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‘How I beat Alzheimer’s’

Reading time: 13 minutes

John Blackburn (not his real name) first began to think there was a problem with his brain at age 52, while he was renovating the bungalow he shared with his wife in Leicester, England. He took a measurement, and by the time he walked to the next room, he’d forgotten it. He took the measurement again, deliberately focusing this time, but he just couldn’t hold the figure in his head. He had never experienced anything like it before. His wife had noticed his forgetfulness too. “I found it hard even having a conversation,” he says.

John was referred to a memory clinic and then a neurologist. Scans showed his brain was shrinking, and in October 2014 he was diagnosed with early-onset Alzheimer’s disease.

Today, Alzheimer’s affects 5.5 million Americans and 47 million people globally. Its signature ‘neurofibrillary tangles’ and ‘senile plaques,’ made of a toxic protein called amyloid-beta in the brain, are poorly understood but thought to disrupt communication between neurons and interfere with proper brain function.

Alzheimer’s erases personalities and robs patients of their memories, their independence and their lives. It is currently the sixth leading cause of death in the United States. Today, if you live beyond the age of 85, your odds of facing the disease are 50/50.1 And its prevalence is predicted to soar – affecting more than 150 million people by 2050.

At best, the currently available drugs can only temporarily manage symptoms. According to the prestigious Mayo Clinic, “Alzheimer’s drugs don’t work for everyone, and they can’t cure the disease or stop its progression. Over time, their effects wear off.” They have side effects, too. Namenda (memantine) can cause nausea and vomiting, confusion and hallucinations, for example. Aricept (donepezil) is linked to nausea, tremors, stomach ulcers and seizures.

And despite countless clinical trials of ‘promising’ new drugs, no new drugs have been approved for Alzheimer’s disease since 2003.

John knew the treatment odds for his diagnosis were zero, but he was certain why he was losing his mind, and he thought this was key to fixing his problem. For 26 years he had worked building aluminium railway cars. “The shop I worked in was called ‘Death Bay.’ You couldn’t see from one end to the other because it was so filled with aluminium dust.” The huge bay housed at least two dozen welders and numerous machines to grind and buff the aluminium carriages, and there was no extraction filter.

“You could see the aluminium particles shining in the air, and our overalls were covered in very fine dust,” he recalls. “We were eating the stuff. It made your skin black, and you couldn’t scrub it off.”

There was some concern about the exposure at higher levels of the company. Sometime in the early 1990s, a group of “university types” came in and requested 11 men to provide urine samples. John and a friend of his volunteered, and when the academics returned to meet with operations personnel, the two men peeked in on their presentation through a window.

They saw figures on an overhead screen, each matched to the birthday of a volunteer. “Bloody hell,” said his friend. “My number is high.” John saw that his own number was lower, but didn’t know what they meant. That friend was diagnosed with Alzheimer’s in his late 60s, institutionalized, and died from the disease at age 70.

Clues from Camelford

John’s research was helped by clues from the worst mass poisoning incident in British history, the subject of a government inquest around the time he was diagnosed. In 1988, a truck driver mistakenly deposited 20 tons of aluminium sulfate into the household water supply instead of a reservoir tank in the village of Camelford in Cornwall, England. Aluminium is commonly used to clarify water, but the Camelford villagers received doses between 500 and 3,000 times the level that’s considered safe.

The villagers noticed the effects within minutes. The cloudy, sticky water burned children in their baths, blistered skin, caused hands and lips to stick together, turned fingernails blue and hair green and induced stomach cramps and diarrhea. In the quarter-century that followed, several of the exposed residents had documented cognitive impairment, high blood aluminium levels and complained of joint pain.2 Camelford has also seen a number of suspicious suicides and residents who developed dementia symptoms and early-onset Alzheimer’s disease.3

One of them was Carole Cross, who was 44 at the time of the disaster. She developed Alzheimer’s in her early 50s and died from it at 58. A coroner found that her brain was riddled with amyloid plaques and other abnormal protein aggregates.

Frozen samples of her brain were sent to the lab of Christopher Exley, a professor of bioinorganic chemistry at Keele University in England. Exley and his team have been studying the effects of aluminium in biological systems for more than 30 years – in fish gills, breast tissue, baby formula, mice, bumblebees, heroin addicts – and the brains of Alzheimer’s patients.

Exley found that Cross’ brain cortex contained high levels of aluminium, ranging from values typical of Alzheimer’s (3-7 micrograms per gram of dry weight, or roughly 2-4 times the amount in non-Alzheimer’s brain) to one sample with an astonishing 23 micrograms per gram.4

A potent neurotoxin

Cross’ high aluminium levels were similar to that seen in ‘dialysis-associated encephalopathy,’ a condition identified in the 1970s in dialysis patients who developed cognitive decline, memory loss and other symptoms similar to Alzheimer’s because, it turned out, their kidneys could not filter the aluminium in ordinary tap water, which then found its way to their brains. As a consequence, water used for dialysis today is carefully purified to exclude any trace of the metal.

Aluminium’s toxicity to neurons is well established. Research has shown that it interferes in at least 200 biochemical pathways, disrupts the blood brain barrier, kills neurons and glial cells, causes brain inflammation, increases oxidative stress, damages mitochondria – the energy powerhouses in every cell of the body – and alters gene expression. It’s been suspected in a number of other nervous system diseases including autism, ALS (amyotropic lateral sclerosis) and Parkinson’s.5

In the early 1990s, scientists established that aluminium is linked to redistribution of proteins related to the ‘tangles’ in the brains of both Alzheimer’s and dialysis patients.6 They showed that aluminium binds to amyloid-beta and that just a tiny amount of the metal can disrupt its normal configuration, causing it to form structures linked to neurotoxicity. A 2002 study showed tha
t transgenic mice fed a diet high in aluminium developed amyloid-beta plaque deposits.7 Through these studies and dozens more, the ‘aluminium-amyloid cascade hypothesis’ for Alzheimer’s gradually crystallized.8

Out of fashion

The theory fell out of fashion in the 1990s. Some scientists doubted the data on aluminium content in Alzheimer’s brains and some disagreed about whether aluminium-induced changes in lab animals’ brains were the same as those in humans. But they did not refute the theory.

The Alzheimer’s Association, like most advocacy groups, dismisses the aluminium connection as a ‘myth’ – an outdated idea, thoroughly explored way back in the 1960s and ’70s.

“Since then,” the association says, “studies have failed to confirm any role for aluminium in causing Alzheimer’s.”

Skeptics cite a review claiming the ‘Aluminium Hypothesis Dead’ by Theodore Lidsky, a paid consultant to the $168 billion International Aluminium Institute.

However, a review by Japanese researchers counters these criticisms, citing new evidence for the role of aluminium and other metals in Alzheimer’s.9

A number of independent laboratories have shown that diets and/or drinking water containing aluminium significantly enhance amyloid-beta pathology and inflammation and induce Alzheimer’s disease-like changes compared to controls – albeit in mice.10

A 2016 study of 10,567 individuals found that those with chronic aluminium exposure had a 71 percent increased risk of developing Alzheimer’s,11 and a 2009 study clearly showed aluminium at the core of senile plaques of amyloid-beta.12 Exley’s team in the UK published a study this year in which they looked at rare brain tissue samples from 12 people who had died from an inherited form of Alzheimer’s involving genetic mutations in amyloid-beta, which strikes people in their 30s and 40s as opposed to their 60s and 70s.

The researchers found extremely high aluminium levels in every brain sample tested.13

This familial form of the disease may be rare, affecting only two to three per cent of Alzheimer’s sufferers, but they are like canaries in a coal mine. About 200,000 Americans and about 40,000 Brits are living with early onset Alzheimer’s, but understanding how these susceptible patients are affected is key to understanding the disease as a whole.

“Concentrations of aluminium found in these familial [Alzheimer’s] brains… are highly likely to have contributed to both the onset and the aggressive nature of any ongoing [disease] in these individuals,” the paper concludes.

Put into the context of what is already known about aluminium, says Exley, the significance of the latest study findings is “overwhelming and compelling” evidence of aluminium as a causal factor in Alzheimer’s disease.

Age of aluminium

It is hard to avoid neurotoxic aluminium. Although it is an abundant metal in the earth’s crust, it wasn’t until industry began mining and processing it from its naturally locked state that it became dangerous. The very first case of Alzheimer’s was identified in Germany in 1901, less than a decade after the birth of the aluminium industry there in the 1890s. Today, aluminium is the most predominant structural metal in use. About 50 billion tons are produced annually, which is expected to rise to 80 billion by 2023.

But its architectural use is probably the least of our health worries (see Sources of aluminium, page 37). Aluminium may be in your water, if your municipality adds it to the treatment process. It’s in food (preservatives, colorants, caking agents, baking powders, self-rising flour and as a contaminant from packaging and from cooking with aluminium pots and pans) and even baby formula.

It is also a primary component of many vaccines, where it serves as an ‘adjuvant’ to artificially stimulate the immune system into action. In the current vaccination schedule recommended by the US Centers for Disease Control, babies’ exposure to the toxic metal can reach 4,925 micrograms.14

A single hepatitis B vaccine given at birth contains 250 micrograms of aluminium – 20 times higher than permitted safety levels. Pregnant women also receive an aluminium-containing pertussis vaccine (Tdap), and aluminium crosses the placenta and accumulates in fetal tissue.

This would be fine if injected aluminium were all excreted, as public health officials claim, but recent research has demonstrated how aluminium from vaccines can gradually migrate from its injection site in muscle to the lymph nodes, spleen and brain. This mechanism has been implicated in the newly documented fatigue disorder macrophagic myofasciitis, which may follow vaccinations with aluminium adjuvants.15

A large emerging body of evidence has documented how aluminium in vaccines can induce chronic immune inflammation and a host of neurological and autoimmune diseases such as Guillain-Barré syndrome and multiple sclerosis.16

The water solution

Exley’s team has been working for decades on how to remove toxic aluminium from the body once it gets in. In his studies with aluminium-intoxicated salmon more than 25 years ago, Exley had a ‘Eureka’ moment when he discovered that the mineral silica in water bound to toxic aluminium and removed it from poisoned fish, which then recovered.

Since then, Exley has demonstrated that drinking 1.5 litres (about 50 fl oz) of mineral water high in aqueous silica content, such as Volvic or Fiji water, an hour before 30-minute workouts increases aluminium excretion in sweat up to 10-fold, and drinking just one liter of silica-rich mineral water (34 fl oz) increased aluminium excretion in the urine of Alzheimer’s patients. What’s more, after just three months of doing this, three of 15 patients showed cognitive improvements.

That may not sound very impressive, but considering that the pharmaceutical industry spends $3 billion each year treating Alzheimer’s but only claims to perhaps be able to slow disease progression, never reverse the condition at all, it is very promising.

When John Blackburn was faced with the terrifying prospect of Alzheimer’s in his 50s, he wrote to Exley’s lab and asked the researcher what to do.

Exley told John to exercise vigorously to sweat the aluminium out, and John started religiously drinking 1.5 litres of Volvic water each
day and working out to a sweat at least three times a week.

Fat: the brain’s alternate fuel

John also learned about the benefits of coconut oil. Coconut oil was made famous by neonatologist Mary Newport, whose husband Steve had spent five years in declining health from Alzheimer’s disease. In studying how to help her husband, she found that an early feature of Alzheimer’s is a decline in the brain’s ability to burn its usual fuel, glucose, which is broken down from carbohydrates and sugar, and this translates into impaired brain function.

However, the brain, like a hybrid engine, has the ability to run on an alternate fuel – ketone bodies, which are normally produced from stored fat when glucose is limited, such as when people are fasting or on a very low carbohydrate diet. Another way to boost ketones is to consume fats called medium-chain triglycerides (MCTs), which the liver converts to ketones.

Coconut and palm oil are rich sources of MCT, and Newport chose coconut oil because it was readily available, known to be anti-inflammatory and antioxidant, and has a long history of use in traditional medicine.

In 2008 she began adding a few teaspoons of coconut oil to her husband’s oatmeal in the morning, and the results, which she described in her book Alzheimer’s Disease: What If There Was a Cure? The Story of Ketones (Basic Health Publications, 2011), were remarkable. Within a few weeks he went from being inactive and unable to draw a simple clock to reading and gardening as he hadn’t in years and drawing a recognizable clock.

Steve Newport’s decline eventually resumed, but Newport received hundreds of testimonials from people who said they saw similar improvements in their loved ones with the disease. Now her story has triggered a wave of research into ‘ketogenic’ diets for Alzheimer’s and other neurodegenerative disorders.17

In one recent study, amyloid increased oxidation and disrupted energy production in neurons grown in a lab, but ketones reversed these effects. What’s more, ketones reduced amyloid levels, protected neurons from amyloid-related damage and restored normal memory performance, at least in mice with Alzheimer’s, which of course may not apply to humans.18

The Indian spice cure

The vibrant orange-yellow spice turmeric has a long history of use in Indian and Chinese medicine for treating wounds, inflammation and many other conditions. It has been shown to be anti-inflammatory, antioxidant, antidepressant, liver-protective, anti-arthritic, neuroprotective and more, and a number of studies have documented its potential benefits to the brain and in ameliorating Alzheimer’s symptoms.

Curcuminoids, the active ingredients that give the spice its bright hue, are able to penetrate the blood brain barrier and can inhibit amyloid-beta from clumping together into plaques, suggesting that turmeric may be a promising therapy in Alzheimer’s.19

John also read about how black pepper can massively enhance the effect of turmeric. Just a pinch of black pepper – 1/20th of a teaspoon – which contains an active molecule called piperine, skyrockets the ‘bioavailability’ or body’s absorption capability of curcumins in turmeric. (No wonder most curry dishes contain turmeric and black pepper together.)

A nasty but effective “cocktail”

John told his doctors about his previous high aluminium exposures, but he says they dismissed it. When he asked about using coconut oil and turmeric, his doctor said it was “useless”, but John thought it was worth a try and better than what was being offered – a life of slow, steady decline.

He made himself a daily warm morning “cocktail” by mixing a heaping teaspoon each of coconut oil and turmeric powder in boiled water, stirred in cold milk to cool with a dash of ground black pepper to spike the curcumin absorption.

“It tastes really nasty,” admits John. “I’ll never like it.” But now, three years after his Alzheimer’s diagnosis, John says, “I am doing massively better.” He noticed improvements within a few months of drinking Volvic water, exercising and drinking his coconut-curcumin mixture in the morning.

When he returned for a scan a few months later, he says, the printout returned with a handwritten scrawl saying “What steroid is this guy taking?” He wasn’t taking any steroids, but it seemed to him that they could see the improvement. He continues to get scans, but his doctor now says that he must not have had Alzheimer’s to begin with, which John laughs at. It took a full 18 months for him to feel like he had recovered, although he says, “I am frightened to stop drinking my Volvic water.” He won’t stop taking his nasty morning tea anytime soon, either.

Nasty, but it works

It tastes nasty, says John Blackburn, but since his reversal of early-onset Alzheimer’s, he is afraid to not drink this concoction every day.

• One heaping teaspoon of extra virgin coconut oil.

• One heaping teaspoon of ground turmeric

Combine these in a cup and stir to a paste. Add boiling water from the kettle to dissolve. John adds milk to cool the drink, then grinds on some fresh black pepper and puts it down the hatch.

Suggestion: Made with coconut milk and a dash of cinnamon and ground ginger, or with a half teaspoon of cacao and honey, this might be more anti-inflammatory and palatable.

Don’t forget: drink 1.5 litres (about 50 fl oz) of high-silica mineral water such as Fiji or Volvic and exercise or sit in a sauna until you sweat.

Sources of toxic aluminium

Today, aluminium is everywhere. It is in architecture as siding and roofing, airplanes, trains, automobiles, pots and pans and foil. In minute quantities, it’s even in the air we breathe, generally ranging from 0.18 to 6.36 micrograms per cubic foot depending on location and weather, but perhaps as high as 14 to 280 micrograms per cubic foot in urban and industrialized areas, according to the Centers for Disease Control and Prevention (CDC).1

Don’t cook with aluminium

Scientists have demonstrated that when you cook with aluminium pots and pans or wrap food in aluminium foil, the aluminium leaches into the food. Heating, as well as salt and acid in food
s, increase this effect. After studying the aluminium content in foods after cooking, researchers concluded, “It is also possible that excessive consumption of food baked with aluminium foil may carry a serious health risk.”2

Watch your medicines

Antacids contain approximately 104-208 milligrams (mg) of aluminium per tablet, capsule or 5-milliliter (mL) liquid dose.1 So just one dose could exceed the World Health Organization’s safety threshold for oral aluminium exposure of one milligram per kilogram of body weight per day.

While heartburn drugs like proton pump inhibitors have been linked to a 44 percent increased risk of dementia, some doctors have wondered if this is really due to the aluminium-containing antacids people take for the same condition.3

Buffered aspirin. Aspirin that is designed to decrease gastrointestinal bleeding is frequently buffered with aluminium hydroxide, 10 to 20 mg per tablet, according to the CDC.1

Vaccines. Aluminium is added to many vaccines to prime the immune system into action. It is found in the 5-in-1 vaccines, Pediacel and Infanrix; the pneumococcal conjugate vaccine Prevenar 13; the preschool booster vaccines Repevax, Infanrix IPV and Boostrix-IPV; the HPV vaccine Gardasil; the teenage booster shot Revaxis; and in hepatitis and meningitis vaccines.

Allergy shots. In Europe, most allergy injections (systemic allergen immunotherapy) have added aluminium. Over a course of treatment, patients receive up to 54 injections totaling 45 to 67.5 mg of aluminium.4

It’s in your pantry

Baking powders frequently are about one-quarter sodium aluminium sulfate. So if you buy anything baked and sold in a wrapper – like muffins, cakes and cookies – it likely contains aluminium. You can buy aluminium-free baking powder, however, to avoid the neurotoxin.

Baking soda is just pure bicarbonate of soda, and whether it is labeled aluminium-free or not, it should not contain aluminium.

It’s in your toiletries

Antiperspirants. Antiperspirants contain aluminium salts that block sweat pores. Since aluminium in deodorant can enter the bloodstream through skin abrasions and has been linked to breast cancer, some scientists advise avoiding it.5 Aluminium-free deodorants such as Tom’s of Maine work, but be warned that many deodorant ‘crystals’ that claim to be aluminium-free actually contain aluminium salts.

See WDDTY‘s Healthy Shopping guide from July 2016 for a roundup of 100 percent natural, aluminium-free deodorants.

Cosmetics. Besides containing parabens and other nasty chemicals, many makeup products including foundations, lipsticks and powders contain aluminium in nanoparticle form, which is so tiny it can cross cell barriers and enter into organisms.

Main

References

1

Hirosaki Igaku, 2010; 61: S111-24

2

BMJ, 1999; 319: 807-11

3

Daily Mail, article 2608449

4

J Neurol Neurosurg Psychiatry, 2006; 77: 877-9

5

Biomed Pharmacother, 2016; 83: 746-54

6

Lancet, 1994; 343: 993-7

7

7. FASEB J, 2002; 16: 1138-40

8

Subcell Biochem, 2005; 38: 225-34

9

Int J Alzheimers Dis, 2011; 2011: 276393

10

J Inorg Biochem, 2015; 152: 206-9

11

Neurosci Lett, 2016; 610: 200-6

12

J Inorg Biochem, 2009; 103: 1579-84

13

J Trace Elem Med Biol, 2017; 40: 30-6

14

JPandS, 2016; 21: 109-17

15

Front Neurol. 2015; 6: 4; Sci Rep, 2016; 6: 31578

16

Vaccines & Autoimmunity, 2015, Wiley-Blackwell

17

Br J Nutr, 2015; 114: 1-14

18

Nutr Metab (Lond), 2005; 2: 28

19

Phytother Res, 2014, 28: 517-25

Sources of toxic aluminum

1

CDC, Public Health Statement, September 2008, CAS#: 7429-90-5

2

Int J Electrochem Sci, 2012; 7: 4498-509

3

JAMA Neurol, 2016; 73: 1025

4

World Allergy Organ J, 2015; 8: 7

5

Federal Institute for Risk Assessment, Germany, BfR opinion No. 007/2014, 26 February 2014

Article Topics: aluminium
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