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 ingestive behaviour, this post focusses on medications:
Medications and Drugs That Affect Hunger and Appetite
A wide range of medications and illicit drugs can promote hunger and appetite. These include some oral anti‐diabetic agents, antidepressants, atypical antipsychotics, anticonvulsants, certain hormonal preparations including corticosteroids and oral contraceptives, as well as the medicinal and recreational use of marihuana. Alcohol and other mind‐altering drugs can also promote over‐eating by increasing appetite, reducing dietary restraint and promoting disinhibition. Patients presenting with weight gain and obesity need a careful review of their medication and substance abuse history.
Commentary: Obviously this a complex topic as the number of medications and recreational substances that can affect appetite and eating behaviour is long. Nevertheless, assessing the possibility that a change in appetite and weight gain are due to this factor is an essential part of clinical assessment.
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.
Physiological or Homeostatic Factors
In contrast to excess caloric consumption that results largely from environmental determinants, over‐eating in response to increased hunger or reduced satiety can be viewed as a physiological response to a perturbation of the homeostatic system and is perhaps best termed homeostatic hyperphagia. Primary homeostatic hyperphagia can result from genetic defects in the homeostatic system (e.g. leptin deficiency, melanocortin type 4 receptor mutation or Prader Willi Syndrome) and are rare. Secondary homeostatic hyperphagia can result from acquired defects or perturbations in the homeostatic system (e.g. head trauma, craniopharyngeoma, insulinoma). Tertiary homeostatic hyperphagia, by far the most common category, is largely the result of inappropriate feeding intervals and/or nutrient selection. Thus, skipping meals, resulting in a compensatory hyperphagic response (rapid ingestion of energy‐dense foods), is perhaps the most prevalent form of homeostatic hyperphagia. Ingestion of high‐glycemic foods resulting in a rapid rise and fall in blood glucose and insulin levels (‘crash and crave’) may prompt increased snacking and overconsumption, although this notion remains controversial. Meal duration and composition can also affect satiety response, whereby delayed or reduced satiation (e.g. in response to hasty eating, energy‐dense foods, low fibre intake, liquid calories) can result in excess caloric intake. The presence of homeostatic hyperphagia (characterized by over‐eating in response to increased hunger and/or reduced satiety) will likely call for interventions that specifically address the underlying perturbation in this system (e.g. administration of leptin, excision of the insulinoma, correction of meal pattern, nutritional hygiene, portion control, etc.). Patients with obesity resulting from tertiary homeostatic hyperphagia are the most likely to benefit from dietary counselling.
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 ingestive behaviour. Once you have quickly established that weight gain is not primarily driven by a change (decrease) in metabolic requirements, you turn to the most likely cause of weight gain – eating more calories than your body actually needs:
Ingestive behaviour, which includes both eating and drinking, accounts for 100% of total energy intake. In contrast to total energy expenditure, caloric intake (on a daily basis) can vary from zero (fasting) to several times that of total energy requirements (e.g. during a binge eating episode). Given the ease with which it is possible for energy intake to exceed caloric expenditure, it is therefore not surprising that caloric hyperalimentation is a major determinant of weight gain. Any assessment of obesity or increase in body weight thus requires a careful assessment of ingestive behaviour. Evidence for caloric hyperalimentation or hyperphagia should in turn prompt systematic exploration of the determinants of this behaviour. In this context, it helps to view over‐eating as a symptom of an underlying perturbation of ingestive behaviour rather than simply a wilful behavioural choice.
While the socio‐psycho‐neurobiological determinants of ingestive behaviour are exceedingly complex, in clinical practice, it is possible to divide them into four domains: socio‐cultural factors, biomedical or physiological (homeostatic) factors, psychological (hedonic) factors and medications. In a given individual, these domains are intimately connected and show considerable variation and overlap. Nevertheless, in practice it is often possible to determine the primary domain that explains the excess caloric intake in a given individual and can thus provide the key to developing a treatment plan that addresses the root cause of this behaviour.
More on the various factors affecting ingestive behaviour in coming posts.