A variety of epidemiological trials have suggested that higher intake of lycopene-containing foods (primarily tomato products) or blood lycopene concentrations are associated with decreased cardiovascular disease and prostate cancer risk. Of the carotenoids tested, lycopene has been demonstrated to be the most potent in vitro antioxidant leading many researchers to conclude that the antioxidant properties of lycopene are responsible for disease prevention. In our review of human and animal trials with lycopene, lycopene-containing extracts, or tomato products, there is limited support for the in vivo antioxidant function for lycopene. Moreover, tissue levels of lycopene appear to be too low to play a meaningful antioxidant role. We conclude that there is an overall shortage of supportive evidence for the “antioxidant hypothesis” as lycopene’s major in vivo mechanism of action. Our laboratory has postulated that metabolic products of lycopene, the lycopenoids, may be responsible for some of lycopene’s reported bioactivity.

Recent studies suggest that lower survival among gravid squamate reptiles may be partially the result of decreased locomotor ability during gestation. In this study, we compared the speed and endurance of female garter snakes (Thamnophis marcianus), before, during, and after pregnancy. Gravid snakes had significantly lower locomotor performance than did non-gravid females, and performance varied among stages of gestation, reaching a minimum 0-6 weeks prior to parturition. Both number of offspring and relative clutch mass were inversely correlated with locomotor performance; as females increased these traits, locomotor ability decreased. If reduced locomotor performance results in greater risk of predation and/or lowered foraging ability, then natural selection (operating via differential mortality or feeding rates of gravid females) may result in important constraints on both clutch size and relative clutch mass in squamates.

Consumers are often confused about nutrition research findings and recommendations. As content experts, it is essential that nutrition scientists communicate effectively. A case-study of the history of dietary fat science and recommendations is presented, summarizing presentations from an Experimental Biology Symposium that addressed techniques for effective scientific communication and used the scientific discourse of public understanding of dietary fats and health as an example of challenges in scientific communication. Decades of dietary recommendations have focused on balancing calorie intake and energy expenditure and decreasing fat. Reducing saturated fat has been a cornerstone of dietary recommendations for cardiovascular disease (CVD) risk reduction. However, evidence from observational studies and randomized clinical trials demonstrates that replacing saturated fat with carbohydrates, specifically refined, has no benefit on CVD risk, while substituting polyunsaturated fats for either saturated fat or carbohydrate reduces risk. A significant body of research supports the unique health benefits of dietary patterns and foods that contain plant and marine sources of unsaturated fats. Yet, after decades of focus on low-fat diets, many consumers, food manufacturers, and restauranteurs remain confused about the role of dietary fats on disease risk and sources of healthy fats. Shifting dietary recommendations to focus on food-based dietary patterns would facilitate translation to the public and potentially remedy widespread misperceptions about what constitutes a healthful dietary pattern.

A number of recent studies have indicated that life history characteristics (e.g., number of offspring, offspring size, age at sexual maturity) are strongly affected by proximate environmental factors such as prey availability. Evaluating this phenotypic plasticity will be crucial to a complete understanding of the evolution oflife history traits, because the occurrence of such variability casts doubt on the common assumption that the values of life history characteristics expressed in nature are the outcome of long-term natural selection. In this study, we manipulated the diets of a captive-bred colony of the viviparous snake Thamnophis marcianus to determine to what degree the reproductive characteristics of this species were determined by food intake. We found that both number of offspring and clutch mass were significantly affected by prey availability, but that relative clutch mass and offspring size were fixed relative to diet. Our data suggest that like other organisms, T. marcianus shows a gradient in phenotypic plasticity, with some traits more canalized than others. Therefore, intraspecific comparisons of life history characteristics should not be made without information on which traits are subject to phenotypic plasticity.

Calorie restriction (CR) is one of the most potent broadly acting dietary interventions for inducing weight loss and for inhibiting cancer in experimental models. Translation of the mechanistic lessons learned from research on CR to cancer prevention strategies in human beings is important given the high prevalence of excess energy intake, obesity, and metabolic syndrome in many parts of the world and the established links between obesity-associated metabolic perturbations and increased risk or progression of many types of cancer. This review synthesizes findings on the biological mechanisms underlying many of the anticancer effects of CR, with emphasis on the impact of CR on growth factor signaling pathways, inflammation, cellular and systemic energy homeostasis pathways, vascular perturbations, and the tumor microenvironment. These CR-responsive pathways and processes represent targets for translating CR research into effective cancer prevention strategies in human beings.

Lycopene is associated with a reduced risk of prostate cancer. However, lycopene may not be wholly responsible for the effects seen in vivo or in cell culture systems. Apo-lycopenals or other lycopene metabolites, whether produced by cleavage enzymes within the body or consumed with tomato products, can be found in tissues at concentrations equivalent to physiological retinoid concentrations. Therefore, it is plausible that lycopenoids, like retinoids, are bioactive within tissues. Androgen-independent DU145 prostate cancer cells were treated with lycopene, apo-8'-lycopenal, or apo-12'-lycopenal. DU145 cell proliferation was significantly reduced by supra-physiological levels of lycopene and apo-12'-lycopenal, in part, through alteration of the normal cell cycle. Levels of the gap junction protein, connexin 43, were unaltered by lycopene or apo-lycopenal treatment while cell apoptosis rates significantly decreased. We further confirmed that connexin 43 protein levels were unaltered by lycopene treatment in mouse embryonic fibroblasts, or in Dunning R3327-H rat prostate tumor. The present data indicate that lycopene and apo-12'-lycopenal reduce the proliferation of prostate cancer cells, in part, by inhibiting normal cell cycle progression.

Two enzymes have been identified for the oxidative metabolism of carotenoids in mammals. Carotene-15,15'-monooxygenase (CMO-I) primarily centrally cleaves β,β-carotene to form vitamin A. We hypothesize that carotene-9',10'-monooxygenase (CMO-II) plays a key role in metabolism of acyclic nonprovitamin A carotenoids such as lycopene. We investigated carotenoid bioaccumulation in young adult, male, wild-type (WT) mice or mice lacking CMO-II (CMO-II KO). Mice were fed an AIN-93G diet or identical diets supplemented with 10% tomato powder, 130 mg lycopene/kg diet (10% lycopene beadlets), or placebo beadlets for 4 or 30 d. Lycopene preferentially accumulated in CMO-II KO mouse tissues and serum compared with WT mouse tissues. β-Carotene preferentially accumulated in some CMO-II KO mouse tissues compared with WT mouse tissues. Relative tissue mRNA expression of CMO-I and CMO-II was differentially expressed in mouse tissues, and CMO-II, but not CMO-I, was expressed in mouse prostate. In conclusion, the loss of CMO-II expression leads to increased serum and tissue concentrations of lycopene in tomato-fed mice.

No abstract