Exacting Responses: Lack of Endocrine Cephalic Phase Responses Upon Oro-Sensory Exposure

Abstract

Oro-sensory exposure (OSE) to food plays an important role in the regulation of food intake. One proposed underlying mechanism is the occurrence of cephalic phase responses (CPRs). CPRs include the pre-digestive endocrine responses induced by food-related sensory input. Yet, whether OSE duration or sweetness intensity affects CPRs is unknown. The objective of this study was to determine the independent and interactive effects of oro-sensory duration (chewing) and stimulation intensity (sweetness) on endocrine CPRs and satiation. Eighteen males (22 ± 2 years, BMI 22 ± 2 kg/m2) participated in a 2 × 2 randomized study with a control condition. Each session participants performed modified sham feeding (MSF) with one of the four gel-based model foods. During the control session no MSF was performed. Model foods differed in chewing duration (hard or soft texture) and sweetness (low or high intensity). During each session, eight blood samples were collected up till 25 min after MSF onset. Subsequently, food intake from an ad libitum lunch was measured. No typical CPR was found for insulin, pancreatic polypeptide (PP), and ghrelin. However, the overall PP response was 1.1 times greater for the hard sweet MSF condition compared to control (p = 0.02). Overall ghrelin responses were 1.1 times greater for the hard model food compared to the soft model food conditions (p = 0.003). These differences in endocrine response were not associated with differences in food intake at the subsequent meal. Exploratory sub-analysis of the responsive insulin curves showed that after 2.5 min of MSF the hard texture model foods insulin concentrations were 1.2 greater compared to the soft texture. These findings indicate that texture hardness and sweetness increase the overall PP response and that MSF on hard texture increases the overall ghrelin response compared to soft texture model foods. However, MSF on model foods does not lead to a typical CPR. This study, among others, shows that there are major dissimilarities in the endocrine responses to food stimulation between individuals. This emphasizes the importance of considering cephalic responders and non-responders. More research is needed to understand CPRs in relation to food texture and taste properties.

Measured energy content of frequently purchased restaurant meals: multi-country cross sectional study

“… 25 27 This may be due in part to the cephalic phase initiation of digestion, which is a normal physiologic mechanism whereby the sight and smell of food causes parasympathetic mediated preparations for digestion that include increased hunger, enlarged stomach lumen, and greater gastric motility. 48 49 Effectively, the human body is in equilibration with the immediate food environment via its cephalic phase, with the result that human eating patterns tend to synchronize with the available amount of food, whatever that amount is. Another innate mechanism that may contribute to overeating when portion sizes are very large is an increase in bite size without a compensatory decrease in the rate of bites, which results in a faster rate of energy ingestion.…”

Endocrine Cephalic Phase Responses to Food Cues: A Systematic Review

“…Instead, the size of the response relative to its (baseline) variation should be taken into consideration when drawing conclusions ( 103 ). The changes of a type I or II error depend on the sample size; only 8% of the studies did a power calculation prior to the study and the sample size in these studies ranged from 14 to 22 participants ( 4 , 32 , 66 , 86 ). Future studies should take the above-mentioned methodological issues into account and focus on individual (phenotype) differences in food perception and appreciation in relation to cephalic insulin and PP responses.…”

“…To summarize, endocrine CPRs are found consistently in animal ( 27–31 ), but not in human ( 4 , 32–39 ) studies, which could be due to individual characteristics and specificity to certain food cues ( 45 ). In previous review articles the literature on human CPIR and CPPPR has been summarized and hypotheses have been posited on their roles in satiation and glucose homeostasis.…”

“…Simple sucrose solutions have shown to be sufficient to trigger CPIR in rodents ( 28 , 31 ). However, in humans, studies have failed to observe a CPIR or CPPPR ( 4 , 32–39 ). A wide range of food cues have been used to study CPIR and CPPPR in humans.…”

“…For example, the response may be dependent of weight status, basal insulin concentrations, and eating behavior such as restrained eating or disordered eating ( 46–50 ). Studies also report cephalic phase insulin responders and nonresponders, but have not found a common divider among responders as yet ( 18 , 32 , 45 , 51 ).…”