Halloween Scares Me to Death Because of Aluminum

Halloween Scares Me to Death Because of Aluminum

I remember when the scariest thing on my doorstep at Halloween was a child in a monster or alien costume.  Now I find the scariest thing to be the bags of chocolate and brightly colored candy that are clutched in the hands of small children on my doorstep.  My fear stems from aluminum in both chocolate and the food dyes used for candy.  This aluminum is a neurotoxin that will continue to kill neurons in these children’s brains long after Halloween.  Aluminum has been linked to autism in children and should not be allowed in candy.  Cocoa trees are the source of chocolate. Cocoa trees prefer a clay soil that is rich in aluminum.  This results in 84 samples of chocolate from different sources containing from 170 to 4,260 mcg of aluminum per ounce.

The following table taken from my book “Prevent Alzheimer’s, Autism, and Stroke” shows how much aluminum is in food and candy.

Foods and Sweets Containing Aluminum Lake as an AFC397
Food or Sweets Colored with Aluminum Lake (Serving Size in Parentheses)	AFC per Serving (mg/Serv.)	Estimated* Amount of Aluminum per Serving (mcg/Serv.)
Kellogg Frosted Cherry Poptart (1) – Red 40	10.1	1,110
Marsh Green Sprinkles Cookie (1) – Yellow 5, Blue 1	1.4	154
Hostess Orange Cupcake (1) – Yellow 5 & 6	3.5	470
Betty Crocker’s Blue Cupcake (1) – Blue 1	1.2	84
Betty Crocker’s Red Cupcake (1) – Red 40	34.7	3,470
Okedoke Cheesy Popcorn (1 cup) – Red 40	3.8	420
Combos (1/3 cup) – Yellow 5 & 6, Blue 1	3.2	350
Hamburger Helper (1 cup prepared) – Yellow 5 & 6	7.7	1040
Scalloped Potatoes (1/2 cup prepared) – Yellow 5 & 6	1.4	190
M&M Milk Chocolate (48 Pieces) – Blue 1 & 2, Yellow 5 & 6, Red 40	29.5	2,950
M&M Peanuts (15) – Blue 1 & 2, Yellow 5 & 6, Red 40	14.1	1,410
Skittles Original(61) –Blue 1 & 2, Yellow 5 & 6, Red 40	33.2	3,320
Reese’s Pieces (51) – Blue 1, Yellow 5 & 6, Red 40	6.6	660
Rainbow Nerds (1 tablespoon) – Blue 1 & 2, Yellow 5 & 6, Red 40	3.7	370
Sprees (8 pieces) – Blue 2, Yellow 5, Red 40	1.9	230
Red Jawbreakers (3) – Red 40	1.2	130
Orange Jawbreakers (3) – Yellow 5 & 6, Red 40	0.4	50
Purple Jawbreakers (3) – Blue 1 & 2, Red 40	0.7	70
Green Jawbreakers (3) – Blue 1 & 2, Yellow 5 & 6	0.5	50
Yellow Jawbreakers (3) – Yellow 5 & 6	0.2	27

AFC stands for artificial food colorant * Assumes no alumina extender and 2 atoms of aluminum per molecule of colorant, except 3 for Yellow 5, and assumes a mixture of 4 colors to be approximately 10% aluminum.

At the beginning of the 20^th century a number of synthetic dyes and pigments became available.  They were synthesized from bituminous coal and were called “coal-tar dyes”.  These dyes were less costly to produce and superior in color when compared with natural dyes available at the time.   In the U.S. only seven of these synthetic dyes were initially approved for food under the U.S. Pure Food and Drug Act of 1906. These dyes are in general soluble in water.  In order to add color to candy and prevent the color from “bleeding”, the aluminum salts of these dyes are used as an “Aluminum Lake” in the candy. 

Currently some manufacturers of candy are promising to remove aluminum from candy in the future but for now both chocolate and colored candy is neurotoxic and should not be given to children.  For Halloween this year my wife and I are giving the children on our doorstep rubber spiders and erasers that are too big to swallow.

 

 

An Aluminum Free Cake for My Mother's 90th Birthday

A Cake for My Mother’s 90^th Birthday

My mother has been suffering from short term memory loss for 4 years.  For the last two years she has followed the recommendations in my book “Prevent Alzheimer’s, Autism, and Stroke” including eliminating all major sources of aluminum from her diet and drinking 3 to 4 cups of Fiji water a day in order to lower her accumulation and increase her excretion of aluminum. Following these recommendations has stopped her declining short term memory loss and stabilized her cognition.

As my mother’s 90^th birthday approached I needed to order a decorated vanilla birthday cake that was aluminum free.  Three possible sources of aluminum in a birthday cake are baking powder, food color dyes, and the aluminum baking pan. Calling most of the bake shops in the area revealed that most of them made their standard cakes with baking powder containing alum.  However I finally found Sarah at Iced Bakery who was a baker in town willing to make a custom aluminum-free birthday cake for my mother.

      

Baking Powder

Most baking powders contain alum. Alum is a combination of aluminum and sulfate ions making a salt that sometimes contains additional ions, such as ammonium, potassium, or sodium.  Alum is acidic and when combined with other acids and baking soda is sold as double acting baking powder. Baking powder releases a gas (e.g. carbon dioxide) when heated causing bread and cake to rise.   The use of alum in baking powder continues today but should be banned due to the neurotoxicity of the aluminum it contains (approximately 50mg/tsp.). Other non-aluminum containing acidic salts can be used in place of alum to make baking powder and these salts include mono calcium phosphate and cream of tartar.  “Aluminum-free” baking powder made with mono calcium phosphate and baking soda still contains some aluminum as an impurity (approximately 1mg/tsp.).  Homemade baking powder made with cream of tartar and baking soda has a much lower level of aluminum (less than 0.004mg/tsp.). The recipe for this baking powder is:

                                                2 Tbsp.                  Cream of Tartar (for leavening)

                                                1 Tbsp.                  Baking Soda (for leavening)

                                                1 Tbsp.                  Corn Starch (for anti-clumping)

History of Baking Powder

The first scientist to make the observation that alum in bread is a health problem is the English epidemiologist Dr. James Snow, M.D.  In 1857 Dr. Snow published an article in a British medical journal, “The Lancet”, pointing out that the incidence of rickets in children is higher in London than in towns north and west of London. Rickets in children and osteomalacia in adults is due to a lack of sufficient calcium and phosphate for bone strength and vitamin D for calcium absorption. With the help of a chemist, by the name of Dr. Arthur Hill Hassall, Dr. Snow had found that baker’s bread made in London contained alum while homemade bread made in towns north and west of London contained no alum. Dr. Snow suggested that aluminum complexed with phosphate preventing the absorption of phosphate in the gut required for strong bones. It took 128 years for research to fully explain why aluminum can cause rickets and osteomalacia. In early 1980s J.A. Roberston, et al. (1983), W.G. Goodman, et al. (1984), and G.L. Klein, et al. (1985) found in rats, dogs, and humans that aluminum inhibits the biosynthesis of the active form of vitamin D that is required for calcium absorption.  More recently it has been discovered that neurotoxic forms of aluminum, such as alum, also cause a wide variety of neurologic diseases, such as Alzheimer’s, autism, and stroke.

The Royal Baking Company of Fort Wayne, Indiana was organized in 1873 and through extensive advertising and branding became the premier manufacturer of baking powder in the U.S during the late 1800s.  Their baking powder was made from cream of tartar (a by-product of wine production) and baking soda (a.k.a. sodium bicarbonate).  The recipe was developed by Brothers Joseph and Cornelius Hoagland and pharmacist William Ziegler. Their business grew and was moved to New York in 1890 to become the largest producer of baking powder in the U.S.  In 1889 William M. Wright with the help of chemist George Campbell Rew developed double acting baking soda made with baking soda and two acids, monocalcium phosphate and alum (sodium aluminum sulfate).  This mixture was less expensive than using cream of tartar and the baking powder was advertised as releasing carbon dioxide over a wider temperature range. They marketed their product under the name Calumet Baking Powder. In 1928 the firm was sold to General Foods and it became the largest producer of baking powder in the U.S.

The popularity of alum containing baking powder is in spite of health warnings by dietary experts and a bitter metallic flavor that is experienced by approximately 30% of those who eat the resulting bake-goods. In 1897 eight years after alum containing double acting baking powder was developed, N.Y. University Professor of Clinical Medicine, W. Gilman Thompson, M.D. warned in his book “Practical Dietetics” that “Baking Powder … should be free from alum …”.  In spite of warnings and research showing aluminum is a neurotoxin, double acting baking powder is still recommended today in popular books on baking such as James Peterson’s “Baking” published in 2009.

Artificial Food Color Dyes

Many artificial food color dyes (AFCs) contain the aluminum salt of the colorant and in some cases colorants are combined with alumina (a.k.a. aluminum oxide).  The total amount of AFCs added to food per person in the U.S. rose 5-fold from 1950 (12mg/person/day) to 2012 (62mg/person/day). On average 10% of aluminum containing AFCs is aluminum.

Although Sarah agreed to make an aluminum free cake for my mother, she did not realize until reading the ingredients that her colorants for the icing contained “Aluminum Lakes”.  Manufacturers of AFCs are required to list aluminum salts of colorants as “Aluminum Lake” on the package.  In order to eliminate aluminum and still color the icing on my mother’s cake I agreed to send Sarah a set of pink, blue, and yellow natural food dyes made by ColorKitchen.  These natural dyes use beet juice extract for pink, an extract of blue-green algae (a.k.a. spirulina) for blue, and turmeric extract for yellow.  These natural dyes do not contain aluminum but look just as good as AFCs that do contain aluminum.

History of Artificial Food Dyes

At the beginning of the 20^th century a number of synthetic dyes and pigments became available.  They were synthesized from bituminous coal and were called “coal-tar dyes”.  These dyes were less costly to produce and superior in color when compared with natural dyes available at the time.   In the U.S. only seven of these synthetic dyes were initially approved for food under the U.S. Pure Food and Drug Act of 1906. These dyes are in general soluble in water but not soluble in fats and oils. In order to add color to icing used on cakes, the aluminum salts of these dyes are used as an “Aluminum Lake” in the icing.  The Lakes are not soluble, but are dispersible in the icing. In general Lakes are more stable than natural dyes.  In addition to cake icing these “Aluminum Lake” dyes are used for coated tablets, candies and chewing gums, lipsticks, soaps, shampoos, and talcs.

Aluminum Baking Pan

Acidic and/or fluoride containing cake mix, baking powder, and water used to prepare the cake mix will corrode the aluminum baking pan releasing neurotoxic aluminum ions into the cake during baking.  The easiest way to eliminate this source of aluminum is to use a stainless steel baking pan.  There are also thin plastic sheet liners for baking pans that will withstand baking temperatures up to 400 degrees Fahrenheit. These disposable liners, made of PET (a.k.a. polyethylene terephthalate, PTL, PETE, CPET), not only allow baking in an aluminum pan without adding aluminum to the cake but also make cleanup easier. Likewise the use of an aluminum baking pan lined with parchment paper will prevent aluminum corrosion from adding neurotoxic aluminum ions to the cake.

 

History of Aluminum Cookware

At the 1901 Pan-American Exposition in Buffalo, New York, aluminum cookware was first introduced to housewives, who wisely viewed it with suspicion because of concerns about the quality of the cookware and the toxicity of aluminum. It took approximately 50 years before aluminum pots and pans gained acceptance. Because it is lighter and less costly than the alternatives, currently aluminum is the most common cookware on the market.

Conclusion

With Sarah’s help as the baker, I can give my mother a beautiful custom aluminum-free birthday cake for her 90^th birthday party.

From the historical data presented here it is evident that this custom aluminum-free cake would have been the standard cake in the late 1800’s.  Since 1900 aluminum containing double acting baking powder, “Aluminum Lake” containing artificial food dyes, and aluminum baking pans have become popular.  All of these add aluminum to cakes that we currently consider the new standard cake. This aluminum contamination extends to all commercial baked goods, such as bread, muffins, cupcakes, pancakes, waffles, and biscuits.

The fact that aluminum containing double acting baking powder, “Aluminum Lake” artificial food dyes, and aluminum cookware all became popular in the early 1900’s explains why Alzheimer’s and autism are modern diseases  first observed in the early 1900’s.  It is time that consumers demand aluminum free food, including bake-goods, for our brain health and the brain health of our family. For more details on how to eliminate aluminum from your body and your diet, please read my book entitled “Prevent Alzheimer’s, Autism, and Stroke With 7 Supplements, 7 Lifestyle Choices, and a Dissolved Mineral”.

For more information about sources of Aluminum view the video my wife and I made on YouTube titled:
Brain Fitness in the Aluminum Age - Eliminating Aluminum.  https://www.youtube.com/watch?v=Gt5gfKxpHZU&t=2s

Introduction to the blog

Introduction

Welcome to my blog. This blog introduces you to the culprit responsible for Alzheimer’s, autism, and stroke.  This monster lurks in our food, drinking water, pharmaceuticals, and brains.  This blog also introduces you to 7 supplements, 7 lifestyle choices, and one dissolved mineral which work together to prevent the monster from causing Alzheimer’s, autism, and stroke in your brain and the brains of those you love. 

My interest in dementia started after an acquaintance died of the after-effects of a stroke and my mother and a friend’s mother, both 86 years old, began suffering severe frustration and panic attacks due to short term memory failure.  Having no preconceived notions about dementia and autism, I spent a number of years reading research articles in scientific journals. The search for the causes of Alzheimer’s, autism, and stroke started as a mystery and once solved it transformed into a crusade to rid my life of an evil monster.  I found this monster lurking in my medicine cabinet, food pantries, refrigerator, and the water pipes leading into my home.   This monster has been damaging the brains of newborn infants, elderly family members, and everyone in between for years.  It has remained undetected because of our lack of information and false reassurances by those in positions of responsibility who we have trusted with our health. It is time to take on this monster as both individuals and as a culture.  Wake up, read this blog and my book, and become informed before this monster claims your brain and the brains of those you love. I had not originally planned to write a blog or a book but once the monster was unveiled, I had no other choice. 

The close relationship of Alzheimer’s disease (AD) to autism, and stoke will be discussed.  These diseases are modern mismatch diseases created by our carefully evolved brains attempting to function in the presence of a chemical monster not experienced during the brain’s evolution.

The underlying goal of this blog is to create a cultural change in the way we view Alzheimer’s, autism, and stroke.  This blog encourages preventative measures to be taken by you and your family. It also encourages cultural changes on a larger scale than your family. For these changes to take place we need more people all wanting the same changes. So please tell family and friends about this blog. 

My book, Prevent Alzheimer's Autism and Stroke with 7 Supplements, 7 Lifestyle Choices and a Dissolved Mineral, is available on Amazon in print and kindle.  

Introduction to my book Prevent Alzheimer's, autisim and stroke with 7 Supplements, 7 Lifestyle Choices, and a Dissolved Mineral

 

Chapter 1 Conclusion - Prevalence, Symptoms, Diagnosis of AD

Chapter 1 Part 8 The Case for Aluminum Being the Cause of AD - continued

8)      Analogy of metal neurotoxicity to diseases similar to AD:

The two best analogies for a trace metal in the environment causing a disease, such as aluminum causing AD, are the effects of lead or mercury accumulation in our brains. Like aluminum both of these metals slowly accumulate in our bodies over our lifetime and cause mental illness.

Low level lead exposure was common during the Roman Empire.  The people of this period used lead to make water pipes, cookware, and cosmetics.  Corrosion of lead in contact with their drinking water and application of leaded cosmetics to their skin resulted in lead accumulation in their bones and brains¹⁴¹.  Judging from the amount of lead found in their bones, these people suffered from mild to severe lead poisoning resulting in brain swelling that caused severe headaches, confusion, irritability, seizures, and possibly death. Lead exposure continues today as there is lead in drinking water due to lead water pipes and lead pollution in ground water. For more information on the analogy between lead and aluminum exposure see Chapter 8.

Low level mercury exposure is currently common.  Mercury gets into the environment from both human-generated sources, such as coal-burning power plants, and natural sources, such as volcanoes. Consumption of fish is the primary ingestion-related source of mercury in humans.  The mercury in both salt and fresh water organisms is bio-concentrated in the food-chain that ends up in fish and humans. Symptoms of mercury poisoning typically include lack of coordination and sensory impairment, such as vision, hearing, speech, and sensation.  Although these symptoms indicate brain damage, mercury also damages the kidneys and lungs and can lead to death.   

9)      Experimental evidence showing that AD can be prevented:   

The primary goal of this book is to show that diseases caused by aluminum can be prevented by 7 supplements, 7 lifestyle choices, and a dissolved mineral.  For example AD may be prevented by, antioxidants that counteract the oxidative effects of aluminum (Chapter 3), avoidance or minimization of aluminum exposure (Chapter 4), a complexation agent and vitamin that lower brain aluminum accumulation (Chapter 3 and 5), and a combination of aerobic exercise and sleep (Chapter 6).      

·         The antioxidant PQQ protects the brain from low level aluminum exposure by inhibiting the formation of reactive oxygen species (ROS) and reducing ROS as they form in the brain due to aluminum accumulation.

·         Avoiding foods and pharmaceuticals, like antacids, that are high in aluminum, filtering drinking water, and cooking in non-aluminum cookware minimizes aluminum exposure.

·         Orthosilicic acid taken orally is absorbed into the blood and complexes with aluminum facilitating its excretion by the kidneys.

·         Vitamin D3 taken orally is converted by the body to vitamin D that facilitates the excretion of aluminum by the kidneys, even in the case of damaged kidneys due to kidney disease. 

·         Aerobic exercise and sleep help to cleanse the brain of Aβ peptides and oligomers that are complexed with aluminum.

 The best evidence that AD can be prevented is comparing the AD rate in countries with high levels orthosilicic acid in their drinking water, such as Singapore and Malaysia, with countries with low levels of orthosilicic acid in their drinking water, such as the U.S. and Iceland.  

 

With comparable life expectancy and higher orthosilicic acid in their drinking water, people who live in Malaysia and Singapore have a much lower death rate due to AD.  Since orthosilicic acid facilitates the excretion of aluminum by the kidneys, there is evidence that lowering aluminum will prevent AD.

 Conclusion: The nine criteria of causality originally set out by Sir Austin Bradford Hill⁷² and applied to neuropsychiatric conditions, such as AD, by Robert Van Reekum⁷³ have been applied using primarily human data taken from studying AD patients and controls. The conclusions are that aluminum is the likely cause of AD and AD is a human form of chronic aluminum neurotoxicity.  Given these conclusions we as individuals and a society have a responsibility to take action.  This book proposes what action can and needs to be taken to avoid or lower our exposure to aluminum and prevent diseases caused by aluminum.      

Aluminum an Unrequired and Unwanted Intruder

People representing the aluminum industry routinely point to aluminum’s omnipresence in our bodies as a sign of its essentiality. It is true that we all currently have a body-burden of aluminum but there has been no proven benefit of aluminum in our bodies.  In fact aluminum is a neurotoxin and aluminum exposure is the known cause of a number human diseases¹⁴². 

The brain relies on a delicate balance of monovalent (e.g. potassium and sodium) and divalent (e.g. calcium, magnesium, and zinc) cations in order to function properly.  These cations bind reversibly and not tightly with aminoacids, such as histidine and lysine that are involved in the active sites of key enzymes (e.g. protein phosphatase) or on the backbones of key proteins (e.g. β-amyloid and α-synuclein).  Aluminum is a small trivalent cation that can bind tightly to both key enzymes and proteins in the brain.  For instance magnesium regulates over 300 proteins and aluminum competes for magnesium binding. Aluminum binds to some of these proteins 10 million times stronger and dissociates 10 thousand times slower than magnesium¹⁴³. This property results in aluminum’s slow accumulation in select areas of the brain and aluminum’s inhibition of enzymes that causes the onset and progression of AD and possibly other forms of dementia. Aluminum is an unrequired neurotoxic element and not a nutrient for normal body function.  This makes aluminum an unwanted intruder. 

Chapter 1 Part 7 The Case for Aluminum Being the Cause of AD - continued

4)      Temporality of aluminum accumulation occurring before AD: 

This criterion requires that the causative agent occurs prior to the outcome.  Therefore chronic aluminum exposure must precede AD if chronic aluminum intake is the environmental cause of AD.

For the last 125 years we have lived in the “aluminum age” during which there has been a steady increase in our exposure to aluminum. We ingest food, pharmaceuticals, and drink water containing aluminum, we apply aluminum containing products to our skin, we are vaccinated with aluminum containing vaccines, and we inhale air containing aluminum¹¹².  This results in a slow accumulation of aluminum in our brains from the fetal stage to old age^{28,49,113,114}.      Therefore humans living in an industrialized society accumulate aluminum in certain regions of their brains many years before the onset of AD.  There are three sub-cellular changes in brain physiology that occur prior to overt AD in humans and all three lead to AD:

·         Progressive aluminum accumulation in neurons

·         Hyperphosphorylation of tau due to aluminum inhibition of an enzyme

·         Oxidative stress due to aluminum

Increasing aluminum exposure and accumulation is in lock-step with the increasing frequency of AD.  AD was described as a rare disease in The Lancet fifteen years after Alzheimer’s 1911 paper¹¹⁵. The reported number of AD cases rose from one in 1907 to more than 90 by 1935¹¹⁶.  Subsequently the age-adjusted death rate for AD in the U.S. rose from 0.4 per 100,000 in 1979 to 25 per 100,000 in 2010^117,118. In the 25 year span from 1980 to 2004 the annual U.S. death rate from AD in those over 65 rose from 1,037 to 65,313 per year¹¹⁷.     

It is estimated that in North America the mean aluminum intake is 24mg of aluminum per day, equivalent to more than 8.76 grams per year¹¹⁸.   The demand for aluminum products has increased requiring more and more aluminum be extracted and refined from bauxite deposits.  The current annual global demand for aluminum is 11 kg per person¹¹⁹.  This means approximately 0.08% of the aluminum produced each year is ingested.  Demand for aluminum has increased 30-fold since 1950 and is estimated to increase by 3-fold current levels by 2050¹¹⁹.  Using these data on aluminum demand, it is estimated that human exposure to aluminum has and will continue to increase at a rate of 90 fold over the 100 year period from 1950 to 2050³⁹.  This means we only ingested 0.29 grams of aluminum per year in 1950 and by 2050 we will be ingesting more than 26 grams per year. 

So temporality exists as aluminum accumulates in our bodies prior to the onset of AD.  In addition the rate of ingestion and accumulation of aluminum is increasing and this accounts for the rising prevalence of AD.

5)      Biological Gradient with Dose-response Effects of Aluminum and AD: 

In 1996 McLachlan, et al. observed a dose-response in the amount of aluminum in drinking water with the risk of AD in humans⁷⁵.  Each subject’s residential and drinking water history for the 10-year period prior to death were taken into account.  The drinking water subjects were exposed to varied from less than 100mcg/L to 175mcg/L.  A single pathologist performed a histopathological examination of all 614 brains included in this study. The brains were assigned to AD or control groups based upon clinical history and the presence or absence of plaques and NFTs. The results in the following table demonstrate a dose-response relationship between aluminum in drinking water and AD.

6)      Biological Plausibility of Aluminum Neurotoxicity Causing AD:

It is known that aluminum facilitates the formation of Aβ plaques and NFTs in the brain that are two hallmarks of AD^16,17,24,25. Aluminum causes oxidative stress that kills mitochondria and ultimately kills neurons⁵³.  This results in mitochondrial disease and increased atrophy of some brain regions both of which are clinical symptoms of AD. Aluminum also disrupts memory storage that is a behavioral symptom of AD⁴⁴. 

Some metal ions, such as aluminum, act as physiological stressors in the brain by stimulating brain cells to produce oxidizing chemicals (a.k.a. ROS)^121,122. This ROS can damage and kill mitochondria and neurons creating inflammation in the brain. Aluminum tops the list of metal ion inducers of ROS in human brain’s glial cells⁵⁸.

It has been observed from microscopic evidence that aluminum causes lesions in the brain’s perforant pathway that result in short term memory loss⁴⁴.  Aluminum also acts as individual ions to block the neurochemistry of long and short term memory storage¹²³. This mechanism of action explains why very small amounts of aluminum in the brain (i.e. on the order of several parts per million or micrograms per gram of brain on a dry weight basis) can have a very large impact on memory storage.

Calmodulin is a calcium-binding messenger protein required for memory formation and storage.  Aluminum ions modify its structure thereby inhibiting its function¹²³.  This prevents calmodulin from regulating calcium levels in neurons and also prevents the activation of four key enzymes that control memory formation and storage in neurons.

The neurochemical explanation of how memories are stored in neural networks is still evolving. However considerable detail has already been discovered.  The ground-work was laid by Donald Hebb in 1949¹²⁴ when he described a theory of neuronal learning as:

“Neurons that fire together - wire together and neurons that are out of sync - do not link”.

The neurochemical mechanism that supports Hebbian Theory involves the synchronized firing of several different types of neuroreceptors at a synapse between two neurons.  When this occurs in synchrony it leads first to stronger or potentiated neuronal connection between the two neurons.  This connection is then made even stronger by several types of neuroreceptors moving their location in order to increase their density at the synapse.  The theory that describes this two- step process of strengthening neuro-circuits is called spike-timing dependent plasticity (STDP)¹²⁵.  The successful result of this process is called long term potentiation (LTP).  STDP and LTP are theorized to be the way memories are stored.  A lack of synchrony in the process leads to no potentiation and is called long term depression (LTD) or lost memories.  Aluminum ions inhibit calmodulin from activating four key enzymes involved in LTP^{16,101,123,126-129}. Thereby aluminum ions encourage LTD and cause memory loss (see Neurochemistry of Memory Impairment by Aluminum for details on role of these four enzymes in memory storage).

The biological plausibility of aluminum causing AD is well established by those studies that have connected aluminum’s neurotoxicity with the hallmarks and symptoms of AD.

7)      Coherence of what we know about how aluminum neurotoxicity causes AD:

Aluminum taken in by ingestion alone is estimated to be 24mg a day of which approximately 0.2% is absorbed into our blood^118,130,131.  We know that aluminum accumulates more in some areas of the human brain such as memory processing regions⁸⁶.  This accumulation likely results in chronic aluminum neurotoxicity and the hallmarks and symptoms of AD.  The cells in these regions have very high energy needs.  The high rate of energy utilization increases the demand for iron.  Transferrin is the molecule that carries iron to these cells.  Therefore these cells have a high density of transferrin receptors on their membrane in order to facilitate iron uptake.  Aluminum and iron ions are almost equivalent in size and can have the same ionic charge.  This allows aluminum to be carried by transferrin into these cells in higher than normal amounts even though the cells have no need for aluminum. 

Some metal ions act as physiological stressors in the brain by stimulating brain cells to produce oxidizing chemicals (a.k.a. ROS)^121,122. The metal ions stimulate inducible nitric oxide synthase (iNOS) in microglial and astroglial cells of the brain to produce nitric oxide (NO) that reacts to produce ROS¹²². This ROS can damage and kill neurons creating inflammation in the brain.  The following table shows how much ROS is produced from a cell culture of human glial cells exposed to 50nM aqueous solutions of various common metal ions⁵⁸.  Aluminum tops the list of metal ion inducers of ROS in human brain’s glial cells.

The brain damage caused by aluminum inducing ROS could partially account for the neuronal death that underlies brain atrophy. This atrophy is seen in those areas the brain that are aluminum “hot spots” and it parallels aluminum accumulation in those areas of our brains as we age^86,94.

Neurofibrillary tangle (NFT) formation in the brain is a hallmark of AD.  Aluminum has been shown to participate in NFT formation in both pre-tangle and tangle-bearing cells¹³².   Aluminum inhibits the activity of enzyme PP2A that clips off excess phosphoryl groups on a structural protein of the brain called tau^22,133. Aluminum also inhibits the expression of a gene involved in making PP2A¹⁰⁰. Aluminum creates a lack of active PP2A that results in tau being coated with more than the normal number of phosphoryl groups. This accounts for low PP2A activity and paired helical filaments (PHFt) found in the brains of AD patients¹³³. In AD brains aluminum secondarily aggregates the PHFt into granules that fuse and grow into cytoplasmic pools of PHFt and aluminum that give rise to NFT filaments¹³². Aluminum and PHFt give rise to NFTs in brain cells, including large pyramidal and stellate cells, particularly in the brains of those with AD¹³².   Pyramidal cells are found in many regions of the brain, including the hippocampus, entorhinal, and prefrontal cortex.

Aβ plaque formation in the brain is another hallmark of AD.  Aβ plaques form from Aβ peptides that are cleaved from large Aβ precursor proteins (APP).  This process is called amyloidogenic cleavage and alteration of this process is a key feature of AD¹³⁴.  Beneficial non-amyloidogenic cleavage of APP leads to a secreted product that is important for promoting neurite growth and maintaining brain tissue.  Protein phosphorylation stimulates the beneficial non-amyloidogenic pathway.  Both protein kinase C (PKC) activity that increases phosphorylation and protein phosphatase 2A (PP2A) activity that decreases phosphorylation are involved in the control of how much of each competing pathway is used for APP cleavage¹³⁵. Activation of PKC decreases production of Aβ peptides by 50-80% and increases the beneficial non-amyloidogenic cleavage by 30-50%¹³⁵. Nanomolar concentrations of aluminum reduce PKC activity by 90%¹³⁶.  Therefore inhibition of PKC activity by aluminum directs APP to the amyloidogenic pathway resulting in more Aβ peptide¹³⁵.   This situation is partially modulated by aluminum’s inhibition of PP2A¹³⁵.

Microtubules are important neuronal structural features that are required for strength, rigidity, and transportation of cell constituents between the nucleus of the cell and the synapses.  Human pyramidal cells that contain NFTs and/or high levels of aluminum accumulation are microtubule-depleted⁴⁴.  Aluminum-induced microtubule depletion is possibly more fundamental to AD neuropathology than AB oligomers, AB plaques, or NFTs⁷⁴. This is because microtubule depletion is more damaging to neuronal connectivity and function than these hallmarks of AD neuropathology that may represent protective cell responses to aluminum ^132,137. Aluminum-induced microtubule depleted cells have axonal and dendritic dieback that is consistent with AD being associated with neuronal disconnection.   In addition aluminum-induced microtubule depletion leads to synapse breakdown and depletion^44,138. This explains why humans with AD have impaired axonal transport^139,140.

Neuronal death is marked in the brain by ghost NFTs that can be the result of aluminum accumulation in the neuron prior to death.  NFTs inside the pyramidal cells tend to displace the cell nucleus to the periphery resulting in denucleation. The denucleated cell is unable to renew cellular membranes and eventually the cell membrane ruptures⁷⁴.  This results in an extracellular ghost NFTs that act as tombstones of former neurons and a hallmark of AD.