IngredientsChemical name and symbol: Boron (symbol: B) is element number 5 on the periodic table. It is a semimetal (metalloid) of main Group 13 (IIIa, or boron group) of the periodic table, essential to plant growth and of wide industrial application. As a metalloid, it exhibits the properties of both metals and nonmetals.
Physical forms: Pure crystalline boron is a black, lustrous semiconductor; it conducts electricity like a metal at high temperatures and is almost an insulator at low temperatures. It is hard enough (9.3 on Mohs scale) to scratch some abrasives, such as carborundum, but too brittle for use in tools. It has allotropes in the form of an amorphous powder and three major crystalline forms.
Isotopes: Naturally occurring boron has two stable isotopes with mass numbers 10 and 11. Boron-11 is the most prevalent isotope with an abundance of 80%, while the remaining 20% are completely made up of boron-10.
Occurrence in nature: Boron does not occur in its elemental state on Earth, but various borate minerals are found in natural deposits worldwide. It constitutes about 0.001 percent by weight of Earth's crust. It is concentrated on Earth by the water-solubility of its more common naturally occurring compounds, the borate minerals. Boron occurs as an orthoboric acid in some volcanic spring waters, and as borates in the minerals borax and colemanite. At a concentration of 4.6 ppm, seawater contains trace amounts of boron.
Important mineral sources: Boron occurs combined as borax, kernite, and tincalconite (hydrated sodium borates), the major commercial boron minerals, especially concentrated in the arid regions of California, and as widely dispersed minerals such as colemanite, ulexite, and tourmaline. There are over 200 minerals which contain boron, but only a few, such as colemanite and borax, are commercially important. By far the most important source of boron is rasorite (kernite), found in the Mojave Desert in California, USA.
Global production: The largest global borax deposits are in Central and Western Turkey. Global proven boron mineral mining reserves exceed one billion metric tonnes, against a yearly production of about four million tonnes. Turkey and the United States are the largest producers of boron products.
In dietary supplements, boron is present in many different forms, including sodium borate, sodium tetraborate, boron amino acid chelate, boron ascorbate, boron aspartate, boron citrate, boron gluconate, boron glycinate, boron picolinate, and calcium fructoborate.
Scientists do not know if one form of boron is better than others. In a small human study, boron as sodium tetraborate significantly increased plasma boron levels within 4–6 hours of consumption, but no data are available on the relative bioavailability of different forms of supplemental boron.
Dietary sources: Plant foods—including fruit, tubers, and legumes—contain the largest amounts of boron. Wine, cider, and beer also contain boron. The main sources of boron in the diets of people in the United States are coffee, milk, apples, dried and cooked beans, and potatoes, primarily because people tend to consume large amounts of these foods. Most adults in the United States get about 1 milligram (mg) of boron a day from food. People who eat more plant foods tend to get more boron than people who eat fewer plant foods.
Boron is a mineral easily absorbed through the gastrointestinal epithelium, and may reach an absorption rate of about 90%. When it enters the body, it is hydrolyzed to boric acid, which is absorbed by enterocytes and transported. Dietary boron, derived mainly from plant-based foods, is efficiently absorbed and predominantly excreted by the kidneys, showing a strong correlation between intake and urinary levels.
Boron compounds may have been known for about 6,000 years, starting with the Babylonians. Boron may have first been used thousands of years ago in ancient Babylonian and Egyptian societies in the form of borax. The first definitive evidence of boron being used was in the form of mineral borax (tincal), imported to Mecca, Medina, and China by Arab transporters.
Borax was first discovered in dry lake beds in Tibet. Native tincal from Tibet, Persia, and other parts of Asia was traded via the Silk Road to the Arabian Peninsula in the 8th century AD. Borax was first extracted from dry lakebeds in Persia and Tibet and traded to Arabia and India over a thousand years ago.
The Egyptians, Chinese, Tibetans, and Arabians are reported to have used boron compounds. The Arabic word for borax, baurach, which also represents a number of other minerals, is found in old manuscripts from Persia and Arabia. Specimens of Chinese pottery utilizing colorful borax glazes made in the third century exist today.
The Egyptians used borax in mummification, and Marco Polo reportedly brought some back from his Far East travels in the 13th century. Ancient civilizations, such as the Egyptians and Romans, used borax for various purposes, including as a cleaning agent, a flux to assist with soldering metals, and as a preservative for food. It was also used in traditional medicine and in the production of glass and ceramics.
In ancient times, borax was not a bulk industrial material—it was a luxury good, accessible only to kings, artisans, and wealthy merchants. During the Middle Ages and Renaissance, borax became essential for European crafts, glassmaking, and alchemy. Since old times, borax has been an important raw material used particularly in the metal and ceramic industries, first for soldering and brazing, second as a flux to give certain glazes an appropriate fusibility.
Borax is a mineral-origin drug that belongs to the traditional system of medicine. In the late 1800s, boron compounds were a household staple, used in medicines, food additives, and household cleaners.
The element itself was first isolated as a substance distinct from its mineral compounds in the early 19th century. In 1808, Louis-Josef Gay-Lussac and Louis-Jacques Thénard working in Paris, and Sir Humphry Davy in London, independently extracted boron by heating borax with potassium metal. The first nearly pure boron was produced in 1909 by American chemist Ezekiel Weintraub, which was found to have very different properties to those previously reported.
The World Health Organization (WHO) has concluded that boron is a "probably essential" nutrient in humans. However, this has not been conclusively proven, because no specific biochemical function of boron has been identified.
Although boron has not been formally recognized by many organizations as an essential element for humans, and there is no official RDA, certain safe intake limits have been established. The Food and Nutrition Board (FNB) found the existing data insufficient to derive an RDA, AI, or EAR for boron.
The World Health Organization estimates that an acceptable safe range of boron intakes for adults is 1–13 mg/day. The adult median boron intake from supplements was approximately 0.14 mg/day. The median intake of dietary and supplemental boron was approximately 1.0 to 1.5 mg/day for adults.
Although only traces are required, boron is an essential plant nutrient. In plants, boron is widely considered an essential element: it stabilizes cell walls through esterification with pectins, regulates ion transport, and influences meristem growth. Its deficiency leads to tissue deformation, inhibited root growth, and deterioration of cell wall structure, while excess boron can be toxic, indicating a narrow range of homeostasis.
Although present in organisms at very low concentrations, boron participates in key physiological processes, including mineral metabolism, bone homeostasis, hormonal regulation, immune modulation, and redox balance. Its unique electronic structure—characterized by electron deficiency and the ability to form multi-center bonds—gives rise to diverse allotropic, cluster, and coordination chemistries, enabling the formation of biologically active complexes and therapeutic agents.
Boron can form reversible covalent bonds with sugars, amino acids, and hydroxamic acids — a feature that allows it to act as a Lewis acid in chemical reactions, catalyzing various processes. Boron's primary biological mechanism is reversible Lewis acid complexation with cis-diol-containing biomolecules (including NAD⁺ and ribose sugars) — it does not bind classical hormone receptors but modulates steroidogenic enzymes, vitamin D activation pathways, and NF-κB inflammatory signaling indirectly.
Experimental data have suggested that steroid hormone levels in plasma change after boric acid administration, but a clear mechanism behind these variations has not been established. One hypothesis is that boric acid disrupts the interactions between steroid hormones and several carriers in plasma. In particular, it is proposed that there is an uncoupling of the interactions between sex hormone binding globulin (SHBG) and estrogens and testosterone, and that there are alterations in the binding of hydrophobic ligands by other carrier proteins in plasma.
One review indicates that boron influences the activity of 25-hydroxyvitamin D and may modify calcium metabolism by influencing parathyroid hormone and calcitonin secretion. Findings suggest that boron may play a role in the extent of hydroxylation or the half-life of vitamin D3, based on its ability to form complexes with hydroxyl groups in organic compounds. Therefore, boron could affect bone metabolism and improve bone strength. The influence of vitamin D3 on cartilage and bone mineralization is mediated in part through its role as a regulator of energy substrate utilization. There is considerable evidence that dietary boron alleviates perturbations in mineral metabolism that are characteristic of vitamin D3 deficiency.
The interaction of boron with calcium suggests that boron supplementation leads to a reduction in urinary calcium excretion and increased ionized calcium levels in the plasma. About 60% of the magnesium present in the human body is found in the bone, where it acts as a cofactor for numerous enzymes that regulate the metabolism of calcium. Boron appears to significantly improve the absorption of magnesium and its deposition at the bone level, as suggested by a study conducted in rats in which a significant increase in the bone content of magnesium was observed in animals given a diet low in vitamin D but supplemented with boron, compared to those fed a diet low in both vitamin D and boron.
Support for the hypothesis that boron bioactivity could be associated with S-adenosylmethionine (SAM-e) includes findings that plasma homocysteine increased and liver S-adenosylmethionine and S-adenosylhomocysteine decreased in boron-deprived rats compared with boron-supplemented rats.
Boron apparently has diverse effects through influencing a cell signaling system or the formation and/or activity of an entity involved in many biochemical processes. Boron exerts its healing properties through multiple pathways, including anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects. Inflammation is a crucial component of the wound-healing process, and boron has been shown to modulate inflammatory responses by inhibiting pro-inflammatory cytokines and promoting the resolution of inflammation.
Literature reviews indicate that boron supplementation may positively affect bone mineral density by modulating calcium, vitamin D, and sex hormone metabolism. Boron, a trace mineral, supports bone health by influencing calcium, magnesium, and vitamin D metabolism, and shows promise in reducing inflammation and enhancing antioxidant enzymes.
A foundational human study, described in the scientific literature, is the metabolic ward study by Nielsen et al. In this seminal metabolic ward study by Nielsen et al., boron supplementation (3 mg/day) in postmenopausal women reduced urinary calcium excretion by 44% and urinary magnesium excretion, while significantly elevating serum 17β-estradiol concentrations. A clinical trial has demonstrated that both 17-beta-estradiol and testosterone levels significantly increased in postmenopausal women consuming 3 mg/day of boron for 7 weeks. In this study, boron supplementation caused a twofold increase in testosterone concentrations and a significant increase in calcium retention.
A 2024 pilot study in postmenopausal Jordanian women (n = 66) investigated dietary boron and osteoporosis. The study showed a strong correlation between boron intake and bone mineral density in these women with osteoporosis and a negative correlation between boron intake and serum calcium (p < .05). However, no significant correlation was found between boron intake and serum vitamin D, dietary habits, BMI, waist circumference, or other lifestyle parameters. A significant link was found between boron intake and bone mineral density, highlighting the importance of nutritional and lifestyle factors affecting bone health.
A narrative review in Journal of Trace Elements in Medicine and Biology (2020) covering 11 eligible studies—7 regarding boron supplementation alone and 4 regarding boron combined with other nutrients—concluded: Considering the evidence currently available, it seems reasonable to assume that boron also plays a favorable role in calcium metabolism, a figure of great importance for the prevention of osteoporosis and bone loss.
Evidence strength: Although animal studies have shown positive effects on bone mineralization, human studies remain limited. Boron's potential role in bone health is supported by multiple lines of evidence, though the data remain preliminary. The proposed mechanisms include reducing urinary calcium excretion, modulating vitamin D metabolism, influencing osteoblast and osteoclast activity, and affecting steroid hormone levels relevant to bone maintenance. Robustly powered randomized controlled trials in humans are still lacking.
A frequently cited 2011 pilot study (Naghii et al., Journal of Trace Elements in Medicine and Biology) administered boron to healthy male subjects. Subjects consumed a capsule of 10 mg boron every day with breakfast, and after one week, blood was collected. Boron in plasma increased significantly following hourly and weekly consumption. Six hours of supplementation showed a significant decrease in sex hormone binding globulin (SHBG), high-sensitivity CRP (hsCRP), and TNF-α levels. After one week, the mean plasma free testosterone increased and the mean plasma estradiol decreased significantly. Dihydrotestosterone, cortisol, and vitamin D were elevated. Also, concentrations of all three inflammatory biomarkers decreased after supplementation.
In another study, men given 10 mg of boron a day for 4 weeks experienced a significant increase in 17-beta-estradiol levels and an increase in plasma testosterone.
Evidence strength: There is conflicting evidence to support the use of boron in hormonal regulation. The studies on hormonal outcomes are small, short-duration, and not consistently replicated in well-powered randomized controlled trials. The proposed mechanism of SHBG uncoupling from steroid hormones is plausible but not definitively confirmed in humans.
Epidemiological observation has noted that in areas of the world where people eat relatively high amounts of boron—between 3 and 10 mg per day—the incidence of osteoarthritis is below 10 percent. However, in regions with less boron in the diet—1 mg or less per day—the incidence of arthritis is much higher. These are ecological correlations, not causation.
Clinical evidence includes a small double-blind pilot study (Travers et al., Journal of Nutritional Medicine, 1990) and randomized trials using calcium fructoborate. Reported beneficial actions of boron include arthritis alleviation or risk reduction, bone growth and maintenance, central nervous system function, cancer risk reduction, hormone facilitation, and immune response, inflammation, and oxidative stress modulation.
Evidence strength: Although studies assessing the use of boron for osteoarthritis and osteoporosis are in preliminary stages, reports are promising. Boron is sometimes recommended as a treatment for rheumatoid arthritis, but there is no evidence to support this use. The evidence for osteoarthritis specifically is based primarily on small trials and epidemiological data; larger randomized controlled trials are needed.
Research by Penland (published in Environmental Health Perspectives, 1994) found associations between dietary boron and cognitive performance. Changes reversed when boron was repleted at 3 mg/day. The same research program found that low-boron, low-magnesium diets were associated with poorer performance on tasks measuring eye-hand coordination, attention and perception, dexterity, and both short-term and long-term memory compared to diets higher in boron (3 mg/day) and magnesium. Importantly, the cognitive deficits were observed when both boron and magnesium were low, making it difficult to attribute the effects to boron alone.
Regarding cognitive function, there is experimental and observational data that low boron status may be associated with impaired cognitive performance and neurological function.
Evidence strength: The evidence for cognitive benefits is preliminary and largely based on dietary deprivation studies and small human trials. There is conflicting evidence to support the use of boron in cognitive function. No large-scale randomized controlled trials have examined boron supplementation and cognitive outcomes as a primary endpoint.
Chronic wounds present a significant clinical challenge due to their prolonged healing time and susceptibility to infection. Boron, a trace element with diverse biological functions, has emerged as a promising therapeutic agent in wound healing. A 2024 review comprehensively investigated the mechanisms underlying the beneficial effects of boron compounds in wound healing. Boron has been shown to modulate inflammatory responses by inhibiting pro-inflammatory cytokines and promoting the resolution of inflammation. Furthermore, boron exhibits antimicrobial activity against a wide range of pathogens commonly associated with chronic wounds. The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing. Additionally, boron stimulates cell proliferation and migration, as well as essential tissue regeneration and wound closure processes.
Evidence strength: Much of the wound healing evidence comes from in vitro and animal models. Other suggested therapeutic uses that need additional study include using boron as an immune system booster and aiding in wound healing. Human clinical trial data remain limited.
Epidemiological data have associated higher boron intakes with reduced risk of certain cancers. Boron is sometimes explored as a natural supplement for reducing the risk of prostate cancer, although more research is needed to confirm these claims. One large observational study suggests that a higher intake of boron may reduce the risk of prostate cancer.
Findings have shown that boron is associated with decreased risk for some cancers. A separate area of medical research involves boron neutron capture therapy (BNCT), a targeted radiation treatment that exploits the stable, non-radioactive isotope boron-10's well-known use as a neutron-capturing agent.
Evidence strength: Evidence for boron reducing cancer risk is primarily observational and epidemiological. No interventional clinical trial has established boron supplementation as a cancer-preventive agent. The BNCT application is a specialized radiological procedure distinct from dietary supplementation.
Six hours of supplementation with 10 mg boron showed a significant decrease in sex hormone binding globulin (SHBG), high-sensitivity CRP (hsCRP), and TNF-α levels in the Naghii et al. 2011 study cited above. Boron beneficially impacted the body's use of estrogen, testosterone, and vitamin D; and significantly improved magnesium absorption and deposition in bone. In a human trial, a significant increase in concentrations of plasma boron after supplementation was coupled with decreased levels of inflammatory biomarkers and increased levels of antioxidant enzymes.
Regarding the immune system, boron and boron compounds have been shown to modulate both innate and adaptive immune responses.
Evidence strength: Human evidence for anti-inflammatory effects is limited to small, short-duration studies. The findings are consistent and mechanistically plausible but require confirmation in larger, properly controlled trials.
There is fair negative evidence regarding the use of boron as an anticoagulant, a bodybuilding aid, for menopausal symptoms, or for psoriasis. Future randomized controlled trials are warranted across most of boron's proposed health applications.
In dietary supplements, boron is present in many different forms, including sodium borate, sodium tetraborate, boron amino acid chelate, boron ascorbate, boron aspartate, boron citrate, boron gluconate, boron glycinate, boron picolinate, and calcium fructoborate.
The following dosages have been reported in clinical and human studies, as documented in the sources consulted:
It is unclear whether boron supplements are better taken with food or on an empty stomach. There is no requirement to take boron with a fat-containing meal, and the relatively small doses used (1–6 mg) mean that differences in absorption between forms may be clinically insignificant.
The Tolerable Upper Intake Level (UL)—the maximum dose at which no harmful effects would be expected—is 20 mg per day for adults and pregnant or breastfeeding women over 19 years of age. For adolescents 14 to 18 years of age and pregnant or breastfeeding women 14 to 18 years of age, the UL is 17 mg per day. For children 9 to 13 years old, the UL is 11 mg per day; children 4 to 8 years old, 6 mg per day; and children 1 to 3 years old, 3 mg per day. A UL has not been established for infants.
Data are limited regarding adverse effects of boron when used at doses less than the upper intake level. Recommendations regarding the oral dosage below which adverse reactions are unlikely range from 10 mg/day to 20 mg/day.
Boron is possibly unsafe for adults and children when taken by mouth in high doses. Large quantities of boron can cause poisoning. Signs of poisoning include skin inflammation and peeling, irritability, tremors, convulsions, weakness, headaches, depression, diarrhea, vomiting, and other symptoms.
Long-term use of boric acid orally at 1 g/day or boric tartrate 15 g/day can cause dermatitis, alopecia, anorexia, lethargy, and indigestion. At the systemic level, severe acute toxicity can induce metabolic acidosis and renal failure due to the accumulation of boric acid, which exceeds the kidney's clearance capacity.
There is some concern that doses over 20 mg per day, the UL for adults, might harm a man's ability to father a child. In terms of reproductive toxicity—the most sensitive endpoint in animal studies—excess boron specifically targets Sertoli cells in the testes. The mechanism involves the disruption of DNA synthesis and inhibition of histone deacetylases (HDACs), leading to germ cell apoptosis and testicular atrophy.
Intravaginal boric acid, when used during the first 4 months of pregnancy, has been associated with birth defects. Both boron deficiency and excess can disrupt delicate signaling cascades, leading to teratogenic effects (e.g., skeletal and cardiovascular malformations) observed in toxicological studies at high doses.
Boric acid, a common form of boron, is likely safe when used vaginally for up to six months. It can cause a sensation of vaginal burning. Although boric acid, borates, and other compounds containing boron are used medicinally, they can be toxic if ingested at high doses or absorbed through nonintact skin.
Boron is not known to interact or interfere with any medicines or dietary supplements. However, supplementation may result in changes in plasma levels of phosphorus and magnesium. The Institute of Medicine has established a Tolerable Upper Intake Level (UL) of 20 mg elemental boron/day for adults; exceeding this level chronically increases risk of GI, dermatological, and potentially reproductive adverse effects, while acute gram-level exposures are associated with systemic toxicity.
One specific interaction noted in the literature involves vaginal progesterone formulations: vaginal antifungal boric acid agents may diminish the therapeutic effect of progesterone, and this combination should be avoided.
The combined intake of boron from the background diet and a calcium fructoborate novel food supplement is in the range of 9.6–9.9 mg/day (corresponding to up to 0.14 mg/kg body weight per day given a default body weight of 70 kg). This is in the range of the acceptable daily intake (ADI) of 0.16 mg/kg bw per day. Under conditions mimicking the gastrointestinal environment, the novel food is fully hydrolyzed. The EFSA Panel considers that there is no concern with respect to genotoxicity of calcium fructoborate.
Health conditions that Boron may help support.
Boron is a trace mineral with documented 'androgen amplifier effects'; a meta-analysis found boron supplementation significantly increased free testosterone in men after as little as one week of supplementation. It also reduces sex hormone-binding globulin (SHBG), which rises with age and limits testosterone bioavailability—a central concern in andropause. Boron additionally supports vitamin D metabolism, further augmenting testosterone-supporting pathways in aging men.
PMC and peer-reviewed reviews document that boron supplementation raises levels of key antioxidant enzymes—superoxide dismutase (SOD), catalase, and glutathione peroxidase—in human and animal studies. A human trial using sodium tetraborate supplementation demonstrated increased antioxidant enzyme levels alongside decreased inflammatory biomarkers.
The NIH ODS states that observational evidence combined with small clinical studies suggests boron may reduce osteoarthritis symptoms, possibly by inhibiting inflammation. An Australian double-blind pilot RCT (6 mg/day, 8 weeks, n=20) found 50% of the boron-treated group improved versus 10% on placebo. Boron concentrations in bone and synovial fluid are lower in arthritis patients than in healthy controls.
Boron is a trace mineral that modulates vitamin D hydroxylation, delays estrogen and vitamin D degradation, and influences calcium and magnesium metabolism relevant to bone. The NIH ODS and National Academy of Sciences include boron among micronutrients relevant to bone metabolism, and boron deprivation impairs bone composition in animal studies. However, direct large-scale RCT evidence for BMD improvement in humans remains limited.
Boron is a trace mineral that influences cartilage health through regulation of vitamin D, calcium, and magnesium metabolism, and direct stimulation of chondrocyte extracellular matrix synthesis. Epidemiological data show lower OA incidence in populations with higher boron intake. A small double-blind clinical trial found boron supplementation (6 mg/day) significantly reduced OA symptoms versus placebo.
Multiple small RCTs show boron supplementation reduces circulating inflammatory biomarkers including hs-CRP and TNF-α. A 60-person study found reductions in CRP and fibrinogen after 1.5–6 mg/day for two weeks. Evidence is promising but limited by small sample sizes and short durations.
Observational data show decreased plasma boron is associated with increased Alzheimer's disease severity and cognitive decline in amnestic MCI patients (Lin et al., 2021). Reduced plasma boron was also found in APOE ε4 carriers (a major AD genetic risk factor). Experimental boron deprivation in older adults impaired multiple cognitive domains including memory, attention, and psychomotor function.
Human dietary intervention studies, beginning with the landmark 1987 USDA/Nielsen trial in postmenopausal women, show that boron repletion (3 mg/day) markedly elevates serum 17β-estradiol and testosterone. A 2011 Iranian trial further demonstrated increased free testosterone and reduced pro-inflammatory cytokines after boron supplementation in healthy men. Effects appear most pronounced under low-magnesium conditions.
Boron is a trace mineral that influences bone and joint health by modulating calcium metabolism, sex steroid hormones, and inflammatory cytokines. Epidemiological data show lower OA prevalence in regions with higher boron soil/water content. A small RCT in OA patients found boron supplementation (6 mg/day for 8 weeks) significantly reduced pain and improved joint function compared to placebo.
Three within-subject EEG and cognitive performance studies in healthy older adults (Penland, 1994, Environ Health Perspect) found that low dietary boron (~0.25 mg/2000 kcal/day) produced significantly poorer performance on attention tasks compared to adequate intake (~3.25 mg/day). Brain electrical activity also shifted toward patterns associated with lower alertness under boron deprivation.
Boron influences multiple aging-relevant pathways: reducing chronic low-grade inflammation (inflammaging), raising antioxidant enzyme activity, supporting steroid hormone levels that decline with age, and protecting mitochondrial integrity. A rat accelerated-aging model (D-galactose, 2025) showed boron mitigated aging-like phenotypes. Human data tie low boron to poorer cognitive and physiological function in older adults.
A Journals of SAGEPUB review (Nielsen & Meacham, 2011) states that 'limited evidence suggests that boron can facilitate insulin action.' Mechanistically, boron may influence thyroid hormone conversion (T4→T3), which in turn affects insulin sensitivity; animal and limited human data support this pathway.
Boron is a trace mineral that influences testosterone metabolism by reducing sex hormone-binding globulin (SHBG), thereby increasing free testosterone. A 2011 pilot study found 10 mg/day boron for 7 days significantly increased free testosterone by 28% and decreased SHBG and estradiol in healthy men. ConsumerLab lists it among evaluated testosterone-support nutrients.
The same USDA dietary manipulation studies (Penland, 1994) found that low boron significantly impaired encoding, short-term memory (all three studies), and long-term memory (one study) in older adults versus adequate intake. EEG data corroborated poorer neural processing during the low-boron condition.
The NIH ODS identifies low boron intake as specifically impacting postmenopausal women, who experience reduced estrogen alongside altered calcium, vitamin D, and osteocalcin metabolism. Boron repletion in postmenopausal women raised 17β-estradiol and improved calcium retention in the Nielsen 1987 FASEB study. Boron may partially mimic or support estrogen's role in bone mineral conservation during menopause.
A 2015 triple-blind RCT (n=113 university students with primary dysmenorrhea, Shahid Beheshti University) found that 10 mg/day boron taken from two days before menstrual flow until the third day of flow significantly reduced both the severity and duration of pain over two consecutive cycles compared to placebo (p=0.001 for severity; p=0.032 for duration).
Boron is a trace mineral that supports bone health by reducing urinary excretion of calcium and magnesium and by raising serum vitamin D levels. A 2020 research review found boron supplementation may help prevent bone loss, with an intake of 3 mg/day suggested as sufficient. A 2024 pilot study found improved bone density with increased boron intake in postmenopausal women.
Epidemiological studies link higher dietary boron intake to lower prostate cancer risk and lower PSA levels in men. Boron inhibits aromatase activity, modulates sex hormone metabolism, and has anti-inflammatory effects relevant to prostate size. It is a recognized micronutrient in published BPH prostate supplement formulations alongside beta-sitosterol and zinc, supported by mechanistic, epidemiological, and in vivo evidence.
Boron is a trace mineral with evidence for supporting collagen synthesis and extracellular matrix integrity through enzyme cofactor activity and enhancement of vitamin D, estradiol, and magnesium bioavailability. Evidence from embryonic bone studies shows boron deprivation reduces collagen content and alters collagen cross-link profiles, while boron supplementation normalizes these parameters.
Boron supplementation has been shown in human clinical studies to significantly reduce SHBG, increase free testosterone, and reduce estradiol. A 2011 study in men using 10 mg/day of boron showed significantly increased free testosterone and decreased SHBG after one week. A classic study in postmenopausal women showed a near-doubling of testosterone with 3 mg/day boron for 7 weeks.
Intravaginal boric acid restores acidic vaginal pH, disrupts pathogenic biofilms, and supports Lactobacillus-dominant flora. Clinical evidence shows efficacy in recurrent vulvovaginal candidiasis and adjunctive benefit in BV, with a large RCT ongoing. The mechanism includes antimicrobial, anti-biofilm, and pH-acidifying properties independent of systemic boron supplementation.
A 2024 Frontiers in Bioengineering and Biotechnology comprehensive review confirmed that boron compounds promote wound healing through anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative mechanisms, with both preclinical and several clinical studies supporting benefit. Topical boric acid has been used clinically for wound management for decades.
Body systems that Boron may help support.
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