COMMENTARY

Why Is Obesity so Challenging?

Amy E. Rothberg, MD, PhD

Disclosures

March 01, 2018

Editorial Collaboration

Medscape &

About one third of Americans are living with obesity, and it's the second leading cause of preventable death, after smoking. Yet, many clinicians default to treating the conditions caused by obesity—diabetes, hypertension, heart disease, hepatic steatosis, and many cancers—rather than managing the underlying problem.

Why is obesity, per se, so challenging and frustrating to address in clinical practice?

To answer that, it's important to establish what we know about the biology and behaviors associated with obesity, and to sort the myths from the science.

Obesity conforms to the first law of thermodynamics—that is, it results from the imbalance between calories in and calories out. Although that simple equation remains true, we now recognize the complexity of appetite regulation, physical activity patterns, eating behaviors, and the downstream consequences associated with obesity. Therefore, managing a patient with obesity requires a personalized approach that involves many permutations of the traditional "eat less, exercise more" adage.

Is There a Genetic Component?

Obesity is highly heritable, and studies in twins support this. For example, monozygotic twins reared apart have body weights more similar to those of their biological parents compared with those of their adoptive parents with whom they shared the same environment. Genome-wide association studies report an increasing number of alleles associated with adiposity.

Conversely, genetic variations have shown only a modest effect size and therefore cannot explain fully the predisposition to obesity. For example, the fat mass and obesity-associated (FTO) gene polymorphism affects the susceptibility to obesity but accounts for less than 0.5% of the overall variance in body mass index (BMI).

Obesity in a mother prior to conception also increases the risk in her offspring for obesity and other cardiometabolic consequences. These effects are attributed not only to genetic changes but to epigenetic changes (ie, post-DNA modifications that occur throughout the lifespan) that modulate gene expression. And if an obese woman has a daughter who then becomes obese, these effects can be perpetuated into the next generation, creating a vicious cycle of obesity.

Our Fat-Friendly World

Why we eat, what we eat, and how much we eat are determined by a number of factors, such as portion size, taste, caloric density, and setting. Peripheral signals from our gut and fat stores relay information in a bidirectional pathway to our brain to tell us when we are hungry or full.

While some of these signals translate to conscious decision-making, many do not. So, what determines when we eat, particularly when food is always available? Habit, convenience, opportunity, cost, and social factors.

Eating patterns are affected by more than the caloric and nutritional value of food. Our consumptive behaviors are driven by previous experiences, timing, and the emotional and pleasurable aspects of eating. Modern foods and drinks are not only ultra-processed with added sugar and fat, but they are also ultra-appealing to many of our senses, seducing us to consume even more, to the extent that we become almost "addicted" to some of these highly palatable foods.

Often, we are simply unaware that we are eating too much. Even when we try to count calories in an effort to control our weight, we underestimate. A study by Lichtman and colleagues[1] showed a difference of 1000 calories, on average, per day between an individual's perceived intake versus the actual intake.

Still other factors play a role in perpetuating obesity. More than ever, we spend more time sitting: hours in our cars commuting, hours sitting in front of the TV or computer. With so much automation, we do little physical labor at work or for leisure. In our homes, we have electric dishwashers, washing machines, and electric toothbrushes that take away even the most modest of physical activity.

Unfortunately, despite the number of modalities for treating obesity (pharmacologic management, endoscopic treatment, and surgery), there's no quick fix. Even with the most extreme of interventions (ie, weight loss surgery), without making lifestyle modifications, the weight loss will not be maintained.

Why Is Losing Weight so Hard?

Losing weight—and more important, maintaining that weight loss (two distinct entities)—require a lifelong commitment to lifestyle modifications.

When a person loses weight, adaptive responses of the metabolic, neuroendocrine, and autonomic pathways are invoked to reset weight to the previous higher weight, such as:

  • Levels of the hunger hormone, ghrelin, rise robustly;

  • Levels of leptin, the key adipostat or suppressor of food intake, fall;

  • The resting metabolic rate (the biggest contributor to energy expenditure) declines;

  • Skeletal muscle adapts to become more efficient, requiring fewer calories for the same work.

Also, despite initial adherence and discipline to lifestyle changes, the novelty of weight loss begins to wear off and behavioral "fatigue" sets in. Many weight-loss interventions fail because of a short-term duration and lack of follow-up.

The failure to maintain any one diet is governed by a person's underlying biology that defends their fat mass. Only when that individual perseveres and incorporates long-term lifestyle changes will he or she prevail at keeping the weight off.

How Important Is Exercise?

How often have you heard patients say that they are exercising vigorously on the elliptical and lifting weights every day but are not losing any weight?

Although it's important to move more, exercise alone contributes little to weight loss; it does play an important role in maintaining reduced weight.

Exercise confers a wealth of other benefits, such as improving insulin sensitivity, reducing blood pressure, redistributing fat (such as abdominal fat), and improving mood and well-being, so it should be part of any lifestyle intervention. But some patients may be relieved to hear that they don't have to focus so much on exercise.

Those who have trouble getting started on an exercise regimen should be encouraged to get more NEAT (non-exercise activity thermogenesis)—ie, standing more than sitting, parking the car farther away from the store or work site. These activities may contribute to a modest increase in energy expenditure and are a way to gradually add in exercise.

Taking a Realistic Approach

Despite our resistant physiology, many studies have shown that even modest weight loss can result in health benefits and a higher health-related quality of life.[2] We need to disabuse patients of the "all or none" mentality so that when they experience recidivism, they don't give up.

In 2012, the US Preventive Services Task Force recommended that all patients be screened for obesity and that those with a BMI over 30 be offered or referred to high-intensity lifestyle intervention programs. The task force also found that there was adequate evidence to support the use of these high-intensity interventions to prevent diabetes.

Clinicians can refer obese patients to programs that are part of a nationwide network overseen by the Centers for Disease Control and Prevention as part of the Diabetes Prevention Program (DPP), which has reported promising results in its first 4 years.

The DPP website provides information for both patients and clinicians, including links for finding a lifestyle program in a particular city, referral forms for clinicians, and information on how to be reimbursed by Medicare for assessing and referring an eligible patient.

Addressing obesity in clinical practice is challenging, but neither patient nor clinician should despair. We need to help patients remain motivated and engaged by offering continued support to optimize behavioral change. We need to work with our patients to develop a treatment plan with attainable objectives to maximize success, and recognize that the plan may evolve over time and require a different set of strategies.

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