[1] As someone pointed out, in response to a thread on vitamin K2 & bone health, boron is essential too. Deficiency has been linked to osteoporosis [1a, 1b]. I would not want to be deficient. Although boron toxicity in humans is rare, there doesn't seem to be much point in supplementing beyond 3 mg / day (6 mg for those who don't eat fruit or many vegetables).
Deficiency has a negative effect on testosterone [T], & PCa cases tend to have lower T than matched controls.
[1c] (2011) "Eight healthy male volunteers attended the laboratory on three occasions (days 0, 1 and 7). On the first day (day 0), a blood sample collection at 8.00 A.M was followed by ingestion of placebo with the breakfast. On the next day (supplementation-day 1), similar procedure was followed by ingestion of a capsule containing 10mg of boron. On both occasions blood was collected every 2h for the next 6h. Subjects were requested to consume a capsule of 10mg boron every day with their breakfast, and on the day 7, the blood collection was carried out at 8.00 A.M, again."
"Boron in plasma increased significantly following hours and weekly consumption. Six hours supplementation showed a significant decrease on sex hormone binding globulin (SHBG), high sensitive CRP (hsCRP) and TNF-α level."
"After one week (in samples taken at 8.00 A.M, only), the mean plasma free testosterone increased and the mean plasma estradiol decreased significantly."
"... concentrations of all three inflammatory biomarkers decreased after supplementation."
My own view is that, with age, many men become badly in need of improving the T:estradiol ratio.
One way of assessing boron status might be to have a hair mineral test. If levels are below the norm, supplementation might be useful. The 'norm' isn't the same as 'optimal, of course.
[2] Curtis Eckhert (UCLA David Geffen School of Medicin) has done much of the PCa-boron research (there isn't a lot of it).
[2a] (2004) "boron intake of 95 prostate cancer cases {&} 8,720 male controls"
"After controlling for age, race, education, smoking, body mass index, dietary caloric intake, and alcohol consumption, increased dietary boron intake was associated with a decreased risk of prostate cancer with a dose-response pattern. The adjusted odds ratio was 0.46 ... for the highest quartile of boron intake comparing to the lowest quartile ..." Small number of cases, though. But enough to build a hypothesis?
[2b] (2007) "To determine: ... the correlation of prostate cancer incidence and mortality with groundwater boron ..."
"Increased groundwater boron concentrations, across the state of Texas, correlate with reduced risk of prostate cancer incidence and mortality."
Also: "To determine: ... the impact of boron on prostate cancer cell proliferation during co-treatment with alternative chemo-preventative agents, along with boron pre-treatment effects on cell sensitivity to ionizing radiation."
"Growth inhibition was greater during combined treatments of boric acid and selenomethionine, or boric acid and genistein, versus singular treatments. 8-day boric acid pre-exposure enhanced the toxicity of ionizing radiation treatment, while dose-dependently decreasing the expression of anti-apoptotic protein Bcl-2."
[2c] (2009) Calcium "signaling is a central regulator of cell proliferation, but has received little attention in cancer prevention. We and others have reported a strong dose-dependent reduction in the incidence of prostate and lung cancer within populations exposed to boron (B) in drinking water and food; and in tumor and cell proliferation in animal and cell culture models."
"In conclusion, {boric acid} has previously been reported to reduce the risk of prostate cancer in humans and reduce tumor growth and prostate cancer cell proliferation, migration, and invasion. Our results demonstrate that physiological levels of {boric acid} inhibit agonist stimulated release of stored {calcium} in a dose dependent manner and lower stored {calcium} storage levels. This suggests that {boric acid's} ability to dampen {calcium} signaling in cancer cells underlies its ability to reduce clinical cancer risk."
[2d] (2009) Similar to [2c], but here the emphasis is on boron toxicity at high levels probably being due to impaired calcium signaling.
[2e] (2004) cell study
"Here we report that boric acid, the dominant form of boron in plasma, inhibits the proliferation of prostate cancer cell lines, DU-145 and LNCaP, in a dose-dependent manner. Non-tumorigenic prostate cell lines, PWR-1E and RWPE-1, and the cancer line PC-3 were also inhibited, but required concentrations higher than observed human blood levels. Studies using DU-145 cells showed that boric acid induced a cell death-independent proliferative inhibition, with little effect on cell cycle stage distribution and mitochondrial function."
The cell lines LNCaP, DU-145 & PC-3 were derived from lymph node, brain & bone mets. Seems that the latter required a higher level of boron than found in the blood.
[2f] (2005) Boric acid & cell changes in DU-145 PCa.
I understand why the study was done:
"The rationale for this study was based on the fact that {boric acid} is (i) a natural constitute of human blood, (ii) readily absorbed with plasma levels determined by dietary intake, and (iii) there is epidemiological, animal, and cell culture evidence supporting its antiproliferative capacity in prostate cancer."
However, DU-145, derived from a brain met, might not tell us much about the effect on bone mets. (Also, I don't know how the blood-brain barrier affects brain levels of boric acid.) I wonder why Eckhert did not opt for the LNCaP cell line.
[3a] (2007) Part of the VITamins And Lifestyle (VITAL) study. Far bigger study than [2a].
"This cohort study provides no evidence for a preventive role of boron intake on prostate cancer. Since few studies exist on this topic, future research is needed to better elucidate any role that boron may play in the prevention of prostate cancer."
Studies [2a] & [3a] had quite different designs. A similarity, though, was the use of a food questionnaire. There is no indication whether local water sources were considered as a boron source. Water can be a very significant source of boron, as study [2b] seems to indicate.
Googling <Boron deficiency "u.s.">, I get sites on boron deficiency in tomatoes, palms in Hawaii, cotton, alfalfa & peaches - all on the first page. Nothing about humans. I can't find an estimate of deficiency in the U.S. Perhaps not surprising, since there is no RDA.
Could the VITAL cohort have had less defiency?:
"Supplement users were targeted in recruitment, therefore supplement use by cohort members is both high and of long duration." [3b]
[4] The Romanian researcher Scorei has produced a dozen papers on the benefits of calcium fructoborate, a bioavailable patented form of borate, similar to complexes found in edible plants [FruiteX-B]. It appears in various products, such as:
swansonvitamins.com/swanson...
[4a] (2015) A human study of the effect of two different doses of Calcium fructoborate (CFB) on inflammation markers:
"CFB-1 showed a reduction in blood levels of CRP {C-reactive protein} by 31.3 % compared to baseline. CFB-1 and CFB-2 reduced LDL levels by 9.8 and 9.4 %, respectively. CFB-1 decreased blood homocysteine by 5.5 % compared with baseline, whereas CFB-2 did not have a significant effect. Blood levels of TG {triglycerides} were reduced by 9.1 and 8.8 % for CFB-1 and CFB-2, respectively. Use of both CFB-1 and CFB-2 resulted in significantly reduced IL-6 levels, when compared within and between groups. IL-1β was reduced by 29.2 % in the CFB-1 group. Finally, CFB-1 and CFB-2 reduced MCP-1 by 31 and 26 %, respectively."
-Patrick
[1a] ncbi.nlm.nih.gov/pubmed/222...
[1b] ncbi.nlm.nih.gov/pubmed/114...
[1c] ncbi.nlm.nih.gov/pubmed/211...
[2a] ncbi.nlm.nih.gov/pubmed/150...
[2c] ncbi.nlm.nih.gov/pmc/articl...
[2d] ncbi.nlm.nih.gov/pubmed/185...
[2e] ncbi.nlm.nih.gov/pubmed/155...
[2f] ncbi.nlm.nih.gov/pmc/articl...
[3a] ncbi.nlm.nih.gov/pubmed/178...
