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A year later, blood samples were collected from the patients for analysis of fasting and postprandial levels of ghrelin, leptin, peptide YY, amylin and other hormones. The dieters had lost an average of 30 pounds during the initial intervention, and then gained back about a dozen pounds over the months that followed, when they were given advice on healthy nutrition and exercise habits, but were allowed to eat as they liked.
Their endocrine markers showed a similar acute effect, followed by a partial rebound. Levels of the satiety-inducing hormone leptin, for example, initially dropped by almost two-thirds during weight loss when they were on the calorie-per-day diet, but remained more than one-third reduced one year later, after all those months without dietary supervision. Similar patterns were seen for the other assays: across the board, it looked like dieting induced a rapid shift in hormone levels that would tend to favor increased appetite and thus weight gain ; and this effect would not return to baseline even after many months had passed.
Again, there was some murkiness regarding cause and effect. But the hormonal changes could just as well have followed from the weight loss. Leptin levels in the plasma are known to drop during a very low-calorie diet, as well as when a person has been shedding fat. Contestants on The Biggest Loser , for example, saw their concentrations founder by almost 95 percent over the course of the weight-loss competition.
That changes such as these might still be detectable, to some degree, 12 months down the road could just as well reflect the fact that the patients had maintained some degree of weight loss across that time, too.
A more comprehensive theory of weight regain, accounting for a broad array of mechanisms, may help address some of the confusion in this field. Researchers Marleen van Baak and Edwin Mariman of Maastricht University, for example, have proposed that the compensatory reflex begins with changes to the shape of fat cells.
As these cells drain and shrink, their membranes pull away against the points of adhesion to the nearby extracellular matrix, creating mechanical stress. According to their preliminary model, which is based on both in vitro studies of adipocytes and examinations of protein expression during and after weight loss, the mechanical tension that shedding weight creates at the fat-cell membranes inhibits further fat release and primes those cells to be filled again.
At the same time, they theorize caloric restriction may deprive adipose tissue of the energy it would need to relieve this stress through remodeling of the extracellular matrix. This was followed by a brief weight-stabilization period in which they received about as many calories as they would need to keep a constant weight and then further check-ins for the next nine months.
The team took biopsies of adipose tissue at the end of each study phase, measured changes to its gene activity, and checked to see which, if any, might be correlated with weight regain.
In a subgroup analysis of the crash diet participants, 15 genes related to the extracellular matrix were identified, and 8 more associated with stress response. Others are looking for answers in the genome. But a genome-wide association study to determine whether genes that have been linked to the development of obesity might also be predictive of weight regain failed to turn up any positive results. That could be on account of its insufficient sample size, McCaffery explains.
The study had about 3, people in the weight-loss condition, whereas similar studies of the genetics of obesity have been far larger in scope. For one, many participants self-reported their weight by phone or mail rather than having their weight measured on a scale by an impartial source. Also, the studies have very low follow-up rates — eight of the studies had follow-up rates lower than 50 percent, and those who responded may not have been representative of the entire group, since people who gain back large amounts of weight are generally unlikely to show up for follow-up tests, Mann said.
One study found that both men and women who participated in formal weight-loss programs gained significantly more weight over a two-year period than those who had not participated in a weight-loss program, she said. In several studies, people in control groups who did not diet were not that much worse off — and in many cases were better off — than those who did diet, she said. Exercise may well be the key factor leading to sustained weight loss. Studies consistently find that people who reported the most exercise also had the most weight loss.
Diet studies of less than two years are too short to show whether dieters have regained the weight they lost, Mann said. One study of dieting obese patients followed them for varying lengths of time. Among those who were followed for fewer than two years, 23 percent gained back more weight than they had lost, while of those who were followed for at least two years, 83 percent gained back more weight than they had lost, Mann said.
One study found that 50 percent of dieters weighed more than 11 pounds over their starting weight five years after the diet, she said. Evidence suggests that repeatedly losing and gaining weight is linked to cardiovascular disease, stroke, diabetes and altered immune function. Mann and Tomiyama recommend that more research be conducted on the health effects of losing and gaining weight, noting that scientists do not fully understand how such weight cycling leads to adverse health effects.
Mann notes that her mother has tried different diets, and has not succeeded in keeping the weight off.
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