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 joints^2,3. 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 (pK_a1 = 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 19^th 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 pain^8,9. 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 acid^8,9

·       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)

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 - 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 

"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.   

  

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mTOR is higher than normal in Alzheimer’s disease (AD) brains making it a risk factor for AD

 

mTOR Activity Increases in AD Brains Due to Inhibition of PP2A by Aluminum

Dennis N. Crouse

mTOR Complex 1 (mTORC1) includes mTOR a serine/threonine kinase that is found in all eukaryotic cells, phosphorylates several targets, and acts as a master regulator of protein synthesis and degradation. The activity of mTOR is higher than normal in Alzheimer’s disease (AD) brains making it a risk factor for AD that is independent of the ApoE status of patients. (Yates 2013) mTOR activation is a biomarker of autoimmune disorders, cancer, obesity, aging, and possibly AD. (Perl 2015) The activation of mTOR results in an AD associated increase in phosphorylation of both mTOR and downstream targets of mTOR in neurons of AD brains:

·         mTOR phosphorylated at Ser2481 (3-fold higher than normal) and Ser2448 (2.6-fold higher in those with AD than normal) (Pei 2008,  Li 2005, Griffin 2005)

·         p70S6K, a downstream target of mTOR, phosphorylated at Thr421 and Ser424 (phosphorylation is 4-fold higher in those with AD than normal) (An 2003)

·         eIF4E eukaryotic translation factor 4E a downstream target of mTOR 28 (eIF4E’s phosphorylation level is 100-fold higher in those with AD than normal) (Li 2004)

The phosphorylated forms of mTOR and p70S6K may represent putative indicators of cognitive impairments in AD. (Pei 2008) This higher mTOR activity is likely due to higher-than-normal phosphorylation of mTOR at Ser2481 and Ser2448. (Li 2005, Griffin 2005) Also, higher-than-normal levels of phosphorylation of p70S6K and eIF4E were significantly increased in AD brains and correlated with Baark’s stage and the levels of p-tau a biomarker of AD. (An 2003, Li 2004) Also, levels of phosphorylated p70S6K are higher in neurons that later develop NFTs a biomarker of AD. (An 2003)

The enzyme PP2A lowers the phosphorylation level of the mTORC1 complex and by doing so suppresses activity of mTORC1 complex. (Apostolidis 2016) However, aluminum inhibits PP2A in the AD brain thereby preventing suppression of mTORC1 and increasing the activity of the mTORC1 complex. (Yamamoto 1990)  Therefore, aluminum, a biomarker of AD, inhibits PP2A causing both increased mTORC1 activity and increased risk of AD. Facilitating aluminum excretion by drinking OSA rich water will likely allow PP2A to suppress mTORC1 activity and decreased the risk of AD.

Sirolimus (a.k.a. rapamycin) is a macrolide that both lowers mTORC1’s activity and inhibits cell proliferation and growth by interaction with FK506-binding protein. Sirolimus functions as an immunosuppressant and is used to prevent organ transplant rejection by inhibiting the activation of T-cells and B-cells required  by the immune system. (Mukherjee 2009) Taking sirolimus can lower the bodies resistance to bacterial and viral infection, such as COVID-19. Sirolimus can also cause lung toxicity as interstitial pneumonitis. (Chhajed 2006) Therefore, drinking OSA rich water to facilitate the elimination of aluminum and lower mTOR activity is safer than taking sirolimus.

References

An, W.-L., et al.; Up-regulation of phosphorylated/activated p70 S6 kinase and its relationship to neurofibrillary pathology in Alzheimer’s disease; Am. J. Pathol.; Aug.; 163(2):591-607 (2003)

Chhajed, P.N., et al.; Patterns of pulmonary complications associated with sirolimus; Respriation; 73:367-74 (2006)

Griffin, R.J., et al.; Acrivation of Akt/PKB, increased phosphorylation of Akt substrates and loss and altered distribution of Akt and PTEN are features of Alzheimer’s disease pathology; J. Neurochem. 93:105-17 (2005) 

Li, X., et al.; Phosphorylated eukaryotic translation factor 4E is elevated in Alzheimer brain; Neuroreport; Oct.; 15(14):2237-40 (2004) 

Li, X., et al.; Levels of mTOR and its downstream targets 4E-BP1, eEF2, and eEF2 kinase in relationships with tau in Alzheimer’s disease brain; FEBS J.; 272:4211-20 (2005)

Mukherjee, S., and Mukherjee, U.; A comprehensive review of immunosuppression used for liver transplantation; J. Transplantation; Article ID 701464 p1-20 (2009)

Pei, J.-J., and Hugon, J.; mTOR-dependent signalling in Alzheimer’s disease; J. Cell. Mol. Med.; 12(6B):2525-32 (2008)

Perl, A.; mTOR activation is a biomarker and a central pathway to autoimmune disorders, cancer, obesity, and aging; Ann. N. Y. Acad. Sci.; June; 1346(1):33-44 (2015)

Yamamoto, H., et al.; Dephosphorylation of tau factor by protein phosphatase 2A in synaptosomal cytosol fractions, and inhibition by aluminum; J. Neuroscience; 55:683-90 (1990)

Yates, S.C., et al.; Dysfunction of the mTOR pathway is a risk factor for Alzheimer’s disease; Acta Neuropath. Comm.; 1:3 (2013)

Why Drinking Silica Water Is An Alternative To Following A Keto Diet

 

Why Drinking Silica Water Is An Alternative To Following A Keto Diet

There are two primary energy sources for the body:

·  Carbohydrates in the form of sugars (i.e. glucose) produce energy by glycolysis to make acetyl CoA for the citric acid cycle.
·  Fats in the form of triglycerides produce energy by beta-oxidation to make acetyl CoA for the citric acid cycle.

Carbohydrates and fats are converted to energy in cellular organelles called mitochondria. Energy is produced by both glycolysis and the citric acid cycle.  Environmental toxins can inhibit the production of energy from both carbohydrates and stored fats resulting in obesity. For instance aluminum at a concentration of some drinking water in the U.S. inhibits glycolysis.

Since development of the Bayer process for aluminum purification from bauxite in 1888, there has been a steady increase in the amount of aluminum humans ingest and accumulate.  Aluminum, at levels found in some drinking water (108ppb,108mcg/liter, 4mcM), inhibits hexokinase, an enzyme that catalyzes the first step in carbohydrate  metabolism (i.e. glycolysis)1.  The biochemical response to the inhibition of glycolysis is the conversion of carbohydrates to fat as triglycerides comprised of long chain fatty acids2.  This fat can be stored in adipose tissue or metabolized for energy.  However, aluminum also inhibits the production of L-carnitine required for movement of long chain fatty acids in stored fat to the mitochondria for conversion to energy3-6.   Therefore aluminum inhibits two key steps in metabolizing carbohydrates and fats for energy generation:

·      Aluminum inhibits the first step of carbohydrate metabolism called glycolysis1. Inhibition of glycolysis promotes the conversion of carbohydrates to stored fats (e.g. lipogenesis)2.
·      Aluminum inhibits the biosynthesis of L-carnitine3-6. L-carnitine is required for mobilizing stored fat as long chain triglycerides for mitochondrial energy production7.

The result of aluminum ingestion is therefore, more fat from carbohydrate, more fat being stored, and less fat being utilized for energy, resulting in obesity that does not respond to dieting.

Ketogenic Diet of Medium Chain Triglycerides for Coping with Aluminum Toxicity

Switching from a low fat – moderate carbohydrate diet to a high fat – low carbohydrate diet results in higher than normal levels of chemicals called ketones in the blood.  For this reason the high fat diet is called a ketogenic diet.  The source of fat on a ketogenic diet can be from plant and/or animal sources, such as canola oil, coconut oil, and/or beef tallow.  All fats are primarily triglycerides comprised of fatty acids of varying chain length and unsaturation that are esterified to glycerol. These fatty acids are of three types: 
·         Long chain essential fatty acids (e.g. linoleic and alpha-linolenic acids)
·         Long chain non-essential fatty acids (i.e. EPA and 22C DHA)
·         Medium chain fatty acids  (i.e. lauric acid found as 50% of coconut oil)

History of the Ketogenic Diet

The fact that the human body can switch from carbohydrates to triglycerides as its primary source of energy is called the “Schwatka Imperative”.  This is named after Lieutenant Frederick Schwatka who volunteered for a 19 month 3,000 mile Arctic mission, taking with him only enough carbohydrate to last 10 months8.  On June 15th of 1879 he ate his last hard bread and then it became imperative that his body switch to a diet of primarily fresh-killed reindeer meat with occasional fish. For the first two or three weeks on the ketogenic diet he felt “… an apparent weakness and inability to perform severe exertive, fatiguing journeys.”  Then miraculously after two to three weeks on the ketogenic diet his strength and stamina returned to normal. For example, during the last two days of the expedition he hiked 75 miles.

Lieutenant Schwatka was looking for information on why the men of the Franklin Expedition perished in the Arctic a quarter century earlier. Schwatka was lucky he traveled ten years before the Bayer Process for aluminum purification from bauxite was developed in 1888. Since 1888 people in general have been dosed with ever increasing levels of aluminum that is impacting how their mitochondria generate energy. 

           
Moderate Carbohydrate Diet with Supplements for Losing Weight and Aluminum

Johnston in 2006 compared 10 overweight people on a low fat and moderate carbohydrate diet with 9 overweight people on a ketogenic diet with high fat and low carbohydrate diet.  The groups were fed diets providing the following percentages of energy:

Moderate Carbohydrate Diet:    30% fat   –   40% carbohydrate   –   30% protein
Ketogenic Diet:   60% fat   –     5% carbohydrate   –   35% protein

After eight weeks the moderate carbohydrate dieters lost more weight than the ketogenic dieters.  The researchers concluded that the ketogenic diet did not offer any significant metabolic advantage over the moderate carbohydrate diet12.There are supplements of biochemicals naturally found in your body that taken daily will result in improved stored fat utilization and weight loss.  These supplements are:

·         Dissolved silica (a.k.a. OSA) for lowering your body-burden of aluminum13-15
·         CoQ10 for improving your energy and cognition16
·         PQQ for increasing mitochondrial biogenesis and cognition16-18
 

By lowering aluminum levels in your body, glycolysis and fat metabolism will return to normal.  This coupled with new mitochondria will allow you to metabolize or “burn” stored fat resulting in dieting with weight loss.

 There are also supplements of biochemicals naturally found in your body that will lower LDL and triglycerides, both of which are linked to an increased risk of vascular disease, such as stroke and heart attack: 
·         EPA (eicosapentaenoic acid) for reducing triglycerides by 5 to 10%19
·         PA (palmitoleic acid) for reducing triglycerides by 15% and LDL by 8%20
·         Vitamin D for reducing triglycerides by 23%21

Lowering triglycerides and LDL decreases the risk of vascular disease, heart attack, and stroke.  For more details on these supplements see my book “Prevent Alzheimer’s, Autism, and Stroke”22.

Ketogenic Diet with Fat from Medium Chain Triglycerides

Medium chain triglycerides (MCT), as opposed to long chain (i.e. 18 carbon atoms) triglycerides (LCT), do not require L-carnitine for mobilization and conversion into energy by the mitochondria10.  Therefore the metabolism of MCT is not inhibited by aluminum. Also the oxidative utilization (sum of digestion, absorption, and oxidation) of MCT can be 3 to 4 times greater than for LCT10.  These results were obtained with animals preconditioned to survive, like Lieutenant Schwatka, on a ketogenic diet10.  Therefore the modern equivalent of the “Schwatka Imperative” is to either:

·         Remain obese while surviving on a diet of medium chain triglycerides or
·         Lose some weight by decreasing aluminum accumulation and eating a moderate carbohydrate diet.  

Many people are opting for the MCT diet, such as coconut oil, without lowering aluminum.  This will provide more energy and improved cognition. Unfortunately it will not result in weight loss since aluminum is still inhibiting the mobilization and conversion of stored long chain fatty acids to energy. Also:·         

MCT or Coconut oil does not contain essential fatty acids (e.g. linoleic and alpha-linolenic acid)
·         Lauric acid, comprising 50% of coconut oil, increases LDL by 16% in humans and LDL is linked to vascular disease, such as stroke and heart attack11

References
1. Lai, J.C., and Blass, J.P.; Inhibition of brain glycolysis by aluminum; J. Neurochem.; Feb.; 42(2):438-46 (1984)
2. Mailloux, R.J., et al.; Hepatic response to aluminum toxicity: Dsylipidemia and liver diseases; Exper. Cell Res.; 317:2231-2238 (2011)
3. Gaballa, I.F., et al.; Dyslipidemia and disruption of L-carnitine in aluminm exposed workers; Egyptian J. Occup. Med.; 37(1):33-46 (2013)
4. Lemire, J., et al.; The disruption of L-carnitine metabolism by aluminum toxicity and oxidative stress promotes dyslipemia in human astrocytes and hepatic cells; Toxicol. Lett.; Jun.; 203(3):219-26 (2011)
5. Waly, M. I-A., et al.; Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal; Mol. Psychiatry; 9:358-70 (2004)
6. Waly, M. I-A., and Deth, R.; Neurodevelopmental toxins deplete glutathione and inhibit folate and vitamin B12-dependent methionine synthase activity – a link between oxidative stress and autism, FASEB J.; 22:894 1 (2008)
7. Fritz, I.B., Kaplan, E., Yue, K.T.; Specificity of carnitine action on fatty acid oxidation by heart muscle; Am. J. Physiol.; Jan.; 202:117-21 (1962)
8. Schwatka, F.; The Long Arctic Search; Stackpole, E.A., Editor; No. 44; The Marine Historical Association, Inc.; Mystic, CT (1965)
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