Cross-sectional studies have associated numerous health benefits with regular nut consumption [7, 21], and the literature describing the inverse association between nut consumption and body weight is robust [22–24]. Theoretical explanations for this association include enhanced satiety and caloric compensation, a strong thermic response following ingestion, and incomplete digestion with enhanced fecal fat losses [5, 7, 25]. Yet, randomized intervention trials that have examined the impact of daily nut consumption on body weight demonstrated only neutral effects [13–15, 26–29], possibly a consequence of the high caloric value of the nut allotments (240–1374 kcal). In the present report, the nut dosage was modest (1 serving or 170 kcal) and consumed as a preload 1-hour prior to mealtime to maximize purported satiety potential; however, daily nut ingestion did not impact body weight over time.
The favorable effects of grain bar ingestion, the control treatment, in both the acute and long-term trials were unexpected as others have used this control treatment with neutral effects . Furthermore, preloads composed of glycemic carbohydrate increased energy consumption at mealtime in several studies [17, 30]. In the acute trial, in comparison to the peanut and/or water treatments, grain bar consumption one hour prior to the test meal was associated with greater perceived satiety at 60, 90, and 120 minutes postmeal and with greater blood glucose concentrations at the time the test meal was consumed. Thus, grain bar ingestion was associated with a strong, sustained satiety response that was not observed for peanut ingestion. The observed increase in perceived satiety noted with the consumption of a food item that displays a relatively high-glycemic-response contradicts a body of literature demonstrating that postprandial glycemia is directly associated with appetite [8, 9, 31, 32].
Anderson and colleagues  proposed an explanation for these seemingly contradictory responses by suggesting that high glycemic carbohydrates promote satiety in the short-term (one hour after ingestion) whereas low glycemic carbohydrates are associated with a delayed satiety (2 to 3 hours post-ingestion) consistent with their delayed impact on blood glucose concentrations. Indeed, controlled trials demonstrate increased fullness  and lower mealtime energy intakes  one hour after the ingestion of high glycemic preloads versus low glycemic preloads and three hours after the ingestion of a fiber-rich carbohydrate preload versus an isocaloric bread preload . Furthermore, the glucostatic theory, proposed by Mayer in 1952 , suggested that food intake is regulated by glucoreceptors in the hypothalamus that sense glucose utilization and adjust food intake to maintain metabolic glucose at a steady-state. Accordingly, satiety is maximized when blood glucose concentrations are high. Hence, the timing of the preloads in the present report (one hour prior to a meal) likely contributed to the strong satiating effects of the grain bar 1.5 hours later.
Interestingly, although both glucose and insulin concentrations were significantly elevated 1-hour following the ingestion of the grain bar as compared to peanut or water ingestion, the incremental area-under-curve for glucose during the postprandial period (0–120 min postmeal) did not differ significantly between treatments. However, it is likely that these results do not accurately portray the magnitude of total glycemia following grain bar ingestion since blood samples were not collected at the 30-minute interval after preload ingestion. Regardless, grain bar ingestion had an immediate, glycemic and insulinemic response that was not sustained once the test meal was ingested.
The rise in both blood glucose and insulin one hour after grain bar ingestion coincided with the test meal ingestion and may have contributed to the attenuation of the postprandial glycemic response and to the rise in satiety ratings. Following nut ingestion a rise in insulin but not glucose concentrations was observed at 60 minutes, and although postprandial glycemia at 30 min was similar to the grain bar treatment, perceived satiety was not impacted throughout the postprandial period relative to control. The insulintropic action of dietary protein is well documented and believed to relate to bioactive peptides or specific amino acids [38–40]. The rise in insulin following peanut ingestion may have abetted the reduction in postmeal glycemia, but the absence of a glycemic response prior to the ingestion of the test meal may be linked to the low satiety ratings observed for peanut ingestion.
Glucagon-like peptide (GLP)-1, an incretin hormone released from mucosal cells in response to nutritive and non-nutritive agents, contributes to the suppression of appetite during the postprandial period by direct central nervous system action . Although not assessed in the present report, others have shown that carbohydrates and nuts appear to have differing effects on GLP-1 release, a fact that may help explain the results reported herein. Stimulation of the sodium-glucose cotransporter-1 is believed to play a role in GLP-1 release  and both high-glycemic and low-glycemic carbohydrates effectively stimulate GLP-1 release, an effect which is sustained for over 3 hours [35, 43]. Nut ingestion, however, displayed a more moderate effect on GLP-1 release, and blood concentrations fell to below baseline after 60 minutes . Further studies examining the role of preloads in promoting postmeal satiety and incretin hormone release are needed to elucidate mechanisms.
In the 8-week trial, a single serving of peanuts (170 kcal) or the control treatment, a grain bar (140 kcal), were ingested in a structured manner, one hour prior to the evening meal. Theoretically, consuming a modest serving of peanuts as a preload to the evening meal would maximize their purported satiating effects and possibly contribute to weight loss over time [16, 17]. However, consistent with the previous trials, daily consumption of nuts did not impact 24-h energy intakes or body weight. It may be that greater quantities of nuts (>48 g) are necessary to increase satiation [26, 45]; but, given the caloric load of this quantity of nuts, measurable losses in body mass are not likely to be noted, at least over the short-term. Surprisingly, daily grain bar ingestion did reduce body weight significantly after 8 weeks. The favorable impact of grain bar ingestion on body weight was also noted at study weeks 2 and 6 as well as at the 4-week follow-up (Figure 3).
The success of grain bar ingestion for managing energy intake was realized early in the trial. Although the change from baseline for mean energy intakes in the first week of the trial did not differ significantly between groups, the change in energy intake was weakly related to change in body weight at week 2 for all participants (r = 0.339, p = 0.077). The decision to preload the evening meal in this trial may have revealed an unforeseen benefit. The significant reductions in mid-day mealtime energy intakes reported by Farajian et al.  for a fiber-rich carbohydrate preload were not sustained after a 24 h period indicating that energy compensation occurred later that day. In the present trial, by preloading the final meal of the day, the mealtime energy reductions related to the grain bar preload appeared not to have been compensated for prior to bedtime. Moreover, daily grain bar ingestion lowered hemoglobin A1c significantly after 8 weeks compared to peanut ingestion. The favorable impact for regular grain bar ingestion on diabetic biomarkers is novel and deserves further investigation.
Limitations of this study include the use of diet records to estimate energy intakes and compliance to the feeding study protocol. Although compliance did not differ significantly between groups, compliance may have impacted study outcomes. However, the significance for weight loss between groups was retained when only the compliant participants were examined (p = 0.047). Participants were overweight but healthy by self-report; hence, these results may not apply to normal weight populations or those with cardiovascular disease or diabetes. When considering the glucostatic theory as presented by Mayer , glycemic carbohydrates are not well utilized in the diabetic state; hence, a glycemic carbohydrate preload one hour prior to mealtime may not curb hunger in individuals with insulin resistance or diabetes. However, study participants were free-living allowing for natural eating behaviors and contributing to the external validity of the study. The lack of glucose and insulin data at 30 minutes following the ingestion of the preloads is another important limitation in this trial. Future trials should closely follow satiety and glycemic responses after preload ingestion and prior to meal ingestion. Trials of longer duration (6–12 months) are needed to better understand the role of glycemic carbohydrate preloads for weight management, and the measurement of the satiety peptides, e.g., GLP-1, will provide useful physiological information regarding mechanisms.
These data indicate that a low-energy, glycemic carbohydrate preload to the evening meal reduced 24-h energy intakes in healthy, overweight adults, resulting in significant reductions in body weight. A peanut preload (28 g) did not impact 24-h intakes or body weight in this population. Simple, inexpensive, and practical weight loss strategies, easily adopted by children and adults across diverse populations groups, are needed to help combat obesity. Although glycemic carbohydrates are a controversial topic in the recent literature, low-energy, glycemic carbohydrates may have a useful role as a preload. More research is needed to investigate the usefulness of preloads on eating behaviors and weight loss.