Compiled By Rich Murray, MA
Room For All
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Posted: 19 July 2012

MM Kini and JR Cooper 1962 show aerobic respiration in mitichrondria shut down by low level formaldehyde [in humans only, made in situ by ADH1 enzyme from methanol], leading to blindness, weakness, acidosis: WC Monte paradigm: Rich Murray 2012.06.27

"It is our observation that formaldehyde is an extremely potent inhibitor of respiration and glycolysis; formate exercises only weak respiratory inhibition, and methanol itself has no effect."

[Selection from Chapter Six: How Methanol Kills in While Science Sleeps text]

Formaldehyde has the ability, even in extremely small concentrations, to prevent phosphate from attaching to ADP. 113

The article I reference, Biochemistry of methanol poisoning. 4. The effect of methanol and its metabolites on retinal metabolism, 113 reports research performed in 1960 at the Department of Pharmacology of Yale University School of Medicine.

To this day, these results have never been refuted, but much like other good science proving formaldehyde dangerous, it has been ignored.

The authors, Kini and Cooper, begin by stating, "It is generally accepted that formaldehyde is the toxic agent in methanol poisoning."

The article proceeds to provide evidence in support of that proposition. If you are a scientist, this paper is a must read. While the brain is dependent on oxygen and without it will die within a short period of time, cells have alternative methods for generating ATP that require no oxygen.

Both of these forms of energy production are sensitive to -- and can be stopped by -- varying but extremely low levels of formaldehyde. Kini and Cooper establish that formaldehyde, in very low concentrations, can cause considerable damage to key enzymes required by cellular respiration.

They also tested, in an identical manner, formic acid and acetaldehyde, demonstrating that between ten and one hundred times higher concentration levels would be required to get the same results.

It would be physically impossible to shove enough formic acid (formates) down the throat of a living organism to match the effects of formaldehyde.

Kini and Cooper conclude by noting that present evidence shows "support for the contention that formaldehyde is responsible for all the manifestations of methanol poisoning"

They continue, "It is our observation that formaldehyde is an extremely potent inhibitor of respiration and glycolysis; formate exercises only weak respiratory inhibition, and methanol itself has no effect."

Now, just what does this all mean?

Most significantly, formaldehyde has the power to severely hamper aerobic respiration and, in so doing, cause cells that can switch to anaerobic respiration to do so.

In turn, this causes a buildup of lactic acid within the cell, which quickly leaks into the blood.

This partly explains the quick development of acidosis in the blood of methanol poisoning victims, a development that occurs long before the liver has a chance to produce detectable levels of formic acid in the bloodstream. 400

This also explains the symptoms of shortness of breath, fatigue, and muscle pains in the limbs and elsewhere, even before acidosis develops in the bloodstream.

Kini M, Cooper J.
Biochemistry of methanol poisoning:
4. The effect of methanol and its metabolites on retinal metabolism.
Biochemical Journal 1962. 82, 164-172.
Department of Pharmacology, Yale University School of Medicine

Research:Mitochondria and MS progression

Posted: 25 Jun 2012 05:45 AM PDT

Campbell et al.
Clonally expanded mitochondrial DNA deletions within the choroid plexus in multiple sclerosis.
Acta Neuropathol. 2012 Jun 12.
Campbell GR, Kraytsberg Y, Krishnan KJ, Ohno N, Ziabreva I, Reeve A, Trapp BD, Newcombe J, Reynolds R, Lassmann H, Khrapko K, Turnbull DM, Mahad DJ.


Mitochondrial DNA deletions (mtDNA) have been implicated in the pathogenesis of Alzheimer's disease (AD), MS and Parkinson's disease (PD), as well as ageing. Clonal expansion = replication of mtDNA is the process by which a mutant mtDNA molecule increases to high levels within a single cell containing both wild-type and mutant mtDNA. Unlike in AD and PD, the diffuse inflammatory process in MS involves the choroid plexus, and mitochondria are exposed to reactive oxygen and nitrogen species over a prolonged period. The extent of respiratory enzyme deficiency and mtDNA at a single cell level within choroid plexus epithelial cells in MS as well as in AD, PD and controls. The respiratory enzyme-deficient (lacking complex IV and with intact complex II activity) cells were more prevalent within the choroid plexus in AD, MS and PD compared with controls. The main catalytic subunit of complex IV (subunit-I of cytochrome coxidase) was lacking in significantly more respiratory enzyme-deficient cells in MS compared with AD, PD and controls. The single cell analysis showed a fourfold increase in the percentage of respiratory enzyme-deficient choroid plexus epithelial cells harbouring clonally expanded mtDNA in MS. Our findings establish clonal expansion of mtDNA as a feature relatively more prominent within the choroid plexus epithelium in MS than AD, PD or controls. We propose clonal expansion of mtDNA as a molecular link between inflammation and part of a delayed cellular energy failure in MS.

[Prof. Gavin Giovannoni comment]
"Mitochondrial DNA (mtDNA) is the DNA located in organelles called mitochondria, structures that convert the chemical energy from food into a form that cells can use, adenosine triphosphate (ATP). Most other DNA present in eukaryotic organisms is found in the cell nucleus. In most species, including humans, mtDNA is inherited solely from the mother. These are the power houses of cells and create energy for the cell. In MS we think that there is a mitochondrial deficit that results in less energy for the cell, this could because it has to work harder when nerves are demyelinated. This study found expansions of mtDNA and associated this with influences of the respiratory chain enzymes. Is this a cause of pathology or a consequence of the nerves in the choroid plexus having to work harder? This is difficult to know."

Mult Scler. 2012 Jun 21. [Epub ahead of print]
Accumulation of cortical hyperphosphorylated neurofilaments as a marker of neurodegeneration in multiple sclerosis.
Gray E, Rice C, Nightingale H, Ginty M, Hares K, Kemp K, Cohen N, Love S, Scolding N, Wilkins
1 MS Labs, Burden Centre,
University of Bristol Institute of Clinical Neurosciences,
Frenchay Hospital, UK.
1MS Labs, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, UK
PMID: 22723571 C. M. Rice


Axonal loss and grey matter neuronal injury are pathological processes that contribute to disease progression in MS.

Axon damage has been associated with changes in the phosphorylation state (phosphate groups) of neurofilaments and the presence of axonal spheroids (ball at the end of axons when they are transected).

Perikaryal accumulation of abnormally phosphorylated neurofilament proteins has been reported in some neurodegenerative diseases.

The objective of this article is to determine whether abnormally phosphorylated neurofilament accumulates in neuronal perikarya in demyelinated MS cortex.

We used an antibody to hyperphosphorylated neurofilament-H (SMI-34) to assess the level and distribution of this antigen in paraffin sections of cerebral cortex from cases of neuropathologically confirmed MS and controls.

We also examined the relationship of neurofilament phosphorylation to cortical demyelination.

The number of SMI-34-positive neuronal somata was significantly higher in the MS cortex than the control cortex. As a proportion of the total number of neurons present (i.e. taking account of neuronal loss), the proportion of SMI-34-positive neurons was also significantly higher in the demyelinated and non-demyelinated MS cortex than the control cortex.

MS is associated with the widespread accumulation of hyperphosphorylated neurofilament protein in neuronal somata, with the most marked accumulation in regions of cortical demyelination.

This aberrant localisation of hyperphosphorylated neurofilament protein may contribute to neuronal dysfunction and degeneration in MS patients.

[Prof. Gavin Giovannoni comment]
"This work is not new and reproduces what has been shown in other labs. It shows that the cortex or surface of the brain in MS is affected by pathological processes and affects the cytoskeleton of axons and nerves. Yet more evidence that MS is turning out to be more a disease of grey, rather than white, matter. The problem we have is that the gray matter pathology is not picked up with routine imaging techniques."

CNS Neurol Disord Drug Targets. 2012 May 11. [Epub ahead of print]
Clonal Expansion of Mitochondrial DNA Deletions and the Progression of Multiple Sclerosis.
Campbell GR, Mahad, DJ Graham R. Campbell Mres, Don J. Mahad MD, PhD


Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Mechanisms of disease progression in MS are poorly understood but are thought to relate to both focal pathology as well as diffuse inflammation in the white and grey matter. Evidence points to neurodegeneration combined with a loss of cellular function in the remaining tissue as an important factor to the progression of MS. Mitochondria are implicated to play a role in the pathogenesis of MS with evidence of loss of mitochondrial respiratory chain activity, down regulation of both nuclear DNA and mitochondrial DNA (mtDNA) encoded transcripts as well as oxidative damage to, and deletions of, the mitochondrial DNA (mtDNA).

The double stranded circle of mtDNA (16.6 kb) encompasses genes encoding key subunits within the mitochondrial respiratory chain required for the production of ATP as well as transfer RNA and ribosomal RNA molecules within the cell.

The stability of mtDNA is essential for a healthy CNS as highlighted by the patients with primary mitochondrial disease.

In this review, we focus on the potential role of mtDNA mutations, in particular somatic mtDNA deletions, in the pathogenesis of the progressive stage of MS.

We propose clonal expansion of somatic mtDNA deletions as a potential molecular link between early inflammatory events and a delayed cellular energy failure, dysfunction and degeneration.

The high level of somatic mtDNA deletions within single cells in MS is likely to cause cellular dysfunction as well as increase the susceptibility of the CNS tissue to additional stress.

PMID: 22583438

Curr Opin Neurol. 2012 Jun;25(3):221-30.
Mitochondrial changes within axons in multiple sclerosis: an update.
Campbell GR, Ohno N, Turnbull DM, Mahad DJ.
Centre for Neuroregeneration, University of Edinburgh, Chancellor's Building, Edinburgh, UK.


Here, we discuss the recent developments in axonal mitochondrial response to demyelination and remyelination in multiple sclerosis (MS), and following experimental demyelination as well as myelination.

There is a gathering body of evidence implicating an energy-deficient state in the pathogenesis of MS, and mitochondrial defects have been the subject of a number of previous reviews.

In myelinated axons within the central nervous system, over 90% of mitochondria are located within juxtaparanodal and internodal axoplasm.

The electrogenic machinery, mitochondria and myelin form a triad that is disrupted in MS.

The axonal mitochondrial content increases following demyelination and persists despite the residual inflammatory reaction subsiding to levels seen in control cases.

The changes in axonal mitochondrial content following demyelination in MS and experimental demyelination in vivo and in vitro do not return to the levels in nondemyelinated and myelinated axons following remyelination.

Understanding the mechanisms of axonal mitochondrial response to a disturbance in myelin and determining if certain aspects of the axonal mitochondrial response to demyelinated and remyelinated axons are beneficial may identify potential therapeutic targets for the progressive forms of MS.

PMID: 22543429

Autoimmune Dis. 2011 Feb 8;2011:262847.
Mitochondria as crucial players in demyelinated axons: lessons from neuropathology and experimental demyelination.
Campbell GR, Mahad DJ.
Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK.


Mitochondria are the most efficient producers of energy in the form of ATP.

Energy demands of axons, placed at relatively great distances from the neuronal cell body, are met by mitochondria, which when functionally compromised, produce reactive oxygen species (ROS) in excess.

Axons are made metabolically efficient by myelination, which enables saltatory conduction.

The importance of mitochondria for maintaining the structural integrity of myelinated axons is illustrated by neuroaxonal degeneration in primary mitochondrial disorders.

When demyelinated, the compartmentalisation of ion channels along axons is disrupted.

The redistribution of electrogenic machinery is thought to increase the energy demand of demyelinated axons.

We review related studies that focus on mitochondria within unmyelinated, demyelinated and dysmyelinated axons in the central nervous system. Based on neuropathological observations we propose the increase in mitochondrial presence within demyelinated axons as an adaptive process to the increased energy need.

An increased presence of mitochondria would also increase the capacity to produce deleterious agents such as ROS when functionally compromised. Given the lack of direct evidence of a beneficial or harmful effect of mitochondrial changes, the precise role of increased mitochondrial presence within axons due to demyelination needs to be further explored in experimental demyelination in-vivo and in-vitro.

PMID: 21331147 [PubMed] PMCID: PMC3038418 Free PMC Article
Free full text of an excellent review

Eur J Neurosci. 2012 Jun;35(12):1887-93. doi: 10.1111/j.1460-9568.2012.08150.x.
Mitochondrial sirtuins - a new therapeutic target for repair and protection in multiple sclerosis.
Rice CM, Sun M, Kemp K, Gray E, Wilkins A, Scolding NJ.


Given the significant socioeconomic impact of progressive multiple sclerosis (MS) and the paucity of treatment options, there is an urgent need to develop new and effective therapies for this disabling condition.

The relatively recent appreciation that progressive disability is largely driven by neuronal loss has focused considerable research attention on neuroprotective strategies.

This has coincided with the emergence of oxidative damage as a prominent effector mechanism of axonal damage in studies of MS pathogenesis, which has opened up a new range of putative targets for neuroprotective therapy in MS.

Mitochondrial sirtuins are NAD(+) -dependent protein deacetylases associated with the control of metabolism, aging, and stem cell proliferation and differentiation. Their role in inflammatory demyelinating disease has not been fully characterized, and is the subject of ongoing research.

Here, we expound the rationale behind selecting mitochondrial sirtuins as a therapeutic target in demyelinating disease, and report preliminary data that warrant further investigation.

© 2012 The Authors. European Journal of Neuroscience
© 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd.

Aspartame diet drink rise after 1983 -- 22 mg methanol each drink is made into formaldehyde inside cells of brain blood vessel walls by ADH1 enzyme, in humans only: Rich Murray 2012.06.27

Re: Sex ratio of multiple sclerosis in the National Swedish MS Register (SMSreg).

Sir Augustus d'Esté, born 1794 grandson of King George III of England, was the first MS case, starting 1822, died 1848 -- may be from methanol from pectins in wet preserved fruits juices vegetables in containers for rich people, invented in France in 1807 for Napoleon's army -- probably the cause for more MS in colder climates, along with smoke from wood and peat fires.

Methanol also is supplied by cigarette smoke.

Tobacco is usually smoked over wood fires -- a pack of unfiltered cigarettes gives as much methanol as a litre of diet drink, 62 mg.

Cigarettes are well known to be a causal agent for MS -- but few indeed know the simple fact that cigarettes give more methanol than formaldehyde, which serves as a stealth "Trojan Horse"in the blood to all parts of the body, to be made, in humans only, by the ADH1 enzyme into free floating, highly reactive, hydrated formaldehyde inside the cells of the blood vessel walls at the base of the brain, retina, and about 20 other specific tissues.

Formaldehyde in smoke mainly bonds to the first tissues encountered during inhalation, and can not travel far in the blood or plasma, so its direct toxic range is limited.

Where the local cuisine is smoked over wood or peat (three times more methanol) fires, there is much more MS -- Scotland, Shetland Islands and Iceland, with the same genetic population as the Faroese Islands.

The Faroese Islands, treeless, have fish preserved by air drying, with no MS until the first 20 cases after the English army came in WWII with cigarettes and canned fruits juices vegetables.

MS was a largely male disease a century ago, as males worked with methanol solvents in paper-making, chemical, leather, and paint industries, while few females smoked.

In the USA during WWII, women workers were given free cigarettes and exposed to methanol in industries.

The largest source of methanol is from aspartame, legalized in 1983 for beverages in the USA, with increasing use by weight conscious females, and increasing use in hot climates in recent decades.

Methanol from many sources is the key to the puzzling global epidemiology of MS.

Methanol is the cause of MS, with substantial unequivocal anatomical and biochemical evidence.

Yet another co-factor is ethanol, which preempts the ADH1 enzyme, preventing formaldehyde formation from methanol, until after the ethanol levels have fallen to very low levels -- hence, the classic symptoms of alcohol hangovers, "the morning after the night before", when the person wakes up sober, but soon has the panoply of formaldehyde neurotoxicity symptoms from methanol blood levels, about double above normal.

The classic treatment for emergency cases of methanol toxicity is to use ethanol to keep the patient drunk for days, until the methanol has been excreted from the blood.

A drink a day protects most people from methanol/formaldehyde toxicity, thus making light drinkers less prone to many chronic "diseases of civilization" than nondrinkers.

Methanol from aspartame, wood and cigarette smoke, and many sources is made by ADH1 enzyme into formaldehyde within cells inside walls of human blood vessels, harming adjacent tissues, the WC Monte paradigm: Rich Murray 2012.06.24

The 200 mg aspartame in a 12-oz can of aspartame drink is 11% by weight methanol, 22 mg, which is soon released from the GI tract into the blood, where quickly any tissues with high levels of the ADH1 enzyme within the cells of blood capillary walls and adjacent tissues, especially liver, kidney, brain, retina, etc., in humans only, turn the methanol into formaldehyde within these cells, which, being highly reactive, quickly binds with and disables DNA, RNA, and proteins inside the cells, causing cell death, attracting macrophages (white blood cells), which also die, creating durable, cumulative, evolving complex micro lesions.

This affects the fetus, as well, or not so well...

So, there are many resulting novel modern "diseases of civilization" in humans only, for each type of damaged tissue, including Alzheimer's, multiple sclerosis, lupus, arthritis, the birth defects spina bifida, autism, and Asperger's, many specific cancers, and chronic ailments of liver, kidney, heart, lung, joint, skin, muscle, etc.

The Monte methanol/formaldehyde toxicity paradigm MMFTP is backed by 740 references, given free online as full pdf texts by Prof. (retired 2004, Arizona State University, Nutrition and Food Sciences) Woodrow C. Monte, along with his 2012 January 240 page text "While Science Sleeps", with two free chapters on "Autism and Other Birth Defects", and "Multiple Sclerosis", and free full earlier articles and references on MMFTP.

Other methanol/formaldehyde sources include wood, peat and cigarette smoke, some fresh coffees, fermented and smoked foods, fruits juices vegetables heated and sealed wet in jars and cans, some dark wines and liquors, bacteria in the colon, genetic flaws in metabolism, vehicle fumes, leaky fossil fuel stoves and heaters, processed wood products of all kinds, mobile homes, old Ditto type purple ink mimeograph duplicating machines in schools and offices, chemical biology autopsy mortuary facilities, heated wood in particleboard, pressed wood and paper factories, and many personal care cleaners and products...

Methanol/formaldehyde paradigm for multiple sclerosis, free full 56 page chapter 9 pdf, While Science Sleeps, 146 full text references online, Prof. Woodrow C. Monte: Rich Murray 2012.03.20
List of 745 free full text pdf medical research references

Aspartame: The hidden danger [methanol/formaldehyde] in our midst and how it kills us, 12 page review of While Science Sleeps text (Woodrow C Monte), International Health News, whole June issue, Editor: William R Ware PhD: Rich Murray 2012.06.08
Free full text pdf 16 pages

Fwd: Aspartame Submission from Prof. Woodrow C. Monte to EFSA: While Science Sleeps: A Sweetener Kills 241 p -- Ch 12 Autism and other Birth Defects 26 p -- 740 references full pdfs: Rich Murray 2011.11.03\(ref).pdf
Free Chapter 12 of the book "While Science Sleeps", "Autism and Other Birth Defects", with 100 free online full text references

While Science Sleeps, methanol from cigarettes and aspartame becomes formaldehyde inside human cells -- Table of Contents, WC Monte bio, Kindle electronic book version $ 9.80 Rich Murray 2012.01.26

Methyl alcohol ingestion as a model etiologic agent in multiple sclerosis, WC Monte, D Glanzman, C Johnston; Methanol induced neuropathology in the mammalian central nervous system, Woodrow C. Monte, Renee Ann Zeising, both reports 1989.12.04: Murray 2007.12.28 2012.05.01

WC Monte finally got secret FDA memo 37 years after Searle Co. labs found birth defects in rabbits from aspartame (methanol, becomes formaldehyde via ADH1 enzyme within human cells) and its phenylalanine: Rich Murray 2012.06.02

Monte, Woodrow C. (2011-12-30). While Science Sleeps (Kindle Locations 5542-5612). Amazon. Kindle Edition. Free Chapter 12 "Autism and Other Birth Defects" with 100 free online full text pdf medical research references\(ref).pdf

Top MS incidence in Shetland Islands re methanol from smoked foods via wood and peat fires, Prof. WC Monte, While Science Sleeps text 2012 Jan -- methanol and formaldehyde in particleboard, plywood, paper factories: Rich Murray 2012.05.15

Similar macular harm in multiple sclerosis as from formaldehyde made by ADH enzyme inside retina capillary walls from methanol, Prof. Woodrow C. Monte text "While Science Sleeps" 2012 Jan -- some quotes re retina harm: Rich Murray 2012.05.10

Prof. Resia Pretorius letter re aspartame to EJCN cites Prof. Woodrow C. Monte "While Science Sleeps" text, re methanol/formaldehyde toxicity paradigm: Rich Murray 2012.05.21

Victoria Inness-Brown, 3 books and 5-part video on 2.5 year study on many large tumors in 60 rats fed NutraSweet (aspartame, dextrose, maltodextrine): Joseph Mercola: Rich Murray 2011.06.23

See WC Monte's two 1-hour video lectures May 2012:

Rich Murray
MA Boston University Graduate School 1967 psychology,
BS MIT 1964 history and physics,
Rich Murray
254-A Donax Avenue, Imperial Beach, CA 91932-1918
505-819-7388 cell
619-623-3468 home
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