The more damaged you are, the more carbohydrate restriction is likely to benefit you long term.
– Peter @Hyperlipid
I don’t think there are too many people out there familiar with the mechanisms of diabetes and insulin resistance that would disagree with that statement.
But just because a low-carb diet causes fat loss in this population, that doesn’t mean that carbs caused the fat gain or damaged metabolism in the first place.
I wrote about this in a previous article, There is No Single Cause of (or Treatment or) Obesity, but based on some of the comments and discussion I’ve been seeing online recently, I think it bears repeating: in order to properly frame this debate, it’s essential to separate the causes and treatment of obesity. If we don’t do this, we might as well not even have a debate at all because we won’t be talking about the same thing.
We know without a doubt that statins lower cholesterol. But does that mean high cholesterol is caused by a statin deficiency? If you break your arm, your doctor will probably put a cast on to help it heal. Does that mean we should all wear casts on our arms to make sure they don’t break?
Metabolically damaged vs. healthy: apples & oranges
Another important distinction that should be made – but often isn’t – is the difference between how people that are metabolically healthy and metabolically damaged respond to food. Of course excess carbohydrates are more likely to cause problems in someone with leptin and insulin resistance and impaired glucose tolerance. But it doesn’t follow that the same will be true in someone without metabolic problems.
People without gall bladders don’t digest fat very well. Does that mean fat causes indigestion? I have patients with iron overload due to a genetic condition called hemachromatosis. They need to limit their red meat intake because of this. Does this mean we should all avoid red meat to prevent iron overload?
We’re not robot clones. We have different genes, lifestyles, gut flora, immune fitness and exposures to toxins, stress and infections, as well as different emotional and psychological relationships with food. All of these factors play a role in weight regulation.
This explains why two people can react to the same diet in entirely different ways. And it also explains why it’s so ridiculous to extrapolate something that you experience personally to everyone else. (If I read another comment from someone saying that a low-carb diet worked for them, so the insulin-carb theory must be correct, I’m going to lose it. And it takes a lot to make me lose it!)
My unified theory of obesity
For what it’s worth, here’s my “unified theory” on what causes obesity.
Modern lifestyle + genetic predisposition = obesity.
It really is that simple.
Modern lifestyle includes processed, refined and highly rewarding and palatable foods, excess fructose, unprepared grains (especially flour), industrial seed oils, environmental toxins, sedentary behavior, stress, infections and dysregulated gut flora.
But the modern lifestyle doesn’t cause obesity in all people. I’m sure we all know someone who eats a horrible diet, doesn’t exercise, is under tons of stress and lives a shockingly unhealthy lifestyle – but doesn’t gain a single pound.
That’s where genetics come in.
Human evolution didn’t stop in the Paleolithic
A commonly held belief in the Paleo-sphere (I held it myself, until fairly recently) is that our genes haven’t changed much since the Paleolithic era. But recent evidence suggests a much more rapid pace of genetic change in humans than was previously estimated.
The birth of agriculture introduced significant selection pressure, and thus mutation, because humans were not well-adapted to this new way of life. And the evolutionary response to agricultural diet differs because different peoples adopted agriculture at different times and in different places.
Agriculture began in the Middle East 10,000 years ago, but it was never adopted by Aboriginal Australians. Might we expect the descendants of people from these two regions to have different responses when exposed to agricultural diets?
Absolutely. Researchers in Iceland have discovered a gene that regulates blood sugar tolerance. (I discussed the role of genetics in obesity and diabetes in a previous article, Are You At Risk For Diabetes and Obesity?) And we know that Aboriginal Australians have a 4 times greater risk of developing adult-onset diabetes than Australians of European descent.
Lactase persistence is another example. During Paleolithic times, humans stopped producing lactase (the enzyme required to digest lactose, the sugar in milk) shortly after weaning. There was no need for it, since Paleo people didn’t raise cattle or drink milk. Skeletal remains from northern Europeans 8,000 – 9,000 years ago confirm that there was no lactose tolerance at that time.
However, skeletal remains from northern Europeans living in the Bronze Age 3,000 years ago show roughly 25% of adults produced lactase. And today, in certain Scandanavian countries, more than 95% of adults are now lactose tolerant. 1
All of these genetic changes happened within the last 8,000 years, after the advent of agriculture.
The hand you were dealt: life isn’t always fair
What this means is that some of us are likely better adapted to the modern lifestyle, while others are more susceptible to being harmed by it. Those are very likely the ones that become obese when exposed to a western diet.
But as far as I can tell, they didn’t get obese by eating natural, whole-food carbohydrates. I’ve yet to see a population that got fat eating sweet potatoes, fruit and white rice – without any exposure to modern food. If anyone knows of such a population, please let me know.
Does it even matter what causes obesity? I just want to lose weight!
Some might argue that this discussion is irrelevant, since once someone become obese it’s clear their metabolism is damaged. There are two main problems with that argument.
First, not all obese people have deranged metabolisms. Research over the past several years has defined a subset of “metabolically healthy obese” (MHO) people with normal fasting glucose, triglycerides, insulin sensitivity and other markers. I wrote about this in my article Not All Fat People Get Diabetes, and Not All Diabetics Are Fat.
Second, separating the cause and treatment of obesity is necessary to prevent confusion. Something I see all the time in my practice and in the blogosphere is normal or even underweight people following zero- or very-low-carb diets. Why? Because they’ve absorbed the notion that “carbs are bad” from the “carbs-insulin-fat gain” theory, and they avoid them in a misguided attempt to promote health. While this may work for some people, it doesn’t for many others. I know because they end up coming to me with complaints like low energy, hair loss, bad breath, constipation and more.
Food reward vs. the carbohydrate hypothesis: setting the ground rules
I’d like to see a discussion of obesity that acknowledges the difference between cause and effect, considers the varying impact of food on the metabolically healthy and unhealthy, and recognizes the role of genetics in weight regulation.
Unfortunately, these important distinctions seem to be missing from the current debate – which, in my mind, makes it far less compelling.
- Cochran, G. Harpending, H. The 10,000 year explosion – how civilization accelerated human evolution. Basic Books. 2009. pp. 77 ↩
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