain, where it inhibits feeding. Its levels vary exponentially with fat mass, such that higher levels of body fat result in increased leptin secretion and thus, in theory, a decreased drive to eat. Levels also vary with time of day, rising between midnight and the early hours of the morning - presumably to deter dangerous nightime foraging. This makes sense evolutionarily: humans rely predominantly on visual input for their perception of the world but lack detailed night vision, so motivation to find food at night would be disadvantageous. Leptin concentrations are also suppressed in stressful situations, such as sleep deprivation or emotional stress. Again, while this makes sense historically, when any environmental stress would likely present a physical challenge that required a physical response and increased energy requirements, but in modern society, where many of our sources of stress come from behind a screen, the increased drive to eat serves no real purpose and instead might be leading to damaging health effects.
Mutations anywhere along the pathways controlling food intake, such as congenital leptin insufficiency, can also lead to long term obesity. These are not just restricted to humans – a significant proportion of labrador dogs, for example, have mutations in the protein POMC that lead to uncontrollable hunger and a lack of satiety. Therefore, they have the highest rates of canine obesity out of all breeds - but this comes with some advantages for humans, as their voracious appetite renders them highly trainable! Nevertheless, such changes likely reflect random mutations rather than an old evolutionary advantage.
There is even some widely contested evidence that survival methods can kick in as early as during fetal development in utero. The notorious thrifty phenotype hypothesis outlines that babies born to mothers who were experiencing food restriction during pregnancy are more likely to develop obesity and type II diabetes later in life. This most likely reflects changes that occurred to optimise survival of the newborn in a nutrient-poor environment – but if adequate food was available throughout life, lead to pathological change.
In reality, the development of obesity stems past simply an abundance of food. This is a complex disease produced by several interacting factors that may well have evolved to give survival advantages in terms of food acquisition. Whatever the basis, obesity remains an important issue that should continue to be given importance, both from healthcare services and on an individual level.