Fat and Carbohydrate: Clarifications and Details

The last two posts on fat and carbohydrate were written to answer a few important, but relatively narrow, questions that I feel are particularly pertinent at the moment:

• Was the US obesity epidemic caused by an increase in calorie intake?
• Could it have been caused by an increase in carbohydrate intake, independent of the increase in calorie intake?
• Does an unrestricted high-carbohydrate diet lead to a higher calorie intake and body fatness than an unrestricted high-fat diet, or vice versa?
• Could the US government's advice to eat a low-fat diet have caused the obesity epidemic by causing a dietary shift toward carbohydrate?

However, those posts left a few loose ends that I'd like to tie up in this post.  Here, I'll lay out my opinions on the relationship between macronutrient intake and obesity in more detail.  I'll give my opinions on the following questions:

• What dietary macronutrient composition is the least likely to cause obesity over a lifetime?
• What dietary macronutrient composition is best for a person who is already overweight or obese?
• Is fat inherently fattening and/or unhealthy?

From the beginning

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Has Obesity Research Failed?

I frequently encounter the argument that obesity research has failed because it hasn't stopped the global increase in obesity rates.  According to this argument, we need to re-think our approach to obesity research because the current approach just isn't working.

Grant funding for obesity research keeps increasing in the US, and the prevalence of obesity also keeps increasing*.  What gives?  Maybe if we just scrapped the whole endeavor we'd be better off.

Let's take a closer look at this argument and see how it holds up.

Why Do Research?

There are two fundamental reasons why we do research:

1. To gather accurate information about the natural world.  This information is intrinsically valuable because we like knowing how the world works, and it may eventually have practical value that's not immediately obvious.
2. Practical applications.  We want to solve problems and improve our lives.

If we want to determine whether or not obesity research has failed, we should evaluate it using those two metrics.

Has Obesity Research Gathered Accurate Information?

Calorie Intake and Body Fatness on Unrestricted High-fat vs. High-carbohydrate Diets

In recent posts, we've explored the association between calorie intake and the US obesity epidemic, and the reasons why this association almost certainly represents a cause-and-effect relationship.  I also reviewed the evidence suggesting that carbohydrate and fat are equally fattening in humans, calorie for calorie.

One valid objection that came up in the comments is that calorie-controlled diets in a research setting may not reflect what happens in real life.  For example, in a context where calorie intake isn't tightly controlled, diet composition can impact calorie intake, in turn affecting body fatness.  This, of course, is true, and it forms one of the central pillars of our fat loss program the Ideal Weight Program.

Some low-carbohydrate diet advocates argue that the obesity epidemic was caused by US dietary guidelines that emphasize a carbohydrate-rich diet*.  The idea here is that the increase in calorie intake was due to the diet shifting in a more carbohydrate-heavy direction.  In other words, they're hypothesizing that a carbohydrate-rich eating style increases food intake, which increases body fatness**.  According to this hypothesis, if we had received advice to eat a fat-rich diet instead, we wouldn't be in the midst of an obesity epidemic.

Fortunately for us, this hypothesis has been tested-- many times!  Which eating style leads to higher calorie intake and body fatness when calories aren't controlled: a carbohydrate-rich diet, or a fat-rich diet?

Short-term Studies

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A New Understanding of an Old "Obesity Gene"

As you know if you've been following this blog for a while, obesity risk has a strong genetic component.  Genome-wide association studies (GWAS) attempt to identify the specific locations of genetic differences (single-nucleotide polymorphisms or SNPs) that are associated with a particular trait.  In the case of obesity, GWAS studies have had limited success in identifying obesity-associated genes.  However, one cluster of SNPs consistently show up at the top of the list in these studies: those that are near the gene FTO.

As with many of the genes in our genome, different people carry different versions of FTO.  People with two copies of the "fat" version of the FTO SNPs average about 7 pounds (3 kg) heavier than people with two copies of the "thin" version, and they also tend to eat more calories (1, 2).  

Despite being the most consistent hit in these genetic studies, FTO has remained a mystery.  As with most obesity-associated genes, it's expressed in the brain and it seems to respond somewhat to nutritional status.  Yet its function is difficult to reconcile with a role in weight regulation: 

• It's an enzyme that removes methyl groups from RNA, which doesn't immediately suggest a weight-specific function.
• It's not primarily expressed in the brain or in body fat, but in all tissues.
• Most importantly, as far as we know, the different versions of the gene do not result in different tissue levels of FTO, or different activity of the FTO enzyme, so it's hard to understand how they would impact anything at all.  

An important thing to keep in mind is that GWAS studies don't usually pinpoint specific genes.  Typically, they tell us that obesity risk is associated with variability in a particular region of the genome.  If the region corresponds to the location of a single gene, it's a pretty good guess that the gene is the culprit.  However, that's not always the case...

Fat vs. Carbohydrate Overeating: Which Causes More Fat Gain?

Two human studies, published in 1995 and 2000, tested the effect of carbohydrate vs. fat overfeeding on body fat gain in humans.  What did they find, and why is it important?

We know that daily calorie intake has increased the US, in parallel with the dramatic increase in body fatness.  These excess calories appear to have come from fat, carbohydrate, and protein all at the same time (although carbohydrate increased the most).  Since the increase in calories, carbohydrate, fat, and protein all happened at the same time, how do we know that the obesity epidemic was due to increased calorie intake and not just increased carbohydrate or fat intake?  If our calorie intake had increased solely by the addition of carbohydrate or fat, would we be in the midst of an obesity epidemic?

The best way to answer this question is to examine the controlled studies that have compared carbohydrate and fat overfeeding in humans.

Horton et al.