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

---

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

THE OBESITY EPIDEMIC (part 1): What is obesity and what are its consequences?

Obesity.   It seems that nearly every month we hear of yet another potential cause.  It’s due to viruses.  Your gut flora is responsible.  It’s your mother’s fault.  It’s in your genes.  You have a bad thyroid.  Etc., etc., etc.

But in truth, the obesity epidemic that is underway all over the world is probably NOT due to thyroid problems or even a drift in our gene pool toward higher numbers of obesity genes.  It wasn’t a significant problem 100 years ago.  Or even 50 years ago.  And there simply hasn’t been enough time for all of us to develop bad thyroids. 

And to say that obesity is an epidemic is no exaggeration.  It’s not even controversial.  We may argue about whether global warming is caused by human activity, we may debate evolution, and we may disagree about the use of embryonic stem cells.  But I don’t think anyone could disagree that obesity has increased dramatically within the last generation or two.

The data is unequivocal—the world has gotten fatter.  And the United States, ever out in front, is a world leader, along with Samoa, the Solomon Islands, Kuwait, Barbados, the Bahamas, and Micronesia (the fattest of all).

Here in the U.S., the percentage of obese individuals has increased from about 15% in 1976 to 35% in 2004. 

http://en.wikipedia.org/wiki/File:USObesityRate1960-2004.svg

From this graph, you can see that about 70% of the adult population in the U.S. is either overweight or obese.  It is clear that obesity has been increasing for several decades, but surprisingly, the percentage of people who are overweight has not changed.  (I’d like to know more about this phenomenon, but I haven’t been able to find a discussion about it anywhere.  However, it seems to me that in order for people to be classified as obese, they must first have been overweight, so shouldn’t we see an increase in overweight along with—or prior to—the increase in obesity?  Maybe the answer is that large numbers of people who used to be merely overweight have now become obese, and by chance, just enough formerly normal-weight people have moved into the overweight category to keep the size of that group unchanged.)

And what has happened since 2004, the last year covered by the above graph?  According a 2012 report by the National Center for Health Statistics, there has been no significant change in the prevalence of overall obesity in the United States during recent years.  However, the incidence of obesity was previously higher in women than in men, and during the last decade, the men have caught up.

In order to be sure that we understand what we’re talking about, let’s define our terms.  What do “obese” and “overweight” really mean?

Human body fat percentage is commonly estimated by something called the “body mass index” (BMI), which is computed by dividing a person’s weight in kilograms by the square of their height in meters.  It is a far from perfect index—a body builder with lots of muscle may have a high BMI, for example—but it has the benefit of being very simple and straightforward.

Here are the definitions of “obese” and “overweight” as they relate to BMI:

In the United States a BMI of 18.5 to 25 represents “normal” body weight; a BMI between 25 and 29.9 is considered “overweight;” and a BMI above 30 is classified as “obese.”  Since the “above 30” category encompasses a large range of BMI values, it has been further divided into several rough sub-categories:  “severe obesity”  (a BMI of 35–40), “morbid obesity” (a BMI of 40-45 or 40-50), and “super obese” (a BMI greater than 45 or 50, depending on who you ask).  And since BMI is dependent on body type, these categories may change for different ethic groups.   In Asian populations, for example, a BMI of 18.5 to 22.9 is “normal,” and 23 to 27 is “overweight.”

Of course, the most accurate measure of “fatness” involves calculating the percentage of a person’s weight that is due to his or her fat cells.  This is a difficult calculation to make, but it can be done by weighing an individual both in and out of water to obtain a measure of that person’s “density.”  Density can then be related to body fat percentage by a formula first developed in 1953 and then refined in 1963.  

There are also other ways of estimating fatness, including X-ray absorptiometry, near-infrared interactance (using a beam of infrared light directed into the biceps), ultrasound, waist-to-hip ratio, and the “pinch test” (in which a fold of skin is measured by calipers).  But underwater weighing is thought to be the most accurate by far.

Since BMI is so widely used, it is logical to ask how well it is correlated with body fat percentage.  The answer is that it IS correlated—but the variation is substantial.  Here is a graph in which the BMI of 8,550 men is plotted on the horizontal axis and their actual body fat percentage is plotted on the vertical axis.

http://en.wikipedia.org/wiki/File:Correlation_between_BMI_and_Percent_Body_Fat_for_Men_in_NCHS%27_NHANES_1994_Data.PNG

If each person’s BMI were perfectly correlated with his body fat percentage, this graph would be a straight line because their BMI and their percent body fat would always be the same number.  You can see, however, that the graph is actually shaped more like a jellybean, which means that many of the men tested had an actual body fat percentage that that was higher or lower than suggested by their BMI.  For example, you would expect those in the lower right quadrant to be overweight since they all had a BMI above 25.  But when their body fat was actually measured, it was found to be below 25% (sometimes WAY below).  These men were not fat at all—indeed, they were probably quite muscular.

But the fact that BMI mis-identifies some people as overweight is not the real problem.  The primary purpose of BMI, after all, is to identify people whose body fat percentage is higher than it should be for optimum health.  And just as BMI OVER-estimates fatness in people who are lean and muscular (those in the lower right quadrant), it UNDER-estimates fatness in people who have relatively little lean muscle mass (those in the upper left quadrant).  Therefore, it often fails to sound the alarm for people who actually ARE overweight, which suggests in turn that BMI is underestimating obesity as well.

Obesity is correlated with many diseases, including diabetes type 2, high blood pressure, cardiovascular disease, osteoarthritis, various cancers, sleep apnea, systemic inflammation . . . . the list goes on and on.   At least 50, by my count.  But even though the obese as a class have more health problems than the non-obese, they are not a uniform group.  A very recent (2013) study has shown that approximately 46% of people classified as obese were “metabolically healthy” and otherwise “fit”—and showed no higher percentage of mortality or cardiovascular disease than normal-weight people who were also metabolically healthy. 

As a result, the authors of this study advocate the classification of obese people as either “fit” or “not fit.”  At this point, it is unknown what the differences between these two groups might be, but researchers speculate that that they may actually have different types of fat (more on that in another blog, perhaps). 

It should also be mentioned that obesity is correlated with the so-called “survival paradox.”  First described in 1999, this is a phenomenon in which people with heart failure and a BMI between 30 and 35 (obese) had greater chances of survival than those of a normal weight. 

And a 2006 paper that reviewed 40 studies involving 250,152 patients found that those with a BMI lower than 20 (underweight) had an increased risk for total mortality and cardiovascular mortality, while those with a BMI of 25-29.9 (overweight) had the lowest risk among all the groups for both total mortality and cardiovascular mortality.  Remarkably, the obese patients (BMI 30-35) had NO increased risk for either total mortality or cardiovascular mortality.  And the severely obese (BMI greater than 35) did not have increased total mortality, although they did have greater cardiovascular mortality.

In spite of the results outlined in this paper, it is pretty obvious that the authors did not really believe that obesity has no health consequence—they postulated, correctly it seems, that the results may have something to do with the inaccuracies of the BMI calculation. 

And, yes, according to a 2013 paper, almost ALL research studies reporting the “obesity paradox” used BMI as their measure of obesity.  The authors went on to say that more recent indices of obesity, such as large waist circumference and high waist-to-hip ratio, ARE positively correlated with cardiovascular events and mortality. 

Another aspect of obesity that is of great concern is the increasing financial burden that it places on society.  As reported in 2009, medical expenses for obese individuals in the United States average about $1,429 each year—42% higher than the expenses incurred by those of normal weight.   Further, this same report estimated that the medical costs of obesity, which totaled $78.5 billion in 1998, had risen to $147 billion by 2008, a figure that represents 9.1% of all medical expenses in the U.S.

And that was in 2008.  I wonder what it is today. 

Next time we will begin a discussion of the reasons for obesity.

Useful references

http://www.sciencedirect.com/science/article/pii/S0140673606692519

http://eurheartj.oxfordjournals.org/content/34/5/389.long

http://content.healthaffairs.org/content/28/5/w822.long

http://wood-ridge. schoolwires.net/cms/lib6/NJ01001835/Centricity/Domain/

175/Obesity%20Article.pdf

THE WONDERS OF CARBON—and the difficulties of making money on new technology

Now I’m not a chemist, and there may be other elements in the periodic table that are cooler than carbon, but I can’t think of one.  First off, it’s the 4^th most prevalent element in the universe, after hydrogen, helium, and oxygen, and the 15^th most abundant element in the earth’s crust.  It makes up all living things on earth, not to mention other important stuff like oil, natural gas, and carbon dioxide.  And most scientists believe that if life is found outside earth, it will be based on carbon.

Carbon is very interesting at the molecular level, that is, in the varied shapes that molecules made of pure carbon atoms can assume and the surprisingly different properties that a simple shape change can provide.  For example, a diamond and a lump of coal are identical at the atomic level—they are made solely of carbon atoms.  But they differ widely at the molecular level.  The carbon atoms in a diamond are arranged in a lattice design while those in a coal molecule have no structure—they are amorphous.  And of course, the lattice design of a diamond makes it transparent, while the amorphous structure of coal makes it just the opposite.

But coal and diamonds are not the forms of carbon I’m going to talk about today.  I’m more interested in the “chicken wire” forms. 

That’s right, chicken wire.  Think of all the different shapes  you can make with chicken wire—and carbon can probably manage every single one of them.

I’d really like to focus on just three shapes:  sheets of chicken wire, spheres of chicken wire, and tubes of chicken wire.  To see examples of these and other forms of carbon, take a look at the diagram below:   diamond (a), graphene (b), ionsdaleite (c), buckyballs (d, e, f), amorphous carbon (g), and a nanotube (h).

Let’s start with buckyballs.  Now stay with me here.  Buckyballs (as well as nanotubes) are classed as “fullerenes,” a word that comes from the last name of the very famous inventor and futurist Buckminster Fuller, whose first name also gave us the “bucky” in buckyballs.   Fuller popularized dome homes, which he patented as a “Geodesic Dome” as U.S. Patent No. 2,682,235 in 1954 (the first geodesic dome was actually developed and built in 1923 by Walther Bauersfeld, a German engineer, which makes me wonder if Fuller’s patent was valid).  Certainly the spheroid dome shape has in some ways come to symbolize science, technology, and the future.  Think of the dome at Epcot, for example.  And so in this way Buckminster Fuller has become associated with really cool space-age technology.

Now, spherical shapes can be constructed out of a number of geometric forms.  Fuller’s dome homes had triangular faces, but a soccer ball made by Adidas in 1970 was constructed of 12 black pentagons and 20 white hexagons; it was called the Telstar soccer ball.  (Does this give you a strong urge to run out and grab up a soccer ball to see if you have a Telstar or not?  I wish I had known this when my kids were younger—there was a teaching moment there!)

The word Telstar comes from the Telstar 1 and 2 satellites launched back in 1962 and 1963, and you’d like to think that as the progenitor of the soccer ball, they were also made of pentagons and hexagons—but no such luck.  The satellites were made up of rectangles and squares in a roughly spheroid shape.

Okay, back to buckyballs.  The theoretical existence of buckyballs was first discussed in the 1960’s and 1970’s, and in 1980 it was predicted that spherical particles of carbon could be created in the laboratory.  However, it was not until 1985 that researchers published a paper reporting that spherical molecules consisting of 60 carbon atoms, labeled C₆₀, had been produced at Rice University.  Although the scientists who conducted this experiment couldn’t actually “see” the structure formed by this carbon molecule, it was eventually found to be a sphere composed of 12 pentagons and 20 hexagons.  And their groundbreaking article actually included a photo of an Adidas soccer ball to illustrate the point!

The original paper was authored by five chemists (three of whom were awarded the Nobel Prize in 1996—R. Curl, H. Kroto, and R. Smalley), and they came up with the name “buckminsterfullerene” for the spherical carbon molecule they had created.  With a touch of humor seldom found in scientific journals, they also suggested that perhaps it should have been named “soccerene” or “carbosoccer.”  Personally I think these molecules should have been called “Telstar balls” or even “Adidas balls”, but I suspect that kind of industrial affiliation would have been anathema to these academic researchers.

Soon afterwards, thousands of papers were published examining buckyball chemistry and production.  Their spherical shape, plus the possibility of trapping metals and other elements inside, caused a veritable land rush of scientists who immediately embarked on new research programs to investigate potential ramifications and applications.  Many possible uses of buckyballs have been identified, including superconductors, lubricants, catalysts, drug delivery systems, hydrogen storage, optics, chemical sensors, and even cosmetics. 

So here we are, 28 years after this momentous discovery, and it is reasonable to ask whether the early commercial promise of buckyballs has been realized.  (I don’t consider buckyballs produced for research purposes to be commercial products.  You can, however, purchase them by the gram from SES Research in Houston, Texas, for $45.  At 454 grams per pound, that’s $20,430, so it will be a long time before you see buckyballs in your oil change. )

It seems that a medical buckyball product may be the one that is closest to market.  It is a C₈₀ spheroid that can be manufactured in such a way as to trap several different types of metals, including scandium, yttrium, erbium, lutetium, and gadolinium.  These strange-sounding metals (which are “related” to aluminum) have many very specialized uses.  For example, gadolinium is used as a contrast agent for magnetic resonance imaging (MRI) because it helps improve the visibility of internal organs and other structures.  Virginia Tech University discovered and patented the method of making these metal-trapping buckyballs and licensed its rights to a Virginia company called Luna Nanoworks.  The company has developed one C₈₀ spheroid called Trimetasphere that contains three metals, and they are investigating its use as a new MRI contrast agent.  Oh, and H. Kroto, one of the Nobel Prize winners, is an advisor to the company.  

So how well is Luna Nanoworks doing financially?  It is a publically-traded company with a market capitalization of $17 million.  Its stock has been selling at around $1.25 since 2011 (down from about $5 a share in 2009), so I presume it hasn’t had much in the way of commercial sales.

Unfortunately I think we can put buckyballs in the category of really really cool science that has an equally cool name but that doesn’t have a commercial application—yet.  It’s hard making money on science, even really really cool science.  Think about that.

Next up is the other fullerene that you’ve probably heard about:  nanotubes (see “f” in the diagram at the beginning of this blog).

Now, when it comes to the question of who discovered what and when in the nanotube world, the story can get pretty contentions.  Some give the award to Sumio Lijima, a Japanese physicist with the NEC company who reportedly succeeded in producing nanotubes in the lab in 1991.  He also examined these new structures under an electron microscope and correctly speculated on their structure (Lijima’s diagram looks like rolled-up chicken wire).  But others believe that carbon nanotubes were actually produced and photographed decades earlier.  They point to two Russians who published an article in 1951 along with pictures of what some people claim to be nanotubes—but the paper was written in Russian and, due in part to the Cold War, wasn’t available to Western scientists for a long time.  Since I myself don’t read Russian, I can’t tell you how these scientists came up with their nanotubes (if nanotubes they were), but they definitely didn’t clearly lay out the molecular structure the way Lijima did in 1991.

One of the coolest things about a carbon nanotube is its long length compared to its width, with a ratio of 132,000,000:1, which is greater than that of any other molecule found so far.  So if you had a nanotube that was an inch wide, it would be 2,000 miles long!  Nanotubes are also the strongest and stiffest materials known—with tensile strength equivalent to that of a 1 mm² cable capable of supporting 14,158 pounds.  In addition, nanotubes can conduct electricity 1,000 times better than copper, and some scientists claim that they are capable of behaving like a superconductor (although this is somewhat controversial). 

On the negative side, nanotubes have been shown to induce an inflammatory response, and because their structure is somewhat similar to that of asbestos fibers, concerns have been raised about possible carcinogenicity.  

Although the nanotube’s interesting properties have caused speculation about many different types of applications, the actual products sold so far are designed to capitalize primarily on the molecule’s strength.   Consequently nanotubes have been used in such things as bicycle components, skis, hockey sticks, hunting arrows, clothing, and resins and paints for wind turbines and boats.

But I would have to give the award for the “Most Bizarre Use of Nanotubes” (I hesitate to use the word “cool” yet again, but that is what I am thinking) to an application that would take advantage of the nanotube’s high length-to-width ratio:  a space elevator with one end tethered to the ground and the other end, well, out in space.  For transporting stuff back and forth between the earth and the International Space Station maybe. 

Certainly one of the coolest (neatest?!) near-term applications of nanotubes has got to be the paper battery.  Originally reported in the scientific literature by scientists at Rensselaer Polytechnic Institute in 2007, these batteries are composed of cellulose (paper), an ionic liquid (1-ethyl-3-methylimidazolium chloride), and nanotubes.  They produce between 2 and 8 volts of electricity, and since they are paper thin, they appear to be ideally suited for electronic devices such as cell phones and medical devices.  A new venture founded in 2008 (with the unsurprising name of Paper Battery Co.) plans to have a commercial product on the market by 2014.

And finally, the most recent carbon cousin—graphene.  Think of a single sheet of chicken wire.  The world got its first real glimpse of this molecular structure in 2004, when Andre Geim and Konstantin Novoselov at the University of Manchester, England, isolated graphene using Scotch tape.  Yes, indeed—they took some commercially available graphite, and stuck it to some Scotch tape.  Then they peeled the Scotch Tape off and, voila, they found that they had single layers of graphene.  Kind of like lifting pancakes off your plate with duct tape wrapped around your hand.  You get the idea.

This little experiment started another virtual gold rush of entrepreneurs hunting for commercial applications.  Like its buckyball and nanotube cousins, graphene has many unique properties—like being very strong and a great conductor of electricity, as well as having the ability to absorb and re-emit light over a greater range of wavelengths than any other known material.  And being only one atom thick, it is also the thinnest material known.  So graphene is currently being investigated for a wide variety of not-yet-commercial products, including electronic newspapers (e-paper), batteries, flexible electric circuits, and touch screens, not to mention desalinating water, sequencing DNA, and strengthening a wide array of other products.

For example, researchers at Michigan Technological University have shown that platinum (a very expensive metal) can be replaced with graphene in solar cell electrodes.  And scientists at Monash University in Australia have made graphene “supercapacitors” (batteries that can charge and recharge instantly) with as much energy density as a car battery.

And as an example of how one discovery can lead to another, scientists in 2012 reported that they have been able to grow glass on graphene.  That’s right, for the first time ever, researchers have produced a layer of glass only two atoms thick—on top of a layer of graphene.  And just like graphene, the glass looks like chicken wire , but since it is glass, it is composed of silicon and oxygen rather than carbon (glass is SiO₂).  And who knows what its possible uses are—the authors speculate that it might be used in semiconductors or in “layered graphene electronics as a passivated starting layer for gate insulators.”  Whatever that is.

The problem is that, like nanotubes, graphene is expensive to produce.  As a result, Graphenea, a Spanish company founded in 2010, will sell you a mere ½-inch square of single-layer graphene mounted on silicon dioxide for the whopping price of $330.   Or you can buy 250 ml of graphene oxide (advertised for use in batteries, solar cells, supercapacitors, and graphene research) for the slightly-less-shocking sum of $131. 

So graphene won’t be widely used in commercial products until the cost comes down.  Unless, of course, you are selling small and very expensive products—like high-end graphene tennis rackets, which are currently being offered for sale by the Head company.  But it will definitely be awhile before you see graphene in TV screens or e-paper.

So let’s summarize—buckyballs were discovered in 1985 and to date there are no commercial products on the market, but they are getting close.  Nanotubes were discovered in 1991 and commercial products have only recently entered the market.  And graphene, first isolated in 2004, has not yet found its way into commercial products to a significant extent. 

Lesson:  it is really REALLY hard to make money on even the most promising (i.e., coolest) new technologies.  And even if you eventually succeed, it often takes a really long time—due to the existence of competing products that are only so-so in terms of performance, but a lot cheaper to manufacture. 

These fantastic carbon molecules effectively illustrate the position that innovators of revolutionary technologies often find themselves in:  they are trying to “push” a product out the door to buyers who are not yet “pulling.”

Or simply, these are technologies in search of a market.  But with some inspired engineering, the market will come.   And then our lives will be a just a little bit better.

Useful references

http://www.nature.com/nature/journal/v318/n6042/pdf/318162a0.pdf

http://www.sciencedirect.com/science/article/pii/0022024880900135

http://www.nature.com/nature/journal/v354/n6348/pdf/354056a0.pdf

http://www.condmat.physics.manchester.ac.uk/pdf/mesoscopic/publications/graphene/Science_2004.pdf

http://www.pnas.org/content/104/34/13574.full.pdf