The health effects of (poly)phenols (PPs) depend upon their bioavailability that, in general, is very low and shows a high interindividual variability. The low bioavailability of PPs is mainly attributed to their low absorption in the upper gastrointestinal tract as a result of their low water solubility, their presence in foods as polymers or in glycosylated forms, and their tight bond to food matrices. Although many studies have investigated how technological and biotechnological processes affect the phenolic composition of fruits and vegetables, limited information exists regarding their effects on PP bioavailability in humans. In the present review, the effect of food processing (mechanical, thermal, and non-thermal treatments), oral-delivery nanoformulations, enzymatic hydrolysis, fermentation, co-administration with probiotics, and generation of postbiotics in PP bioavailability have been overviewed, focusing in the evidence provided in humans.

Recent clinical trials suggest that early nutritional support might block the induction of autophagy in critically ill patients leading to the development of organ failure. However, the regulation of autophagy, especially by nutrients, in critical illness is largely unclear. The autophagy flux (AF) in relation to critical illness and nutrition was investigated by using an in vitro model of human primary myotubes incubated with serum from critically ill patients (ICU). AF was calculated as the difference of p62 expression in the presence and absence of chloroquine (50 µM, 6 h), in primary myotubes incubated for 24 h with serum from healthy volunteers (n = 10) and ICU patients (n = 93). We observed 3 different phenotypes in AF, non-altered (ICU non-responder group), increased (ICU inducer group) or blocked (ICU blocker group). This block was not associate with a change in amino acids serum levels and was located at the accumulation of autophagosomes. The increase in the AF was associated with lower serum levels of non-essential amino acids. Thus, early nutrition during critical illness might not block autophagy but could attenuate the beneficial effect of starvation on reactivation of the autophagy process. This could be of clinical importance in the individual patients in whom this process is inhibited by the critical illness insult.

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