How to test for Aluminum, Lead, Mercury, and Arsenic in the Body

 Measuring the Body Burden of Toxic Trace Metals in Humans

Dennis N. Crouse

3/24/2021

 

Aluminum – Drinking water containing orthosilicic acid (OSA) has been proven to remove aluminum from most organs of the body including bone and brain. Therefore, the best way to measure your body burden of aluminum is to drink a liter of Fiji water or Silicade that contains 124ppm of OSA and then collect your urine for 24 hours. Measure the total volume of the collected urine and have total aluminum concentration (in units of nanomolar) and total creatinine (in units of micromolar) both quantified in the collected urine. The ratio of aluminum to creatinine concentrations reflects the urine aluminum through-out the body over a 24-hour period. This is more representative of your aluminum body burden than a blood sample that is only representative of the time and place where the blood sample is taken. It is also more reliable than hair samples as some shampoo and hair colorants have aluminum as an ingredient.

Based upon the color of your urine you know that it is sometimes more dilute than at other times. This can be due to inhibition of diuretic hormone by substances, such as alcohol, that reduce the reabsorption of water from the urine resulting in dilute urine. Both aluminum and creatinine once in the kidney are not reabsorbed back into the blood, unlike water. Creatinine is a breakdown waste product from muscle and is present in a narrow concentration range in urine. Therefore, a ratio of aluminum to creatinine concentrations minimizes the effect of urine dilution.

For 10 healthy adults who had not consumed 1 liter of OSA rich water the mean of urinary aluminum (nM/mM creatinine) is 43 and silicon (mcM/mM creatinine) is 32. These numbers are dependent upon the health of an individual and amount of aluminum and silicon in their diet and drinking water. For instance, secondary progressive multiple sclerosis (SPMS) is a disease in which aluminum accumulates in the brain at levels higher than normal. Patients with SPMS who drank 1 to 1.5 liters per day of OSA rich water for twelve weeks had mean urinary aluminum levels of 135 (nM/mM creatinine) before drinking OSA rich water and 349 (nM/mM creatinine) after 12 weeks or drinking OSA rich water.

Here is a link to a lab that does this type of testing.  https://requestatest.com/aluminum-urine-test

If you are outside the US here is what you need to look for when choosing a lab.   

Measuring Accumulated Aluminum – The best way to measure your body burden of accumulated aluminum is to have your urine tested for total aluminum excreted in 24 hours. This test can be performed by a laboratory, such as LabCorp (test no. 071555)³⁴. The 24-hour total aluminum test has three requirements:

·       Aluminum must be measured in units of mg/L or mM/L by the laboratory

·       Aluminum must be detected down to a level of 3mg/L that is equivalent to 0.11 mM/L

·       The total volume of urine must be measured in liters (L)

There are laboratories that only report aluminum/creatinine ratios and/or can’t detect aluminum at sufficiently low levels. Check with the laboratory first before submitting your urine for testing. 

The 24-hour aluminum test is usually performed by collecting your urine for 24 hours in a container provided by the testing laboratory. Do not pour anything but urine into the container and do not pour anything out of the container. The  container should be kept at a cool temperature throughout the collection period and during travel to the laboratory. Follow these instructions for collecting your 24-hour urine specimen:

1.     Upon arising in the morning, urinate into the toilet, emptying your bladder completely. Do not collect this sample. Note the exact time and print it on the container.

2.     Collect in the provided container, optionally using a plastic collection pan, all urine voided for 24 hours after this time, including urine passed during bowel movements. 

3.     At exactly the same time the following morning, void completely again after awakening. This completes the 24-hour urine specimen that must be taken to the lab.

Test results can indicate “Aluminum, Urine 24 Hr.”  as the number of micrograms of aluminum excreted in 24 hours (mg/24hr). Divide mg/24hr by 27 to get micromoles of aluminum excreted in 24 hours (mM/24hr). If your test results are in units of mg/L or mM/L, multiply by the number of liters of urine that was collected in order to get total 24-hour aluminum in units of mg/24hr or mM/24hr. For interpreting your test results see table 4 where the units of measure are mM/24hr.

 

Lead – Exposure to lead can be measured with a whole blood test. However, the blood lead level (BLL) is not a reliable indicator of prior or cumulative dose or total body burden of lead. An indicator of prior lead exposure is a buildup of erythrocyte protoporphyrin in red blood cells. Tests are used to measure free erythrocyte protoporphyrin (FEP) and zinc protoporphyrin (ZPP) in the blood. When BLLs reach or exceed 25mcg/dL an increase in FEP and/or ZPP can be detected. These increases in FEP and ZPP usually lag increases in BLL by two to six weeks.  When BLLs reach 40mcg/dL the FEP or ZPP levels increase abruptly and stay elevated for 3-4 months which is the average life span of a red blood cell.

·       Elevated BLL and Normal FEP/ZPP = Recent exposure to lead in last 2-6 weeks

·       Elevated BLL and Elevated FEP/ZPP = Chronic/ongoing exposure to lead

There is no safe level of lead and all adults have some body burden of lead. The U.S. National Institute for Occupational Health and Safety (NIOSH) in 2015 indicated 5mcg/dL as a reference BLL above which action should be taken to target the detox of lead.

Mercury – Mercury in the body can be in three chemical forms: organic mercury, such as methylmercury from eating fish, inorganic mercury, such as mercuric ion and mercury selenide, and metallic mercury, such as the mercury in dental fillings and some thermometers.

·       Methylmercury is measured in a whole blood sample taken from a vein.

·       Inorganic mercury and metallic mercury are measured in a random or 24-hour urine sample.

A hair sample can be measured to indicate exposure to increased levels of methyl mercury. However, hair samples are rarely used due to hair exposure to mercury containing dyes, bleach, and shampoo.

The Centers for Disease Control and Prevention (CDC) define the laboratory criteria for a diagnosis of excessive mercury exposure is blood mercury level greater than 10mcg/L. Most people have hair mercury levels well below 1mcg/gr (ppm). Adults with average hair mercury level of 4.2mcg/gr have neuropsychological function deficits.  Maternal hair mercury levels of 0.3 to 1.2mcg/gr have been associated with prenatal neurodevelopmental effects. If you have levels over these limits, stop eating fish and begin augmenting your diet with L-selenomethionine.

 

Arsenic – Significant exposure to arsenic results in greater than 12nanograms/ml in blood taken 4 to 6 hours after exposure. Blood concentration of arsenic are elevated for only a short period of time after exposure. This is because arsenic has a high affinity for tissue proteins. The body treats arsenic like phosphate and incorporates it in place of phosphate.  Arsenic is excreted at the same rate as phosphate with an excretion half-life of 12 days because most of ingested arsenic is in tissues, not in the blood where it has a half-life of 4 to 6 hours. Therefore, 24-hour total urine samples, not blood samples, are most useful for measuring the body burden of arsenic. The concentration of inorganic arsenic and its metabolites (i.e., MMA and DMA) in urine reflects the body burden of absorbed arsenic due to acute or chronic arsenic exposure.

Hair analysis can only be used as a screening tool for arsenic intoxication as there can be arsenic deposition in hair due to hair exposure to arsenic containing dyes, bleach, and shampoo. Also, there are uncertainties about the normal levels of arsenic in hair.     

Aluminum, Mercury, and Genetics as Causal Factors of ADHD

Dennis N. Crouse 

This is an excerpt from my book titled

Increasing IQ, Cognition and COVID-19 Cure Rate with Essential Nutrients

Targeted Detox Improves Children’s IQ, ADHD Behavior, and Adult Cognition 

 https://www.amazon.com/Dennis-N-Crouse-PhD/e/B01LFW4782?ref=sr_ntt_srch_lnk_1&qid=1614692140&sr=8-1

Research has made it clear that environmental factors modulate the symptomology of those with a genetic predisposition to attention deficit hyperactivity disorder (ADHD). Herein is a review of how this research has cast light on mechanisms that explain why both environmental aluminum and mercury are modulators and thereby causal factors of ADHD.

Introduction

Sometimes anecdotal information forces us to ask: Why? The following anecdotal information was received shortly after publishing the book “Silica Water the Secret of Healthy Blue Zone Longevity in the Aluminum Age”¹⁸:

1.      “My son has been on Fiji water for about 5 months, and his ADHD is basically gone. We saw a change in him after one week on Fiji. He had ALL the symptoms of ADHD to the max. He had little control over his physical movements or his emotions. But that has really changed since the Fiji.” Nov. 2018

2.      “Personally, I have used Acilis silica water for my child who has ADHD and monitored any changes. As you may know silica rich water removes accumulated aluminium from the body. I can now say after several months of use my son who is 12 has gained better focus to the point where he is refusing to use ADHD medicating presently (which I am monitoring). He feels he can now focus without it, and so far, I have had no indication from school to negate that. He has improved in his self-regulation, his skin is less dry and minor eczema and dry scalp have gone. After some dietary research it has been noted he is no longer craving aluminium affected foods which he did previously. So, I believe he has been affected by aluminium toxicity” Aug. 2019

These two reports from the U.S. and U.K. indicate that by drinking one of two different silica waters, Fiji with 124ppm of orthosilicic acid (OSA) or Acilis with 88ppm of OSA, the symptoms of ADHD are significantly diminished. This review of the scientific literature answers the question: “Why can drinking silica water rich in OSA decrease the symptoms associated with ADHD?”   

Diagnosis of ADHD

A diagnosis of ADHD depends on meeting the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition’s (DSM-V 2013) criteria for symptoms of ADHD¹. Criteria for symptoms of ADHD have remained about the same since 1995 when the fourth edition was published. In DSM-V ADHD is defined as a neurodevelopmental disorder characterized by symptoms of inattention, hyperactivity, and impulsivity that “interfere with or reduce the quality of performance in important life domains”¹. Formerly in DSM-IV an ADHD diagnosis was characterized by the same symptoms but required “clinically significant impairment”. In 2009 ADHD was the most common psychiatric disorder among children with 3 – 4 fold increased prevalence in males². Although usually diagnosed in childhood, 60% of these ADHD cases persist into adulthood³. Those diagnosed with ADHD are divided into three presentations:

·         Predominantly inattentive presentation

·         Hyperactive-impulsivity presentation

·         Combined presentation – at least 6 inattentive and 6 hyperactive-impulsive symptoms

Because of this variety of presentations among individuals diagnosed with ADHD, more than just one neurotransmitter/hormone system must be involved⁴. The primary factors in the development of ADHD are generally accepted to be the failed ability of several monoamine systems in the brain to produce sufficient serotonin, dopamine, norepinephrine, epinephrine and/or acetylcholine^2,5.

Pharmacology of ADHD

Based upon the insufficient monoamine premise underlying ADHD, the pharmaceutical industry has demonstrated to the satisfaction of the US Food and Drug Administration (FDA) that certain manmade chemicals (i.e. drugs) that impact these monoamine systems can be used to treat the symptoms ADHD. These drugs do not increase the total number of monoamine neurotransmitter molecules in the brain, instead these drugs provide palliative relief by blocking transporters of monoamine neurotransmitter molecules in the brain and thereby inhibiting reuptake of monoamine transporters in certain locations. For example Ritalin, Adderall, and Strattera all potentiate norepinephrine by blocking its transporter and thereby inhibiting its reuptake. Unfortunately, most of these drugs have serious side effects and the process of reuptake inhibition may deplete monoamine neurotransmitters/hormone throughout the body⁵. These factors lower the efficacy of these drugs through the course of treatment.

Genetic Component of ADHD

Twin, adoption, and molecular genetic studies all have shown that ADHD is heritable and therefore has genetic components^2,6-8. A genetic variant in the gene (SLC6A2) that encodes the norepinephrine transporter (NET) has been found. This genetic variant has an abnormal T allele at nucleotide 3081 that reduces gene expression of NET by 50% in individuals with this polymorphism. This genetic variation in expression of NET significantly increases the risk for ADHD⁶. A genetic variant in the gene (SLC5A7) that encodes the presynaptic choline transporter (CHT) is found in 6% of the human population. This genetic variant encodes a substitution of valine for isoleucine at position 89 resulting in a CHT polymorph that exhibits only 50-60% of the maximal rate of normal choline uptake⁷.  This genetic variation in CHT lowers acetylcholine production and significantly increases the risk for ADHD, particularly in children with the combined presentation². 

Epidemiology of ADHD

Epidemiology studies indicate that the prevalence of an ADHD diagnosis in young children is increasing in the U.S. and worldwide. Using The National Survey of Children’s Health (2007-2008, 2011-2012, and 2016) it was found that 1% of U.S. children aged 2 to 5 had an ADHD diagnosis in 2007-2008, 1.5% had an ADHD diagnosis in 2011-2012, and 2.0% had an ADHD diagnosis in 2017^9,10. This data is consistent with a study of insurance claims for children 2 to 5 receiving clinical care for ADHD showing a similar increase from 2008 to 2014¹¹. All of these increases in the U.S. were seen during a period of time when there was no change in the criteria for symptoms of ADHD published in the DSM IV and DSM V. The worldwide pooled prevalence of ADHD is also rising with 5.29% of children in 2007, 5.9-7.1% in 2012, and 7.2% in 2014^12-14.     

Environmental Causal Factors of ADHD

Assuming this increase in ADHD as seen in epidemiology studies is real, then the cause of ADHD must have an environmental component as a genetic change due to one or more mutations does not move through  the population fast enough to account for the increased prevalence of ADHD. Identifying causal environmental factors of ADHD requires brain analysis and a mechanism accounting for how environmental factors cause the pathology seen in those with ADHD.  Clues would include the identification of one or more environmental factors that lower the biosynthetic production of the four monoamine neurotransmitters in the brain: serotonin, dopamine, norepinephrine, and acetylcholine, in addition to the monoamine hormone epinephrine (a.k.a. adrenaline). All of these monoamines are biosynthesized in the body from three amino acids: L-tryptophan (TRP), L-phenylalanine (PHE), and L-serine (SER). These three amino acids are among the 20 amino acids that are made into proteins by our body. The biosynthesis from TRP, PHE, and SER of monoamine neurotransmitters/hormone in the body is shown in figures 1-3.

 

Aluminum Causes THB Deficiency

Without sufficient THB as a cofactor for either the enzymatic conversion of TRP to 5-HTP (figure 1) or PHE to L-DOPA (figure 2), the production of serotonin, dopamine, norepinephrine, and epinephrine will decrease. In addition, without sufficient THB the level of PHE in the blood will increase (figure 2).  An elevated level of PHE in the blood is in some cases associated with ADHD symptomology¹⁵.and in other cases with phenylketonuria (PKU) symptomology¹⁶. PKU is an inherited genetic condition involving lower levels of the enzyme phenylalanine hydroxylase. This results in impaired breakdown of PHE to L-tyrosine (TYR) in the liver that also leads to detrimental PHE accumulation in the brain¹⁶.  It was found that 57% of those diagnosed with PKU responded to THB treatment lowering their PHE levels by at least 20%. Of those who responded to THB treatment, 32% had ADHD symptoms prior to treatment and 85% of these were not on medication for ADHD. After 13 weeks of THB treatment there was a significant improvement in the attentiveness score of the 32% with ADHD symptoms as compared to the group given a placebo¹⁵.   

When THB is used as a cofactor in the conversions diagrammed in figures 1 and 2 it is oxidized to DHB (dihydrobiopterin).  In order to maintain levels of THB, the body regenerates THB from DHB with either of two enzymes: dihydrobiopteridine reductase (DHPR) and dihydrofolate reductase (DHFR)¹⁷. An enzyme is a protein that facilitates the conversion of chemicals and in this case two enzymes can facilitate the regeneration of THB from DHB. Both of these enzymes have active sites where DHB can bind and be more easily reduced to THB. This process of regenerating THB from DHB is diagrammed in figure 4. 

Aluminum is an environmental pollutant whose production is increasing exponentially worldwide¹⁸. Because of this, worldwide aluminum exposure is also increasing exponentially¹⁸ and could be a causal factor of ADHD accounting for the increasing rate of ADHD in the U.S. and worldwide. Aluminum inhibits regeneration of THB by reducing the activity of DHPR by 40%^19,20. What inhibits DHPR also likely inhibits DHFR as both of these enzymes have similar amino acid sequences at their active sites. Both of these amino acid sequences involve the amino acids tyrosine (TYR) and lysine (LYS) separated by three amino acids²¹. Aluminum is known to bind tightly with both TYR and LYS²². Therefore aluminum likely inhibits DHFR as well as DHPR.

When aluminum inhibits the regeneration of THB from DHB there is a less THB. Less THB results in less production of both 5-hydroxytrypthophan (5-HTP) and L-DOPA (see figures 1 and 2). Since 5-HTP and L-DOPA are the precursors of serotonin, dopamine, norepinephrine, and epinephrine, the question is: does administration of 5-HTP and L-DOPA reverse the symptoms of ADHD? Just such a protocol was tested with 85 patients, aged 4-18 years, diagnosed with ADHD. The results published in 2011 demonstrated that the efficacy of this protocol appears superior to some ADHD prescription drugs⁵.  This work supports the contention that environmental pollutants, such as aluminum, that reduce the activity of DHPR and DHFR and thereby lower DHB to THB regeneration, may be a casual factor of ADHD.

Lower than normal THB levels in the cerebrospinal fluid is a characteristic of several neurodevelopmental disorders, including autism (ASD)^23-25. Children diagnosed with ASD compared with normal children have 42% lower than normal THB levels in the cerebrospinal fluid²⁵. ASD is symptomatically a clinically heterogeneous neurodevelopmental disorder. Some children with ASD have a high rate of executive function problems, inattention, and hyperactivity and these ADHD-like symptoms suggest dopamine and norepinephrine deficits^26-28. The DSM-V diagnostic criteria permit ADHD to be diagnosed in conjunction with ASD¹. In the past it was felt that ADHD symptoms were always better explained by the child’s autism.

By administering drugs that are designed to increase dopamine and norepinephrine levels, these ADHD like behaviors are mitigated in some children diagnosed with ADHD and ASD^29,30.  Therefore it is not surprising that oral administration of THB as Kuvan has been shown to improve these behaviors of some children with ADHD and ASD^15,31. Also administration of a chelator of aluminum (desferoxamine) reverses DHPR inhibition by aluminum in humans²⁰. Since drinking silica rich water has been shown to lower aluminum in all major organs of the body, including the brain, it is not surprising that drinking silica rich water also improves these behaviors in some children with ASD¹⁸ and ADHD (see anecdotal information in the introduction). Recently much higher than normal levels of aluminum has been found in the brains of those diagnosed with ASD³². Currently levels of aluminum have not been tested in the brains of those diagnosed with ADHD.

Aluminum Causes SAM Deficiency

There is experimental evidence that acetylcholine increases the response to major stimuli of cortical circuits in the brain while suppressing minor background stimuli and enhancing encoding of memory for specific stimuli resulting in improved attention³³. Therefore acetylcholine improves attention and an attention deficit will be observed when its biosynthesis is inhibited.  The biosynthesis of acetylcholine requires three molecules of SAM (S-adenosyl-methionine, SAMe) to trimethylate each molecule of 2-aminoethanol to choline (figure 3). Also the biosynthesis of epinephrine from norepinephrine requires SAM (figure 2) and the enzyme phenylethanolamine N-methyltransferase (PNMT).

Aluminum inhibits the activation of methionine synthase, an enzyme involved in SAM biosynthesis, thereby lowering availability of SAM and decreasing production of acetylcholine and epinephrine^34,35. SAM also increases the half-life of PNMT by protecting it from degradation³⁶. Aluminum inhibition of SAM biosynthesis results in less PNMT and less epinephrine. This inhibition by aluminum may be reversed by drinking silica rich water¹⁸. 

Aluminum Inhalation Increases the Prevalence of ADHD

A study of 65 aluminum welders revealed above normal levels of aluminum in their urine and serum when compared with 25 mild steel welders. Concentration and memory difficulties were the two most prevalent symptoms among the aluminum welders. The severity of these symptoms correlated with urine and serum aluminum levels (P-values 0.005 and <0.001 respectively) ³⁷. These attentional deficits seen in adult welders due to the inhalation of aluminum vapor is also seen in children of mothers who smoked during pregnancy. Tobacco and cannabis contain aluminum, as much as 3.7mg per gram, and it is vaporized, inhaled, and absorbed by the lungs during smoking³⁸. A study of 209 preschool children in New York found that maternal smoking during pregnancy was associated with an increased risk of ADHD³⁹.  In a second case-control study of 222 children it was found that maternal smoking during pregnancy increased the odds of ADHD⁴⁰.    

Mercury Inhibits Acetylcholine Biosynthesis  

Inorganic mercury ions (Hg²⁺) inhibit the biosynthesis of acetylcholine at concentrations of 1 micromolar by inhibiting the enzyme, choline acetyltransferase (ChAT)⁴¹. Organic methylmercury chloride (MMC) at concentrations of 20 micromolar has also been shown to inhibit ChAT and lower both choline uptake and the production of acetylcholine in vitro⁴².  Both organic and inorganic mercury had no effect on cholinesterase activity. This result proves that lower levels of acetylcholine are due to ChAT inhibition by mercury and not increased acetylcholine metabolism. Chronic in vivo treatment of rats with MMC lowers acetylcholine levels in their brains⁴³. In vivo mercury inhibition of ChAT is reversed with mercury chelators, such as 2,3-dimercapto-propanol (BAL)³⁹. This inhibition by organic and inorganic mercury can also be reversed by taking a daily selenomethionine supplement⁴⁴.

Mercury Inhibits AADC and Serotonin Biosynthesis

Inorganic mercury ions (Hg²⁺) from mercuric acetate and organic methylmercury chloride (MMC) at a level of 100 micromolar have both been shown to inhibit AADC (aromatic amino acid decarboxylase) an enzyme required for biosynthesis of three monoamine neurotransmitters and serotonin⁴⁵. Because of this it is not surprising that chronic treatment of rats with MMC lowers serotonin levels in their brains⁴³. 

Mercury Exposure Increased the Prevalence of ADHD

A meta-analysis of epidemiology studies looking at the association between ADHD and environmental mercury exposure during embryo and early infancy found the odds of ADHD being 1.6 fold greater among those exposed to organic (methylmercury chloride) and inorganic (Hg²⁺) environmental mercury⁴⁶.  

This meta-analysis also found exposure to Thiomersal (a.k.a. mercury((o-carboxyphenyl)thio)ethyl sodium salt) used clinically to protect vaccines from biological contamination had no associated risk of ASD or ADHD6⁵. This finding is supported by fact that the rate of ASD in the U.S. continues to climb exponentially despite elimination of Thiomersal from routine childhood vaccines in the summer of 2001¹⁸.

Aluminum, used as an adjuvant in vaccines, is a much more likely candidate for being a causal factor of the recent dramatic rise in the rates of ASD¹⁸ and possibly ADHD.  Aluminum (inhaled, ingested, and injected), environmental organic (e.g. methylmercury chloride), and environmental inorganic (e.g. Hg²⁺) mercury exposures are casual factors of ADHD as described herein. 

Conclusion

Although a casual factor of ADHD is genetics, this does not explain a two fold increase in ADHD prevalence seen in the decade between 2007 and 2017 using diagnostic criteria published in 2013 with no change in ADHD symptoms from diagnostic criteria published in 1995. This increased prevalence of ADHD suggests that environmental factors are modulating the severity of ADHD symptoms, resulting in the doubling of diagnosed cases of ADHD. The two environmental factors that have been implicated by scientific research as causal factors of ADHD are aluminum and mercury. The data linking these environmental factors to ADHD and a mechanism showing how these factors modulate monoamine systems in the brain is presented in this review of the recent scientific literature. There are two recommended ways to reverse the effects of these two environmental factors:

·         Silicic (e.g. OSA) rich drinking water for aluminum detox and facilitated aluminum elimination in the urine and sweat³⁶

·         Selenomethionine supplementation for mercury detox and facilitated mercury elimination in the urine⁴⁴          

These treatments are proven safe by multiyear daily use and involve only supplementing substances normally found in our bodies^18,47. These treatments remove the environmental causes of ADHD and offer hope that ADHD can be treated in some cases without drugs. Palliative relief of ADHD symptoms with THB as Kuvan, 5-HTP, L-DOPA, and SAM supplementation is possible, but taking these supplements does not remove causal factors and these supplements have numerous undesirable side effects^48-52.   

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