Weight loss and biomedical health improvement on a very low calorie diet: the moderating role of history of weight cycling

Weight loss and biomedical health improvement on a very low calorie diet: the moderating role of history of weight cyclingAlthough weight-loss programs appear to result in significant short-term improvements in health, (1-3) only a small percentage (less than 25%) of individuals actually maintain their lowered weight over substantial time periods during the post-loss follow-up period. (4-6) As a result of widespread relapsing, a large percentage of dieters attempt numerous dieting programs and experience repetitive bouts of short-term weight loss followed by subsequent weight regain. This is commonly referred to as weight cycling or yo-yo dieting. Because of the high level of recidivism or negative rebounding, controversy has ensued about the desirability of losing weight only to regain it.

Results from a seminal study by Brownell et al. (7) suggested that history of weight cycling may adversely impact the outcome of future diets. In this early animal study, obese male rats with a history of weight cycling had more difficulty losing weight (2 times slower) when subsequently placed on a calorie-restricted diet. These yo-yo-dieting rats also regained their weight more quickly following the test diet than did their non-cycling counterparts. In a more recent animal study, Gerardo-Gettens et al. (8) studied obese female rats using a repeated-measures design and found a decrease in the amount of weight lost for the second weight-loss attempt as compared with the first weight-loss attempt.

Research studies of obese human participants have also found a reduced amount and rate of weight loss across consecutive weight-loss attempts, (9,10) suggesting findings based on animal models may be able to be generalized for humans as well. In this connection, the data are mixed. Other studies, for example, have failed to find an association between the history of weight cycling and greater difficulties in weight loss over the course of a particular treatment program. (11-14) Other studies involving humans have shown that a greater history of weight cycling may increase the probability and amount of eventual weight regain. (15)

Longitudinal studies consistently report a higher risk of mortality resulting from coronary heart disease (CHD) for individuals with a history of greater variability in their weight. This mortality effect of (apparent) weight cycling remains significant even after adjusting for age and other known CHD risk factors. (16-19) The physiological mechanisms underlying this increased risk and the extent to which these exaggerated levels of weight fluctuation were actually due to voluntary dieting efforts still remains unclear.

One proposed mechanism may be that repeated weight loss attempts may lead to reductions in metabolic rates that may render the body more efficient at storing fats, which in turn makes subsequent weight loss more difficult and regain easier. (20,21) In this connection, research shows that higher levels of body fat, especially in centrally located adipose tissue, can greatly increase the risk of morbidity and mortality associated with CHD. (22) Other supporting evidence comes from findings that indicate lower resting and exercise energy expenditure in samples of nonobese female cyclic dieters relative to nondieting controls. (23,24) However, successive decreases in resting metabolic rate were not evident in a prospective study of obese women followed over the course of 3 consecutive weight-loss and regain cycles. (10)

A second mechanism involves the suggestion that yo-yo dieting may promote the accumulation of higher levels of body fat. Such an association has been observed in weight cycling studies of rats (8,25,26) and normal-weight humans. (23,27) Also, in comparison to obese controls of stable weight, increased preferences for food with higher contents of sugar and fat have been reported in rats with a history of weight cycling (8) and in obese human weight cyclers. (28,29) There are inconsistencies in the literature, however, and it should be noted that no association has been found linking cycling to body fat in the vast majority of animal studies (30) or in samples of obese men and women. (14,31)

Yet another possible mechanism to account for the apparent deleterious health effects of repeated bouts of weight loss and regain may be that weight cycling contributes to alterations in serum glucose or lipid metabolism. (32) In this regard, Sea et al. (33) reported that weight cycling in rats resulted in significant alterations in measures of both lipid (serum cholesterol and triglyceride levels) and glucose metabolism (serum glucose, insulin, and glucagon levels). Similarly, Olson et al. (34) found that reduced levels of high-density lipoprotein cholesterol were associated with a positive history of weight cycling in a sample of 485 women at risk for CHD. There are some inconsistencies, however, given that earlier research with obese adults did not show that history of weight fluctuations (a proxy measure of weight cycling) was associated with disturbances in glucose tolerance or levels of total serum cholesterol. (31,35-37)

Finally, individuals with a positive history of weight cycling may be at elevated risk of CHD by virtue of the mediating influence of higher levels of blood pressure. Ernsberger and Nelson (38) reported that rats with a history of weight cycling had significantly higher systolic blood pressure than control rats without a history of cycling fed either a high sucrose or regular diet. However, other animal studies have been unable to replicate these results. (39,40)

Studies of the impact of weight cycling on blood pressure among human samples have also yielded mixed results. Kajioka et al. (24) employed a repeated measures design and reported significant elevations in systolic and diastolic blood pressure in nonobese young women subjected to a cycle of weight loss, regain, and subsequent loss. Recent prospective studies suggest that weight cycling may serve as a risk factor (or marker) for the development of hypertension among obese women. (41,42) In contrast, other research has failed to find associations between the history of weight cycling and hypertension in obese adults (35,36) and in mixed normal-weight and overweight samples of women (43) and men. (44)

Although longitudinal studies consistently report a higher risk of mortality resulting from CHD for individuals with greater variability in their weight, mixed results have emerged from existing research of authors who have attempted to pinpoint the possible physiological mechanisms for this increased risk. Inconsistent findings may be attributable to differences in sample characteristics (eg, age, sex, and starting weight), variable adherence to the treatment programs investigated, or heterogeneity in operational definitions of weight cycling or outcomes. (21,45)


In the present investigation, we sought to extend and refine previous weight cycling research that has examined clinical samples of obese weight loss patients. In particular, we examined the association of the history of weight cycling to a variety of treatment-related outcome measures in the context of an aggressive multifaceted weight-loss program based on a liquid supplemented fast. Refining previous human research involving clinical samples, we statistically controlled for a host of possible confounding factors--influences that are likely correlated with weight cycling. In particular, we sought to examine whether the medical health benefits of professionally assisted intentional weight loss are moderated by the history of weight cycling independent of (a) age, (b) gender, (c) preexisting medical conditions, (d) depression, (e) starting weight, and (f) treatment program adherence. Because previous studies have employed different means of assessing outcomes, we examined the effects of weight cycling history on treatment outcome using 2 commonly applied operations: (1) absolute and percent difference between baseline and post-treatment and (2) rate of change.