Given that obesity has profound effects on all organ systems, it is not surprising that excess body fat is also associated with a decrease in muscle function.
The complex biology of the molecular, structural, and functional changes that have been associated with obesity are now extensively discussed in a review article by James Tallin and colleagues, published in the Journal of Experimental Biology.
Without going into the molecular details here, suffice it to say that there is considerable evidence to show and explain why muscular function is impaired in both animal models and humans with excess body fat. (For e.g. at a cellular level, the dominant effects of obesity are disrupted calcium signalling and 5′-adenosine monophosphate-activated protein kinase (AMPK) activity. As a result, there is a shift from slow to fast muscle fibre types. There is also evidence for an impairment in myogenesis resulting from disruption of muscle satellite cell activation. Furthermore, muscle function is affected by insulin resistance and decreased adiponectin levels generally associated with obesity).
Although individuals with obesity will often have a larger muscle mass and may well be stronger than “normal-weight” individuals, when corrected for the amount of extra muscle, it is evident that the muscles are less efficient.
In fact, many of the biochemical and structural changes that occur in obesity are very similar to those found with aging. Not surprisingly, when aging meets obesity, things get even worse.
Although the paper does not discuss the reversibility of these changes with weight loss (or obesity treatment in general), I am aware of other data showing that much of the loss of muscle contractile function associated with obesity can be reversed with weight loss.
A clinical correlate of this is the fact that, following weight loss, individuals often find that it takes far more exercise to burn the same number of calories than before (this is not just because the person is now carrying less weight).
Given the increased recognition that lean body mass is an important determinant of overall health and function, clearly this topic is of continuing interest.
To conclude this series of 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, it is important to consider some limitations of this (and any other) etiological approach to obesity management:
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, 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.
Commentary: While the proposed etiological framework can help understand why a given person may have obesity, and, more importantly, help identify important barriers to weight management, we must also realise that virtually every patient, irrespective of the underlying drivers or weight gain will face the same biological challenges when it comes to long-term weight loss – the fact remains, that our bodies can harness a host of powerful neuroendocrine mechanisms to defend against weight loss and promote weight regain. This is why in clinical practice, I often see that the best that addressing the underlying cause of weight gain achieves is the slowing or elimination of further weight gain. Thus, for example, even if painful arthritis and immobility may have caused weight gain in a given patient, a joint replacement will not automatically result in weight loss. Similarly, taking a patient of an atypical anti-pyschotic will not lead to much weight loss, nor will treatment of sleep apnea. When you remove the cause of weight gain – you stop weight gain – you do not generally reverse the process and end up with significant persistent weight loss. Thus, identifying and addressing the drivers of weight gain is only the first step in obesity management. Once weight is stabilized, we can proceed with developing a treatment plan for sustainable weight loss (as indicated).
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.
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. Once we have established that weight gain in a given individual is not primarily driven by a change (decrease) in metabolic requirements, or primarily driven by ingestive behaviour, we turn to the issue of a decrease in physical activity as a drier of weight gain:
Barriers to Physical Activity
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. 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.
As with nutrition, the factors that determine physical activity can be divided into four domains: socio‐cultural factors, biomedical factors, psychological factors and medications. 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.
We will consider each of these factors in subsequent posts.
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.