Here's another one in favor of caution. It's a great review that supports the assumption that if selenium has an useful role in cancer, it comes associated with its pro-oxidant effects. Travisord, you posted a study on colon cancer, but it was in vitro if I'm not wrong. They claim that there's no specificity, you can't control where the excess of selenomethionine is going to be spilling, which is why the other authors above mentioned that perhaps encapsulating and delivering the selenium to the colon cancer region (just like curcumin) is a reasonable approach. All in all, one thing is for sure: a slight excess has pro-oxidant action, and this is unnecessary stress for maintenance. And now it raises the question if it's indeed good for cancer since the data is conflicting and there wasn't anything exceptional happening in trials. Supplementing 200mcg of selenomethionine will give you 250mcg or more when added to dietary intake, is this sufficient to stress and insufficient to make a difference? I don't know.
The Epidemiology of Selenium and Human Cancer - ScienceDirect
"the amount and activity of antioxidant selenoproteins, particularly glutathione peroxidases and plasma selenoprotein P, have been frequently used as indirect indicators of selenium intake, and their low levels have been frequently interpreted as a consequence and a biomarker of selenium deficiency (Fairweather-Tait et al., 2011; Jablonska & Vinceti, 2015; Labunskyy et al., 2014; Vinceti et al., 2009). However, this approach overlooks the fact that selenoprotein levels and activity increase as a compensatory response to oxidative stress, and therefore,
several stressors with pro-oxidant activity, including high amounts of some selenium species, may upregulate selenoproteins (as well as other antioxidant enzymes) thanks to this mechanism (Hafeman, Sunde, & Hoekstra, 1974; Jablonska & Vinceti, 2015; Touat-Hamici et al., 2014; Vinceti et al., 2009). In addition, no clear relation between selenoprotein activity per se and health outcomes has been established so far in epidemiologic studies. These
complex relations between selenium exposure and selenoprotein activity may explain why some regulatory agencies have not adopted a proteomic approach based on maximal upregulation of selenoprotein levels by ingested selenium when setting the dietary reference values for this element (Jablonska & Vinceti, 2015; Vinceti et al., 2017)."
"With specific reference to cancer, interest in a possible etiological role of selenium was first sparked by laboratory animal studies, suggesting the ability of selenium to enhance cancer growth (Nelson, Fitzhugh, & Calvery, 1943; Schroeder & Mitchener, 1972; Seifter, Ehrich, Hudyma, & Mueller, 1946) and later to counteract it (Clayton & Baumann, 1949; Shamberger & Rudolph, 1966). Similarly, ambiguous effects have been observed in more recent studies, which have reported that
forms of selenium may enhance carcinogenesis (Birt et al., 1988; Chen et al., 2000; National Toxicology Program, 2011; Novoselov et al., 2005; Su, Tang, Tang, & Gao, 2005; Woutersen, Appel, & Van Garderen-Hoetmer, 1999)
, reduce it (Guo, Hsia, Hsiung, & Chen, 2015; INCHEM, 1987; Nakahara et al., 2013; Steinbrenner, Speckmann, & Sies, 2013; Wang, Sun, Tan, Wu, & Zhang, 2014; Wrobel, Wolff, Xiao, Power, & Toborek, 2016; Yang, Jia, Chen, Yang, & Li, 2012)
, or exert ambivalent effects through the selenoproteins (Brigelius-Flohe & Kipp, 2016; Hatfield, Yoo, Carlson, & Gladyshev, 2009; Kasaikina et al., 2013; Varlamova & Cheremushkina, 2017)."
Davezord, remember our talk about references? Words spoke louder than words.
"For decades, controversies regarding selenium have abounded, with claims of health benefits met with counterclaims of harm. An atmosphere of selenophobia, or fear of the health effects of selenium, in the early 1970s (Frost, 1972) gave way to a culture of selenophilia focused on the health benefits of selenium in the late 1980s (Casey, 1988). Driving the selenophilia side of the debate has been the fascinating possibility that changes of just a few μg/day in dietary intake of selenium may modify the risk of cancer."
"
Smoking, for example, is a source of selenium exposure, but it also paradoxically leads to lower levels of selenium in blood, possibly due to an interaction with cadmium ( Jossa et al., 1991; Vinceti, Grill, et al., 2015)."
"The SELECT was conducted as a response to the apparent prostate cancer risk reduction findings of the NPC trial and of a trial of vitamin E (The Alpha-Tocopherol Beta Carotene Cancer Prevention Study Group, 1994), and findings from other trials examining a combination of vitamin E and selenium and other antioxidant substances (Lippman et al., 2009). This trial, a major effort by groups of oncology investigators and supported by the US National Cancer Institute, is for its size, cost (over 114 million US $), and soundness of scientific design not only the most important trial for selenium but also one of the most important trials ever implemented in the field of nutritional epidemiology and cancer chemoprevention (Goodman et al., 2013; Lippman et al., 2005)."
"
The trials have consistently shown that selenium administration, in the form of 200 μg/day of organic selenium exclusively or predominantly as selenomethionine, with the exception of 250 μg/day of inorganic selenium in the Polish trial,
does not reduce the risk of overall cancer or of major cancer types (Table 1). This conclusion is also reached when performing summary meta-analyses of these trials, as reported in Fig. 3."
"As shown in Fig. 3, summary estimates
did not show evidence of any beneficial effect of selenium supplementation on cancer risk when looking at all cancers (Fig. 3A)
and major cancer types such as colorectal cancer, melanoma and nonmelanoma skin cancer, and lung, breast, bladder, and prostate cancers (Fig. 3B–H). Limiting the analysis to the RCTs with the best methodological quality, these results were confirmed and suggested
if anything a potential excess risk for breast and lung cancer and for melanoma. In a single study in patients with a history of resected lung cancer (Karp et al., 2013),
selenium supplementation was also unexpectedly associated with a statistically unstable increase of some cancers such as hepatobiliary cancer, though the small number of cases made it difficult to evaluate the results."
"Subjects in the lowest baseline selenium status tertile in the NBT trial (Algotar et al., 2013) did not show a prostate cancer reduction despite being comparable (Table IV of that paper and Fig. 2) with the two NPC trial lowest and middle baseline selenium tertiles, which showed strong reductions in all cancer and prostate cancer incidence (Duffield-Lillico, Dalkin, et al., 2003; Duffield-Lillico et al., 2002)."
Simply correcting a deficiency?
"Overall, despite the heterogeneity of the study populations, the results of RCTs are consistent in ruling out a beneficial effect of selenium supplementation, further confirming the SELECT results. This is particularly true when limiting the analysis to the high-quality, low-bias studies (Fig. 3).
Therefore, it is now clear that selenium intakes of around 250 μg/day [what you get from diet + supplement]
or above have no effect on cancer risk compared with lower amounts, and they might also have adverse effects on the risk of cancer or other chronic diseases, contrary to previous claims about the possible benefits of supranutritional selenium intakes (Rayman, 2002)."
As part of a therapy:
"The mechanisms underlying the anticancer and antiproliferative properties of selenium compounds are not well established and are still under active investigation. They encompass a spectrum of effects including
pro-oxidant and proteomic activities, which ultimately induce apoptosis, necrosis, and paraptosis (Bao et al., 2015; Fernandes & Gandin, 2015; Zhao et al., 2016). Therefore, the potential use of intermediate to high doses of selenium species in cancer therapy and more generally in human disease appears to be
driven by its toxicological properties (Forceville, 2013; Jablonska & Vinceti, 2015; Nogueira & Rocha, 2011), and selenium compounds when used in this context must be considered drugs and tested as such in appropriate animal and human studies."
"Results of these trials indicate that raising exposure of organic selenium to supranutritional levels of about 300 μg/day is not effective in reducing cancer risk and may even increase it, and it also appears to increase the incidence of type 2 diabetes. As far as lower amounts of selenium intake (falling in the nutritional range) and their relation with cancer risk are concerned, no evidence from high-quality trials is available and no conclusion can be drawn from observational studies due to their methodological limitations, such as unmeasured confounding and exposure misclassification."