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Keywords:

  • Causation;
  • emotions;
  • management;
  • psychology

Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

The lack of significant treatment and prevention progress highlights the need for a more expanded strategy. Given the robust association between socioeconomic factors and obesity, combined with new insights into how socioeconomic disadvantage affects both behaviour and biology, a new causal model is proposed. The model posits that psychological and emotional distress is a fundamental link between socioeconomic disadvantage and weight gain. At particular risk are children growing up in a disharmonious family environment, mainly caused by parental socioeconomic disadvantage, where they are exposed to parental frustrations, relationship discord, a lack of support and cohesion, negative belief systems, unmet emotional needs and general insecurity. Without adequate resilience, such experiences increase the risk of psychological and emotional distress, including low self-esteem and self-worth, negative emotions, negative self-belief, powerlessness, depression, anxiety, insecurity and a heightened sensitivity to stress. These inner disturbances eventually cause a psycho-emotional overload, triggering a cascade of weight gain-inducing effects including maladaptive coping strategies such as eating to suppress negative emotions, chronic stress, appetite up-regulation, low-grade inflammation and possibly reduced basal metabolism. Over time, this causes obesity, circular causality and further weight gain. Tackling these proposed root causes of weight gain could potentially improve both treatment and prevention outcomes.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

A better understanding of what causes obesity is essential for improving both prevention and treatment efforts. The strength of association between obesity and the two main perceived culprits, a poor diet and a sedentary lifestyle, tends to be weak or inconsistent [1-4]. While diet can be difficult to measure accurately, which could partly explain why the evidence is not clearer, accelerometers and other objective methods that acquire detailed, valid and reliable physical activity data have been available for at least 15 years [5].

A more likely explanation why the evidence is not more supportive of the big two as the main culprits, given their direct influence on energy homeostasis, is that other causal factors are more influential, particularly in the early parts of the causal chain leading up to the changes in energy intake and expenditure. Most prevention programmes nevertheless continue to focus upon diet and exercise [2, 6, 7]. Treatment programmes are also mainly targeting increased behavioural control of diet and exercise, with minimal long-term impact [8, 9]. Indeed, one could argue that there has been little improvement in effectiveness of either prevention or treatment programmes, given that the obesity epidemic continues to spread across the world, and the vast majority of patients are still not managing to maintain initial weight losses in the long term [8-10].

Arguably, the one exposure that has consistently been linked with obesity is socioeconomic disadvantage, where the strength of association has been considerably stronger than either diet or physical inactivity, and also appears to be growing in strength [1, 11-14]. However, given the lack of an apparent biological link to energy balance, socioeconomic factors have rarely been ascribed a causal role. This may be in error.

The potentially causal role of psychological and emotional distress has been less well researched, but this manuscript argues that this may be a vital link between socioeconomic adversity and the start of weight gain. Important psychological and emotional distress factors include low self-esteem and self-worth, powerlessness and apathy, negative emotions, depression, anxiety, negative self-belief, insecurity and stress.

The aim of this study is to present the case for a new causal model, showing that socioeconomic disadvantage, immediately followed by psychological and emotional distress, represents the starting point for a cascade of events leading to disrupted energy homeostasis, weight gain and obesity. Since the path to weight gain and obesity usually starts in childhood, the model places particular emphasis on risk factors leading up to children's initial weight gain and subsequent obesity. The potential connection to the set-point theory [15] is discussed as well as implications for both prevention and treatment.

A proposed new model of obesity causation

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

Step 1: socioeconomic disadvantage causes psychological and emotional distress

There is a wealth of evidence linking socioeconomic disadvantage with disease, including weight gain and obesity, as well as mental health problems, poor self-rated health and mortality [16, 17]. The effects of socioeconomic factors on mental health problems are particularly noteworthy, with a more or less linear association between income inequality and mood disorders such as depression and anxiety [18-20]. As an illustration, a UK study found that a poor self-rated health was 5.5 times more common at age 50 in individuals born in the lowest socioeconomic quintile compared to the top quintile [21]. The adverse health effects of socioeconomic disadvantage are also found in children [22, 23].

There is clear evidence linking downward social mobility, e.g. by immigrating from a poor to a rich country, to depression and other mental health problems [24, 25]. Another marker of socioeconomic disadvantage is unemployment, which is also strongly associated with numerous adverse health outcomes, including increased mortality [26]. Unemployed adults report 2.5–3 times higher rates of self-reported poor health in cross-country studies [27]. The effect was also more pronounced in countries with less welfare [27].

Longitudinal data from the Whitehall II study found that job insecurity was strongly associated with poor self-rated health and depression [28]. Data from the United States showed that adults with insecure employment were more likely to report minor depression (odds ratio [OR]: 6.8) and anxiety attacks (OR: 3.7) than secure workers, after adjustment for multiple confounding variables [29]. Other studies show similar associations between insecure employment and mental health problems in Japan [30].

Families suffering from outright poverty have been found to eat more processed junk food with high sugar and fat content, but minimal nutritional value [31, 32]. Interestingly, there is a significant association between the price of a Big Mac, as a global indicator of junk food prices, and prevalence of obesity [33].

Having a low education is associated with an increased risk of low self-esteem [34], a major protective factor against poor mental health and strongly related to obesity [35]. Likewise, living in a slum or otherwise deprived neighbourhood predicted poor self-rated health, inflammation, obesity and the metabolic syndrome [36-38], as was living in a neighbourhood with high racial segregation [39].

Another effect of socioeconomic disadvantage is an increased risk of persistent negative emotions (emotions comprise affective, cognitive and behavioural traits that tend to cluster) [40]. Negative emotions are further characterized by their inappropriateness, frequency, intensity and duration, e.g. anger, depression, anxiety, anger, hostility and hopelessness, and are closely linked with a negative self-belief and self-doubt [40]. Negative emotions have been identified as an important link between socioeconomic adversity and a coronary heart disease [40, 41], and socioeconomic disadvantage has been found to greatly increase risk of negative emotions such as anger, life dissatisfaction and hopelessness [40-42].

Step 2: a disharmonious family environment

The distress originally caused by socioeconomic disadvantage is thereafter transferred to the family (Fig. 1) and increases the risk of a disharmonious family environment, characterized by externalization of psychological distress and frustrations, marital discord, negative belief systems and pervading pessimism, inter-parental violence, lack of family cohesion and support, neglect, abuse, parental addiction, excessively harsh or disinterested upbringing methods, and food insecurity [43, 44].

figure

Figure 1. Proposed step-by-step model of obesity causation. Although the figure only shows reverse causality in step 6, all steps in the model are likely to be more or less bidirectional, especially once severe obesity has been established. Skipping of intermediary steps can also occur, e.g. in adult-onset obesity.

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Starting a family and becoming a parent is a major life-changing event that drastically elevates demands and responsibilities, not least financially. Parenting is associated with stress and depression in both mother and fathers, especially when there is pre-existing psychopathology [45-47]. Interpersonal risk factors for increased family distress include parents with pre-existing low self-esteem, low education, addiction and relationship strain, i.e. common results of socioeconomic disadvantage [48-50].

Belonging to a certain ethnic group also appears to play an important part in determining stress levels for parents, and the creation of the disharmonious family environment, particularly in the United States through its marked structural disadvantages, segregation and inequality, with African-American, Hispanics and Asians experiencing significantly higher stress levels when starting a family than Caucasian [51]. A lower community cohesion is likewise linked to increased stress levels for new parents [47].

Step 3: psychological and emotional distress in the offspring

A disharmonious family environment and parental mental health problems have been associated with a range of negative psychological and emotional outcomes in the offspring, including eating disorders, addiction, violence, heightened sensitivity to stress, poor school performance, negative emotions, behavioural problems, low self-esteem, low self-worth, lower education, a lack of confidence, sleeping problems, eating disorders, anxiety and depression [52-62].

Children also tend to adopt parental values and beliefs. If parental values are mainly negative, e.g. excessive hopelessness and pessimism as a result of socioeconomic disadvantage, the child is likely to adopt the same negative values, thereby creating a negative mindset and the perception that change for the better is not possible [63].

Evidence suggests that a disharmonious family environment is particularly damaging for children [57]. Firstly, children have not yet built up sufficient protective mechanisms, such as resilience, coping skills or self-esteem. Secondly, children also tend to internalize (negative emotions, depression, anxiety) parent's frustrations, thereby promoting further psychological and emotional distress [60]. Externalization (aggressiveness, hyperactivity, behavioural problems) of parent psychological and emotional problems is also common [57, 60]. Thirdly, childhood is a very intensive developmental period, meaning that children are extra sensitive to disharmonious social environments [57, 60, 64]. Furthermore, earlier parts of the proposed causal chain, such as family socioeconomic disadvantage, have also been found to increase risk of poor self-rated health, and emotional and behavioural problems in the children [65-69].

Step 4: psychological and emotional overload

Step 4 symbolizes the point where the individual, often a child, is not able to cope with the high amount of experienced psychological and emotional distress, since buffering mechanisms such as coping, resilience and external support are materially insufficient.

The psychological and emotional overload leads to maladaptive coping strategies (e.g. eating to suppress negative emotions and stress, eating disorders, passivity, addiction, increased stress sensitivity), over-reactive emotional responses to outside stressors, feeling insecure and a need for increased security [61, 65, 70-79].

There are also direct physiological perturbations in the energy homeostasis systems, possibly as a response to the increased need for security and survival [70]. Stress levels are now much increased causing hypothalamic–pituitary–adrenal axis dysregulation and increased levels of cortisol, ghrelin, insulin and pro-inflammatory cytokines [80-84]. Stress, negative emotions and inflammation therefore appear to be important mediators between the psycho-emotional overload and disruption of energy homeostasis and metabolism [79, 81-83, 85-87].

Step 5: disruption of energy homeostasis and start of weight gain

The increased circulation of appetite stimulating hormones and peptides, such as ghrelin, cortisol and insulin, causes an increase in appetite and attraction to calorie-dense foods, with concomitant changes in eating behaviour and energy intake [82, 83, 86, 87].

Stress could also have adverse effects on energy expenditure, arguably the main physiological regulator of energy homeostasis and therefore body weight [88-90]. Interestingly, the resting energy expenditure per kilogram has been found to be much lower in the obese than normal weight [91], suggesting that the obese are indeed in calorie-saving mode, possibly as a result of stress (Habash, Fagundes, Kiecolt-Glaser et al., unpubl. data) and thereby increased ability to handle future insults. Stress also appears to induce other adverse metabolic effects such as reduced triglyceride clearance, which promotes fat storage [92].

Behavioural disturbances in energy homeostasis include emotional eating, i.e. eating to find relief from negative emotions and stress [79, 81, 83, 86, 93]. Food, and especially so-called comfort foods rich in fat and sugar, is a readily available form of self-medication from many types of negative emotions and stress [86, 94]. Sleep patterns and physical activity levels are also affected adversely by the more or less chronic exposure to stress, which will further increase metabolic disturbances and inflammation [95].

Possibly the largest adverse impact of psychological and emotional distress, particularly in children, is that the altered profile of hormones and metabolites (e.g. glucocorticoids) affecting the amygdala and hippocampus as a result of negative emotions, facilitate memory and formation of habits [83]. Children in disharmonious families are therefore very likely to rapidly learn that eating comfort foods significantly reduce distress, which then starts to form a maladaptive habit. Emotions have a profound impact on habituation of behaviour through basal ganglia, with little interference from the conscious parts of the brain [83, 86].

Moreover, individuals with this type of maladaptive emotional conditioning can easily progress to using the same strategy after smaller stressors such as school-related problems, tiredness or body dissatisfaction, promoting a reflex-like automatic chain of events that the cognitive parts of the brain struggles to contain [83, 86]. Development of other maladaptive coping behaviours such as eating disorders can also occur [96].

A deliberate psychological reason behind disrupting energy homeostasis is the desire to induce obesity as protection from childhood abuse, particularly sexual abuse [70].

Step 6: manifested obesity and reverse causality

Once obesity has been established, there exist a large number of reverse causality situations. This includes the direct impact of obesity on mental health, social disadvantage, psychological and emotional distress, stress, inflammation and hyperinsulinemia, thereby creating a very potent negative circle. Although Fig. 1 only shows a bidirectional association for step 6, all steps in the model are likely to be more or less bidirectional, especially for severe obesity. There can also be causal processes that bypass intermediary steps in the model, e.g. where obesity (step 6) connects all the way back to socioeconomic disadvantage, and so on.

There are several other examples of reverse causality. Obese children have, e.g. been found to be twice as likely as normal weight children to develop mental health problems [97]. Childhood obesity is also a major risk factor for developing low self-esteem [98, 99], social discrimination and bullying [74, 100, 101], and body dissatisfaction [73, 102]. Moreover, obesity makes it harder to move up the social ladder, and increases the risk of moving down the social ladder [103]. Similarly, obese young men are less likely than normal weight to achieve higher education [104]. In adults, obesity is associated with low self-esteem, body dissatisfaction and a pre-occupation with dieting, mainly due to childhood weight-related teasing and failure to live up to unrealistic body shape ideals [105].

In terms of physiology, adipose tissue is a major source of pro-inflammatory cytokines, which fuels pre-existing inflammation even further [106], leading to multiple knock-on effects such as cognitive impairment and depression [87]. Other examples include obesity as a barrier to be physically active [107-109].

Protective factors

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

There are a number of factors that protect against psychological and emotional distress. Self-esteem protects against future mental health issues, particularly anxiety [99, 110]. Self-esteem can be a particular challenge for the obese individual given the stigmatizing effect of obesity. High self-esteem improves the likelihood of not experiencing mental health problems as a result of life adversity [35]. Peer support can also help to protect children and adolescents against low self-esteem when parental closeness is low [56]. Similarly, having a high self-worth helps to protect against social adversity such as bullying [111].

Resilience, sometimes defined as the combination of self-efficacy, optimism and self-esteem but also intact social, emotional and behavioural functioning, is linked to lower distress levels and high quality of life [112, 113]. Resilience has also been found to moderate the association between childhood neglect and later psychiatric symptoms [114]. Conversely, low resilience is linked with greater use of maladaptive coping strategies [112]. Interestingly, neuroimaging studies suggest that individuals with high resilience have more effective processing of brain circuitries involved in regulating stress and emotions [115].

Functional coping skills are critical for children exposed to family adversity such as violence or witnessing violence [116]. Functional coping of children in abusive families include self-organization skills, ability to remain self-esteem and self-worth, self-reliance and problem solving, emotion regulation and adaptable personalities [117]. Children of alcoholic parents, e.g. commonly develop multiple coping strategies to protect themselves [118].

Connection to set-point theory

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

The body weight set-point posits that deviations from a stable weight, e.g. through overfeeding, is relatively quickly balanced by increased energy expenditure or decreased energy intake to return to the body weight set-point [15, 119, 120]. The deliberate deviation from the body weight set-point, and subsequent return, is largely what happens during obesity treatment programmes, since weight regain is the norm for the vast majority of participants [8, 9].

Indeed, efforts to improve weight loss maintenance have not improved significantly during the last decades [8, 9], and the epidemic continues more or less unabated, especially in socioeconomically disadvantaged populations [11, 12]. This apparent failure can be considered empirical evidence for the existence of a body weight set-point.

It is speculated here that the body weight set-point is heavily influenced by psychological and emotional factors, commonly established already in childhood. In essence, our amount of body fat constitutes a balancing act between protective factors, such as resilience, coping and self-esteem and accumulated psychological and emotional distress (see Fig. 2 for a conceptual overview). This conceptual model of body weight regulation can also allow for other risk factors that have a weak or non-existent association with socioeconomic status, such as genetics, epigenetics, physiology and medication to be included.

figure

Figure 2. A conceptual overview of the potential influence of psychological and emotional distress on body weight/body mass index (BMI) set-point. The current calibration translates medium distress with BMI = 30 kg m−2, low distress with BMI = 25 and high distress with BMI = 35. Further individual calibration is also possible through changing the scoring of the BMI scale. The combined influence of other factors involved in the regulation of body weight, such as genetics, physiology and lifestyle, can also be allowed through vertical movement of the balance point.

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Implications for prevention

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

One of the main purposes of the proposed causal model (Fig. 1) was to highlight the many steps that can take place before weight gain typically starts. Obviously, some individuals will be exposed to all four preliminary steps in the model without triggering fat storage programmes, possibly through adequate coping and inner resilience, and some will become obese without having suffered much adversity. Nevertheless, the model argues that socioeconomic disadvantage and psychological distress constitute a breeding ground for weight gain and obesity in general, i.e. a gradual stacking of the odds (Fig. 2).

Unless prevention programmes start to seriously tackle the many root causes of the disease, the obesity epidemic will likely continue unabated with ever increasing consequences for individuals and societies alike. Prevention programmes could include, e.g. creation of equal opportunities, minimization of financial and job insecurity, creation of safe neighbourhoods, increased education, promotion of mental health and reduced stress for parents, and interventions for challenged families and particularly children with signs of psychological distress. Such efforts may then lead to increased adherence to more established prevention efforts such as healthy eating and regular physical activity.

Implications for treatment

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

The implications for treatment are similar to prevention. Since treatment programmes almost exclusively target step 6 and the discontinuation of the negative weight gain circle, and thereby ignore the steady flood of calories generated by earlier steps, we are unlikely to significantly improve treatment effectiveness unless we go higher up the causal chain.

The main sign of treatment failure is the poor long-term results due to weight regain. Indeed, a recent meta-analysis of weight loss maintenance showed that there were few diet, exercise or anti-obesity drugs that reduced weight regain by more than 1–2 kg, and this was mainly from short-term studies (majority <1 year follow-up) [8]. Long-term studies, such as the 10-year follow-up form the Diabetes Prevention Project, show minimal difference in body weight between treated and controls after 4–5 years [9].

If the proposed model's connection to set-point theory is correct, a de-regulated body weight set-point could potentially be possible through interventions that reduce psychological and emotional distress (Figs 1 and 2). Long-term follow-up data of weight loss maintenance after cognitive behaviour therapy are encouraging [121].

Another important treatment implication is to foster greater body acceptance (e.g. Health At Every Size), which can help to alleviate negative emotions such as shame and guilt and reduce preoccupation with dieting and food, all of which act as barriers to progress [105].

Implications for reducing negative obesity stereotypes

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

By moving away from the strict focus on an excessive food intake and a lack of physical activity as the perceived main drivers of obesity, we may also be able to reduce the common stereotypes that obese individuals are lazy, self-indulgent and lacking discipline [122, 123]. The bullying and discrimination of the obese is particularly upsetting given that many obese already have to cope with a disharmonious childhood, socioeconomic disadvantage and health problems. This review suggests that obesity causation is much more complex than mere gluttony or sloth [124, 125], and could in fact have very little to do with a lack of effort or self-discipline.

Model boundaries

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

There are two important boundaries associated with the proposed causal model. The first boundary pertains to the deliberate focus on psychological and emotional distress as the missing link between socioeconomic adversity and weight gain. The model is not meant to be a grand-unified theory of obesity causation, and the lack of emphasis on other risk factors (genetics, epigenetics, drugs, diseases, etc.) [126] should not be interpreted to mean that they are not part of the causal process.

The second boundary is that the model only applies to countries with an inverse association between socioeconomic factors and obesity, i.e. mainly North America and Europe. It is not intended to be applied to emerging economies that are in the midst of, or have only recently made, the nutrition transition, where obesity is still positively associated with wealth.

Need for further research

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

The potentially causal role of psychological and emotional distress in weight gain and obesity can be much clarified by three research approaches. The first approach would be to quantify the potentially mediating effect of psychological and emotional distress in the association between socioeconomic disadvantage and obesity, ideally using a longitudinal design including adjustment for other causal factors such as diet and exercise. This has already been done in studies testing the mediating role of negative emotions in the association between socioeconomic disadvantage and coronary heart disease [40, 41].

The second approach would be to test the effectiveness of counselling for improving psychological and emotional distress on intermediary causal factors such as stress, emotional eating, appetite and metabolism.

The third approach would be a final empirical validation of the model by evaluating the effectiveness of interventions that target psychological and emotional distress in both obesity prevention and treatment efforts, ideally by adding such therapy to standard care practices with long-term follow-up, particularly to see whether weight loss maintenance has been improved, which could suggest a lasting de-regulation of the body weight set-point.

Conclusion and summary

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References

This conceptual review presented a new causal model suggesting that psychological and emotional distress, mainly established during childhood as a result of socioeconomic disadvantage and family disharmony, is a common starting point for weight gain and obesity. This, in turn, sets off a cascade of maladaptive behavioural and physiological changes, including eating to suppress negative emotions, mental health problems, weight gain as a protective mechanism, stress, inflammation, increased appetite and possibly reduced metabolism. Both prevention and treatment efforts may benefit from addressing these potential root causes of weight gain and obesity.

References

  1. Top of page
  2. Summary
  3. Introduction
  4. A proposed new model of obesity causation
  5. Protective factors
  6. Connection to set-point theory
  7. Implications for prevention
  8. Implications for treatment
  9. Implications for reducing negative obesity stereotypes
  10. Model boundaries
  11. Need for further research
  12. Conclusion and summary
  13. Conflict of interest statement
  14. Acknowledgements
  15. References