Here Comes The Judge

What got me to actually sit down at the computer and start writing was a recent news report in my local newspaper (the Columbia Daily Tribune, Friday, October 21, 2011, page 5B; columbiatribune.com) that U.S. District Judge Consuelo Marshall issued a ruling that a false advertising lawsuit filed by the sugar industry against the CRA could go forward.  The CRA had argued that the lawsuit should be dismissed because HFCS is equivalent to sugar in the way it is metabolized and that the lawsuit was “an attempt to stifle a national conversation about the merits of HFCS versus sugar.”  In addition, the CRA lawyers argued that educational campaigns form the CRA shouldn’t be considered advertising.  The judge dismissed those claims stating that the CRA’s educational campaigns constitute commercial speech and that the industry group is not insulated from federal false advertising regulations just because its “educational” statements relate to a public health issue.  I almost forgot to mention that the CRA had asked the FDA’s permission to use the term “corn sugar” rather than HFCS in both advertising and product labeling.  As far as I know, the FDA has not ruled on the request.  So, what is this all about?

What is HFCS anyway?

To understand what HFCS is and isn’t, we need to discuss a little basic chemistry.  Don’t be afraid, it’s not complicated.  To most people, the word “sugar” means good old table sugar, a sweet-tasting white crystalline substance called sucrose and which is composed of a molecule of glucose and a molecule of fructose.  Another word for sugar is saccharide.  So,  sucrose is a disaccharide; glucose and fructose are six-carbon monosacharides.  Another important disaccharide is lactose (milk sugar), which is composed of a molecule of glucose and a molecule of galactose.  Saccharides are a class of carbohydrates, molecules that are composed of carbon, hydrogen, and oxygen.  Carbohydrates, along with proteins and fats are the basic body building blocks.  Sugars can be composed of many monosaccharide molecules linked together, called polysaccharides, which are important storage forms of sugars in both animals and plants.  Although all sugars (by definition) are sweet, there is a large difference in the sweetness of individual sugars: fructose is the sweetest sugar, almost twice as sweet as glucose.

Sucrose comes mainly from sugar cane (60%) and from sugar beets (40%).  Sugar cane was first found in Papua New Guinea and was domesticated about 10,000 years ago.  The discovery of beet sugar was not until about 250 years ago.  The history of sugar is a fascinating one which has been chronicled by N Deerr in The History of Sugar (volumes 1 and 2, London, Chapman and Hill Ltd., 1949 v-258/1950 v-259-636).  An excellent summary of the subject was written by M. Gracey, N Kretchmer, and E. Rossi (A glimpse into the history of sugar, in: Sugars in Nutrition, Ed. M. Gracey, N. Kretchmer, and E. Rossi.  Nestle Nutrition Workshop Series, Vol 25; Nestec Ltd., Vevey/Raven Press, Ltd., N.Y., 1991).  I can assure you that HFCS is no more controversial than sugar itself, which has been considered by many historians to be most responsible for slavery (both in the U.S. and globally).

Anyway, for a variety of reasons, beginning in the 1970′s, HFCS was introduced as an ingredient in many processed foods.  HFCS is made from corn syrup, a liquid composed mostly of glucose molecules.  It is commercially available from a number of manufacturers, but perhaps, the best known form of corn syrup is Karo Syrup (ACH Food Companies, Inc.).  Corn syrup is made first by milling corn into corn starch, and then adding an enzyme, alpha-amylase, which breaks the starch into oligosaccharides (small chains of glucose molecules).  The next step is adding another enzyme, glucoamylase (also know as gamma-amylase) which results in a syrup consisting of only glucose molecules.  To make HFCS, the corn syrup is converted into fructose by another enzyme, D-xylose.  The manufacturing process results in HFCS with 90% fructose (HFCS 90) or 42% fructose (HFCS 42).  HFCS 90 is used to make HCFS 55, which is used to sweeten sodas and various sport drinks.  HFCS 42 is used in many processed foods including some yogurts, frozen desserts, breakfast cereals, and baked goods, and has about the same composition as sucrose.

How much sucrose and HFCS do Americans actually consume?

You may find it hard to believe, but since 1970, U.S. consumption of HFCS has risen from zero to about 40 lbs/yr/person.  At the same time, consumption of sucrose has decreased from about 70 lbs per person to about 40 lbs per person.  Net (total) sugar consumption has risen from about 80 lbs/yr to about 100-120 lbs/yr.  Thus, virtually all of the increase in total sugar consumption is the result of increased consumption of HFCS in its various forms.  But, the ratio of fructose to glucose intake has remained about the same over time

Why is HFCS so widely-used?

The development of HFCS was to a great extent the result of political and economic circumstrances.  Cane sugar quotas in the U.S. have kept the price of can sugar high while corn subsidies have made growing corn relatively inexpensive.  The bottom line is that it is cheaper to make HFCS than to process cane sugar.  It is also important to note that HFCS has some desirable qualities; It mixes well with foods and keeps foods moist.

How is HFCS metabolized?

Remember that HFCS and sucrose are composed of glucose and fructose molecules.  It is the fructose that most experts have focused on as a possible health culprit, beyond the fact that sugar in the form of glucose, sucrose or fructose add calories to the diet- about 4 calories/gram consumed.  Metabolism of glucose is relatively simple.  Glucose can be used by all cells in the body for energy, it can be stored in the form of glycogen (long chains of glucose molecules, much like starch, and used as a building block for polysaccharides.  Fructose, on the other hand, is taken up mainly by the liver and can be converted into glucose, glycogen, triglycerides  and some fatty acids.  It is the role of fructose in fat metabolism that has generated the most controversy.  There are considerable data in both animal and humans that consumption of large amounts of fructose raise triglyceride levels and increase insulin levels, promoting insulin resistance.  Does fructose promote cardiovascular disease?  Does fructose promote the development of diabetes mellitus? Does high fructose intake stress the liver?  These are just some of the questions that have been raised about dietary consumption of fructose, and by extension, consumption of HFCS.

Is HFCS metabolized differently than sucrose derived from cane and beet sugars?

There is considerable controversy whether HFCS has unique properties such that it is metabolized differently than sucrose derived from cane or beet sugar.  In my opinion, there are no credible data to show that HFCS and sucrose are metabolized differently or that the fructose in HFCS is any different than frucose in sucrose or fructose in fruits, honey, maple sugar, agave syrup or brown rice.

So, what’s the problem?

In my opinion, the problem is that we in the U.S., consume far more calories than we need and many of those calories come from foods containing various sugars, including HFCS.  The latest data show that Americans currently consume, on average,  about 130 lbs of sugar a year which works out to be almost 40 teaspoons of sugar every day.  It’s extraordinary.  We have twin epidemics of obesity and diabetes mellitus and plenty of cardiovascular disease to go around.  We don’t need to single out a single food or food additive (i.e., HFCS) as the reason for our many ills; there is plenty of blame to go around, including our fondness for inactivity.  But, it is clear that if we curb our sugar intake, we will benefit.  I am neither defending or condemning the use of HFCS in foods.  I seriously doubt that if tomorrow, the use of HFCS in foods and drinks were banned, it would have any impact on the prevalence of obesity, diabetes or heart disease.  We  will still eat too much (including an extraordinary amount of the various sugars) and exercise too little.

If you find this subject interesting, I urge you to read an article by Mary Franz (“High-fructose corn syrup: what’s the fuss about?,” published in Diabetes Self-Management, May/June 2011, pages 33-37) and an article by Gary Taubes (“Is sugar toxic?,” published in the New York times Magazine, April 17, 2011).  The Taubes article discusses the highly controversial views of Robet Lustig, a physician from the University of California San Francisco.  Don’t miss the Lustig video on You-Tube which is a lecture he gave in 2009 entitled “Sugar: the bitter truth.”  I’m not saying whether I agree or disagree with Lustig’s views, but………..

Finally, what about calling HFCS corn sugar?  In my opinion, it’s clearly false advertising.  Why don’t the corn growers just call HFCS something like “sugar derived from corn?”  Or, maybe, just continue to call it HFCS?

The second media piece was in the Business section, page 5 of the New York Times, Sunday March 26, 2010.  The piece is entitled “Carrots, Sticks and Lower Premiums” written by Steve Lohr.   The article addresses the mostly unspoken truth that health care reform in the U.S. would benefit in an extraordinary way if all of us lived healthier lives.  Data do show that 50-70% of our nation’s health care costs are preventable, mostly attributable to treatment for chronic complications that mostly related to unhealthy behaviors.  The article is about how employers are beginning to wake up to the fact that it is good business to have healthy employees.  Read the article.

The third piece is an article that appeared the other day in the New England Journal of Medicine (March 25, 2010).  The title of the article was “Prevalence of Diabetes among Men and Women in China” and written by Wenying Yang and colleagues.  The investigators studied whether the rapid change in lifestyle in China has increased diabetes prevalence.  The study population included 46,239 adults, 20 years of age or older, from 14 provinces and municipalities tested between June 2007 and May 2008. The results were astonishing.  China is catching up with the U.S., and I’m not talking about their economy.   The age-standardized prevalences of total diabetes (previously undiagnosed and previously diagnosed diabetes)  were 10.6% in men and 9.7% in women.  For prediabetes (abnormal blood glucose levels but not diagnostic for diabetes), the prevalences were 16.1% in men and 14.9% in women.  The data showed a sharp and steady increase in the national prevalence of diabetes from surveys conducted in 1980, 1994, and 2001 (e.g., prevalence in 1994 was 2.5%).  Not surprisingly , the prevalence was considerably higher in urban residents than among rural residents.  The investigators concluded the following: “that diabetes has become a major public health problem in China and that strategies aimed at the prevention and treatment of diabetes are needed.”

So?

I don’t think I really need to explain how the 3 media pieces relate to one another.  The prevalence of diabetes in China is now just about the same as the prevalence in the U.S. (prevalence of 9.6% based on the National Health and Nutrition Examination Survey 2003-2006).  It’s the price we now pay globally for our economic advances coupled with our genetic predisposition to obesity and diabetes (check out some of my old entries if you have forgotten).   Jamie Oliver knows what do do about the problem in both the U.S. and China and so do employers trying to get their employees healthier, and so do you.

In Summary

Taken together the two studies show quite convincingly that bariatric surgery (from an earlier posting you may remember that the term “bariatric” comes from the Greek word “baros” which means weight) has a statistically significant effect on mortality from cardiovascular diseases, diabetes, and cancer. The Swedish study had a rather impressive duration of follow-up with a mean of almost 11 years. The data support earlier cross-sectional studies showing clear-cut benefits from bariatric surgery in people with obesity (BMIs over 40 or over 35 with obesity complications).

Any pitfalls?

I was a bit surprised to find that the Swedish study which was a non-randomized longitudinal design showed so many deaths in the surgery group (101 vs. 129 in the controls) and many more deaths from non-typical obesity-related conditions (e.g., accidents, suicide) than the control group. I have no idea what this means. My main concern with the data is that the only way to really tell how much the surgery works and what the non-obesity-related deaths are all about is to have a randomized trial. This would be a study design where potential study volunteers agree to be in a study about bariatric surgery and would agree to be in either the surgery or control group, as determined by a “flip of the coin.” The problem with both the Swedish and Utah studies was that controls were not selected on a randomized basis. Regardless of their limitations, these data are important and support the use of bariatric surgery in selected patients.

We still have much to learn about this subject. I fear that there will be a steady increase in surgery for patients with lower and lower BMIs, where the long-term benefits are unknown. To all you bariatric surgeons out there- temper your enthusiasm with a dose of good judgment in selecting cases.

What does TV have to do with blood sugar control?

In people with diabetes, many factors affect the blood sugar level but in general it is a tug-of-war of sorts between factors that use up sugar in the blood and those that increase the sugar level (let’s use the term “glucose” instead of “sugar,” since it’s really the molecule glucose we are talking about when when use the word “sugar” when referring to the “blood sugar level’). Anyway, eating food will increase the blood glucose level as will insufficient insulin which allows the liver to release stored glucose into the blood. It’s not so simple; there are other things that will tend to increase the blood glucose level including stress (hormones such as cortisol and adrenaline (epinephrine) raise the blood glucose level) but these factors all do it through effects on the liver’s glucose stores.

Factors that tend to lower the blood glucose level include the hormone insulin, through decreases in the liver’s release of stored glucose and increases in tissue use of glucose, and through exercise, which can stimulate glucose uptake by muscles even independent of insulin.

So, sitting around and watching TV means less exercise and it may mean more munchies, both of which would tend to result in higher blood glucose levels.

Is this information of any relevance to people who do not have type 1 diabetes?

For people who do not have type 1 diabetes, this report is a reminder that sitting around watching TV for hours and hours might not be such a good idea- what we see as higher blood glucose levels in people with type 1 diabetes will likely be seen as weight increases in people who do not have diabetes (in people with type 1 diabetes, high blood glucose levels usually mean high urine glucose levels and thus loss in calories, limiting weight gain if the high blood glucose levels are due to excessive caloric intake). Is there anything much worth watching on TV anyway?

What causes insulin deficiency?

There are many causes of insulin deficiency. The easiest to understand is the type of insulin deficiency because the beta cells are decreased in number or totally missing from the pancreas as in type 1 diabetes (T1DM). Type 1 diabetes is the type of diabetes that is most often diagnosed in childhood- it used to be called juvenile-onset diabetes. In most instances T1DM is a genetic disorder caused by autoimmune destruction of the beta cells. About 10% of diabetes in the U.S. is classified as T1DM.

Another kind of insulin deficiency is what I would call “relative deficiency.” This means that the beta cells are producing insulin but the person is resistant to the insulin- it just doesn’t work well. This is typically present in people who have type 2 diabetes (T2DM), the most common form of diabetes in the U.S. This form of diabetes is also inherited but in most instances requires that the person be overweight (all overweight people are somewhat resistant to insulin). It is all a bit complicated, but in most instances of type 2 diabetes there are several factors involved including insulin resistance, impaired insulin release from the pancreas in response to high blood glucose levels, and some element of actual deficiency. Anyway, the end result is not enough insulin to prevent high blood glucose levels or hyperglycemia, the second feature in all forms of diabetes.

Hyperglycemia

It is not enough to have insulin deficiency (either actual deficiency, resistance to insulin action, or both) to call it diabetes. The end result must be hyperglycemia, the hallmark of diabetes. In my last entry I discussed the specific blood glucose levels that define a diagnosis of diabetes.

The third feature

The last component of all types of diabetes is a tendency to develop serious complications. Most people know something about these problems- eye disease, called retinopathy, kidney disease, called nephropathy, and nerve disease, called neuropathy. Together these three “opathies” account for much of the misery associated with diabetes and are often called “microvascular” complications even though they do not all affect the microvasculature (don’t ask me to explain that). The microvascular complications are to be distinguished from the “macrovasular” complications of diabetes, peripheral vascular disease, stroke, and heart disease.

Diabetes mellitus as a syndrome

In summary, diabetes is a group of distinct disorders that share 3 things in common- insulin deficiency, hyperglycemia as a result, and high risks for developing medical complications. There are many different types of diabetes but probably 99% are either T1DM or T2DM. Maybe sometime in the future we will discuss the other 1%. We will definitely come back to further discussions about T1DM and T2DM.

What does interval training have to do with “prediabetes?”

The paragraph above really has nothing to do with prediabetes except that in the article, the author wrote the following: “weight watchers, prediabetics, and those who simply want to increase their fitness all stand to gain,” referring to the technique of interval training. I would be willing to bet that most of the people who read the article do not have any idea what prediabetes is. I’m here to help.

Prediabetes is an old term in the diabetes field but which has been “reinvented” recently. It used to mean a more-or-less theoretical state in which a person was at genetic risk for developing diabetes mellitus or “sugar diabetes” (to distinguish it from diabetes insipidus, a condition related to water balance) but had normal blood sugar levels. More recently, the term is used to define a group of people who are at increased risk for developing diabetes based on specific blood sugar levels, which are above normal but not high enough to allow one to definitively diagnose diabetes. Are you with me so far?

Definitions

Diabetes is defined by certain blood sugar levels, either in the “fasting state,” which usually means with no caloric intake for the previous 12 hours, or after a standard sugar water drink called a glucose tolerance test. Technically speaking what is measured is the “plasma glucose level” even though many people talk about the “blood sugar level.” Anyway, for a variety of reasons, some scientifically sound and some more politically sound, a person is said to have diabetes if either the fasting plasma glucose is 126 mg/dl or greater on two occasions, or the value two hours after 75 grams of oral glucose is 200 mg.dl or greater. The diagnosis can also be made if a “casual” plasma glucose value (this means testing without regard to interval since the previous meal) is 200 mg/dl or greater with typical symptoms of diabetes- excessive thirst, excessive urination, etc.  There are a number of conditions that need to be met before the diagnosis can be made, such as the person must be well-nourished, not acutely ill, etc. Also, a definitive diagnosis cannot be made using the little portable blood glucose meters that we see advertised on TV; the test must be carried out in a laboratory with actual measurement of the plasma glucose level.

Impaired fasting plasma glucose, impaired glucose tolerance, and prediabetes

This brings us to “prediabetes” states. Diabetes experts define impaired fasting plasma glucose (IFG) as fasting plasma glucose of 100-125 mg/dl; impaired glucose tolerance (IGT) is defined as fasting plasma glucose <126 mg/dl but 2-hour plasma glucose after a glucose tolerance test of 140-199 mg/dl. Finally, prediabetes is defined as either IFG, IGT, or both. Recent studies show that people who have prediabetes are at great risk to develop diabetes within a few years. As it turns out, things are not quite so simple. For example, if the fasting plasma glucose is 100-109 mg/dl, the risk for progression to diabetes from IFG is rather low- much higher if the fasting plasma glucose is in the range 110-125 mg/dl.

So?

THe reason it is important to understand these definitions is that recent studies have shown that treating patients with prediabetes can slow progression to diabetes. Thus the very recent American Diabetes Association’s Consensus Statement entitled ” Impaired Fasting Glucose and Impaired Glucose Tolerance” (Diabetes Care 30:753-759) in which it is recommended to treat all people who have either IFG, IGT, or both.  Depending on a number of factors, the treatment would be lifestyle modification and moderate intensity phycical activity (defined as roughly 30 minutes/day) or the above and medications. All of this is to decrease the risk for progression from prediabetes to the real thing, diabetes.

So?

These are bold recommendations that if followed by all medical practitioners would lead to an astonishing increase in testing for IFG and IGT. What I find so amazing is that despite these recommendations, the American Diabetes Association (ADA) and many of the experts who wrote the Consensus Statement discussed above are ambivalent about testing for prediabetes. To quote the recently published ADA’s Clinical Practice Recommendations 2007 (Diabetes Care 30 (suppl 1.):S1-S104, 2007) for diabetes screening: “Screening to detect prediabetes (IGF or IGT) should be considered in individuals >45 yeares of age, particularly in those with a BMI >25 kg/mXm.” They go on to say that screening should be considered in people <45 years of age who are overweight if they have other risk factors for diabetes. How seriously should we take a recommendation of "should be considered."? On the one hand the "experts" tell us we should be treated for prediabetes but our doctors should only "consider" testing us for it. Does any of this make sense to you?

What should we do?

Given that about 60% of people in the U.S. are overweight and that we have a diabetes epidemic, we should (not should consider) begin testing on a regular basis (e.g., every 1-2 years) for prediabetes or diabetes in all adults who are overweight. It is the only logical thing to do based on the available scientific information. Why are the “experts” so afraid to speak up? I’m not sure but I suspect there are powerful health-care industry lobbyists who do not feel insurers can cope with the expense of making so many diagnoses of prediabetes and diabetes and then having to treat the patients? Of course, they need not worry; our health-care system is so disorganized that we couldn’t possibly find a way to actually carry out the testing and provide the proper treatment. Am I being unfair? I don’t think so.

The good news

All is not lost. It is still possible for people, children and grown-ups, to lose weight or, at least, not gain excess weight year after year as most people do. It does, however, require that a person recognize his or her problem and commit to a solution long-term. Dealing with obesity is no place for the timid.

Where to start: Goldstein’s principles

1. First, I do not really believe in “diets” as most people use the term. In most instances a diet implies some plan to consume fewer calories until whatever weight goal is achieved. Thereafter, most “diets” get a little fuzzy about what to do and inevitably most people (note- I didn’t say everyone) regain all the weight they have lost and then some. I believe the primary reason most “diets” fail is that they do not really give a person a satisfactory way of eating life-long. In fact, there are considerable data showing that the best way to lose weight and keep it off is to lose weight slowly through a new approach to eating that can be sustained long-term. We should stop taking about “diets” and begin talking about healthy eating plans. A healthy eating plan should be the way all of us eat, overweight or not.

2. People who are significantly overweight (BMI >35) need to face their situation squarely in the mirror- literally and figuratively; they are at great risk for serious consequences of their obesity. They have to come to the conclusion themselves. For children it’s a bit tricky and parents need to be very sensitive to the psychological side of their child’s obesity. This is particularly true for teen-age girls. I have encountered many mothers who create enormous stress by continually nagging about their child’s “problem.” The mothers clearly mean well and are genuinely concerned about the short- and long-term consequences of their child’s obesity; many of these mothers struggled with their weight as teens and many are still struggling. Parents must not press too hard, despite the seriousness of the situation. I was told about a recent report on CNN describing a high prevelance of bulimia in teenage girls placed on diets (there’s that word again!).

3. Let’s forget about “guilt trips” and anti-obesity bias. Most people got overweight by just living in a “machines can do almost everything for us” era and by listening to their brain appetite centers. Most people who are overweight are not suffering from serious personality disorders characterized by lack of restraint. It’s not a disease (it could be a symptom of a disease such as hypothyroidism), although over time it certainly can have serious health consequences. Those of us who are lucky enough to have desirable BMIs need to stop looking at overweight people with some measure of distain or even revulsion. It’s an irrational bias that doesn’t often help people who are overweight deal with their situation (our society has the same type of bias against short people- that’s called heightism. We’ll discuss it at another time). Many physicians have trouble working with people who are overweight simply because of this anti-obesity bias and their belief (probably subconscious) that the patient is to blame for his or her problem.

4. Keep it simple. While a very complicated weight management plan might be a great idea for a neurotically obsessive-compulsive person, most people do best with simple, easy to understand plans that are also easy to implement. I already discussed my aversion to “diets” and I especially do not like diets that offer a gimmicks as their draw; usually it’s completely avoiding a certain type of food (e.g., don’t eat anything that is white in color, don’t eat bread or pasta) and often the plan includes purchasing expensive foods or supplements. It’s amazing- just because someone writes a book (or a blog?) people tend to “believe.” Certain diet plans are also trendy and come and go as quickly as the “beautiful people” find they are hard to follow or, as is usually the case, do not work long-term.

I confess that I am being a bit heavy-handed with my criticisms of many diet plans out there but in my experience simple and nutritionally sound eating plans work best.

5. People who are overweight need to know as much as possible about nutrition principles. They need to understand the differences between carbohydrates, proteins, and fats. They also need to know about saturated fats and trans fats. They need to know how to read food labels (maybe we’ll cover that subject in the future?); if whatever food they are contemplating purchasing has 18 grams of fat in each portion and that fat is mostly saturated fat, they need to appreciate what that means for their eating plan (answer- maybe good tasting but not anything very good for their eating plan). Children as young as 6-7 years can be taught quite a bit about nutrition.
Not to be overly critical of physicians, but most don’t have a clue about good nutrition; it is generally not taught at all in medical school or in residency/fellowship training or if it is taught, addressed in a very cursory way. Even though I think I have a better-than-average understanding of nutrition principles, the program I direct for children with obesity (it’s called the University of Missouri Children’s Hospital Health and Fitness Clinic) relies on a pediatric dietitian to help educate patients and their families.

6. Healthy eating plans must be individualized and the specifics depend on the unique characteristics of the overweight person and his or her family. Unfortunately, developing a customized healthy eating plan requires that the health-care provider know a great deal about the overweight person and family; the plan will be doomed to failure unless it takes into account the way the overweight person and family “operate.”

For example, if an overweight child comes home after school and is all alone, maybe a major contributor to the overweight is the afternoon megasnack? Is it a very busy family, always on the run, with many meals at fast-food restaurants (or meals eaten in the car to or from some activity?). Does the family tend to spend many evenings watching TV and snacking? You get the picture? It helps to know a great deal about how the overweight person and family eat and live before trying to fashion a healthy eating plan. Of course, in many instances given the genetic aspects of obesity, the healty eating plan is appropriate for the entire family.

It is clear that once a person is overweight, psychological factors can contribute to the obesity and make it more difficult for a person to trim down. For example, some people deny their obesity and refuse to confront the problem. Denial is a powerful psychological mechanism for relieving anxiety and I suspect this is a fairly common feature, especially in people who are very overweight (i.e., BMIs > 35-40). In other people, it’s more like giving up rather than denial- they may have tried losing weight and maybe even lost a bit but regained all they had lost and then some. There is not much evidence that psychotherapy is a highly effective method of treating obesity. Of course, every person is different and there are certainly some people whose overweight is primarily related to psycholoigical factors. But, let’s not forget that the single common pathway to obesity remains more calories in than are burned up.

Clearly, one important component of the obesity epidemic in the U.S. is our rather alarming state of inactivity. But, lack of exercise can not fully explain things. For example, we all know some people who get virtually no exercise and are not overweight. Some people do try hard to get regular exercise and still gain weight year after year. It can’t be just inactivity. I do not mean to imply that lack of at least reasonable physical activity (I won’t try to define what I mean by “reasonable”) is not an important factor in explaining the obesity epidemic. Even 100-200 “extra” calories burned per day through physical activities, can have a profound effect on energy balance; all other things equal, each 100 calories per day in increased energy expenditure translates into about 12 pounds of fat not gained per year!

What about the caloric intake side of the energy balance equation?

If a person has an appropriate body weight at time-point A and then increases calorie intake by 100 calories per day (assume no change in energy expenditure),there would be about a 12 pound increase in body weight at at point B one year later- I bet you figured it out before I told you the answer! So can we put part of the “blame” for the obesity epidemic on increases in calorie intake? The answer is “you bet.” Studies have shown that on average, people in the U.S. are eating about 200 calories more per day than in 1977- that’s a 10% increase in calories consumed per day. How can this be? Well, I can’t give you an easy answer but I can give you some possibilities.

Food is cheap

Food in the U.S. is really cheap. I know that some families still struggle to afford enough high quality foods to allow good nutrition and adequate calories. But for most people in the U.S. it’s almost a free-for-all; at present, we spend only about 17% of our incomes on food, including eating out. That’s far less than what we spent on food 30 years ago as percent of income. We already know that many of us have brain appetitie centers that are not satisfied with just enough calories in to maintain body weight (or to gain weight appropriately for a child). So easy access to really cheap food helps to explain where the 200 “extra” calories per day come from.

Portion sizes and types of foods

Partly because food is so cheap, we as a nation have made drastic changes in portion sizes. We do it at home and restaurants have done it to us when we eat out. I remember when a “regular” hamburger was the only size available at McDonalds (it only cost 15 cents then). Now at McDonalds or any other fast food chain resturant that sells hamburgers, we can feast on a a megasandwich, which is incredibly cheap considering the gigantic number of calories (mostly fat calories, of course). At home and in resturants we use much bigger plates than in the past- about 30% bigger over the past 30 years so I am told. The psychology of plate size is fascinating. Left to our own devices, we will take about 30% more food if our plates are 30% bigger. It’s the same for glasses; people using a short fat glass will take about 30% more liquid to drink than if the glass is tall and slender.

Who is to blame for portion-size inflation and for such cheap food?

I don’t know that anyone in particular is to blame for the mess we have created. The “why” of our cheap food is complicated and I refer you to the books I mentioned in an earlier posting (“The Omnivore’s Dilemma,” by Michael Pollen, and “Fast Food Nation,” by Eric Schlosser). In a nut-shell, our government subsidizes the production of much of the food we eat, particulary soy bean and corn-based products (in about 70% of what we eat!). That’s why it’s so cheap. Don’t get me wrong, I am not advocating more expensive food just to keep us from eating as much and as much that is not very good for us. It’s all so complicated. We are weak (at least our appetite centers are) and the food advertisers are strong. The food industry has a big problem. They have become so efficient at food production that we have gigantic surpluses; the food industry produces about 500 calories more per day per person in the U.S. than we can stuff into our mouths. Of course, no one is forcing us to eat so much and so much that is of questionable nutritional value.

What about the children?

The one real problem I have with the food industry is the way it puts so much energy into getting children to eat more and more of what is of questionable nutritional value. Children are bombarded with food advertising on television, billboards, and even at the schools. The entertainment industry plays a part in all of this too by working with the fast food industry to entice children to go eat fast food because they can get some little toy creature. Even so, parents could control this if they would. And of course they should take control; remember, most overweight children become overweight adults.

We have discussed that net body weight is the sum of two opposing forces, calories in and calories burned. If a person eats more than he or she burns up through basal metabolism and additional activities, there is weight gain. Of course, for growing children it is okay to gain weight, but it should be appropriate for the gain in height. Anyway, it should be clear to you by now that a person’s activity level can have a profound effect on his weight. With genetic influences already in place, the only mechanisms to lose weight or to maintain an appropriate weight, independent of drugs and/or surgery, are related to activity and calories.

There is no doubt that steadily decreasing amounts of activity contribute to the obesity upsurge in the U.S. Why has this happened? The answer is a multifactorial one but a major contributor is technology; many tasks that in the past required intense physical labor now are performed by machines. How many farmers weed their crops by hand? How many people walk to the shopping mall and to the grocery store? How many people mow their own lawns? Of those that do, how many use a manual “push” mower? You get the point; we are an affluent people and we are good at getting other people or machines to do much of what used to be physical activity for each of us. Many of us do try to conmpensate by going to a gym or jogging, or whatever, but the statistics show that very few people have regular exercise programs long-term that amount to much in the way of caloric expeniture.

What about the children?

It’s particularly worrisome for the children. Computers and television have largely replaced outdoor play after school. In the school setting, things are as bad; most schools have cut back drastically on physical education programs because of funding formulas that favor academic classes. The five-day-a week physical education programs that used to be standard in the schools are rare indeed; many high school students have phycical education classes only as an optional activity. Certainly many students do participate in organized school sports and in non-school sponsored sports such as community baseball leagues, but fewer and fewer children are getting much exercise. What is very important to understand is that it’s not a question of children getting no exercise, but rather, less exercise than in the past.
The situation is particulary bad for teenage girls. Studies have shown that girls participate in exercise activities less and less beginning at about age 14 years; by age 18 years, fewer than 20% of girls get any meaningful physical activity on a regular basis (unless you consider turning a key to start a car and holding a cell phone to one’s ear as meaningful exercise).