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The Last 10 Pounds

by Kristine Clark, PhD, RD on Apr 01, 2004

Research Update

A scientific look at why the weight can cling so tenaciously

While the obesity epidemic affects thousands of individuals nationwide, scores of nonobese women and men struggle with their own battle against fat. They are doing all they can to shed the final 10 (or fewer) pounds that have plagued them over the years. These may be the same people who successfully lost 30 or more pounds over the course of several years but never quite managed to reach their desired weight. Researchers have begun exploring the more complicated side to weight loss and studying the biochemical pathways that control energy intake and expenditure.

I advise people on weight loss efforts every day and my goals are threefold: to encourage physical activity; counsel clients on reducing a portion of their total daily caloric intake (depending on their typical diet); and stress portion control. If a client has successfully lost weight by following a healthy lower-calorie eating plan plus exercising, simply sticking to the routine is often good advice. However, when a plateau causes cessation of weight loss and a frustrated client insists he is sticking to his diet and exercise program, what explanation can we provide?

New Research

Researchers are teaching us that weight loss is not just about energy balance. Losing that last 10 pounds may be complicated by complex signaling systems in the brain, intestines and hormones, as well as in the fat cells themselves, now considered part of the endocrine system. In addition our metabolic rate—the number of calories we burn—may adapt for a period of time by becoming slower.

In one study investigating how weight loss alters metabolic rate, researchers compared 24 weight-reduced women to 24 never-overweight women in two 10-day study periods (Weinsier et al. 2000). (The overweight women were previously studied over two 10-day study periods in a clinical research setting during their weight loss phase.) Once the weight-reduced women were matched to the never-overweight women, their resting metabolic rates (RMRs) were measured using indirect calorimetry (the subject reclines in a relaxed position and breathes into a machine that collects data on oxygen inhaled and carbon dioxide exhaled. These samples can be used to assess the number of calories burned at rest); their body composition was measured through hydrostatic weighing; and several thyroid hormones were tested.

The results of this study showed that for the overweight women, RMR and thyroid hormones fell during the entire energy restriction phase of weight loss but returned to normal once ideal weight had been achieved and energy intake had been normalized (because energy balance had been restored). In addition, once the weight-reduced women had achieved energy balance, their RMR values were not significantly different from those of the never-overweight women. The researchers concluded that “energy restriction produces a transient hypothyroid-hypometabolic state that normalizes on return to energy-balanced conditions.”

From an application standpoint, this study indicates that during weight loss over time, metabolic adaptations take place. As a result, weight loss will not be consistent. During some point in the weight loss process, clients may get frustrated and either quit exercising or stray from their reduced-calorie programs, feeling “it’s not worth it.” If energy balance helps normalize metabolism, it’s arguable that perhaps it is advisable for these clients to stick with their basic programs, but possibly even add more calories (500 to 1,000, depending on the number of calories they are currently consuming).

One of my clients provided a strong example of how this works. Marlon lost all but 6 pounds to reach his goal weight by both cutting back on calories and being more consistent with his running (5 miles daily). When he consulted me about the plateau he was experiencing, his carefully recorded food logs revealed a 649 calorie per day diet! I explained that he was underconsuming energy and needed to increase his calories by approximately 1,000 per day to begin losing weight again. Although this approach is not precise, the concept of needing more calories proved accurate in this case. Within one week Marlon reported a weight loss.

A research article by Dr. Rudolph Leibel (2002) suggests that how we eat may influence weight loss. Leibel pointed out that the way the body controls food intake is affected by meal frequency and meal size, with meal size playing the predominant role. Studies evaluating why meal size matters have found that once food is absorbed, a series of digestive signals from the small intestine (such as cholecystokinin, in response to the presence of food, or glucagon-like peptide) interact with chemical signals that signal the brain (such as leptin or estrogen). These integrated systems of signaling appear to influence hunger and satiety, leading to decisions about meal termination.

Melanocortin, Leptin and Ghrelin

Research has shown that three bodily systems influence weight loss. Cells throughout the human body communicate with each other through hormone, enzyme and neurotransmitter systems.


The body’s ability to make or lose adipose (fatty) tissue may be dependent on cell-to-cell communication. The melanocortin system appears to be one of the critical pathways in controlling human obesity. As a signaling molecule, this complex protein structure seems to play a key role in the central nervous system’s control of eating behavior and calories burned during exercise. (Yang & Harmon 2003).


Leptin, known as the “satiety hormone,” is produced by fat cells and appears to regulate body fat. Leptin circulates as a protein in human plasma, providing feedback to the hypothalamus (the “appetite center”) regarding body fat stores. Low leptin levels result in reduced metabolic rate, increased hunger and food intake, and reduction in immune function. Leptin levels appear to decrease after weight loss in humans, which may partially explain the difficulty of maintaining weight loss (Friedman 2002).

When weight loss occurs, leptin levels fall. This stimulates a starvation response, which can trigger an increase in food intake, a reduction in energy expenditure and decreased body temperature. Conversely weight gain triggers higher leptin levels, which stimulates decreased food intake and increased energy expenditure. (For more information, see “The Lowdown on Leptin,” IDEA Health & Fitness Source, April 2003, pp 31-35.)


Like leptin, ghrelin (pronounced grr-hel-in), the “hunger hormone,” is produced largely in the stomach. Several studies have shown that in dieting humans, plasma levels of ghrelin increase, stimulating appetite and the desire to eat more. Ghrelin levels appear to be high before a meal and then taper off after eating. If calories are too low, ghrelin levels remain high, conserving body fat and weight (Cummings et al. 2002). Both of these mechanisms act as the body’s attempt to maintain homeostasis and protect the body. The body cannot distinguish between purposeful weight loss and starvation.

What Lies Ahead?

As more mechanisms influencing weight loss are understood, strategies for losing those last few pounds should be revealed. For now we are not sure how these added factors can be manipulated to achieve weight loss goals. In the meantime, guiding clients on exercise frequency, intensity and duration as well as encouraging adequate, but reduced, calorie intake through a well-balanced, varied diet is worthwhile. In addition it never hurts to remind our clients—and ourselves—that no matter how much new information researchers reveal on this topic, 1 pound of weight will always equal 3,500 calories, muscle burns more calories than fat and perhaps the last few pounds may not be that important to lose.

Kristine Clark, PhD, RD, FACSM, is director of sports nutrition for the athletic department at Pennsylvania State University. She is also the nutritionist for the U.S. Soccer Federation, U.S. Olympic Women’s Soccer Team and U.S. Olympic Women’s Field Hockey Team.


Cummings, D.E., et al. 2002. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery.

New England Journal of Medicine, 346 (21), 1623-30.

Friedman, J.M. 2002. The function of leptin in nutrition, weight, and physiology. Nutrition Reviews, 60 (10),


Leibel, R.L. 2002. The role of leptin in the control of body weight. Nutrition Reviews, 60 (10), S15-9.

Weinsier, R.L., et al. 2000. Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. American Journal of Clinical Nutrition, 72, 1088-94.

Yang, Y.K., & Harmon, C.M. 2003. Recent developments in our understanding of melanocortin system in the regulation of food intake. Obesity Reviews, 4, 239-48.

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About the Author

Kristine Clark, PhD, RD

Kristine Clark, PhD, RD IDEA Author/Presenter

Kristine Clark, PhD, RD, FACSM, is director of sports nutrition for the athletic department at Pennsylvania State University. She is also the nutritionist for the U.S. Soccer Federation, U.S. Olympic Women’s Soccer Team and U.S. Olympic Women’s Field Hockey Team.