Continuing with citations from my article in Obesity Reviews on an aeteological framework for assessing obesity, that guides us through a systematic assessment of factors influencing energy metabolism, ingestive behaviour, and physical activity, we ca now apply this framework in clinical practice:
This paper provides a comprehensive framework, which should enable clinicians to systematically assess and identify the socio‐cultural, biophysical, psychological and iatrogenic determinants of increased energy intake and reduced energy expenditure in patients presenting with excess weight or weight gain. Beginning with an assessment of energy requirements and metabolism, clinicians should systematically assess the role and determinants of ingestive and activity behaviour to identify the factors promoting positive energy balance. This will enable clinicians to develop management plans that address the root causes of weight gain and move beyond the simplistic and generally ineffective recommendation to ‘eat less and move more’.
Thus for example, in a listless patient ‘self‐medicating’ with food, identification and treatment of depression may be the first step to reducing food intake and preventing further weight gain. In a patient with socioeconomic barriers to healthy eating or physical activity, referral to a social worker who can assist in identifying and accessing community resources may be important. Identification and effective treatment of obstructive sleep apnoea may be the key to increasing activity in someone with this disorder. Psychological counselling to manage alcohol or substance abuse or to help patients deal with binge eating resulting from past trauma, emotional neglect or grief, can put patients on a path to successful weight management. Clearly, the common notion that all forms of obesity can be addressed simply by counselling patients on diet and exercise should be considered ineffective and obsolete.
To conclude this series, we will tomorrow look at some of the potential limitations of this system.
Continuing with citations from my article in Obesity Reviews on an aeteological framework for assessing obesity, we now turn to the some of the factors that can affect physical activity. Similar to the factors that can affect ingestive behaviour, there are a host of factors that can significantly affect physical activity:
A wide range of socio‐cultural determinants of physical activity exist. These range from factors related to the built environment (e.g. urban sprawl, walkability, street connectivity), neighbourhood safety, social networks, and public transportation to socioeconomic limitations as well as customs and beliefs that can influence vocational or recreational physical activity. For example, being promoted from a physically active outdoor job to a sedentary indoor job, moving from a dense urban location to a rural or suburban residence, immigration to a Western country, pregnancy and change in familial status or time constraints can all promote sedentariness and increase the risk of weight gain. Indentifying and addressing the socio‐cultural barriers to physical activity can be a key to successful weight management. Patients facing significant socio‐cultural barriers to activity may specifically benefit from counselling by an occupational and/or recreational therapist.
Numerous medical conditions can lead to a reduction in or inability to engage in physical activity. These include musculoskeletal pain or immobility resulting from injury, osteoarthritis or fibromyalgia as well as any other condition that can affect physical performance such as cardiorespiratory disease, obstructive sleep apnoea, chronic fatigue, stroke or urinary incontinence. Alleviating these factors and thereby reducing immobility may be the first step in addressing weight management in these patients. Given the predominant role of musculoskeletal disorders and pain as a barrier to mobility and physical activity, these patients may benefit most from physiotherapeutic interventions and pain management.
Psychological factors and mental health
Lack of motivation, low energy levels and disinterest in exercise (especially in a previously active individual) can be a symptom of depression. Social anxiety disorder, agarophobia, sleep disorders or substance abuse can all affect physical activity levels. Body image issues and self‐efficacy can likewise pose important psychological barriers that may require specific professional counselling and intervention to promote a more active lifestyle.
Although published research on this issue is limited, it is reasonable to assume that medications, which reduce energy levels, promote drowsiness, impair coordination or limit cardiorespiratory function can pose significant barriers to physical activity.
Now that we have discussed why it is important to asses the many factors that can affect energy metabolism, ingestive behaviour, and physical activity, in coming posts, we can explore how to apply this framework to patients presenting with weight gain.
Psychological or Hedonic Factors
In contrast to hyperphagia resulting from physical hunger, over‐eating for emotional reward or as a coping strategy is regulated by the hedonic system and has little to do with the body’s real or perceived need for calories. The range of psychological or emotional factors that can initiate and influence eating encompass virtually the entire range of emotional responses including stress, frustration, loneliness, anxiety, anger, disgust, fear, grief, joy, relief, all of which can significantly alter dietary restraint or promote disinhibition. Typically, hedonic hyperphagia is associated with the selection and consumption of highly palatable energy‐dense ‘comfort’ foods, although homeostatic hyperphagia also tends to be associated with the preferential consumption of palatable foods.
In addition to simple ‘emotional’ over‐eating, specific psychiatric conditions that affect food intake or can pose important barriers to maintaining a healthy diet must be considered. Increased appetite is a feature of atypical depression and can be interpreted as ‘self‐medicating’ with food – particularly in cases where these foods affect the serotonergic and reward systems to improve mood. Binge eating, night eating and other abnormal eating behaviours must also be seen in the context of underlying emotional or psychological processes that are distinct from homeostatic ingestive behaviour. Other mental health conditions that can significantly affect eating include attention deficit disorders, post‐traumatic stress syndrome, sleep disorders, chronic pain, anxiety disorders, addictions, seasonal affective disorder and cognitive disorders. Particularly sleep deprivation has been associated with increased appetite and ingestion of highly palatable snacks as well as increased risk for diabetes. Patients with obesity resulting from emotional eating or hedonic hyperphagia are most likely to benefit more from psychological and/or psychiatric interventions rather than simply from dietary counselling.
Commentary: Although for didactic and practical purposes I find it helpful to distinguish between what I have referred to as “homeostatic” vs. “hedonic” hyperphagia, it is important to note that at a physiological level, the distinction between the “homeostatic” and “hedonic” pathways is not as clear cut as is often assumed. In fact, there is close and complex cross talk between these pathways. For example, hunger, a feature of the “homeostatic” pathway, is also a powerful activator of the “hedonic” pathway, thus leading to seeking out and consumption of caloric-dense foods. On the other hand, “hedonic” drivers to eat can override satiety and lead to eating even when not hungry. This, physiology, however, does not take away from the fact that in clinical evaluation, trying to distinguish between homeostatic and hedonistic is often helpful in determining the appropriate treatment path.
Several years ago, my colleague Raj Padwal and I published a paper in Obesity Reviews, where we outline a rational approach to an aetiological assessment of obesity.
As many readers may not have seen this paper, I will repost several of the key elements we discussed in it. Although some of our thinking has evolved since then, I believe the overall reasoning remain as relevant today, as when we first wrote the paper back in 2010:
Obesity is characterized by the accumulation of excess body fat and can be conceptualized as the physical manifestation of chronic energy excess. Using the analogy of oedema, which is the consequence of positive fluid balance or fluid retention, obesity can be seen as the consequence of positive energy balance or caloric retention. Just as the positive fluid balance of oedema can result from a host of underlying aetiologies including cardiac, hepatic, renal, endocrine, infectious, venous, lymphatic or drug‐related causes, obesity can result from a wide range of aetiologies that promote positive energy balance.
As with oedema, assessment and management of obesity requires an exploration of the root causes and underlying pathologies. To extend the obesity–oedema analogy, addressing all forms of obesity simply with caloric restriction and exercise (‘eat less and move more’) would be akin to addressing all forms of oedema simply with fluid restriction and diuretics. As this narrowly focused approach is not considered standard‐of‐care in managing patients with oedema, why should it be considered as the preferred method of treating obesity?
The classical treatment of obesity, based on increased physical activity and decreased calorie intake, has not been successful. Approximately two‐thirds of the people who lose weight will regain it within 1 year, and almost all of them within 5 years. In our opinion, the lack of efficiency in these therapeutic approaches is likely due to an incomplete understanding of the precise aetiology or aetiologies of obesity and, consequently a failure to address the root causes of energy imbalance.
In this paper, we present a theoretical diagnostic paradigm that provides an aetiological framework for the systematic assessment of obesity and discuss how this framework can enhance our ability to diagnose and manage obesity in clinical practice. The framework considers socio‐cultural, physiological, biomedical, psychological and iatrogenic factors that can determine energy input, metabolism and expenditure.
Comment: In hindsight, I would note that apart from failure to address the underlying pathology and drivers of weight gain, the “failure’ of conventional “eat-less – move-more” approaches to obesity management, relying largely on willpower, primarily fail because these efforts are counteracted by powerful neuroendocrine factors that both defend against continuing weight loss and promote weight regain. At the time we wrote this paper, we had perhaps not given the powerful nature of these effects full consideration. Nevertheless, I still believe that trying to understand exactly why a given person has gained excess weight is a good start to any obesity management endeavour.
More to follow…
There is no doubt that some people gain weight when started on anti-depressant medications. However, it is also true that the increased appetite and listlessness that accompanies “atypical” depression can contribute to weight gain. Finally, there is evidence that weight-gain in turn may decrease mood, which in turn may further exacerbate weight gain.
Trying to cut through all of this is a study by Rafael Gafoor and colleagues from King’s College London, in a paper published in BMJ.
They examined data from the UK Clinical Practice Research Datalink, 2004-14, which included data on 136,762 men and 157,957 women with three or more records for body mass index (BMI).
In the year of study entry, 17,803 (13.0%) men and 35,307 (22.4%) women with a mean age of 51.5 years were prescribed anti-depressants.
While during 1, 836,452 person years of follow-up, the incidence of new episodes of ≥5 weight gain in participants not prescribed anti-depressants was 8.1 per 100 person years, it was slightly higher at 11.2 per 100 person years in those prescribed an anti-depressant.
In the second year of treatment the number of participants treated with antidepressants for one year for one additional episode of ≥5% weight gain was 27.
Thus, there appears to be a slight but discernible increased risk of weight gain associated with the prescription of anti-depressants, which may persist over time and appears highest during the second and third year of treatment.
However, as the authors caution, these associations may not be causal, and residual confounding might contribute to overestimation of associations.
Nevertheless, the notion that there may be a distinct weight-promoting pharmacological effect of some anti-depressants is supported by the finding that certain anti-depressants (e.g. mirtazapine) carry a far greater risk of weight gain than others (e.g. paroxetine).
Given the frequency with which anti-depressants are prescribed, it could be argued that the contribution of anti-depressants to the overall obesity epidemic (particularly in adults) may be greater than previously appreciated.
If nothing else, patients prescribed anti-depressants should be carefully monitored for weight gain and preventive measures may need to be instituted early if weight gain becomes noticeable.