Why diets make you fat

To date, I have not heard back from her. No surprise there as pushing diets and the thin ideal sells more magazines than supporting Health At Every Size, but I will still hold out hope that she will write the story and enlighten her readers with the truth. Subscribe to Robyn's Newsletter! April 29, I will get to the details in a minute, but first, a story… Recently, a reporter put out a request for a Registered Dietitian to help her with a story she was writing about the pitfalls of dieting.

When you diet, you will lose weight, but eventually, it will come back on, and bring a few extra pounds with it. The more you start a diet, the higher your body will set your set point. Hence, dieting makes you fatter. Back to the reporter… To date, I have not heard back from her. What is Size Acceptance? April Anxiety, Fidgeting and Gadgets June October Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Your weight set point is a combination of several factors, including your:.

Weight set point and metabolism play for the same team: Your metabolism burns energy at a rate that will maintain your weight set point, even if that point is heavier than is healthy. Beware of the quick-fix, Dr. Griebeler warns. You can successfully lose weight for a while, but at some point, your body simply adjusts to need fewer calories to function. Which means weight loss will eventually stop, unless you start eating even less than your diet calls for.

You can see where this is going. Your body is also a survivor. As soon as calories drop, it starts doing everything in its power to prevent starvation, including:. These effects stick around for the long-term. Remember the television show The Biggest Loser? As smoking status remained stable from 16 to 18 years, 17 baseline smoking was assessed based on information at 18 years and if this was missing, answers from 16 and 17 years were used.

Information on the frequency of eating breakfast every morning, about 3—4 mornings a week and once a week or less often was obtained at all ages, but used only at 16 years. Father's socio-economic status at twin age 16 years was determined based on questions concerning occupation, employment and education. Socio-economic status was classified into five categories white collar, blue collar, manual worker, self-employed and farmer by following the criteria of the Finnish Classification of Socio-economic Groups.

All statistical analyses were performed by using the Stata statistical software 9. Differences in the rate of weight gain between IWL groups were tested by using linear regression models.

Then, an additional term of the interaction of age with IWL group was added, and the change in fit between models was assessed by using a likelihood ratio test.

The ORs for having become overweight at 25 in previously non-overweight subjects by IWL categories was assessed by using logistic regression models that controlled for the same confounding factors as listed above. The effect of the twin-sampling design on standard errors was taken into account in the individual-level analyses by computing robust standard errors by using the cluster option in Stata.

In MZ twins, the differences within pairs are by definition independent of genetic factors. As DZ twins share half of their segregating genes, differences within pairs are partially but not fully adjusted for genetic factors.

In both zygosities, the co-twins are matched for age and most environmental factors in utero , and in childhood and same-sex twins also for gender. The prevalence of overweight was similar in females and in males at age 16 years, but after age 18, males were significantly more overweight than females Table 1.

In a multivariate analysis using BMI, physical activity, smoking, breakfast eating, parent's BMI and father's socioeconomic status at baseline, growth in height from 16 to 18 years, age of menarche in females and number of children at 25 years as confounding factors, the odds for having at least one IWL was higher in males and females who had higher BMI at 16 years, smoked daily, skipped breakfast and were in the blue collar in females also self-employed socioeconomic group Table 2.

BMI The effects were especially large in those with the greatest BMI at baseline. Males gained much more weight than females, especially when the baseline BMI was low. The risk of becoming overweight by 25 years in the initially non-overweight participants was proportional to the IWL frequency.

Males with one OR 1. Adjusting for the possible confounders and baseline BMI did not change the result. Of the confounders, BMI at age 16 years highly significantly and independently predicted the risk of overweight at 25 years in the models in both genders. Further, in females, low physical activity at 25 years, low socio-economic status and father's overweight also predicted the risk of overweight Table 3. Next, we used the co-twin control approach to examine the effects of weight loss on later weight development adjusting fully in MZ; Figure 3a or partially DZ twins; Figure 3b for genetic effects.

Further, in opposite-sex twins, we studied the effects of gender on weight loss and BMI development Figure 3c. Twins with a history of IWLs were heavier at all ages for example, 2. At the age of 16 years, the weights of the co-twins of these pairs were similar. By age 25 years, co-twins with IWLs were slightly but significantly 0.

In the opposite-sex DZ twins, males gained more weight than females in pairs where co-twins were concordant for IWL Figure 3c. In IWL-discordant pairs, we examined the results separately by the gender of the dieting twin. Compared with their male co-twins, female twins with IWLs were 1. In discordant pairs where the male had a history of IWLs, male twins were consistently much heavier than their twin sisters: 2.

The results presented above show that twin pairs where both co-twins have IWL episodes are heavier throughout their adolescence and young adulthood than pairs where neither of the co-twins had IWLs. Such group differences may depend on an underlying genetic background, where the group, which later ends up experiencing IWLs, is in fact heavier and more susceptible to obesity in the first place.

Further, the fact that in the DZ twins co-twins who had IWLs were clearly heavier already at age 16 than their non-IWL twin pair members would suggest that the need to diet only arises in co-twins who are more genetically predisposed to obesity. BMIs In pairs discordant for IWL, mother's The physical activity of subjects with and without IWLs differed only slightly at age16 and no differences were found at 25 years data not shown. Among females with IWLs, those who were physically passive at age 16 gained more weight 3.

Passive females also had an increased risk of becoming overweight Table 3. This was not observed in males. Our findings of a dose-dependent association between the number of lifetime weight losses, gain in BMI and risk of overweight in a large population-based twin cohort with a follow-up from adolescence to young adulthood confirm the results of several previous studies. The novelty of the present study was its ability to distinguish between genetic and environmental influences on the dieting-induced weight gain.

These results suggest a causal relationship, although clinically modest in magnitude, between IWL and subsequent weight gain. The weight loss pattern of weight-discordant DZ twins suggests that dieting may be a response to predisposition to obesity.

DZ twins who had tried to lose weight were significantly heavier already at age 16 and remained so at 25 years as compared with their co-twins who had no history of weight loss.

Further evidence for the genetic underpinning of weight gain and subsequent efforts to control weight by dieting came from MZ and DZ pairs where both co-twins had frequent IWLs: These twins had identical weight development at a much higher level than those pairs in which neither co-twin had ever lost weight.

Inherited predisposition to higher weight in the dieters was also confirmed by the fact that twins with a history of IWL had heavier parents than twins with no dieting history. There are several possible non-genetic explanations for why short-term success in weight loss may turn into long-term failure. The psycho-physiological explanation suggests that restricted eating may lead to an increase in the sensation of hunger and overeating as a physiological response to restore body energy stores.

This phenomenon was first illustrated in in the classic Minnesota Starvation Study, 26 where 36 normal-weight men were given a restricted diet providing only half of their caloric needs for a 6-month semi-starvation period. This pattern of behaviours with overeating continued in the rehabilitation phase with restoration of the energy needs, and have been observed also in later studies of adolescents 11 and adults.

Therefore, some patients choose to starve occasionally rather than follow an energy-deficient diet regularly—a fact that maintains the weight loss—regain cycle. Recurrent weight losses and weight cycling have been proposed to exacerbate obesity by increasing metabolic efficiency both in animals 29 and in humans.

Thus, the detrimental effects of weight loss seem to be most significant in initially normal-weight subjects. Studies to date do not unequivocally support the theory that energy expenditure is permanently depressed by dieting, 35 , 36 nor do they provide a biological explanation for why recurrent weight loss attempts paradoxically seem to lead to subsequent weight gain.

One important factor not addressed in previous studies is genetics. It is well known that susceptibility to obesity is partly determined by genes, as are body weight and composition changes. We also found evidence that dieting may promote weight gain independent of genetic effects in weight loss-discordant MZ pairs, although such effects are probably very small.

However, given the well-documented high failure rate in weight maintenance and the observed potential of excessive regain, special efforts are clearly warranted to ensure improved and sustainable outcomes.

This could reduce the pressure for excessive repeated dieting and counteract the obsession with weight loss that may in part be responsible for the current obesity epidemic. Weight cycling has been shown to predict subsequent weight gain and the risk of obesity even in the athletes. However, the group best protected from long-term excess weight gain was athletes without weight cycling 3. Thus, weight loss strategies, which combine physical activity, may prevent subsequent weight re-gain.

The advantages of physical activity were shown in a recent study, where none of the dietary approaches alone predicted weight change; however, in combination with frequent exercise, limiting portion sizes proved to be the most successful strategy for weight gain prevention.

Among sedentary subjects, risk alleles are associated with weight gain, but among physical activity subjects, the same risk alleles predict weight loss. Thus, there is a complex interaction of genetic predisposition and physical activity in the trajectory of weight over time. In summary, our results suggest that one important explanation for the poor long-term success in dieting is genetic susceptibility to weight gain. The findings in MZ twins suggesting that dieting per se is associated with later weight gain even independent of genetic effects merit further studies.

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