Physiology of Fat Replacement and Fat Reduction: Effects of Dietary Fat and Fat Substitutes on...

May 1998: (ll)S29549

Physiology of Fat Replacement and Fat Reduction: Effects of Dietary Fat and Fat Substitutes on Energy Regulation Susan B. Roberts, PhD, TuRs University, Boston MA(Co-chair); F. Xavier Pi-Sunyer, MD, St-Luke's Roosevelt Hospital, Columbia University9 New York NY (Co-chair); Mark Dreher, PhD, Nabisco Foods Group, East Hanover NJ; Robert Hahn, JD, MPH, Public Voice for Food and Health Policy, Washington DC; James 0. Hill, PhD, University of Colorado, Denver CO; Ronald E. Kleinman, MD, Massachusetts General Hospital, Boston MA; John C. Peters, PhD, Procter & Gamble, Cincinnati OH; Eric Ravussh, PhD, National Institutes of Health, Phoenix AZ; Barbara J. Rolls, PhD, Pennsylvania State University, University Park PA; Elizabeth Yetley, PhD, Food and Drug Administration, Washington DC; Sarah L. Booth, PhD, Tufts University, Boston MA'

w

Introduction

Excess dietary fat has been hypothesized to be a risk factor for the development of numerous chronic diseases, including obesity, certain types of cancer, cardiovascular disease, hypertension, and diabetes.' In the case of obesity, excess fat intake is widely assumed to be one of the most important environmental factors, exerting its effect on energy balance through an influence on energy intake and possibly also on energy

The purpose of this review is to evaluate data from epidemiologic studies and clinical trials on the effects of dietary fat and fat substitutes on obesity and energy regulation, and to relate these data to current theories on the effects of dietary fat on energy regulation. These results will then provide a theoretical framework that can be used to examine the effects of fat-modified foods on energy regulation and body fatness. Fat-modified foods will also be examined in terms of their effects on fat-soluble vitamin status.

Dietary Fat and Energy Regulations

Theoretical Models for Effects of Dietary Fat on Energy Regulation Until recently, our understanding about the cause of differences in body fat mass ,between individuals has been primarily influenced by the guiding principle of energy balance:

Energy Stored = Energy Intake -Energy Expenditure. Thus, it has been recognized that high levels of body

fat (i.e., energy) must be accumulated as the result of en-

ergy intake being unusually high or energy expenditure being unusually low, or a combination of these two op- tions.

As an extension of the energy balance principles de- tailed abwe, it has been recently suggested that body' carbohydrate balance may play a critical role in overall energy regulation? The basic principle behind this theory, which is in keeping with the glucostatic theory of energy reg~lation,~ is that balances of the primary energy substrates-fat and carbohydrate-have to be considered ~eparately:~

Fat Stored = Fat Intake -Fat Oxidation, and Carbohydrate Stored = Carbohydrate Intake

- Carbohydrate Oxidation. Because the energy in carbohydrate stores is very

small in relation to that in fat stores, the carbohydrate stores have a high turnover rate and are liable to be de- pleted quickly and frequently. The essential requirement of key tissues for glucose suggests that signals should exist to efficiently monitor and correct body carbohydrate balance. An extension to this theory of nutrient regulation is that dietary macronutrient composition may play an important role in determining body fat content." The higher the dietary fat content, the more total food (and energy) must be consumed to maintain carbohydrate intake and therefore carbohydrate stores, and the fatter the individual will be because of increased energy intake. Flatt4 has also suggested that the increase in body fat induced by a high- fat diet may be self-limiting, because reduced insulin sen- sitivity and increased circulating free fatty acids tend to occur with increased body fat content. This promotes in-

'Reprint requests to Sarah L. Booth, PhD, Tufts University, 71 1 Washington St, Boston MA 021 11-1525.

Nutrition Reviews, Vol. 56, No. 5 S29

creased fat oxidation and preservation of carbohydrate stores, resulting in a stabilization of hunger and satiety signals &om body carbohydrate and stability of food intake and body fat stores. This model is entirely consistent with the hypothesis and data of fried ma^^^.^ suggesting that the regulation of body weight may occur through the control. of food intake, which is in turn influenced by the metabolic availability of primary substrates: glucose and free fatty acids (FFA).

Support for the importance of nutrient balance in the overall regulation of energy balance can be derived from several sources. Of critical importance is Flatt’s4 work with mice demonstrating that energy balance is indeed adjusted on a day-to-day basis to maintain stable body carbohydrate balance through adaptive fluctuations in food intake. Studies in humans have indicated that carbohydrate balance may be more closely regulated than fat balance,*S9 while animal studies have repeatedly demonstrated that hyperphagia and obesity can be induced in many strains of normal-weight rodents by the feeding,of a high-fat dietOL0J1

Observational Studies of the Relationship Between Dietary Fat and Obesity Comparisons of diets and the prevalence of obesity between affluent and poor countries have been used to support a causal association between dietary fat and obesity.12 There are very few populations around the world who eat a low-fat diet and yet have a significant problem with obesity, which supports the suggestion that consumption of low-fat diets may be protective, while high- fat diets may promote obesity. However, these contrasts could be confounded by differences in food availability9 physical activity, cultural differences in eating patterns, and a genetic predisposition to obesity. l3

However, body fatness is typically negatively corre- lated with energy intakes in the same studies, while at the same time there is increasing underreporting of energy intake with increasing body fatness.14J5 Thus, reports of a positive association between dietary fat and body fat within population groups are confounded by the accu- racy ofreporting by fatter individuals. The extent to which the observed associations are valid will depend on whether the macronutrient composition of the unreported food is the same as or different from the reported foods.

Trends in fat consumption and body fatness over time are also of interest when examining the relationship between dietary fat and obesity. The U.S. National Health and Nutrition Examination Surveys (NHANES) I, 11, and I11 data indicate a substantial decline in the percentage of energy from fat during the last two decades16parallel with a considerable increase in the prevalence of obesity.17 However, these declines in percentage energy from fat have occurred in the context of increased total energy

intake and decreased physical activity, with the total intake of fat remaining constant. For these reasons, the NHESMANES data may be of limited value for evaluating any causal associations between dietary fat intake and excess body weight. Similarly, data from developing countries continue to show that both obesity and dietary fat are increasing. However, other dietary changes, together with declines in physical activity, are also occur- ring simultaneously with increases in dietary fat intake.18

Clinical Trials of Dietary Fat and Energy Regulation Effects of dietary fat on energy intake. Randomized clinical trials may be a preferable method for evaluating the effect of dietary fat on adiposity. Several investigators have examined voluntary energy intake in response to alterations in diet composition. The results, obtained in studies of 1 to 14 days duration, show that access to high- fat (hence, low-carbohydrate) diets generally leads to a higher total energy intake than access to low-fat diet^.^^^^

There have also been several trials examining the effects of dietary fat content on energy intake and/or body fatness over 1 year or longer (Table 1). In these studies, reductions in fat consumption within the range of 18% to 40% of energy intake typically result in a modest 1 kk to 3 kg reduction in body fat, an amount comparable to that seen in many of the short-term studies described above.

The reason for the perhaps surprising finding of similar weight reduction in both short-term and long-term trials of dietary fat and energy regulation is not known. One possible explanation is that dietary fat has only transient effects on energy intake, resulting in the same response when measured in short-term and long-term investigations. However, it is also possible that there is a lower degree of compliance in the long-term studies and that larger effects could potentially be seen with better control of various study parameters. It is additionally possible that the body’s energy regulation mechanisms act to prevent weight loss better than weight gain.26 If this is the case, the long-term trials of lower-fat diets and energy regulation may not reflect the true magnitude of which dietary fat promotes weight gain, even if they accurately reflect the long-term effects of fat reduction on energy intake and energy regulation.

There have also been a large number of studies in which subjects have been instructed to reduce the percentage fat in their diet, without any specific advice on reducing total energy intake. A weight loss of approximately 0.3 kg of weight loss for every 1% reduction in dietary fat has typically been reported in studies of overweight subjects, and the amount of weight loss appears to vary directly with the reduction of dietary fat.27-3’ There have also been several studies of the impact of an ad libitum low-fat diet on body weight in normal weight sub-

S30 Nutrition Reviews, Vol. 56, No. 5

Table 1. Dietary intervention Studies with Ad Libitum Intakes Greater than 2 Months

Normal weight subjects Sample Sue A in % Fat Energy Duration Mean Weight Loss (kg)

Raben et al. (1 995) 24 37-+26 1 1 weeks 13 Sheppard et al. (1991) 171 39 + 21 6 months 32 Boyar et al. (1998) 20 36 -+ 22 6 months 13

Boyd et al. (1990) 100 37 + 21 12 months 1 .O

Siggaard et al. (1996) 50 39 + 28 12 weeks 3.4 Shahetal. (1991) 47 34+21 6 months 4.4

Bloemberg et al. (1991) 39 39 + 34 26 weeks 0.9

Gorbach et al. (1 990) 173 39 + 22 12 months 3.1 Overweight or obese subjects

jects. 32-4' These studies all produced some weight loss, but in general, it was modest and less than that seen in nonobese subjects subjected to comparable dietary regi- mens. It is important to point out that dietary intake in these studies was assessed by self-reporting. Since many subjects tend to underreport total energy intake, it is often difficult to determine whether subjects intentionally reduced total energy intake in addition to reductions in total fat intake. Furthermore, some of the studie; involved advice to increase physical activity so that is not possible to separate effects of dietary fat from effects of the combination of dietary fat and physical activity. For these reasons, these studies may tend to overestimate the effects of a change in dietary fat alone on energy regulation. This could help to explain the somewhat greater effects seen in comparison to the more carehlly controlled clinical trials.

Effects of dietaty fat on energy expenditure, substrate oxidation, and body composition when energy intake is held constant. Several investigators have also examined how dietary fat content influences body composition in- directly through energy expenditure, substrate oxidation, and macronutrient balance in humans under laboratory conditions. Whether and to what extent dietary composition affects energy balance is determined by its impact on energy expenditure as well as energy intake. For these reasons, studies of energy expenditure are an important component of any general understanding of the effects of dietary composition on energy regulation and obesity.

There are several studies in which diet composition has been varied while total energy intake was fixed at main- tenance levels. Liebel et a1.,42 Saltzman et al.,25 and Yost et al.43 all showed no significant effect of dietary fat content on daily energy expenditure. However, in the Yost subjects required an average of 156 kcallday more to maintain a constant body weight when eating a low-fat (20%) diet versus a high-fat (50%) diet. While the difference was not statistically significant, the magnitude is such that it could have an impact on body weight if confirmed in larger investigations with sufficient statistical power to detect that magnitude of a difference.

The effects of dietary composition on energy expenditure have also been investigated when energy intake is

above that required to maintain weight. One study by Horton et a1.44 demonstrated that significantly more energy is stored during overeating when the excess comes from fat rather than from carbohydrate. The same study also showed that carbohydrate overfeeding increases total energy expenditure to a greater extent than does fat overfeeding.

Several investigators have also examined the effects of varying the dietary fat content in energy-restricted diets on body weight and body As expected, there was no effect of diet composition on weight loss or reduction in body fat content during food restriction.

Dietary Fat Versus Energy Density Because fat is more energy dense compared to other macronutrients, it has the potential to profoundly influence the overall energy density of the diet. Thus, in addition to any specific metabolic effects of consuming energy as fat versus carbohydrate, and the effects of fat on diet palatability, some of the effects of dietary fat on energy regulation may be mediated by energy density.

In the studies described above, both the fat content and the energy density of the diets varied. In those studies, the greater the fat content and energy density, the greater the energy intake. Participants tended to eat a similar weight of food, regardless of changes in fat content andor energy d e n ~ i t y . 2 ~ ~ ~ ' J ~ ~ ~ ~ These studies raise the question of whether the effects of dietary fat on voluntary energy intake are entirely attributable to the high energy density of fat, or whether fat can promote excess energy intake, independent of its effects on energy density. Sev- eral studies have addressed this by independently manipulating the fat content and energy density of diets. When the fat content varied by as much as 40%, but energy density was held constant, the macronutrient content had no effect on food or energy intake.49s50J6 On the other hand, when the fat content was controlled but energy density varied, subjects ate a constant weight of food; therefore, the greater the energy density, the greater was the energy intake.*' Although energy intake was reduced on the diet of low energy density in this study, and

\ I

Nutrition Reviews, Vol. 56, No. 5 S3 1

also in other studies when diets were low in both fat content and energy density, in general, hunger was not increased.

Thus, some research suggests that energy density may be a more important determinant of voluntary energy intake than is dietary fat per se when the effects of fat on palatability are not controlled. The question of whether there may be subtle effects of dietary fat on appetite and energy balance that are independent of its contribution to dietary energy density remains c o n t r ~ v e r s i a l , ~ ~ ~ ~ ~ and further studies in this area are needed. Several methodologic issues are also important in consideration of studies in this area. In particular, it is possible that systematic manipulations of diets or of a range of foods may well pro- duce poorer caloric compensation than manipulations of specific meal^.^^,'^ Compensation appears to be more accurate in response to deficits than to increments in energy intake. Furthermore, the degree of food selection and the familiarity of those foods to the subject determine the degree of constraint that the dietary aspects of the experimental design place on the subjects’ behavioral response.

The Influence of Other Environmental Factors on the Relationship of Dietary Fat to Body Weight

e

The impact of high-fat, energy-dense diets on energy intake may also depend on the concomitant influence of other factors, especially exercise.56 Tremblay et al?’ reported that exercise may attenuate the hyperphagic effect of a high-fat, energy-dense diet in association with increased fat oxidation. The physiologic significance of changes in fat oxidation during exercise was confirmed in a subsequent study, which revealed that a reduced exercise respiratory quotient predicts a better capacity to be in negative energy balance after exercise.5s The implications of these findings have been examined in an epidemiologic conte~t.~~High-fat consumers are typically fatter than low-fat consumers, but when this comparison is controlled for differences in physical activity and alcohol consumption, the maximal difference in adiposity is found between individuals characterized by alcohol intake and physical activity rather than dietary fat.

Taken together, these observations suggest that variations in fat intake can affect daily energy intake and balance. Moreover, the overall impact of variations in fat intake on fat and energy balance may potentially be accentuated or attenuated by other environmental factors that have the potential to promote better weight control.

Genetic Susceptibility to High-Fat Diets It is well accepted that, in addition to environmental factors, genetic factors also influence body fatness.60 One recent review of the data suggested that as much as 40% to 50% of between-subject variability in body fat may be genetically determined.6’ It is possible that some of this

apparent individual susceptibility to fatness may be mediated by differing susceptibility to dietary fat-through either the tendency to overeat high-fat diets or metabolic responses to them. Consistent with this speculation, Tho- mas et a1.2* reported that lean individuals tend to increase lipid oxidation after 7 days on a high-fat diet, whereas obese individuals fail to do so. In addition, when postobese subjects are exposed to a eucaloric diet, they tend to have low rates of fat oxidation. This results in positive fat balance, which may explain their propensity to regain weight.62 This effect appears more evident in children with a familial history of obesity, which further supports the possibility of an inherited metabolic deficiency in the control of fat balance.63 As well, studies in Pima Indians and Caucasians indicate that people with a high respiratory quotient, i.e., a low rate of fat oxidation, are at greater risk of gaining body weight than those with a low respiratory

Respiratory quotient has been shown to be a familial trait.M Finally, Saltzman et a1.26 recently reported a significant familial tendency toward hyperphagia in high- fat diets matched in energy density and palatability to low-fat diets. The underlying metabolic reason for a possible genetic influence on responsiveness to high-fat diets is not known.

Fat-modified Foods and Energy Regulation I

Overview of Fat Substitutes in the Food Supply Fat-modified foods represent a broad range of foods in which the fat content of the traditional full-fat version of the food has been modified by either omission of the fat or replacement of the fat with a reduced-fat or nonfat ingre- dient. For example, snack foods that are baked instead of fried would represent fat-modified foods in which the fat content was modified by omission of the fat. Reduced-fat or fat-free salad dressings in which a water-holding gum is used in the formulation instead of fat represent foods in which the fat content is modified by fat replacement.

The use of foods produced with these technologies offers a number of potential benefits, including reduced dietary fat intake, caloric intake, and energy density, and decreased bioavailability of dietary cholesterol. However, there are also several concerns about potential adverse effects of fat substitution as a strategy for dietary change, including: 1) decreased micronutrient bioavailability, 2) gastrointestinal or other specific side effects, 3) unpre- dictable or undesirable changes in overall food or nutrient consumption patterns, 4) decreased motivation to under- take other “desirable” dietary and lifestyle behaviors, and 5 ) increased food costs.

Materials used to replace or substitute for fat can be classified in a variety of ways, based on chemical, nutritional, functional, or other qualities. Typical fat replacers include several classes of ingredients such as nonabsorb-


able fatlike products (olestra), partially absorbable struc- tured lipids (salatrim), and fat mimetics based on microparticulated proteins or various forms of carbohydrate.‘j7 The differences between specific fat replacement technologies and ingredients may be highly relevant to the particular benefits or adverse effects noted above, but many of the prominent issues relate to fat reduction in foods as a general strategy.

A large volume of research has addressed the nutrition and health implications of reduced fat consumption, and regulatory bodies have required manufacturers to assess a wide range of potential hazards associated with specific technologies. Although there are still unresolved issues relating to those points, there are far fewer data that have directly addressed broader issues relating to the actual benefits of reduced-fat product usage. Answers to these can come from predictive modeling, epidemiologic, and intervention studies.

Predictive model^^^.^^ suggest that substantial reductions in fat consumption can be accomplished through the use of reduced-fat foods. However, the resulfs of such analyses are dependent upon a set of assumptions about the food selection and eating behaviors of consumers using these products. National survey data based on trends in consumption patterns will help to characterize the dietary, anthropometric, and iifestyle correlates of reduced- fat product usage. These data would arguably provide valuable information about actual consumer behavior, although there are well-known difficulties with the interpre- tation of cross-sectional data.

As will be discussed in further detail, the results of intervention studies suggest a generally positive impact on dietary change from the use of reduced-fat products. However, the effects under actual conditions of use will depend upon both the composition of the products themselves (degree of fat reduction, type of fat replaced, energy density, etc.) and the volitional behavior of consumers. Reduced-fat products tend to be lower in fat and energy density than their full-fat counterparts. However, this is not true for all products and categories, and the effect of each different product on the total diet ultimately needs to be evaluated separately.

Fat Substitutes, Hunger, Satiety, and Food Intake One of the important questions that arises when consid- ering the growing availability of fat-modified foods in the marketplace is their potential net impact on dietary intakes of fat and energy. Researchers have shown that taste is the primary determinant of the foods people choose to eat. Fats contribute heavily to the richness of food flavor and overall palatability of foods, and therefore foods high in fat are often selected and preferred. In response to both current medical opinions about the harmful effects of high- fat diets and consumer demand for reduced-fat products

that taste good, a number of fat substitutes have been developed and incorporated into a variety of foods. As with sugar substitutes, it is important to assess the impact that these fat substitutes will have on hunger, satiety, and food intake.

“Satiety” refers to the effects of a food or meal after eating has ended. One technique for studying satiety is to administer a fixed amount of a given food or nutrient as 8

preload. After a predetermined delay, the effects on subsequent food intake in an ad libitum test meal are mea- ~ u r e d . ~ ~ The aim of a preloading study is to determine whether intake in the test meal varies in relation to the calories in the preload-that is, is there caloric compensation? As indicators of satiety, ratings of subjective sensa- tions such as hunger and fullness are usually made before and after the preload and in the interval before the test meal. Although subjective ratings provide a useful indica- tor of what the test subjects are experiencing, they do not always accurately predict subsequent food intake.

The influence of a preload on subsequent food intake depends upon a number of variables that often differ between studies, such as macronutrient composition or caloric content of the preloads and characteristics of the subjects. For example, older rnen,’O as well as obese individuals and those concerned with their body weight? showed less accurate caloric compensation than younger participants of normal weight. It is important to note that variables such as these could account for differences between studies. Attempts to apply the results of a particular study to broad generalizations about the effects of fat substitutes may be inappropriate.

Much of the published research in humans has focused on the sucrose polyesters (SPE), with an emphasis on olestra. Preloading studies have tested whether olestra consumption is associated with reductions in energy intake and changes in macronutrient composition. Short-term studies have been conducted with lean adults, obese ad~l t s , ’~*~~ and also children.83 All studies examined the effects of dilut- ing the energy density and reducing the fat content of the diet by substituting fat with olestra, on aspects of feeding behavior and energy balance. In most of these studies the substitution was covert, although two studies examined the effect of overt fat s~bstitution.’~,”

Lean adults showed generally incomplete compensation for a decrease in the energy density of the diet by replacement of fat with SPE in short-term studies. In a series of 2-day studies, in which subjects were allowed to eat ad libitum from a variety of familiar foods following a mandatory intake of either SPE-containing or full-fat foods, the maximal average compensation observed for the energy deficit produced by olestra was 27%.75 In another study from the nether land^:^ SPE was incorporated into croissants and the effects on subsequent intake were determined after different intervals between the preload and

Nutrition Reviews, Vol. 56, No. 5 s33

the test meal. At all intervals, the subjects showed incomplete compensation for the calorie reduction associated with SPE-an overall decrease in energy intake. No compensation was seen for the reduction in fat intake, so that the daily proportion of calories consumed as fat was reduced. In another series of 2-day studies, lean male subjects were fed a fixed diet containing either fbll-fat or SPE throughout day 1; on day 2 subjects were allowed ad libitum intake. No energy compensation was seen and fat energy was reduced from 40% to about 30% of energy.78 However, when a more severe reduction was imposed (fiom 32% energy as fat to 20%) the subjects compensated for 74% of the energy deficit." The explanation for the stron- ger compensatory response under these particular dietary conditions is unclear.

In contrast to these studies in which relatively poor energy compensation was observed, two replicate short- term studies in lean male subjects found complete energy compensation when the entire olestra intake was provided solely at the breakfast meal. Using an identical protocol, two separate, blinded, dose-response studieg were car- ried out by independent investigator^?^,^^ At each site, olestra was used covertly to replace 20 grams or 36 grams of fat at a compulsory breakfast in 24 lean, nondieting young male subjects. When intakes at lunch, dinner, and the evening snack were analyzed, the data showed that the consumption of olestra did not affect daily energy intake because subjects compensated for the reduction in calories associated with the olestra. However, subjects did not eat more fat to compensate for the reduction in calories from fat. The substitution led to a significant dose- dependent reduction in daily fat intake and a reciprocal increase in carbohydrate intake. There were no systematic differences in ratings of hunger or fullness between conditions.

In a study of the effects of olestra substitution for fat in the diets of 2- to 5-year-old children,83 approximately 123 kcal of fat were replaced over the first part of day 1 of the study, and intake was recorded until the end of day 2. As in adults, ingestion of the substitute resulted in a significant reduction in overall fat intake but was not associated with a decline in total energy intake.

Longer-term studies lasting from 12 days to 12 weeks in men and women have found that compensation for both fat and energy is incomplete when dietary fat is replaced with olestra in foods in the diet. De Graaf and colleagues" studied the effects of replacing 52 grams of regular fat with SPE at evening meals. The subjects were normal weight men and women in two within-subjects experiments in which the reduced-fat and placebo treatments each lasted 12 days. In one study (n= 28 men, 20 women), fat replacement was covert. In the second study (n=27 men, 20 women), subjects were provided information about the fat replacement. In both studies, men and women consumed

less fat and less energy each day when SPE replaced fat in the dinner meal; this effect persisted throughout the 12- day treatment. Mean compensation for energy was 3% in men and 19% in women in the covert study, while compensation reached 46% for men and 14% for women when information about the fat manipulation was provided. There was no evidence for fat-specific compensation in either study among men or women. Average dietary fat-energy intakes were 43% on placebo and 32% during the fat replacement condition. It should be noted, however, that as in the short-term studies and the studies described below, these investigations compared diets that differed in both dietary fat content and energy density. Thus, the effects observed may be an indirect effect of fat on density, rather than a direct metabolic effect of fat itself.

The effect of covertly replacing one-third of the dietary fat with olestra (with a corresponding change in energy density) was also studied in lean male volunteers (n=lO) in a two-period crossover study with 1 week of baseline control (40% fat energy) followed by 14 days of olestra (30% fat energy).76 During each treatment period, subjects had ad libitum access to food modules of fixed diet composition. Food intake was measured throughout the study. Energy and fat intakes decreased significantly during the olestratreatment (2790 f 570 kcdday to 2552 f 5 13 kchday and f?om 120 f 25 gramdday to 86f 18 grams/ day, respectively) compared with control. Energy compensation in response to the fat replacement averaged 35%.

In another 14-day study, Hill et al.*' conducted a double-blind, placebo-controlled, within-subject crossover study to investigate the effects of covert olestra substitution for regular fat on food selection and energy intake ( ~ 2 8 females, 23 males; BMI 19-36, ages 25-63). Over- all compensation for energy averaged 20% across all groups. (For lean and obese females compensation was 33% and 13%, respectively. For lean and obese males, compensation was 6% and 29%, respectively.) There was no apparent specific compensation for dietary fat, resulting in a significant reduction from 32% to 25% of dietary fat energy.

Another issue to be considered in relation to fat substitutes is whether the sensory properties imparted by fat substitutes can interfere with energy intake regulation when low-fat foods are consumed. That is, if a low-energy, low- fat food has the taste and texture of a high-fat food, will some people compensate for the food as if it were high in fat and energy? This question arises from evidence that humans can make physiologic associations between the sensory cues provided by a food and its energy content.86*87 The use of an energy-free fat substitute such as olestra could potentially alter this regulatory process.

To test this hypothesis, soups were developed in three versions: fat-free, fat-free plus olestra (33 grams olestra),

s34 Nutrition Reviews, Vol. 56, No. 5

and high-fat (33 grams of fat).8o The olestra soup had the nutrient composition of the fat-free soup but retained the sensory properties (thickness, creaminess) of the high-fat soup. Lean or obese men and women consumed either no preload or a fixed amount of one of the soups before lunch. Food intake over the rest of the day was similar following all three soups. The subjects compensated completely for the energy in the fat-free and olestra soups, in that total intake (soup plus lunch) was equivalent to intake in the no-preload condition. However, total intake was significantly greater when the high-fat soup was consumed than in the other conditions. Because there were no differences in the response to the two low-€at conditions-one with the taste of fat and one without-it appears that the sensory properties of fat alone, apart from the physiologic effects of fat, do not disturb short-term energy intake regulation. Further long-term studies are needed to evaluate whether comparable responses occur when fat substitutes are consumed regularly over an extended period of time.

In one other study, snacks of regular or Qt-free potato chips were offered to determine how changes in the fat content of foods affect satiation, or the amount consumed in a Habitual consumers (lean and obese men and women) of potato chips were given free access to either regular potato chips (5.3 kcaygram, 60% energy from fat) or chips made with olestra (2.8 kcdgram, 0% fat). The palatability of the chips did not differ. When no nutrition information was given, the subjects had to rely on physiologic cues if they were to adjust intake in relation to calorie content. All subjects ate similar amounts of both the no-fat and regular chips over the 1 0-day periods, indi- cating that they were not responsive to caloric differences.

Because of the fat and calorie reduction in the olestra chips, all participants ate less fat and calories in the snack when eating the olestra chips than when eating the regular chips. The results were similar when participants were given nutrition information about the chips, in that amounts consumed of both types of chips were similar. However, some individuals who were concerned about their body weight ate significantly more (1 0 grams) of the no-fat chips. Because the no-fat chips contained only half the calories of the regular chips, this slight increase in amount consumed did not negate the reductions in fat and energy intakes. In this study of satiation, when offered two equally palatable foods, the strategy that subjects em- ployed was to eat the same amount in granis regardless of the energy content of the foods. Even knowing the caloric content of the foods, or repeatedly eating them for 10 days, did not alter the strategy of eating a particular portion size.

Overall, the collective results of these studies with one particular fat replacer, olestra, resemble the broader literature on the effects of low-fat diets on energy intake and weight regulation. They are consistent with the hy-

pothesis that ad libitum consumption of reduced-fat diets, in association with reduced energy density, is associated with lower energy intakes and can be predicted to lead to modest weight loss if the results are comparable to the long-term studies on the relationship between dietary fat content and body weight.

Fat-soluble Vitamin Absorption Issues Wekated to Fat-modified Foods The process by which fat-modified foods might affect fat- soluble vitamins (A, D, E, and K) and phytochemical intake and absorption is complex.89 It can be influenced by a large number of factors, both related and unrelated to the characteristics of the foodstuff. These include: 1) the physical and chemical properties of a food such as lipophilicity, form, and structural characteristics, 2) the quantity of foods or dose, 3) individual diversity such as efficiency of digestiodtransit, age, and gender, 4) the presence of gastrointestinal disorders, 5 ) other products with which food is consumed, 6) the prior treatment of the food, particularly cooking or processing, and 7) time of consumption.

Because fat replacers have the potential to be used at substantial levels in human diets, an important question is the Bxtent to which they affect nutrient consumptkm patterns. One study demonstrated that the impact of replacing fat with modified starches in a variety of traditional fat-containing food products (e.g., baked goods, margarines and salad dressings) has only a modest effect on the intake of fat-soluble vitamin^.^' A 6-month, free- living, randomized, parallel, controlled intervention study showed that individuals consuming diets with reduced- fat products consume significantly less vitamin E compared with diets with regular fat products.w However, plasma alpha-tocopherol concentrations were not significantly affected by the intervention. The fact that vitamin E intake was the nutrient most compromised was predict- able because the richest food sources are vegetable oils, shortenings, and nuts?'

The introduction of nonabsorbable and partially absorbable fat replacers into the gastrointestinal tract raises the general question of whether the replacement substance might affect the availability of fat-soluble vitamins, cholesterol, and c a r o t e n o i d ~ . ~ ~ . ~ ~ Dietary fat undergoes lipolysis in the intestine, and the resulting fatty acids and monoglycerides form mixed micelles with bile acids. Lipo- philic molecules such as fat-soluble vitamins are incorporated into the mixed micelles and transported to the intestinal villi where they are absorbed. Any nonfat replacer will reduce absorption, so lipophilic fat replacers should only compete with absorption in those meals that are al- ready high in fat. When lipophilic fat replacers are consumed, it is likely that some portion of the fat-soluble vitamins will partition into the replacer and become un-


available to the intestinal micelles. Given this mechanism, the impact of a fat replacer on fat-soluble vitamins and carotenoids is dependent on its degree of lipophilicity, dose, presence of other digestible fat in the meal, and time of consumption relative to other foods.

The degree to which a lipid-based fat substitute might affect the absorption of fat-soluble vitamins can be predicted from knowledge of the lipophilicity of the sub- s t a n ~ e . ~ ~ - ~ ~ The lipophilicity of a molecule is based on its equilibrium distribution, expressed as a partition coefficient between the aqueous and oil phases?’ Fat replacers vary widely in their lipophilicity, such that the impact on fat-soluble vitamins varies among products. Since olestra is not absorbed and has the highest lipophilicity among currently approved fat replacers, it has the greatest potential for impact. Olestra’s effect on absorption of another substance in the gut is a function of the lipophilicity of that such that only the absorption of those molecules that are highly lipophilic are affected by olestra. Olestra has no significant effect on water-soluble components such as carbohydrates, proteins, vitamin-C, folate, flavonoids, and polyphenols because of their low lipophilicity. On the other hand, fat-soluble vitamins and cholesterol are influenced in direct relation to lipophilicity. Clinical studies demonstrate that sucrose polyester can affect the absorption of fat-soluble vitamins, cholesterol, and carotenoids, as would be expected from the partitioning mechanism. The more lipophilic the nutrient, the larger the e f f e ~ t . ~ ~ ” ~

There must be physical interaction in the lumen of the gastrointestinal tract between the olestra and fat-soluble vitamins before partitioning can affect absorption. Sepa- rating the time between the consumption of the olestra and the foods or supplements containing fat-soluble vitamins and carotenoids may help reduce the capacity for interference. Olestra’s capacity to reduce the availability of the fat-soluble vitamins can be offset by adding specific amounts of these vitamins to olestra or olestra-containing foods. Human and pig studies established the relationship between the dietary concentration of olestra and the amounts of extra vitamins required to offset the olestra effect^.^-%^^^^'^^ Vitamins A, D, E, and K are supple- mented in olestra-containing foods at levels that are similar to amounts found in common foods, and are added to simply maintain tissue concentrations at levels they would be if olestra were not eaten.

In contrast, there is currently no carotenoid (i.e., beta- carotene, alpha-carotene, lycopene, and lutein) supple- mentation in olestra-containing foods. It is beyond the scope of this review to assess the current data on the impact that dietary fat reduction and modification has on carotenoids and health. This was the topic of a recent workshop, which concluded that more long-term studies are required to determine the long-term health effects of

reducing individual caxotenoid concentrations though the use of fat-modified foods.lO’ Whereas much ofthe existing data are limited to beta-carotene, the putative roles of carotenoids in human health are not limited to a single carotenoid.

Discussion Based on the existing laboratory and clinical data, dietary fat appears to be one of the environmental factors that contributes to energy regulation and body weight. Ani- mal studies and laboratory studies in humans are consistent in that high-fat diets promote acutely increased energy intake. However, both short-term and long-term clinical studies suggest that switching from an ad libitum high- fat diet to an ad libitum low-fat diet results in only a modest weight loss, within the range of 1-3 kg. It is possible that dietary fat plays a greater role in weight gain during ad libitum eating than in weight loss (since the body may defend itself against weight loss more effectively than weight gain), but more studies are needed to address this possibility. Moreover, generalizations about the effect of dietary fat on voluntary energy intake and body weight are difficult, given the possible heterogeneity in genetic susceptibility to overeating with increased dietary fat, changes,in energy regulation with age, and the effect Of existing body composition on body fat stores. For example, although there is a perception that obese subjects respond differently than lean subjects to high-fat diets, the existing data require confirmation. Likewise, the overall impact of variations in fat intake on fat and energy balance may be attenuated or accentuated by other environmental factors, including physical activity. However, further data in this area are needed.

To further understand the effects of dietary fat on energy regulation and body weight, it is important to independently consider the separate impacts of related factors such as palatability, energy density, and fiber. Exist- ing discrepancies in the rate of weight loss between short- term and long-term studies may be an indication of the variation in the degree of constraint that the dietary aspects of the experimental design place on the subjects’ behavioral response. Declines in compliance with low-fat diets may also contribute to the modest long-term impact of low-fat diets. Conversely, there may be fundamental metabolic consequences of the longer-term use of a different intake of dietary fat. The impact of a prescription, such as the impact of low-fat foods on body weight, may be very powerfbl at the onset of the manipulation, but there may be compensation over time, such that there may be a point at which the effect can no longer be measured.

Results of a few short-term studies that control for palatability suggest that the effects of dietary fat may be mediated by energy density. In the current U.S. food supply, most of the difference in energy density of foods is


due to differences in dietary fat content. There may possibly be a small additional specific effect of dietary fat on energy regulation that is not mediated by energy density, but more studies are required to assess this possibility. Although there are some existing data not presented here that have studied the effects of dietary fat on palatability, there have been few studies directly linking palatability of dietary fat to food intake or body weight.

If all the other dietary components are included, such as replacement carbohydrate, protein, and water, a food that derives a low percentage of its energy from fat is not invariably a low-energy-density food. The distinction between dietary fat and energy density is important, given the dietary recommendations to reduce dietary fat intake and the wide availability of fat-modified foods. Although many reduced-fat products are lower in energy density than their fill-fat counterparts, this generalization does not hold for all products. As more low-fat, high-density food products become available, the dissociation between dietary fat and energy density becomes more distinct. Some low-fat products, such as yogurt, cookies, and cLe , may actually contain as much energy in a given portion than the full-fat versions. Results from a study by Shide et al.lM suggest that low-fat labels may give individuals license to eat more during other parts of the day, perhaps because they perceive the low-fat message to be synonymous with low energy density.

Overall, the studies based on the one sucrose polyester fat replacer, olestra, have produced results similar to the broader literature on the effects of low-fat diets (using other fat-reduction strategies) on energy intake and regulation. Both the short- and longer-term studies consistently show that fat replacement with olestra reduces total fat intakes. There has been no indication of fat-specific compensation when dietary fat is reduced. In the longer- term studies, energy compensation was incomplete in all studies, and did not exceed 50%.

The use of reduced-fat foods seems likely to help reduce total and relative fat intake, and thus have a modest impact on loss of body weight. However, as previ- ously stated, it cannot be assumed that different forms of fat substitutes have similar effects, and direct evaluation of each different product will be needed. The effects will likely depend on overall composition of food products, and on the cognitive effects of actual food choices and dietary patterns. Fat replacement and reduction technologies offer one potentially useful tool for achieving reductions in total dietary fat, but are likely to be effective only as one part of a broader and more conscious effort to control diet and lifestyle. The data on the few fat-modified foods that have been available for decades (e.g., low-fat and skim milk) suggest that it takes many years for a significant proportion of the population to adopt consistent use of these products in the diet.Io3 However, among those

consumers who consistently use such products, overall diet composition and nutrient intakes improve toward rec- ommended dietary g0als.lo3 Based on current understanding of how the use of such products is adopted within the population, it may be years before the net effect of reduced-fat and fat-modified foods on fat and energy intakes in the population can be assessed.

Based on laboratory studies, it seems likely that the use of low-fat or fat-modified diets by themselves will have only a modest impact on preexisting obesity, although it could be argued that even small amounts of weight loss by a significant fraction of the population could reduce the overall prevalence of obesity and reduce the risk for other chronic diseases. Given this, it may be more reason- able to look at the question of whether fat reduction strategies may help prevent excess energy consumption, and hence prevent body weight gain in the first place.

Summary and Recommendations Given the modest weight loss potential of 1-3 kg associated with a realistic reduction in dietary fat, this mea- sure alone is unlikely to be an effective treatment of preexisting obesity. It is possible that reduced-fat diets may be more effective in preventing weight gain than in treating it, but studies are needed to address this possibility. ' Recent work suggests that many of the effects of dietary fat on energy regulation appear to be mediated by the effects of fat on energy density. However, more research is needed. There are disparities in the rate of weight loss between short-term and longer-term clinical studies investigat- ing the role of dietary fat in energy regulation and body weight. Therefore, additional long-term (21 year) studies are needed that separately investigate the effects of fat, energy density, and palatability in both overweight and normal-weight individuals. In view of the typically modest long-term effects of dietary fat on energy regulation, further research is needed to identify those individuals and/or populations that may most benefit from long-term dietary fat reduction. Examples of these comparisons are obese versus lean individuals, dieting versus nondieting individuals, sed- entary versus active adults, alcohol versus nonalcohol consumers, and younger versus older adults. Many of the studies to date have examined the short-term role of dietary fat on weight loss. The extent to which these data adequately reflect the real-life role of fat in the etiology of weight gain, and hence in prevention of obesity, is not known. Differences in susceptibility to high-fat and high-energy-density diets may partly be of genetic origin. There are current genome-wide searches for genes respon- sible for susceptibility to high-fat diets, and there is

%


.

some evidence to suggest genotypic interactions that increase susceptibility among certain individuals. Theo- retically, symmetrical phenomena may also exist, resulting in some individuals being susceptible to low-fat diets, high-carbohydrate diets, or diets high in energy density, for example. These have yet to be explored. Most of the existing data on the impact of fat-modified foods on overall dietary energy and fat intakes have been based on studies using olestra. Direct comparisons of other fat substitutes will be required before generalizations can be made. More research is also needed to determine how individuals incorporate fat substitutes into their diets to ensure that the substitutions do not replace healthy rather than unhealthy al- ternatives. Moreover, some limited research shows that in certain situations, the consumption of foods that contain fat substitutes-particularly those labeled low- fat-may be used as an excuse to eat more of other less- than-desirable foods. Consumers may assume that fat substitutes are always associated with a reduction in the calorie content of foods, althoughaome foods are of equivalent energy density. Likewise, certain fat substitutes have the potential to displace consumption or interfere with absorption of fat-soluble vitamins, and research is needed to further evaluate this overall impact on total dietary intakes of key nutrients and phytochemicals.

Acknowledgments. Additional contributors to this report include: David Mela, PhD, Institute of Food Research, Reading, UK; James Stubbs, PhD, Rowett Research Insti- tute, Aberdeen, Scotland; Andre Tremblay, PhD, Lava1 University, Ste Foy, Quebec, Canada; Walter Willett, MD, PhD, Harvard School ofhbl ic Health, Boston MA.

1.

2.

3.

4.

5.

6.

7.

8.

S38

Kuller LH. Dietary fat and chronic diseases: epidemiologic overview. J Am Diet Assoc 1997;97:S% S15 Astrup A, Toubro S, Raben A, et al. The role of low- fat diets and fat substitutes in body weight man- agement: what have we learned from clinical studies? J Am Diet Assoc 1997;97:S82-S87 Blundell JE, MacDiarmid J. Fat as a risk factor for overconsumption: Satiation, satiety and eating patterns. J Am Diet Assoc 1997;97:S63-S69 Flatt JI? Importance of nutrient balance in body weight regulation. Diab Metab Rev 1988;4:571-81 Van ltallie TB, Smith NS, Quartermain D. Short-term and long-term components in the regulation of food intake: evidence for a modulatory role of carbohydrate status. Am J Clin Nutr 1977;30:742-57 Friedman MI. Body fat and the metabolic control of food intake. Int J Obesity Re1 Metab Dis 1990;3:53- 67 Friedman MI, Ramirez 1. Relationship of fat metabolism to food intake. Am J Clin Nutr 1993;57:35-42 Flatt JP, Ravussin E, Acheson KJ, et al. Effects of dietary fat on postprandial substrate oxidation and

9.

10.

11.

12.

13.

14.

15.

16.

17. I

18.

19.

20 *

21.

22.

23.

24.

25.

26.

on carbohydrate and fat balances. J Cliin Bravest

Abbott WGH, Howard BE, Christin b, et d. Short- term energy balance: relationship with protein, carbohydrate, and fat balances. Am J Physiol

Trayhurn I? The development of obesity in animals: the role of genetic susceptibility. Clin Endocr Metab

Sclafani A. Dietary-induced overeating. Ann NY Acad Sci 1989;575:281-91 Popkin BM, Paeratakul S, Zhai F, et al. A review of dietary and environmental correlates of obesity with emphasis on developing countries. Obes Res

Willett WC. Is dietary fat a major determinant of body fat? Am J Clin Nutr 1998;67:5558-5628 Schoellet DA. How accurate is self-reported dietary energy intake? Nutr Rev 1990;48:373-9 Black AE, Goldberg GR, Jebb SA, et al. Critical evaluation of energy intake data using fundamental principles of energy physiology. 2. Evaluation the results of published surveys. Eur J Clin Nutr

Ernst ND, Sempos CT, Briefel RR, et al. Consis- tency between US dietary fat intake and serum total cholesterol concentrations: the National Health and Examination Surveys. Am J Clin Nutr

Kuczmarski RJ, Flegal KM, Campbell SM, el al. In- creasing prevalence of overweight among U.S. adults. The National Health and Examination Sur- veys, 1960-1 991. JAMA 1994;272:205-11 Popkin BM, Paeratakul S, Zhai F, et al. Dietary and environmental correlates of obesity in a population study in China. Obes Res 1995;3:1358-1438 Sacks FM, Castelli WP, Donner A, et al. Plasma lipids and lipoproteins in vegetarians and controls.

Ussner L, Levistsky DA, Strupp BJ, et al. Dietary fat and the regulation of energy intake in human subjects. Am J Clin Nutr 1987;46:886-92 Kendall A, Levitsky DA, Strupp BJ, et al. Weight loss on a low-fat diet; consequence of the impreci- sion of the control of food intake in humans. Am J Clin Nutr 1991 ;53:1124-29 Thomas CD, Peters JC, Reed GW, et al. Nutrient balance and energy expenditure during ad libitum feding of high-fat and high-carbohydrate diets in humans. Am J Clin Nutr 1992;55:934-42 Stubbs RJ, Harbron CG, Murgatroyd PR, et al. Co- vert manipulation of dietary fat and energy density: effect on substrate flux and food intake in men eating ad libitum. Am J Clin Nutr 1995;62:31&29 Stubbs RJ, Ritz F Coward WA, et al. Covert manipulation of dietary fat and energy density: effect on food intake and energy balance in free-living men eating ad libitum. Am J Clin Nutr 1995;62:330- 7 Golay A, Allaz AF, Morel V, et al. Similar weight loss with low- or high-carbohydrate diets. Am J Clin Nutr

Saltzman E, Dallal GE, Roberts SB. The effect of high-fat and low-fat diets on voluntary energy intake and substrate oxidation: studies in identical

1985;76:1019-24

1988;255:E332-7

1984; 13:451-74

1995;3:145S-1533

1991 ;45:583-99

1 997; 66: 965s-72s

NEJM 1975;292:1148-51

1996;63:174-8

Nutrition Reviews, Vol. 56, No. 5

27.

28.

29.

30.

31 0

32.

33

34 *

35.

36.

37.

38.

39.

40.

41.

twins using diets matched for energy density, fiber, and palatability. Am J Clin Nutr 1997;66:1332-39 Shintani TT, Hughes CK, Beckham, S, et al. Obe- sity and cardiovascular risk intervention through the ad libitum feeding of traditional Hawaiian diet. Am J Clin Nutr 1991;53:1647S-51S Shah M, McGovern P, French S, et al. Comparison of a low-fat, ad libitum complex-carbohydrate diet with a low-energy diet in moderately obese women. Am J Clin Nutr 1994;59:980-4 Jeffery RW, Hellerstedt WL, French SA, et al. A randomized trial of counseling for fat restriction versus calorie restriction in the treatment of obesity. Int J Obesity Re1 Metab Dis 1995;19:132-7 Sigaard R, Rabe A, Astrup A. Weight loss during 12 week’s ad libitum carbohydrate-rich diet in overweight and normal-weight subjects at a Danish work site. Obesity Res 1996;4:347-56 Toubro S, Astrup A. Randomized comparison of diets for maintaining obese subjects’ weight after major weight loss: ad lib, low-fat, high carbohydrate diet v. fixed energy intake. BMJ 1997;314:29- 34 Boyar AP, Rose DP, Loughridge JR, et al. Response to a diet low in total fat in women with postmeno- pausal breast cancer: a pilot study. Nutr Canc

bee-Han H, Cousins M, Beaton M, et al. Compli- ance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia. Am J Clin Nutr 1988;48:575-86 Boyd NF, Cousins M, Beaton M, et al. Quantitative changes in dietary fat intake and serum cholesterol in women: results from a randomized, controlled trial. Am J Clin Nutr 1990;52:470-6 Gorbach SL, Morrill-LaBrode A, Woods MN, et al. Changes in food patterns during a low-fat dietary intervention in women. J Am Diet Assoc

Bloemberg BPM, Kromhout D, Goddijn HE, et al. The impact of the Guidelines for Healthy Diet of the Netherlands Nutrition Council on total and high density lipoprotein cholesterol in hypercholester- olemic free-living men. Am J Epidemiol

Sheppard L, Kristal AR, Kushi LH. Weight loss in women participating in a randomized trial of low- fat diets. Am J Clin Nutr 1991;53:821-8 Singh, RB, Rastogi SS, Verma R, et al. Randomised controlled trial of cardioprotective diet in patients with recent acute myocardial infarction: results of one-year follow-up. BMF 1992;304:1015-19 Hunninghake DB, Stein EA, Dujovne CA, et al. The efficacy of intensive dietary therapy alone or com- bined with lovastatin in outpatients with hypercho- lesterolemia. NEJM 1993;328:1213-I 9 Kasirn SE, Martino S, Kim PN, et al. Dietary and anthropometric determinants of plasma lipoproteins during a long-term low-fat diet in healthy women. Am J Clin Nutr 1993;57:146-53 Raben A, Jensen ND, Marckmann P, et al. Sponta- neous weight loss during 11 weeks ad libitum intake of a low-fat/high fiber diet in young, normal weight subjects. Int J Obesity Re1 Metabol Dis

1988; 1 1 :93-9

1990;90:802-9

1991 :134:39-48

1 995; 1 9191 6-22

42.

43

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

Liebel RRL, Hirsch J, Appel BE, eta!. Energy intake required to maintain body weight is not affected by wide variation in diet composition. Am J Clin Nutr

Yost TJ, Jensen DR, Hill JO, Eckell RH. The effects of dietary macronutrient composition on full substate utilization and balance on normal weight humans. Obesity Res 1997;5:875 Horton TJ, Drougas H, Brachey A, et al. Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am J Clin Nutr

Rumpler WV, Seale JL, Miles CWp et al. Energy- intake restriction and diet-composition effects on energy expenditure in men. Am J Clin Nutr

Peterson CM, Jovanovic-Peterson L. Randomized crossover study of 40% versus 55% carbohydrate weight loss diet strategies in women with previous gestational diabetes mellitus and non-diabetic women of 130-200% ideal body weight. J Am Coll Nutr 1995;14:369-75 Racette SB, Schoeller DA, Kushner RF, et al. Ef- fects of aerobic exercise and dietary carbohydrate on energy expenditure and body composition during weight reduction in obese women. Am J Cli Nutr 1995;61:486-94 Golay A, Eigenheer C, Morel Y, et al. Similar weight loss with low or high-carbohydrate diets. Am J Clin Nutr 1996;63:174-8 Van Stratum P, Lussenburg RN, van Wezel LA, et al. The effect of dietary carbohydrate:fat ratio on energy intake by adult women. Am J Clin Nutr

Stubbs RJ, Habron CG, Prentice AM. The effect of covertly manipulating the dietary fat to carbohydrate ratio of isoenergetically dense diets on ad libitum food intake in free-living humans. Int J Obe- sity Re1 Metab Dis 1996;20:651-60 Bell EA, Castellanos VH, Pelkman CL, et al. En- ergy density of foods affects energy intake in normal weight women. Am J Clin Nutr 1998;67:412- 20 Rolls BJ. Carbohydrate, fats, and satiety. Am J Clin Nutr 1995;61:960S-967S Rolls BJ, Hammer VA. Fat, carbohydrate and the regulation of fat intake. Am J Clin Nutr 1995;

Foltin RW, Fischman MW, Moran TH, et al. Caloric compensation for lunches varying in fat and carbohydrate content by humans in a residential laboratory. Am J Clin Nutr 1992;55:331-42 Foltin RW, Rolls BJ, Moran TH, et al. Caloric, but not macronutrient, compensation by humans for required-eating occasions with meals and snack varying in fat and carbohydrate. Am J Clin Nutr

Bouchard C. Obesity in adulthood-the importance of childhood and parental obesity. NEJM

Tremblay A, Plourde G, Despres JP, et al. Impact of dietary fat content and fat oxidation on energy intake in humans. Am J Clin Nutr 1989;49:824-31 Almeras N, Lavallee N, Despres JF! et al. Exercise and energy intake: effect of substrate oxidation.

1992;55:350-5

1995;62:19-29

1991 ;53:430-6

1978;31:206-12

62:S1086-S1095

1992;55:341-2

1997;337:926-7


59.

60.

61.

62.

63.

64.

65.

66.

67.

68.

69.

70.

71.

72.

73.

74.

75.

76.

Phys Behav 1995;57:995-1000 Tremblay A, Buemann B, Theriault G, et al. Body fatness in active individuals reporting low lipid and alcohol intake. Eur J Clin Nutr 1995;49:824-31 Ravussin E, Tataranni PA. Dietary fat and human obesity. J Am Diet Assoc 1997;97:S42-S46 Bouchard C. The Genetics of Obesity. Boca Raton, FL. CRC Press;l994 Larson DE, Ferraro RT, Robertson DS, et al. Energy metabolism in weight-stable postobese individuals. Am J Clin Nutr 1995;62:735-9 Eck LH, Klesges RC, Hanson CL, et al. Children at familial risk for obesity: an examination of dietary intake, physical activity and weight status. Int J Obesity Re1 Metab Dis 1992;16:71-8 Zurlo F, Lillioja S, Esposito-Del Puente A, et al. Low ratio of fat to carbohydrate oxidation as predictor of weight gain. Seidell JC, Muller DC, Sorkin JD, et al. Fasting respiratory exchange ratio and resting metabolic rfate as predictors of weight gain: The Baltimore Longi- tudinal Study on Aging. Int J Obesity Re1 Metab Dis

Froidevaux F, Schutz Y, Christin L, et al. Energy expenditure in obese women before,and during weight loss, after refeeding, and in the weight-re- lapse period. Am J Clin Nutr 1993;57:35-42 Munro IC, McGirr LG, Nestman ER, et al. Alterna- tive approaches to the safety assessment of macronutrient substitutes. Regul Toxic Pharmacol

Lyle BJ, McMahon KE, Kreutler PA. Assessing the potential dietary impact of replacing dietary fat with other macronutrients. J Nutr 1991 ;122:211-I6 Beaton GH, Tarasuk V, Anderson GH. Estimation of possible impact on non-caloric fat and carbohydrate substitutes of macronutrient intake in the human. Appetite 1992;19:87-103 Rolls BJ. Dimeo KA, Shide DH. Age-related impair- ments in the regulation of food intake. Am J Clin Nutr 1995;62:923-31 Rolls BJ, Kim-Harris S, Fischman MW, et al. Satiety after preloads with different levels of fat and carbohydrate: implications for obesity. Am J Clin Nutr

Blundell JE, Burley V, Peters JC. Dietary fat and human appetite: effects of non-absorbable fat on energy and nutrient intakes. Obesity: Dietary factors and Control. Tokyo, Japan. Science Society Press;l991;3-13 Rolls BJ, Pirraglia PA, Jones MB, et al. Effects of olestra, a non-caloric fat substitute on daily energy and fat intake in lean men. Am J Clin Nutr

Burley VJ, Cotton JR, Westrate JA, et al. Effect of replacing natural fat with sucrose polyester in meals or snacks across one whole day. Obesity in Eu- rope. Fitschuneit H, Gnes FA, Houner H, Schusdziarra V, Wechsler JG, eds. London UK. John Libbey & Company;l993:213-9 Hulshof T. Fat and non-absorbable fat and the regulation of food intake 1994; Wageningen Agricul- tural University Bray G, Sparti A, Windhauser M, et al. Effect of two weeks fat replacement by olestra on food intake

1992;16:667-74

1996;23:S6-S14

1994;60:476-87

1992;56:48-92

77.

78.

79.

80.

81.

82.

83.

84.

85.

86.

87.

88.

89.

90.

91.

92.

93.

94.

and energy metabolism. FASEB J 1995;78:34-65 Miller DL, Jammer VA, Peters JC. Effects of substituting fat-free (olestra) potato chips on 24-hOUr fat and energy intake. Obesity Res 1995;3:S327 Cotton JR, Burley VJ, Westrate HA, et al. Fat substitution and food intake: effect of replacing fat with sucrose polyester at lunch or evening meals. Brit J Nutr 1996;75:545-56 Cotton JR, Westrate JA, Blundell JE. Replacement of dietary fat with sucrose polyester: effects on energy intake and appetite control in non-obese males. Am J Clin Nutr 1996;63:891-6 Rolls BJ, Castellanos VH, Shide DJ, et al. Sensory properties of a non-absorbable fat substitute did not affect regulation of energy intake. Am J Clin Nutr 1997;65:1375-83 Hill J, Seagle H, Johnson S, et al. Effects of 14 days of covert substitution of olestra on spontaneous food intake. Am J Clin Nutr 1998; (in press) Glueck CJ, Hastings MM, Allen C, et al. Sucrose polyester and covert calorie dilution. Am J Clin Nutr

Birch LL, Johnson SL, Jones MB, et al. Effects of a non-energy fat substitute on children’s energy and macronutrient intake. Am J Clin Nutr 1993;58:326- 33 de Graaf C, Hulshof T, Westrate J, et al. Nonab- sorbable fat (sucrose polyester) and the regulation of energy intake and body weight. Am J Physiol

Mulshof T, de Graaf C, Westrate JA. Short-term effects of high-fat and low-fat/high SPE croissants on appetite and energy intake at three deprivation periods. Physiol Behav 1995;57:377-83 Booth DA, Mather F1 Fuller J. Starch content of ordi- nary foods associatively conditions human appetite and satiation, indexed by intake and eating pleasantness of starch-paired flavors. Appetite

Birch LL, McPhee L, Steinberg L, et at. Conditioned flavor preferences in children. Phys Behav

Miller DL, Hammer VA, Shide DJ, et al. Impact of fat- free potato chips with and without nutrition information labels on fat and energy intakes. Am J Clin Nutr 1998; (in press) Jackson MJ. The assessment of bioavailability of micronutrients: introduction. Eur J Clin Nutr

Velthius-te Wierik EJM, van den Berg H, Westrate JA, et al. Consumption of reduced-fat products: effects of parameters of anti-oxidative capacity. Eur J Clin Nutr 1996;50:214-9 Hoffman-LaRoche. Vitamins . Encyclopedia of Food Science and Technology. Hui YH, ed. New York, NY. John Wiley and Sons;4:2701-32 Lawson KD, Middleton SJ, Hassall CD. Olestra, a nonabsorbed, noncaloric replacement for dietary fat: a review. Drug Metab Rev 1997;29:651-703 Peters JC, Lawson KD, Middleton SJ, et al. Assess- ment of the nutritional effects of olestra, a nonabsorbed fat replacement: introduction and overview. J Nutr 1997;127:1539S-I546S Jandacek RJ. The effect of nonabsorbable lipids on the intestinal absorption of lipophiles. Drug

1982;35: 1352-9

1996;270:R1386-93 \

1 982 ;3: 1 63-84

1989;47:501-5

1997;51 :SI-S2


95.

96.

97.

98.

99.

Metab Rev 1982;13:695-714 Schlagheck TG, Kesler JM, Jones MB, et al. Olestra’s effect on vitamins D and E in humans can be offset by increasing dietary levels of these vitamins. J Nutr 1997;127:16668-1685S Schlagheck TG, Riccardi KA, Zorich NL, et al. Olestra dose reponse on fat soluble and water soluble nutrients in humans. J Nutr 19973 27:

Lyman WJ. Octanol/water partition coefficient. Handbook of Chemical Property Estimation Meth- ods. Lyman WJ, Reehl WF, Rosenblatt DH, eds. Washington DC. American Chemical Society; 1990 Westrate JA, van het Hof KH. Sucrose polyester and plasma carotenoid concentrations in healthy subjects. Am J Clin Nutr 1995;62:591-7 Cooper DA, Berry DA, Spendel VA, et al. Nutritional status of pigs fed olestra with and without increased

16468-1 6658

dietary levels of vitamins A and E in long-term studies. J Nutr 19973 27:1609S-16358

100. Cooper DA. Design of a study to determine the relationship between olestra intake and serum carotenoids and fat-soluble vitamins in the United States. Sixth World Congress on Clinical Nutrition, Banff, Alberta, Canada; 1997

101. Anderson D (ed). Potential effects of reducing carotenoid levels on human health. Proceedings of the Workshop. Harvard School of Public Health, Bos- ton MA. 1996

102. Shide DJ, Rolls BJ. Information about the fat content of preloads influences energy intake in healthy females. J Am Diet Assoc 1995;95:993-8

103. Sigman-Grant M. Can you have your low-fat cake and eat it too? The role of fat-modified products. J Am Diet Assoc 1997;97:S76-S81

Discussion

* Rosenberg: If working group one had the task of examining the evolution of the science relating to dietary fat to disease and health outcomes, group two was charged with the responsibility of bringing together the information that we have accumulated over the same period of time about what happens at the physiologic level when one modifies fat in the diet, with or without fat-modified foods. Are there questions or clarifications with which we should begin? Bieber: Dr. Roberts mentioned that a majority ofthe studies using olestra show incomplete caloric compensation. Do you think that this might have been due to people feeling sick from any adverse side effects from olestra? Maybe that’s why they didn’t compensate? Pi-Sunyer: There doesn’t seem to be evidence in the literature that this was a defining pattern that would cause the lack of compensation. Rosenberg: In fact, I think it is true. One of the points you made in the working paper is we do need more information about compensation f o r - o r lack thereof-with respect to other forms of fat-modified foods. Pi-Sunyer: There’s very little data outside of olestra. Rosenberg: But you do have data, as you pointed out this morning, that there is some experience with other kinds of substitutions in the case of calories substituted or artifi- cial sweeteners. Leveille: This is a very quick question. You talked about the impact of palatability. Did you tease that out in terms of the many factors that influence palatability? Fat, for example, carries flavors but it also has myriad textural effects in food products which make products either more or less pleasant. Did you get at those, or did you just look at palatability in a broad sense? Roberts: These are very important issues. I think that when

you really tightly control diets differing in fat or palatability and texture (which at least one study has done), you see no significant effect of fat. It’s very hard to pin a number on what the effect of texture is versus the learned associatiyns that you may get between the post- \ ingestional consequences of a food and its taste. Denke: I have an issue with your review of the diet studies and looking at the incidental weight loss that might have been seen on the low-fat component. This isn’t really, as you billed it, “a randomized clinical trial looking at the fat issue.” Most of these studies were either done to look at the efficacy of a low-fat diet in people at risk for breast cancer, or people with high cholesterol or people with established coronary disease. It brings up an issue of why people follow a diet. There’s also a motivational issue. And the therapeutic diet for these people was the lower-fat diet. So I think I’d be very careful in presenting this because you’re asking whether a low-fat diet gives you incidental weight loss but you’re using data that were not designed to answer that question. Rosenberg: The point being that weight loss was not the outcome variable that was in the design of the study? Denke: Yes, nor was it the motivation of the participants. And you combine two different types of studies-between-subject and within-subject studies. But remember, all those subjects were participating for therapeutic health benefits, and the low-fat diet was a therapeutic diet. Pi-Sunyer: That’s correct. Some of it was done for those reasons. My personal feeling, and I may be totally wrong, is that those people who are doing this for therapeutic reasons are more likely be successful. In a sense, they’d be more motivated to stay on the diet and lose weight if the diet leads to weight loss. And yet, they’re the ones who have not done very well on these diets. This is an

Nutrition Reviews, Vol. 56, No. 5 S4 1

Physiology of Fat Replacement and Fat Reduction: Effects of Dietary Fat and Fat Substitutes on...

Documents

Transcript of Physiology of Fat Replacement and Fat Reduction: Effects of Dietary Fat and Fat Substitutes on...