Obesity is increasingly recognised as a major health issue and clear links exist between it and serious cases of covid-19, especially fatal ones.

We need a rethink of our understanding and attitudes to fat, large bodies and linked health issues, and become more aware of how obesity is linked to socio-political issues, stress and childhood trauma. There is real danger that discourses about food and obesity become another way of blaming the poor for their poverty and its effects. The overweight are often criticised for being lazy, greedy, lacking control or selfish, yet often what drives eating is far outside consciousness and developed for sensible evolutionary reasons.

Obesity is often described in alarmist language, such as ‘an ‘epidemic’ or ‘public health crisis’. Prejudice against fat is endemic, with common narratives often evoking fear, disgust and blame [1] , attitudes often overlaid with social class and ethnic prejudice [2]. Prejudice against fat is one of the last remaining allowable ones, and most of us have feelings about food, fat and weight that we do not want to admit to. There are thankfully some alternative discourses, such as the Health At Any Size [3] and Fat Studies  [4] movements, which critique many poor quality scientific claims, such as those which automatically equate bodyfat and ill-health. Such movements have highlighted the overt discrimination in many health narratives about fat, including discrimination against large black female bodies [5].

Fat shaming and fat blaming is of course pernicious, and indeed shame cycles are common contributors to unhealthy food issues such as binge eating. Over the decades I have seen too many clients full of self-blame, wracked with self-hate, feeling awful about their bodies and indulging in solutions which simply don’t work,  issues that many, such as Orbach [6] have brought to our attention over recent decades.

Science, biology, evolution and why diets don’t work

The recent science about body set-points and how bodies fight hard to protect fat stores, explains why diets don’t work in the long-term [7]. Dieting only gives short-term gains as the human body strives for homeostasis, so as we consume less calories, our body responds by using less energy, hence in time feeling tired, weak and ‘hangry’, and nearly always, reverting to old eating patterns.  In fact, nothing in our evolutionary history prepared us for living in an environment where calorie rich food was so abundantly on-tap. Our bodies evolved to conserve energy via storing fat, and our adipose tissue (fat cells), are packed with masses of important goodies set aside for future use, such as vitamins and minerals. Fat cells are alive, communicating and signalling, and have been a brilliant survival-aiding resource of millions of years [8], although they can also give rise to more worrying inflammatory processes [9].

Such science is partly why I despair about much policy discourse and health advice, which is simplistic and prosaic, and centred on behavioural advice, like ‘consume less,’ ‘eat healthier’, and ‘move more’. Such an approach shows little understanding of basic biological processes, let alone the social, psychological, political and biological complexities of increased obesity levels. Shifting of responsibility onto individuals anyway reinforces dominant medical individualistic models [10], giving rise to worryingly pathologizing discourses, blaming the obese, and also, the parents of obese children.

Adverse Experiences and Obesity

The area of science which I think is too often missed is the link between obesity and adverse early life experiences, and how life-histories and our socio/political/economic contexts are expressed and ‘lived’ through our bodies, brains, minds and behaviours.  There is a growing literature on the relationship between obesity and both stress and trauma, with childhood trauma associated not only with obesity but also with a hugely increased likelihood of diseases loosely grouped under the heading of metabolic syndrome, including heart disease, diabetes and strokes [11]. The links between ACE’s (Adverse Childhood Experiences) and health issues such as obesity, diabetes, heart-disease and metabolic syndrome, is staggeringly clear, as highlighted for example in this radio 4 program. Stress and anxiety of course have many other worrying psychobiological effects, including increasing the chances of almost every kind of illness, physical and psychological, and indeed of early death [12], [13].

One study, analysing 112,000 subjects, found a very clear link between early childhood trauma and adult obesity [14], [15]. How might this happen? It seems that high stress levels disrupt our metabolisms, having an effect on our body chemistry and on weight-regulating hormones such as leptin and adiponectin, particularly in people who suffered abuse or trauma [16].  We also know that obesity also profoundly affects autoimmunity [17], hence  the possible link between obesity and covid-19 mortality. To dive into the science, in diabetes low insulin signalling undermines glutathione production which is central to antiviral action. Fructose, especially high-fructose corn syrup but also even table sugar, reduces antiviral activity, and indeed whether glucose is controlled or not is very linked to covid outcomes [18].

There is much new science about  the obesogenic effects of stress [19], poor sleep [20], and  the cascade of endocrinological and other effects of stress, including links to poor sleep which in turn links to higher body mass index, less healthy eating [21] and greater risk for obesity [22]. In addition, when stressed, anxious or traumatised a range of things happen to our bodies and brains, including less ability to self-regulate, as well as a drive towards more sweet, fatty and salty ‘obesogenic’ foods, which would have aided survival in our human ancestral past.  In experiments, those induced into stressful states of mind  are much more likely to go for fatty and sugary foods than those in a calm state [23], including even generally restrained eaters [24].

We can blame people for being ‘weak-willed’ or lazy, but it is ‘our evolution what done it’, for sensible survival-based reasons. We know from decades of developmental and evolutionary research [25] how extraordinarily adaptable humans are to their contexts, especially the earliest ones. Our brains, bodies and minds mould to fit into our environments, both in the physical world, where we can survive in artic cold and Saharan heat, and also in emotional worlds where we adapt to violent or abusive or loving or cut-off families and communities. Obesity is in many ways another example of our adaptability, as we see if we look at the research. Indeed childhood obesity is linked to increased numbers of fat cells that remain stable throughout the lifespan [26], as if messages about food, such as likely shortages, predispose to conserving fat stores. The more adipocytes the more desire to  consume calories, and the long-term effect is that childhood obesity is predictive of later health issues [27].

Storing Fat when times are tough

Food insecurity and other stressors lead to increased fat storage, as bodies naturally try to insure against future risks [28]. Stress. including facing an uncertain future, makes us attracted to fattening foods [29]. Linked to this, poverty and inequality induce a propensity to seek high calorie foods  [30]. If you subliminally give people messages suggesting that harsh economic times are around the corner and then you offer them both high and low-calorie food, they tend to choose more fattening food than those given more hopeful messages. Indeed, when both groups are offered the same food, but some are told that this food is high calorie, those receiving messages of economic trouble or hard times consume considerably more of the supposedly high rather than food designated low calorie.

Extraordinarily, if we have a stressful or depressing event 6 hours before eating a high fat meal, then our metabolism slows down and we are more likely to put on weight than someone not experiencing stressors. This can translate to around an 11kg weight difference over a year for stressed or depressed people compared to a non-stressed control groups [31]. Stress and anxiety actually alter the bodies inflammatory responses, which in turn effects how we metabolise foods, which is one way in which stress increases the propensity for obesity [32], again presumably for good evolutionary reasons.

Life-history here makes a surprising difference. Extraordinarily the same meal in the same fast-food outlet has a different effect on disadvantaged populations to the affluent [33], allostatic load and its likely effects on the microbiome seeming to be central in this process. The way our bodies respond to a food is in part determined by people’s whole lived experience, including both long-term lifetime and environmental stressors. This is another reason why just legislating about fast or processed food sales is not enough, we must also look at stress and life-history.

Linked to this, parents with an insecure attachment style who struggle to regulate their own emotions are more likely to have kids who indulge in foods that are less healthy, and who are likely to become obese [34]. This is partly due to using food as a comforter to compensate for unhappy feelings, but the stress is likely to drive both children and adults to not only comfort eat but also to store fat.

This all makes sense from an evolutionary perspective. In our hunter-gatherer pasts when the environment and food sources were uncertain and there was little sustenance available, our bodies pushed to stock up on calories and fat. These are not conscious decisions but bodily-led non-conscious instinctual ones.

Benefits of psychological wellbeing

On the other hand, feeling good about our lives will lead to consuming less. In fact people who do the same activity, such as running a race, and find it pleasurable are less likely to eat high calorie foods than those who are dissatisfied or unhappy about the same run [35]. If you get people to do exercise and tell some it is a pleasurable, relaxing activity while others are told it is exercise, the latter afterwards tend to consume more calories and less healthy foods. Feeling good helps you to eat healthily, creating a virtuous cycle for those without stressors. Clinical experience adds plenty of important angles to these issues. The push to eat when stressed and anxious often of course leads to ‘eating down’ feelings, and self-punishment linked to high levels of self-disgust about body-shape in both obese and non-obese people.

Given all this it seems imperative to challenge belief systems replete with blame and factually dubious assumptions. Current discourse has remained primarily at the level of individual responsibility. The British Prime Minister,  Boris Johnson, whose covid-linked scrape with mortality was probably diabetes/obesity linked, has naively exhorted us to, Tebbit-like, get on our bikes to exercise as well as eat better. This is not enough, especially when factors such as early adversity and its relationship to biological mechanisms are not considered, let alone the power of the food industry.

Addiction and Big-Food

Important here is the ‘addictive’ nature of eating and cravings, powerfully fuelled by the addictive nature of much processed food. Our biological and psychological systems drive us towards pleasurable experiences which aid species reproduction, such as sex and food, such drives being linked to the dopaminergic system,  and centrally involved in all addictive processes. While in some clients we see too low a drive and ‘appetitive’ system, in others we see a very high one, and more often one which has lost touch with ‘real’ needs, such as in drug, alcohol, and other addictions. We can add food addiction to this list, and following high stress, we see worse poor interoceptive abilities, ie less capacity to read bodily signals and know if one is hungry. The propensity for both worse interoception and heightened addictive states is massively increased in trauma, stress and abuse.

Particularly worrying are the obesogenic effects of easy to access high sugar/fat/salty foods designed to stimulate reward pathways. Food companies invest huge sums into researching exactly what quantities of, especially, sugar, fat and salt, and also which tastes, stimulate addictive food urges and the likelihood of customers returning for more.  Alongside this supermarkets invest vast sums in not only marketing but also product placement, such as where exactly to place, at what height etc , the  high profit, less healthy more addictive processed foods.  Calling for a ‘sin tax’ is a wrong-sighted redirection of responsibilities onto individuals and away from culprits such as poverty, childhood trauma, inequality, stressful environments and of course the powerful food industry.

Lessons

What are some of the lessons from this kind of research? Firstly, it does not mean that we should not continue to campaign against advertising which suggests that skinny prepubescent looking bodies are what is attractive. Nor should we let up on arguing that companies who basically sell addictive products should be brought to rights. Such practices are as pernicious and dangerous as selling cigarettes and other addictive health damaging substances. Indeed, it might well be the combination of the fairly recent availability of high calorie, high fat foods with the biological predisposition to consume these in times of stress that has given rise to such an obesity epidemic.

This kind of research could be used to try to halt the tendency of certain already marginalised sectors of society to be blamed for what are basically the effects of stress, fear, unhappiness, inequality, poverty and bad luck, plus a manipulative food industry. Such issues need addressing on a macro-socio-political level, but also with community interventions, improving neighbourhoods. We also do need interventions to help individuals feel better about their lives through wellbeing enhancing help, whether therapy, mindfulness, yoga, exercise, dietary advice and the like. These can make a huge difference but will be but a drop in the ocean if we don’t address the wider, macro socio-political issues such as poverty, inequality, poor economic prospects for so many, degraded neighbourhoods, the lack of hope for increasing numbers of our population and the power of Big Food.

We know that the current climate is particularly dangerous given  how economic downturns gives rise to a reduction of food spending,  buying foods higher in calories and fats [36], and our bodies retaining more fat when stressed. In the face of what is being described as an obesity epidemic we must avoid simplistic and judgmental solutions, many of which blame sufferers. Instead we badly need scientifically valid yet potentially liberating understandings, with the blame, guilt and judgement stripped out, allowing for macro-social, community, family and individual level responses that might lead to better overall mental and physical health, including the reduction in obesity.​

This is truly deadly serious. Obesity has been shown to increase death by covid-19 by nearly 50%, hospital admissions by 113% and ICU admission by 74%  [37]. Incredibly a recent government report  [38] suggested that obesity costs the NHS more than the police, fire-services and judicial systems combined.  Given the clear link between obesity, covid mortality and a range of health issues, we cannot afford not to act.

[1]        A. Ravary, M. W. Baldwin, and J. A. Bartz, “Shaping the body politic: Mass media fat-shaming affects implicit anti-fat attitudes,” Pers. Soc. Psychol. Bull., vol. 45, no. 11, pp. 1580–1589, 2019.

[2]        C. L. Hoyt, J. L. Burnette, L. Auster-Gussman, A. Blodorn, and B. Major, “The obesity stigma asymmetry model: The indirect and divergent effects of blame and changeability beliefs on antifat prejudice.,” Stigma Health, vol. 2, no. 1, p. 53, 2017.

[3]        A. N. Taylor, “Fat Cyborgs: Body Positive Activism, Shifting Rhetorics and Identity Politics in the Fatosphere,” Bowling Green State University, 2016.

[4]        E. Rothblum and S. Solovay, The Fat Studies Reader. New York: NYU Press, 2009.

[5]        S. Strings, Fearing the black body: The racial origins of fat phobia. NYU Press, 2019.

[6]        S. Orbach, Fat is a feminist issue. Random House, 2010.

[7]        J. Fung, The obesity code: Unlocking the secrets of weight loss. Greystone Books, 2016.

[8]        C. A. Wagner, P. H. I. Silva, and I. Rubio-Aliaga, “And the fat lady sings about phosphate and calcium,” Kidney Int., vol. 91, no. 2, pp. 270–272, 2017.

[9]        L. Boutens, G. J. Hooiveld, S. Dhingra, R. A. Cramer, M. G. Netea, and R. Stienstra, “Unique metabolic activation of adipose tissue macrophages in obesity promotes inflammatory responses,” Diabetologia, vol. 61, no. 4, pp. 942–953, 2018.

[10]      V. McFarland, “Neoliberal bodies: ideology and obesity,” Laurentian University of Sudbury, 2020.

[11]      O. M. Farr, D. M. Sloan, T. M. Keane, and C. S. Mantzoros, “Stress-and PTSD-associated obesity and metabolic dysfunction: A growing problem requiring further research and novel treatments,” Metab.-Clin. Exp., 2014.

[12]      C. Van Niel, L. M. Pachter, R. Wade Jr, V. J. Felitti, and M. T. Stein, “Adverse Events in Children: Predictors of Adult Physical and Mental Conditions.,” J. Dev. Behav. Pediatr. JDBP, vol. 35, no. 8, pp. 549–551, 2014.

[13]      S. R. Dube, V. J. Felitti, M. Dong, W. H. Giles, and R. F. Anda, “The impact of adverse childhood experiences on health problems: evidence from four birth cohorts dating back to 1900,” Prev. Med., vol. 37, no. 3, pp. 268–277, 2003.

[14]      E. Hemmingsson, K. Johansson, and S. Reynisdottir, “Effects of childhood abuse on adult obesity: a systematic review and meta‐analysis,” Obes. Rev., vol. 15, no. 11, pp. 882–893, 2014.

[15]      R. Cox, H. Skouteris, E. Hemmingsson, M. Fuller-Tyszkiewicz, and L. L. Hardy, “4.1 Narrative Review,” ACCESS THESIS-A, p. 53, 2015.

[16]      M. Dalamaga, S. H. Chou, K. Shields, P. Papageorgiou, S. A. Polyzos, and C. S. Mantzoros, “Leptin at the intersection of neuroendocrinology and metabolism: current evidence and therapeutic perspectives,” Cell Metab., vol. 18, no. 1, pp. 29–42, 2013.

[17]      C. Tsigalou, N. Vallianou, and M. Dalamaga, “Autoantibody Production in Obesity: Is There Evidence for a Link Between Obesity and Autoimmunity?,” Curr. Obes. Rep., pp. 1–10, 2020.

[18]      L. Zhu et al., “Association of blood glucose control and outcomes in patients with COVID-19 and pre-existing type 2 diabetes,” Cell Metab., 2020.

[19]      A. J. Tomiyama, “Stress and obesity,” Annu. Rev. Psychol., vol. 70, pp. 703–718, 2019.

[20]      M.-P. St‐Onge, “Sleep–obesity relation: underlying mechanisms and consequences for treatment,” Obes. Rev., vol. 18, pp. 34–39, 2017.

[21]      J. S. Kjeldsen et al., “Short sleep duration and large variability in sleep duration are independently associated with dietary risk factors for obesity in Danish school children,” Int. J. Obes., 2013.

[22]      J. S. Dweck, S. M. Jenkins, and L. J. Nolan, “The role of emotional eating and stress in the influence of short sleep on food consumption,” Appetite, vol. 72, pp. 106–113, 2014.

[23]      G. Oliver, J. Wardle, and E. L. Gibson, “Stress and food choice: a laboratory study,” Psychosom. Med., vol. 62, no. 6, pp. 853–865, 2000.

[24]      C. Evers, A. Dingemans, A. F. Junghans, and A. Boevé, “Feeling bad or feeling good, does emotion affect your consumption of food? A meta-analysis of the experimental evidence,” Neurosci. Biobehav. Rev., vol. 92, pp. 195–208, 2018.

[25]      G. Music, Nurturing Natures: Attachment and Children’s Emotional, Social and Brain Development. London: Psychology Press, 2016.

[26]      K. L. Spalding et al., “Dynamics of fat cell turnover in humans,” Nature, vol. 453, no. 7196, pp. 783–787, 2008.

[27]      S. Kumar and A. S. Kelly, “Review of Childhood Obesity: From Epidemiology, Etiology, and Comorbidities to Clinical Assessment and Treatment,” Mayo Clin. Proc., vol. 92, no. 2, pp. 251–265, Feb. 2017, doi: 10.1016/j.mayocp.2016.09.017.

[28]      D. Nettle, C. Andrews, and M. Bateson, “Food insecurity as a driver of obesity in humans: The insurance hypothesis,” Behav. Brain Sci., vol. 40, 2017.

[29]      J. Laran and A. Salerno, “Life-history strategy, food choice, and caloric consumption,” Psychol. Sci., vol. 24, no. 2, pp. 167–173, 2013.

[30]      B. Bratanova, S. Loughnan, O. Klein, A. Claassen, and R. Wood, “Poverty, inequality, and increased consumption of high calorie food: Experimental evidence for a causal link,” Appetite, vol. 100, pp. 162–171, May 2016.

[31]      J. K. Kiecolt-Glaser et al., “Daily Stressors, Past Depression, and Metabolic Responses to High-Fat Meals: A Novel Path to Obesity,” Biol. Psychiatry, 2014.

[32]      J. K. Kiecolt-Glaser et al., “Depression, daily stressors and inflammatory responses to high-fat meals: when stress overrides healthier food choices,” Mol. Psychiatry, vol. 22, no. 3, pp. 476–482, 2017.

[33]      S. L. Prescott and A. C. Logan, “Each meal matters in the exposome: Biological and community considerations in fast-food-socioeconomic associations,” Econ. Hum. Biol., vol. 27, pp. 328–335, 2017.

[34]      B. H. Fiese and K. K. Bost, “Family Ecologies and Child Risk for Obesity: Focus on Regulatory Processes,” Fam. Relat., vol. 65, no. 1, pp. 94–107, Feb. 2016, doi: 10.1111/fare.12170.

[35]      C. O. Werle, B. Wansink, and C. R. Payne, “Is it fun or exercise? The framing of physical activity biases subsequent snacking,” Mark. Lett., pp. 1–12, 2014.

[36]      R. Griffith, M. O’Connell, and K. Smith, “Shopping around? Households’ ability to maintain nutritional quality over the Great Recession,” 2014.

[37]      S. B. H. editor, “Obesity increases risk of Covid-19 death by 48%, study finds,” The Guardian, Aug. 26, 2020.

[38]      “Health matters: obesity and the food environment,” GOV.UK, 2017. https://www.gov.uk/government/publications/health-matters-obesity-and-the-food-environment/health-matters-obesity-and-the-food-environment–2 (accessed Dec. 30, 2019).