Tag Archives: weight loss tablets
Back in The Real Bathroom Scales, we learned that obesity has less to do with excess consumption than with insufficient energy expenditure, and that energy expenditure is very tightly regulated by our bodies, such that we cannot fool our fat-making machinery with simple changes to diet and exercise. Then, in my most recent post, Through Thick and Thin, we looked at a couple of major physiological determinants of that regulatory process—specifically, the degree of alpha and beta adrenergic stimulation and the amount of insulin our bodies produce. In this post, we’ll continue that discussion by examining a study of several drugs in the so-called “appetite suppressant” class, and look at how they really get the job done. “Back to the Future” Unless you’ve been living under a rock or aren’t yet 12 years old, you’ve no doubt heard of the infamous “fen-phen” diet drug combination. Fen-phen was short for Fenfluramine and Phentermine, two drugs classified as appetite suppressants, which were at one time heralded as the answer to obesity when used together. Unfortunately, the propensity of Fenfluramine to increase the risk of primary pulmonary hypertension resulted in that drug being removed from the marketplace, but fortunately, Phentermine is still available, and contrary to the mythology of the day, works just as well, if not better, by itself, than in combination with Fen. Some less well-known drugs in this class are Diethylproprion, Mazindol, Sibutramine, and more recently, Bupropion (Wellbutrin), originally intended as a smoking-cessation aid. All of these drugs have a broadly similar mechanism—they alter the ebb and flow of neurotransmitters in the brain in such a way that thermogenesis is increased, either through direct stimulation of the beta adrenergic receptors or by inhibition of insulin release via the alpha adrenergic receptors. I’ll get further into the mechanics of these actions in another post, but for those of you who are looking for answers now, let’s get down to the brass tacks of what we can expect from drugs in this class. “Back to School” I’d like to review a study that compared the four most common diet drugs of its day (1981). In this study, researchers gave Phentermine, Mazindol, Fenfluramine, and Diethylpropion to four groups of mice, allowing them to eat freely as their respective appetites directed, for a period of 28 days. A group of unmedicated, ad libitum fed mice served as controls, while one other group, also unmedicated, were fed a restricted calorie diet for comparison. Although it is a mouse study and not a human study, I chose this one because of its excellent design, which eliminates the common confounding variables found in most diet drug studies, namely, caloric restriction and added exercise. Due to the pervasive mythology about the cause of obesity, the vast majority of diet medications are tested in conjunction with a reduced calorie regimen and/or exercise program, which completely obscures the actual effects of the drugs. Since we know that reducing calories and increasing exercise causes both a temporary period of weight loss and a gradual metabolic slowdown, adding these variables into a medication trial is clearly…well, stupid! It makes a fair evaluation of the drug’s effects impossible to tease out. By allowing the subjects in this study to eat and exercise at will, the researchers were able to give a useful assessment of the drugs themselves. Okay, back to the study. As you can see in these graphs, all of the study treatments resulted in voluntarily reduced intake and some weight loss, but what’s important to note here is the relationship between the reduction in food intake and the amount of weight lost. Notice the bar lengths do not track—the highest intakes, relative to the control group, resulted in the lowest amount of body fat. Phentermine and Mazindol clearly offer a greater bang for the buck than Fenfluramine, Diethylpropion, and the standard caloric restriction. Here are the numbers as percentage reductions from control:
What this is telling us is that for the 22% reduction in calories experienced by the Low-Calorie mice, there was only a 12% drop in fat mass, relative to the controls, while for the lucky mice on Phentermine, there was a mere 6.6% decrease in intake, yet a whopping 15.9% decline in bodyfat, 2.4 times the change in intake. Looking at the numbers this way, Phentermine and Mazindol are again the clear winners.
“Get Your Back into It!”
So where do these differences in results come from? At the risk of charting you to death, let’s look at another interesting and critical statistic from this study: energy expenditure.
I keep saying that it is innate EE and not intake that ultimately determines our bodily fat content; well, here is more proof of that concept. If you compare the body fat mass graph (above) with this EE graph, you will see that these bars do track–the drugs which induced the greatest energy expenditure (as measured during the six hours post-medication at four time points) resulted in the least fat mass. Among these four drugs, again, Phentermine is the obvious star, raising EE by 43% over control.
Before I leave this informative study, I would like to point out one more set of measurements the researchers made—body water and lean mass. At this point, it shouldn’t surprise you to learn that only Phentermine and Mazindol increased both body water and lean mass by a statistically significant amount compared to control. Good luck getting that result with any old low-calorie diet regimen!
If the underlying cause of obesity is actually low energy expenditure and not high calorie intake, then isn’t the obvious solution something that increases EE rather than decreases intake? From the results of this study, it should seem clear that a good diet medication will be a poor appetite suppressant and a powerful energy enhancer.
Through Thick and Thin
In The Real Bathroom Scales, we verified two important facts. First, we confirmed that the body responds to alterations in calorie balance with a combination of adjustments to energy storage (body mass) and to energy usage, the latter being mostly via changes to TEF and NEAT. Second, we saw that there was a wide variance between individuals in their rate and degree of adaption via the energy expenditure variables. In fact, in the Mayo Clinic NEAT study, the change in expenditure in response to an added 1,000 calories per day ranged from a low of +107 cals to a high of +917 cals, a nine-fold difference!1 So what drives these vast differences in our ability to adapt to changes in intake, such that some of us pile on the pounds, while others never seem to gain an ounce? While there are myriad biological abnormalities that can lead to obesity, most of them are uncommon, such as leptin deficiency, adrenal tumors, or genetic diseases such as Prader-Willi Syndrome. Most common obesities, on the other hand, can be directly linked to poor function or signaling of the sympathetic nervous system. The SNS is a primary regulator of many of the body’s homeostatic mechanisms, not the least of which is energy balance. The effects of the SNS on energy balance are achieved through the binding of catecholamines (adrenaline and noradrenaline) to a series of receptors known as the adrenergic receptors. “Greek Alphabet Soup” There are two basic types of adrenergic receptors, the alphas and the betas, and while both play a role in the management of body fat, the beta adrenergic receptors have been much more extensively studied with regard to energy balance, so we’ll start there. There are three beta receptors, and all are involved in the automatic regulation of energy expenditure, with some ability of each to compensate for the others. When these receptors are sufficiently stimulated by endogenous catecholamines or pharmacologic substitutes, the body is relatively resistant to weight gain. High levels of beta adrenergic stimulation probably underlie the “lean ‘n hungry” phenotype referred to in The Calculus of Calorie Counting. Without that stimulation, eating the same amount of food and doing the same amount of exercise, you will simply burn less of it as heat and energy and store more of it as fat. Like the patient in the Mayo Clinic NEAT study who only increased his energy expenditure by 107 calories per day, you would have what researchers call “defective thermogenesis”. Although the concept of thermogenesis has been around for at least half a century, the definitive proof that the beta-adrenergic receptors mediate thermogenesis took some time to develop. In a revealing study of mice specially bred to lack all three beta receptors, researchers at Harvard Medical School showed how profoundly the beta receptors effect our ability to dispense with our caloric intake. In two separate experiments, these beta-null mice were compared with normals under free-feeding situations with first, ordinary lab chow, and second, with more palatable high-fat chow. All the mice consumed more calories with the more palatable chow, however, in both situations, beta-nulls ate exactly the same amount as normal mice and engaged in similar amounts of activity. The difference in the outcomes, however, was startling. The beta-nulls had consistently lower energy expenditure, and as the graph shows, consistently higher weight gain; on lab chow, it was about 70% higher, and on the palatable diet, it was three times higher! Now, while the beta adrenergic receptors are clearly important to fat-burning, the alpha adrenergics should not be ignored. The alpha adrenergics are often described as being anti-lipolytic, because the alpha-2 adrenoreceptors reduce levels of cyclic adenosine monophosphate, an important second messenger in the thermogenic process. This characterization is somewhat lopsided, however, as the alpha-2’s also have a generally inhibitory effect on the pituitary hormones, putting the brakes on excessive levels of insulin, prolactin, cortisol2, and thyroid. These are not hormones that we necessarily want to inhibit, but neither do we benefit from excess; all of these hormones have optimal levels, and too much is just as problematic as too little. With regard to controlling our weight, we particularly need to keep our levels of insulin in check. “Insulination” Recall from Dr. Segal’s research in Calculus, how the presence of insulin resistance dramatically reduces the thermic effect of feeding (TEF), in both the lean and the obese.3 Besides just impacting TEF, however, insulin reduces the overall fat-burning ability of the body. In fact, insulin reduces the effect of beta-adrenergic stimulation in a dose-dependent manner; in one study, the calorigenic effect of norepinephrine was decreased by the presence of elevated insulin levels by as much as 50%.4 Just how powerfully does insulin sensitivity impact our ability to burn fat? Consider this interesting study: a group of researchers in Canada bred a strain of mice with a mutation in their insulin receptors, such that the same amount of insulin would keep the receptor active longer, thereby reducing the amount of insulin needed to return blood sugar to basal levels. In other words, these mutant mice were exquisitely insulin-sensitive. The researchers then placed the mutants and a control group of wild-type mice on a high-calorie diet designed to cause weight gain. While on the diet, the mutant mice maintained slightly lower blood glucose levels, despite secreting approximately half the amount of insulin as the controls. Because of the reduction in insulin, weight gain was significantly lower, too. After 10 weeks on the diet, the mutants had added 27% to their weight, while the wild-types gained 50%–all while eating and exercising in a similar fashion. So here we have two common physiologic aberrations–insulin resistance and decreased adrenergc stimulation–that lead to decreased energy expenditure without any difference in diet or exercise patterns. For those who have any degree of either or both of these conditions, fat will tend to accumulate easily and be difficult to lose, while those on the other end of the spectrum, our (annoying) “lean ‘n hungry” friends, can’t gain weight to save their lives. Now, the important thing is, is there anything we can do about this? Well, it just so happens there is. If nature left a little something out of your gene pool, you can get it back. In my next post, You Can Get There From Here, I’ll start showing you which products, both prescription and OTC, can truly change your metabolism.
- Levine, J.A., et. al. Role of Nonexercise Activity Thermogenesis. Science 1999; 283(5399): 212–214. ↩
- Price, L.H., et. al. Alpha 2-adrenergic receptor function in depression. The cortisol response to yohimbine. Arch Gen Psychiatry 1986 Sep; 43(9): 849-58 ↩
- Segal, K.R., et al. Independent Effects of Obesity and Insulin Resistance on Postprandial Thermogenesis in men. J Clin Invest 1992; 89:824-833. ↩
- Marette, A. and Bukowiecki, L. J. Stimulation of glucose transport by insulin and norepinephrine in isolated rat brown adipocytes. Am J Physiol Cell Physiol 1989; 257: C714-C721. ↩
The Real Bathroom Scales
In The Biggest Medical Myth of All Time and The Calculus of Calorie Counting, we examined research exploring the futility of low-calorie dieting and exercise as methods of long-term weight loss. In this post, we’ll delve into a few more specifics on how our bodies actually react to alterations in calorie intake. “The lean ‘n hungry type” Besides a flashback to a musical era I’d just as soon forget, the phrase “lean and hungry” has been used in obesity research to describe those naturally thin folks who have difficulty gaining weight, no matter how much they eat—much like Sims’ prisoners in Medical Myth. That such a type exists at one end of the body-fatness spectrum is rarely denied by medical science nowadays, though it’s generally assumed that those folks are some sort of natural super-athletes who are always engaging in sports and exercise activities. As Sims’ research showed, however, that assumption is incorrect; these folks stay thin even if they sit around with a TV remote growing out of their arm. In fact, a 1985 study analyzing data from the National Health and Nutrition Survey (NHANES) examined the relationship between ordinary dietary intake and body weight and showed the distinct lack of positive correlation there. The NHANES gathers information about the diet and exercise habits of the entire U.S. population via a statistical sampling method. The data is collected by experienced interviewers, trained to request information in multiple forms, so that the validity of the responses can be verified. In other words, it’s as reliable as self-reported data can be. The following chart displays results for caloric intake by relative weight class (as a percentage of ideal body weight) for adult men and women. As you can see, it appears that the leannest individuals actually eat the most. Even if you have doubts about self-reported intake, it’s pretty clear that weight is not proportional to consumption; that is, people who are 30, 40, or 50% above normal weight eat nowhere near 30, 40, or 50% more than their lean ‘n hungry counterparts. So how are variations in caloric intake actually dealt with by our bodies? “A calorie is a calorie is a calorie…NOT!” In Calculus, we looked at each of the elements that make up daily energy expenditure, culminating in the equation: Total Energy Expenditure (TEE) = Resting Energy Expenditure (REE) + the Thermic Effect of Food (TEF) + the energy expended in activity, exercise (EE) and non-exercise (NEAT). The response of each of these elements to a situation of extended overnutrition was explored in a 1998 Mayo Clinic study. In this study, sixteen weight-stable, non-obese subjects had 1,000 extra calories added to their daily diet for eight weeks, while simultaneously agreeing not to engage in any exercise outside of normal daily activities (that is, EE=0). Traditional wisdom holds that the human body has a relatively fixed rate of energy expenditure, like a car, so any major change in intake would automatically be converted to added body mass, mostly fat. In this situation, that would be: 1,000 extra calories X 56 days, divided by 3,500 calories per added pound = 16 lbs of added mass. Even if we refine the calculation to allow for 10% of the calories to be used in food processing (TEF), we’re still looking at more than a 14 lb. gain. In theory. In reality, the researchers found two things. One, the average weight gain was considerably less than predicted, and two, the pattern of weight gain varied greatly between individuals and depended largely on changes in NEAT and TEF. The average gain was 10.4 lbs, only half of which was fat (5.26 lbs), with one person gaining less than a single pound of fat. So what happened to all the “missing” calories? Well, that is precisely what these researchers were after. During the run-in period, when subjects’ intake and weight were stable, their energy expenditure variables were measured by the most reliable scientific methods available (doubly-labeled water, indirect calorimetry, etc.). The same was done at the conclusion of the study, and the comparison was remarkable. Total energy intake was increased by 35%, from 2,824 to 3,824 kcal/day, while total energy expenditure increased by just over half that amount, from 2,824 to 3,350 (18.6%), by the end of the eight weeks. If the subjects were not exercising (a fact verified by accelerometer use), how did their daily energy expenditure increase? The measurement processes showed the following: REE increased 4.8% for a total of 79 calories, which is about what we’d expect from the increase in body mass. Calories attributable to TEF increased by an impressive 62%, moving from 218 to 354 calories per day. And the calories burned in Non-Exercise Activity Thermogenesis (NEAT), changed from 913 to 1,224 per day, an increase of 311 kcal, or 37%. Thus, TEE, after eight weeks of eating 1,000 additional calories, was automatically raised by the body to the tune of 527 calories per day, or 53% of the increase in intake—the equivalent of a 4-5 mile walk. To summarize:
“Time in a bottle”
Now there are two points I want to make here. The first is that this study only looked at two time points—baseline and eight weeks. It would have been really nifty if the measurements had been taken weekly to show how the variables changed over time, and it would have been super cool to see what happened during the next eight weeks, but alas, research costs money, and there was no blockbuster drug at the end of this rainbow, so they did what they could. In all likelihood, the change in energy expenditure was a gradual adaptation over the study period, with most of the weight gain coming early and slowly decreasing, as seen in other studies, and if I make my guess, the energy expenditure rate would have continued to increase in the following weeks to the point that all the excess calories were being burned and no more weight was being gained.
My other point is with regard to the NEAT. As the researchers pointed out, despite the inter-subject variability in changes to energy expenditure, the change in NEAT correlated very tightly and negatively with the change in fat gain (R=-.7). That is, subjects whose NEAT increased the most gained the least. Contrast this with what we saw in the Thomas and Miller rat study in Calculus, where forced exercise was met with a concomitant decrease in NEAT. From these data, it can be surmised that NEAT is a primary defense mechanism against exogenous alterations in energy balance. Changes you make to diet and exercise will be countered with adjustments to NEAT—your body’s subconscious drive to fidget, wiggle, whistle, talk, laugh, dance, hug, kiss, and yes, even change the channel.
What we’ve shown here is that the difference in people’s weights has precious little to do with how many cheeseburgers we eat or how many marathons we run, but rather much to do with energy expenditure variables we cannot voluntarily control—TEF and NEAT. All we have proven so far is that when our bodies sense a surfeit or deficit in energy supply, they attempt to balance it with changes to both energy storage and energy use, the relative percentages of which are highly variable between individuals. But what makes some folks more prone to the storage side and others more prone to “use”? We’ll explore that question in my next post, Through Thick and Thin.
|Variable||Mean Change||%||Std Deviation||Minimum||Maximum|
|Weight Gained (lbs)||10.4||7.2%||3.8||3.1||15.6|
|Fat Gained (lbs)||5.3||N/A||2.5||0.8||9.3|
|TEE Change (kcal)||+527||+18.6%||+264||+107||+917|
|REE Change (kcal)||+79||+4.8%||+126||-100||+360|
|TEF Change (kcal)||+137||+63%||+83||+29||+256|
|NEAT Change (kcal)||+311||+37%||+276||-172||+696|
The Calculus of Calorie Counting
In The Biggest Medical Myth of All Time, we reviewed some of the evidence that losing excess body fat is not as simple as the supposedly tried-and-true formula of eating less and exercising more. And that’s because our bodies are not simple machines, like cars or televisions or the iPhone 3GS. In this post, we’re going to examine the calorie balance theory: Calories In – Calories Out = Fat Lost/Gained, and build an understanding of why we can’t fool our fat-o-stats with a step-aerobics video and a freezerful of Lean Cuisines.“The New Math” As far back as the beginning of the last century, scientists were questioning the simple calorie balance theory. In 1902, researcher R.O. Neumann, experimenting on himself, showed that his body could adjust to significant changes in caloric intake, with only minimal changes in weight. He theorized that the apparently lost calories were being given off as greater or lesser amounts of heat by his body, and called this phenomenon “luxuskonsumption” (luxury consumption).1 Since that time, the subject has been studied exhaustively, with both support and refutation for the idea that the human body can adjust to differing levels of calorie intake without fulling accounting for the ingested energy differential through changes in body mass and/or energy output. When you sift through it all, two conclusions seem irrefutable: 1) that our bodies do indeed have the ability to adjust to sustained alterations in intake, though not in the fashion Neumann first proposed, and 2) that the means and methods of accomplishing this task are highly variable between individuals. To begin understanding the real mathematics behind calorie balance, we need to understand the parts that make up our daily total energy expenditure—the “Calories Out”—because this is the piece over which we lack voluntary control. The acronyms and terms are constantly changing, but the currently accepted model for daily total energy expenditure looks something like this: TEE = REE + TEF + EEE + NEAT, where:
- TEE=Total Energy Expenditure.
- REE=Resting Energy Expenditure, the rate of oxygen consumption when fasting and completely at rest.
- TEF=Thermic Effect of Food, the increment in oxygen consumption seen just before, during, and after a meal.
- EEE=Exercise Energy Expenditure, the increment in oxygen consumption attributable to volitious exercise, such as jogging, playing hockey, etc.
- NEAT=Non-Exercise Activity Thermogenesis, all non-volitious activity over and above lying completely still.
Resting Energy Expenditure (REE)Much research has compared the REE between lean and obese persons, and, while slight differences are sometimes reported, for the most part, REE can be attributed to the maintenance of lean body mass—muscle, bone, skin, hair, etc. Even highly trained athletes don’t show a significantly higher REE than couch potatoes of the same size and body composition.2 When people alter their intake acutely for a short period of time, or modestly for a long period of time, however, the REE, when measured per unit of lean body mass, will show a commensurate adjustment, albeit a small one. Let me make that clear: if a person has dieted (or gorged) for a suitable length of time, he will burn a different number of calories at complete rest than will a person of exactly the same size and body composition who hasn’t altered his diet. Some studies will fail to show this, but likely only due to methodological differences (sample size, study length, measurement technique). As an example, in 2006, researchers showed that the metabolic rate of mildly overweight people during non-movement sleep (a decent proxy for REE) decreased after just three months of a 25% calorie deficit, created through diet alone or diet + exercise. In the graph, you see sleep energy expenditure (SEE) predicted from baseline SEE and three-month LBM, compared to the actual three-month SEE. The difference is small, but significant: 7.7% for the diet-only group, and 4.9% for the diet+exercise group. The difference persisted over the next three months, when the subjects were fed the amount necessary to maintain the three-month loss.
Thermic Effect of Food (TEF)Now here’s where things get interesting. As far back as the 19th century, scientists were fascinated by what was then called Specific Dynamic Action, the significant increase in metabolic rate that occurs when we eat and for several hours after. Early researchers observed that TEF varied with the size and composition of the meal and so logically drew the conclusion that TEF represented the energy cost of digestion and assimilation of the meal, which is how it is still often defined today. This isn’t entirely accurate, however. Researchers began to notice that there were significant variances in TEF between individuals, even when eating the same exact meal under the same circumstances. That fact suggested that TEF was not solely the processing cost of food. In fact, many studies found that TEF was consistently higher in lean vs. overweight folks, which led to explorations of what else might be involved in TEF. In a series of elegantly designed experiments, Dr. Karen Segal and her team showed that insulin resistance and body fatness are independently and negatively associated with TEF. In this image, we can see that insulin-sensitive, lean persons burn considerably more calories in response to a given meal than do insulin-resistant or obese persons, matched for LBM and RMR. Clearly, there is much we have to learn from studying TEF, even if it is a relatively small portion of our daily TEE, and I’ll get into that more deeply in another post.
Exercise Energy Expenditure (EEE) and Non-Exercise Activity Thermogenesis (NEAT)The calories burned as a result of activity over and above REE can be divided into Exercise Energy Expenditure (jogging, tennis, pilates, etc.) and Non-Exercise Activity Thermogenesis (showering, fidgeting, channel-changing). The former is pretty straight-forward; it’s basic physics: work = mass X distance and force=mass X acceleration. The distance you move something—like your arm or a barbell—through space, and the force you use to do so can be combined to calculate the calories burned in the process. Okay, there’s a bit more to it than that, as there are effects from exercise training and efficiency, and interactions with the fuel source (sugar or fat), but for the most part, moving a given weight a given distance at a given intensity has a set value, regardless of our body’s fat content. The same could be said of NEAT, except for one important difference. For most of us, EEE is the result of a willful, conscious act; whether we enjoy the activity or not, we make the decision to spend 30 minutes or an hour or the whole afternoon playing golf, painting the den, or using the elliptical trainer. NEAT is much more about unconscious movements—the number of times we get up and walk to the window to look outside, how often we feel the urge to head to the water cooler for a gossip-fest, whether or not we are drumming out our favorite song on our desk while reading email—in short, how inclined we are to fidget, pace, or otherwise “waste” energy. So why do we make this distinction? Because our inclination toward non-exercise activity is a key element in balancing the energy expenditure equation. Let’s look at some science behind that statement. A group of researchers at Mayo Clinic was given a great deal of credit for their research into the NEAT concept about a decade ago, but in reality, the idea of compensatory changes in NEAT goes way back to the mid-twentieth century. In a delightful study performed just down the road at UNC-Chapel Hill, a group of Sprague-Dawley rats (a strain of rat disinclined to high levels of activity) showed researchers what happens to NEAT when sudden changes are made in EEE. The scientists forced the rats to run on little rat treadmills for a specified distance and at a specified speed for the first three days of each week, then allowed them to rest the other four. This experiment went on for five weeks, and during the final week, spontaneous activity of the animals was measured during their non-exercise period and compared to matched controls. What the researchers discovered was quite fascinating. Spontaneous activity was greatly reduced on the three exercise days and modestly reduced on the four non-exercise days. That is, the forced increase in EEE was compensated for by an unconscious decrease in NEAT. Furthermore, following cessation of the experiment, there was a “persistent depression of spontaneous activity” for “a very considerable period of time”. The rats’ little bodies were battling back against the attempt to use a lot more energy than they were naturally designed for. “The dieter’s playground” So what is all this telling us? Well, the next time someone refers to weight loss dieting as a roller coaster, you can correct them—it’s not a roller coaster, or a merry-go-round, and it’s certainly not “The Fun House”. It’s more like a see-saw—the harder you push down on your end, the higher up you’re going to bounce when your body pushes back. In my next post, The Real Bathroom Scales, I’ll review a detailed example of how the elements of the energy expenditure equation respond to overeating in different body types.
- Neumann R.O. Experimental determination of human food requirements with particular consideration of essential protein need. Arch Hyg 45: 1–87, 1902 ↩
- Schulz, LO. Effect of endurance training on sedentary energy expenditure measured in a respiratory chamber. Am J Physiol. 1991 Feb;260(2 Pt 1):E257-61. ↩
The Biggest Medical Myth of All Time
Without a doubt, the greatest medical myth of all time is that obesity, or any degree of excessive body fatness, is the direct result of excessive food intake and/or insufficient exercise. Ask anybody. Literally. Ask 100 people, including scientists and health care practitioners, and 99 will tell you this. Ask 100,000, and 99,999 will give the same answer. The other one doesn’t speak English. Yet despite this widespread belief, there is no good research to back this up, and plenty of scientific evidence to the contrary. “Eat Less and Exercise More” I’ve heard it said that obesity must be the result of a caloric imbalance, because the First Law of Thermodynamics cannot be controverted, and indeed, this is the case. What people are failing to understand is that we cannot control our caloric balance via diet and exercise. Although we can adjust the amount of food we put into our mouths and how much physical activity we perform every day, our bodies determine what percentage of the available energy to use in the production of heat and physical energy and how much to store as fat. This is the real reason that overweight people often feel tired, sickly, and run-down—their bodies apportion input calories more in the direction of fat storage than energy production, and reducing calorie intake or increasing physical exercise only makes the situation worse. Let’s look at some numbers…or better yet, a few graphs (statisticians love graphs). Typical research studies on diet and exercise last three months. It’s considered a sufficient amount of time to measure significant changes in body parameters. Funny thing about three months, though—it happens to be just about the amount of time the average person’s body needs to completely adjust to a caloric imbalance. Here’s a graph showing what happened when a group of overweight people were treated with a medically-supervised, low-calorie diet, moderate exercise, and “behavior modification” program for longer than three months. I’ve looked at a lot of similar graphs over the years; the pattern is predictable—initial rapid weight loss, then slowing, then stopping. And all of this happens while still sticking to the original regimen. Of course, the diet “counselors”, friends, and family doubt that the patient is still sticking, but they shouldn’t. As numerous studies have shown, this is what will happen to 95% of overly fat people when a caloric deficit is created through diet and exercise. (We’ll cover the reasons why in another post.) So is life just not fair? Well, no, it is fair, because happily, the opposite relationship between caloric balance and weight also exists. That is, intentionally increasing caloric intake above current maintenance levels results first in rapid weight gain, then slower weight gain, and finally, weight maintenance at the new higher levels of both weight and calories. “Just push yourself toward the table!” Studies have shown that it is just as hard for an otherwise weight-stable person to gain beyond a certain level (~10% of current weight) and to “keep it on”, as the reverse. Notice the trend in this graph from an early study on the subject; weight is increasing, but less so with each passing week, and if one were to extrapolate (this study ended at 4 wks), it’s clear that the weight increase was approaching a level maximum. In what was probably the seminal study on the issue, E.A. Sims, an obesity researcher in Vermont, enlisted a group of naturally lean prison inmates to willingly overeat their way into obesity in order to study the effects of the disease as separate from the genetic factors that cause it. Well, much to his dismay, he found that, despite their best efforts—which included eating 6-7,000 calories a day and refraining from all work and exercise—the prisoners struggled to add and then retain the requisite 25% to their weights, even though they were eating 200% of their previous intake. One particularly lean fellow could never gain more than twelve pounds (9% of his initial weight) after months of stuffing his face and lounging around in his striped pajamas. In an alternate universe where “Weight Watchers” is a support group for overly thin people trying to bulk up, this poor guy would have been labelled lazy, undisciplined, and probably stupid, as well, for not doing what was needed to meet his weight goal. “Energy is neither created nor destroyed…” So now we might be agreed that diets do not continue to cause weight loss, but many would argue that they can still be used to cause some weight loss, which could then be maintained by eating a “normal intake” (which assumes the overweight eat more than the thin to begin with—an errorneous assumption to be dealt with another day). Well, as it turns out, even a brief period of reduced calorie intake will cause the body to adjust its current level of “energetic efficiency”—the rate at which calories are partitioned toward energy versus fat storage. Let’s see what happened when a group of rats decided to lose a few for bikini season. In a cleverly designed experiment by long-time obesity researchers Dulloo and Girardier, half of a group of young rats were put on a diet, while the others were allowed to eat whatever they wanted (the “ad libitum” group). The dieters were fed exactly 50% of what the ad lib group ate spontaneously, for a period of 30 days. At the end of that time, the dieting group was then matched to a third group of rats by both weight and body composition (that is, their total weight and percentage body fat were similar). For the next 25 days, the previously food-restricted rats were fed exactly what these similar-sized, non-dieted rats chose to eat naturally. If there was no adaptive mechanism, the two groups of animals would be expected to dispose of the calories in a similar fashion, but in fact, that was not at all what happened. Since they were young rats, they all gained weight during the 25 days of pair-feeding, but the gain and relative proportions of fat and lean tissue were vastly different, as the chart illustrates. The dieted rats gained the same amount of lean tissue, but more than twice the fat of their free-eating counterparts, on the same number of calories. This experiment clearly shows that the bodies of the dieted rats made not just minor, but rather gross adjustments to their calorie-burning efficiency and to the preferential deposition of lean and fat tissue. Thus, when dieters return to eating “normally”, where normal is the amount eaten by a person of similar size and body composition, they will lay down fat like nobody’s business. So what makes this seemingly implausible variance possible? That will be the subject of my next post, “The Calculus of Calorie Counting”.