Food Reward Friday

This week's lucky "winner"... Lay's milk chocolate-dipped potato chips!!

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.

Garden Update: A Banner Year

Things are warming up here in Seattle and the flowers are blooming.  I just planted my first crops of the year-- potatoes and strawberries.

2013 was a banner year for my 500-square-foot urban vegetable garden, including my first experience growing and processing a grain.  I never got around to posting about it last year-- so here it is.

Interbay mulch technique

The bed on the right has been mulched with leaves, spent coffee
grounds, and burlap sacks ($1/sack at the local hardware store).
The beds on the left were planted with a rye-clover-vetch-pea
cover crop.  Paths are mulched with wood chips.

In the fall of 2012, I tried a new technique for improving the soil called "Interbay mulching".  This is a variation on sheet mulching, which involves placing uncomposted organic matter directly onto the garden soil in fall and letting it compost until the next growing season.  To Interbay mulch, you simply cover your sheet mulch with burlap.  This keeps everything moist, protects earthworms from bird predation so they can munch freely, and suppresses weeds.  I used leaves (carbon) and spent coffee grounds from a local coffee shop (nitrogen) for my organic matter.

When I pulled back the burlap last spring, I was initially disappointed.  The coffee grounds had disappeared completely, but there was still a lot of leaf matter left on the soil, indicating that it had only partially composted.  However, I later decided that it had worked well, because the soil structure underneath was improved and it seemed to be enriched with significant organic matter as well as a large population of fat earthworms.  The mulch suppressed weeds remarkably well, and the beds remained mostly clean for the rest of the season.

Those observations, combined with huge yields from the mulched beds, convinced me that it was worthwhile.

New tools

More Graphs of Calorie Intake vs. BMI

In the last post, a reader commented that the correlation would be more convincing if I graphed calories vs. average BMI rather than the prevalence of obesity.  It was a valid point, so I went searching for average BMI values from NHANES surveys.  I dug up a CDC document that contains data from surveys between 1960 and 2002 (1).  Because these data only cover five survey periods, we only get five data points to analyze, as opposed to the eight used in the last post.  The document contains BMI values for men and women separately, so I averaged the two to approximate average BMI in the general adult population.  It's also worth noting that I use the approximate midpoint of the survey period as the year.

First, a graph of average BMI over time.  It went up:

Now, let's see how well average BMI correlates with calorie intake:

The correlation between calorie intake and obesity prevalence was remarkable, but this correlation is simply incredible.  An R-squared value of 0.98 indicates that daily calorie intake and average BMI are almost perfectly correlated.

We can further deduce that each 100-calorie increase in daily food intake is associated with an 0.62-point increase in average BMI among US adults.  

Calorie Intake and the US Obesity Epidemic

Between 1960 and 2008, the prevalence of obesity in US adults increased from 13 to 34 percent, and the prevalence of extreme obesity increased from 0.9 to 6 percent (NHANES surveys).  This major shift in population fatness is called the "obesity epidemic".

What caused the obesity epidemic?  As I've noted in my writing and talks, the obesity epidemic was paralleled by an increase in daily calorie intake that was sufficiently large to fully account for it.  There are two main sources of data for US calorie intake.  The first is NHANES surveys conducted by the Centers for Disease Control.  They periodically collect data on food intake using questionnaires, and these surveys confirm that calorie intake has increased.  The problem with the NHANES food intake data is that they're self-reported and therefore subject to major reporting errors.  However, NHANES surveys provide the best quality (objectively measured) data on obesity prevalence since 1960, which we'll be using in this post.

Uncovering the True Health Costs of Excess Weight

Is excess weight hazardous to health, or can it actually be protective?  This question has provoked intense debate in the academic community, in some cases even leading researchers to angrily denounce the work of others (1).  There is good evidence to suggest that excess body fat increases the risk of specific diseases, including many of our major killers: diabetes, heart attack, stroke, heart failure, cancer, and kidney failure (2).  Yet strangely, the studies relating excess weight to the total risk of dying-- an overall measure of health that's hard to argue with-- are inconsistent.  Why?