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The Effects of Obesity on Skeletal Muscle Contractile Function

Skeletal muscle

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.

@DrSharma
Edmonton, AB

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Some Limitations In Applying The Etiological Framework To Obesity Assessment

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).

@DrSharma
Edmonton, AB

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Applying The Etiological Framework For Obesity Assessment In Clinical Practice

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.

@DrSharma
Edmonton, AB

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Etiological Assessment of Obesity: Factors That Affect Physical Activity

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.

@DrSharma
Edmonton, AB

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Factors That Can Affect Ingestive Behaviour: Drugs and Medications

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.

@DrSharma
Edmonton, AB

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