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Stop the Patient Blame Game: What Actually Causes Obesity?

Updated: March 04, 2019

Stop the Patient Blame Game: What Actually Causes Obesity?

This article was first published on Medscape on March 01, 2019.

https://www.medscape.com/viewarticle/909500#vp_4

By: Nikhil V. Dhurandhar

Successful prevention or treatment of obesity is fraught with many difficulties, including challenges in having open patient-clinician conversations[1] and overcoming stigma.[2]

These difficulties are further heightened because obesity is often considered to have a simple cause, when in fact it is a complex disease with a multifactorial etiology.

Effective treatment of obesity requires a careful understanding of the facts and myths surrounding this disease and its various causes. Here, I will provide evidence-based explanations for the various causes of obesity as we examine some popular misconceptions.

‘Food Causes Obesity’

To address this misconception, let’s first consider the example of edema. Water balance is usually precisely controlled by the body through multiple hormones and mechanisms. Edema results from an impairment of the controls of water balance, not from drinking excessive amounts of water.

Similarly, the body has mechanisms to regulate energy intake and expenditure. The net result of these mechanisms could be a state of energy balance, negative energy balance, or positive energy balance, leading to maintenance, loss, or gain of weight, respectively.

“Blaming food for causing obesity is like blaming water intake for edema or the glucose bolus for diabetes.”

As declared by the American Medical Association and other professional organizations, such as the Obesity Society, obesity is a disease. The defect in energy balance regulation leading to excessive energy storage in the form of fat is the disease. Food does not cause that defect. Hence, food does not cause obesity.

But food allows obesity to be expressed, just like water allows the defect in heart or kidney functions to express edema, or as a load of glucose allows the detection of impaired glucose clearance in diagnosing diabetes.

Blaming food for causing obesity is like blaming water intake for edema or blaming the glucose bolus for diabetes. An individual with an impairment in energy balance will find it easier to gain weight on energy-dense food than another individual eating the same food who does not have an impairment in energy balance.

Although obesity has many causes, as we’ll discuss below, its current treatment involves creating an energy deficit by reducing food intake. The fact that reducing food intake may produce weight loss is often considered proof that obesity is caused by food. However, that does not demonstrate its role in causing obesity. Often, cause and treatment are not two sides of the same coin. Excessive exposure to UV radiation may contribute to skin cancer, but its treatment does not involve placing a person in a dark room, away from sunlight.

‘Obesity Is a Choice’

A popular and simplistic assumption is that energy balance is completely under volitional control, which stems from the observation that individuals control their food intake and physical activity. However, the numerous controls up- and downstream that collectively determine energy balance are ignored.

There are numerous physiologic factors beyond volitional control that influence energy balance and keep energy storage within a reasonable range. Such nonvolitional controls may explain why some individuals eat seemingly huge amounts of food but have lean body weight.

Factors that regulate energy balance include acute, medium, and long-term control of energy intake and expenditure, and may have some overlapping functions.

Besides the executive function by higher brain centers, satiety hormones such as GLP-1 (glucagon-like peptide 1) and PYY (peptide tyrosine tyrosine), and the hunger hormones, such as ghrelin, help regulate food intake acutely.[3] As blood ghrelin levels rise, hunger sets in. As food intake proceeds, ghrelin levels start dropping and the satiety hormones GLP1 and PYY start rising, signaling satiety and enabling meal termination.

Leptin, a protein made by adipocytes, gives the brain a biochemical estimate of the amount of adipose tissue in the body and allows the brain to take longer-term actions to increase or decrease adipose tissue over time.[4] Recent studies raise the possibility that gut microbe composition influences the extraction of additional calories from food.[5] Brown adipose tissue, which consumes energy instead of storing it, influences energy expenditure over the medium term.[6]

An example of long-term regulation of energy deposition is suggested by the seasonal regulation of the enzyme lipoprotein lipase (LPL), which is present on adipose tissue and skeletal muscle cells, and which facilitates the entry of triglycerides into those cells.[7] Typically, the entry of triglycerides into skeletal muscle cells leads to its “burning” for energy production, and entry into adipocytes indicates storage.

It appears that in winter, adipose tissue LPL activity increases, suggesting that energy storage is favored in winter,[8] perhaps to provide insulating fat for protection. The potential for adipose tissue LPL activity to increase or the skeletal muscle LPL to decrease in response to a meal predicts weight gain over time.[9]

‘Calories In, Calories Out’

A popular misconception is that weight gain can be predicted using a simple math of calories: If you gain 1 lb, you have eaten 3500 calories more than your requirement.

Not quite. The Vermont prisoner study was one of the early studies showing how difficult it is to make willing participants gain weight by forced overfeeding.[10] Although conventional wisdom calculates that 3500 excess calories leads to 1 lb of weight gain, these participants required a many-fold greater calorie surplus to gain 1 lb.

Bouchard and colleagues[11] reported another such compelling example. They enrolled twin participants who underwent an 84-day forced overfeeding inpatient trial. Under constant monitoring and surveillance, the participants received a surplus of 1000 kcal per day.

The calculated weight gain expected during the trial was 24 lb. Instead, the actual range of weight gain was 9-30 lb. Despite identical surplus energy intakes, some individuals were very resistant to storage of surplus energy, whereas others had a physiology very conducive to weight gain. Moreover, the difference was greater between twin pairs but not as much within twin pairs, indicating a strong genetic influence on the propensity to gain weight. 
A prominent example of the genetic control of weight regulation is the study conducted by Stunkard and colleagues[12] of twins separated at birth and reared separately. They observed that even when reared separately, body weights of the twins matched closely with each other. They concluded that “genetic influences on body-mass index are substantial, whereas the childhood environment has little or no influence.” 
The dominance of genetic over environmental influence on body weight was also demonstrated in a study that showed a strong link between the body weights of adopted children and their biological parents, but not at all with their adoptive parents.[13] These studies indicate a stronger influence of genetics on determining body weight than food or related habits of a household.

Furthermore, the body has mechanisms to resist changes in body energy stores, which can offset mathematical expectations based on calorie intake calculations. Leibel and colleagues[14] showed that bodies that were overfed resisted weight gain by increasing metabolic rate.

Alternatively, on a weight loss diet, metabolic rate was decreased and weight loss was resisted. These studies suggest that mechanisms beyond a person’s voluntary control regulate energy stores and can make it easier or harder for different individuals to gain weight.

‘It’s Just a Lack of Willpower’

Impairments in energy balance mechanisms that lead to energy surplus cannot be changed with willpower. Thyroid disorders can increase or decrease energy reserves by influencing metabolic rate. Or, suboptimally functioning ghrelin, PYY, or GLP1 may cause difficulties regulating food intake.[15,16]

In obesity, there is delayed reduction of ghrelin and delayed induction of satiety hormones. Two individuals offered identical meals will consume different quantities depending on their individual meal termination signals conveyed by their satiety and hunger hormones.

“If we were asked to reduce the rate of breathing to 10 times per minute, we would certainly be able to comply. The critical question is, for how long?”

They may appear to volitionally eat more or less, even if they are both responding to their respective internal satiety signals. Although food intake is noticeable, the factors that regulate the intake are not apparent, lending support to simplistic assumptions about an individual’s willpower.

Some individuals may harbor a gut microbe composition that is conducive to greater calorie extraction and weight gain,[17] or some may have less brown fat, which may result in reduced utilization of calories.[18]

If energy balance is influenced by impairments in the brain, satiety and hunger hormones, other hormones and enzymes, gut microbes, or the amount of brown adipose tissue, lack of willpower cannot be solely to blame for energy surplus.

Often, the “faulty” eating pattern of individuals, particularly in relation to fast food, is blamed for their obesity. This question was addressed nearly 40 years ago by Stunkard and colleagues.[19]

Eating styles of 30 obese women and 37 matched women of normal weight were observed unobtrusively in a fast-food restaurant in the search for an “obese eating style” or other differences between the two groups. The size and character of the food was carefully matched by giving each woman a coupon entitling her to a free meal of either 985 or 1800 calories. There were only small and inconsistent differences between obese and normal-weight women. No evidence of an “obese eating style” was found.

I have heard people say, “We hold a fork in hand and put that food in our mouth. So, we have total control over the quantity we eat.” This is only partly correct. True, people have some volitional control over when to terminate a meal. This is very similar to the control we have over our breathing.

If we were asked to reduce the rate of breathing to 10 times per minute instead of the usual 16-18, we would certainly be able to comply. The critical question is, for how long?

Similarly, it is a tall order to expect a person to volitionally eat substantially less than what the person’s brain, gut, and physiology are asking for, for months and years on end. This is not an issue of willpower for only a select few; it is unrealistic and unsustainable for most individuals.

‘Who Cares About Why? Just Eat Less.’

The word “cancer” encompasses many different conditions, with etiologies as varied as smoking, UV light exposure, or viral infection, depending on the cancer type. Similarly, the multiple etiologies of obesity indicate that it is a collection of diseases, better referred to as “obesities.”

Cancer treatment depends on the type of cancer. Similarly, “obesities” require that the various causes and contributors are identified for effective treatment.

Current obesity treatments include diet and lifestyle management, some pharmacotherapy, and bariatric surgery on a limited scale. These are blanket treatment approaches regardless of the cause. If the individual causes of obesity were to be correctly identified, treatment could be directed to the specific causes, which may be more effective than current approaches.

A prominent example from the field of gastric ulcer treatment highlights the significance of accurately understanding the cause of an illness. The role of gastric acid in gastric ulcer was recognized even in the early 1900s, and subsequent efforts were made to modify the diet, neutralize acid, or reduce its secretion.

It required the 2004 Nobel Prize–winning research to discover Helicobacter pylori infection as an upstream cause of gastric acidity and ulcer. As a result, antibacterial medications became an important and effective treatment for gastric ulcer.

 A comparable example in obesity treatment would be the discovery and use of leptin for weight loss. Most people with obesity are resistant to leptin action and have excess leptin as a result. Some individuals are born without any leptin. These cases typically present as kids with a very high degree of obesity.
Their obesity is not due to excess TV watching or eating junk food, as popularly believed. This type of obesity develops because leptin is absent to provide the usual feedback to the brain about energy status. Hence, the brain fails to take corrective action in response to accumulating fat.

The treatment of obesity due to leptin deficiency is not diet or lifestyle modification but simply leptin replacement injections.

Another example is the treatment of obesity that results from proopiomelanocortin (POMC) deficiency in the brain. Melanocyte-stimulating hormone is produced from POMC and conveys the anorexic effect of leptin via the melanocortin-4 receptor (MC4). POMC deficiency leads to impaired stimulation of MC4, resulting in greater energy intake. This condition is effectively treated with a MC4 agonist drug.[20]

Deficiency of leptin or POMC are obesities of genetic origin that are successfully treated with a cause-specific approach. Other examples of contributors to obesity that inform treatment include endocrine disorders such as hypothyroidism, Cushing syndrome, or inadequate or poor sleep quality. These few examples underscore the need for further research to uncover additional causes of obesity and how they could be effectively treated.

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