Higher intake of total flavonoids was linked to a significantly elevated risk of prostate cancer, decreased risk in women-specific cancers

demonstrating higher consumption of isoflavones with a decreased risk of endometrial cancer among case–control studies and the higher intake category of total flavonoids with an elevated risk of prostate cancer confined to prospective studies. Nevertheless, a meta-analysis of randomized controlled trials (RCTs) revealed an effect by higher isoflavone intake for a lower risk of prostate cancer [90].

So meta analyses of randomized controlled trials showed isoflavones DECREASED prostate cancer risk.

Here is the study they reference: https://sci-hub.se/10.1111/bju.12435

They also say this:

>On the contrary, there are some limitations and challenges to be settled in the research. As only observational studies were included, evidence power is not very strong yet. The sample size of individual studies is small and there
may still be other unknown confounding factors affecting the results. This limits the opportunities for extrapolation. Further intervention studies are needed to confirm our conclusion. The number of eligible studies is still limited, especially for certain cancers, thus flavonoid subclasses cannot be synthetically analyzed. Further, the criteria for the included studies allowed no subgroup analyses based on dietary and other sources (urine/serum/plasma) of flavonoids to be performed. For the sake of avoiding unnecessary heterogeneity, RCTs were not included in our meta-analysis. Limited clinical trials have prevented our results from providing more conclusive evidence.

>Sensitivity analyses for total flavonoids and HRCs were performed (Fig. 5 and Supplementary Table S8). When any study except Ghanavati’s [81] was eliminated, there was no evidence that total flavonoids had a detrimental
effect on prostate cancer. When Wang’ study [77] was eliminated, the dangerous effect of total flavonoids on men-specific cancers disappeared. For other cancers, no statistically significant change in combined effect sizes was detected after excluding each study separately.

Here are those cited studies:

https://academic.oup.com/aje/article-pdf/179/8/974/252775/kwu006.pdf

https://sci-hub.se/10.1111/ecc.13364

So if you eliminate the single study from Wang, the correlation between isoflavones and prostate cancer risk disappear. If you read that study, it is not as clear as it seems.

To our knowledge, the present study was the first prospective study to comprehensively examine dietary flavonoid andproanthocyanidin intakes with prostate cancer risk by tumor grade and stage in US men. Overall, greater flavonoid intake was positively associated with total prostate cancer risk, mostly driven by associations during the first 2 years of follow-up. Total flavonoids, especially proanthocyanidins, showed suggestive protective associations with high-grade prostate cancer among men who were followed from 2 years after returning the 1999 survey. No subclass of flavonoids was significantly associated with advanced disease. Several potential explanations may account for the positive associations with overall prostate cancer seen in our study. First, higher dietary flavonoid intake was associated with several healthier lifestyle factors, such as less smoking, less overweight or obesity, and lower prevalence of type 2 diabetes. Being overweight and having a history of diabetes have been associated with a lower risk of overall prostate cancer in the CPS-II cohort (33, 35). Although body mass index and history of diabetes were included in the multivariable models, residual confounding may exist and contribute to the positive associations for total flavonoids and some subclasses with overall prostate cancer risk. Secondly, the prevalence of PSA screening was higher in men in the top categories of dietary total flavonoid intake than in men in the lowest category, and a history of PSA screening was positively associated with nonaggressive prostate cancer in this cohort. As reported by other studies, PSA screening has increased the likelihood of diagnosis of early-stage tumors (36, 37). Third, the positive associations of total flavonoids and some individual flavonoids with high-grade prostate cancer risk within the first 2 years of follow-up, mostly driven by the top quintile, also need to be interpreted with caution. These associations might be due to reverse causality, in that men who had symptoms were likely to improve their diets. Isoflavones are the most commonly studied flavonoid class in relation to prostate cancer because of the hypothesized protective effects of phytoestrogens on hormone-related cancers (38), but associations remain inconclusive.

LOL, so that study doesn't even prove any causality at all. It's counfounded to shit! Even then, some of their findings shows that soem flavonoids DECREASED prostate cancer risk. The other increases are likely due to the fact that people who consume flavonoids are healthier overall, and are less likely to be overweight with diabetes. Well being overweight with diabetes lowers risks of prostate cancer, surprisingly enough. Does that mean we all go get fat and eat sugar to lower our prostate cancer risk? Moreover, they couldn't rule out reverse causality, where people who had symptoms of prostate cancer improved their diets, which increased flavonoid consumption. So this study really doesn't show what people think it does. Remove that study from the meta-analysis you posted, and the correlation goes away.

Let's look at the Ghanavati study.

After adjusting the impact of confounders, individual in the highest tertile of flavone intake (OR=0.3 95% CI=0.12–0.87), flavanone intake (OR=0.10; 95% CI=0.03–0.31) and flavanol intake (OR=0.24; 95% CI=0.08–0.67) compared with those in the lowest quartile of intake showed a significant decrease in the risk of PCa. As detailed in Table 5, there was no significant association between dietary TAC and PCa after adjusting for the effect of confounders

So a decrease in the risk of prostate cancer with flavone intake...

In our study, there was a significant inverse relationship between total flavonoid intake, and subgroups including flavonols, flavones, flavanones, anthocyanidins and isoflavones, and the risk of PCa. Indeed, recent studies have shown the putative protective role of flavonoids and subgroups against some types of cancer (Cui et al., 2016; Hui et al., 2013; Tang et al., 2009). A meta-analysis by He et al. found that procyanidin and isoflavones were protective against colon cancer; however, there was insufficient evidence to support a relationship between increased total flavonoid intake and reduced risk of colon cancer (He & Sun, 2016). Despite the large number of studies to have investigated the effect of flavonoid intake and the risk of PCa, much of the reported results are equivocal. Consistent with our results, in a meta-analysis published in 2016, a significant relationship was observed between high intake of anthocyanidine and reduced PCa risk (Guo et al., 2016). Lewis et al. (2009) in acase–control study in Japan, found a significant inverse relationship between high isoflavone (daidzein and genistein) consumption and risk of PCa (Lewis et al., 2009), whilst, in another case–control study, individuals receiving high amounts of isoflavones (genistein and daidzein) had a 14% and 20% lower chance of developing PCa, respectively (Nagata et al., 2016). In addition, it has been reported that higher intake of soya, as an important source of isoflavones, may be associated with reduced risk of PCa (Applegate et al., 2018).

So that study is showing dietary flavone/flavonoid intake is associated with lower instances of prostate cancer. I am not seeing where they get the conclusion they are making. All I am seeing is a clear correlation to DECREASED prostate cancer risk, and confounding variables in the single study showing a positive correlation.