Life

UW Lecture: Why is it so hard to lose weight?

May 13, 2015
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One of my friends told me that the University of Washington was hosting a “Weight and Wellness” lecture series (thanks, Tracy!) So, this evening I attended a two hour talk called “Why is it so hard to lose weight?”  It was presented by Dr. Ellen Schur, who does extensive research in obesity medicine and the brain’s appetite regulation.

I took detailed notes on the lecture, and wanted to share some of the key takeaways from Schur’s lecture. So, why is it so hard to lose weight?

Introduction

More people are overweight and obese than ever before. Why? What is causing this shift?  In 20 years, obesity rates have rapidly risen. Yet, people’s genes haven’t changed drastically in 20 years.  How is this possible?

One study that suggests an explanation is Claude Richarde’s, where 12 twin pairs were overfed by 1000 calories per day.  There was some individual variability, but twins’ weight gain was more similar to each other than to unrelated individuals. In short: the amount of weight twins gained when their environment changed to one of high nutritional availability was directly related to their genes. What this tells us is that genes not only influence your ultimate body weight, but how much weight a person gains when the environment changes. 

(Kimberly’s aside: obesity researchers also suggest that if overweight or obese people, e.g. those with that genetic predisposition, reproduce with each other, that actually could create a genetic shift among the population.)

Is obesity a disease?

In short, the answer is “yes”.  In the last 15-20 years, medical research and thinking has shifted from viewing obesity as a personal problem to a medical problem.  

It used to be that people with weight issues were viewed has having a personal failing, and that it was a matter of willpower.  Now, the understanding is that obesity is an impairment of the body’s ability to regulate its weight.  

Additionally, research shows that the body resists weight being lost once the weight is gained. 

A disease model of obesity

Schur had two participants get up onstage and inflate balloons. One inflated a small balloon. The other inflated a larger balloon. Understandably, the larger balloon could hold more air than the smaller balloon. Moreover, when you let all the air out of either balloon and reinflate it, it inflates easier the second time.

How does this apply to obesity? In a few ways:

  • Inflating a larger balloon is easier than inflating a smaller ballon -> some people are genetically predisposed to gain more weight than others. Additionally, like balloons, people’s genes cause their bodies to have many different shapes and sizes.
  • Up until a certain point, you have to blow pretty hard to inflate a balloon -> the body has a weight regulatory system, but when you pass that point, this weight system gets impaired and it’s easier to gain weight.
  • Once a balloon has been inflated and deflated once, it’s easier to inflate it the second time -> when overweight people lose weight, this “weight system” does not regain its functional integrity. Schur said, “It stays a little wrinkled; the next time you regain weight, it’s easier than it was before.”

Genes and environment matter

There is no one obesity gene, but studies on twins estimate that 90% of BMI variation is genetic.  

  • Identical (monozygotic) twins have about 99.99% genetic similarity, and are virtually identical in terms of body shape and size even later on in life, regardless of whether they shared the same childhood environment or not.
  • In contrast, fraternal (dizygotic) twins share only about 50% of their genes, and may have various body shapes and risk of obesity, even when they do share the same childhood environment.

Thus: genetics play a huge factor in body shape, size, and predisposition toward weight gain, while environment appears to play a much smaller role. 

Maintaining the status quo

Bodies resist weight gain

A properly functioning metabolism fights against weight gain with energy homeostasis:

  • Your body regulates fat and energy stores just like it does your blood pressure, body temperature, etc.
  • Adiposity (body fat) signals like insulin and leptin are part of the endocrine system and communicate between the brain and body about the status of energy stores.
  • These signals release hormones into the bloodstream, which circulate to the brain and interact with neurons that either suppress food intake (through reduced hunger signals) and raise energy expenditure, or increase food intake (through increased hunger signals) and lower energy expenditure.
  • When fat stores rise, a normally-functioning body will raise the metabolic rate and decrease hunger to maintain weight.

The role of leptin

Leptin, a hormone produced by adipose (fat) cells, was discovered in 1994.  Its discovery had an almost immediate, dramatic impact on weight research.

  • When leptin was first discovered, everyone was excited and thought it was going to be the solution to obesity.  This is because when leptin is absent, mice become obese, eat a lot, don’t move much, and have a low metabolic rate.
  • However, leptin levels are high in obese individuals because it’s your body’s signal of body fat levels to the brain. In fact, they increase exponentially relative to your body weight.
  • High leptin regulates fat stores, suppresses appetite, and raises metabolism.
  • One theory: obesity may be a disease in which leptin is no longer effective at regulating appetite and metabolism like it should.  Obesity may, in fact, partially be “leptin resistance”.

However, leptin isn’t the only factor, because…

Bodies also resist weight loss. When you lose weight…

Leptin levels fall

Using the balloon analogy, it becomes easier and easier to inflate a balloon (regain weight) as leptin becomes ineffective. When you lose weight, even as little as 10% of your body weight, circulating leptin concentrations drastically fall. 

In one study on the effects of weight loss on leptin, researchers looked at both overweight and non-overweight individuals and had them lose weight.  As expected, heavier individuals had more leptin to begin with, less heavy people had less leptin.  

However, once people lose 10% of their weight, their leptin falls by 32%.  

In other words, your body overreacts to weight loss and leptin levels drop disproportionately, regardless of whether you are lean or obese.  The body does not “see” an individual’s weight, just that they’re “starving” and losing energy stores.

Hunger increases

Ghrelin, a hunger hormone, was discovered in 1999.  Research has found that caloric restriction increases ghrelin (hunger) levels. After weight loss, ghrelin levels rise. Losing weight makes you hungrier! Your body is trying to restore energy balance.

Your metabolism slows down

Studies show that 65% of metabolism is resting metabolic rate, 10% is energy expended towards food and digestion, and 25% is physical activity.  

Schur said that we have a little control over a small portion (physical activity), but a majority is set by our resting metabolic rate.  

Resting metabolic rate is fairly predictable and varies based on age, gender, weight, height, lean mass, exercise, and, critically, whether the individual is weight-reduced. She gave the following example:

  • A 90 kg man who has not lost any weight has a resting metabolic rate of 2000 kcal a day
  • A 90 kg man who originally weighed 100 kg has a resting metabolic rate of 1850 kcal a day

Resting energy expenditure decreases by 15 calories for every kg of body weight lost.  Your system changes in a way that encourages weight regain, even if you are eating less than you were before. The more weight you lose, the less you can eat, because your metabolism keeps slowing down.

Brain + food environment = trouble

Our brains are designed to quickly identify and acquire food. In fact, brains are able to distinguish high-energy food within 300 ms.  The motivation to eat is a powerful – and necessary! – process.  However, studies show that the brain is highly excited by “fattening” foods:

  • In FMRI scans, the hypothalmus and dopamine centers of the brain respond strongly to images of foods like burgers, pizza, chocolate, and sweets. However, when shown pictures of vegetables, fruit, etc., people’s brains responded to those images no differently than a picture of furniture (literally, the other picture shown to participants was a couch, and there was no difference in their brain response.)
  • Additional studies revealed that individuals who are more hungry respond more strongly to images of fattening foods – their amygdala and medial cortex were strongly activated compared to non-hungry individuals.  
  • Lastly, obese women responded more to pictures of high calorie foods than control women.  This could be a sign that leptin is less effective in obese individuals, because a separate study showed that leptin helps reduce the brain response to so-called “rewarding foods” in children who are genetically deficient in leptin.

In short: brains are highly attuned to food in their environments. A properly functioning metabolic system means that attention to high calorie food should be suppressed after eating, because hormones that regulate body weight should cause satiety, which removes the motivation to seek out food. In individuals with obesity, this process may be altered. 

Obesity is a disease process

Schur wrapped up by saying that there is absolutely a disease process happening in individuals with obesity.  Medical organizations like AMA, WHO, the FDA, NIH, and more agree that it’s a disease.  She emphasized that physicians need to change their approach. In the past, the onus has been put on patients, with much finger-shaking and reproach being directed at individuals who are overweight.  She said that obesity instead must be managed as a chronic disease: “We wouldn’t tell someone with high blood pressure to regulate their blood pressure themselves, so we shouldn’t be telling people with high body weight that they’re on their own.”

It’s treatable, but there’s no magic bullet 

Some important lessons learned from the talk:

  • Both genes and environment matter, but genetics paint 90% of the picture when it comes to body shape and weight
  • Body weight is regulated, but once weight passes a certain point this can cause the system to break down
  • Bodies are resistant to weight loss whether an individual is overweight or not
  • Losing weight puts the body in a “starvation” state that makes weight regain easier
    • For individuals who have chronic, weight-related health issues:  Losing as little as 10 pounds can have drastic health improvements.  You don’t have to lose 50 pounds to change your health.
    • For individuals who want to lose weight for social or appearance reasons:  Losing weight can put your body in a slowed metabolic state and can cause more weight gain in the long run.
  • We cannot cure obesity, yet – more research is needed to understand what’s going on and offer more effective, durable treatments.

On a more personal note, I’m very hopeful that more and more conversations are being had about the fact that obesity is a disease and is not a personal failing. There’s so much stigma against people who are overweight, and yet more and more research is coming out to suggest that obesity is a matter of genetics.  Now if only social opinions would catch up with medical research!

Thanks to the UW and Dr. Schur for this informative and helpful talk. I’m very much looking forward to going to the series conclusion next week, called “Women and Body Image”.  I will be sure to post my notes from that talk as well!


Photo credit: kizette / Ashley Modern / CC BY-NC-ND


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