Neurons and Exercise

Neurons and Exercise

Monday, September 5, 2016

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.