Sulfur Cycle, Interrupted: or, Why Sea Breeze is Becoming Odorless (The Second Great Dying – Holocene Extinction Event)

Part I

The Sulfur Cycle

The Sulfur Cycle is a biogeochemical (biological, geological and chemical) cycle. Steps of the sulfur cycle are, in short:

1. Mineralization of organic sulfur into inorganic forms.
2. Oxidation of hydrogen sulfide, sulfide, and elemental sulfur (S) to sulfate (SO42–).
3. Reduction of sulfate to sulfide.
4. Incorporation of sulfide into organic compounds (including metal-containing derivatives).1

For our purposes, we are concerned with the sulfur cycle as it pertains to dimethylsulfide (DMS), which is produced by the decomposition of dimethylsulfonioproprionate.

Dimethylsulfonioproprionate (DMSP) is a zwitterionic (a neutral molecule with a positive and negative electrical charge) metabolite found in marine phytoplankton. Agents for primary production, phytoplankton are photosynthesizing microscopic organisms found in seawater. Primary production refers to the process whereby which organic compounds are synthesized by phytoplankton from the carbon dioxide dissolved in the water. One such organic compound is oxygen. It is estimated that no less than half of the Earth’s oxygen is generated by the photosynthetic action of phytoplankton.

When phytoplankton die, dimethylsulfonioproprionate decomposes and produces the biogenic gas, dimethylsulfide. The distinct odor associated with sea breeze is dimethylsulfide. When oxidized, dimethylsulfide is transformed into several sulfur-containing compounds, including dimethylsulfoxide (DMSO), sulfur dioxide and sulfuric acid. It is this last compound, sulfuric acid, which rapidly aerosolizes, producing cloud seeds, or cloud condensation nuclei, which are non-gaseous particulate surfaces on which water undergoes a transition from vapor to liquid.

When phytoplankton populations are disrupted, atmospheric dimethylsulfide concentrations are subsequently diminished, as is the concentration of cloud-seeding sulfuric acid; planetary homeostasis is thus disrupted, as the potentiating elements required for cloud generation have been compromised. In a word, absent a preponderance of cloud condensation nuclei, water does not possess the naturally-produced non-gaseous particulate surfaces over which to transition from vapor to liquid.

The Ozone Layer

Hydrogen Fluoride (HF) is not only a direct byproduct of weapons, phosphate fertilizer, metals smelting, power generation, and chemical manufacturing industries, but is also a product of the breakdown (dissociation) of chlorofluorocarbons (CFCs) in the stratosphere (e.g., chlorofluoromethane (CFM)). Chlorine atoms are released following HF dissociation which react with and destroy the Ozone Layer. What is more, HF is a catalyst: its molecules are not used up in their destructive reaction with stratospheric ozone, but are regenerated — the reaction is hence repeated, over and over again. According to the Langley Research Center’s Halogen Occultation Experiment (HALOE) team, “For every chlorine atom formed in the middle atmosphere by dissociation of the CFM molecules, approximately 1,000 ozone molecules are destroyed.”2 Other common CFCs and Ozone-Depleting Substances (ODS) which produce atomic chlorine when broken down include, but are not limited to, methyl chloroform, carbon tetrachloride, and halons, all of which have long atmospheric lifetimes.

Due to unchecked degradation of the Ozone Layer, UV radiation has increased and one of the microorganisms that is dying en-masse as a consequence is phytoplankton. Resultantly, although underreported, one of the Earth’s most important Sulfur Cycles on which planetary homeostasis depends, has been permanently and progressively disrupted. The interruption of the dimethylsulfide sulfur cycle has ushered in The Second Great Dying (See: Permian-Triassic Extinction Event). As phytoplankton populations are diminished, oceanic concentrations of carbon dioxide increase, and without conversion by photosynthetic microorganisms, atmospheric oxygen is displaced and oceans are acidified.


In an effort to forestall the inevitable, remediation efforts have been underway since the 80s, at which time the criticality of the ozone layer and depletion cascade effects were identified. While working as an electrical engineer and Global Systems Scientist for Oak Ridge National Laboratory, James E. Phelps was instrumental in the development of an emergency atmospheric remediation technique referred to as air pharmacology (or: “Insolation-Modulating Scattering System” Teller). Today, air pharmacology is colloquially referred to as chemtrails.

Air pharmacology is not harmless, but it is not altogether sinister either. It’s aims are many: the aerial dispersal of aluminum oxides (often originating as the jet fuel additive trimethylaluminum – Al2(CH3)6) not only reflects harmful ultraviolet radiation back into space by increasing the albedo of the stratosphere via Mie Scattering, but also reacts with sulfuric acid to produce the hygroscopic (moisture-retaining) aluminum sulfate (Al2(SO4)3) which in-turn forms the cloud-inducing octadecahydrate, Al2(SO4)3·18H2O. Effective Mie Scattering requires that the dispersed particles be of a similar size as the target wavelength.3 In the context of air pharmacology, then, alpha alumina (Al2O3) or aluminum oxide particulates must possess a size between 290 and 320 nm in order to effectively scatter UV-b radiation.4

The logic behind the inclusion of highly photoelectric (“Conducting Sheets” Teller) barium oxide (BaO) is multipartite: It is introduced in an effort to simulate cloud condensation nuclei (a process, you will remember, dependent upon the failing dimethylsulfide sulfur cycle), induce rain, absorb CO2, spontaneously generate ozone, draw complexed HF from the atmosphere, as well as to actively transform the atmosphere’s pressure gradient, thus altering, in theory, the intensity of storm systems. More recently, titanium dioxide (titanium sulfate [Ti(SO4)2·9H2O] in the atmosphere) has been included in an effort to mitigate the adverse effects of elevated levels of aluminofluoride (AlFx) complexes in the food chain. Additionally, like barium sulfate, titanium sulfates readily complex with the CFC, nitrogen oxide (NO). Unfortunately, recent studies (which although not untrue, do aim to misdirect) suggest that when suspended in sea water and excited by UV-b radiation, electrons from titanium dioxide particulates react with H2O to form reactive oxygen species (described below) which attack phytoplankton.5 Suspiciously, the studies do not ask the obvious question: how did the particulate TiO2 get there?

Today, our scientific knowledge and our technological capability already are likely sufficient to provide solutions to these problems; both knowledge and capability in time-to-come will certainly be greater. Whether exercising of present capability can be done in an internationally acceptable way is an undeniably difficult issue, but one seemingly far simpler than securing international consensus on near-term, large-scale reductions in fossil fuel-based energy production, especially in a world exhibiting very large geographical and cultural differences in per capita energy use, past, present and future.

We believe that, prior to any actual deployment of any scattering system aimed at full-scale 1% insolation modulation, completely transparent and fully international research in sub-scale could result in public opinion conducive to a reasonable technology-based approach to prevention of large-scale climatic failures of all types. International cooperation in the research phase, based on complete openness, is necessary and may be sufficient to secure the understanding and support without which any of these approaches will fail.

—Edward Teller, et. al., LLNL, 1997

At-Home Remediation

Like titanium dioxide (introduced into the food chain through air pharmacology, and which in the atmosphere becomes titanium sulfate), supplemental and dietary boron has been shown conclusively to counteract adverse physiological reactions due to elevated levels of fluorine complexes/heavy metals in the body. Regions with soil rich in boron have demonstrated so-called dietary paradoxes around which fads have sprung over the last several decades. The Mediterranean Diet, for instance, comes to mind, as does the so-called “French Paradox.” These are regions in which food is grown in soil that is rich with boron (e.g. olives/olive oil, French, Italian and Peruvian red wines, nuts, raisins, apples, etc.); it isn’t the wine, per se, but the boron in the wine, or in the bread, or in the nuts… In North America, we are not so lucky. In most regions of North America, soil levels of boron are statistically insignificant, and consequently, foods rich in boron must either be imported or fortified after-the-fact.

Red Herring

Industry has scrambled to isolate and knight compounds in wine (e.g. resveratrol-as-red herring), and even gone so far as to laud a popular folk remedy (gin-soaked raisins [sulphur-as-red herring]) in a frenzied effort to deflect attention from the common denominator present in health-imparting foods, as an explicit identification of boron would disperse an elaborate intra-governmental smokescreen designed to prevent the public from becoming cognizant of what will one day soon be referred to as “The Second Great Dying.”

Part II

Why Boron?


All that glitters is not gold, but sometimes it is boron, and that is even better.

—David Duff

In order to understand the intrinsic value of the metalloid boron in relation to our study of the dimethylsulfide-specific sulfur cycle and its breakdown as a consequence of Ozone-Depleting Substances and their ongoing impact on stratospheric ozone, it is vital that we understand those factors which necessitate the introduction of supplemental/dietary boron, the most pressing of which is the electronegative halide, fluoride.

Elemental fluorine, the chemical element from which fluoride is reduced by electrolysis, is critical to uranium enrichment. Uranium Tetrafluoride (UF4), an intermediate in the conversion of Uranium Hexafluoride (HF6), is a molten fluoride salt coolant in which nuclear fuel is dissolved in a type of nuclear fission reactor known as a Molten-Salt Reactor (MSR). The Oak Ridge National Laboratory Molten-Salt Reactor Experiment (MSRE), which went critical (the nuclear fission chain-reaction became self-sustaining) in 1964 and was operated until 1969, was an example of a reactor in which UF6 was utilized as a coolant. Although inactive, the decommissioning process for the MSRE was not commenced until a build-up of fluoride gas at the site was detected in 1994. The cleanup, led by Bechtel Jacobs, was not completed until 2009; the removal and disposition of UF6 necessitated the infusion of the salts with excess fluoride. A detailed description of the process may be downloaded here: “Alternatives for the Removal and Disposition of Molten-Salt Reactor Experiment Fluoride Salts.” The Molten-Salt Reactor design was succeeded by Liquid Metal Cooled Reactor designs which use coolants other than fluoride salts (mercury, sodium-potassium alloys, lead, and lead-bismuth eutectics). [IAEA-TECDOC-1569]

Uranium-enrichment is not the only source of fluoride emissions into the atmosphere, although it remains a key offender, albeit without the same data that may be extrapolated from sources of emissions that are not subject to similar levels of concealment, such as metals smelting and coal-fired power plants. The MSRE was described in an effort to expose the risks associated with a number of nuclear reactors, in North America and abroad, that although mothballed, passively release an unprecedented volume of fluoride gases into the environment, very often over decades, as the cost of cleanup (“decommissioning”), is prohibitive.

Why does this matter?

We have already described the impact of fluorine reductions on stratospheric ozone and its subsequent cascade effects. How do fluoride complexes impact the health of mammals?

Due to its electronegativity, fluorine atoms have the highest propensity of all elements to attract electrons and to react with preexisting trace metals in skeletal bone. “With this effect,” says James E. Phelps, formerly of Oak Ridge National Laboratory, “comes the depletion of beneficial trace metals used in the enzyme repair process of immune cells.” “Fluorides building in the bone,” says Phelps, “and its extremely high affinity to react with metals in the bone creates a problem that leads to immune dysfunction, brain damage, illness, rapid aging, and early death.”

Not only do fluorides accumulate in skeletal bone, but complexes of fluoride also have a propensity to accumulate in the pineal, pituitary and thyroid glands. The light-transducing pineal gland is responsible for synthesizing the structurally simple hormone melatonin from serotonin. Fluoride is a melatonin receptor (G protein-coupled cell surfaces – Mel1A and Mel1B) antagonist, which is to say, fluoride complexes will bind to active receptor sites reserved for melatonin agonists, disrupting normal neuronal connectivity. The longevity of the fluoride-antagonist-receptor complex is high, due to the electronegativity of fluorides. The ionic non-covalent bond formed between the fluoride complex (cation) and the receptor site (anion) is a strong and long one. Resultantly, as Mel1A and Mel1B-type receptor sites are found in largest concentration in the anterior pituitary, hypothalamus and retina, the antagonistic behavior of fluorides impact reproductive functions and sleep activity in mammals. Melatonin has been shown to inhibit the secretion of luteinizing and follicle stimulating hormones, both of which control seasonal reproduction cycles — fluorides prevent this biological delimiter to unchecked multi-seasonal reproduction in mammals. G protein-coupled cell surface antagonism in the retina also leads to sleep disturbances, as light-dark information is not carried properly from the retina to the pineal gland; this, in-turn, disrupts the pituitary’s thyroid-stimulating hormone (TSH).

The Strontium 90 (90Sr) — Fluoride Connection

90Sr, not to be confused with natural strontium which is nonradioactive and nontoxic, is a radioactive isotope of strontium produced in nuclear fission that, like calcium, “seeks bone.”9 90Sr is ubiquitous in the environment due to above-ground nuclear weapons tests from 1963-1980, the Chernobyl and Fukushima disasters, as well as unintentional but fairly regular releases from nuclear power plants in incidents unrelated to meltdown scenarios.

The action of 90Sr in skeletal bone is not dissimilar to the action of fluorides. 90Sr lodged in bone and soft tissue emits high energy electrons and beta particles. When beta particles strike DNA, spontaneous and irreversible mutations arise. Chronic low-dose beta particle emissions also increase reactive oxygen species formation (free radical reactions), which compete for trace metals in bone.

“The closely-related process (90Sr/low-dose beta ray emissions),” says Oak Ridge’s James E. Phelps, “is the prime vector behind the immune system problems associated with fluoride … The radiation and oxygen radical process usually related to development of cancers and loss of control of certain cancer-related viruses by the immune system. In the case for the fluorine process, the problems are also related to loss of control of viruses like CMV, EBV and others. This contributes to fatigue. Both effects tend to shut down the cell’s ability to repair DNA using the enzymes that have been damaged due to losses of essential trace metals.”

Phelps continues:

Almost all the immune-linked illnesses are due to this principle mechanism of this degenerative loss of essential trace metals. Adding to these problems is the losses of essential trace metals in the soils due to acid effects, and these compound and worsen the health effects, as these trace metals in the food chain would normally go to lessen the retention of fluorine in the body.

Glutathione and final words…

In Part I, we studied the causative factors behind rising levels of heavy metals (e.g., aluminum, barium, titanium, etc.) in the environment/food-chain (air pharmacology) and in Part II, the impact of fluorides in the body. Taken together, when fluorides complex with aluminum (AlFx), they create G protein-coupled cell surface antagonists which compete with trace metals and disrupt basic neuronal and hormonal communication and contribute to the subsequent depletion of glutathione (GSH), a major cellular endogenous antioxidant.6 Oxidative stress from fluoride exposure is shown as levels of GSH decrease when fluoride levels increase. Concomitantly, levels of oxidized GSH (GSSH) increase, which is the primary indicator of oxidative stress. (See: GLUTATHIONE METABOLISM IN RATS EXPOSED TO HIGH- FLUORIDE WATER AND EFFECT OF SPIRULINA TREATMENT)

There are few systems in the body that do not depend, in some measure, upon glutathione. It is required for DNA synthesis and repair, an issue already exacerbated by low-dose beta ray emissions from 90Sr; it is required for protein synthesis, prostaglandin synthesis, amino acid transport and enzyme activation. Absent sufficient levels of glutathione, the immune, neurological, pulmonary, and gastrointestinal systems are at risk of collapse. James E. Phelps elaborates:

The GSH damage process then allowed toxic metals to build up in the body as the phase I and phase II glutathione clearance was impaired. The loss of the liver bile pathway placed more clearance of metals demand on the kidneys, which set the stage to metabolic acidosis and shift of the blood pH toward acid, which further impaired toxic metal clearance. The rise of the toxic metals caused the cell mitochondria to produce increased rates of free radicals, which required the up regulation of the superoxide dimutase enzymes (Mn-SOD). These enzymes employed all the trace metal manganese, which upset the production of the cytokine interferon (IFN) and the production of effective 2-5A [-signaled] RNase L enzymes.

The high oxidative stress in the cells caused the mutation of the 2-5A [-signaled] RNase L enzyme from its normal 83 kDa MW to an ineffectual 37 kDa MW. This is the prime enzyme within cells that kills viral RNA by cleaving it, sets up cell apoptosis, and calls in the NK and macrophage cells. The mutation of this enzyme is the prime effect that allows cancer viruses to grow, HIV to grow, and CFS problems with EBV, CMV, and mycoplasma to affect long-term health.

Boron, once again…

Environmental 90Sr, fluoride, barium, and aluminum levels are rising. Phytoplankton populations are dying. Planetary homeostasis has been critically disrupted and oceans are acidifying at an alarming rate. No meaningful solutions to the crisis are hovering on the horizon. It would appear that we all have ring-side seats for “The End,” or, “The Second Great Dying.” The impact of CFCs and ODS on stratospheric ozone may be irremediable, but the impact of these same substances on the human body are not. Fluoride, fluoride complexes and the reactive oxygen species resulting from low-dose 90Sr exposure, which compete for the trace minerals critical for proper immune function, may be counteracted — simply and cheaply.

Boron, like table salt, has low toxicity in mammals (the same cannot be said for arthropods), and has been shown to efficiently detoxify the body of fluoride/fluoride complexes. Below you will find a number of sources that attest to the value of supplemental/dietary boron. Other valuable trace elements and compounds that will work synergistically with boron to rebalance the body’s trace metal/element profile include selenium more, manganese, zinc, and alpha lipoic acid.

Mechanism-of-Action: Chelation

Magnesium (Mg) is responsible for the production of no fewer than 300 enzymes vital for systemic homeostasis and fluoride (F-) ions are instrumental in critical Mg deficiency. F- has a not inconsiderable affinity for Mg ions, and bonds with Mg to form MgF+ and MgF2, both of which prevent the proper absorption of Mg through intestinal cell walls.7 Diets deficient in Mg create an opportunistic environment for F- accumulation. Dietary and supplemental boron has been shown to 1.) elevate concentrations of assimilable Mg 2.) increase urinary fluoride excretion and 3.) via chelation, prevent the complexing of F- with Mg (the F- ions are the ligands which form metal complexes [coordination complexes] with boron). Specifically, dietary and supplemental boron (as amino acid chelate) in the stomach, prevents the complexing of Mg and other trace metals and elements with electronegative sodium fluoride (NaF), by forming coordination complexes8 with F- ions, rendering NaF chemically inert (Refer to: Sodium Fluoride (NaF) Chelation Demystified – “The Complexation Reaction”). F-, consequently, also is unable to complex with aluminum to form AlFx.

Lastly, F- may additionally act by reacting with adjacent thiol residues (organosulfur compounds) on metabolic enzymes, creating a chelate complex that inhibits the affected enzyme’s activity. Boron, like the anti-Lewisite Dimercaprol or alpha lipoic acid, competes with the thiol groups for binding the F- ion, which is then excreted in the urine.

Further Reading

1: Hideghety K, Sauerwein W, Wittig A, Gotz C, Paquis P, Grochulla F, Haselsberger K, Wolbers J, Moss R, Huiskamp R, Fankhauser H, de Vries M, Gabel D.
Tissue uptake of BSH in patients with glioblastoma in the EORTC 11961 phase I BNCT trial.
J Neurooncol. 2003 Mar-Apr;62(1-2):145-56.
PMID: 12749710

2: Gibson CR, Staubus AE, Barth RF, Yang W, Ferketich AK, Moeschberger MM.
Pharmacokinetics of sodium borocaptate: a critical assessment of dosing paradigms for boron neutron capture therapy.
J Neurooncol. 2003 Mar-Apr;62(1-2):157-69.
PMID: 12749711

3: Wallace JM, Hannon-Fletcher MP, Robson PJ, Gilmore WS, Hubbard SA, Strain JJ.
Boron supplementation and activated factor VII in healthy men.
Eur J Clin Nutr. 2002 Nov;56(11):1102-7.
PMID: 12428176

4: Pan XQ, Wang H, Lee RJ.
Boron delivery to a murine lung carcinoma using folate receptor-targeted liposomes.
Anticancer Res. 2002 May-Jun;22(3):1629-33.
PMID: 12168846

5: Yanagie H, Kobayashi H, Takeda Y, Yoshizaki I, Nonaka Y, Naka S, Nojiri A, Shinnkawa H, Furuya Y, Niwa H, Ariki K, Yasuhara H, Eriguchi M.
Inhibition of growth of human breast cancer cells in culture by neutron capture using liposomes containing 10B.
Biomed Pharmacother. 2002 Mar;56(2):93-9.
PMID: 12000141

6: Fort DJ, Rogers RL, McLaughlin DW, Sellers CM, Schlekat CL.
Impact of boron deficiency on Xenopus laevis: a summary of biological effects and potential biochemical roles.
Biol Trace Elem Res. 2002 Winter;90(1-3):117-42. Review.
PMID: 12666830

7: Armstrong TA, Spears JW.
Effect of dietary boron on growth performance, calcium and phosphorus metabolism, and bone mechanical properties in growing barrows.
J Anim Sci. 2001 Dec;79(12):3120-7.
PMID: 11811468

8: Kurtoglu V, Kurtoglu F, Coskun B.
Effects of boron supplementation of adequate and inadequate vitamin D3-containing diet on performance and serum biochemical characters of broiler chickens.
Res Vet Sci. 2001 Dec;71(3):183-7.
PMID: 11798292

9: Smith DR, Chandra S, Barth RF, Yang W, Joel DD, Coderre JA.
Quantitative imaging and microlocalization of boron-10 in brain tumors and infiltrating tumor cells by SIMS ion microscopy: relevance to neutron capture therapy.
Cancer Res. 2001 Nov 15;61(22):8179-87.
PMID: 11719448

10: Sheng MH, Taper LJ, Veit H, Thomas EA, Ritchey SJ, Lau KH.
Dietary boron supplementation enhances the effects of estrogen on bone mineral balance in ovariectomized rats.
Biol Trace Elem Res. 2001 Jul;81(1):29-45.
PMID: 11508330

11: Armstrong TA, Spears JW, Lloyd KE.
Inflammatory response, growth, and thyroid hormone concentrations are affected by long-term boron supplementation in gilts.
J Anim Sci. 2001 Jun;79(6):1549-56.
PMID: 11424693

12: Schaafsma A, de Vries PJ, Saris WH.
Delay of natural bone loss by higher intakes of specific minerals and vitamins.
Crit Rev Food Sci Nutr. 2001 May;41(4):225-49. Review.
PMID: 11401244

13: Stacewicz-Sapuntzakis M, Bowen PE, Hussain EA, Damayanti-Wood BI, Farnsworth NR.
Chemical composition and potential health effects of prunes: a functional food?
Crit Rev Food Sci Nutr. 2001 May;41(4):251-86. Review.
PMID: 11401245

14: Sheng MH, Taper LJ, Veit H, Qian H, Ritchey SJ, Lau KH.
Dietary boron supplementation enhanced the action of estrogen, but not that of parathyroid hormone, to improve trabecular bone quality in ovariectomized rats.
Biol Trace Elem Res. 2001 Summer;82(1-3):109-23.
PMID: 11697760

15: Armstrong TA, Spears JW, Crenshaw TD, Nielsen FH.
Boron supplementation of a semipurified diet for weanling pigs improves feed efficiency and bone strength characteristics and alters plasma lipid metabolites.
J Nutr. 2000 Oct;130(10):2575-81.
PMID: 11015492

16: Fort DJ, Stover EL, Strong PL, Murray FJ, Keen CL.
Chronic feeding of a low boron diet adversely affects reproduction and development in Xenopus laevis.
J Nutr. 1999 Nov;129(11):2055-60.
PMID: 10539784

17: Gaby AR.
Natural treatments for osteoarthritis.
Altern Med Rev. 1999 Oct;4(5):330-41. Review.
PMID: 10559548

18: Naghii MR.
The significance of dietary boron, with particular reference to athletes.
Nutr Health. 1999;13(1):31-7. Review.
PMID: 10376277

19: Sayli BS.
An assessment of fertility in boron-exposed Turkish subpopulations: 2. Evidence that boron has no effect on human reproduction.
Biol Trace Elem Res. 1998 Winter;66(1-3):409-22.
PMID: 10050934

20: Penland JG.
The importance of boron nutrition for brain and psychological function.
Biol Trace Elem Res. 1998 Winter;66(1-3):299-317. Review.
PMID: 10050926

21: Lanoue L, Taubeneck MW, Muniz J, Hanna LA, Strong PL, Murray FJ, Nielsen FH, Hunt CD, Keen CL.
Assessing the effects of low boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems.
Biol Trace Elem Res. 1998 Winter;66(1-3):271-98.
PMID: 10050925

22: Fort DJ, Propst TL, Stover EL, Strong PL, Murray FJ.
Adverse reproductive and developmental effects in Xenopus from insufficient boron.
Biol Trace Elem Res. 1998 Winter;66(1-3):237-59.
PMID: 10050923

23: Samman S, Naghii MR, Lyons Wall PM, Verus AP.
The nutritional and metabolic effects of boron in humans and animals.
Biol Trace Elem Res. 1998 Winter;66(1-3):227-35. Review.
PMID: 10050922

24: Hunt CD.
Regulation of enzymatic activity: one possible role of dietary boron in higher animals and humans.
Biol Trace Elem Res. 1998 Winter;66(1-3):205-25. Review.
PMID: 10050921

25: Sutherland B, Strong P, King JC.
Determining human dietary requirements for boron.
Biol Trace Elem Res. 1998 Winter;66(1-3):193-204.
PMID: 10050920

26: Hunt CD, Herbel JL, Nielsen FH.
Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations.
Am J Clin Nutr. 1997 Mar;65(3):803-13.
PMID: 9062533

27: Wilson JH, Ruszler PL.
Effects of boron on growing pullets.
Biol Trace Elem Res. 1997 Mar;56(3):287-94.
PMID: 9197925

28: Naghii MR, Samman S.
The effect of boron supplementation on its urinary excretion and selected cardiovascular risk factors in healthy male subjects.
Biol Trace Elem Res. 1997 Mar;56(3):273-86.
PMID: 9197924

29: Naghii MR, Wall PM, Samman S.
The boron content of selected foods and the estimation of its daily intake among free-living subjects.
J Am Coll Nutr. 1996 Dec;15(6):614-9.
PMID: 8951740

30: Meacham SL, Taper LJ, Volpe SL.
Effect of boron supplementation on blood and urinary calcium, magnesium, and phosphorus, and urinary boron in athletic and sedentary women.
Am J Clin Nutr. 1995 Feb;61(2):341-5.
PMID: 7840072

31: Hunt CD.
The biochemical effects of physiologic amounts of dietary boron in animal nutrition models.
Environ Health Perspect. 1994 Nov;102 Suppl 7:35-43. Review.
PMID: 7889878

32: Penland JG.
Dietary boron, brain function, and cognitive performance.
Environ Health Perspect. 1994 Nov;102 Suppl 7:65-72.
PMID: 7889884

33: Newnham RE.
Essentiality of boron for healthy bones and joints.
Environ Health Perspect. 1994 Nov;102 Suppl 7:83-5.
PMID: 7889887

34: Meacham SL, Taper LJ, Volpe SL.
Effects of boron supplementation on bone mineral density and dietary, blood, and urinary calcium, phosphorus, magnesium, and boron in female athletes.
Environ Health Perspect. 1994 Nov;102 Suppl 7:79-82.
PMID: 7889886

35: Hunt CD, Herbel JL, Idso JP.
Dietary boron modifies the effects of vitamin D3 nutrition on indices of energy substrate utilization and mineral metabolism in the chick.
J Bone Miner Res. 1994 Feb;9(2):171-82.
PMID: 8140930

36: Nielsen FH.
New essential trace elements for the life sciences.
Biol Trace Elem Res. 1990 Jul-Dec;26-27:599-611.
PMID: 1704767

37: Massie HR, Whitney SJ, Aiello VR, Sternick SM.
Changes in boron concentration during development and ageing of Drosophila and effect of dietary boron on life span.
Mech Ageing Dev. 1990 Mar 31;53(1):1-7.
PMID: 2325439

38: Nielsen FH, Hunt CD, Mullen LM, Hunt JR.
Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women.
FASEB J. 1987 Nov;1(5):394-7.
PMID: 3678698

39: Teller, E., Wood, L., Hyde, R.
Global Warming and Ice Ages: I. Prospects for Physics-Based Modulation of Global Change.
This paper was prepared for submittal to the 22nd International Seminar on Planetary Emergencies – Sicily, Italy August 20-23, 1997)


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Sodium Fluoride (NaF) Chelation Demystified – “The Complexation Reaction” (T. Fahy, Z. Li, et. al.)

Summary: Sodium Fluoride (NaF) complexing agents/chelating agents, referred to herein as “ligands,” react with boron metalloid ions to form a chelate (complex ion/metal coordination complex)

Boron ions in a hydrochloric acid (HCl)/potassium chloride (KCl)/sodium chloride (NaCl) solution (gastric acid) with a pH of 1.5 to 3.5 are solvated and a number of solvent molecules are bound to the boron ions. It is with these solvent molecules that NaF reacts, forming metal complexes or metal coordination compounds →

The NaF molecules which displace the solvent molecules are called ligands. The ligands, arranged symmetrically about a central atom (octahedron), serve as electron-donating entities, which when bonded with boron ions, form insoluble complexes.


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