Chronic and immediate refined carbohydrate consumption and facial attractiveness.

The Western diet has undergone a massive switch since the second half of the 20th century, with the massive increase of the consumption of refined carbohydrate associated with many adverse health effects. The physiological mechanisms linked to this consumption, such as hyperglycaemia and hyperinsulinemia, may impact non medical traits such as facial attractiveness. To explore this issue, the relationship between facial attractiveness and immediate and chronic refined carbohydrate consumption estimated by glycemic load was studied for 104 French subjects. Facial attractiveness was assessed by opposite sex raters using pictures taken two hours after a controlled breakfast. Chronic consumption was assessed considering three high glycemic risk meals: breakfast, afternoon snacking and between-meal snacking. Immediate consumption of a high glycemic breakfast decreased facial attractiveness for men and women while controlling for several control variables, including energy intake. Chronic refined carbohydrate consumption had different effects on attractiveness depending on the meal and/or the sex. Chronic refined carbohydrate consumption, estimated by the glycemic load, during the three studied meals reduced attractiveness, while a high energy intake increased it. Nevertheless, the effect was reversed for men concerning the afternoon snack, for which a high energy intake reduced attractiveness and a high glycemic load increased it. These effects were maintained when potential confounders for facial attractiveness were controlled such as age, age departure from actual age, masculinity/femininity (perceived and measured), BMI, physical activity, parental home ownership, smoking, couple status, hormonal contraceptive use (for women), and facial hairiness (for men). Results were possibly mediated by an increase in age appearance for women and a decrease in perceived masculinity for men. The physiological differences between the three meals studied and the interpretation of the results from an adaptive/maladaptive point of view in relation to our new dietary environment are discussed.

Can postfertile life stages evolve as an anticancer mechanism?

Why a postfertile stage has evolved in females of some species has puzzled evolutionary biologists for over 50 years. We propose that existing adaptive explanations have underestimated in their formulation an important parameter operating both at the specific and the individual levels: the balance between cancer risks and cancer defenses. During their life, most multicellular organisms naturally accumulate oncogenic processes in their body. In parallel, reproduction, notably the pregnancy process in mammals, exacerbates the progression of existing tumors in females. When, for various ecological or evolutionary reasons, anticancer defenses are too weak, given cancer risk, older females could not pursue their reproduction without triggering fatal metastatic cancers, nor even maintain a normal reproductive physiology if the latter also promotes the growth of existing oncogenic processes, e.g., hormone-dependent malignancies. At least until stronger anticancer defenses are selected for in these species, females could achieve higher inclusive fitness by ceasing their reproduction and/or going through menopause (assuming that these traits are easier to select than anticancer defenses), thereby limiting the risk of premature death due to metastatic cancers. Because relatively few species experience such an evolutionary mismatch between anticancer defenses and cancer risks, the evolution of prolonged life after reproduction could also be a rare, potentially transient, anticancer adaptation in the animal kingdom.

Changes in diet associated with cancer: An evolutionary perspective.

Changes in diet are frequently correlated with the occurrence and progression of malignant tumors (i.e., cancer) in both humans and other animals, but an integrated conceptual framework to interpret these changes still needs to be developed. Our aim is to provide a new perspective on dietary changes in tumor-bearing individuals by adapting concepts from parasitology. Dietary changes may occur alongside tumor progression for several reasons: (i) as a pathological side effect with no adaptive value, (ii) as the result of self-medication by the host to eradicate the tumor and/or to slow down its progression, (iii) as a result of host manipulation by the tumor that benefits its progression, and finally (iv) as a host tolerance strategy, to alleviate and repair damages caused by tumor progression. Surprisingly, this tolerance strategy can be beneficial for the host even if diet changes are beneficial to tumor progression, provided that cancer-induced death occurs sufficiently late (i.e., when natural selection is weak). We argue that more data and a unifying evolutionary framework, especially during the early stages of tumorigenesis, are needed to understand the links between changes in diet and tumor progression. We argue that a focus on dietary changes accompanying tumor progression can offer novel preventive and therapeutic strategies against cancer.

In Vivo imaging reveals extracellular vesicle-mediated phenocopying of metastatic behavior.

Most cancer cells release heterogeneous populations of extracellular vesicles (EVs) containing proteins, lipids, and nucleic acids. In vitro experiments showed that EV uptake can lead to transfer of functional mRNA and altered cellular behavior. However, similar in vivo experiments remain challenging because cells that take up EVs cannot be discriminated from non-EV-receiving cells. Here, we used the Cre-LoxP system to directly identify tumor cells that take up EVs in vivo. We show that EVs released by malignant tumor cells are taken up by less malignant tumor cells located within the same and within distant tumors and that these EVs carry mRNAs involved in migration and metastasis. By intravital imaging, we show that the less malignant tumor cells that take up EVs display enhanced migratory behavior and metastatic capacity. We postulate that tumor cells locally and systemically share molecules carried by EVs in vivo and that this affects cellular behavior.