One of the most hotly debated subjects over the past few years has been the cause of the obesity epidemic, and along with that, the best strategy for weight loss.
Some folks (Atkins, Taubes, Eades, etc.) believe that carbohydrates are to blame. Others (Ornish, Campbell, Esselstyn, Fuhrman, etc.) believe that fat is the problem. More recently, researchers like Seth Roberts and Stephan Guyenet and clinicians like Dr. Sharma have raised awareness of another hypothesis, called the food reward theory, which holds that the consumption of highly palatable foods leads to overeating and weight gain. And Paul Jaminet and others have argued that micronutrient deficiencies, toxins and infections may play a significant role in the obesity epidemic.
Here’s what I think: the most accurate answer to “why do people get fat?” and “what’s the most effective weight loss strategy?” is: “it depends.”
Separating Cause from Mechanism and Effect
While it’s tempting to make such an assumption, the logic is faulty. It’s kind of like saying “Advil cures headaches. Therefore, headaches must be caused by Advil deficiency.”
Let’s look at some definitions.
Cause: something that brings about an effect or a result
Mechanism: the fundamental processes involved in or responsible for an action, reaction, or other natural phenomenon
Effect: an outward sign
Obesity is an effect. Insulin resistance, leptin resistance, lipotoxicity, disruption of the mesolimbic dopamine reward pathway and inflammation of the hypothalamus are presumed mechanisms. Excess consumption of carbohydrates, fat, highly palatable food and food toxins (wheat, seed oils, liquid fructose, etc.), exposure to environmental toxins (chemicals), stress, infections, etc. are presumed causes.
Say we do a study on obese people and we observe that they eat a lot of carbohydrates and are insulin and leptin resistant. It’s easy to assume that the chain of causality worked like this: normal weight person eats high-carbohydrate diet, becomes insulin and leptin resistant, and then becomes obese.
But again, this is faulty logic. There’s no proof that A (high carbohydrate intake) was what led to B (insulin and leptin resistance) was what led to C (obesity).
In fact, we could disprove that theory simply by observing another individual or group that eats a very high carbohydrate diet, but does not develop insulin or leptin resistance and obesity. Guess what? Such individuals and groups most certainly exist. There goes that theory.
Likewise, we could also disprove this theory by observing people that are insulin and leptin resistant, but don’t become obese. Such people do exist, and I’ve written about them in my series on diabesity and metabolic syndrome.
A More Rigorous Approach
How have we developed our theories on obesity and weight regulation? It seems to me they come from a blend of personal experience, belief and facts. And I think it’s time to become more rigorous about keeping them separate. Here’s an example of what I mean:
Personal experience: I lose weight on an low-carb diet, therefore low-carb diets must be best for weight loss.
Belief: carbohydrates are responsible for the obesity epidemic, via their effects on insulin.
Fact: many cultures around the world eat high-carbohydrate diets and are exceptionally lean.
Those who’ve lost a lot of weight on a low-carb diet have a tendency to become convinced that their wife, friends, family, plumber and everyone else will also lose weight following the same diet.
This is especially true if our reputation or financial livelihood is tied to said belief. As Upton Sinclair famously said:
It’s difficult to get a man to understand something when his salary is dependent upon him not understanding it.
When a belief like “carbs cause obesity” is shared between enough individuals, it becomes a meme. Once that happens, it is accepted by most as fact – regardless of whether it has any scientific basis. Hence we had the idea for decades that eating fat makes you fat, and now the more recent idea that eating carbs makes you fat.
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There’s No Single Cause (Or Treatment) of Obesity
Perhaps one of the reasons it’s so easy to confuse cause, mechanism and effect and personal experience, belief and fact is that obesity is an incredibly complex disease. Just how complex is it?
Click on the Obesity Systems Influence Diagram below to find out.
Wow. That should give you a rough idea of how many variables are potentially involved in weight regulation. Now you know why it has been such a challenge to come up with a single, unified theory of obesity.
That said, of all of the hypotheses advanced to explain the mechanisms behind obesity, I think the food reward theory is the most inclusive.
However, as even its proponents would agree, it doesn’t tell the whole story because there are people and groups that eat large amounts of highly palatable foods that do not become obese.
My opinion is that the modern lifestyle (i.e. food and environmental toxins, stress, poor gut health, infections, micronutrient deficiencies, sleep deprivation, etc.) interfere with hypothalamic hormonal regulation, dopamine signaling, leptin and insulin sensitivity at the cellular level, glucose metabolism and a range of other mechanisms that lead to obesity.
This is consistent with the observation that obesity is extremely rare or nonexistent in traditional cultures that do not consume modern foods and do not live a “modern” lifestyle.
But even this theory is incomplete, because there are people fully exposed to the modern lifestyle that do not become overweight or obese. This suggests that genetics, and perhaps other undiscovered factors, also play a role.
We’re Not Robots
Humans are not robots. We’re living, breathing, dynamic organisms influenced by varying genetics and environmental conditions.
Anthropological evidence combined with modern research has helped us to reveal the basic template of a species-appropriate diet. However, it has also shown us that humans can thrive on a wide variety of macronutrient ratios and foods within that basic template.
This is not a belief. It’s a fact, supported by the evidence as a whole. Ignoring the evidence doesn’t make it go away. Believing passionately in something doesn’t make it true. Experiencing something personally doesn’t make it fact for everybody else.
19th century philosopher Charles Peirce said:
The state of belief is a calm and satisfactory state which we do not wish to avoid, or to change to a belief in anything else.
And Tolstoy said:
I know that most men, including those at ease with problems of the greatest complexity, can seldom accept even the simplest and most obvious truth if it be such as would oblige them to admit the falsity of conclusions which they have delighted in explaining to colleagues, which they have proudly taught to others, and which they have woven, thread by thread, into the fabric of their lives.
Recognizing this basic human trait, philosopher of science Karl Popper advised every researcher to earnestly try to discredit their own hypotheses.
That is no easy task, and it asks a lot of us. Yet intellectual rigor, emotional maturity and personal integrity are characterized by the capacity to question our own beliefs, no matter how deeply cherished they are or how much is at stake.
I sometimes wonder why we’re all so sure of ourselves. It helps me to remember that at every point in history scientists (and the general public) were convinced they had the right answers. At one time the world was flat, the earth was the center of the solar system and disease was caused by foul humors and could be cured by bloodletting.
Nowadays we look back on those fallacies with a smirk. But are we so arrogant to assume that our great-grandchildren won’t do the same?
The truth is, there’s far more we don’t know than we do know.
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