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Keywords:

  • Clinical assessment;
  • energy metabolism;
  • ingestive behaviour;
  • obesity management

Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

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, the consequence of positive fluid balance or fluid retention, obesity can be seen as the consequence of positive energy balance or calorie ‘retention’. Just as the assessment of oedema requires a comprehensive assessment of factors related to fluid balance, the assessment of obesity requires a systematic assessment of factors potentially affecting energy intake, metabolism and expenditure. Rather than just identifying and describing a behaviour (‘this patient eats too much’), clinicians should seek to identify the determinants of this behaviour (‘why, does this patient eat too much?’). This paper provides an aetiological framework for the systematic assessment of the socio-cultural, biomedical, psychological and iatrogenic factors that influence energy input, metabolism and expenditure. The paper discusses factors that affect metabolism (age, sex, genetics, neuroendocrine factors, sarcopenia, metabolically active fat, medications, prior weight loss), energy intake (socio-cultural factors, mindless eating, physical hunger, emotional eating, mental health, medications) and activity (socio-cultural factors, physical and emotional barriers, medications). It is expected that the clinical application of this framework can help clinicians systematically assess, identify and thereby address the aetiological determinants of positive energy balance resulting in more effective obesity prevention and management.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

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 (1). 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 (2).

In this paper, we present a theoretical diagnostic paradigm that provides an aetiological framework for thesystematic 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.

A problem of energy in and energy out

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

In the same manner in which a complete understanding of oedema requires the assessment of the complex physiological systems affecting fluid and sodium homeostasis, understanding obesity requires a comprehensive appreciation of the multitude of factors affecting energy intake and expenditure. Energy expenditure can be further subdivided into non-activity (= resting metabolic rate + dietary-induced thermogenesis) and activity thermogenesis (= non-exercise + exercise activity thermogenesis). For simplicity's sake, these three elements can be termed diet, metabolism and activity (Fig. 1). A change in any one of these elements, if not balanced by corrective changes in the others, will result in a net change in energy balance, which, if positive, will result in caloric ‘retention’ and weight gain.

image

Figure 1. Schematic of factors that can influence energy balance.

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A. Low metabolic rate predisposes to obesity

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

Any assessment of obesity should begin with an estimate of energy requirement – specifically recognizing that any decrease in metabolic rate, without a corresponding decrease in energy intake and/or increase in activity will result in weight gain. Thus, in anyone presenting with weight gain, without any notable change in energy intake or activity levels, it is safe to assume that the only explanation can be a reduction in energy metabolism (Fig. 2).

image

Figure 2. Weight gain can result from a combination of reduced metabolism, increased energy intake and/or reduced activity.

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As a rule of thumb: the lower the total energy requirements, the greater the risk of obesity (3) (simply stated: over-eating is less likely for someone who needs 4000 kcal d−1 than for someone who needs 1500 kcal d−1). In sedentary individuals, resting metabolic rate is responsible for dissipating the vast majority of daily ingested calories (60–75%) and is therefore a key determinant of energy expenditure (4). Thus, even a small, sustainedpercentage reduction in resting metabolic rate, without a compensatory adjustment of energy intake or activity, can account for a large cumulative caloric excess over time (e.g. an unbalanced 3% reduction in resting metabolic rate in an individual with a total energy expenditure of 1800 calories can lead to a caloric excess of 32.4 kcal d−1, which can translate into 972 kcal excess per month).

Numerous factors can determine and/or affect metabolic rate. These include genetic and epigenetic factors, gender, aging, neuroendocrine function, sarcopenia, metabolically active fat, certain medications and prior weight loss.

Genetics

Because heritable factors appear to be responsible for 45–75% of the inter-individual variation in body mass index (BMI), the potential impact of genetic determinants of metabolic rate upon the predisposition to obesity must be considered (5). While numerous somatic and mitochondrial genes with potential effects on metabolic rate have been identified, their contribution to human obesity has yet to be defined (6). Likewise, although there is preliminary evidence for intrauterine and perinatal programming of genes involved in energy metabolism (7), their role in human obesity remain unclear. What is apparent is that the genetic predisposition to obesity (including both energy intake and metabolism) is not explainable on the basis of a small number of common mutations exerting substantial effects on the individual tendency to weight gain (7). Thus, a great deal of work is still required before investigation into the multitude of genetic determinants of body weight can potentially impact clinical management. Currently, a careful clinical assessment of family history of obesity and related risk factors remains the best measure of genetic risk for obesity.

Sex

There is a clear effect of gender on metabolic requirements, whereby, for the same BMI, women consistently display lower metabolic rates (approximately 20% less) than men, largely accounted for by differences in fat-free mass (FFM) (8).

Aging

Aging is an important determinant of a decline in metabolic rate (9), with an estimated reduction of around 150 kcal per decade of adult life (10). Factors that result in the age-related decline in energy requirements include changes in neuroendocrine factors (e.g. sympathetic activity, thyroid function, etc.) (11) as well as a reduction in skeletal muscle quantity and quality (resulting from reduced physical activity, reduced protein intake and other less-well-understood factors) (12,13).

Neuroendocrine factors

Across the entire age continuum, a wide range of neuroendocrine factors can not only affect metabolic rate, but also substrate partitioning and utilization, which may directly or indirectly contribute to weight gain. The latter point is of particular significance as low rates of fat oxidation are associated with an increased risk of weight gain (14). A wide range of neuroendocrine hormones and biomarkers can affect energy metabolism; sympathetic nervous system activity and thyroid function are two major factors directly influencing resting energy expenditure (15). Sympathetic nervous activity is also a major determinant of post-prandial thermogenesis and the thermogenic response to a glucose load has been shown to be significantly lower in obese individuals, a finding that persists even with substantial weight loss (16). Specific examples of endocrine hormones that affect energy metabolism and substrate partitioning include cortisol, growth hormone (GH) and testosterone. Catabolism associated with hypercortisolism or Cushing's syndrome can reduce energy requirements and increase the deposition of truncal fat (17). Discontinuation of GH treatment at the end of childhood growth in individuals with GH deficiency markedly increases fat mass and decreases metabolic rate (18), whereas GH treatment in GH-deficient adults has beneficial effects on protein metabolism, energy expenditure and thyroid metabolism (19). Testosterone deficiency can also result in abnormal energy partitioning, which adversely alters anabolism and reduces metabolic rate (20). It is important to note that a careful history and physical examination should precede any endocrine testing for these disorders, as testing should be reserved for patients with an above-normal pretest probability for one of these conditions (21).

Sarcopenia

The importance of FFM as the key determinant of resting metabolic rate, even in a very obese individual, cannot be over emphasized (22). Obese individuals can present with wide variations in lean body mass, almost entirely accounted for by differences in skeletal muscle mass (23). Thus, any change in muscle mass can markedly affect basal energy requirements. In this context it is important to remember that in ambulatory individuals, the mass of weight-bearing muscles is directly proportional to BMI, as heavier individuals require a greater skeletal muscle mass to support and move their excess weight. This alone accounts for much of the higher basal and activity-related energy requirements of larger individuals (24).

Although inactivity may be the most common cause of decreased skeletal muscle mass and reduced basal metabolic needs in obese individuals (25,26), it is important to consider other causes of muscular atrophy that can likewise markedly reduce energy demands. A wide range of nutritional, neuromuscular, endocrine, renal, cardiac, pulmonary, inflammatory, infectious or neoplastic conditions can result in muscular wasting and sarcopenia (27). Reduced skeletal muscle mass and weight gain is also noted after many cancer treatments, although the mechanisms remain unclear (28). Any reduction in skeletal muscle mass not accounted for by a decrease in physical activity and ambulation should prompt investigations for other causes of muscular wasting.

Metabolically active fat

Recent evidence suggests that brown adipose tissue (BAT) exists into adult hood and can, when present account for as much as 20% of daily resting energy expenditure (29). While the exact contribution of BAT (or lack thereof) to obesity remains to be determined, the presence and inducibility of BAT by cold exposure is inversely related to BMI, appears higher in women, and diminishes with aging (30–32). Given the role of cold exposure in the expression of BAT, it can be speculated that an increase in ambient temperature may promote weight gain by significantly reducing BAT and, thus, metabolic rate in some individuals. In rodents, increased production of neuropeptide Y in the hypothalamus can not only increase food intake but also reduce energy expenditure via a reduction in non-shivering thermogenesis in BAT and facilitate triglyceride deposition through increased insulin levels (33).

Medications

A wide range of medications can affect metabolic rate. Notably, the use of beta-blockers has been shown to significantly reduce thermogenesis, resulting in clinically relevant weight gain (34). Metabolic rates can also be reduced by the discontinuation of drugs that promote thermogenesis such as beta-adrenergic agents (35), stimulants (including performance-enhancing and illicit drugs like crack/cocaine) (36,37), coffee (38) or nicotine (39), resulting in weight gain.

Weight reduction

Finally, weight loss can markedly reduce energy requirements with a 5–10% reduction in body weight reducing resting metabolic rate by as much as 20% in some individuals (40), thereby substantially increasing the susceptibility to weight regain in the post-obese state.

B. Eating too much

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

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 (41). 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 (Fig. 1). 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.

Socio-cultural factors

A wide range of socio-cultural and environmental factors can determine changes in ingestive behaviour (42). Thus, traditions or habitual patterns, belief systems, peer pressure, availability of foods, and the context in which these are presented and consumed can all significantly predispose to or prompt increased caloric consumption. Moving to a neighbourhood with more fast food outlets, exposure to food advertising, decreasing affordability of healthy foods, or increased professional or social pressure can all influence eating behaviour. Thus, for example, taking up a job that requires extensive wining and dining of clients is likely to increase caloric consumption. Similarly, regularly partaking in social activities that revolve around eating and drinking can promote caloric excess. Not surprisingly, the frequency of eating out is an important determinant of food quality (43). As many of the factors that influence overconsumption are subtle (e.g. plate size, food variety, ambient distractions, etc.) and do not generally involve conscious decision-making, exposure to an environment that promotes ‘mindless’ over-eating will promote weight gain (44). For individuals in lower socioeconomic class, affordability and availability may limit access to a healthy nutritious diet (45). Lack of knowledge about healthy eating may also contribute. When present, identifying, recognizing and acknowledging the possible role of the socio-cultural factors that promote overconsumption or pose important barriers to eating a healthy, calorically balanced diet is the first step to devising strategies to mitigate these influences or overcome these barriers. In addition to nutritional counselling patients in whom strong socio-cultural determinants of obesity are identified may benefit from counselling by a social or public health worker.

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 (46). 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 (47). Secondary homeostatic hyperphagia can result from acquired defects or perturbations in the homeostatic system (e.g. head trauma, craniopharyngeoma, insulinoma) (48,49). 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 (50). 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 (51), although this notion remains controversial (52). 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 (53). 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.

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 (54). 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 (55). Typically, hedonic hyperphagia is associated with the selection and consumption of highly palatable energy-dense ‘comfort’ foods (56), 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 (57). 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 (58). 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 (59,60). Particularly sleep deprivation has been associated with increased appetite and ingestion of highly palatable snacks (61) as well as increased risk for diabetes (62). 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.

Medications and drugs that affect hunger and appetite

A wide range of medications and illicit drugs can promote hunger and appetite (63). 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 (64), reducing dietary restraint and promoting disinhibition (65). Patients presenting with weight gain and obesity need a careful review of their medication and substance abuse history.

C. Barriers to physical activity

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

As with caloric intake, activity-related caloric expenditure can vary from virtually zero (as in a bedridden individual) to several thousand calories a day (as in a competitive athlete). In considering physical activity, it is important to note that in sedentary individuals, the majority of activity thermogenesis results from non-exercise activity thermogenesis (NEAT) simply from performing the acts of daily living, walking, posture and fidgeting (66). Any reduction in NEAT, even with no change in planned exercise frequency, duration or intensity, would result in reduced energy requirements. Evidence suggests that some individual's resistance to weight gain is linked largely to their innate ability to spontaneously increase NEAT to defend against caloric excess (67).

As with nutrition, the factors that determine physical activity can be divided into four domains: socio-cultural factors, biomedical factors, psychological factors and medications (Fig. 1). Determining which of these domains is predominantly responsible for reduced physical activity or sedentariness can allow the clinician to specifically address those barriers in the management plan.

Socio-cultural factors

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 (68,69). 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.

Biomedical factors

Numerous medical conditions can lead to a reduction in or inability to engage in physical activity (70). 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 (71). Social anxiety disorder, agarophobia, sleep disorders or substance abuse can all affect physical activity levels (72). Body image issues and self-efficacy can likewise pose important psychological barriers (73) that may require specific professional counselling and intervention to promote a more active lifestyle.

Medications

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.

Applying this aetiological framework to obesity management

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

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.

Limitations of the proposed system

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

While we have taken efforts to provide a comprehensive and wide-ranging list of considerations in the assessment of obesity, we fully recognize that a full work-up of all permutations of the proposed factors may well be beyond the scope of a busy practitioner. In this regard, the old saying applies: ‘when you hear hoofs, think of horses not zebras’. Thus, consideration should be first given to the most common and obvious reasons laid out in this paper, many of which should be immediately apparent to the experienced clinician (e.g. homeostatic hyperphagia resulting from meal skipping, hedonic hyperphagia related to depression, immobility due to osteoarthritis, weight gain due to atypical antipsychotics, etc.). Also, the use of comprehensive self-directed questionnaires such as the Weight and Lifestyle Inventory (74), a multiple-page self-report questionnaire that the patient completes before treatment visits, designed to identify the root causes of obesity and perform an environmental analysis, may be helpful in this regard. Future efforts must also aim to provide simple clinical algorithms that will guide the busy clinician through the maze of factors that can potentially precipitate and/or exacerbate positive energy balance.

Nevertheless, as in a patient with oedema, despite complete recognition of the underlying factors, the clinician often has no option but to manage the patient with the judicious use of fluid restriction and diuretics. Similarly, in patients presenting with obesity, the underlying contributing factors (e.g. genetics, addiction, depression, back pain, etc.) may not be easily amenable to causal treatment. In these cases, ‘symptomatic’ treatment of obesity with caloric restriction and exercise regimens may well in many cases prove to be the only option. Nevertheless, we maintain that careful identification and management of the possible socio-cultural, psychological and biomedical barriers will likely increase the feasibility, compliance and adherence to these measures. Recognition of the causes and barriers will also help set out realistic expectations regarding the degree of weight loss that is likely to be achievable and sustainable, an important aspect of weight management. Despite the increased time required for the comprehensive work-up of an obese patient, we believe that this framework will eventually save costs by allowing clinicians to specifically identify and target the causes and barriers of positive energy balance, rather than resorting to the ‘one-size-fits-all’ (eat less – move more) approach to obesity, which given its limited efficacy, can only be considered wasteful.

Conclusion

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

Obesity can be seen as a clinical sign of chronic caloric ‘retention’ and as such, requires a systematic assessment of factors potentially affecting energy intake and expenditure. Rather than simply identifying and describing a behaviour (this patient eats too much), clinicians should seek to identify the determinants of this behaviour (why, does this patient eat too much?). This paper provides a theoretical framework that can help clinicians systematically assess, identify and thereby address the aetiological determinants of positive energy balance. It is expected that the clinical application of this framework will improve obesity prevention and management.

Acknowledgements

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References

A. M. S. is supported by an Alberta Health Services Chair in Obesity Research and Management and funding from the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada and the Networks of Centres of Excellence Program. R. P. is supported by funding from the Canadian Institutes of Health Research. Both authors are grateful to William F. Colmers, University of Alberta, for his thoughtful editorial comments.

References

  1. Top of page
  2. Summary
  3. Introduction
  4. A problem of energy in and energy out
  5. A. Low metabolic rate predisposes to obesity
  6. B. Eating too much
  7. C. Barriers to physical activity
  8. Applying this aetiological framework to obesity management
  9. Limitations of the proposed system
  10. Conclusion
  11. Conflict of Interest Statement
  12. Acknowledgements
  13. References