With a third of Americans facing the medical, emotional and social implications of obesity, weight loss has become a sensitive topic. Fitness instructors, life coaches, and your girlfriends all think they know exactly how you can lose a few extra pounds, but much of their advice is anecdotal or condescending. To avoid the previously mentioned pitfalls, I’ve grounded this article in solid scientific research from the New England Journal of Medicine (NEJM), which is one of the most read journals in medicine and therefore has the best oversight by the entire medical community. If one doctor disagrees with a paper’s conclusion, he is able to craft an editorial or a perspective article for the whole community to read. This will be the first article on a series on obesity. If you have any questions that you would like me to answer in future posts, please post a comment or write to me using my contact page.
The New York Times recently publish a phenomenal expose on the current weight of contestants of the Biggest Loser in season 8. As it turns out, all but one contestant gained a significant amount of the weight back. Danny, the winner of season 8 and one of my fitness inspirations, lost 239 pounds just to gain 100 pounds back (1). So, obviously, something is wrong. Did he lack self control? Did he not have the right support system? Before we even attempt to find out the answer, let’s ground ourselves in research.
That’s my hormones talking
In one Australian study, the researchers put healthy obese patients on a very low calorie diet for 8 weeks, slowly introduced ordinary food on weeks 9 and 10, and then gave them rigorous dietary and fitness counseling for the next year. During this time, they measured the weight, hunger, and hormones related to fat storage, hunger and digestion. During the first 10 weeks, each participants lost 13.5 kg on average. However, by the end of the year, they gained 5.5 kg back (2). Whamp, whamp, whamp! (That was the trumpet sound that they used to play for cartoons after something disappointing but expected happened.)
Oh, and this study was almost 70% female; I just wanted to mention that.
Now, let’s talk about hormones. Don’t get scared. I’ll guide you through this. Leptin is secreted by fat cells and acts on the brain to reduce how much you eat (food intake) and increase the amount of calories that your body burns (energy expenditure). During this study, they found that the participants had very low leptin levels after the fast, which we expected. Less fat equals less leptin, which implies that the participants were more hungry and less motivated to exercise. As they gained weight back, the leptin levels rose as the participants gained weight. Also, this is logical. However, these leptin levels did not completely normalize after one year.
A group of digestive hormones that prevent your from eating too much were also recorded. Guess what happened to them? They also went down and stayed down for a year. Gastric inhibitory polypeptide, which is thought to cause your body to store instead of expend energy went down and stayed down. This means that the participant’s brain is being told “you’re hungry” and “you should be lazy” even after one year after the initial weight loss. As expected, the participants reported a higher hunger score a year later.
If you look back at the study NY Times article was based on, they found that the leptin levels of the participants were low even after they regained all the weight back. So, even after they were back to their original weight, their body was shouting “You’re hungry!!!!” It’s not surprise that some contestants gained back more weight than they lost.
What the heck, body? What’s going on?
We can’t take every study as fact, and there are reasons why we can’t completely trust this study. First, a group of 34 Australians (16 participants dropped out) might not represent each individual’s situation. Moreover, we know that genetics contribute to weight balance, which brings us to the next article.
In this article, researchers found that a transcription factor, a type of gene, acted like an on-off switch for obesity in mice. A transcription factor can cause other proteins to be made or not made and determine how much is being made, so some are light switches some are dimmers. Proteins are the muscle of the cell–they are the power generators, repairmen, building materials, and computer processors of the cell. So, researchers put this transcription factor inside a group of mice and studied what happened. What they found is that with the right triggers, this gene activates significant weight gain–almost doubling the fat tissue in the mouse. However, without the trigger, these mutant mice are the same as their genetically normal furry friends. The strange thing about the whole experiment is that the mutant mice had the same metabolism regardless if they were obese or not (3).
So, perhaps obesity that occurs from this gene has stages rather than a continuum. If this little mouse starts falling off the obesity cliff, it’s going to keep falling until it plops onto its new body weight set point. If this fluff ball never get the trigger, it’s going to have a shot at being a model in mousy fashion week.
You, like me, probably want to know what the triggers are. The only one that they studied is in the form of epigenetics. Epigenetics is kind of how your body takes notes on your DNA strands. If you went through a stressful time, your body would tag genes on your DNA that have to do with stress so that they can find them easier and produce the proteins from the genes faster. Anyway, epigenetics is an accumulation of your body’s response to the environment.
Epigenetics are inheritable. A study was done on the grandchildren of a group of people who almost starved to death in Nazi, Germany. They found that the grandchildren had those hunger and energy storing genes tagged as if they had gone through starvation. Trippy, right?
The problem with this paper is that, while they have identified the same gene in humans, this experiment was still done on an animal model. We don’t know how this fully applies to humans.
Opinion: Why your fitness instructor is wrong
Retailers of fitness and nutrition products have shamed the masses for too many years. They want you to think that weight gain was just accidentally “letting yourself go,” and losing the weight is a simple as “caring about yourself more.” Much of the conventional wisdom about combating obesity is spread for more selfish reasons than scientific ones. The medical community has not been much better. However, as the researchers and physicians themselves plump up, they are forced to realize that once again, medicine is trailing behind the complexities of the human body and the ever-evolving human race.
These two articles are apart of a shift in physician thinking: obesity is a biology-based medical problem and not a self control issue. While weight gain is probably initially due to lifestyle choices, losing weight is not as simple as changing your lifestyle back to what it used to be. An obese person cannot stop their cravings any more than a person with migraines can will their pain to go away. This is actually great news; medicinal and surgical treatments for obesity are being aggressively researched as we speak.
To those who are on a weight loss journey, keep at it! Keep making good choices, and find a community who will support you on this journey. For the most up-to-date resources on healthy lifestyle, to visit the resources page of this blog and stay tuned for more posts!
Take home messages
- If you’re trying to lose weight, your body is fighting you. If you’re trying to keep the weight off, it’s still fighting you over one year later.
- As far as we know, if you’re trying to maintain weight loss, you won’t be able to eat like your skinny friend after a year of keeping the weight off.
- We have not yet studied the hormonal profile of someone who has maintained weight loss many years, and we don’t know if losing weight slowly causes a better hormone profile
- Obesity may be a switch in some organisms, but we still need to identify who has these mutations and how it works in humans.