“Few individuals ever truly recover from obesity; rather they suffer from ‘obesity in remission,” said Dr. Christopher Ochner. “They are biologically very different from individuals of the same age, sex and body weight who never had obesity.”
or more than a half century physicians have told people who struggle with maintaining a healthy weight that they must eat less and exercise more. Entire industries have made billions of dollars from people unable to get slim or maintain a svelte figure.
I wanted to know whether obese people really eat more than thin people and exercise less than their slimmer peers and why it is so difficult for those who lose the weight to keep it off. What I concluded after digging into all of the research data is—science doesn’t know for sure why fat people are fat, but it is finally getting a clue. And it isn’t as simple as calorie intake and exercise levels. It’s a lot more complex than that.
I also found that despite the lack of factual data that supports the notion that fat people eat to excess and do not exercise enough, the area is rife with moral judgment against the obese. In other words, fat people are considered to have major character flaws, such as lack of self-control and sloth. But the reality is that fat people may actually have a metabolic disease, as some scientific literature suggests. To put it bluntly, the belief in the simple equation of energy in and energy out as the sum cause of obesity is a bit like believing in Santa.
Before digging into the metabolic data, however, I do have to come clean that I arrive at the table with some presuppositions, such as a belief that those people who are not health conscious at all and who willfully eat excessive amounts of sugar and processed food with no thought to the high amount of empty calories they are consuming, will continue to gain exponentially and at a dangerous rate. This is just irresponsible behavior. Sugar is a metabolic drug and anyone who has willfully torn down the firewall of their built-in oven is going to suffer a metabolic breakdown. I consider this group of people to have additional issues, such as a sugar addiction and psychological and emotional issues, so let’s just take this group off the table for now.
My other supposition is that the human body is a complex machine, and the theory that obesity is a simple energy equation seems far too simplistic to be a good measure of why some people get fat and others do not, particularly if diet and activity levels of obese people are nearly identical when compared to slim people. And a half century of telling people to just eat less historically does not work. Surely, we are missing something here.
In fact, the data is clear that there is a DNA cause of obesity and we can’t continue to ignore that more than 60 relatively common genetic markers have been implicated in causing a higher susceptibility to obesity, which also suggests that the etiological cause of obesity is far more complicated than the old energy consumed and expended theory.
So this brings us to the great conundrum. If obesity is a genetically inherited “disease,” then telling people to restrict their caloric intake to 1,200 calories or less a day for the remainder of their lives and to work out at least four times a week, quite honestly, is a draconian life sentence of deprivation that even your average gym rat is not going to be able to sustain for more than a decade at best. Worse, it may cause more metabolic damage.
According to Asheley Skinner, a pediatrician at the University of North Carolina Chapel Hill School of Medicine. “Even if someone loses weight, they will always [my emphasis] need fewer calories and need to exercise more,” says Skinner. “So we’re putting people through something we know will probably not be successful anyway. Who knows what we’re doing to their metabolisms.”
How complex is obesity? Scientists have discovered that there are several obesity variant gene sequences known to cause monogenetic obesity, particularly MC4R, a known obesity gene. But what exactly does monogenetic mean? Monogenetic diseases result when modifications in a single gene occur in all cells of the body. Though relatively rare, monogenetic diseases affect millions of people worldwide. Scientists currently estimate that more than 10,000 human diseases are monogenetic. In contrast, pure genetic diseases are caused by a single error in a single gene in the human DNA.
The nature of disease depends on the functions performed by the modified gene. The single gene, or monogenetic diseases, can be classified into three main categories: dominant, recessive, and X-linked. If the obesity gene is a monogenetic disease, it is no wonder then that there is no one elixir to solve a complex disease. It also confirms my suspicion that a dieter such as myself will always have to eat less to maintain any weight loss. And over a lifetime, this becomes extremely draining.
A recent study in Skien, Norway’s Department of Laboratory Medicine, looked at the medical genetics of next-generation sequencing of the obesity genes LEP, LEPR, MC4R, PCSK1 and POMC using 485 patients with morbid obesity and 327 normal weight controls. The test detected 151 variants in the genes with 18.5 percent of these being rare, coding or splice variants and 3.3 percent being novel. All individuals, except one control were heterozygous for the 28 variants, and the distribution of the rare variants showed a significantly higher carrier frequency among cases than controls, or 9.9 percent versus 4.9 percent. And four variants in MC4R were classified as pathogenic or likely pathogenic.
The scientists concluded that there are significant differences in carrier frequencies among patients with morbid obesity and those who are normal weight, which suggests an association between heterozygous rare coding variants.
Dr. Christopher Ochner, assistant professor of pediatrics and psychiatry at the Icahn School of Medicine in New York and lead author of the paper, said that in those with chronic obesity “body weight seems to become biologically stamped in and defended.”
“Few individuals ever truly recover from obesity; rather they suffer from ‘obesity in remission,” he said. “They are biologically very different from individuals of the same age, sex and body weight who never had obesity.” This is epic but not unknown to those of us who fight our weight every single day of our lives. Without being told, we know that the minute we are not vigilant in counting calories and actually giving in to our desire to eat something fatty, we inevitably gain weight and at a faster rate.
Clearly, there is such a thing as a fat gene and if the science is to be believed, there is little a person can do to change their DNA or their “stamped-in” body weight. It really isn’t good news to be told that once a fatty, always a fatty, but it would nice if the virtue signaling, militant health community would save their condemnation of the obese to something more factual.
The diet industry is huge, and it is imperative that overweight people have hope, however, degrading people who struggle with their weight as somehow being morally deficient is unconscionable, particularly in light of the scientific data. It’s tough to be a big girl in a thin world, but it does help to know that I am not any more morally deficient than my thinner peers. So here’s to continuing the battle of the bulge and mindful, healthy eating, just leave the guilt on the editing room floor. Reign well.