Neurons and Exercise

Neurons and Exercise

Friday, May 5, 2023

Silicade - Measuring Spoons Alert - Change in product 2023

 

Measuring Spoons for Making Silicade 5/5/23

In 2014, when the recipe for Silicade was developed, measuring spoons listed as Norpro 3061D Mini Measuring Sets were available online at Dine Company’s Restaurant Store.

                                         


By 2023 Norpro and Dine no longer sell 3061D measuring spoons and Norpro now sells newly designed 3061 oversized measuring spoons. Beware online as some companies, such as “Lily’s TV Items”, claim to sell Norpro 3061D measuring spoons but they ship only the new 3061 oversized measuring spoons.

In 2023 there are a number of similar commercially available measuring spoons, some of which are nearly identical to the 3061D and some of which are not identical in spite of attempts at standardization (see references).  In 2023 a half dozen of these similar commercially available measuring spoons were tested by filling them to level, not heaping, with water on a balance with 1mg resolution.  The measuring spoons sold on Amazon by three companies: Yellrin, Beryler, and Dostien, were found to be nearly identical to 2014 Norpro 3061D measuring spoons (see below table).

Do not buy Norpro 3061 or 3080 or Table Craft H723 measuring spoons as they all have over-sized level smidgens and the Norpro spoons also have non-standard incorrect level dash volumes.

Water Volume in Cubic Centimeters (cc) of Level Dash and Smidgen Measuring Spoons

Vendor / Year Purchased

ASIN (Amazon Number)

Bar Code

Each Engraved with Fraction of tsp

Volume of Level Dash

Volume of Level Smidgen

Norpro 3061D (Dine) / 2014

No Longer Available

---

No

0.50cc

0.16cc

Yellrin (Amazon)   / 2023

B0958CDQS4

X0031NIPLZ

Yes

0.52cc

0.15cc

Beryler (Amazon) / 2023

B091SW8BD5

X002UZ3227

Yes

0.51cc

0.15cc

Dostien MS-5PC (Amazon) / 2023

B0BBKRJXGK

---

Yes

0.51cc

0.15cc

The Following Measuring Spoons are Not Recommended

Norpro 3080  (Amazon) / 2023

B016VDB512

28901 03080 3

No

0.42cc

0.17cc

Norpro 3061 (Amazon) / 2023

B0002IK4PQ

28901 03061 2

No

0.72cc

0.25cc

TableCraft H723 / 2023

Available from Webstaurant

27875 05972 7

No

0.52cc

0.21cc

Note: making Silicade with Norpro 3061 measuring spoons will make it 40% stronger and making Silicade with Norpro 3080 measuring spoons will make it 17% weaker than recommended.

In the Silicade recipe one dash and two smidgens of sodium silicate monohydrate and one dash of sodium bisulfate are dissolved together in a gallon of tap water.  The following table shows the amount of these chemicals per dash and smidgen:

Volume (mg) of Level Dash and Smidgens of Silicade Ingredients

Measuring Spoon Type

Volume of a Level Dash of Sodium Silicate

Volume of a Level Smidgen of Sodium Silicate

Volume of a Level Dash of Sodium Bisulfate

Yellrin

350mg

125mg

830mg

Beryler

350mg

125mg

830mg

Dostien

350mg

125mg

830mg

 

Note: All three of these recommended measuring spoon types have their fraction of a teaspoon (tsp) engraved on the handle. Spoons that do not have this fraction of a tsp engraved on their handles are not recommended.

The Silicade recipe calls for a level dash and two level smidgens totaling 600mg (6.17mM) of sodium silicate monohydrate and a level dash of 830mg (6.01mM) of sodium bisulfate monohydrate added to a gallon of tap water (pH <8.5) resulting in Silicade (pH 4-5). If your tap water’s pH is greater than or equal to 8.5, in order to get the pH to just below 5 may require an added smidgen of sodium bisulfate monohydrate. After filtration through a Brita filter, two smidgens of sodium bicarbonate (i.e., baking soda) are added in order to elevate the pH of Silicade to 6.5 or greater.

References

1)     Pinch, Dash, and Smidgen; Internet Accuracy Project; https://www.accuracyproject.org/pinchdash.html (2009)

2)     Rowlett, Russ; How Many? A Dictionary of Units of Measurement; Univ. North Carolina at Chapel Hill; http://alltootechnical.weebly.com/uploads/4/0/7/5/4075543/dict_units.pdf (December 2003) The following is quoted from this document:

“dash (ds) an informal unit of volume used in food and drink recipes. Originally the dash was usually a liquid measure, small but indefinite in amount, roughly 1/8 teaspoon or a little less. More recently it has been used as both a liquid and dry measure. Kitchen supply stores in the U.S. and other countries have begun selling sets of “minispoons” in which the dash spoon is designed to hold exactly 1/8 teaspoon, which is roughly 0.02 fluid ounce or 0.6 milliliter.” Note that this definition is of a heaping liquid 1/8 teaspoon not a level 1/8 teaspoon that is 0.51cc (0.51 milliliter).  

“smidgen a very small quantity of material. Until recently, no one thought a smidgen was an actual unit of measure, but recently kitchen supply stores in the U.S. and other countries have begun selling sets of “minispoons” in which the smallest spoon, labeled “smidgen,” is designed to hold exactly 1/2 pinch or 1/32 teaspoon, which is roughly 0.005 fluid ounce or 0.15 milliliter. The word is a diminutive of “smutch” or “smudge”; it originally meant a small spot.”

Note” milliliter is equal to cubic centimeter (cc) and 1 gram of water

Links for ordering measuring spoons:

Yellrin  https://www.amazon.com/Measuring-Spoons-Stainless-Liquid-Ingredients/dp/B09J8CDQS4/ref=sr_1_6?crid=210UDC16DVRZE&keywords=Mini%2BMeasuring%2BSpoons%2BSet%2Byellrin&qid=1683303844&s=home-garden&sprefix=mini%2Bmeasuring%2Bspoons%2Bset%2Byellrin%2Cgarden%2C85&sr=1-6&th=1

Beryler https://www.amazon.com/dp/B091SW8BD5?ref=ppx_yo2ov_dt_b_product_details&th=1

Dsotien https://www.amazon.com/dp/B0BBKRJXGK?psc=1&ref=ppx_yo2ov_dt_b_product_details

Saturday, March 11, 2023

Gouty Arthritis - drinking silica water reduces pain

 

Silicia Water for Gouty Arthritis by Dennis N. Crouse 2/20/23

Gouty arthritis (a.k.a. gout) is characterized by rapid onset of severe pain, redness of the skin, and swelling1. The etiology of gout involves excessive production of monosodium urate monohydrate crystals (a.k.a. trophi) in the synovial fluid of joints2,3. Approximately 10% of patients with hyperuricemia (i.e., excessive uric acid in the blood) develop gout in their lifetime4. Overall prevalence of gout in the U.S. doubled from 1969 to 1986 with 3 million adults having gout in 20055. Exponential growth in prevalence suggests an environmental cause of gout.

           


                    Figure 1. Forms of uric acid with the sodium salt of the urate ion being the form found in trophi

The three forms of uric acid are diagrammed in figure 1. Uric acid exists in the body above pH 5.4 (pKa1 = 5.4) as a urate ion bonded ionically to cations, such as sodium, aluminum, and iron. Uric acid crystallizes in the body as monosodium urate monohydrate and these crystals preferentially absorb small trivalent metal cations such as aluminum and iron6. This absorption is an ion exchange, thermodynamically favoring the complexation of small trivalent cations over monovalent cations, such, as sodium. This transfers aluminum and iron from blood to synovial fluid in people with gout, lowering blood levels of aluminum (Al) and iron (Fe) by 25% (fig. 2)7.




 

Figure 2. Bar plot showing the average change in levels of four detected elements in blood serum of gout patients versus healthy controls. Healthy controls are indicated as 1.0-fold on the bar plot, compared with gout patients who have levels of aluminum (Al), titanium (Ti), and iron (Fe) all approximately 0.75-fold equal to 25% less than healthy controls. Gout patients also have lithium (Li) 2.5-fold higher than normal. Lithium is a 19th century treatment for gout and is likely being used by gout patients in China even though it is ineffective. Gout-SH: n=65 from Shanghai, Gout-SD: n=32 from Shandong,  Gout-BJ: n=42 from Beijing. Number of people tested is n.7

The biosynthesis of uric acid involves the enzyme xanthine oxidase (XO) converting hypoxanthine to uric acid in two steps diagrammed in figure 3. In both steps reactive oxygen species (ROS) as hydrogen peroxide (H2O2) are produced. For those with gout, ROS causes inflammation and pain in joints. Both aluminum and iron have been shown to activate XO in a dose dependent manner resulting in more uric acid, ROS, and pain8,9. Iron also increases the expression of XO mRNA in the hippocampus resulting in more uric acid, ROS, and pain9.

                                 


         Figure 3. Biosynthesis of uric acid and hydrogen peroxide (H2O2) from hypoxanthine by XO

Desferrioximine (DFO), a chelator of both aluminum and iron, can remove these ions from both synovial fluid and urate crystals lowering the activity of XO and its’ generation of ROS, such as H2O2, that causes inflammation and pain in joints6.  DFO injected into twelve patients with gouty arthritis induced remission of gouty attacks in all cases11. Attacks averaged 48 and 53 per year prior to DFO treatment to 32 during the first year of treatment and 11 during the second year. Also, during DFO treatment gouty attacks were most often of milder severity11. These patients had aluminum and iron reduced by DFO for 28 months. High-dose DFO injections resulting in near-iron deficiency (NID) levels carries the risk of ocular and cerebral toxicity.

Compared with DFO injections, there is a safer and easier way of removing aluminum from the synovial fluid and urate crystals in vivo and this is drinking water rich in orthosilicic acid (a.k.a. silica water). Drinking silica water only lowers aluminum levels and does not lower  iron levels in the body. Therefore, drinking silica water does not require subjecting the patient to NID levels of iron risking ocular and cerebral toxicity. Removing aluminum by drinking silica water has been reported in several cases to reduce gout symptomology likely because of the following:

·       Aluminum enhances xanthine oxidase (XO) activity causing more uric acid8,9

·       Aluminum induces more ROS as hydrogen peroxide than does iron11

·       Aluminum as a vaccine adjuvant causes both more uric acid and inflammation12

References

1.     Wallace, S.L., et al.; Preliminary criteria for the classification of the acute arthritis of primary gout; Arthritus Rheum.; 20(3):895-900 (1977)

2.     Onal, S., et al.; Effects of different medical treatments on serum copper, selenium and zinc levels in patients with rheumatoid arthritis; Biol. Trace Elem. Res.; 142(3):447-455 (2011)

3.     Terkeltaub, R.; Update on gout: new therapeutic strategies and options; Nat. Rev. Rheumatol.; 6(1):30-8 (2010)

4.     Wortmann, R.L.; Gout and hyperuricemia; Curr. Opin. Rheumatol.; 143);28106 (2002)

5.     Lawrence, R.C., et al.; Estimates of the prevalence of arthritis and other rheumatic conditions in the United States; Part II; Arthritis Rheum.; 58(1):26-35 (2008)

6.     Ghio, A.J., et al.; Complexation of iron cation by sodium urate crystals and gouty inflammation; Arch. Biochem. Biophys.; Sep.; 313(2):215-21 (1994)

7.     Su, M., et al.; Human gouty arthritis is associated with a distinct serum trace element profile; Metallomic; 4:244-52 (2012)

8.     Moumen, R., et al.; Aluminium increases xanthine oxidase activity and disturbs antioxidant status in the rat; J. Trace Elem. Med. Biol.; 15(2-3):89-93 (2001)

9.     Ji, P., et al.; Excess iron enhances purine catabolism through activation of xanthine oxidase and impairs myelination in the hippocampus of nursing piglets; J. Nutr.;  149:1911-19 (2019)

10.  Facchini, F.S.; Near-iron deficiency-induced remission of gouty arthritis; Rheumatology; 42:1550-5 (2003)

11.  Pogue, A.I., et al.; Metal-sulfate induced generation of ROS in human brain cells: detection using an isomeric mixture of 5- and 6-carboxy-2’,7’-dichlorofluoresin diacetate (carboxy-DCFDA) as a cell permeant tracer; Int. J. Mol.; 13:9615-26 (2012)

12.  Kool, M., et al.; Alum adjuvant boosts adaptive immunity by inducing uric acid and activating inflammatory dendritic cells; JEM; Apr.; 205(4):869-82 (2008)

Wednesday, August 3, 2022

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 




 

 


Saturday, April 2, 2022

Finding a Cause and Potential Cures for Alzheimer’s Disease Climbing the Ladder of AD Causation - Colored Figures

 

Color Figures in the Book (i.e., figure 9, 13, 18, 19, 20, 21, 34, 38, and 39)

Page 41 


Page 13 



Page 61

Page 61 




Page 63 


Page 67

Page 86 


Page 96 




Wednesday, March 23, 2022

"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 AD180,181. 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 AD315-318.





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 AD200,209. 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 water42,43. 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 Indianapolis321,322. 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 AD321,322. 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.   

  

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