All:
Coming in late on this, hoping to avoid a premature decision:
As of now my ideas are change are:
Removing all carotenoids, including the beta-carotene, lutein, lycopene, etc. supplemental carotenoids have consistantly been linked to various types of cancer and imo, are not worth the risk.
I don't believe there's any evidence that supplemtnal lycopene has been linked to increased cancer risk; lutein, as noted elsewhere on VITAL, was only thus linked at very high doses. On lycopene:
lycopene seems to be a negative for prostate cancer. Other recent references find it neutral, while one finds benefit from lycopene in people with a particular MNSOD SNP.
I wouldn't put any real weight on the first study above. First, it was a case-control study, which is a weak methodology and not justified in a relatively common disease like PCA. Second, and more importantly, they didn't actually even
evaluate outcomes for
prostate cancer: they found an outcome for
PSA, which (as USPTFS and multiple bodies have concluded) is useless for
screening of prostate cancer (as opposed to its
diagnostic and monitoring uses, which were not addressed in this study). For all we know, lycopene raises PSA for reasons that have nothing to do with PCA, or that are even protective. Also, even if there were a real PCA signal here, it might yet be protective: some nutrients appear to be unassociated with, or increase the incidence of, non-life-threatening, 'indolent' cancers, but
decrease the risk of aggressive cancer (or vice-versa), and serum/plasma lycopene is one of them: plasma "lycopene and the sum of carotenoids ... were not associated with the risk of localized disease but were inversely associated with the risk of advanced disease. The risk of advanced disease for men in the highest fifth of plasma concentrations compared with men in the lowest fifth was 0.40 (95% CI: 0.19, 0.88) for lycopene and 0.35 (95% CI: 0.17, 0.78) for the sum of carotenoids" (
here).
And also, even if (again) PSA in this study is a real signal of undiagnosed prostate tumors, retrospective bias is especially likely here, as people who have reason to suspect they might have PCA are (after all the promotion by supplement hawkers and Hunt's) all the more likely to start upping their tomato product intake and/or taking lycopene supplements. The same is true, to a lesser extent, of age, as the authors note, along with other reasons to not take their finding too seriously:
The finding that lycopene was positively associated with a tPSA threshold level is inconsistent with current knowledge [31–42]. Previous studies have mostly implied either no association or a protective effect of lycopene against PCa. For instance, a recent meta-analysis of seven studies suggested that serum lycopene was inversely related to PCa risk [RR = 0.74 (0.59–0.92)] [43]. In our study, it is plausible that the distinct relationships observed between serum levels of lycopene and tPSA before and after adjustment for selected characteristics are due to strong confounding by at least one of the variables that we adjusted for. We performed separate analyses for each of the selected characteristics and identified age as being the strongest confounder, based on changes in the estimated odds ratios for the hypothesized relationship. In addition, adjusting for age, but not for other characteristics, was sufficient to change the direction of the relationship between lycopene and tPSA from inverse in the unadjusted model to direct in the adjusted model. In our study, unadjusted results overwhelmingly support an inverse association between lycopene and tPSA level, as hypothesized. However, this association changed to positive after simply adjusting for age. Confounding bias by older age is plausible as it is associated with both higher PSA levels and potentially higher lycopene intake (through supplements or diet) as a consequence of prostate health awareness. These relationships would result in an upward bias, as is seen in the adjusted models.
Major epidemiologic studies of the inverse association between lycopene intake and PCa were published in the late 1990s and early 2000s, which could have influenced lycopene intake among older men with higher PSA levels (and perhaps undiagnosed, underlying disease) in the current study period from 2001–2006. Furthermore, the effect of lycopene at the 2.5 ng/ml threshold was shown to be different from its effect at the 4 and 10 ng/ml thresholds of tPSA. This finding implies the need for further investigation into the possibility of a non-linear relationship between lycopene and tPSA levels.
According to Erdman and colleagues [44], lycopene has been shown to be the most potent in vitro antioxidant of all carotenoids tested, yet in vivo studies do not support the hypothesis that lycopene (found at low concentrations in animal and human tissues) can protect against PCa through its antioxidative properties [44]. The authors suggest alternative mediators of the protective effect of lycopene on screen-detected PCa, namely apoptosis, cell cycle inhibition, insulin-like growth factor 1 axis, gap junction communication, androgen status, detoxification enzymes, and C-reactive protein [44].
The
2004 meta-analysis the cite (which is the latest systematic evaluation of the evidence AFAICS) found that "Our results show that tomato products may play a role in the prevention of prostate cancer. However, this effect is modest and restricted to high amounts of tomato intake." Later studies include the EPIC serum lycopene study above and
this one, and my impression (and evidently the investigators in this newest study) are on balance favorable.
Also anyone eating even a moderate amount of fruits and veggies will blow the DRI for vitamin A out the window.
Sure, but the same is true for very nearly everything else. remember my COM analysis of a Big Mac, large fries, and a chocolate milkshake. This is inevitable with multivitamins; we have to either abandon the project, or accept that people will need to take a partial dose and tweak, and still be less than perfectly balanced.