The Big, Fat Lie
It’s not what you weigh, but what you eat.
Posted Jan 19, 2018
“It’s a New Year!
It’s a New You!”Blah, blah, blah.
How many times have we heard that twaddle, as a depression emanating from our image in the mirror settles in around us like some January freezing fog. With the free pass of “It’s the holidays,” checked, validated, and used; bodily reality parks on the couch like some unwanted, obnoxious Patriots fan at a Super Bowl party; constantly reminding us that not only is Tom Brady obviously the GOAT (Greatest Of All Time), but that Tom Terrific looks, well, terrific.
And we hear all the time, from all the various experts, that as a nation we are increasingly obese and increasingly sick (the latter is beyond questioning). Their logic dictates that one follows the other and that both the cause and correlation are vetted with 100% certainty.
But as we watch Brady’s potbellied left tackle pancake a would-be-sacker, we catch a glimpse of what everyone in the medical field understands. There is heavy, there’s obese, and there’s a difference.
Anyone who has spent time clinically treating patients has seen them; overweight, plump, and in perfect health. Just a matter of time, we all think, as we recite the 50-cent obligatory “Got to lose that weight and get in shape” rote from memory and repeated use. But is it all really an inevitable matter of time till they crash and burn?
The BMI is the body mass index, calculated by using the height and weight measurements. It is what is currently used to define normal, overweight, and the three classes of obese individuals.
“Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health,” according to both the Centers for Disease Control and the World Health Organization. The WHO continues, “A crude population measure of obesity is the body mass index (BMI), a person’s weight (in kilograms) divided by the square of his or her height (in meters). A person with a BMI of 30 or more is generally considered obese. A person with a BMI equal to or more than 25 is considered overweight.” How arbitrary are these divisions? What about the folks that are just overweight and mildly obese (class 1), do those three extra fat cells confer triple the risk?
The BMI was developed in the 19th century by Belgian polymath Lambert Adolphe Jacques Quetelet. It was made popular in the 1970s in a study performed by Ancel Keys where the Quetelet Index, as it was originally known, proved the most accurate of several easily performed clinical measurements used to correlate with fat. Keys renamed the measure the BMI.
There are many issues with the BMI as a measure of obesity which by definition infers an increased risk to health. In fact, the Council on Science and Public Health, which had studied the issue of declaring obesity a disease delivered their final opinion “that obesity should not be considered a disease mainly because the measure usually used to define obesity, the body mass index, is simplistic and flawed.”
The BMI is indeed a poor measure of obesity. Because it does not take into account lean body mass such as muscle, it can overestimate obesity in certain ethnic groups, while underestimating it in others. Many physically fit people, including actors and athletes with very low percentages of body fat, register as obese when judged solely by their BMI.
For example, some world-class athletes like rugby player Jonah Lomu or basketball superstar LeBron James have a high BMI. According to BMI measurements, Arnold Schwarzenegger and Sylvester Stallone are or were all obese or overweight at one time (like when they were buff during the Rocky and Terminator days). Genetics may also play a role as those who tend to have larger frames and more muscle mass, like African-Americans, may be over-diagnosed; while those who are of slighter frame, such as those of Asian descent, may be underdiagnosed when relying completely on the BMI.
But there are significant questions and issues beyond just the BMI. In one of my previous books, The Fallacy of the Calorie, I discussed the problems of the ecological fallacy and the obesity paradox. Both Quetelet and Keys warned against applying conclusions drawn from measuring the BMI in populations to any given individual. What applies in large groups may lose predictive significance when trying to apply it to any individual. This is known as the ecological fallacy. Yet, this is precisely what we attempt to do by basing all actions and treatments solely on the BMI.
At the population level, various grades of obesity have been associated with the development of various disabilities and diseases; among them diabetes and cardiovascular disease. However, among those suffering from such disabilities and diseases, for certain conditions, the presence of obesity is associated with a reduction in mortality. In other words, in certain situations being overweight or obese puts you at less risk than those in the normal or ideal body weight category. This is known as the “obesity paradox.”
After the publication of The Fallacy of the Calorie, my colleague Dr. Carl Lavie, from Ochsner Medical Center in New Orleans, covered this in extensive detail in his excellent book, The Obesity Paradox: When Thinner Means Sicker and Heavier Means Healthier. As if to emphasize this point, in one of the most extensive studies done to date, the healthiest group of people in terms of survival were not those at the “normal” or “ideal” BMI.
This meta-analysis of almost three million people around the world found that the lowest mortality rates were in the overweight group. They had a statistically significant six percent reduction over the ideal group. Interestingly, the mortality rate of the ideal group was actually the same as the Grade 1 (mildly) obese group.
Those persons with Grades 2 and 3 obesity did show a significantly increased risk, but individuals in those groups represent a small fraction of the 67 percent of all Americans who are classified as either overweight or obese (though they are among the most rapidly expanding groups). At some level of increasing weight, there is always going to be an increased risk of mortality, but where that boundary is, that is far from clearly defined.
Many other studies of patients with various diseases have shown that the best survival rates occur not at the ideal BMI, but in those groups that are either overweight or mildly obese—counter-intuitive, obviously, to the conventional wisdom.
And the paradox is growing.
Obesity is repeatedly emphasized as a risk factor for atrial fibrillation, a condition that is estimated to affect up to 1-in-4 persons during their lifetime. It is associated with a series of adverse effects, such as lower health-related quality of life, dementia, heart failure, stroke, and even early death. Even with advances in other areas of cardiovascular disease, atrial fibrillation stubbornly remains one of the few heart diseases with increasing incidence.
A recent Danish study of nearly 4,000 people with atrial fibrillation (AF) examined risk factors. The research revealed “a spectacularly simple pattern, which suggests that lean body mass was the predominant anthropometric driver of AF risk, whereas none [emphasis mine] of the traditional obesity-related measures proved to have any independent influence. The pattern was consistent between the sexes and over time.”[i]
Another potent risk factor for AF, a process believed to be involved in the etiology of this disease, is inflammation. Chronic, continuous low-level inflammation that brings us back to the table for an examination of diet (not examined in the previous study). True obesity associated with the development of disability and disease is universally linked to an increased state of inflammation, and oft-derided as its genesis.
Perhaps, just perhaps, obesity is the result of diet-derived inflammation. In essence, a marker of gut injury that leads to chronic continuous inflammation and subsequently the disabilities and diseases associated with the modern Western diet. Not, as it is so often perceived, as the cause of said inflammation.
The idea is not far-fetched. Another recent study examined otherwise healthy college students. They were not obese, nor ill by any measure. After eating a typical Western meal (pizza) many had an over 500% increase in blood markers of inflammation; including endotoxin, triglycerides, and interleukins IL-12p70 and IL-1β, as well as ghrelin, the hormone responsible for making you “hangry” and overeat.[ii]
The modern Western diet (MWD) alters our gut microbiome and our innate physiology in a way that encourages the development of just such a pathologic, pro-inflammatory state. In light of the preponderance of data destroying “calories in, calories out," the quantity hypothesis of obesity, we must look beyond the same banal “New Year, New You” epithets that have been hurled at us over the last half-century in the name of conventional wisdom.
The alternative hypothesis may be that it is not simply the mass of food of we ingest, but the quality that makes the difference. Grading simply by size is like judging a movie solely based on its length, and ignoring its story, content, acting and emotional impact. An action we would all immediately agree is preposterous. We must evolve in thought and perception to recognize that it is not merely the quantity—calories, carbs, percent sat fat, or any other villain of the moment—but the value of the food experience which determines who we are.
If we truly are what we eat, shouldn’t we eat authentic, quality, and wholesome food? It’s all about the taste, keep it real.
[i] (Fenger-Grøn, Overvad, Tjønneland, & Frost, 2017)
[ii] (McFarlin, Henning, Bowman, Gary, & Carbajal, 2017)