Good News ! Reduction of aluminum in body by 40%

My wife, Laurie and I have been drinking silica water for 8 years and did our first test for aluminum 2 years ago. We recently did another 24 hour urine test for aluminum (October 2023). We reduced our body burden of aluminum by 40% in the past 2 years by drinking silica rich mineral water.

We are now below the Healthy Adult category. I am 77 and Laurie is 69 years old. See table below.

Here is a link for ordering the test in the US. You have to have a lab near you and some states do not allow you to use this service. order 24 hour urine test

These results are incredible as they prove that drinking 4 cups of OSA rich water each day and avoiding dietary aluminum can lower “aluminum accumulation”. This AD biomarker, can be reduced and maintained at levels below that of an average 22-year-old by drinking Silicade daily for 6 years and can be further reduced 40% by drinking Silicade daily for 2 more years. (Silicade is the recipe Dennis developed for making your own silica water)

Here are our results for 2021 and 2023

· Total 24-hour urinary aluminum levels in 2021:

· 0.74mmoles/24hr for Dennis

· 0.44mmoles/24hr for Laurie

· 2021 Healthy young adult category

· Total 24-hour urinary aluminum levels in 2023:

· 0.55mmoles/24hr for Dennis

· 0.33mmoles/24hr for Laurie

We also work hard at eliminating sources of aluminum we are exposed to.

Here is the table.

Here is a link with more information on doing a 24 hour urine test for aluminum and how to interpret the results. How to test for aluminum

Improvements we have seen from drinking silica water:

Laurie and I did not have any noticeable cognitive issues prior to drinking silica water but we have seen improvements in our cognition. 

At 77 I have no major medical conditions and I am in shape enough to lead a large group of new parents on a 1 ½ hour 3 mile hike in the woods every week. My skin is still very flexible and my hairdresser commented that my face does not have any wrinkles despite the fact I have a few wrinkles. I have no pain in my joints, hips, and knees. My eyesight is good with no pathology. 

My brain power remains undiminished as evidenced by the publication of my 4th book this year. Do I attribute this all to drinking silica water for 7 years, no. Silica water is responsible for my continuing to have low blood pressure (both my parents had/have heart disease). Silica water has helped maintain and improve my cognition. My word recall and my ability to retain what I have read and apply it have improved. I also attribute my good health to routine daily aerobic exercise which I have being doing my entire adult life (45 minutes every other day). In the morning I sometimes experience stiffness and for the first few minutes hiking. This has decreased somewhat since starting silica water.  

The cognitive changes Laurie has noticed from drinking silica water are a “sharper brain”. For example, less word finding problems, less “senior moments” and her thinking is clearer and faster. The biggest surprise was we lost weight. We did not consider ourselves needing to loose weight when we started drinking silica water. We lost the weight slowly over a year or so. I am now back to the weight I was in high school. Dennis is back to his weight in college.  Aluminum inhibits two key steps in metabolizing carbohydrates and fats for energy generation.   Here is more information.  Remove aluminum loose weight

Here is a link to more anecdotal information from people with MCI and Alzheimer's.  Improvements

Silicade Frequently asked questions

      Frequently asked questions about making Silicade 

 

1.     Can I use RO, distilled water instead of tap water to make Silicade?

 

Yes you can.  However, these waters do not have minerals so you should add calcium and magnesium.  Directions for this at the end of the recipe.

 

2.     Can I heat the sodium silicate solution to boiling stovetop instead of using a microwave? 

 

Yes.  You can use a small stainless steel/glass pan and boil the solution stovetop.

 

3.     Do I have to use a Brita filter in the recipe or can use the filter I already own?

 

You must use the Brita filter.  The Brita filter removes more than 90% of aluminum, lead and mercury but does not remove the OSA (which is the form of silica in Silicade). Some water filters made by other manufacturers add aluminum to the water.  Some filters remove OSA.   

 

4.     I am using RO water do I still need to use a Brita filter?

 

Yes. There are impurities in the ingredients and the Brita will remove these impurities.

 

5.     My water tastes funny?

 

Check the pH of the Silicade you made.  Everyone’s taste buds are different.  You want the water to be between 6.5 to 8.5.  At the lower end water is acidic and at the upper end the water is basic.  Adjust the pH with the baking soda for your taste.

 

6.     I see crystals after I boil the sodium silicate solution, should I boil longer?

 

No.  What you are seeing is 0.5% water insoluble impurities in the sodium silicate.

 

7.     Can I use another vendor/manufacture for purchasing the sodium silicate?

 

No.  Many other forms of sodium silicate from other vendors have been tested and do not have the required amount of OSA to make the recipe.

 

8.     I cannot get the ingredients in my country ? 

 

Here is a company which gives you an address in the US.  https://www.myus.com/

How much Silicade can I make with the 2 pounds of sodium silicate ?  

The 2 pounds of sodium silicate will make 1,1511 gallons. This is 6,044 days per person of silica water (4 cups a day).  You will need 9- 4 ounce bottles of sodium bisulfate to make this amount of Silicade.  

9.      Can I make a concentrated form of Silicade ?   No. OSA over 200 ppm is unstable. resulting in polymeric OSA. 

 

10.  Can I use metasilicate instead of sodium silicate?  No.  Metailicate is a polymere of silica which can not be readily converted into OSA. 

 

11.   Can I store Silicade and for how long?  Yes.  Don’t store in direct sunlight. Silicade is stable for more than a month and is probably stable much longer. 

 

12.   Can I double the recipe?  Yes. 

Here is a link to the Recipe for making Silicade 

 

 

"Finding a Cause and Potential Cures for Alzheimer’s Disease Climbing the Ladder of AD Causation" Introduction to my 4th book

Finding a Cause and Potential Cures for Alzheimer’s Disease

Climbing the Ladder of AD Causation

Publication Spring 2022 available on Amazon

 

 

Author:  Dr. Dennis N. Crouse, BSc Biochemistry, - Harvard College, Ph.D. Organic Chemistry - Harvard University Chemistry Department, Post-graduate courses:  Understanding Dementia - Wicking Faculty of Health, University of Tasmania, Fundamentals of Neuroscience - Harvard.

 

Introduction

Alzheimer’s disease (AD) is prevalent in the U.S. with an estimated 6.2 million people age 65 and older currently living with AD. Unfortunately, my mother is one of those people. Her short-term memory was going from bad to worse when she was 85. Her doctor was following this trend with the mini-mental state exam (MMSE) and reported that she had MCI that could lead to AD. Several years later, magnetic resonance imaging (MRI) of her brain indicated she had “accelerated brain atrophy” that is a characteristic biomarker of AD used to diagnose AD.

Being trained in biochemistry and chemistry at Harvard College and Harvard University, respectively, I decided to take action with the goal of identifying causal factors of AD so a cure for mom might be found. After several years of researching the scientific literature on AD, a causal factor of AD was identified and a potential cure for mom was tried with some success! Mom’s MMSE score improved and thankfully by age 89 she could describe the daily news she read or heard. This potential cure for some symptomologies of AD is also a preventative as documented in my 2016 book titled: “Prevent Alzheimer’s, Autism, and Stroke with 7 Supplements, 7 Lifestyle Choices, and a Dissolved Mineral”²¹¹.

Most AD cases are sporadic and result from hereditary and environmental causes. A subset (i.e., 66%) of sporadic AD cases, that are usually diagnosed before age 70, are associated with a specific genotype (i.e., ApoE e4 allele) increasing the risk of AD and amount of cerebral beta-amyloid protein (Ab-42)¹⁷⁸. Less than 2% of total AD cases are familial early-onset AD (EOAD) that is associated with mutations in presenilin 1 and 2 genes. EOAD is usually diagnosed before age 65 and is also characterized as having an increased amount of Ab-42¹⁷⁹. At least one third of AD patients do not have an ApoE e4 allele. In addition, half of those with two copies of the ApoE e4 allele, do not get AD and survive to age 80¹⁷⁸. Also, 24% of people with high levels of Ab-42 do not have in vivo biomarkers of AD^180,181. Therefore, logically there must be one or more environmental causes of sporadic AD that are made worse by increased amounts of cerebral beta-amyloid Ab-42. 

My mother has the ApoE e3/e4 alleles and I have the ApoE e2/e4 alleles. I got the ApoE e4 allele from my mother and the ApoE e2 allele from my father who had ApoE e2/e3 alleles . Carriers of the ApoE e4 allele have increased odds of getting AD as compared to carriers of two ApoE e3 alleles, like my sister who has ApoE e3/e3 alleles.

The odds of getting sporadic AD are based upon environmental factors, age and sex of the carrier, and if the carrier has one or two copies of the ApoE e4 allele (see two graphs below)¹⁷⁸. At age 65 I had approximately 2-fold greater odds of getting AD due to my genetics as compared with my sister¹⁷⁸. My mother’s odds of getting AD at age 65 were 4.5-fold greater than my sister¹⁷⁸. Men and women with ApoE e4/e4 alleles at age 60 have 11-fold and 12-fold greater odds of getting AD, respectively¹⁷⁸. But in spite of these greater odds, studies of twin pairs have demonstrated the ApoE e4 allele accounts for only 10.7% of the variance in Ab-42 accumulation, suggesting significant environmental factor(s) as cause(s) of sporadic AD^315-318.

Relative odds of getting AD based upon Caucasian subjects in clinical and autopsy studies¹⁷⁸

When I began researching AD in 2012 it became apparent that the field had become dominated by some very large and financially powerful players (e.g., aluminum industry, pharmaceutical industry and their partner the Alzheimer’s Organization) They had decided for their own financial gain that scientists in the U.S. and U.K. should play by their rule: if you are not working on decreasing beta-amyloid protein (Ab-42) you are not working on AD. In spite of their rule there are three proposed theories, not just one, on the cause of AD:

·       Aluminum Accumulation

·       Beta-amyloid Accumulation

·       Calcium  Dyshomeostasis

Playing by their rule required that you ignore two of these theories and don’t work on hypothesizing a fourth or fifth theory. Being close-minded does not facilitate finding cure(s) for a disease. Ironically at an Alzheimer’s Organization talk in 2015 by Claudia Kawas on the 90+ study it was pointed out those with just neuronal beta-amyloid accumulation do not have a high risk of AD dementia. Two other cerebral pathologies are required to significantly increase odds of AD dementia. A significant number of people are resilient to beta-amyloid accumulation¹⁸¹.     

Even before Claudia’s talk, I decided to not play by their rule. I read research papers on all three proposed theories with the goal of building a unified theory of AD.

Molecular epidemiological data is available that can be used to find causal factors of AD and cures for AD.  Looking for correlations in this data, revealed a causal factor of AD. I found that there is molecular epidemiological data providing convincing evidence that aluminum is both a causal factor of AD and drinking silica rich water is a preventative intervention for AD and a potential cure for some symptomology of AD.

Finding the cause of a disease facilitates finding the cure and finding factors that mediate or modulate the disease can reveal the cause of a disease. A literature search for modulators of AD uncovered two independent French epidemiology studies published in 2005 and 2008 that used two different data sets and surprisingly found drinking water containing greater than 4mg/day of silica as orthosilicic acid (OSA) or drinking water greater than 12mg/liter of OSA significantly lowered the odds of getting AD^200,209. With further searching I found a small 2006 study where 3 out of 15 patients with AD had an improvement in cognition after just 12 weeks of daily drinking OSA rich water^42,43. The 2008 French epidemiology study also found that aluminum levels in drinking water of 100mcg/liter or more significantly increased the odds of getting AD²⁰⁰. These studies were the primary inspiration for my first book²¹¹. My second book looked at the health of people who drank OSA rich water for their entire life²³⁹.

Does drinking OSA rich water significantly lower the odds of getting AD in those, like my mother and I, who are carriers of the ApoE e4 allele? This question was answered during the writing of my second book when I discovered Ibadan, Nigeria. The drinking water of Ibadan has a high level of OSA (i.e., 35ppm) compared with average level in the U.S. (i.e., 11ppm)^319,320.

From 1992 to 2006 a cohort of 2,245 elderly Nigerians living in Ibadan were genotyped and clinically diagnosed. Also, a cohort of 2,147 elderly African Americans living in Indianapolis, Indiana, were genotyped and diagnosed. In this latter cohort, people with the ApoE e4 allele had increased odds of getting AD. In general people living in Ibadan have 2-fold less risk of AD that those living in Indianapolis^321,322. Importantly, unlike the cohort of African Americans living in Indianapolis, the cohort of people with the ApoE e4 allele living in Ibadan did not have increased odds of getting AD^321,322. Therefore, drinking OSA rich water is an environmental factor that significantly lowers the odds of getting AD even in those with the ApoE e4 allele.

Based upon these studies I began in September of 2015 drinking 4 cups a day of OSA rich water (i.e., Silicade) spaced throughout the day. After 6 years I had my body burden of accumulated aluminum tested and it was found to be in the range of a healthy 22-year-old. These test results made me feel much younger than my 75 years and also made me confident that even with the ApoE e4 allele I would not get AD.

In addition to aluminum there are many environmental factors that negatively impact cognitive health. These environmental factors could also be potential causal factors of AD. The scientific literature was searched without success for links between these “brain drainers” and AD. This search revealed that essential nutrients could be used to detoxify these brain drainers as summarized in my third book titled “Increased IQ, Cognition, and Covid 19 Cure Rate with Essential Nutrients”⁴⁰.  

In 2018 I began reading about the new science of cause and effect called “causal inference” and applying it to finding causes, mediators, and modulators of AD. Having acquired a large amount of data on causal factors of AD, I found it could be logically organized as a “ladder of AD causation” inspired by causal inference. The result is a data-based logical argument for aluminum being the cause of AD based upon the current scientific literature and is the subject of this my fourth book.   

  

Buy Book

 

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.     

Safety of Fiji Water

 

How Safe is Bottled Fiji Water

Dennis N. Crouse

March 15, 2021 updated in January 2025

 

Fiji water is sold in recyclable polyethylene terephthalate (PET) bottles¹. Fiji water is a unique bottled water because the bottle is made of 100% PET that is more economic to recycle than bottles made of mixed plastics¹. Both glass and PET bottles were used to store water from the same spring and in both cases no endocrine disrupters were released into the water^2,3. This suggests that known endocrine disruptors, such as di-2-ethyhexyl phthalate (DEP)⁴, optionally added to some PET as a plasticizer, may be the cause of endocrine disruption seen with water stored in some non-Fiji PET bottles². Fiji water has been tested and found to contain no detectable DEP⁵. Also, it is claimed the PET Fiji uses, does not contain phthalate plasticizers¹.

Fiji water is also a unique bottled water because of its high concentration of orthosilicic acid (OSA) which is a water-soluble form of silica. OSA exists as single molecules [i.e., Si(OH)₄] at a concentration of 124-149ppm⁶. Drinking water containing less than 160ppm of OSA (equivalent to 100ppm of dissolved silica) is generally regarded as safe (GRAS) by the U.S. FDA⁷.

In addition to OSA, Fiji water also contains bicarbonate, calcium, chloride, magnesium, sodium, and sulfate, all of which are considered harmless⁵. In addition, Fiji water contains the following trace metals including arsenic (1.2ppb), and fluoride (0.24ppm)^5,8 that are well below the maximum contaminant levels [MCL or SMCL set by the U.S. EPA]. Also, Fiji water was filtered through a 0.45micron filter and then the filter was examined using a 45x power microscope to reveal 12 particles of unknown composition/liter⁹.

·       Aluminum: 0 ppb¹⁰ (levels of aluminum over 100ppb have been linked to Alzheimer’s)¹⁰

·       Antimony: 0 ppb⁵ (6 ppb MCL)^{Note 1}

·       Arsenic: 0.59ppb¹⁴ to 1.2ppb⁵ (10ppb MCL)

·       Fluoride: 0.24ppm^5,8 (2.0ppm SMCL)

·       Lead: 0 ppb⁵ (0ppb MCL)

·       Mercury: 0 ppb⁵ (2ppb MCL)

·       Particles: 12/liter⁹ where usually only 1 in 3000 is a micro- or nanoplastic particle^{Note 2,3}

Therefore, Fiji water is safe to drink. 

 Note 1: An insignificant amount antimony is leached out of PET into bottled water after 3 months of storage at 22^oC (71.6^oF)¹¹. However, storage of drinking water in PET containers at greater than 70^oC (the glass transition temperature of PET) has been shown to add antimony to the stored water¹¹.

Note 2: Fiji water is “micron-filtered” prior to bottling in order to remove particles⁵. A study that found 12 particles larger than 0.45 microns per liter of Fiji water, used a microscope that could not identify the composition of the particles⁹. When looking at small particles with just a microscope it is impossible to discern their composition¹².   People who use equipment that can discern composition of particles (e.g., Raman spectrometer) have not examined the particles in Fiji water. However, they have found that only 1 particle in 3000 particles in river water is microplastic¹². The toxicology of microplastic particles is currently unknown but in spite of this, plastic microbeads were used for a number of years in some toothpastes and cosmetics. Because microbeads may be mistaken as food by fish, the Microbead Free Waters Act of 2015 by the U.S. FDA outlaws the manufacture, delivery, and sale of any rinse-off products (e.g., toothpastes, cosmetics, and over the counter drugs) containing microbeads smaller than 5 millimeters¹³.

Note 3: Research in 2024 on humans by analysis of their olfactory lobes indicates that inhalation and not ingestion of micro and nanoplastics in the air is the major pathway for micro and nanoplastics to enter the brain¹⁵.  The inhalation route of entry does not involve crossing the blood-brain barrier. The amount of micro and nanoplastic in the frontal cortex of human brains were as high as 0.48% by weight in 2016 and 0.88% in 2024¹⁶. This 2-fold rise is not surprising when compared to rising nano and microplastics in the atmosphere and with a similar 2-fold rise of microplastic concentrations observed in Greenland Sea water during the time period 2005 to 2014^17,18.  

References

1. Lynch, I., et al.; Fiji water A sustainability report; University of Vermont (2010)

2. Wagner, M., and Oehlmann, J.; Endocrine disruptors in bottled mineral water: total estrogenic burden and migration from plastic bottles; Environ. Sci. Pollut. Res.; 16:278-86 (2009)

 3. Chung, B.Y., et al.; Uterotropic and Hershberger assays for endocrine disruption properties of plastic food contact materials polypropylene (PP) and polyethylene terephthalate (PET); J. Toxicol. Envrion. Health, Part A; 76(10):624-34 (2013)

4. Latini, G., et al.; Di-2-ethylhexyl phthalate and endocrine disruption: a review; Curr. Drug Targets Immune Endocr. Metabol. Disord.; Mar.; 4(1):37-40 (2004)

5. Fiji Water; Bottled water quality report; January (2017)

6. Crouse, D.N.; Silica water the secret of healthy blue zone longevity in the aluminum age, Etiological Publishing (2018)

7. Select committee on GRAS substances – SCOGS-61, NTIS Pb 301-402/AS (1979)

8. Delaney, J. as Client; Tweed Laboratory Centre; NSW Australia; Laboratory report on Fiji water (2019)

9. Barrows, A.P.W., Anthropogenic microparticle contamination in bottled water for human consumption; (2018)

10. Crouse, D.N.; Prevent Alzheimer’s, autism, and stroke with 7 supplements, 7 lifestyle choices, and a dissolved mineral; Etiological Publishing (2016)

11. Westerhoff, P., et al.; Antimony leaching from polyethylene terephthalate (PET) plastic used for bottled drinking water; Water Res.; Feb.; 42(3):551-6 (2018)

12. Ivleva, N.; Technical University Munich; How dangerous is microplastic?  https://phys.org/news/2019-01-dangerous-microplastic.html

13. The microbead-free waters act: FAQs; U.S. FDA (2020)

14. Leavy-Roach, S., et al.; Heavy metals in bottled natural spring water; J. Environ. Health; June; 73(10):8-13 (2011)

15. Amato-Lourenco, L.F., et al.; Microplastics in the olfactory bulb of the human brain; Environ. Health; JAMA Open; 7(9):e2440018 (2024)

16. Campen, M., et al.; Bioaccumulation of microplastics in decedent human brains assessed by pyrolysis gas chromatography-mass spectrometry; https://orcid.org/0000-0002-4873-0454 (2024)

17. Zhang, Y., et al.; Atmospheric microplastics: A review on current status and perspectives; Earth-Sci. Rev.; 203:103118 (2020)

18. Amelineau, F.;  Microplastic pollution in the Greenland sea: background levels and selective contamination of planktivorous diving seabirds; Environ. Pollut. Dec.; 219:1131-39 (2016)