Evidence Unlinking Fat From Obesity

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A number of observational studies have suggested that the role of fat in obesity development may be exaggerated, and suggest that the population differences in weight do not appear to be due primarily to the fat intake (30). For instance, in a recent literature review, it was found that short-term hy-pophagia on low fat diets is compensated in the longer term (18). A report from the National Centre for Health Statistics has shown that Americans today eat less fat but more calories than earlier, a finding that may explain the rise in obesity, but acquits the role of fat (31). In addition, results from prospective observational studies give inconsistent results, and do not support the relation between a high fat intake and subsequent weight gain. Klesges et al. (32), for instance, found a clear positive association between dietary fat and subsequent weight changes, while Colditz et al. (33), using the same dietary instrument, and Kant et al. (34), using a different instrument, could not find such an association. Other studies have also shown inconsistent results (35-37). Indeed, Katan (38) recently reviewed the literature on long-term fat trials, and found that low fat diets in these trials had resulted in decreases in body weight of only 0.4-2.6 kg relative to control diets. Based on this, he concluded that the evidence from the long-term trials could not support the idea that a high proportion of fat in the diet could be responsible for the 10-15 kg weight gain that people in affluent societies experienced between adolescence and middle age.

Results from feeding studies in humans, with covert manipulation of energy density in the diet, suggest that increase in the fat content does not result in an increase in energy intake, when density is constant (39). Also Stubbs et al. (40,41) manipulated macronutrient intake in iso-caloric diets and found that the energy density of the diet was dissociated from the fat content, since spontaneous energy intake remained unchanged as the fat increased from 20% to 60%.

In experimental animals, Ramirez and Friedman (42) demonstrated that increasing the energy density of the chow food led to an increase in energy intake, but did not affect the weight of the food eaten. Results like these suggest that fat is only less satiating than carbohydrate if the energy density is tied to the fat content, and hence, challenge the specific role that has been attributed to fat in obesity development. Rather, results like these imply that it is the bulk, or the weight, of food that controls satiety. Indeed, Westerterp et al. (43) recently demonstrated that change in the fat content of the diet resulted in change in body composition only when energy intake was simultaneously changed, and several studies have found the weight of food eaten to be more constant than daily energy intake (20,22,44). Hence, an increasing energy density may result in passive over-consumption only because individuals habitually eat a constant weight of food per day (40,41).

Finally, it has been suggested that the benefits of decreasing the density of one meal, by removing selected high fat items from the diet, may be compensated by the inclusion of high fat items in a later meal (45). On the other hand, this leaves a greater potential for diluting diets, for instance with fibre. In fact, it may be argued that the benefits of a low fat diet with regard to obesity may depend not on the low fat per se, but on the accopanying high fibre content (Table 10.1).


Genetic susceptibility for weight gain may be influenced by dietary factors, such as fat intake (46). Indeed, a few studies have indicated that development of obesity is, in part, due to differential effects of fat in the diet for those who are genetically predisposed, compared to those who are not (47-49). In this context, studies in both animals and humans have demonstrated that food intake seems to play a specific role for obesity development in association with a predisposition to obesity (37,50,51). For instance, Sclefani and Assimon (52) found that obesity prone mice ate more high fat, but less sugar-rich foods than leanness prone mice. In addition, obesity prone mice have been found to gain weight at a much faster rate than wild-type mice fed the same high fat diets (50), suggesting a gene-environment interaction between the high fat diet and the subsequent weight gain. Furthermore, compared to non-obese controls, impaired ability to increase the fat/ carbohydrate oxidation ratio in response to a high fat diet has been suggested in post-obese women (51), implying that this obesity prone group is particularly susceptible to weight gain on such a diet. Although not all studies have been able to document gene-environment interactions relating a high fat intake to weight gain (53,54), a study using identical twins found that weight gain in response to controlled overfeeding was more similar within identical twin pairs than between pairs of twins, suggesting a specific genetic influence (47). Finally, the specific role of fat in obesity development may be restricted to those who are predisposed, only. This was the case in one study where women with a familial history of obesity had a stronger risk of major weight gain compared to women without such a predisposition, when consuming a high fat diet (37).

Several genes have been proposed, for instance

Table 10.2 Evidence for and against a genetic component

♦ Obesity prone mice have been found to prefer high fat diets.

♦ Weight gain in obesity prone mice is higher than in wild type mice fed the same high fat diets

♦ Subjects with a familial predisposition to obesity seem to have an impaired ability to increase the fat/carbohydrate oxidation ratio in response to a high fat diet.

♦ One study found that women with a familial history of obesity had a stronger risk of dietary fat-related weight gain compared to women without such a predisposition.

♦ Two studies found no evidence of a genetic predisposition for dietary fat-related weight gain.

lipid oxidation after consumption of a high fat diet may vary greatly among individuals, and may depend on both physiological and genetic factors.

Finally, the genetically determined ability to taste bitter substances relates to obesity and may also be associated to fat preferences. Obese subjects are less sensitive to the bitterness of phenylthiocarbamide, and hence, the gene that determines this bitter taste polymorphism may either have effects on both dietary fat perception and body weight, or be linked to genes contributing to these phenotypes (60) (Table 10.2).

the family of uncoupling proteins, apparently used by cells to convert excess calories to heat. These may provide insight into identifying subjects predisposed for obesity, since this gene is thought to be involved in overall metabolic rate. It may be that rodents with this gene have the ability to burn off excess calories, while animals without the gene store the extra calories. Furthermore, the gene seems to be activated by dietary fat, and the fat intake seems to play a differential role for activation of the gene in different strains of mice (55).

Lean and obese/obesity prone individuals seem to vary in their response to fat manipulation, since obese individuals have been found to compensate less well than lean unrestrained individuals for energy intake in response to preloads of varying energy densities (56). Furthermore, not only do obese subjects generally report liking high fat foods more so than lean subjects (57,58) they also may not be as sensitive to the satiety value of fat as lean subjects (20,59). Indeed, the literature suggests that the selection of macronutrients is, in part, heritable (60). For instance, obese rodents have been found to avoid sweets compared to their lean littermates, and genus that mediate the consumption of sugar have been mapped, and are being isolated and characterized. For sweet taste preference, major gene effects have been described, mapping studies of genetic loci have been published, and single-gene mutants have been discovered. However, only a few studies have assessed the role of genetic variability in dietary fat preference, but so far no genes have been characterized (60,61). In addition, it has been proposed that the development of obesity may be viewed as a regulatory mechanism by which the impaired lipid oxidation rate in the body is raised to match the dietary fat intake (27). This capacity to increase

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