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Background Longer oral processing decreases food intake. This can be attributed to greater oro-sensory exposure (OSE) and a lower eating rate (ER). How these factors contribute to food intake, and the underlying physiological mechanisms, remain unclear. Objectives We aimed to determine the independent and simultaneous effects of OSE and ER on satiation and associated endocrine responses. Methods Forty participants in study 1 [mean ± SD age: 24 ± 4 y; BMI (in kg/m2): 22 ± 2] and 20 in study 2 (mean ± SD age: 23 ± 3 y; BMI: 23 ± 2) participated in a 2 × 2 randomized trial. In both studies, participants ate chocolate custard with added caramel sauce (low OSE) or caramel fudge (high OSE) and with short (fast ER) or long breaks (slow ER) in between bites, until fullness. In study 2, endocrine responses were measured during the meal. Results In study 1, participants ate (mean ± SEM) 42 ± 15 g less in the slow- than in the fast-ER condition, only within the high-OSE condition (P = 0.04). In study 2, participants ate 66 ± 21 g less in the high- than in the low-OSE condition and there were no intake differences between slow and fast ER (P = 0.35). Eight minutes after starting to eat, insulin concentrations increased by 42%–65% in all treatments compared with the control. At the end of the meal, insulin concentrations were 81% higher in the high-OSE, slow-ER than in the low-OSE, fast-ER condition (P = 0.049). Pancreatic polypeptide (PP) increased by 62%, 5 min after meal onset in the low-OSE, fast-ER condition (P = 0.005). Ghrelin concentrations did not change. Conclusions Greater OSE increases insulin responsiveness. In contrast, PP responses are stronger when OSE is reduced and ER is fast. Insulin and PP responses may mediate the independent effects of OSE and ER on food intake. These may be beneficial eating strategies, particularly for type 2 diabetic patients, to control food intake and maintain glucose homeostasis. This trial was registered at trialregister.nl as NL6544.

An expert panel was successfully trained to assess characterising odours in cigarettes and roll-your-own tobacco. This method could be applied to other product types such as e-cigarettes. Regulatory decisions on the choice of reference products and significance level are needed which directly influences the products being assessed as having a characterising odour.

This is the first fMRI study to report increased activation to large portions in a brain region that is involved in inhibitory control. These findings may contribute to understanding why some children overeat when presented with large portions of palatable food.

Large portions promote intake of energy dense foods (i.e., the portion size effect--PSE), but the neurobiological drivers of this effect are not known. We tested the association between blood oxygen level dependent (BOLD) brain response to food images varied by portion size (PS) and energy density (ED) and children's intake at test-meals of high- and low-ED foods served at varying portions. Children (N = 47; age 7-10 years) participated in a within-subjects, crossover study consisting of 4 meals of increasing PS of high- and low-ED foods and 1 fMRI to evaluate food images at 2 levels of PS (Large, Small) and 2 levels of ED (High, Low). Contrast values between PS conditions (e.g., Large PS - Small PS) were calculated from BOLD signal in brain regions implicated in cognitive control and reward and input as covariates in mixed models to determine if they moderated the PSE curve. Results showed a significant effect of PS on intake. Responses to Large relative to Small PS in brain regions implicated in salience (e.g., ventromedial prefrontal cortex and orbitofrontal cortex) were positively associated with the linear slope (i.e., increase in intake from baseline) of the PSE curve, but negatively associated with the quadratic coefficient for the total meal. Responses to Large PS High ED relative to Small PS High ED cues in regions associated with cognitive control (e.g., dorsolateral prefrontal cortex) were negatively associated with the linear slope of the PSE curve for high-ED foods. Brain responses to PS cues were associated with individual differences in children's susceptibility to overeating from large portions. Responses in food salience regions positively associated with PSE susceptibility while activation in control regions negatively associated with PSE susceptibility.

The mouth is the first part of the gastrointestinal tract. During mastication sensory signals from the mouth, so-called oro-sensory exposure, elicit physiological signals that affect satiation and food intake. It has been established that a longer duration of oro-sensory exposure leads to earlier satiation. In addition, foods with more intense sweet or salty taste induce earlier satiation compared to foods that are equally palatable, but with lower taste intensity. Oro-sensory exposure to food affects satiation by direct signaling via the brainstem to higher cortical regions involved in taste and reward, including the nucleus accumbens and the insula. There is little evidence that oro-sensory exposure affects satiation indirectly through either hormone responses or gastric signals. Critical brain areas for satiation, such as the brainstem, should be studied more intensively to better understand the neurophysiological mechanisms underlying the process of satiation. Furthermore, it is essential to increase the understanding of how of highly automated eating behaviors, such as oral processing and eating rate, are formed during early childhood. A better understanding of the aforementioned mechanisms provides fundamental insight in relation to strategies to prevent overconsumption and the development of obesity in future generations.

Cephalic phase responses (CPRs) are conditioned anticipatory physiological responses to food cues. They occur before nutrient absorption and are hypothesized to be important for satiation and glucose homeostasis. Cephalic phase insulin responses (CPIRs) and pancreatic polypeptide responses (CPPPRs) are found consistently in animals, but human literature is inconclusive. We performed a systematic review of human studies to determine the magnitude and onset time of these CPRs. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were used to develop a search strategy. The terms included in the search strategy were cephalic or hormone response or endocrine response combined with insulin and pancreatic polypeptide (PP). The following databases were searched: Scopus (Elsevier), Science Direct, PubMed, Google Scholar, and The Cochrane Library. Initially, 582 original research articles were found, 50 were included for analysis. An insulin increase (≥1μIU/mL) was observed in 41% of the treatments (total n = 119). In 22% of all treatments the increase was significant from baseline. The median (IQR) insulin increase was 2.5 (1.6–4.5) μIU/mL, 30% above baseline at 5± 3 min  after food cue onset (based on study treatments that induced ≥1 μIU/mL insulin increase). A PP increase (>10 pg/mL) was found in 48% of the treatments (total n = 42). In 21% of the treatments, the increase was significant from baseline. The median (IQR) PP increase was 99 (26–156) pg/mL, 68% above baseline at 9± 4 min  after food cue onset (based on study treatments that induced ≥1 μIU/mL insulin increase). In conclusion, CPIRs are small compared with spontaneous fluctuations. Although CPPPRs are of a larger magnitude, both show substantial variation in magnitude and onset time. We found little evidence for CPIR or CPPPR affecting functional outcomes, that is, satiation and glucose homeostasis. Therefore, CPRs do not seem to be biologically meaningful in daily life.