The Obesity Epidemic (part 4): Effects of Sugar

In the last three blogs on obesity, I have made the following points:

1.    The entire world is becoming more obese, and the United States is leading the pack.

2.    The most common measure of obesity is “body mass index” (BMI).

3.    There are many negative health outcomes associated with obesity.

4.    Some studies report that obesity can confer health benefits (the “obesity paradox”), but these results don’t hold up when measures of fatness other than BMI are used.

6.    Recent data indicates that about 40% of obese people are actually “fit” and metabolically normal, and do not have increased morbidity, cancer, or cardiovascular disease.

7.    The primary cause of obesity is probably the consumption of excess calories and/or carbohydrates, most likely sugar.

8.    The research concerning the relationship between energy expenditure and obesity is not conclusive—although there is a correlation in the United States between decreased activity and increased obesity, studies indicate that there is no difference in energy expenditure between developed and developing countries.   

9.    The consumption of excess calories during the last three decades of the 20^th century can fully account for the obesity epidemic.

10.    Sugar, specifically sugar in soft drinks, is probably the single greatest source of excess calories.

In the last blog we ended with a discussion about fructose (fruit sugar), so let’s pick up there. 

Fructose has been much maligned in recent years, with researchers (and pretty much everybody else) finding correlations between fructose consumption and obesity (!), cardiovascular disease, hypertension, diabetes, and nonalcoholic fatty liver disease.  In 2010, this natural sugar was even hailed by some people as an “environmental toxin.”

One of the topics discussed at the 2012 meeting of American Society for Nutrition was “Fructose, Sucrose, HFCS oh my,” proving that scientists do have a sense of humor.  You can tell from the tongue-in-cheek title of this presentation that the discussion was expected to be controversial and heated.  And by all accounts, it was. 

But unfortunately, after all that intense debate, their conclusions concerning the impact of fructose consumption on health can be summarized in less than ten words:  there is not enough good data to say.  The problem is that fructose studies have many of the same problems as other nutritional studies—in order to clearly see the effects of fructose in the diet, the amount consumed must be unrealistically high, and even then, it is difficult to separate the effects of fructose from the confounding effects of other nutrients such as fats, proteins, complex carbohydrates, and other sugars.  For example, sucrose is about half glucose and half fructose, so if you reduce the amount of sucrose in the diet, you are actually decreasing both glucose and fructose, and thus you can’t blame, or credit, either one of them for any observed effects.  As an added complication, fructose is metabolized in the liver—where half of it is converted into glucose.  So are you seeing the effects of fructose or glucose?  And as I mentioned in the previous blog post (The Obesity Epidemic, part 3), U.S. consumption of fructose has declined in the last decade, but the rate of obesity has not.

Since ingesting sugar increases available energy, it is possible that at least some of the results of the various obesity studies are in fact due to excess energy rather than sugar consumption.  The potential causes and effects are such a tangled mess that the best that science can do in terms of identifying the villain is that it is either the sugar itself or the excess energy that results from the sugar.  And of course, it may be both.

Even so, the culprit identified in the last blog—sugar sweetened beverages (SSBs)— seems to be emerging as a principal bad actor in a number of studies that examined the relationship of SSBs with obesity, diabetes, and cardiovascular disease. 

First, obesity.  The following graph is based an 8-year study involving 50,000 nurses, with the data having been adjusted for age, alcohol intake, physical activity, smoking, postmenopausal hormone use, oral contraceptive use, cereal fiber intake, and total fat intake. 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862465/

This graph plots the weight of the test subjects at three different times:  in 1991, 1995, and 1999.  At the start of the study in 1991, the nurses were divided into two categories,  either “low” consumers (those who drank less than one SSB a week) or “high” consumers (those who drank more than one SSB a day).  First off, you will notice that there is a glaring anomaly—in 1991 the low consumers weighed more than the high consumers! (Seems to be counter to the point I’m making, doesn’t it?)  Be that as it may, everyone gained weight over the next eight years, and the “high” consumers gained the most.  Even more telling, when some of the “high” consumers switched in mid-stream to became “low” consumers, they lost weight.   And although this particular graph only reflects the correlation between SSB consumption and weight, the researchers also found that higher consumption of SSBs was also correlated with higher rates of diabetes.

A 6-year study of 40,000 black women (1995-2001) had similar results:  the test subjects who drank more SSBs (and fruit juices) also gained more weight and were more prone to diabetes than those who drank fewer sugary beverages.  And just to show how unpredictable these things can be, a similar German study in 2002 found that consumption of SSBs was correlated with weight gain in men, but not in women.   But all in all, the data seems to slant pretty significantly towards a strong correlation between heavy SSB consumption and obesity, as well as diabetes.

Well, so much for the weight-gain literature.  Let’s discuss SSB consumption and diabetes in more detail, which will lead us to cardiovascular disease and the “metabolic syndrome.”

First let’s talk about diabetes.  There are two types—diabetes type 1 (DT1), and diabetes type 2 (DT2).  We are interested in DT2, as it is the one that’s associated with obesity.  DT2 occurs when the body’s cells become “resistant” to insulin or when the body’s insulin production either increases or decreases.

Insulin “instructs” liver cells, for example, to take up glucose and store it as glycogen (a storage form of glucose in animals, as opposed to starch, which is a storage form of glucose in plants).  Alternatively, the liver may take up the glucose and make fatty acids, which then become “fat.”  In this way, insulin regulates blood glucose and is one of the “controllers” of fat accumulation.

So when insulin resistance results in DT2, we get elevated glucose in the blood, as well as elevated insulin—since the insulin is not being taken up by cells.  What seems to be happening is that elevated glucose in the blood over a period of time causes muscle and liver cells to stop taking up glucose, which means there are even higher levels of glucose in the blood.   The body produces more insulin in an effort to bring those levels down, and if muscle and liver cells develop resistance to this increased insulin, uptake is lowered and insulin levels in the blood rise even higher.  Fat cells, particularly those making up the roll around your waist, respond to the elevated insulin by doing what they are supposed to do—store fat.  So you get fatter because there is more insulin circulating around in your body. 

Confusing?  Yes it is.  It can even be hard to tell what is a cause and what is an effect.  And that puts us right about where the science is at this point in time.  It does seem to be clear is that obesity and DT2 are correlated, but the exact connection between them has yet to be determined.   Some believe that fructose consumption is the main culprit in the development of insulin resistance, but as I mentioned in part 3 of this series, this view is by no means universal. 

That brings us to a phenomenon known as the “metabolic syndrome” (MSYN).  There are several different definitions of MSYN, but according to the International Diabetes Federation, a diagnosis of MSYN requires obesity along with two of the following: raised triglycerides, reduced HDL cholesterol, raised blood pressure, or DT2.  The World Health Organization’s definition for MSYN requires DT2 and two of the following:  elevated blood pressure, elevated triglycerides and cholesterol, or a BMI (body mass index) greater than 30.  And finally, the US National Cholesterol Education Program requires at least three of the following:  “central obesity” (waist circumference greater than 40 inches in men and greater than 35 inches in women), elevated triglycerides, elevated blood pressure, or elevated glucose (probably DT2).

So MSYN is really a constellation of characteristics that may or may not have an underlying common cause, but certainly together increase the risk of DT2 and cardiovascular disease.  And obesity shows up in all of the definitions of MSYN, though most of them allow for a diagnosis of MSYN in patients who are not obese.

And get this:  44% of the US population over the age of 50 has MSYN.  75% of British patients with DT2 or pre-DT2 have MSYN.   50% of patients with coronary heart disease have MSYN. 

YIKES!

So, given what we have learned so far, it seems reasonable to suppose that if you reduced obesity, you might also reduce DT2 and cardiovascular disease.  Scientists love these kinds of experiments.  You see what’s going on here—if we say that obesity increases the likelihood of DT2 and coronary heart disease, then reducing obesity should have the opposite effect, right?  That is a good check of the theory and a classic “if then” experiment. 

An 11-year project called Look AHEAD (Action for Health in Diabetes) was begun in 2001.  This is/was an “intervention” clinical trial involving approximately 5,000 people aged 45-74 with DT2 and a BMI greater than 25.   Therefore, the test subjects were required to be at least minimally classified as “overweight”; they were also required to be cancer-free and not suffering from  cardiovascular disease.  They were divided into two groups:  one group was placed on an aggressive weight-loss program  involving exercise and a diet restricted to 1,200-1,800 calories per day depending on starting weight, and the other group received normal counseling and treatment for DT2 (called the “diabetes support and intervention” group—or DSE).  The goal for each person in the diet/exercise group was to lose at least 7% of body weight within the first year (e.g., 17.5 pounds for a person weighing 250 pounds).  Those who failed to meet this goal received extra counseling. 

To date, at least two publications have come out of this study.  The first one (2012) looked at the effects of weight loss on DT2, and the other (2013) looked at weight loss and cardiovascular disease. 

The 2012 paper showed that, yup, weight loss was correlated with remission of DT2.  Hooray!  But did the reduction in DT2 result from, say, changes in the diet or changes in the fat cells themselves?  Still unknown.

The 2013 paper is rather more interesting because it showed that weight reduction did NOT result in decreased cardiovascular disease.  There was also no effect on death from any cause.  This disappointing result may be due to the relatively small amount of weight actually lost by the test subjects—only 3.5% after 9 years, down from a high of 8.6% after one year.  Or, it may be because folks in the non-diet/exercise group took statins.  But it is encouraging to note that even though the weight-loss group did not experience lower rates of cardiovascular disease, they experienced a number of other benefits, including reduced urinary incontinence, sleep apnea, and depression, and higher levels of physical fitness.

So there you have it.  Increased sugar consumption in general, and sugar-sweetened sodas in particular, seem to account for the majority of our obesity.  And obesity is correlated with a suite (no pun intended) of conditions known as “metabolic syndrome,” which may, in come cases, be reversible with weight loss.  Unfortunately the same can’t be said for cardiovascular disease.

And of the seemingly endless number of issues involved in a discussion of the obesity epidemic, what is left to cover?  Next up are what I think of as the “minor” explanations for obesity (gut flora and genes, for example), and then finally the dreaded topic I was hoping to avoid—dieting.

Useful References:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862465/

http://www.sciencedirect.com/science/article/pii/S0197245603000643

http://jama.jamanetwork.com/article.aspx?articleid=199317

http://www.nejm.org/doi/pdf/10.1056/NEJMoa1212914

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THE OBESITY EPIDEMIC (part 3): Sugar

In the last two blogs on obesity, I made the following points:

1.      The entire world is becoming more obese, and the United States is leading the pack.

2.      The most common measure of obesity is “body mass index” (BMI).

3.      There are many negative health outcomes associated with obesity.

4.      Some studies report that obesity can confer health benefits (the “obesity paradox”), but these results don’t hold up when measures of fatness other than BMI are used.

6.      Recent data indicates that about 40% of obese people are actually “fit” and metabolically normal, and do not have increased morbidity, cancer, or cardiovascular disease.

7.      The primary cause of obesity is probably the consumption of excess calories and/or carbohydrates, most likely sugar.

8.      The research concerning the relationship between energy expenditure and obesity is not conclusive—although there is a correlation in the United States between decreased activity and increased obesity, studies indicate that there is no difference in energy expenditure between developed and developing countries.     

This last point, which is pretty counterintuitive, supports the view that increased obesity is mainly due to the consumption of excess calories.  In fact, a 2009 study found that excess calories ALONE can account for the U.S. obesity epidemic.  When researchers looked at dietary changes since the 1970’s, they found that children are consuming an extra 350 calories per day and adults are consuming an extra 500—equivalent to one can of soda for a child and one hamburger for an adult.

So if we assume that obesity in the United States (if not the world) is generally due to over-eating and/or -drinking, the logical question is whether there is one particular food or drink that is the culprit. 

Since sugar is found large quantities in both food and drink, that seems to be a good place to start.  It turns out that the U.S. has had a long-standing love affair with sugar, and our attachment to it has only grown stronger over time.  As you can see from the following graph, in the early 1800’s the average person consumed 4 pounds of sugar per year; by 1850 it was 50 pounds, and by 2000 it was almost 120 pounds.

http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html

[The data in the graph above is drawn from U.S. Dept. of Commerce and USDA reports concerning sugar production because data concerning consumption wasn’t available.  In order to account for waste, the author of the graph (a researcher at the University of Washington) reduced all the production data by approximately 30% to arrive at estimated sugar consumption.]

This striking graph shows that in the United States, we consume something in the neighborhood of 100 pounds of sugar per person per year.  In this case, the word “sugar” means sweeteners such as high-fructose corn syrup, sugar, and maple syrup, but not naturally-occurring sugars in fruit and vegetables (and probably not lactose, the sugar in milk, but that is just a guess on my part). 

And what do these levels of sugar consumption mean in terms of calories?  It appears from the graph that in the early 1970’s, we were consuming about 80 pounds of “sugar” (sweetener) per year, which is .22 pounds/day or 330 calories/day (assuming that one pound of an “average” sweetener has about 1500 calories).   Today we consume about 100 pounds of sugar/year or 0.27 pounds/day, which is 405 calories.  That’s an increase of 75 calories per day from 1970 to 2010, which doesn’t sound like much, but when you do the math, it turns out to be a whopping 27,375 calories per year.

By using the old rule of thumb commonly found in diet books that says “3,500 calories equals a pound of fat,” you would conclude that if you consume 75 extra calories every day, you will gain 7.8 pounds of fat in a single year—and if you maintain this practice for 20 years, you will be carrying around an extra 156 pounds of fat! 

(Okay, I don’t believe that and neither do you—and indeed, recent research results are rejecting this old “rule.”  But rather than getting into those studies, suffice it to say that an increase of a mere 75 calories per day would probably NOT result in an obesity epidemic.  Yes, those extra calories could result in a weight gain of 6 or 7 pounds over the course of ONE year, but according to more recent models, it would level off after that because extra fat requires additional energy to maintain itself.)

So far we have only accounted for an additional 75 calories/day.  If we assume that the “average” American (both adults and children) consumes about 425 excess calories each day, we still need to find another 350 calories.  Let’s look at soft drinks and fruit drinks, which constitute a prime source of sugar in this country.  In fact, the National Health and Nutrition Examination Survey by the Centers for Disease Control and Prevention estimates that more than 40% of our sugar intake is in the form of this “liquid candy.”

http://advances.nutrition.org/content/4/2/220.full.pdf+html

According to the above graph, it is estimated that in 2005, each person in the United States drank about 50 gallons of soft drinks (sodas):  about half a liter a day.  At about 1,520 calories per gallon, that is 76,000 calories/year or 208 calories/day.  (I can’t explain the discrepancy between the result that we get from the sugar-consumption graph (75 calories/day) and the result from this soda-consumption graph (208 calories/day), unless the sugar estimates in the first graph are way off.   But either way it is clear that the sugar in sodas is probably a major contributor to our excess calorie intake.)

At this point in the story, let’s look more closely at the different KINDS of sugar in the American diet and how that has changed over time.

Sugar, as you may know, is not just one kind of molecule.  There are many, many different types of sugars, but for the purposes of this discussion, I want to focus on just three of them:  sucrose, glucose, and fructose. 

Everyone has heard of sucrose, I’m sure.   Composed of two simpler sugars (glucose and fructose), sucrose is the white granulated stuff you put in your coffee, also called “table sugar.”   It’s dang tasty and it’s everywhere, in spite of being reviled as nothing but empty calories.  And contrary to what a lot of people think, sucrose is completely “natural, “ since it is the sugar found in sugar cane and sugar beets.  It also constitutes 90% of maple sugar and makes up a large portion of floral nectar, which is ingested by bees and then vomited up (along with an enzyme called invertase that breaks the sucrose down into its simpler sugars) to make honey, which itself is about 50% glucose and 50% fructose.

Glucose, also known as “blood sugar,” is the kind of sugar that is first produced by plants from sunlight, and thus can be thought of as the “foundational” energy source upon which all life depends.  Since starches are just chains of glucose molecules linked together, what you get when they are broken down by digestion is glucose, which is readily absorbed by the blood stream and provides fuel for brain and body. 

And finally there is fructose, which is also known as “fruit sugar” because it is found in high concentrations in figs, grapes, pears, and many other fruits.  The majority of people, however, probably know it as “high fructose corn syrup” (HFCS), which has become the primary sweetener in soft drinks during the last 40 years,. 

This next graph tracks sweetener consumption over time just like the first graph did, but this time fructose and obesity are plotted as well.  As you can see, there is a correlation between obesity and the consumption of fructose, as both of them began to rise at about the same time.  But even though consumption of fructose, and all sweeteners, began to decline about 15 years ago, the incidence of obesity did not.

http://advances.nutrition.org/content/4/2/246.full.pdf+html

The last graph (below) tells an interesting story about the consumption of high-fructose corn syrup during the 40-year period from 1970 to 2010.  The process for making HFCS was developed in the 1950’s and fine-tuned during the next couple of decades, but for all intents and purposes, it was largely absent from the American diet until the 1970’s.  Consumption grew rapidly thereafter, particularly in the mid-1980’s when falling corn prices made it the sweetener of choice for soft drinks, and its use continued to increase until the late 1990’s.  But amid concerns about HFCS’s role in the obesity epidemic and its other potential negative effects on human health, consumption has been declining since the turn of the century—even though recent studies indicate that the fault may lie with excess sugar consumption in general rather than HFCS in particular.

. 

When I started searching for those 425 extra calories that appear to be causing the obesity epidemic, I fully expected to find them in a soft drink bottle.  But while soda  is clearly one of the culprits, at this point it doesn’t seem to be the only one.  I’m beginning to think that the answer may be more straightforward:  we are simply consuming too much.  Of everything.

We could stop with our “sugar” story right there, but I can’t help thinking that there is more to be said about fructose and health, as well as carbohydrates in general. 

Also, I can’t get rid of the niggling thoughts in the back of my mind about those studies that found no association between energy expenditure and obesity. 

And with that, I think I’m going to go have a Mountain Dew . . . .

References

http://wholehealthsource.blogspot.com/2012/02/by-2606-us-diet-will-be-100-percent.html

http://ajcn.nutrition.org/content/90/6/1453.long

http://advances.nutrition.org/content/4/2/220.full.pdf+html

http://advances.nutrition.org/content/4/2/246.full.pdf+html

http://ajcn.nutrition.org/content/93/2/427.full.pdf+html

THE OBESITY EPIDEMIC (part 2): Causes

In last blog I made the following observations:

1.            The world’s population is becoming more obese, and the United States is leading the pack.

2.            The most common measure of obesity is “body mass index” or BMI.

3.            Obesity has many negative health implications.

4.            But there have been reports that obesity confers a health advantage (the “obesity paradox”).

5.            The most recent thinking is that the obesity paradox is an artifact of the BMI classification; when measures other than BMI have been used to calculate fatness, the obesity paradox did not hold up.

6.            Recent data indicates that about 40% of obese people are actually “fit” and metabolically normal; they do not have increased cancer, cardiovascular disease, or morbidity.

7.            As of 2008, obesity cost the US $147 billion/year, or $1,429/year for each obese person.

In this blog I want to focus on the two primary explanations for obesity.  But first, there is a “law of nature” and a definition to cover.

The Law of Conservation of Energy (also known as the First Law of Thermodynamics) is usually forgotten when it comes to discussion of diets and dieting.  It tells us that  energy can not be created or destroyed.  This natural law was popularized by Einstein’s famous equation E=mc², which states that mass and energy are interchangeable. 

That means you can’t gain weight (increase your mass) unless you get energy from somewhere.  E=mc² tells us that food, having mass, also has energy.  And since you, as a human, can’t get energy directly from the sun through photosynthesis the way plants do, you get it from food instead.  By eating.  

You can conclude both from everyday experience and the First Law that as long as you are alive, you are expending energy, and if you don’t eat, you will get the energy you need to continue living from energy reserves within your own body.  Energy is stored in your body in several different forms (fat, protein, creatine, etc.), but for purposes of an obesity discussion, the only one that is important is fat. 

If you don’t eat, you will burn fat (and then muscle).  WWII supplied ample evidence of the effects of not eating—through photographs of starving prisoners in concentration camps.  There were no fat people there.  And if you’ve ever read about the exploits of adventurers who ran out of food in such hostile places as Antarctica or the Sahara, you know that the descriptions of their gradual emaciation are quite memorable.  Anyone who stumbles 5-10 miles a day at -20F or +120F on limited or no rations will end up losing weight (fat).  The Law of Conservation of Energy, being a law, applies wherever you are.

It even holds up at your kitchen table.  If you don’t eat, i.e., replace the energy your body expends, you will consume your body fat until there is no more fat to consume.  Your body has to get energy from somewhere.

At this point we should define how energy is measured relative to food.  As I’m sure everyone knows, the unit of measurement is a “calorie,”  defined as the amount of energy it takes to raise one gram of water one degree Celsius.  (Okay, this is actually the definition of a “small calorie.”  The calorie we hear about relative to food and nutrition is a “large calorie,” equal to 1,000 small calories.  I don’t have a clue why there are two different definitions, except that using large calories keeps us from having to deal with a bunch of zeroes when we’re counting them.) 

In any event, the energy in food is measured in calories per unit of weight.  If you read the nutrition information on a candy bar wrapper, for example, you will see that the candy inside has a certain number of calories per gram.  Or per ounce.  Sometimes this is referred to as a food’s “energy density.”

In the course of the next three or four (!) blogs, I want to look at several diet-related explanations for obesity.  There are two “main” theories:  too many calories or not enough exercise.   Then there are what I think of as the “minor” explanations, all of which can be lumped together as the “depends on WHAT you eat, not just calories” theories.

Too many calories.  We take in more energy (consume more calories) than we expend through exercise.  We are simply the victims of our own success in being able to feed ourselves, and the reason for the obesity epidemic is because we’re taking in more calories than we used to.

It is no coincidence that those countries with the highest rates of obesity also consume the most calories.  In fact, the average person in the 10 countries with the highest caloric intake (United States, Austria, Greece, Belgium, Luxemburg, Italy, Malta, Portugal, France, Israel) consumes 3,653 calories each day and has a BMI of 25.1.  On the other hand, the average person in the 10 countries with the lowest caloric intake (Eritrea, Democratic Republic of the Congo, Burundi, Haiti, Comoros, Zambia, Ethiopia, Angola, Central African Republic, Republic of Tanzania) consumes only 1,830 calories each day and has a BMI of 21.36. 

Here is a chart about world energy consumption that pretty much says it all:  we just keep eating more and more.

http://en.wikipedia.org/wiki/File:World_Per_Person_Energy_Consumption.png

The worldwide consumption of calories has been steadily increasing since 1960, and obesity has been increasing at the same time.  Here in the United States, caloric consumption started increasing about 1980, as shown in the graph below.  Interestingly, that is the same time that obesity in the United States started increasing too (see graph in previous blog).

http://www.usda.gov/factbook/chapter2.pdf

So, we have a worldwide correlation between increasing caloric intake and obesity, as well as a similar correlation in the United States. 

Kind of makes you think that obesity has increased as a result of overeating, no?

Not enough exercise.  As you will recall, the other primary explanation for the obesity epidemic is that we’re not getting as much exercise as we used to.  But has energy expenditure really decreased?  That is, have we become more sedentary?  This is important because what makes us gain weight is NET calories, i.e., those that are consumed but not used up by activity.

After all, in order for weight to remain stable, we must adhere to the following equation:  calories in = calories out.

1988–2008 No Leisure-Time Physical Activity Trend Chart

http://www.cdc.gov/nccdphp/dnpa/physical/stats/leisure_time.htm

This graph reflects the percentage of U.S. citizens who engage in no physical activity during their leisure time.  Note that during the 20-year period from 1988 to 2008, the percentage of people who do engage in leisure-time physical activity actually went UP (the sedentary percentage dropped from 30% to 25%). 

Additionally, the Centers for Disease Control has developed a map of the U.S. that correlates particular counties with three related factors:  obesity, no leisure time physical activity, and diabetes. 

                          

Again, the data seem to make a pretty convincing argument that obesity is caused by too many calories—those parts of the U.S. that are the most obese are also the least active, and by inference have the least calorie expenditure.  And conversely, the places with the least obesity expend the most calories.

However, a recent (2011) study reported counterintuitive results when the energy expenditure of developed countries was compared with that of developing countries.  This was a meta-analysis of 98 studies in which the energy expenditure of 4,972 subjects (both male and female) was measured using the “doubly labeled water” technique, considered the gold standard.  In this procedure, the test subject drinks water tagged with heavy isotopes of hydrogen and oxygen, and then several days or even weeks later, the CO₂ in the subject’s respiration is analyzed to determine how much heavy oxygen it contains.  Since CO₂ leaves the body only as a result of metabolism, the heavy oxygen that remains in subject’s CO₂ at the end of the study provides a direct measure of total energy expenditure during the study.  One of the beauties of this technique is that it integrates energy expended in all of a person’s activities, from sleeping to working.  (Interestingly, this same procedure has been used to measure the activity levels of more than 200 wild animals.) 

So, what were the results?  Essentially, they found no difference in energy expenditure between developing and developed countries.  Individuals from developed countries were fatter (as measured by BMI and weight), but their energy expenditure was the same.

The authors conclude that increased obesity is primarily the result of eating too much rather than not exercising enough, and they cite many other studies that have reached the same conclusion.

In the same vein, a widely-cited 2012 study compared the energy expenditure of Tanzanian hunter-gatherers belonging to the Hadza “tribe” with the energy expenditure of U.S. and European males and females (“Westerners”).  Here too, the researchers found no difference between the two populations—their levels of activity were essentially the same even though at the time of the study, the Hadza were actively engaged in both hunting and foraging.  But the Westerners were fatter (more body fat as well as higher BMI’s). 

These two studies strongly suggest that there is no relationship between increased “fatness” and decreased energy expenditure.  And in fact, the study authors state this pretty unequivocally.

Is it what we eat?  When looking at changes in obesity over time, it is important to note that the TYPE of foods we consume has also changed.  Thus our attempts to identify the causes of the obesity epidemic are confounded by the fact that increased caloric intake has been accompanied by a change in diet.

And that brings us to another explanation for our obesity:  it’s related to WHAT we eat rather than just calories in and calories out.  Consider a chunk of firewood, for example.  It has lots of calories—but good luck deriving any energy from it.  Unless you are a termite.

So let’s look at our diet here in the United States.   You can see from the following chart that it changed quite a bit from 1909 to 2000.  In particular, consumption of sugars and sweeteners increased 7%, and fats and oils increased 10%.  But grains actually decreased.  

http://www.cnpp.usda.gov/publications/foodsupply/FoodSupply1909-2000.pdf

Now take a look at the following graph.  Note that consumption of carbohydrates, as a class, remained fairly stable—if anything, our carb consumption in 2005 was a little lower than it was in 1909.  

http://www.ers.usda.gov/data-products/food-availability-(per capita)-

data-system/summary-findings.aspx#.Uknv3WTXhUh

However, carbohydrates are a very big class that includes grains, bread, potatoes, and other starches, as well as sugar.  In fact, what’s happened is that although carbohydrates from grains have decreased, carbohydrates from sugars have increased.  More about sugar later.

It is also interesting to look at the KINDS of fats that we are consuming—and to wonder whether some types of fats might also be correlated with obesity.

Saturated, monounsaturated, and polyunsaturated fat in the U.S. food supply, per capita per day, 1909-20000

http://www.cnpp.usda.gov/publications/foodsupply/FoodSupply1909-2000.pdf

This  graph shows that there was no increase in consumption of saturated fats in the United States from 1909 to 2000, so we can’t blame the obesity epidemic on that.  What HAS increased, however, is the consumption of both monounsaturated and polyunsaturated fats.  I’ve already discussed fats in an earlier blog and I don’t want to bore you by repeating myself, but let me say it again anyway: saturated fats have been unfairly maligned over the years.  Go ahead and enjoy that juicy steak.

So, the conclusions reached here are as follows:

Obesity is correlated with increased caloric intake but probably NOT with decreased activity.  There has also been a substantial increase in consumption of sugars as well as monounsaturated and polyunsaturated fats.

We’ll try to sort out these correlated factors next time.  But, it seems to me that anyone who is interested in losing weight need only read the previous paragraph—and behave accordingly. 

References

http://ajcn.nutrition.org/content/93/2/427.full.pdf+html

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0040503