Passive Overconsumption Research Articles

Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake

Dietary fat has traditionally been viewed as being particularly lipogenic because of its high energy density, metabolic efficiency, and palatability. If these attributes of dietary fat were counteracted by a high satiating power, or if the body made autoregulatory adjustments in fat utilization in response to high fat intakes, energy balance would not necessarily be displaced. However, recent experiments have shown that neither of these hold true: human and animal trials consistently show that covert manipulation of dietary fat can induce hyperphagia, which can readily lead to spontaneous fat storage of 50-100 g/d in humans. Experiments with isoenergy-dense diets show that this high-fat hyperphagia (with diets of similar palatability) is caused by the high energy density of fatty foods rather than by their other attributes. Hyperphagia has therefore been termed passive overconsumption because it occurs unintentionally and without the consumption of excess bulk. When palatability is allowed to vary normally, high-fat foods may additionally induce active overconsumption in response to the enhanced organoleptic qualities of fats. In terms of substrate flux, fat is at the bottom of an oxidative hierarchy that determines fuel selection. Whereas alcohol, carbohydrates, and protein elicit powerful autoregulatory adjustments in their oxidation in response to changes in intake, fat fails to elicit such a response and fat balance is therefore easily displaced. These physiologic observations provide mechanistic support for secular-trend, cross-cultural, and cross-sectional epidemiologic studies investigating the role of energy-dense diets in the etiology of obesity.

Passive overconsumption. Fat intake and short-term energy balance.

Passive overconsumption. Fat intake and short-term energy balance.

Fat as a Risk Factor for Overconsumption: Satiation, Satiety, and Patterns of Eating

Many people experience great difficulty in preventing energy intake from outstripping energy expenditure. Eating high-fat foods can facilitate the development of short-term positive energy balances by influencing satiation and satiety, the processes that control the size of eating episodes and the strength of postingestive appetite inhibition, respectively. An important feature of these processes is the relative potency of orosensory, postingestive (preabsorptive), and postabsorptive signals. Foods high in dietary fat have a weak effect on satiation, which leads to a form of passive overconsumption, and a disproportionately weak effect on satiety joule-for-joule compared with protein and carbohydrate). This overconsumption (high-fat hyperphagia) is dependent upon both the high energy density and the potent sensory qualities (high palatability) of high-fat foods. A positive fat balance does not appear to generate a tendency for behavioral compensation, and there appears to be almost no autoregulatory link between fat oxidation and fat intake. The Leeds High Fat Study has found a higher frequency of obesity among high-fat than low-fat consumers, but the relationship between fat consumption and obesity is not a biologic imperative; analysis of the pathways between daily fat intakes and patterns of eating has revealed high-risk eating episodes. The physiologic responses to fat ingestion appear to be weak compared with the potent orosensory properties of high-fat foods, and such responses cannot prevent overconsumption. A first stage in a health program should be to prevent passive overconsumption. J Am Diet Assoc. 1997;97(suppl):S6S-S69.

Control of human appetite: implications for the intake of dietary fat.

The human appetite system contains central and peripheral mechanisms that interact with environmental features, especially with the physical and nutrient composition of the food supply. Foods varying in nutrient composition exert different physiologic effects, some of which function as satiety signals. High-fat diets (low food quotient) lead to high levels of energy intake. This effect is termed passive overconsumption and overcomes fat-induced physiological satiety signals. High-fat foods exert a weak effect on satiation (intra-meal satiety), and fat has a weaker effect, joule for joule, on postingestive satiety than do other macronutrients. The frequency of obesity is greater among high-fat than low-fat consumers. However, the development of obesity on a high-fat diet is not a biological inevitability. The investigation of people who resist the weight-inducing properties of high-fat diets is a key research strategy. Understanding the appetite control system suggests behavioral, nutritional, and pharmacologic strategies for modifying dietary fat intake.

Nutrition and appetite control: implications for the regulation of body weight

There is an important relationship between the expression of human appetite and the macro nutrient composition of the prevailing diet. Evidence indicates a correlation between the amount of fat consumed and body weight gain or the degree of adiposity. The pattern of eating behaviour is represented by the size and number of eating episodes (meals and snacks). The size of eating episodes is influenced by the process of satiation and the intervals between episodes by post-ingestive satiety. Protein appears to exert the most potent control over appetite. Carbohydrate also generates strong post-ingestive satiety with the intensity and duration depending upon the particular structure of the carbohydrate. High fat foods exert weak control over satiation and generate a weak satiety response relative to the proportion of energy ingested. High fat foods therefore have the potential to generate a form of passive overconsumption. The high energy density and potent oro-sensory qualities of high fat foods allows the rate of ingestion to overcome fat-induced satiety signals. This situation suggests behavioural, nutritional and pharmacological strategies to prevent fat-induced passive overconsumption and to improve the effect of fat on appetite control.

Dietary fat and the control of energy intake: evaluating the effects of fat on meal size and postmeal satiety

Three separate experiments in lean subjects confirmed that a 1.52-MJ (362-kcal) carbohydrate supplement at breakfast suppressed appetite 90 min later but had no effect on a test meal given after 270 min. A 1.52-MJ (362-kcal) fat supplement produced no detectable action on measures of appetite at any time point. Therefore, fat and carbohydrate do not have identical effects on the appetite profile. In a further study in obese subjects, a novel experimental design was used to assess the satiating efficiency and compensatory response of fat. Eating from a range of either high-fat or high-carbohydrate foods, obese subjects voluntarily consumed twice as much energy from the fat items, thereby indicating a weak action of fat on satiation. In turn, this large intake of fat exerted a disproportionately weak effect on satiety. These studies suggest that the appetite-control system may have only weak inhibitory mechanisms to prevent the passive overconsumption of dietary fat. The results indicate how this action could induce a positive energy balance and lead to a gradual upward drift in body mass index.