by John D. MacArthur

“Alzheimer’s disease is an illness that is 100% incurable and 100% fatal. It attacks rich and poor, white-collar and blue, and women and men, without regard to party. A degenerative disease, it steadily robs its victims of memory, judgment and dignity, leaves them unable to care for themselves and destroys their brain and their identity – often depleting their caregivers and families both emotionally and financially.”

This sober assessment is part of Sandra Day O’Connor’s 2010 call for a national Apollo-like program to stop Alzheimer’s by the end of this decade.¹ Three years later, the Alzheimer’s Association says that there is still no way to prevent or even slow the progression of this dreadful disease.

This report suggests otherwise. Minimizing ingestion of two common substances – fluoride and copper – may well prove to be a simple and effective way to help prevent Alzheimer’s disease.

Sleep Disruption and Alzheimer’s Disease

The greatest universal risk factor for Alzheimer’s disease is age, especially because sleep quality decreases with age. Distinct sleep problems appear in Alzheimer’s disease. Clinicians report abnormal excitement at bedtime (sundowning), increased awakenings and sleep fragmentation, reduced slow-wave sleep, and slower EEG frequencies.² “It is very clear that animals’ circadian systems begin to deteriorate as they age,” says UCLA Chancellor Gene Block, professor of biobehavioral and physiological sciences. “Humans have enormous problems with the quality of their sleep as they age.”³

Circadian rhythms govern most aspects of physiology and behavior in mammals, including sleep-wake cycles. These rhythms are generated by the suprachiasmatic nucleus (SCN), the master circadian pacemaker located in the hypothalamus. Disruptions in the SCN lead to disrupted sleep, as well as dysfunction in memory, the cardiovascular system, and the body’s metabolism and immune response.³

The brain’s pineal gland is the central structure in the circadian system that produces the hormone melatonin at night under the control of the SCN. Secretion levels of melatonin are decreased in aging and more severely reduced in Alzheimer’s disease.⁴ Studies indicate that a dysfunction of pineal melatonin synthesis by the SCN is responsible for disrupted circadian rhythms taking place as early as the very first preclinical stages of Alzheimer’s.^5,6

Older adults with insomnia have a greater risk of Alzheimer’s disease (AD), and recent evidence suggests that circadian dysregulation and sleep disruption are not just a consequence of AD, but play roles in the development of this neurodegenerative disorder.^7-9

In 2011, researchers at Washington University School of Medicine (WUSM) reported a mechanism for how inadequate sleep increases the risk of Alzheimer’s disease. They discovered a circadian rhythm to amyloid removal. In the spinal fluid of healthy young people, levels of amyloid-beta rise and fall in a daily pattern that echoes the sleep cycle. However, in older adults with amyloid-beta plaques in their brains, “the ebb and flow is eradicated, and amyloid-beta levels are close to constant.” Inadequate sleep seems to be disrupting clearance of amyloid-beta from the brain through the spinal fluid, a process that normally occurs when the brain is relatively inactive during sleep.¹⁰

In 2013, WUSM researchers confirmed their earlier observations that sleep is disrupted in people who likely have early AD, but don’t yet have the memory loss or other cognitive problems characteristic of full-blown AD. Participants with preclinical AD had poorer sleep efficiency than people without markers of AD. On average, those with preclinical disease spent less time asleep while in bed at night and also napped more often. The worst sleepers were five times more likely to have preclinical AD compared with good sleepers. A vicious cycle: AD disrupts sleep, and lack of sleep promotes AD.¹¹

Pineal Calcification and Fluorosis

Researchers used computed tomography to examine the pineal glands in 279 memory clinic outpatients (AD: 155; other dementia: 25; mild cognitive impairment: 33; depression: 66) and 37 age-matched controls. In patients with AD, the degree of pineal calcification was significantly higher than in patients with other types of dementia, with depression, or in controls – indicating reduction in melatonin production and its circadian properties.¹²

The fact that pineal calcification is significantly higher in patients with Alzheimer’s disease should be a wakeup call to researchers, because the National Research Council (NRC) reported in 2006: “As with other calcifying tissues, the pineal gland can accumulate fluoride. Fluoride has been shown to be present in the pineal glands of older people (14–875 mg of fluoride per kg of gland in persons aged 72–100 years), with the fluoride concentrations being positively related to the calcium concentrations in the pineal gland.”¹³

The pineal gland is not protected by the blood–brain barrier and is therefore exposed to fluoride in the bloodstream. Animal research by Dr. Jennifer Luke showed that “fluoride is associated with depressed pineal melatonin synthesis.”¹⁴

Luke’s human research revealed: “By old age, the human pineal gland has readily accumulated fluoride and its fluoride/calcium ratio is higher than bone.” The pineal gland is a mineralizing tissue. Its calcified concretions are composed of hydroxyapatite similar to that in bone and teeth. The aged pineal gland contains about the same amount of fluoride as teeth (300 mg F/ kg). Fluoride may also accumulate in a child’s pineal gland, because significant amounts of calcification have been demonstrated in the pineals from young children.¹⁵

The NRC concluded, “Fluoride is likely to cause decreased melatonin production and to have other effects on normal pineal function, which in turn could contribute to a variety of effects in humans. Actual effects in any individual depend on age, sex, and probably other factors [e.g., genetic], although at present the mechanisms are not fully understood.” The NRC called for more research to “address the effect of fluoride exposure on pineal function or melatonin production in humans.” Seven years later, however, not a single such study has been published, although more than 700 studies involving “fluorosis” have.

The term pineal fluorosis does not yet exist, but there is evidence of fluorosis in other soft tissues. PET/CT scans show that vascular calcification and fluoride uptake are significantly correlated in most arterial walls. In coronary arteries, there was a significant association between presence of fluoride uptake and history of cardiovascular events.¹⁶ A mechanism of pathology could be fluoride’s ability to induce “dramatic endothelial cell barrier dysfunction.”¹⁷

We still don’t know to what extent decreased melatonin production is caused by fluoride in the pineal gland. We do know melatonin is highly protective against fluoride-induced damage. Recent studies of human blood cells show that melatonin significantly reduces the frequency of primary DNA damage induced by the genotoxicity of fluoride.¹⁸ Melatonin also demonstrated a significant decline in fluoride-induced hemolysis (breakdown of red blood cells).¹⁹

Animal studies show that pineal proteins and melatonin can protect against fluoride-induced neurotoxicity through mechanisms involving enhancement of the antioxidant defense system.²⁰ Pineal proteins significantly protect the activity of a crucial nervous system enzyme, acetylcholinesterase, from adverse changes induced by fluoride.²¹

Fluoride Risks To Young and Old

More people drink artificially fluoridated water in the US alone, than in the rest of the world combined.²² Because fluoride permeates America’s food-and-beverage chain, people can receive a substantial amount of fluoride from beer, soft drinks, and processed foods.²³ The average for children 2 to 5 years old is about 37%, but some children receive as much as 85% of their dietary fluoride from solid foods.²⁴

Children and seniors are also at risk from swallowing fluoride in toothpaste. A brushful of toothpaste contains 1 to 2 mg of fluoride. It’s estimated that children may ingest up to 40% of their toothpaste. Adults with a welldeveloped spitting reflex swallow less than 10%.²⁵ Swallowing disorders, however, are common in the elderly (from 7% to 22%) and dramatically increase to 40% to 50% in older individuals who reside in long-term care facilities.²⁶

Circadian-rhythm sleep disorders may affect between 20% to 30% of young children, but for those with neurodevelopmental disabilities, the prevalence tends to be much greater: about 86% of children aged up to 6 years suffer from severe sleep problems if they have learning disabilities.²⁷ There is increasing evidence that chronic sleep loss can lead to neuronal and cognitive loss in children, although this is generally unrecognized by the medical profession and the public.”²⁸

We don’t really know if sleep disruption is merely a symptom or is also a causative factor of neurodevelopmental disabilities as it is for neurodegeneration. We do know that the EPA’s Neurotoxicology Division has found “substantial evidence” that fluoride is toxic “to the developing mammalian nervous system.”²⁹

Copper and Melatonin

Melatonin is not only vital to the regulation of circadian rhythms, but is also a potent antioxidant. For example, the effective antioxidant dose of melatonin to protect the liver from oxidative stress during malaria is 20 times lower than that of vitamin C and vitamin E.³⁰ Melatonin is also neuroprotective against coppermediated free radical damage.³¹

In a 2001 study that administered copper daily to Wistar rats for a 6-week period, copper significantly reduced the activity of N-acetyltransferase, an enzyme in their pineal glands needed to produce melatonin from serotonin. When melatonin was coadministered, it prevented copper from inhibiting the enzyme.³²

Research suggests “a potential role of rhythmic copper metabolism in pineal and/or retina circadian function.”³³ A 2012 study measured the copper and zinc levels in the serum and hair of 126 adult women. Less sleep was significantly associated with higher copper levels in their hair.³⁴ Other research found elevated levels of copper in the cerebrospinal fluid of women compared with men with Alzheimer’s.³⁵

Serum copper levels rise with age, and high copper/zinc ratios are linked with multiple-cause mortality in the elderly. A 2012 study of 144 frail elderly men identified “specific deficits associated with high copper/zinc ratios that span multiple organ systems and supports earlier studies indicating that serum copper levels and the copper/ zinc ratio may serve as useful predictive biomarkers for poor health in the elderly.”³⁶

Copper and DNA Damage

Two factors are consistently associated with neurodegenerative disorders: DNA damage by reactive oxygen species and excessive levels of copper and iron in regions of the brain associated with the particular disorder. In 2010, the first study to examine genome integrity and its relation to these metals found a “clear correlation between copper and iron levels versus DNA strand breaks in aging brain regions.” Researchers assessed copper, iron, and zinc levels in the hippocampus and frontal cortex of normal brains in three age groups. As one progressed from Group I (under 40) to Group III (over 61) – especially from Group II (41–60) to III – levels of copper and iron were significantly elevated, while zinc was significantly depleted.³⁷

The researchers note that the accumulated DNA fragmentation could be due to decreased DNA repair capacity. Although our DNA is constantly being damaged, complex mechanisms continuously assess and repair our genetic material thousands of times a day in every cell in our bodies.³⁸ In 2011, researchers at University of Texas Medical Branch at Galveston discovered how copper and iron act as a “double-edged sword.” Not only do these metals induce oxidative damage, but they also inhibit the DNA repair process. Iron and copper significantly interfere with the activity of two enzymes that normally would quickly repair DNA damage. “Our results show that by inhibiting NEIL1 and NEIL2, iron and copper play an important role in the accumulation of DNA damage in neurodegenerative diseases,” said lead author Muralidhar Hegde. “We have found multiple toxic mechanisms linking elevated iron and copper levels in the brain and extensive DNA damage.”^39,40

Neuroplasticity, Long-Term Potentiation, and Copper

Another reason why age is the greatest universal risk factor for Alzheimer’s disease is because the biological capacity for neuroplasticity decreases with age. Plasticity – derived from the Greek word meaning “molded” or “formed” – is the fundamental ability of the brain to change in response to experience. Plasticity is the process of modifying the number and strength of connections between neurons that give the brain its structural capacity to learn and remember, to control behavior, and to recover from injury.

Recent studies have shed light on the role of sleep in synaptic plasticity. Evidence suggests that sleep creates a heightened state of plasticity, which may be essential for the consolidation and optimization of synaptic circuits to retain salient memory traces.² Neuroplasticity is impaired in patients with Alzheimer’s disease compared with controls.^41,42 A breakdown of brain plasticity also characterizes the late stages of mild cognitive impairment (MCI),usually a precursor to Alzheimer’s.⁴³

A key mechanism of neuroplasticity is long-term potentiation (LTP), the process of memory formation at the molecular level. LTP produces the synaptic changes necessary to acquire and store new information. LTP occurs in the hippocampus and is required for adult learning.⁴⁴ In Alzheimer’s, dementia severity correlates strongly with decreased synapse density in the hippocampus and cortex.⁴⁵

Inhibition of LTP by copper has been well established, but the exact mechanism is poorly understood.⁴⁶ In animal studies, electrophysiological tests on hippocampal slices indicated absence of LTP in rats that chronically consumed copper dissolved in water, compared with rats who did not consume copper. The research showed that copper reduces synaptic sensibility and represents “a significant disturbance in the plasticity phenomenon associated with learning and memory.”⁴⁷ A 2011 mouse study showed that “copper inhibited NMDA receptor-independent LTP in the CA3 region of the mouse hippocampus.”⁴⁶

Copper and NMDA Receptors

Long-term potentiation requires activation of N-methyl D-aspartate (NMDA) receptors, key neurotransmitter receptors that also regulate neuronal death. NMDA receptors are crucial to learning and memory, and dysregulation of the NMDA receptor is a key underlying mechanism of neurodegenerative disease.

The NMDA receptor is unusually complex. It is regulated by the excitatory neurotransmitter glutamate, but is also voltage sensitive. Homeostasis in the glutamatergic system is crucial. Both hypo- and hyperactivity lead to dysfunction.⁴⁸ The influence of copper on cortical glutamatergic transmission has been extensively demonstrated at a synaptic level. A pilot study suggested that a higher level of body copper reserve parallels lower cortical glutamatergic responsiveness.⁴⁹

When released into neural synapses, copper damps down the activity of NMDA receptors whose high activity causes excitotoxic cell death.⁵⁰ Too much copper, however, inhibits NMDA receptor activity. Animal studies on hippocampal neurons showed that exogenously applied copper can be a potent inhibitor of NMDA receptor mediated responses and that low concentrations of copper can selectively reduce NMDA-mediated potentials and synaptic plasticity, thus inhibiting LTP in the CA1 region of the rodent hippocampus.^51-53

NMDA receptors are also the principal glutamate receptors central to the photic signaling that mediates the effect of light on resetting the brain’s circadian pacemaker in the SCN.^54,55

Copper and Neurodegeneration

Both alpha-synuclein and huntingtin are copper-binding proteins, and both have been associated with NMDA receptor-mediated neuronal toxicity. This raises the possibility of copper modulation of NMDA receptors as a unifying theme in many neurodegenerative disorders.^56-58

Alpha-synuclein is commonly found in the brain, but aberrant accumulation can form the insoluble aggregates implicated in several neurodegenerative diseases. Researchers at the University of Bath have explored how the combination of copper and alpha-synuclein may cause neurodegeneration.⁵⁹ In 2010, they found that a reduction in cellular copper resulted in a great decrease in large aggregates of alpha-synuclein in cells.⁶⁰

Researchers in Korea reported that copper was the most effective metal ion affecting alpha-synuclein to form aggregates. They concluded, “Abnormal copper homoeostasis could be considered as one of the risk factors for the development of disorders such as Alzheimer’s or Parkinson’s disease.”⁶¹ In 2011, North Carolina State University scientists showed how copper induces misfolding in the alphasynuclein protein, which they propose is an initial event in the formation of Lewy bodies and thus in Parkinson’s disease pathogenesis.⁶²

Copper Particulate Matters

Another factor coincident with our modern epidemic of dementia is the worsening environmental problem of copper pollution. For example, 530,000 pounds of copper from human activity entered San Francisco Bay in 2003. An estimated 70,000 to 318,000 pounds of copper pollute Puget Sound each year. About a third of this copper comes from the brake pads of motor vehicles.⁶³

Brake pads contain as much as 25% copper. Each time drivers apply their brakes, tiny particles of copper are released from the pads. Tests show that “full stop” braking produces the highest number and concentrations of fine particles and nanoparticles. Some exposure occurs even when brakes are not being applied. Elevated copper levels in the air have been measured in traffic, including inside vehicles.⁶⁴ High levels of copper were also found in a parking garage.⁶⁵

California and Washington have already passed laws to greatly reduce the copper content in brake pads (by 2023), because copper is toxic to aquatic life, including plankton, the base of the aquatic food chain. In regions of the Mediterranean Sea, significant declines in phytoplankton biomass have been detected after atmospheric aerosol events characterized by high copper concentrations.⁶⁶

Copper is known to interfere with the normal function of the peripheral olfactory nervous system of fish. When juvenile coho salmon were exposed to low levels of dissolved copper (5–20 ppb for 3 hours), they became unresponsive to their chemosensory environment and were significantly less likely to survive an attack.⁶⁷

Human studies show that long-term exposure to traffic-related particulate matter impairs cognitive function in the elderly and is associated with significantly worse cognitive decline in older women.^68,69

Depending on their characteristics, air toxicants can reach the brain through several pathways. The effects of air pollution on the brain then manifest as neuroinflammation, oxidative stress, and neurodegeneration.⁷⁰

A decade of compelling epidemiological and experimental research led by Lilian CalderónGarcidueñas, MD, PhD, has found that particulate matter can reach the brain by uptake through olfactory neurons, and that the olfactory bulb neuropathology associated with urban exposures is very similar to the early stages of Alzheimer’s and Parkinson’s diseases.^71,72 “Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alphasynuclein starting in childhood.”⁷³

What’s more, the researchers’ data suggest that “air pollution moderates the association between ApoE genotype and neurodegenerative changes … An ApoE4 carrier residing in a highly polluted environment will have an acceleration of neurodegenerative changes towards AD.”⁷³ (The increased risk of Alzheimer’s disease for ApoE4 genotypes may relate to the inability of ApoE4 to bind copper and remove it from the brain.)

Calderón-Garcidueñas points out that in 2012, more than 74 million people in the US were being exposed to concentrations of fine particulate matter above the health standard set in 2006. In 2013, the EPA lowered that threshold 20%, so now many more people are being exposed to air pollution particulates that Calderón-Garcidueñas says “likely play a key role in the development of neuroinflammation and neurodegeneration.”⁷¹

Other sources of olfactory exposure to copper are pressure-treated lumber (whose copper content was boosted substantially in 2004) and “high-copper amalgam” dental fillings whose copper content jumped from below 6% to 12% to 30% in 1962. An Israeli company recently began marketing clothing, pillowcases, and even respiratory face masks impregnated with very small particles of copper oxide.

Prevention Is Possible

For more than six years, Dr. George Brewer has continued to publish well-reasoned wake-up calls about our dementia epidemic’s association with our chronic consumption of unprecedented high levels of inorganic copper.⁷⁴ (His latest report, “Too Much Copper, Too Little Zinc, and Cognitive Deterioration in Alzheimer’s Disease,” is in this issue of the Townsend Letter, p. 52)

Brewer has received little support from the scientific-journal community, even though major copper/AD researchers acknowledge that something is disturbing copper homeostasis. For example, Ashley I. Bush, MD, PhD, says, “Brain homeostasis of transition metals is severely perturbed in Alzheimer’s disease.”⁷⁵ And “ … the AD-affected brain suffers from metallostasis, or fatigue of metal trafficking, resulting in redistribution of metals into inappropriate compartments.”⁷⁶ Even the International Copper Association’s researcher concluded, “More research is urgently required to understand why there is an apparent disturbance in metal homeostasis in AD.”⁷⁷

In his comprehensive 2009 review (“Copper in Alzheimer’s Disease: Too Much or Too Little?”), Joseph F. Quinn, MD, concluded, “Disordered copper metabolism is not likely to be the primary cause of AD … however, copper may modulate the primary mechanisms in AD.”⁷⁸ In his subsequent 2010 study (with Brewer), Quinn concluded, “Our data suggests that controlled lowering of systemic copper may achieve antiamyloid effects if initiated early in the disease process.”⁷⁹

How early in the disease process should preventive measures be initiated? As soon as possible. We already know that biochemical harbingers of Alzheimer’s are present 15 to 20 years before any of its currently recognized symptoms become apparent. No doubt the disease begins even sooner, especially for people who have the ApoE4 gene. In a brain-imaging study of young adults (aged 20–35), fMRI scans showed visible differences in the brains of those with ApoE4, compared with others. There was hyperactivity in their hippocampi. Even when these ApoE4 carriers weren’t doing anything, their hippocampi were working harder than in those without ApoE4.⁸⁰

ApoE4 increases the risk for sleep disordered breathing, including obstructive sleep apnea/hypopnea in individuals under age 65.^81,82 A significant portion of sleep-disordered breathing is associated with ApoE4 in the general population.⁸³ Breathing disorders during sleep affect pineal function.⁸⁴ “Sleep apnea skyrockets in the elderly, and this fact hasn’t been given the attention it deserves by the sleep world or the Alzheimer’s world,” says Ricardo S. Osorio, MD. His 2013 research found an association between sleep disordered breathing with hippocampal atrophy and other biomarkers of AD in cognitively normal elders (with a body mass index below 25).⁸⁵

An estimated 77 million Americans carry an ApoE4 gene, and most don’t know they have this risk factor. If you inherit a single ApoE4 from one parent, your AD risk triples. If you inherit a double dose of ApoE4 from both parents, your risk rises by 10 times or more. Also, someone who has a first-degree relative with Alzheimer’s disease (especially a mother) is 4 to 10 times more likely to develop the disease compared with people with no family history.

History Repeats Itself

Benjamin Franklin wrote to a colleague in 1786 about a case of lead poisoning in Europe wherein a whole family was afflicted by drinking rain water from their leaded roof: “This had been drunk several years without mischief; but some young trees planted near the house growing up above the roof, and shedding the leaves upon it, it was supposed that an acid in those leaves had corroded the lead they covered and furnished the water of that with its baneful particles and qualities.”

This problem Franklin that described more than two centuries ago is being repeated in our time. Similar to how acidic leaves leached lead from the roof into the rain water that the family drank, caustic chemicals added to modern tap water are leaching lead and copper from metallic plumbing into the water that we consume.

Research presented at a 2005 Drinking Water Symposium points to copper pipe failure caused by the use of chloramines in California’s water systems. Chloramines are compounds containing a mixture of chlorine and ammonia that extend the disinfecting power of chlorine in drinking water. Chloramine treatment, however, may cause pinhole leaks in the copper tubing carrying the water. Chloramines may be producing what EPA calls “aggressive” water with an ability to leach out the minerals, metals, or other materials from whatever it touches or passes over.⁸⁶

According to corrosion expert Marc A. Edwards, professor of civil and environmental engineering at Virginia Tech, “Copper corrosion by-product release to potable water is a complex function of pipe age, water quality, stagnation time, and type of phosphate inhibitor.”⁸⁷ He says, “A wide range of factors are involved, including natural organic matter, pH, alkalinity, sulfides and other dissolved materials in water. In some cases, particularly bad combinations of these components can cause a new copper pipe to leak in as little as two weeks.”⁸⁸ Edwards points to some water-treatment steps that result in removing natural inhibitors of copper corrosion. For example, pipes dosed with polyphosphate generally had higher levels of particulate copper. In his 1994 and 2001 surveys of US drinking water utilities, more than half reported adding phosphate inhibitors to their water.⁸⁹

Copper pipes are not the only source of copper that contaminates drinking water. Another is brass plumbing fixtures, because brass is about twothirds copper. Water enters most homes through brass water meters and backflow valves, travels through brass elbows and shutoff valves, then flows out of brass faucets. Also, millions of families have water wells equipped with brass-bearing submersible pumps.

Fluoridation Chemicals Leach Copper into Drinking Water

Disinfection and fluoridation chemicals have been added to the tap water that hundreds of millions of people have been drinking their entire lives. Unbelievable as it seems for a society that prides itself on science, no one had looked at brass corrosion caused by combinations of these corrosive chemicals prior to a landmark 2007 study by the nonprofit Environmental Quality Institute at the University of North Carolina in Asheville.

This well-designed study found that when fluosilicic acid (the chemical most often used to fluoridate drinking water) is combined with disinfection chemicals, it worsened the leaching of lead from brass elbows and brass water meters. The researchers note, “Chlorine is known to corrode brass, releasing lead from plumbing devices. It is known that chloramines and chlorine in different ratios with ammonia mobilize copper from brass, which we have found also enhances elution of lead from leaded brass alloys.”⁹⁰

The study’s abstract concludes: “Over the first test week … lead concentrations nearly doubled (from about 100 ppb to nearly 200), but when fluosilicic acid was also included, lead concentrations spiked to over 900 ppb. Lead concentrations from the chlorine-based waters appeared to be decreasing over the study period, while for the chloramines + ammonia + fluosilicic acid combination, lead concentrations seemed to be increasing with time.”⁹⁰

Although increased copper levels were not measured, what happened was that as more copper was leached from the brass, more lead became available for corrosion. The researchers explain: in brass, “lead alloyed with copper is not molecularly distributed, as in a solid solution. Discrete lead nodules are embedded in a copper matrix. Agents that attack copper are likely to foster lead mobility, adding significantly to lead (probably particulate) in drinking water. … This may help to explain the Washington, DC experience that homes with only brass as a possible source of lead, not only had high water lead, but were also experiencing serious pitting of copper pipe.”⁹⁰ (The District of Columbia’s drinking water is treated with both chloramines and fluoridation chemicals.)

The researchers conclude that several factors can produce more corrosion than either of the disinfectants or fluoridating agents alone: “One such factor is that fluosilicic acid, the most widely used fluoridating agent, is a good solvent for lead. Another is that chlorine, ammonia, and chloramine are all hostile to copper in that they induce copper stress cracking and/ or can dissolve it. A third factor is that ammonia added to chlorine to produce chloramine will also react with fluosilicic acid to produce ammonium fluosilicate, an established solvent for copper alloys.”⁹⁰

Related research showed that in communities where fluosilicic acid is added to the drinking water, the “prevalence of children with elevated blood lead (PbB > 10 micrograms/dL) is about double that in non-fluoridated communities.”⁹¹ Recent research suggests that a biological mechanism not yet recognized may underlie this epidemiological association. In rats exposed to low levels of lead, fluoride consistently increased lead concentrations in their blood and calcified tissues. Conversely, lead exacerbated dental fluorosis in these rodents, suggesting that coexposure to lead may affect the degree of fluorosis.^92,93 This may be relevant to the mystery of pineal fluorosis (discussed above).

Evidence of Copper and Lead Leaching from Fluoridation

Westby, Wisconsin (1990): Fluoride equipment malfunctioned and caused the fluoride to surge to 150 ppm, instead of the intended 1 ppm. The fluoride corroded copper off the pipes in area homes. The Westby Council stopped fluoridating its water.⁹⁴

North Branford, Connecticut (1988): When excess hydrofluorosilicic acid was diverted to a 127-home community water supply for 12 hours, fluoride levels peaked at 51 ppm. Water acidification caused copper to leach from the domestic plumbing, raising copper levels to 25 to 41 ppm.⁹⁵ (The EPA’s maximum contaminant level goal for copper is 1.3 ppm.)

As the Environmental Quality Institute study suggests, when lead is leached from brass, so is copper. Several cities have reported increased lead levels in their drinking water because of fluoridation:

Tacoma, Washington (1992): The city had to shut down the fluoridation equipment because fluoride had eaten the pipes. The municipal water had approximately 32 ppb lead, but after fluoridation stopped, the lead level dropped to 17 ppb. When the equipment was fixed, the lead level shot right back up to 32 ppb. The city discontinued the use of fluoride, and the lead level again dropped.⁹⁶

Thurmont, Maryland (1994): Lead levels in town water decreased significantly after town officials stopped adding fluoride. Thurmont then voted to officially ban the use of fluoride.⁹⁷

Lebanon, Oregon (2005): The town’s tap water contained more lead after fluoridation began in 2001. “City Administrator John Hitt said that adding fluoride apparently changed the water chemistry enough to cause more lead to be leached from pipes in some houses dating from before the 1960s.”⁹⁸

When New York City’s fluoridation treatment was shut down for 3 to 4 months, there was approximately a 20% decrease in the lead concentrations in city water.⁹⁹

What To Do?

Over thousands of generations, humans have evolved to require only minute amounts of copper obtained from food. The body contains only 5/1000 of an ounce of copper. Copper is a micronutrient essential to life – especially to brain function – but copper can also be neurotoxic. That’s why special copper “chaperone” proteins have evolved to safely transport this important but dangerous metal through the interior of the cell to specific sites where it’s needed.¹⁰⁰ Now, however, seniors in developed nations have for much of their lives been chronically consuming abnormally high amounts of inorganic copper – especially in vitamin/mineral supplements and tap water.

As for fluoride, humans have no nutritional need for it. In fact, nature has evolved to protect infants from fluoride. Even when a mother’s dietary intake of fluoride is high, fluoride levels in her breast milk remain low.¹⁰¹ Nursing infants also have a similar natural protection against another toxin, lead.¹⁰²

On the one hand, it’s mind boggling. The neurochemistry of copper and the broad toxicity of fluoride are extremely complex.¹⁰³ On the other hand, it’s quite simple. For decades we’ve been overdosing on copper and fluoride – and now dementia is epidemic. We must do something, now. Even if we could simply postpone the onset of Alzheimer’s disease by 5 years, a large share of nursing-home beds in the US would empty.¹

A logical preventive strategy is obvious. Stop consuming copper in multivitamins and in drinking water, especially fluoridated water and the beverages made with it. Make sure that elderly family members do the same. (Eye formulas with high amounts of copper are often recommended for seniors.) Use fluoride-free toothpaste. Minimize exposure to pollution from heavy traffic.

Human societies have always relied on guidance from their elders, whose wisdom comes from a lifetime of experience and memory. If we continue to tolerate the devastation of our elders’ minds, our society cannot thrive. If we fail to prevent the early deterioration of our leaders’ minds, we may not even survive.

We must not allow the gift of consciousness to fade while we wait around for profit-centered interests to create a “cure.” The human brain is the most complex structure in the known universe. Attempts to pharmodulate neurochemistry are guaranteed to have unexpected, dire consequences.

Our levels of fluoride and copper consumption must return to what they were before 1945, when our current plague of dementia was only a horror story in the minds of science-fiction writers.

Notes

1. O’Connor SD, Prusiner S, Dychtwald K. The age of Alzheimer’s. New York Times. October 27, 2010. www.nytimes.com/2010/10/28/opinion/28oconnor. html.

2. Wang G, et al. Synaptic plasticity in sleep: learning, homeostasis, and disease. Trends Neurosci. 2011 September;34(9):452–463. www.ncbi.nlm.nih.gov/ pmc/articles/PMC3385863.

3. Wolpert S. Study shows new evidence of age-related decline in the brain’s master circadian clock. UCLA press release. July 18, 2011. www.eurekalert.org/pub_ releases/20118/15/2013-07/uoc–ssn071811.php.

4. Pappolla MA et al. Melatonin prevents death of neuroblastoma cells exposed to the Alzheimer amyloid peptide. J Neurosci. 1 March 1997, 17(5): 1683–1690. www.jneurosci.org/content/17/5/1683.full.

5. Wu YH, Swaab DF. The human pineal gland and melatonin in aging and Alzheimer’s disease. J Pineal Res. 2005 Apr;38(3):145–152. www.ncbi.nlm.nih.gov/ pubmed/15725334.

6. Wu YH, Swaab DF. Disturbance and strategies for reactivation of the circadian rhythm system in aging and Alzheimer’s disease. Sleep Med. 2007 Sep;8(6):623– 636. www.ncbi.nlm.nih.gov/pubmed/17383938.

7. Osorio RS et al. Greater risk of Alzheimer’s disease in older adults with insomnia. J Am Geriatr Soc. 2011 March; 59(3): 559–562. www.ncbi.nlm.nih.gov/pmc/ articles/PMC3378676.

8. Bedrosian TA, Nelson RJ. Pro: Alzheimer’s disease and circadian dysfunction: chicken or egg? Alzheimers Res Ther. 2012 Aug 13;4(4):25. www.ncbi.nlm.nih.gov/ pmc/articles/PMC3506939.

9. Purdy MC. Sleep loss linked to increase in Alzheimer’s plaques [press release]. Washington University School of Medicine. September 24, 2009. www.eurekalert.org/ pub_releases/2009-09/wuso-sll092209.php.

10. Purdy MC. Marker for Alzheimer’s disease rises during day and falls with sleep [press release]. Washington University School of Medicine. September 26, 2011. www.eurekalert.org/pub_releases/2011-09/wusomfa092611.php.

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John D. MacArthur writes about neuroscience. His previous contribution to the Townsend Letter was “Cell Phones and the Brain” (July 2002). John researched and wrote “The Human Brain” section for the Franklin Institute Science Museum website. This summer, all his neuroscience reports were published in a single volume, Mind Over Gray Matter: Practical Neuroscience for the Best Performance of Your Life (www.createspace.com/4316759).