Each of the macronutrients, carbohydrate, protein and fat, has a unique set of properties that influence health, but all are a source of energy. The optimal balance of their contribution to the diet has been a long-standing matter of debate. Over the past half century, there has been a progression of thinking regarding the mechanisms by which each may contribute to energy balance. At the beginning of this time period, the emphasis was on metabolic signals that initiated eating events (i.e., determined eating frequency). This was followed by an orientation to gut endocrine signals that purportedly modulate the size of eating events (i.e., determined portion size). Most recently, research attention has been directed to the brain where the reward signals elicited by the macronutrients are viewed as potentially problematic (i.e., contribute to disordered eating). At this point the predictive power of the macronutrients for energy intake remains limited.

Berries and other anthocyanin-rich treatments have prevented weight gain and adiposity in rodent models of diet-induced obesity. Their efficacy may be explained by modulation of energy substrate utilization. However, this effect has never been translated to humans. The objective of this study was to evaluate the effects of berry intake on energy substrate use and glucoregulation in volunteers consuming a high-fat diet. Twenty-seven overweight or obese men were enrolled in a randomized, placebo-controlled crossover study with two treatment periods. Subjects were fed an investigator controlled, high-fat (40% of energy from fat) diet which contained either 600 g/day blackberries (BB, 1500 mg/day flavonoids) or a calorie and carbohydrate matched amount of gelatin (GEL, flavonoid-free control) for seven days prior to a meal-based glucose tolerance test (MTT) in combination with a 24 h stay in a room-sized indirect calorimeter. The washout period that separated the treatment periods was also seven days. The BB treatment resulted in a significant reduction in average 24 h respiratory quotient (RQ) (0.810 vs. 0.817, BB vs. GEL, p = 0.040), indicating increased fat oxidation. RQ during the MTT was significantly lower with the BB treatment (0.84) compared to GEL control (0.85), p = 0.004. A 4 h time isolation during dinner showed similar treatment effects, where RQ was reduced and fat oxidation increased with BB (0.818 vs. 0.836, 28 vs. 25 g, respectively; BB vs. GEL treatments). The glucose AUC was not different between the BB and GEL treatments during the MTT (3488 vs. 4070 mg·min/dL, respectively, p = 0.12). However, the insulin AUC was significantly lower with the BB compared to the GEL control (6485 vs. 8245 µU·min/mL, p = 0.0002), and HOMA-IR improved with BB (p = 0.0318). Blackberry consumption may promote increased fat oxidation and improved insulin sensitivity in overweight or obese males fed a high fat diet.

Limited information exists on the effectiveness of potential treatments to reduce levels of opium alkaloids that may be present in seeds from poppy (Papaver somniferum L.). Poppy seeds containing morphine at relatively lower (14.7 mg kg–1) and higher (210.0 mg kg–1) concentrations were subjected to dry heat and steam treatments, water washing, and baking. Sample extracts were then analyzed using liquid chromatography–tandem mass spectrometry for the opium alkaloids morphine, codeine, and thebaine. The results indicated that thermal treatment promoted opium alkaloid degradation in poppy seed samples, with a 50% loss of morphine observed after 30–40 min at 200 °C. Water washing reduced concentrations of opium alkaloids in poppy seeds by approximately 50–80%, while steam treatment resulted in reduction of morphine in only one sample type. Importantly, baking had no significant effect on concentrations of opium alkaloids. Overall, these results indicate that opium alkaloids may not be significantly affected by baking or steam application and that poppy seeds may require water washing or extended thermal treatment to promote reduction of these compounds.

Interest in the application of phenolic compounds from the diet or supplements for the prevention of chronic diseases has grown substantially, but the efficacy of such approaches in humans is largely dependent on the bioavailability and metabolism of these compounds. Although food and dietary factors have been the focus of intense investigation, the impact of disease states such as obesity or diabetes on their absorption, metabolism, and eventual efficacy is important to consider. These factors must be understood in order to develop effective strategies that leverage bioactive phenolic compounds for the prevention of chronic disease. The goal of this review is to discuss the inducible metabolic systems that may be influenced by disease states and how these effects impact the bioavailability and metabolism of dietary phenolic compounds. Because current studies generally report that obesity and/or diabetes alter the absorption and excretion of these compounds, this review includes a description of the absorption, conjugation, and excretion pathways for phenolic compounds and how they are potentially altered in disease states. A possible mechanism that will be discussed related to the modulation of phenolic bioavailability and metabolism may be linked to increased inflammatory status from increased amounts of adipose tissue or elevated plasma glucose concentrations. Although more studies are needed, the translation of benefits derived from dietary phenolic compounds to individuals with obesity or diabetes may require the consideration of dosing strategies or be accompanied by adjunct therapies to improve the bioavailability of these compounds.