The mechanisms underlying beneficial responses to frequent feeding as opposed to an infrequent meal pattern are not fully understood. Frequent feeding has been shown to elicit lower plasma glucose fluctuations than does a more infrequent eating pattern. The absolute amount of carbohydrate eaten at each episode of ingestion in a frequent feeding pattern is simply not great enough to elevate glucose to the same extent as more infrequent eating. Small elevations in plasma insulin seen with frequent feeding are most likely in response to minimal fluctuations in glucose. The mechanisms responsible for the effect of an increased frequency of meal eating on lipid metabolism are not as clear-cut. The lower serum cholesterol levels observed during frequent feeding may be related to lower serum insulin levels. Insulin appears to have a key role in enhancing the hepatic synthesis of cholesterol through its ability to stimulate hydroxymethylglutaryl-coenzyme A reduc-tase (HMG-CoA), the rate-limiting enzyme in hepatic cholesterologenesis. Exogenous insulin quickly increases HMG-CoA reductase activity in rats with diabetes and raises levels of the enzyme in animals without the disorder. It is possible that the reduction of serum cholesterol during a diet of habitual frequent feeding in normal healthy individuals may result from a reduction in hepatic cholesterol synthesis, secondary to the maintenance of euglycemia at lower serum insulin levels. A reduction in cholesterol synthesis would result in an increase in LDL receptors, further lowering total and LDL-C levels.
Alternatively, or in addition, the benefits associated with an increased feeding regimen may reflect unintentional or uncontrolled changes in dietary energy and fat intake that may occur when an individual's meal frequency is altered. It is not clear whether a diet of frequent eating results in any adaptational responses of enzymes or hormones that in turn may be providing additional benefit to the individual.
Much of the research that found these benefits is difficult to interpret due to the variety of methods used, the lack of information available regarding the foods consumed, and the exact nature of the dietary intervention. The majority of measurements are made on fasted blood samples, when in fact most individuals are in a postprandial state for the greater part of every 24-h period. The results of such research must be interpreted with caution for a number of reasons, such as the small sample size used and the interactions with other factors that may prolong absorption time (e.g., soluble fiber, low-glycemic index foods, and the administration of a-glycosides).
As discussed previously, frequent feeding has been demonstrated to lower circulating plasma glucose, insulin, and lipids in both healthy and diabetic subjects in the short term. In addition to the lack of clarity on the mechanisms involved, further research is needed to investigate any medium- and long-term benefits of frequent feeding. It is important that, if deemed desirable in terms of metabolic control, increasing the number of periods of feeding encourages the desired dietary pattern and mix of macro- and micronutrients and is not offset by the failure to decrease meal size.
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