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does methanol (wood alcohol) cause MS?

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    Posted: 18 Aug 2014 at 3:59am
Alzheimer's Stops Here 71 minute free video -- WC Monte gives science since 1807 for 20 new slow chronic human autoimmune diseases from rampant formaldehyde formed from methanol (wood alcohol)  in cells by ADH1 enzyme: Rich Murray 2014.08.16


[ see also:

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
http://rmforall.blogspot.com/2012/03/methanolformaldehyde-paradigm-for.html
http://health.groups.yahoo.com/group/aspartameNM/message/1642 ]



1:11:29  2014.08.15

Alzheimer's Stops Here.
by Woodrow Monte

The link between the consumption of aspartame and the epidemic of Alzheimer's over the last 30 years.
Helps explain why Alzheimer's has increased over 100X in such a short time.


Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004


free searchable archive of 782 pdfs of mostly full text medical science references

from his slides:

Positive news: just 5 grams a day of ethanol [ordinary drinking alcohol], spread out as little sips every hour or two, strongly prevents harm from 50 grams daily of methanol -- this is so low that no change would occur in awareness from the "solvent effect", from about 1/2 shot daily 40 % ethanol liquor [ 80 proof ].


source of methanol --- mg/L food ---  mg/day [ rough data for average intake ]

freshly made juice ---1 --- ?

foods sealed wet in containers of glass, metal, plastics:

juice --- 33 --- 8

vegetables --- 27 --- 6

aspartame diet drink --- 60 --- 43 [ about 3 cans ]

aspartame diet Sprite --- 91 --- 65

A pack of cigarettes in Berlin in a 1926 study gave 40 mg methanol.

Less than 2,000 mg methanol took 48 hours to kill a four year old girl from the typical methanol toxicity brain swelling -- that would indicate the likelihood that the cumulative toxicity for 100 days of aspartame diet drink at one can daily, 22 mg daily methanol for 100 days, 2200 mg methanol, might reasonably be expected to show scattered spots of harm in the 20 vulnerable tissues, where the methanol is concentrated as durable toxic products of formaldehyde, hidden away in sick and dead cells.



768. Nursel Türkmen, 
Bulent Eren,
Gursel Cetin.
FATAL METHANOL INGESTION IN A CHILD; CASE REPORT
-- (severe brain swelling picture). 

ACTA MEDICA (Hradec Králové) 2009;52(3):125–127.

Uludag University Medical Faculty, Forensic Medicine Department, Council of Forensic Medicine of Turkey Bursa
Morgue Department, Bursa, Turkey 1; 

Council of Forensic Medicine of Turkey Bursa Morgue Department, Bursa, Turkey 2;

Istanbul University Medical Faculty, Forensic Medicine Department, Council of Forensic Medicine of Turkey, Istanbul Morgue Department 3.

Summary: 

The records of Forensic Medicine Council of Turkey Bursa Morgue Department reveal the first case of fatal methanol ingestion in a child. 

Household methanol exposures are mostly due to accidental ingestion of washing fluids.

A 4 year-old girl was admitted to the emergency department with her parents with gastrointestinal symptoms; nausea, vomiting and abdominal pain.

Toxicological studies revealed 79 mg/dl blood level of methanol.
[ 790 mg/L blood -- almost a gram -- 60 mg/L has been shown to produce severe symptoms in a laboratory study on male alcoholics. ]

We presented infant autopsy case of methanol toxicity and discussed the case from medicolegal aspect.


Fig. 2: Severe brain edema, flattened brain surface with widened gyri and congested vessels.

page 127

Discussion

Household methanol exposures are mostly due to accidental ingestion of washing fluids.

But rare exposures also have occurred through dermal and pulmonary routes, which cases are reported usually in occupational areas (1, 3, 6, 7). 

The lethal dose of methanol is reported as 1 to 2 mL/kg.

[ 0.8 to 1.6 g/kg body weight = 800 to 1600 mg/kg bw.

Well, the standard  daily safe dose for methanol for humans would usually be set by dividing 800 by 100 to give just 8 mg/kg body weight, while the current USA aspartame safe level is 50 mg/kg bw, with its 11 % methanol being 5.5 mg/kg bw -- but these kinds of estimates don't take into account cumulative formaldehyde  damage inside cells in 20 specific human tissues that actually slowly remove most of any ingested methanol every day, which has a long half-life of 3 hours in the human bloodstream, reaching and entering every cell in the adult and the fetus every minute via the blood flow. 

Thus, the ADH1 enzyme gradually concentrates the methanol as high levels of harm in specific clusters of vulnerable cells, especially the inner walls of blood vessels in brain, retina, and many other tissues. ]

Ingestion of a little amount as 0.1 mL/kg has been reported to be resulted in permanent blindness or death (1).

[ This is 10 to 20 times smaller than the lethal numbers given just above...

0.08 g/kg body weight  = 80 mg/kg bw-- dividing by 100 would set the daily safe level at 
0.8 mg/kg bw -- far below the 5.5 mg/kg methanol safe daily level implied by the aspartame safe level... ]

Methanol is rapidly absorbed via the gastrointestinal tract.

Most household exposures are due to the intentional or accidental ingestion of windshield washing fluids and fuel de-icing agents, cases would be seen more commonly in occupational settings (1).

In the literature from USA it was demonstrated that most accidental exposures were reported in children younger than 6 years, like our case, wheres half of the cases of exposure were reported in children ranging from 6 to 19 years of age (3).

Davies et al. (4) also indicated that toddlers were at the highest risk cluster for
methanol exposure, but on the other hand adolescents and adults were at the highest risk for life-threatening intoxications in concert with investigation of clinical documents of
different study which also revealed that outcomes data in toddlers resulted in complete treatment with no sequelae (3).

Drowsiness, confusion, ataxia, ocular injury, blindness, coma, seizure, and hypotension may be observed (1–7). 

Methanol toxicity has a more significant manifestation in that it affects the optic system more so than any of the other toxic alcohols.

Different patients may report variable degrees of visual symptoms like looking though a snow field, but in the presented case there were no documentation about visual
symptoms. 

Other ophthalmic effects include mydriasis, papilledema, retinal edema, and hyperemia of the optic disc (1). 

These signs and symptoms are able to be seen in varying degrees and are related to the amount and time of methanol ingestion. 

Mortality is often associated in settings where treatment was not initiated quickly or correctly as it was in the presented case (1–7). 

Meyer et al. stated that some patients, in spite of potentially lethal methanol levels of up
to 160 mmol/L, did not develop signs of toxicity (5).

[ There probably was enough ethanol in the blood for those cases to prevent ADH1 enzyme from forming formaldehyde right inside certain cells in 20 specific tissues. ]

Different from the presented case blood methanol levels were above 100 mg/dL in majority (70 %) of their cases in the study of Davies et al. (4), but similar to our findings metabolic acidoses and anion gap were detected in most of the cases.

The patient presented without signs or symptoms of methanol toxicity is suggested to demonstrate difficulties during evaluation process.

For these reason, for the patient who has been poisoned with methanol without evidence of clinical toxicity, the first primacy is to provide specific therapy which can probably decrease the morbidity and mortality associated with this form of poisoning.

References

1. Barceloux DG, Bond GR, Krenzelok EP, Copper H, Vale JA.
American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Methanol Poisoning.
J Toxicol Clin Toxicol 2002;40:415–46.

2. Brown MJ, Shannon MW, Woolf A, Boyer EW.
Childhood methanol ingestion treated with fomepizole and hemodialysis. 
Pediatrics. 2001;108:E77.

3. Bucaretchi F, Baracat E. 
Acute toxic exposure in children: an overview. 
J Pediatri (Rio J) 2005;81(5 Suppl):S212–22.

4. Davis LE, Hudson D, Benson BE, Jones Easom LA, Coleman JK.
Methanol poisoning exposures in the United States: 1993–1998.
J Toxicol Clin Toxicol. 2002;40:499–505.

5. Kruse JA. Methanol poisoning.
Intensive Care Med. 1992;18:391–7.

6. Meyer RJ, Beard ME, Ardagh MW, Henderson S.
Methanol poisoning.
N Z Med J. 2000;113:11–13.

7. Watson WA, Litovitz TL, Rodgers Jr GC, et al.
2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. 
Am J Emerg Med 2005;23:589–666.

Corresponding author:
Dr. Bülent Eren, Council of Forensic Medicine of Turkey Bursa Morgue Department, Heykel, Osmangazi 16010, Bursa, Turkey; e-mail:bulenteren2000@yahoo.com

Bülent Eren <bulenteren2000@yahoo.com>.

Bülent Eren <drbulenteren@gmail.com>,



Citing WC Monte twice, well funded RQ He 3 year study in China shows Alzheimers harm in monkeys from chronic methanol becoming formaldehyde, Part 2/2: Rich Murray 2014.07.27


"Nonetheless, these findings support a growing body of evidence that links methanol and its metabolite formaldehyde to AD pathology."


"It is one of the first studies, if not the first, to show that methanol toxicity inflicted all the major hallmarks of AD; cognitive decline, tau phosphorylation, and the corner stone of AD pathology: amyloid plaque formation, where earlier studies in conventional laboratory rodent systems were unable to."


"In fact, at the longest delay time (5×B), the animals being fed methanol for 1.5 months averaged 3 correct choices out of 6."  [ random guessing in a memory test... ]


"However, one monkey had complications during the regimen (∼1 year in). 

The animal began to eat its fur, which caused a severe intestinal obstruction. [ dementia ]

The methanol feeding was stopped, but the animal did not recover and was euthanized. 

The animal was not available to contribute further data to the memory evaluation but its brain was evaluated histologically for tau phosphorylation and amyloid plaque formation."


"The full extent of how these systems and of toxic exposure contribute to development of AD in relation to formaldehyde and/or methanol is not clearly understood and will require more work to be fully elucidated.

Nonetheless, the neural consequences of these biological interactions may prove to be one of the most important discoveries into AD pathology.

The work presented here in the rhesus monkey has been able to side step what appears to be a confounding problem in the use of the rodent system and provide fruitful new information in the investigation of complex neurological disorders, like AD.

It highlighted the fact that there is a tremendous evolutionary difference between rodents and primates, including both nonhuman and human primates, which may have biased scientific inquiry away from potential and important understandings about human physiology. 

This investigation serves as a very important example to this fact.

It is one of the first studies, if not the first, to show that methanol toxicity inflicted all the major hallmarks of AD; cognitive decline, tau phosphorylation, and the corner stone of AD pathology: amyloid plaque formation, where earlier studies in conventional laboratory rodent systems were unable to.

As most investigations correctly evaluated the contributions of genetic factors to AD, it is possible that previous investigations into AD pathology have missed this major relationship to the progression of the disease because the animal systems used masked the contribution of methanol or formaldehyde. 

Thus, these simpler metabolic contributors which may underlie how genetic vulnerabilities fully engage the disease went unnoticed. 

A full investigation into the importance of methanol and its metabolite formaldehyde to AD pathology by the scientific community may unearth a new understanding into how age, genetics, and metabolic changes contribute to the dementia epidemic that is currently exploding worldwide.

The use of methanol feeding in the rhesus macaque will assuredly provide a new model into the pathology of AD that will allow these future investigations to take place. 

Such an investigation may also reveal new therapeutic avenues, in addition to dietary monitoring, that may reflect a relatively simpler metabolic target than focusing solely on genetic causes."  [ end of body of report ] 

[ much more... ]


California OEHHA sets methanol ingestion level 23 mg daily, same as from 1 can aspartame diet soda, 10 cigarettes, 3 tomatoes, or 4 cans green beans: Rich Murray 2013.07.03

"However, the anticipated exposure to methanol from consumption of aspartame would not be considered an exposure within the meaning of Proposition 65 because aspartame is not listed under Proposition 65."

[ Rich Murray: Many pregnant women drink one 12-oz can aspartame diet drink daily, with 200 mg aspartame that gives 11% methanol, 22 mg, which is just under the OEHHA limit of 23 mg daily.

The smoke from 10 cigarettes gives 20 mg methanol, the same as from 1 can aspartame drink, 3 full size fresh tomatoes, or 4 cans of unfresh green beans. ]


smoke from pack cigarettes gives 40 mg methanol for 20 gr tobacco, 6 tobacco methanol papers, Carl Neuberg 1926-1939, Berlin -- so methanol formaldehyde toxicity paradigm is co-factor in 18 tobacco diseases -- WC Monte gives 23 references: Rich Murray 2013.03.29


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


highly competent, pithy analysis of aspartame cancer study by Eva S.
Schernhammer at Harvard, William R. Ware, PhD, showing relevance of
Woodrow C. Monte methanol-formaldehyde toxicity paradigm: Rich Murray
2012.12.03


confirms WC Monte paradigm: ingested methanol becomes toxic
formaldehyde-induced hydroxymethyl DNA adducts in all tissues in rats,
sensitive C13 test, Kun Lu, James A Swenberg, UNC Chapel Hill
2011.12.08 Toxicol Sci: Rich Murray 2013.01.11



methanol (11% of aspartame), made by body into formaldehyde in many
vulnerable tissues, causes modern diseases of civilization, summary of
a century of research, Woodrow C Monte PhD, Medical Hypotheses
journal: Rich Murray 2009.11.15
Sunday, November 15, 2009

"Formaldehyde produced within the cell immediately reacts with water
to produce formal hydrate,[#27] a strong acid[#114] with twice the
number of available hydrogen ions as the next methanol metabolite,
formic acid.

Formal hydrate produced from methanol by the ADH I sites found in
the intima, media, and adventitia lining of the circulatory system of the
heart and brain[#220] would be expected to diffuse into the localized
tissue, quickly methylating basic molecules such as myelin basic
protein (MS)[#224] and tau protein (Alzheimer's).[#234]"

free full text, 5 pages
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Med Hypotheses 2010;74(3):493-6.


check out methanol as multiple sclerosis toxin -- in humans only, ADH1 enzyme turns it into rampant formaldehyde right inside cells in 20 tissues, the WC Monte paradigm: Rich Murray 2014.06.18


methanol toxicity, not by formate, but by formaldehyde made inside human cells by ADH1 enzyme -- brief by Woodrow C. Monte, with lengthy references: Rich Murray 2013.05.24


Table 5.2 is the key chart -- ADH1 enzyme at high levels in 20 tissues in body and fetus makes methanol into formaldehyde right inside cells, initiating over 20 human diseases, with full text references, WC Monte paradigm: Rich Murray 2013.03.21

"sources of methanol (wood alcohol):

smoke from cigarettes, wood, peat;

aspartame, and chewing gums;

some dark wines and liquors;

fresh tomatoes, black currants;

unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers (including home preserves and jugs of apple cider by farming families);

jams jellies marmalades;

smoked fermented spoiled foods;

some fresh coffees;

approved food additive dimethyl dicarbonate;

vehicle fuels;

medical chemical mortuary facilities, home and industry solvents, factories for processed wood and paper products -- formaldehyde heated to 150 deg C releases methanol." 

"tissues with high levels of ADH1 enzyme inside cells:

liver, kidney, lung;
intima and media (inner walls) of blood vessels, notably base of brain and retina;
rods and cones in retina;
purkinje cells of vermis in cerebellum;
islets of Langerhans in pancreas;
fibroblasts in skin, bone marrow, synovial tissues in joints;
milk ducts of breast;


Men have several times more ADH1 in their GI tract than women, so less methanol gets into the blood to attack other tissues, so now four times as many women get multiple sclerosis as men."
 


MS goes with cigarettes in large Iran survey, S Asadollahi et al, JClinNeurosci -- toxic
cause may be methanol from cigarettes, aspartame diet drinks, unfresh fruits and
vegetables in cans and jars: Rich Murray 2013.09.16


"As a matter of course, every soul citizen of Earth has a priority to quickly find and positively share evidence for healthy and safe food, drink, environment, and society."

within the fellowship of service,

Rich Murray,
MA Boston University Graduate School 1967 psychology,
BS MIT 1964 history and physics,
1039 Emory Street, Imperial Beach, CA 91932
rich.murray11 free Skype audio, video chat
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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 01 Feb 2014 at 4:50am
Thanks marc mineralogy, yes, I've seen Russell Blaylock give many long detailed referenced articles and books on MSG and aspartame toxicity, and many other modern health challenges.

Here's a long summary of my posts from 1999 to 2004:

research on aspartame (methanol, formaldehyde, formic acid) toxicity: Rich Murray 2004.07.11 2014.01.21


Rich Murray, MA Room For All rmforall@gmail.com
254-A Donax Avenue, Imperial Beach, CA 91932  619-623-3468




As part 2, this is the rest of the preceding post, which is part 1 -- the entire post is on my blog at:



within the fellowship of service,
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http://rmforall.blogspot.com
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Post Options Post Options   Thanks (0) Thanks(0)   Quote marc mineralogy Quote  Post ReplyReply Direct Link To This Post Posted: 30 Jan 2014 at 4:19pm
Hi rich marc here if you want to hear a lecture by a brain specialist nurosergion who goes into some of what your saying and more watch dr russell blaylock nutrition and behavior the dangers of aspartame and msg on you tube. Very very interesting. Also check on google gluten causes ms, but it seems aspartame and msg accelerate it by letting poison breach the blood brain barrier and oxygenating your brain by over working the nuerons. Excitotoxins.
Hope this helps,
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Very good info.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 22 Aug 2013 at 4:04am
http://en.wikipedia.org/wiki/Dichloromethane
 
Dichloromethane or Methylene chloride

CCl2H2

Toxicity

DCM is the least toxic of the simple chlorohydrocarbons, but it is not without health risks, as its high volatility makes it an acute inhalation hazard.[4][5]

DCM is also metabolized by the body to carbon monoxide potentially leading to carbon monoxide poisoning.[6]

Acute exposure by inhalation has resulted in optic neuropathy[7] and hepatitis.[8] 

Prolonged skin contact can result in DCM dissolving some of the fatty tissues in skin, resulting in skin irritation or chemical burns.[9]

It may be carcinogenic, as it has been linked to cancer of the lungs, liver, and pancreas in laboratory animals.[10]

DCM crosses the placenta. 

Fetal toxicity in women who are exposed to it during pregnancy, however, has not been proven.[11]

In animal experiments, it was fetotoxic at doses that were maternally toxic but no teratogenic effects were seen.[10]

In many countries, products containing DCM must carry labels warning of its health risks.

In the European Union, the European Parliament voted in 2009 to ban the use of DCM in paint-strippers for consumers and many professionals.[12]

The ban took effect in December 2010.[13]

In Europe, the Scientific Committee on Occupational Exposure Limits (SCOEL) recommends for DCM an occupational exposure limit (8h time-weighted average) of 100 ppm and a short-term exposure limit (15 min) of 200 ppm.[14]

In February 2013, the U.S. Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health warned that 14 bathtub refinishers have died since 2000 from DCM exposure.[15][16]





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Post Options Post Options   Thanks (0) Thanks(0)   Quote anonymouse Quote  Post ReplyReply Direct Link To This Post Posted: 22 Aug 2013 at 12:04am
I don't know about Wood Alcohol but I am drinking a nice Glenmorangie Malt at the moment.

What I did ask myself was did exposure to Dichloromethane or Methylene chloride have anything to do with my MS. 
I worked as a technician in a London school where it was used as a solvent to weld plastics together.
I remember the smell of it every time I had to decant it into small containers for distribution to teachers.


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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 20 Aug 2013 at 7:57am
usual doses of aspartame proven to cause cancers, Michael F. Jacobson PhD, Director, Center for Science in the Public Interest -- also long 1985 statement: Rich Murray 2013.08.15
http://rmforall.blogspot.com/2013/08/usual-doses-of-aspartame-proven-to.html


http://www.cspinet.org/new/201308141.html

Coke Shouldn't Bother Rehabilitating Aspartame's Image, Says CSPI

Statement of CSPI Executive Director Michael F. Jacobson
mjacobson@cspinet.org,
cspi@cspinet.org,

August 14, 2013

Aspartame has been found to cause cancer -- leukemia, lymphoma, and other tumors -- in laboratory animals, and it shouldn’t be in the food supply. 

We certainly want Coca-Cola to shift its product mix toward lower- and no-calorie drinks, but aspartame’s reputation isn’t worth rehabilitating with this propaganda campaign.

The company would be better off phasing out its use of aspartame and accelerating its research into safer, natural sweeteners such as those extracted from the stevia plant.

That said, consumers should know that the greater and more immediate danger to their health is posed not by artificial sweetened products, but by the full-calorie versions of Coke, Pepsi, and other sugar drinks.

Rather than posing small risks of cancer, the high-fructose corn syrup or other sugars in these drinks cause obesity, diabetes, heart disease, and other health problems.

Everyone would be better off drinking water or seltzer water instead.
[ End ]


Eva A. Schernhammer cites Woodrow C. Monte methanol-formaldehyde
paradigm in brave, cautious Harvard team study that confirms more
cancers in aspartame diet soda users over 22 years -- full plain text:
Rich Murray 2012.10.27
http://rmforall.blogspot.com/2012/10/eva-schernhammer-cites-woodrow-c-monte.html


careful expert lifetime study on mice shows liver and lung cancers
from aspartame, M Soffritti et al, Ramazzini Institute, Italy, checked
by US National Toxicology Program experts, confirms many previous
studies from 2001 on: Rich Murray 2011.02.27
http://rmforall.blogspot.com/2011/02/careful-expert-lifetime-study-on-mice.html


Michael F. Jacobson of CSPI now and in 1985 re aspartame
toxicity, letter to FDA Commissioner Lester Crawford;
California OEHHA aspartame critique 2004.03.12;
Center for Consumer Freedom denounces CSPI:
Murray 2004.07.27
http://health.groups.yahoo.com/group/aspartameNM/message/1189




Diet Coke and Pepsi (mostly aspartame) sales fell three times more than regular sugar versions in 2012 -- Diet Pepsi fell 6.2 percent: Rich Murray 2013.08.14
http://rmforall.blogspot.com/2013/08/diet-coke-and-pepsi-mostly-aspartame.html


"In fact, sales of diet sodas are falling at a faster rate than regular sodas in the U.S., according to Beverage Digest.

Last year, for example, sales volume for Coke fell 1 percent,
while Diet Coke fell 3 percent.

Pepsi fell 3.4 percent,
while Diet Pepsi fell 6.2 percent."

http://abcnews.go.com/Business/wireStory/coke-defend-safety-aspartame-ad-19947805#disqus_thread


Here's my comment last night, on Net articles about Coke ads that defend aspartame today:


Only in 2007 did the expert Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, start publishing detailed evidence that the 11% methanol (wood alcohol) part of aspartame quickly reaches the blood flow, with a half-life of 3 hours, reaching all parts of the body and fetus every minute, entering all cells.

In humans only, the cells in 20 tissues have high levels of ADH1 enzyme, that turns methanol into formaldehyde right inside these cells, that lack a functioning defense system that all other animals have. Headache is the first main symptom of harm to the brain, which over many years leads to Alzheimer's, multiple sclerosis, and many cancers.

Monte gives a free online archive of 786 full text medical research references, so experts can assess his breakthrough paradigm -- just Google for "WhileScienceSleeps"...

Other methanol sources include cigarette wood and peat smoke, smoked foods, dark wines and liquors, fresh tomatoes, and unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans and jars. [ End ]


11% of aspartame is methanol, which becomes free floating formaldehyde inside human cells -- methanol also in cigarettes and canned fruits and vegetables: Rich Murray 2013.08.14


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
http://rmforall.blogspot.com/2012/05/similar-macular-harm-in-multiple.html


Human epidemiological studies so far fail to control for additional common methanol sources: cigarettes and wood and peat smoke, smoked foods, fresh tomatoes, and degraded pectins from unfresh fruits juices vegetables preserved wet at room temperature in sealed cans jars plastic containers...


Methanol has 3 hour half-life in blood, enters all cells in body and fetus, and is made into uncontrolled formaldehyde by ADH1 enzyme inside cells of 20 human tissues --Woodrow C. Monte gives 786 free full text references at WhileScienceSleeps.com .


autism as a birth defect from epigenetic methylation by formaldehyde made from methanol by ADH1 enzyme inside Purkinje cells in vermis in cerebellum and in inner walls of brain blood vessels -- Prof. WC Monte paradigm: Rich Murray 2013.04.26
http://rmforall.blogspot.com/2013/04/autism-as-birth-defect-from-epigenetic.html


CA Pardo autism brain autopsy findings in 2005 fit WC Monte paradigm -- methanol with blood half-life 3 hours is made by ADH1 enzyme into free floating formaldehyde in 20 defenseless human cells in 20 tissues: Rich Murray 2013.07.21
http://rmforall.blogspot.com/2013/07/ca-pardo-autism-brain-autopsy-findings.html


The Woodrow C. Monte methanol/formaldehyde toxicity paradigm is that
concentrations of ADH1 enzyme, well known to exist inside blood vessel
wall cells in specific tissues, quickly turn methanol into
formaldehyde inside the vessel cells, in humans only -- the highly
reactive formaldehyde diffuses to penetrate adjacent tissue cells,
binding to DNA, RNA, and proteins, attracting macrophages, which die,
creating complex, expanding micro lesions, leading to many modern
"diseases of civilization", Alzheimer's, arthritis, diabetes, multiple
sclerosis, lupus -- as well as later cancers -- also serious birth
defects in the fetal brain in the fourth week of pregnancy, spinal
bifida and autism.

Aspartame is 11% methanol, 22 mg per can of diet drink -- similar
levels of methanol come from wood and cigarette smoke, heated and
canned fruits juices vegetables, fermented and smoked foods, some
wines and liquors, vehicle fuels, many cleaners and solvents, chemical
medical autopsy mortuary facilities, heated wood in particleboard and
paper factories, and more.


WC Monte submits robust evidence for multiple sclerosis, which he concludes proves methanol to be the proximate toxic cause, since ADH1 enzyme is within the cells of the inner linings of brain blood vessels, the Purkinje cells of the vermis of the cerebellum, and rods and cones of the retina -- ADH1 quickly turns methanol into free floating formaldehyde within these cells, disrupting the blood brain barrier...


California OEHHA sets methanol ingestion level 23 mg daily, same as from 1 can aspartame diet soda, 10 cigarettes, 3 tomatoes, or 4 cans green beans: Rich Murray 2013.07.03
http://rmforall.blogspot.com/2013/07/california-oehha-sets-methanol.html

"However, the anticipated exposure to methanol from consumption of aspartame would not be considered an exposure within the meaning of Proposition 65 because aspartame is not listed under Proposition 65. "

[ Rich Murray: Many pregnant women drink one 12-oz can aspartame diet drink daily, with 200 mg aspartame that gives 11% methanol, 22 mg, which is just under the OEHHA limit of 23 mg daily.

The smoke from 10 cigarettes gives 20 mg methanol, the same as from  3 full size fresh tomatoes, or 4 cans of unfresh green beans. ]


See also:

James McDonald to EFSA, outdated aspartame ADI gives methanol 35 times too high for human safety, ten minute talk at April 9 public sharing, Brussels: Rich Murray 2013.04.15
http://rmforall.blogspot.com/2013/04/james-mcdonald-to-efsa-outdated.html


aspartame harm in rat brain from 75 mg/kg gives human ADI 0.75 mg/kg, 53
times less than EU ADI 40 mg/kg, Ashok Iyyaswamy, SheelaDevi Rathinasamy,
U. Madras 2012.08.03 free full text -- main methanol toxin is formaldehyde,
not formate: Rich Murray 2013.06.01
http://rmforall.blogspot.com/2013/06/aspartame-harm-in-rat-brain-from-75.html


more lower aspartame and methanol ADIs from studies by RH Nair, SheelaDevi
Rathinasamy, WC Monte, PS Jeganathan, A Namasivayam, Hazleton Labs, Searle
Labs: Rich Murray 2013.06.01
http://rmforall.blogspot.com/2013/06/more-lower-aspartame-and-methanol-adis.html


Kate S. Collison et al show prediabetic harm in gene expression in mice fed lifetime aspartame, MSG, trans fats -- reduce human aspartame ADI 1000 times: Rich Murray 2013.07.30
http://rmforall.blogspot.com/2013/07/kate-s-collison-et-al-show-prediabetic.html


aspartame impairment of spatial cognition and insulin sensitivity in
mice, focus on phenylalanine and aspartate [ methanol also crosses
placenta into fetus, turning into teratogenic formaldehyde], Kate S.
Collison et al, PLoS One 2012.04.03: Rich Murray 2012.04.29
http://rmforall.blogspot.com/2012/04/aspartame-impairment-of-spatial.html
http://health.groups.yahoo.com/group/aspartameNM/message/1645


The public EFSA session on aspartame safety on April 9 for 5 hours included an audience of about 50 experts and 10-20 ESFA staff in Brussels.

The release of the final EFSA review on aspartame safety will be delayed from April 15 to November, 2013.

Extremely cogent multiple lines of robust evidence were briefly described that strongly support the methanol formaldehyde toxicity paradigm of Prof. Woodrow C. Monte, Prof. Food Science and Nutrition, Arizona State University, retired 2004 -- supported by an online archive of 782 free full text medical research references at
 www.WhileScienceSleeps.com .

It is clear that methanol is far more dangerous for chronic low level exposures than realized since 1890.

Major sources include the smoke from a pack of cigarettes, 40 mg methanol,the same as from 2 cans aspartame diet drink. It now seems likely that most cigarette diseases are actually methanol toxicity...

Methanol stays in the blood with a half-life of 3 hours, reaching every part of the body and the fetus with the bloodstream, and readily entering all cells.

Humans are uniquely vulnerable to methanol formaldehyde toxicity, as they lack a functioning catalase enzyme system, that in all other creatures serves to protect each cell against the rapid conversion of methanol into free floating formaldehyde right inside the cells of 20 specific tissues that have high levels of ADH1 enzyme.

The effects are used to good advantage in embalming and disinfection, as formaldehyde immediately bonds to and impairs DNA, RNA, and proteins, permanently disrupting cell biochemistry, cell by cell, as long as methanol is ingested -- leading to 20 specific chronic modern novel "diseases of civilization", that progress slowly and erratically, according to the ingestion of methanol from a variety of modern sources:

smoke from cigarettes, wood, and peat;

since 1983, aspartame, including from most chewing gums;

fresh tomatoes and black currants;

unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers;

jams jellies marmalades;

smoked fermented spoiled foods;

many dark wines and liquors;

work at paper and wood factories, mortuaries, medical and chemical facilities;

Research since 2012 specifically shows the presence of formaldehyde bonded to cellular macromolecules inside cells after methanol ingestion -- the paradigm will be confirmed in detail very quickly, as science exponentially explores this simple breakthrough.

This presents the world food industry with an unprecedented opportunity to serve the huge public good by collaborating vigorously to eliminate all methanol exposures from foods and beverages. The Net guarantees that the news and evidence will spread explosively everywhere.


Paul Thomas MD Pediatrics and Integrative Medicine, Portland OR, praises
"While Science Sleeps" at Amazon.com -- WC Monte paradigm of methanol
formaldehyde toxicity via ADH1 enzyme in 20 human tissues, including fetus: Rich Murray 2013.04.03
http://rmforall.blogspot.com/2013/04/paul-thomas-md-pediatrics-integrative.html


highly competent, pithy analysis of aspartame cancer study by Eva S.
Schernhammer at Harvard, William R. Ware, PhD, showing relevance of
Woodrow C. Monte methanol-formaldehyde toxicity paradigm: Rich Murray
2012.12.03
http://rmforall.blogspot.com/2012/12/highly-competent-pithy-analysis-of.html


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
http://rmforall.blogspot.com/2012/05/prof-resia-pretorius-letter-re.html


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
http://rmforall.blogspot.com/2012/06/aspartame-hidden-danger.html


Table 5.2 is the key chart -- ADH1 enzyme at high levels in 20 tissues in body and fetus makes methanol into formaldehyde right inside cells, initiating over 20 human diseases, with full text references, WC Monte paradigm: Rich Murray 2013.03.21
http://rmforall.blogspot.com/2013/03/table-52-is-key-chart-adh1-enzyme-at.html   
http://health.groups.yahoo.com/group/aspartameNM/message/1734


"As a matter of course, every soul citizen of Earth has a priority to
quickly find and positively share evidence for healthy and safe food,
drink, environment, and society."


within the fellowship of service,

Rich Murray,
MA Boston University Graduate School 1967 psychology,
BS MIT 1964 history and physics,
254-A Donax Avenue, Imperial Beach, CA 91932-1918,
rmforall@gmail.com,
505-819-7388 cell,
619-623-3468 home,
http://rmforall.blogspot.com

within the fellowship of service,
Rich Murray
http://rmforall.blogspot.com
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Methanol, furthermore renowned as methyl alcoholic beverage, timber alcoholic beverage,timber naphtha or timber spirits, is a chemical with the equation CH3OH.
The 1980’s was well into the era when laboratories that had been performing methanol toxicity research were being paid by the company who invented Aspartame to prove the safety of its sweetener. Dr. Hugo Henzi, an M.D. now deceased, published a book in 1980 purporting to prove dietary methanol as the cause of multiple sclerosis. His clinical logic and anatomical observations were impeccable, but he made a major mistake. He erroneously believed that the methanol that caused MS came from “fresh” fruits and vegetables, and as a consequence, he proposed a curative diet that we now know had little chance of success. However, several lines of evidence are now converging to support Dr. Henzi’s primary assertion.



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CA Pardo autism brain autopsy findings in 2005 fit WC Monte paradigm -- methanol with blood half-life 3 hours is made by ADH1 enzyme into free floating formaldehyde in 20 defenseless human cells in 20 tissues: Rich Murray 2013.07.21


Dear Prof. Carlos A. Pardo and  colleagues,

I want to express my gratitude for your detailed sharing of evidence in a FAQ on your website, from your two papers in 2005, from a fresh look at the micro anatomy of harm in the brains of autism victims, by sharing the breakthrough methanol formaldehyde toxicity paradigm of Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004.  Your findings fit well with many lines of evidence for his unifying vision.

In humans only, cells lack an effective defense in the peroxisomes against the conversion of methanol into formaldehyde right inside the cells of 20 tissues with high levels of ADH1 enzyme -- notably the inner layers of blood vessels at the base of the brain (the blood brain barrier itself), the Purkinje cells in the vermis of the cerebellum, and the rods and cones of the retina. 

Methanol is about 10 to 100 times more deadly to humans than to any other creature.

In multiple sclerosis the symptoms  are mostly due to a multitude of scattered tiny lesions in the brain from harm initially triggered by ADH1 enzyme inside the cells of the inner walls of blood vessels at the base of the brain, which turns methanol, which has a life-time in the blood of 3 hours, right into formaldehyde in these cells, causing malfunction and death of the cells, (which are the blood brain barrier itself), with leakage of methanol and formaldehyde and other substances directly from the blood into the brain.

The formaldehyde bonds to and thus marks DNA, RNA, and large protein molecules, which then specifically attract three kinds of white blood cells (microglia, monocytes, and macrophages) that eat up the marked molecules, stripping the MBP myelin sheath off the long axons of the nerves, leading to accumulating brain damage and most of the symptoms, according to how much methanol is taken in.  The harm looks like a multitude of tiny inflamed pussy lesions inside the brain and spinal cord.

Major methanol sources are cigarette smoke, aspartame, dark wines and liquors, fresh tomatoes, smoked foods, unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers, jams jellies marmalades, fermented and spoiled foods, and wood and peat smoke.

A positive factor is one shot of alcohol drink taken daily, which at that level is a safe potent antidote to methanol formaldehyde toxicity. 

For over a century experts have noted that symptoms from ethanol drinks mixed with some methanol  result in symptoms only after about half a day later, when the ethanol level, with a half-life of only 1/3 hour, reaches almost zero -- notably in hangovers "the morning after the night before".  Ethanol is supplied by IV to cases of acute methanol toxicity in hospitals  for days, until all the methanol has been eliminated, without conversion by ADH1 enzyme to formaldehyde.

The reduction of harm in those who drink about one shot ethanol drink daily, compared to those who never drink, is a tell tell indicator that methanol formaldehyde is involved for many similar modern novel chronic "diseases of civilization" like Alzheimer's, atheroscelerosis, and diabetes 2.

So, the basic facts are incontrovertible.

Monte's key insight is that the ADH1 enzyme freely floats inside the cells of 20 specific tissues, leading to the formation of uncontrolled, free floating formaldehyde, which promptly hydrates, with two acidic hydrogen donating OH radicals on each side, which rapidly bind firmly to any adjacent DNA, RNA, and huge protein macromolecules, gumming up the cellular biochemistry.

The tiny formaldehyde molecule is hidden against these huge victim molecules -- only in recent years has research found ways to prove their existence within living or dead cells.

Cigarette smoke correlates with all 20 chronic diseases -- a pack gives as much methanol, 40 mg, as 2 cans aspartame diet drink.  Very likely most cigarette diseases are to some degree methanol formaldehyde diseases.  

Fatigue and weakness are caused by formaldehyde strongly blocking 2 key enzymes in the cellular energy centers  (mitochondria) that help the ATP energy metabolism that sustains all cellular biochemistry in the body.

Eye symptoms, including temporary and permanent blindness, are due to a form of ADH1 that is in the rods and cones of the retina.

The symptoms of autism are from ADH1 that is right inside the brain tissue of the Purkinje cells in the vermis of the cerebellum.  The fetus is especially vulnerable at the fourth week of pregnancy, when the brain is first being grown, as methanol reaches every part of the mother and the fetus.

Formaldehyde is a powerful methylation agent, that firmly attaches small methyl groups to the genes on the DNA and RNA, messing them up, and leading birth defects in the fetus, and to later cancers at all ages.

There is damage to all 20 tissues with high levels of ADH1, but it is the brain damage that kills, in the end, as breathing shuts down.

Recently, multitudes of tiny lesions has been found in most brain tissue in MS cases, which suggests that there are low levels of ADH1 enzyme in most parts of human brain tissue -- so far, ADH1 research studies, especially in humans, are few and far between in recent decades.

This is the WC Monte methanol-formaldehyde paradigm.  It applies to many different modern novel chronic human diseases: atherosclerosis, strokes, Alzheimer's, multiple sclerosis, ALS, macular degeneration, lupus, arthritis, diabetes 2, dermatitis, cancers of liver kidney lung breast prostate skin pancreas, COPD, and birth defects autism, Asperger's, spina bifida, preterm birth, Fetal Alcohol Syndrome, infertility.

The many symptoms of MS, acute and chronic methanol toxicity, and aspartame (11% methanol) toxicity are identical, including specific types of reversible blindness.



WC Monte provides a free online archive of 782 full text medical research references at WhileScienceSleeps.com . 


Following are many dense collections of references for the paradigm details:

Table 5.2 is the key chart -- ADH1 enzyme at high levels in 20 tissues in body and fetus makes methanol into formaldehyde right inside cells, initiating over 20 human diseases, with full text references, WC Monte paradigm: Rich Murray 2013.03.21

  
autism as a birth defect from epigenetic methylation by formaldehyde made from methanol by ADH1 enzyme inside Purkinje cells in vermis in cerebellum and in inner walls of brain blood vessels -- Prof. WC Monte paradigm:  Rich Murray 2013.04.26


Chapter 12 "Autism and Other Birth Defects, free at www.WhileScienceSleeps, Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, with 745 free online full text medical research references:

" ... our methanol poisoned rat pups lost Purkinje cells preferentially from a very specific area of the cerebellum called the vermis.  This meant little to me at the time but it has now been discovered the cerebellum is known to be preferentially damaged in human autism, 622   and the vermis 570 and hippocampus are the particular areas of the cerebellum most damaged and reduced in volume by the disease. 571 ..."  


622.  Allen G., Courchesne E. 
Differential effects of developmental cerebellar abnormality on cognitive and motor functions in the cerebellum: an fMRI study of autism. 
Am J Psychiatry 2003;160(2):262-73. 
Eric Courchesne <ecourchesne@ucsd.edu>,


570. Mitchell S, Reiss A, Tatusko D, Ikuta I, Kazmerski D, Botti J, et al.
Neuroanatomic alterations and social and communication deficits in monozygotic twins discordant for autism disorder.
Am J Psychiatry 2009;166(8):917-25.
Wendy R Kates <katesw@upstate.edu>,
"...our study replicates previous findings of an enlarged dorsolateral prefrontal cortex, reduced areas of the corpus callosum, and decreased posterior cerebellar vermis in autism and demonstrates that neuroanatomic alterations are closely associated with phenotypic features of autism in children who are severely affected."


571.  Webb S, Sparks B, Friedman S, Shaw D, Giedd J, Dawson G, et al.
Cerebellar vermal volumes and behavioral correlates in children with autism spectrum disorder.
Psychiatry Res 2009;172(1):61-7. 
Sara Jane Webb <sjwebb@u.washington.edu>,


many strong birth defects in 336 rat fetuses, 3 g/kg bw oral methanol (not toxic dose) in 26 rat litters, thesis done 1987, WC Monte, M Hoque, L Black, CS Johnson: Rich Murray 2013.04.13


With years of expertise in testing toxins on rats, Prof. Woodrow C. Monte, Arizona State University, had his own lab, where he mentored graduate students.

Vivid personal reports led him to test the possibility of birth defects from methanol, 11% of aspartame, 22 mg in the 200 mg aspartame in a 12-ounce can diet drink.

He was unaware that the FDA and Searle Corp. had hidden 6 of their studies that showed birth defects from aspartame in rabbits and mice in 1975.

This dose was planned to swamp the catalase enzyme defense system, which, effective in rats and all animals, except the uniquely vulnerable human species, protects against harm from methanol being made into free floating formaldehyde inside cells with high levels of ADH1 enzyme, notably the inner walls of brain blood vessels and in retina rods and cones.

As the smallest organic molecule, methanol readily enters all cells, while it is carried to all parts of the body and the fetus with the bloodstream — in humans with a blood half-life of 3 hours, circulating through the whole body every minute.

A ten-fold lower dose of 0.3 g/kg body weight was used with 272 fetuses in 21 litters, producing a much lower number of birth defects, compared to 296 fetuses in 22 control litters with no methanol.



gives all photos and figures in “While Science Sleeps” textbook –
Figure 12.5 shows a damaged rat pup brain…

177. Hoque M., Monte WC., Black L., Johnston CS.
Methanol Neuropathy and Teratology A Histological Study on Long-Evans Rats.
FASEB 1988;25(2(6)):A513.

[ See also:

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

posted again Tuesday, May 1, 2012

Friday, December 28 2007

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

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


Download Chapter 12 of the book "While Science Sleeps"
"Autism and Other Birth Defects",
with 100 free online full text references ]


smoke from pack cigarettes gives 40 mg methanol for 20 gr tobacco, 6 tobacco methanol papers, Carl Neuberg 1926-1939, Berlin -- so methanol formaldehyde toxicity paradigm is co-factor in 18 tobacco diseases -- WC Monte gives 23 references: Rich Murray 2013.03.29


welcome to the WC Monte methanol formaldehyde toxicity paradigm via
this treasury of studies -- depression, diabetes, retina harm,
multiple sclerosis, cancer -- crisp Michele Bouchard 2001 review --
hangovers: Rich Murray 2013.02.21


#6 diabetes 2 risk high for 2 cans aspartame diet drink weekly 14
years 66K women study, Guy Fagherazzi et al AJCN 2013 Jan -- methanol
(cigarettes, aspartame) formed into formaldehyde inside cells in
pancreas by ADH1 enzyme, WC Monte paradigm: Rich Murray 2013.02.13


#4 methanol formaldehyde toxicity in alcohol withdrawal syndrome study
on closed hospital ward in 1969, Edward Majchrowicz and Jack H.
Mendelson -- fits WC Monte paradigm: comment on EFSA draft aspartame
review: Rich Murray 2013.02.02


 #3, methanol leaves retained formaldehyde, with similar symptoms as multiple sclerosis for eye and brain, comment re EFSA aspartame review: Rich Murray 2013.01.17

[ 3771 characters ] line 4054
"4054 When 14C-methanol or [14C-methyl]-aspartame were given orally to rats or monkeys in equimolar  doses...(Oppermann, 1984)...In rats, about 40% and in monkeys about 30% of the dose was not accounted for."


Many reports cite similar eye harm from methanol as associated with MS:


The aim of this Blog is for the Barts and The London Neuroimmunology Group to update you on the latest research in MS with an emphasis on the research we are involved in.

Research: Eye Problems in MS
Posted: 08 May 2012 11:08 PM PDT
Epub: Gelfand et al. Microcystic macular oedema in multiple sclerosis is associated with disease severity. Brain. 2012 Apr 25.

"Macular oedema has been reported in MSers on fingolimod (Gilenya);
this study shows that this can occur spontaneously in a small number of MSers.
This was worse in MSers with more advanced disease and occurred more in people that have had optic nerve disease in the past.
Visual disturbances can occur result from macular swelling in addition to that which may also relate to influences on the nerve fibre layer (ganglion cells), which are damaged as nerves in the optic nerve are damaged...The observation that inflammation occurs in the retinae of MSers, where there is no myelin questions the dogma that the autoimmune target in MS is myelin..."
Posted by Prof. Gavin Giovannoni

Prof. Woodrow C. Monte,
page 17, Chapter 3, "While Science Sleeps" textbook 2012 January (Kindle Locations 806-812)

"The ADH enzyme is found dissolved in the cell’s fluid, or cytosol. 531
This makes ADH a free agent that can float around the cell unencumbered, releasing formaldehyde from methanol wherever it happens to be within the cell at the time.
Nothing can then restrain the reactive formaldehyde;
it is free to leave the cell or travel to the nucleus or other sensitive areas within the cell, where serious damage (such as methylation [ of DNA and RNA]) can be done.
Whether within the cell or outside it, the necessary enzyme that would [ safely] convert formaldehyde to the next metabolite, formic acid, is, at the very least, a considerable distance away...

Vision is the one major responsibility of ADH that is well understood,
and the retina is one of the sites where ADH is located.
In fact, ADH is the enzyme that makes vision possible 663 by metabolizing the alcohol form of Vitamin A, which begins the process that initiates the eye’s signal to the brain.
This connection of ADH to vision can account for the phenomenon of blindness, both temporary and permanent, and other strange visual signs and symptoms associated with both methanol toxicity and multiple sclerosis."

663. free full text pdf 10 pages [ total 745 free references available ]
Eur. J. Biochem. 267, 4315-4324 (2000) c FEBS 2000
Families of retinoid dehydrogenases regulating vitamin A function
Production of visual pigment and retinoic acid
Gregg Duester

WSS text, pages 35, Chapter 4.2  (Kindle Locations 1300-1306):

"Formaldehyde is slowly being produced within the lining of the circulatory system of the brain and diffusing outward into the tissue, and attaching itself to the MBP.
The macrophages are then called in to remove all the formaldehyde-damaged MBP that is in its wake. [ Myelin Basic Protein ]

It is the intermittent production of formaldehyde in the lining of the circulatory system of the brain, beyond the blood brain barrier, that turns on when methanol from the diet is high and ethanol [which prevents formaldehyde formation] from [fermentation by bacteria in] the colon is low, that [then] is more likely to lead to the slow progression of the perivascular plaque, which is the discerning feature of multiple sclerosis."
[ end of comment 3 ]


comment 2 on 5.1 methanol Alzheimer's cause from formaldehyde formed
by ADH1 enzyme at "perivascular loci" in brain, EFSA aspartame draft:
Rich Murray 2013.01.15


comment 1 on 5.1 methanol metabolism, EFSA aspartame draft : Rich
Murray 2013.01.14


The half life of methanol in human blood is about 3 hours. Actually,
the huge oral dose is enough to saturate the rats' catalase defense
system, resulting in their ADH1 enzyme making methanol into toxic
formaldehyde inside cells in many tissues, whereas in humans only,
whose defective catalase enzyme fails to safely metabolize
formaldehyde inside the many protective peroxisomes in every cell, the
ADH1 enzyme, in high levels in 19 specific tissues, quickly turns
bloodborne methanol into uncontrolled free floating highly toxic
formaldehyde inside cells, according to Prof. Woodrow C. Monte, Food
Science and Nutrition, Arizona State University, retired 2004, in text
"While Science Sleeps" 2012 January, with 2 free chapters, "Multiple
Sclerosis" and "Autism and other birth defects", summary in Medical
Hypothesis 2010 (not peer reviewed), 3 articles from Fitness Life,
fall 2007, other articles, audio and video lectures and interviews,
slideshows, backed by a free online archive of 745 mostly full text
medical research references:
Monte W.,
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Med Hypotheses 2010;74(3):493-6.


confirms WC Monte paradigm: ingested methanol becomes toxic
formaldehyde-induced hydroxymethyl DNA adducts in all tissues in rats,
sensitive C13 test, Kun Lu, James A Swenberg, UNC Chapel Hill
2011.12.08 Toxicol Sci: Rich Murray 2013.01.11


methanol (11% of aspartame), made by body into formaldehyde in many vulnerable tissues, causes modern diseases of civilization, summary of a century of research, Woodrow C Monte PhD, Medical Hypotheses journal: Rich Murray 2009.11.15
Sunday, November 15, 2009

"Formaldehyde produced within the cell immediately reacts with water
to produce formal hydrate,[#27] a strong acid[#114] with twice the
number of available hydrogen ions as the next methanol metabolite,
formic acid.

Formal hydrate produced from methanol by the ADH I sites found in
the intima, media, and adventitia lining of the circulatory system of the
heart and brain[#220] would be expected to diffuse into the localized
tissue, quickly methylating basic molecules such as myelin basic
protein (MS)[#224] and tau protein (Alzheimer's).[#234]"

free full text, 5 pages
Monte WC.
Methanol: A chemical Trojan horse as the root of the inscrutable U.
Med Hypotheses 2010;74(3):493-6.

Methanol: A Chemical Trojan Horse as the Root of the Inscrutable U
Prepublication Copy; Medical Hypotheses -- 06 November 2009
(10.1016/j.mehy.2009.09.059)
Woodrow C. Monte PhD
[ extracts ]



Int Rev Psychiatry. 2005 Dec;17(6):485-95.
Immunity, neuroglia and neuroinflammation in autism.
Pardo CA, Vargas DL, Zimmerman AW.
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.cpardo@jhmi.edu

Abstract

Autism is a complex neurodevelopmental disorder of early onset that is highly variable in its clinical presentation. 
Although the causes of autism in most patients remain unknown, several lines of research support the view that both genetic and environmental factors influence the development of abnormal cortical circuitry that underlies autistic cognitive processes and behaviors.
The role of the immune system in the development of autism is controversial.
Several studies showing peripheral immune abnormalities support immune hypotheses, however until recently there have been no immune findings in the CNS. 
We recently demonstrated the presence of neuroglial and innate neuroimmune system activation in brain tissue and cerebrospinal fluid of patients with autism, findings that support the view that neuroimmune abnormalities occur in the brain of autistic patients and may contribute to the diversity of the autistic phenotypes.
The role of neuroglial activation and neuroinflammation are still uncertain but could be critical in maintaining, if not also in initiating, some of the CNS abnormalities present in autism. 
A better understanding of the role of neuroinflammation in the pathogenesis of autism may have important clinical and therapeutic implications.
PMID: 16401547


Carlos A. Pardo <cpardo@jhmi.edu>,

Ann Neurol. 2005 Jan;57(1):67-81.
Neuroglial activation and neuroinflammation in the brain of patients with autism.
Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA.
Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA.

Erratum in
Ann Neurol. 2005 Feb;57(2):304.

Abstract

Autism is a neurodevelopmental disorder characterized by impaired communication and social interaction and may be accompanied by mental retardation and epilepsy.
Its cause remains unknown, despite evidence that genetic, environmental, and immunological factors may play a role in its pathogenesis. 
To investigate whether immune-mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme-linked immunosorbent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic patients and determined the magnitude of neuroglial and inflammatory reactions and their cytokine expression profiles. 
Brain tissues from cerebellum, midfrontal, and cingulate gyrus obtained at autopsy from 11 patients with autism were used for morphological studies.
Fresh-frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profiling.
We demonstrate an active neuroinflammatory process in the cerebral cortex, white matter, and notably in cerebellum of autistic patients. 
Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 and tumor growth factor-beta1, derived from neuroglia, were the most prevalent cytokines in brain tissues. 
CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1.
Our findings indicate that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain.
PMID: 15546155



July 17, 2013   Posted by Prof. Gavin Giovannoni

Article of interest: inflammation the brain shredder
How do you feel about having a shredder in your brain? #MSBlog #MSResearch

"A lot of readers don't like me using the analogy of a paper shredder when referring to the effects of inflammation on the brain of someone with MS.

The classic paper of Bruce Trapp and colleagues explains using beautiful pictures and hard data how damaging focal inflammation is in the brain of someone with MS.

In each cubic millimeter of an actively inflammed MS lesions over 11,000 axons were transected or shredded compared to less than 1 axon in a control subject. 

11,000 to 1 that is the ratio you need to keep in your head. 

This is why it is so important to suppress inflammation in the brains of MSers to stop the inflammation from shredding your axons.

The problem is that once these axons are shredded they very little chance of recovering. 

Now you need to scale  this damage up several orders of magnitude as most MS lesions are larger than 1 cubic millimeter, i.e. in the order of 1 cubic centimeter or 1000 cubic millimeters, to get a sense of the magnitude of the shredding that is occurring in MSers with active disease.

This is why I am such an active proponent of anti-inflammatories in MS, this includes RRMS and progressive MS; and is why in the PROXIMUS trial we are adding neuroprotective drugs on top of existing anti-inflammatories.

I would go as far as stating that I doubt an a pure neuroprotective drug will work in MS unless it has anti-inflammatory properties or is added on top of an existing anti-inflammatory drug.

Don't let anyone fool you into believing that progressive MS is non-inflammatory; the brains of progressive MSers, both SPMS and PPMS, are stuffed full of inflammatory cells."


Bruce Trapp and colleagues conducted pathological studies of brain tissues to define the changes in axons in MSers.

free full text with full page color images

Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mörk S, Bö L.
Axonal transection in the lesions of multiple sclerosis.
N Engl J Med. 1998 Jan 29;338(5):278-85.

BACKGROUND:
MS is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults.

Despite antiinflammatory or immunosuppressive therapy, most MSers have progressive neurologic deterioration that may reflect axonal loss.

METHODS: 
Brain tissue was obtained at autopsy from 11 MSers and 4 subjects without brain disease.

Fourteen active multiple-sclerosis lesions, 33 chronic active lesions, and samples of normal-appearing white matter were examined for demyelination, inflammation, and axonal pathologic changes by immunohistochemistry and confocal microscopy.

Axonal transection, identified by the presence of terminal axonal ovoids, was detected in all 47 lesions and quantified in 18 lesions.

RESULTS:
Transected axons were a consistent feature of the lesions of MS, and their frequency was related to the degree of inflammation within the lesion.

The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 
3138 at the hypocellular edges of chronic active lesions,
875 in the hypocellular centers of chronic active lesions,
and less than 1 in normal-appearing white matter from the control brains.

CONCLUSIONS:
Transected axons are common in the lesions of MS, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

A picture tells a thousand words:

This picture is embedded from

free full text with full page color images

The scale bar in Panel A represents 64 um;
the scale bars in Panels B, C, D, and E represent 45 um.

The axonal structure is green in this image and represents neurofilaments the scaffolding that supports axons. 

In panels B & C red indicates myelin. 

When green and red are overlaid you get yellow and this indicates myelinated axons.
 
In panels D and E red stains macrophages or microglia the cells that clear up the myelin debris; the so called garbage collectors.
 
Panels A and D show the centers of active lesions.
 
Panels B, C, and E show the edges of active lesions.
 
Panel A shows green bulbs or terminal axonal ovoids with single axonal connections (arrows), an axonal ovoid with dual axonal connections (arrowhead), and many normal-appearing axons. 

Panel B shows three large, green (neurofilament–positive) axons undergoing active demyelination (arrowheads).

One axon ends in a large terminal ovoid (arrow). 

Panel C shows some axons (green) terminating at the ends of normal-appearing myelin internodes (arrow), and many axons that express neurofilaments surrounded by normal-appearing myelin (arrowheads). 

In Panels D and E, macrophages (red in Panel D) and microglia (red in Panel E) surround and engulf terminal axonal swellings (large arrows) but have no consistent association with normal-appearing axons (arrowheads) or swellings in nontransected axons (Panel E, small arrow).


free full text

Bruce D. Trapp  <trappb@ccf.org>,
Richard M. Ransohoff  <ransohr@ccf.org>,

N Engl J Med. 1998 Jan 29;338(5):278-85.
Axonal transection in the lesions of multiple sclerosis.
Trapp BD, Peterson J, Ransohoff RM, Rudick R, Mörk S, Bö L.
Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.

Comment in
Demyelinating diseases--new pathological insights, new therapeutic targets. [N Engl J Med. 1998]
PMID: 9445407 Free full text

Bruce D. Trapp, Ph.D.,
John Peterson, B.S.,
Richard M. Ransohoff, M.D.,
Richard Rudick, M.D.,
Sverre Mörk, M.D., Ph.D.,
and Lars Bö, M.D.

"Neurologic disability in patients with multiple sclerosis has been correlated with atrophy in the spinal cord,12 cerebellum,13 and cerebral cortex,14 and the neuronal marker N-acetyl aspartate is decreased in multiple-sclerosis lesions according to magnetic resonance spectroscopy.14-17

In patients with relapses, reduced N-acetyl aspartate is restricted to the area of the lesion, whereas patients with chronic progressive multiple sclerosis have reduced N-acetyl aspartate even in normal-appearing white matter.18 

This observation suggests the spread of axonal pathologic changes, wallerian degeneration, or both.19,20"

"Axonal transection was abundant in active and chronic active lesions from patients with durations of clinical disease ranging from 2 weeks to 27 years. 

During relapsing–remitting stages of the disease, the restoration of conduction along demyelinated axons, redundant neuronal pathways, or axonal sprouting may compensate for the destruction of axons.

Our results suggest that a threshold of axonal loss is eventually reached beyond which patients have progressive neurologic deterioration.

If axonal pathologic changes begin at the onset of disease, as our data suggest, aggressive early treatment with neuroprotective agents should be considered."

"Neurofilaments are the principal constituent of the axonal cytoskeleton,45 and their phosphorylation states are dynamically regulated by myelination, demyelination, and intrinsic axonal pathologic changes.

Developmentally, myelination increases neurofilament phosphorylation, which in turn increases the lateral extension of neurofilament side arms.46,47 

This increases neurofilament spacing, axonal caliber, and axonal conduction velocity.42,48

In animal models, demyelination or dysmyelination causes decreased neurofilament phosphorylation, reduced axonal caliber, and an increase in nonphosphorylated neurofilament epitopes.49,50 

Therefore, it was expected that SMI-32 immunoreactivity would be increased in multiple-sclerosis lesions and that most SMI-32–positive axons would appear normal. 

In addition to axonal transection, two patterns of axonal pathologic changes were identified.

Discontinuous SMI-32 staining similar to that described in axonal degeneration (Figure 2C) provided additional evidence of axonal transection in multiple-sclerosis lesions.

Other axons had significant alterations in caliber (Figure 2D) and represented damaged axons that retained active-transport systems and connection to neuronal perikarya.

Axons distant from multiple-sclerosis lesions also displayed alterations in neurofilament phosphorylation. 

Although most appeared normally myelinated, some ended in terminal ovoids.

This finding is consistent with the results of magnetic resonance spectroscopy studies that detected reduced N-acetyl aspartate in regions where there were no visible lesions.20

Reduced N-acetyl aspartate may therefore reflect potentially reversible axonal dysfunction due to demyelination,51 as well as irreversible axonal degeneration distal to sites of transection. 

Since myelin ensheathment governs the activity of the axonal kinases and phosphatases that regulate neurofilament phosphorylation, myelination may also modulate the activity of aspartoacylase, the enzyme that hydrolyzes N-acetyl aspartate to aspartate and acetate. N-Acetyl aspartate–derived acetate can be used to make acetyl coenzyme A.52 N-Acetyl aspartate may therefore be part of an energy-storage system in axons that helps meet the energy demands of saltatory conduction.

In the absence of myelination, axonal energy demands may be reduced and N-acetyl aspartate levels diminished.

The results of this study highlight the considerable importance of clarifying the implications of reduced N-acetyl aspartate in multiple-sclerosis lesions, and they stress the need to develop or improve noninvasive methods of monitoring and treating axonal pathologic changes in patients with multiple sclerosis."




January 31, 2013   Posted by Prof. Gavin Giovannoni

"What does brain atrophy mean for you as someone with MS?

Brain atrophy could mean a lot of things. In general it probably implies ongoing loss of axons and neurones.

Brain atrophy cannot be a good thing and there is data that associates it with a poor prognosis."

'...Imaging correlates of gray matter atrophy indicate that mechanisms differ in RRMS and SPMS....' 

Fisher E, Lee JC, Nakamura K, Rudick RA.
Gray matter atrophy in multiple sclerosis: a longitudinal study.
Ann Neurol. 2008 Sep;64(3):255-65. doi: 10.1002/ana.21436.

OBJECTIVE:
To determine gray matter (GM) atrophy rates in MSers at all stages of disease, and to identify predictors and clinical correlates of GM atrophy.

METHODS:
MSers and healthy control subjects were observed over 4 years with standardized magnetic resonance imaging (MRI) and neurological examinations.

Whole-brain, GM, and white matter atrophy rates were calculated. 

Subjects were categorized by disease status and disability progression to determine the clinical significance of atrophy. MRI predictors of atrophy were determined through multiple regression.

RESULTS:
Subjects included
17 healthy control subjects,
7 subjects with clinically isolated syndromes,
36 MSers with relapsing-remitting MS (RRMS),
and 27 MSers with secondary progressive MS (SPMS).

Expressed as fold increase from control subjects,
GM atrophy rate increased with disease stage, 
from 3.4-fold normal in CISers converting to RRMS
to 14-fold normal in SPMS.

In contrast, white matter atrophy rates were constant across all MS disease stages at approximately 3-fold normal.

GM atrophy correlated with disability.

MRI measures of focal and diffuse tissue damage accounted for 62% of the variance in GM atrophy in RRMS,
but there were no significant predictors of GM atrophy in SPMS.

INTERPRETATION:
Gray matter tissue damage dominates the pathological process as MS progresses, and underlies neurological disabillity.

Imaging correlates of gray matter atrophy indicate that mechanisms differ in RRMS and SPMS. 

These findings demonstrate the clinical relevance of gray matter atrophy in MS, and underscore the need to understand its causes.



February 15, 2013   Posted by Prof. Gavin Giovannoni

Research: brain shrinkage in early MS
#MSBlog: Is your brain, or more importantly your cortex, shrinking?

"This study confirms what we already know from several other studies that MS is associated with progressive brain atrophy that begins early in the disease and is associated with disability progression. 

This is why it is important to treat MS early, aggressively and actively. 

Actively means not to assume a clinical response is good enough, i.e. to monitor with MRI and to switch or escalate treatment if there are signs of a non-response. 

Now that we have drugs that reduce or slow the rate of brain atrophy we need to consider incorporating this variable into our clinical practice."


free full text  Robert Zivadinov <rzivadinov@bnac.net>,
Epub: Robert Zivadinov et al.
Bimonthly Evolution of Cortical Atrophy in Early Relapsing-Remitting Multiple Sclerosis over 2 Years: A Longitudinal Study.
Mult Scler Int. 2013;2013:231345. 
doi: 10.1155/2013/231345. 

"Background: Brain atrophy, in particular cortical atrophy, is an indicator of the neurodegenerative component of MS. 

Objectives: This study investigated the evolution of cortical atrophy in MSers with early relapsing-remitting (RR) MS and its association with lesion volume (LV) accumulation and disability progression. 

...Conclusion:
Significant cortical atrophy, independent of T2-LV accumulation, occurs in early RRMS over 2 years, and it is associated with the disability progression."




Carlos A. Pardo-Villamizar, MD

Dr. Pardo is an Assistant Professor of Neurology and Pathology (Neuropathology) at the Johns Hopkins University School of Medicine.
His main focus of research is on immunological and molecular mechanisms of neurological disorders.
Dr. Pardo's current projects center on studies of neuroimmunopathological mechanisms associated with HIV infection (e.g. HIV dementia and HIV neuropathy), multiple sclerosis, transverse myelitis, epilepsy and autism. 
Dr. Pardo is the principal investigator of a project that studies the role of neuroglia dysfunction in HIV infection and drug abuse (funded by NIH-NIDA K08-DA16160) and and co-investigator in several other NIH funded grants that focus on neurological complications of HIV infection. 
Dr. Pardo also receives funding from Cure Autism Now (CAN) Foundation to study neuroimmune mechanisms involved in pathogenesis of autism and has received previous support from the Epilepsy Foundation of America, Passano Physician Scientist and Johns Hopkins Clinical Scientist Awards.





John Hopkins Neuroimmunopathology Laboratory

FAQs: The meaning of neuroinflammatory findings in autism

1. What type of immune reactions are present in the brain of autistic patients?

In our study, we have demonstrated a marked increase in neuroglial responses, characterized by activation of microglia and astroglia, in the brains of autistic patients.

These increased neuroglial responses are likely part of neuroinflammatory reactions associated with the central nervous system's (CNS) innate immune system.

In innate immune reactions of the CNS, microglial activation is the main cellular response to CNS dysfunction. 

This is in contrast to adaptive immune responses, in which lymphocyte and/or antibody mediated reactions are the dominant responses.

In our sample of autistic patients, microglial and astroglial activation was present in the absence of lymphocyte infiltration or immunoglobulin deposition in the CNS.

It also was associated with increased production of pro-inflammatory and anti-inflammatory cytokines such as MCP-1 and TGFß-1 by neuroglia. 

2. Is neuroinflammation always present in the brain of autistic patients?

NOT necessarily.

Since autism is a disorder that is highly variable in the ways it presents, and may be associated with multiple causes, it is possible that our sample of cases does not represent the entire autistic spectrum.

Also, some of our patients had other associated neurological disorders frequently found in autism, such as epilepsy and mental retardation. 

However, the presence of microscopic and immunological findings showing neuroimmune reactions in all of our autistic patients and the cytokine findings in the cerebrospinal fluid (CSF) support a potential role for neuroglia and neuroinflammation in the CNS effects in a number of individuals with autism. 

3. Why are neuroglial activation and neuroinflammation relevant to the neurobiology of autism?

The presence of increased neuroglial responses is relevant to the neurobiological mechanisms involved in autism, as both microglia and astroglia are essential for neuronal activity and synaptic [neural transmission] function, neuronal-neuroglial interactions, as well as for cerebral cortex modeling, organization and remodeling during brain development.

Furthermore, microglial and astroglial activation seems to play a major role in the neuroimmune mechanisms of disease in the CNS. 

These cells are part of the first-line response of the innate immune system of the CNS. 

They contribute to the modulation of immune responses by producing both pro-inflammatory and anti-inflammatory cytokines as well as growth and differentiation factors. 

4. Are microglial and astroglial reactions always bad for the brain?

NO.

The microglia and astroglia in the CNS may have a two-sided role in the inflammatory responses of the brain: they can act both as direct effectors of injury and on the other hand as protectors of the brain.

In some situations, microglia and astroglia may produce neurotoxic reactions that damage other cells such as neurons and oligodendrocytes in the brain.

However, there is strong evidence from experimental models that in some situations, both microglia and astroglia also contribute to the repair and restoration of neuronal connections and produce growth factors to maintain normal CNS function. 

5. Are microglial and astroglial activation the result of residual damage or ongoing damage to the brain? 

It remains unclear how and when microglia and astroglia become activated in the brain of autistic patients.

Neuroglial responses in autism may be part of primary (intrinsic) reactions that result from disturbances in neuroglial function or neuronal-neuroglial interactions during brain development.

They may also be secondary (extrinsic), resulting from unknown factors that disturb prenatal or postnatal CNS development (e.g. infections, toxins, etc).

Both astrocytes and microglia are critical for brain development.

MHC class II (HLA-DR antigen)-positive microglia colonize the developing CNS during the second trimester of pregnancy. 

It is possible that the presence of activated microglia in the brain in autism may reflect abnormal persistence of fetal patterns of development. 

This may be in response to genetic or environmental (e.g. intrauterine, maternal) factors. 

Our study of brains of autistic patients showed that regardless of age, history of epilepsy, developmental regression or mental retardation, microglial and astroglial reactions were consistently present. 

Our findings support the view that chronic and sustained neuroglial inflammatory responses are part of an ongoing and active process rather than a residual change. 

These changes may be involved in mechanisms associated with abnormal function of neurons and synapses in the brain in autism. 

Although our studies did not show any difference in neuroglial activation among patients with autism with respect to history of developmental regression or mental retardation, further studies that include larger series of cases may help to clarify whether these factors contribute to the ongoing neuroinflammatory responses. 

6. Is the neuroinflammation observed in autism similar to encephalitis or 
meningitis ?

NO.

In meningitis and encephalitis, the most prominent immune reaction is one of adaptive immunity, the main feature being infiltration of the CNS by inflammatory cells such as T lymphocytes and B lymphocytes along with the production of antibodies. 

There is also activation of astroglia and microglia in meningitis and encephalitis, but the dominant immune reaction is due to adaptive immunity.

In contrast, in autism, there is NO evidence of lymphocyte infiltration or antibody mediated reactions; the most prominent immune response is characterized by 
activation of microglia and astrocytes, features that characterize innate immune responses within the CNS.

These observations suggest that the adaptive immune system does not play a significant pathogenic role in this disorder, at least not during its chronic phase, and that the main immune mechanism involves predominantly innate immune reactions. 

Since our study focused on autopsy tissues, we cannot exclude the possibility that specific immune reactions, mediated by T-cell and/or antibody responses, occurred at the onset of disease, during prenatal or postnatal stages of development. 

7. Is there any brain region particularly affected by neuroinflammation?

Yes.

Our study showed the cerebellum exhibited the most prominent neuroglial responses.

The marked neuroglial activity in the cerebellum is consistent with previous observations that the cerebellum is a major focus of pathological abnormalities in microscopic and neuroimaging studies of patients with autism.

Based on our observations, selective processes of neuronal degeneration and neuroglial activation appear to occur predominantly in the Purkinje cell layer (PCL) and granular [needs to be defined] cell layer (GCL) areas of the cerebellum in autistic subjects. 

These findings that are consistent with an active and ongoing postnatal process of neurodegeneration and neuroinflammation. 

Our observations suggest that the pathological changes observed in the cerebellum in
autistic patients do not occur exclusively during prenatal development, but appear to involve an ongoing chronic neuroinflammatory process that involves both microglia and astroglia.

Furthermore, this process continues beyond early neurodevelopment, and is even present at very late stages in the life of patients with autism.

These findings also support the hypothesis that selective vulnerability of Purkinje cells plays a role in the pathological process of autism 

8. Is there any other evidence to support the presence of neuroinflammation in the brain of autistic patients?

Yes. Our study has also demonstrated the presence of unique profiles of cytokine expression in the brain and CSF of subjects with autism. 

Two pro-inflammatory chemokines, MCP-1 and TARC, and an antiinflammatory and modulatory cytokine, TGF-ß1, were consistently elevated in the brain regions studied.
 MCP-1, a chemokine involved in innate immune reactions and an important mediator for monocyte and Tcell activation, and for trafficking into areas of tissue injury, appeared to be one of the most relevant proteins found in cytokine protein array 
studies. 

It was significantly elevated in both brain tissues and CSF. 

The presence of MCP-1 is of particular interest, since it facilitates the infiltration and accumulation of monocytes and macrophages in inflammatory CNS disease. 

Our immunocytochemical studies of the cerebral cortex and cerebellum showed that MCP-1 is produced by activated and reactive astrocytes, showing that these cells play an effector role in the disease process in autism. 

The increased expression of MCP-1 has relevance to the pathogenesis of autism as we believe its elevation in the brain is linked to microglial activation and perhaps also to the recruitment of additional macrophages and microglia to areas of neurodegeneration, such as those we observed in the cerebellum. 

9. . Is the elevation of MCP-1 unique to autism?

No. 

Our observations resemble findings in other neurological disorders in which elevation of MCP-1 is associated with the pathogenesis of neuroinflammation and neuronal injury. 

These diseases include HIV dementia, ALS, stroke and multiple sclerosis.

It remains unclear whether MCP-1 plays multiple roles in the CNS or whether its presence is only associated with inflammatory conditions.

It has been speculated that MCP-1 may be involved in neuronal survival and brain protection mechanisms in addition to monocyte activation and trafficking or even in
non-lymphocytic-mediated neuronal injury. 

Expression of MCP-1 in the CNS appears to be developmentally regulated, and previous studies have shown its expression in the cerebellum during prenatal development, a finding that may suggest an association with maturation of Purkinje cells. 

Like MHC-class II expression in microglia during CNS modeling, MCP-1 elevation in the brain of autistic patients may reflect persistent fetal patterns of brain development. 

10.What is the role of other cytokines found in the brain of autistic patients?

Our study found that other cytokines with pro-inflammatory and antiinflammatory effect were also increased in the brain of patients with autism. 

An example of anti-inflammatory cytokines is TGF-ß1, a key anti-inflammatory cytokine involved in tissue remodeling following injury. 

It can suppress specific immune responses by inhibiting T-cell proliferation and maturation and downregulates MHC class II expression. 

In our immunocytochemical studies, TGF- ß1 was localized mostly within reactive astrocytes and neurons in the cerebellum.

Purkinje cells that exhibited microscopic features of degeneration showed marked 
reactivity for TGF-ß1. 

These findings suggest that the elevation of this cytokine in autism may reflect an attempt to modulate neuroinflammation or remodel and repair injured tissue. 

11.What is the significance of the cerebrospinal fluid findings in autistic patients?

Cerebrospinal fluid (CSF) studies also confirmed a prominent inflammatory cytokine profile in patients with autism. 

The presence of a marked increase of MCP-1 in CSF supports the hypothesis that proinflammatory pathways are activated in the brain of autistic patients.

This increase in MCP-1 may be associated with the mechanisms of 

macrophage/microglia activation observed in the brain tissue studies.

The elevation of MCP-1 in the CSF resembles observations in other conditions in which microglia/macrophage activation is important, such as in HIV dementia and multiple sclerosis, diseases in which neuroinflammation plays a prominent role.

In addition to the marked elevation in MCP-1, the presence of elevated levels of IFN?, IL-8, IP-10, angiogenin and LIF strongly supports the view that active 
neuroinflammatory reactions and a network of multiple cytokines are likely involved in immune-mediated mechanisms in the CNS of autistic patients. 

These cytokines play important roles in immune mediated processes and their presence in the CSF in autistic patients may reflect an ongoing stage of inflammatory reactions associated with neuroglial activation and/or neuronal injury.

There was a greater increase in these cytokines in the CNS compared to the brain tissue. 

The reasons for the difference is unknown.

It could be that the brain cytokines are produced from neuroglial and neuronal sources as demonstrated by our immunocytochemical assessment. 

The cytokines in CSF could result from other sources of production, such as the meningeal lining around the brain or choroid plexus (where CSF is produced).

The persistent elevation of cytokines in CSF also might reflect a neurodevelopmental arrest, as some of the cytokines are normally elevated during phases of neurodevelopment. 

Since the CSF is easily accessible for clinical studies, CSF cytokine profiling may be useful in the future to diagnose, characterize and follow the clinical course of autistic disorders. 

12. If there is neuroinflammation in the brain of some autistic patients, is treatment with anti-inflammatory or immunomodulatory medications indicated? 

At present, THERE IS NO indication for using anti-inflammatory medications in patients with autism. 

Immunomodulatory or antiinflammatory medications such as steroids (e.g. prednisone or methylprednisolone), immunosupressants (e.g. Azathioprine, methotrexate, cyclophosphamide) or modulators of immune reactions (e.g. intravenous immunoglobulins, IVIG) WOULD NOT HAVE a significant effect on neuroglial activation because these drugs work mostly on adaptive immunity by reducing the production of immunoglobulins, decreasing the production of T cells and limiting the 
infiltration of inflammatory cells into areas of tissue injury. 

Our study demonstrated NO EVIDENCE at all for these types of immune reactions. 

There are ongoing experimental studies to examine the effect of drugs that limit the activation of microglia and astrocytes, but their use in humans must await further evidence of their efficacy and safety. [ End ]



"As a matter of course, every soul citizen of Earth has a priority to
quickly find and positively share evidence for healthy and safe food,
drink, environment, and society."

within the fellowship of service,

Rich Murray,
MA Boston University Graduate School 1967 psychology,
BS MIT 1964 history and physics,
254-A Donax Avenue, Imperial Beach, CA 91932-1918,
505-819-7388 cell,
619-623-3468 home,
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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 27 Jul 2013 at 7:00am
global epigenetic DNA methylation goes with insulin resistance in diabetic twins -- Jinying Zhao et al, Diabetes 2012 Feb -- fits WC Monte methanol formaldehyde toxicity paradigm: Rich Murray 2013.07.16
http://rmforall.blogspot.com/2013/07/global-epigenetic-dna-methylation-goes.html


Prof. Woodrow C. Monte, Food Science and Nutrition, Arizona State University, retired 2004, just sent me this article.

WC Monte first shared in fall 2007 a breakthrough paradigm for methanol formaldehyde toxicity, now at WhileScienceSleeps.com with full details and an archive of 782 free full text medical research references:

Briefly, only humans lack a functioning catalase defense system in the peroxisomes in their cells to carefully process formaldehyde as a normal part of normal metabolism.  

Of all creatures, humans are up to a hundred times more vulnerable to ingested methanol (wood alcohol), which goes in the blood with half-life 3 hours to all cells every minute, and, being a very small one-carbon molecule, readily enters all cells, where very quickly the ADH1 enzyme makes it into free floating, uncontrolled highly reactive formaldehyde, which promptly binds to and disables huge molecules of DNA, RNA, and proteins -- just as in its well known use in embalming and sterilizing.

In addition, this rampant formaldehyde acts as a potent epigenetic switch that randomly firmly attaches methyl groups to DNA and RNA, shutting down genes, and so causing complex cellular malfunctioning, birth defects, and later cancers.

Formaldehyde is too reactive to travel far in the blood, so ingested and inhaled formaldehyde is harmful only to the first tissues encountered -- by itself, it cannot reach all parts of the body.

Thus, the methanol acts as a "Trojan Horse" agent that allows deadly formaldehyde toxicity right inside cells in 20 specific tissues with high levels of ADH1 enzyme, including the isles of Langerhans in the pancreas, which make insulin -- when insulin production  is impaired, diabetes 2 slowly evolves.

This paradigm offers vital new vistas for safe, easy, low-cost prevention, diagnosis, treatment, and successful research in over 20 modern novel chronic "Diseases of Civilization".

The major sources of methanol are aspartame, cigarette smoke, fresh tomatoes, and unfresh fruits juices vegetables preserved wet at room temperature in sealed  cans jars plastic containers.

Epigenetic methylation research is surging now for many chronic diseases -- I quickly found 13 promising studies out of 110 since April 1 worldwide, listed in PubMed, and list them after selections from this article.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266395/
free full text 17 pages [ selections herein ]

Diabetes. 2012 Feb;61(2):542-6.
doi: 10.2337/db11-1048.
Epub 2011 Dec 30.

Global DNA methylation is associated with insulin resistance: a monozygotic twin study.
Zhao J,
Goldberg J,
Bremner JD, 
Vaccarino V.
Department of Biostatistics and Epidemiology, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. jinying-zhao@ouhsc.edu

Abstract

Insulin resistance (IR), the hallmark of type 2 diabetes, may be under epigenetic control. 

This study examines the association between global DNA methylation and IR using 84 monozygotic twin pairs.

IR was estimated using homeostasis model assessment (HOMA).

Global DNA methylation of Alu repeats in peripheral blood leukocytes was quantified by bisulfite pyrosequencing.

The association between global DNA methylation and IR was examined using generalized estimating equation (GEE) and within-twin pair analyses, adjusting for potential confounders.

Results show that methylation levels at all four CpG sites were individually associated with IR by GEE (all false discovery rate-adjusted P values≤0.026).

A 10% increase in mean Alu methylation was associated with an increase of 4.55 units (95% CI 2.38-6.73) in HOMA.

Intrapair difference in IR was significantly associated with intrapair difference in global methylation level.

A 10% increase in the difference in mean Alu methylation was associated with an increase of 4.54 units (0.34-8.71; P=0.036) in the difference in HOMA.

Confirmation of the results by intrapair analyses suggests that genetic factors do not confound the association between global DNA methylation and IR.

Exclusion of twins taking diabetes medication (n=17) did not change our results.

PMID: 22210312 [PubMed - indexed for MEDLINE] PMCID: PMC3266395 
Free PMC Article

Diabetes. 2012 February; 61(2): 542–546.
Published online 2012 January 17. doi:  10.2337/db11-1048
PMCID: PMC3266395

Jinying Zhao, 1
Jack Goldberg, 2,3
James D. Bremner, 4 
and Viola Vaccarino 5

1 Department of Biostatistics and Epidemiology, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
2 Seattle Epidemiologic Research & Information Center, Veterans Affairs Office of Research & Development, Seattle, Washington
3 Department of Epidemiology, University of Washington, Seattle, Washington
4 Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
5 Department of Epidemiology, Emory University School of Public Health, Atlanta, Georgia
Corresponding author: Jinying Zhao <jinying-zhao@ouhsc.edu>,

Copyright © 2012 by the American Diabetes Association.
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
This article has been cited by other articles in PMC.
Articles from Diabetes are provided here courtesy of American Diabetes Association


"Insulin resistance (IR) is the hallmark of type 2 diabetes and is also a characteristic feature of various cardiometabolic conditions, such as obesity (1), hypertension (2), and cardiovascular disease (CVD) (3).

IR results from the complex interplay between genetic and environmental factors. 

Despite significant effort, the understanding of the molecular processes underlying IR remains a major challenge.

Epigenetic mechanisms act at the interface between internal genetic makeup and external environmental factors.

Epigenetics provides an appealing explanation for many clinical features of IR (4), such as discordance within monozygotic (MZ) twins, relatively late age of onset, interindividual variation in disease severity, and the close relationship with lifestyle factors.

Therefore, epigenetic modifications, especially DNA methylation, may play a critical role in the pathogenesis of IR and its complications (5).

The human genome contains a large portion of repetitive elements, more than one-third of which are methylated (6).

Alu repeats, with >1 million copies per haploid genome, are the most plentiful families of repetitive sequences, representing >10% of the human genome sequence (7). 

Because of their high copy numbers throughout the genome, Alu repeats have been used as surrogate markers for estimating global DNA methylation levels (8). 

Alterations in global DNA methylation patterns have been associated with various human diseases, such as cancer (9), hypertension (10), CVD (11), and autoimmune disease (12).

Since epigenetic mechanisms are in part under genetic control (13), disentangling the role of epigenetic factors in disease etiology could be confounded by genetic factors in unrelated individuals.

MZ twins are matched on their DNA as well as many other known and unknown factors, thus providing an ideal sample for epigenetic research.

The goal of this study is to examine the association between global DNA methylation and IR within MZ twin pairs."


"Cigarette smoking was classified into current smoker (any number of cigarettes) versus never or past smoker.

A pack year was calculated by multiplying the number of packs of cigarettes a person has smoked per day by the number of years the person has smoked."


"DNA methylation levels of the two members within a pair were highly correlated at each of the four CpG sites (all P values <0.001).

The mean global methylation levels of the two twins within a pair were also significantly correlated (r = 0.46, P < 0.0001).

Regression analysis showed that intrapair difference in IR was significantly associated with intrapair difference in global DNA methylation level at two of the four examined CpG residues, after adjusting for differences in pack years, BMI, lipids, sBP, and depressive symptoms.

On average, a 10% increase in the difference in mean Alu methylation level was associated with an increase of 4.54 units in the difference in HOMA (95% CI 0.34–8.71; P = 0.036).

For both GEE and pairwise analyses, exclusion of twins receiving diabetes treatment did not change our results (Table 2).
[ much more... ]

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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 13 Jul 2013 at 4:56am
http://www.sciencebasedmedicine.org/aspartame-truth-vs-fiction/

[ In case you're interested in a skeptic's views on aspartame: ]

Aspartame – Truth vs Fiction
Posted by Steven Novella on September 15, 2010 (67 Comments)

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[ Continued ]

http://skeptoid.com/blog/2013/02/01/finally-proof-that-aspartame-will-destroy-your-kidneys/#comment-34092

Finally, proof that aspartame will destroy your kidneys?

2.1.2013 | by Josh DeWald

Hot on the heels of claims about a study that supposedly correlated aspartame with lymphoma, but that turned out to be “weak”, a 2011 study linking diet sodas to “increased kidney decline” has been making the rounds of the anti-aspartame sites. I am not sure why it took until early 2013 for it to start popping up on the various blog sites.The way that the conspiracy sites tell it, the study was damning and demonstrated that aspartame will pretty much kill your kidneys.


Some headlines:

  • “Diet Soda, Aspartame Shown to Destroy Kidney Function”
  • “Aspartame alert: Diet soda destroys kidney function”
  • “Aspartame and Kidney Damage”

What does the study say?

But what does the study actually say and how does it fit into the larger body of evidence?

As of this writing, the full text of the study (“Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women” by Julie Lin, published in Clinical Journal of the American Society of Nephrology)  is available for free, so anybody can read it without a subscription.

The results:

Consumption of ≥2 servings per day of artificially sweetened (diet) soda was independently associated with eGFR decline ≥30% (OR 2.02, 95% CI 1.36 to 3.01) and ≥3 ml/min per 1.73 m2 per year (OR 2.20, 95% CI 1.36 to 3.55). No increased risk for eGFR decline was observed for <2 servings per day of diet soda. No associations were noted between diet soda and MA or sugar soda and MA or eGFR decline.

With the simplified conclusion of:

Consumption of ≥2 servings per day of artificially sweetened soda is associated with a 2-fold increased odds for kidney function decline in women.

Basically, the study looked at the results of two tests that are associated with a decline in kidney function. One of them, Estimated Glomerular Filtration Rate or eGFR, had apparently a larger decline for diet than for sugar sodas. The other measure, microalbuminuria or MA, did not have a statistically significant effect for either sugar or diet drinks.

Looking deeper into the study content itself, their Table 3 presents the OR values for eGFR decrease (using <1 day to represent OR=1.0) but they do not present a direct comparison between sugar-sweetened and diet drinks for each level of consumption. They show the 1 to 1.9/day (OR 0.9) and >=2/day (OR 2.02) for diet, but only show >=1/day (OR 1.56) for sugar-sweetened. The authors note:”…only 3% of the women in our study consumed ≥1 sugar soda per day”, versus 22% for >=1 for diet soda, which would obviously generate a much smaller sample set. But it seems like it should have been possible to calculate the >=1 per day for diet soda to at least get a better comparison (and perhaps just show it in the footnotes of the table). Forgetting about any sort of comparison (i.e. pretending that we have essentially two separate studies), the granularity makes sense because it was only after 2/day of diet that the potential problem manifests. But, if the two were nearly identical at >=1,it would imply an issue with soft drinks in general, not specific to diet drinks.

But in any case, there is still the 2-fold (100%) increase in risk from >=2 per day which should be looked at. Also note that from 1 to 1.9 per day actually has an OR < 1 (the authors note “No association between lower levels of artificially sweetened soda intake and eGFR decline was seen, implying a threshold effect rather than one that increases linearly”). I doubt that actually means diet beverages have a “protective” effect. But what must also be noted is the 56% increase for >=1 of sugar sweetened. The study is touted as showing diet beverages to “destroy” kidneys, but nobody talks about the increased risk from sugar-sweetened soft drinks. And if I am at all right and combining the diet data to produce a >=1 figure, it would very possibly come very close to the sugar number.

A little statistical support

As I am certainly no statistical expert, I actually consulted a friend who provides statistical support for research at one of the UC schools, and the relevant parts of his response were (emphasis mine):

It is odd that they would evaluate and report the non-equivalent intakes…my guess is that they are justifying this non-equivalency by trying to show “proof of concept” that artificially sweetened soda is, at higher intakes, associated with increased risk.

But you are right that the odds ratio for artificially sweetened drink does not appear to be statistically different than the odds ratio for sugar soda. You can tell by the confidence intervals (CI) they report. The 95% CI is 1.36 to 3.01 for artificially sweetened, meaning that we can be 95% certain that the true OR in the population is somewhere between 1.36 and 3.01 (this range is due to the fact that we are dealing with a sample – the range would be smaller if the sample was larger and/or variance in the outcome was smaller)… the OR for sugar soda, by contrast, is 1.56 (with CI = .84 to 2.91), which is a value that is captured within the CI for artificially sweetened soda and thus not statistically different from it… So what they are saying is that, on its own, drinking more than 2 artificially sweetened sodas a day is associated with increased risk…But they cannot say that this risk is statistically greater than the risk of drinking 1 sugar soda a day…What does the OR look like for 2 or more sugar sodas a day? Seems like that would be important to know….

 

So this seems to mostly confirm my hunch that perhaps there should be more highlighting the result that consumption of carbonated soft drinks (sugar-sweetened or no) is correlated with a decline in kidney function, in women at least. The authors themselves actually point out that the diet link was not hypothesised so the study was not actually designed to test for that effect. Further studies may nullify it (or strengthen it). This study is in no sense a smoking gun that diet drinks are going to destroy your kidneys.

I want to quickly note that there were two previous studies (both mentioned by the current Lin study). A 2004 study based on the National Health and Nutrition Examination Survey found no association between diet sodas and kidney damage but some association with sugary sodas. A separate 2009 study based on the Multi-Ethnic Study of Atherosclerosis (MESA) also found no association of sugar-sweetened sodas for people with pre-existing chronic kidney disease (CKD).

In all cases the authors mention that it could be other factors in the lifestyle or the beverage itself which relate to the kidney decline, because the studies were not designed to actually figure out what is causing the problem. One crucial thing is that aspartame is never identified as the crucial factor in any of the studies.

Conclusion

So it seems that the analysis here should be tempered — if you consume a lot of sodas (sugary or not), you might be at increased risk for kidney damage versus not consuming soda. But this is not how the anti-aspartame sites present the data, and that is the problem. If anything, this is a great case for moderation, both in consumption and analysis. As is frequently the case with these sort of studies, it seems to warrant further studies specifically intended to isolate the reason for the decline, such as an ingredient common to both sugar-sweetened and artificially-sweetened.

REFERENCES
Lin, Julie, and Gary C. Curhan. “Associations of sugar and artificially sweetened soda with albuminuria and kidney function decline in women.”Clinical Journal of the American Society of Nephrology 6, no. 1 (2011): 160-166.

Shoham, DA, et al. Sugary soda consumption and albuminuria: Results from the National Health and Nutrition Examination Survey, 1999-2004. PloS ONE 3(10): e3431. doi:101371/journal.pone.0003431.

Bomback, AS, et al. Sugar-sweetened beverage consumption and the progression of chronic kidney disease in the Multi-Ethnic Study of Atherosclerosis (MESA). American Journal of Clinical Nutrition, 2009, 90:1172-8.

within the fellowship of service,


Rich Murray,

MA Boston University Graduate School 1967 psychology,

BS MIT 1964 history and physics,

254-A Donax Avenue, Imperial Beach, CA 91932-1918

rmforall@gmail.com

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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 10 Jul 2013 at 11:34pm
highly competent, pithy analysis of aspartame cancer study by Eva S.
Schernhammer at Harvard, William R. Ware, PhD, showing relevance of
Woodrow C. Monte methanol-formaldehyde toxicity paradigm: Rich Murray
2012.12.03
http://rmforall.blogspot.com/2012/12/highly-competent-pithy-analysis-of.html


Ethan Evers gives crisp summary of landmark study linking leukemia and
lymphoma in over 100,000 people using just 1.5 cans aspartame diet
soda daily for 22 years, Eva A. Schernhammer, Harvard expert team:
Rich Murray 2012.11.01
http://rmforall.blogspot.com/2012/11/ethan-evers-gives-crisp-summary-of.html


Eva A. Schernhammer cites Woodrow C. Monte methanol-formaldehyde
paradigm in brave, cautious Harvard team study that confirms more
cancers in aspartame diet soda users over 22 years -- full plain text:
Rich Murray 2012.10.27
http://rmforall.blogspot.com/2012/10/eva-schernhammer-cites-woodrow-c-monte.html


artificial sweeteners (aspartame): suggestive correlations with
multiple myeloma, non-Hodgkin lymphomas, leukemia in huge 22 year
Nurses' Health Study, Harvard, AJCN: Rich Murray 2012.10.24
http://rmforall.blogspot.com/2012/10/artificial-sweeteners-aspartame.html


California OEHHA sets methanol ingestion level 23 mg daily, same as from 1 can aspartame diet soda, 10 cigarettes, 3 tomatoes, or 4 cans green beans: Rich Murray 2013.07.03
http://rmforall.blogspot.com/2013/07/california-oehha-sets-methanol.html


fine critique by Josh DeWald of aspartame kidney harm survey, J Lin, GC Curhan 2011 -- now labs directly prove formaldehyde harm inside cells from blood methanol via ADH1 enzyme -- confirming methanol harm in alcoholics, lab study, E  Majchrowicz 1971 -- WC Monte paradigm: Rich Murray 2013.02.02
http://rmforall.blogspot.com/2013/02/fine-critique-by-josh-dewald-of.html

Josh DeWald, congratulations and thanks for an excellent, lucid, reasonable critique on this widely discussed study -- I will copy it to my blog  rmforall@blogspot.com .

Epidemiological studies seem to me to be mostly a waste of time, especially for methanol-formaldehyde toxicity disorders in humans:

1. ADH1 enzyme, which makes methanol into free floating formaldehyde right inside human cells, is itself free floating inside the cells of 19 specific tissues, especially the inner layers of blood vessels, the rods and cones of the retina, and in fibroblasts in skin and bone marrow -- thus there are as many different disorders, varying with the amount and pace of methanol ingestion, and a host of genetic, dietary, infectious, and toxic co-factors.

2. Folic acid in the blood offers some protection for some people, while many drugs and antibiotics impede folic acid function -- notably aspirin.

3. Ethanol, ordinary drinking alcohol, is a strong antidote for low levels in the blood, about an hourly oral dose of 3 ml 80 proof vodka, which in many people is provided by fermentation by bacteria in the GI tract (so the toxic "side effects" of antibiotics and many drugs may to some unknown degree be via disruption of this ethanol production, leading to formaldehyde toxicity within the cells of vulnerable tissues) -- other ethanol sources include most fruits and many vegetables, which strongly reduce the harm from their high levels of methanol.

Also, this explains the mystery that those who never drink have about twice the level of symptoms from many modern novel chronic diseases as those who drink about one shot (3 ounces volume) of 80 proof vodka daily, while larger daily doses lead to increased harm -- called the U-shaped curve -- which may be a major clue that chronic methanol-formaldehyde toxicity is involved.

Daily heavy drinkers end up with high blood methanol levels, as the ethanol stops the main process of methanol metabolism, so when in a lab experiment the high level of intake was stopped suddenly after two weeks, the resulting high blood methanol levels, with a half-life of 3 hours, dropping 16 fold in 12 hours, generated dangerous alcohol withdrawal symptoms that only started when blood ethanol, with a half life of 20 minutes, dropped 36 fold to effectively zero 16 hours after cessation, allowing the ADH1 enzyme to start making the methanol into formaldehyde within cells.

http://www.whilesciencesleeps.com/references/  745 free full texts

http://www.whilesciencesleeps.com/pdf/133.pdf
133.  Majchrowicz E. Biochemical Pharmacology of Ethanol.
New York: Plenum Press; 1973.

http://www.whilesciencesleeps.com/pdf/134.pdf
134. Majchrowicz E, Mendelson J.
Blood Methanol Concentrations During Experimentally Induced Ethanol Intoxication in Alcoholics.
The Journal of Pharmacology and Experimental Therapeutics 1971;179:293-300.

4. Few indeed know that the smoke from a pack of cigarettes gives as much methanol as a liter of aspartame diet soda -- so most of the long-term chronic symptoms of cigarette use may actually be evidence for methanol-formaldehyde toxicity: Alzheimer's, multiple sclerosis, atherosclerosis, and birth defects spina bifida, autism, preterm birth, many cancers, etc.

Methanol (wood alcohol) comes from wood smoke as well, while peat smoke gives three times higher doses -- hence highest world incidence of multiple sclerosis is in Scotland, where smoked fish is a daily staple.

5. So, modern methanol sources include:
aspartame,
smoke from cigarettes wood peat,
dark wines and liquors,
fresh tomatoes,
unfresh fruits juices vegetables cut up and preserved wet at room temperature in sealed cans jars plastic containers,
smoked, fermented, spoiled foods,
jams jellies marmalades,
mortuary medical chemical industrial facilities, especially wood and paper factories.

6. New precision methods now make it possible to directly confirm toxic formaldehyde products in tissues from methanol:

apoE4 protein scaffold allows growth of human neurons in lab,
Kwang-Min Kim et al, Brown U -- can test harm from formaldehyde made
from methanol by ADH1 enzyme inside cells of inner walls of brain
blood vessels, WC Monte paradigm: Rich Murray 2013.01.29
http://rmforall.blogspot.com/2013/01/apoe4-protein-scaffold-allows-growth-of.html


Initial tests could use micro gram amounts of formaldehyde to show the
typical processes of harm within neurons:

confirms WC Monte paradigm: ingested methanol becomes toxic
formaldehyde-induced hydroxymethyl DNA adducts in all tissues in rats,
sensitive C13 test, Kun Lu, James A Swenberg, UNC Chapel Hill
2011.12.08 Toxicol Sci: Rich Murray 2013.01.11
http://rmforall.blogspot.com/2013/01/confirms-wc-monte-paradigm-ingested.html

Then, if neurons can be grown along with small brain blood vessels,
with ADH1 enzyme free floating within the cells of the inner layers of
the vessels, the effects of formation of formaldehyde in situ from
micro grams of added methanol can be studied, confirming the WC Monte
paradigm, described in detail at www.WhileScienceSleeps.com and backed
by a free online archive of 745 full text medical research references.


Blood methanol concentrations during experimentally induced ethanol intoxication in alcoholics.
Edward Majchrowicz, Jack H. Mendelson.
J. Pharmacol. Exp. Ther. 179: 293-300, 1971.

[ comments by Rich Murray are in square brackets. ]

Abstract

Accumulation of methanol in blood was detected in alcoholic subjects during a 10- to 15-day period of chronic alcohol intake.

Blood methanol levels increased progressively from 2 to 27 mg/l from the 1st to 11th day of drinking, when blood ethanol concentrations ranged between 1500 and 4500 mg/l.

Blood ethanol was eliminated at the rate of 2720 +- 30 mg/l/hr within 14 to 18 hours after cessation of drinking.

Blood methanol levels decreased at the rate of 2.9 +- 0.4 mg/l/hr only after blood ethanol levels decreased to 700 to 200 mg/l.

Blood methanol disappearance lagged behind the linear disappearance of ethanol by approximately six to eight hours, and complete clearance of blood methanol required several days.

The pattern of accumulation and clearance of methanol and ethanol was similar for subjects who consumed either beverage alcohol (bourbon) or methanol-free grain alcohol.

Methanol probably accumulates in the blood as a result of competitive inhibition of alcohol dehydrogenese by ethanol, and the presence of endogenously formed methanol or its metabolites may contribute to the severity of intoxication and/or the alcohol withdrawal syndrome.

[ paper first presented at an April 1970 meeting ]

[ Probably these alcoholics smoked a lot in 1969 --

cigarettes were unrestricted in a small urban psychiatric hospital I worked in as a night therapist in 1988 in Santa Fe, New Mexico.

Few know that the smoke from a pack of cigarettes gives 60 mg methanol, 3 mg per cigarette...

Cigarettes correlate with many modern novel chronic diseases, including Alzheimer's and multiple sclerosis, atherosclerosis, many cancers, and birth defects spina bifida, autism, preterm birth, and fetal alcohol syndrome.

Methanol is actually less toxic than ethanol, unless it meets up with any ADH1 enzyme inside cells without any ethanol present, which quickly turns methanol into toxic formaldehyde inside the cells of 19 specific human tissues, including liver, brain, retina, skin, fetus.

During high daily use of ethanol, the ADH1 enzyme is preoccupied, so it cannot turn blood methanol from any source into formaldehyde, so blood methanol levels rise and rise, not causing any symptoms -- this probably caused much of the increase in blood methanol with large ethanol intake for two weeks.

Without any ethanol, the blood half-life of ethanol is still just 1/3 hour, while the blood half-life of methanol is 3 hours, so every 9 hours, the ethanol falls 27 times, while methanol blood levels would fall 8 fold, but if the men increase their smoking, the methanol levels decline only a little, as happened to many male alcoholics in this study.  After about 16 hours, the ethanol is zero, and then the remaining methanol is quickly made into highly toxic formaldehyde right inside cells by the ADH1 enzyme.  If then the patient is too sick to eat or smoke, he will not be taking in any more methanol, which will drop to 1 mg/l, sometimes a few days later.

Methanol also comes from the pectins in unfresh fruits juices vegetables cut up and preserved wet at room temperature in cans jars plastic containers -- i.e. classic institutional diet.. ]


[ 19 male alcoholics were given 32 ounces by volume of 50% ethanol drink for 10 - 14 days in a closed hospital ward -- blood methanol was measured with 1.0 mg/l accuracy -- 

...All samples from the subjects before the commencement of drinking and three to four days after the cessation of drinking, and from control subjects, had negligible amounts of methanol, whereas the subjects had variable amounts of methanol during the experimental drinking period....

...During the predrinking period, blood methanol levels were always less than 1.0 mg/l. [ 1 ppm ]

On the first day of drinking, blood methanol concentrations were between 1 and 2 mg/l when the mean range of blood ethanol concentrations ranged between 55 and 3540 mg/l.

As drinking continued, mean blood methanol levels ranged between 11 and 27 mg/l when the mean blood ethanol concentrations were between 1570 and 4350 mg/l.

On a few occasions, blood methanol concentrations of 40 mg/l or more were detected in subjects whose blood ethanol concentrations exceeded 5000 mg/l.

[ These methanol blood levels of 11, 27, and 40 or more ppm are the levels that, made by ADH1 enzyme into formaldehyde inside cells in 19 specific human tissues, especially brain blood vessels and the retina rods and cones, may well be the main trigger for the gamut of painful symptoms of alcohol hangover, "the morning after the night before". ]

Although blood ethanol levels fluctuated daily, they were  usually high enough to induce and maintain a significant degree of clinical intoxication.

Blood methanol and blood ethanol concentrations after cessation of drinking are shown in Figure 2.

Blood ethanol values ranged between 2000- and 4000 mg/l at the initiation of the withdrawal period.

Usually, ethanol was not detected in the blood after 14 to 18 hours following cessation of drinking.

However, in a few subjects traces of ethanol approximating 10 mg/l were detected up to 20 hours after ethanol withdrawal.

The concentration of blood methanol remained relatively constant in both groups of subjects until blood ethanol levels decreased to approximately 200 mg/l.

At this blood ethanol level blood methanol concentrations began to decline and, in most instances, blood methanol was cleared within two days after cessation of drinking.

However, in a few cases disappearance of accumulated methanol did not occur until three or four days after termination of drinking.

Figures 3 and 4 present typical blood methanoI and blood ethanol curves as a function of time during drinking and withdrawal for subjects who consumed either bourbon or grain alcohol.

[ Figure 3 shows the data for a bourbon drinker, whose ethanol peaked at  3400 mg/l , and methanol at 24 mg/l, while only after 11 hours after cessation, when ethanol was down to 200 mg/l   and methanol 19 mg/l, until 3 hours later, 14 hours after cessation, with ethanol reaching zero, and methanol falling to 7 mg/l, do we see the abrupt conversion of most of the methanol into formaldehyde, reaching the last measured methanol value of about 1 by about 5 more hours, about 19 hours after cessation -- the authors are not gifted at making clear graphs.

Figure 4 shows the data for a grain alcohol drinkers, whose ethanol peaked at 4500 mg/l, and methanol at 15 mg/l, while only after 16 hours after cessation did ethanol levels fall to zero, with methanol levels then falling steeply from 15 to 1 mg/l 8 hours later, 24 hours after cessation.

We can only speculate how much less they may have eaten and smoked during two weeks of intoxication, and a severe alcohol withdrawal syndrome for a day or two -- hospital food and cigarettes would prolong the methanol-formaldehyde toxic syndrome. ]

Blood methanol levels increased progressively from 2 mg/l on the first day of drinking to 23 mg/l in the bourbon subjects by the 11th day of drinking.

A similar pattern of ascending blood methanol levels is related to the duration of ethanol ingestion.

The concomitant pattern of increase in blood methanol levels was highly consistent and was categorized into four phases.

Low methanol concentrations were found during the first day of drinking (phase I), but as drinking continued, methanol levels progressively increased (phase II).

The highest levels of blood methanol were found at the termination of the drinking period.

After alcohol withdrawal, blood methanol levels remained relatively stable for about 15 to 18 hours (phase III), but when blood ethanol levels decreased to approximately 700 to 200 mg/l, methanol levels began to decline (phase 1V).

Thus, blood  methanol disappearance lagged behind the linear disappearance of ethanol by approximately six to eight hours, and complete clearance of blood methanol accumulation and elimination in grain alcohol drinkers was similar to that of bourbon drinkers.

...methanol content varied between 40 and 55 mg/I of bourbon.

This value is comparable with those reported by the distillers.

The concentration of methanol in 50% grain alcohol was approximately 1 mg/l.

Average daily consumption of bourbon or grain alcohol was 649 and 781 ml/subject; respectively.

Assuming the mean concentration of methanol in the bourbon is 48 mg/I the daily ingestion of methanol was 31 mg/man.

After absorption and equilibration, this dose of methanol would result in a concentration of 6 mg/kg of body water in a 70-kg man.

[ So, 60 mg methanol from smoke from a pack of cigarettes would lead to twice as much, 12 mg/kg of body water in a 70-kg man. ]

[ Probably these alcoholics smoked a lot in 1969 -- cigarettes were unrestricted in a small urban psychiatric hospital I worked in as a night therapist in 1988 in Santa Fe, New Mexico.  Few know that the smoke from a pack of cigarettes gives 60 mg methanol, 3 mg per cigarette... Cigarettes correlate with many modern novel chronic diseases, including Alzheimer's and multiple  sclerosis, atherosclerosis, many cancers, and birth defects spina bifida, autism, preterm birth, and fetal alcohol syndrome.  ]

Furthermore, if the amount of ingested methanol were unaffected by such variables as the intervals of drinking, the rate of drinking, excretion and metabolic processes, the mean concentration of methanol after 14 days of drinking would be  8.4 mg/kg of body water.

It is also calculable that the amount of methanol derived from grain alcohol would be undetectable through most days of drinking.

It is suggested, therefore, that the presence of small amounts of methanol in the bourbon may explain a somewhat higher blood methanol level in the bourbon drinkers as compared with the grain alcohol drinkers, but not the maximal amount of methanol accumulated with either beverage.

Therefore, these data suggest that most of the methanol found in the former group of drinkers and virtually all of the methanol found in the latter group is derived from endogenous sources.

Discussion

Accumulation of methanol in blood was detected in all subjects studied during chronic ethanol intake.

Blood methanol levels were only slightly higher in the bourbon drinkers than in the grain alcohol drinkers.

This may be explained by the greater content of methanol in the bourbon (40-55 mg/l) as compared to the grain alcohol used (1 mg/l).

However, the exogenous source of methanol cannot account for the amount of methanol that accumulated in the blood, which suggests that a major fraction, if not all, of the methanol was more than likely derived from endogenous sources.

It remains to be established if the methanol-producing enzyme system described by Axelrod and Daly (1965) is capable of producing quantities of methanol in blood similar to those found in this study.

Data obtained in this study do not eliminate the possibility that methanol may be derived in part from metabolic processes involving intestinal flora.

What are some possible mechanisms which may underlie the accumulation of blood methanol during chronic ethanol ingestion?

Although both ethanol and methanol can be oxidized by catalase and alcohol dehydrogenase, there are differences in the major metabolic pathways which affect the disposition of these two alcohols.

Tephly et al. (1964) showed that the peroxidative system involving hepatic catalase had played a major role in methanol oxidation in the rat.

Kimi and Cooper (1961) found that the alcohol dehydrogenase system and not the catalase-peroxide system was responsible for the physiological oxidation of methanol in the monkey.

These data have been confirmed in subsequent studies by Goodman and Tephly (1968).

In addition, studies of Mani et al. (1970) indicate that human alcohol dehydrogenase oxidizes methanol at approximate 1/10 of the ethanol rate.  [ Thus, the half-life in human blood for methanol is 3 hours, while for ethanol is 1/3 hour. ]

[ Mani JC, Pietruszko R, Theorell H.
Methanol activity of alcohol dehydrogenases from human liver, horse liver, and yeast.
Arch Biochem Biophys. 1970 Sep;140(1):52-9.
PMID: 4318994 ]

The Km values of 6.8X10E-6 M (330 mg/l) and 1.5X10-4 M (91 mg/l) for methanol and ethanol, respectively, found for human liver alcohol dehydrogenase have good correspondence to the noncompetitive concentrations of ethanol found in this study (approximately 200 ml/l).

Since both methanol and ethanol are metabolized by the same enzyme systems, ethanol competitively inhibits the oxidation of methanol, it is likely that methanol accumulates in the blood, because of competitive inhibition of the enzyme which metabolizes both alcohols.

This conclusion is supported by the finding that during the early part of the withdrawal phase, blood methanol levels remained relatively constant until blood ethanol levels declined from approximately 700 to 200 mg/l. 

We also observed that when alcohol consumption was temporarily interrupted or decreased during the phase of continuous drinking (Fig. 4), blood methanol levels remained relatively unaffected if blood ethanol concentrations were above 700 to 200 mg/l.

These findings suggest the enzyme which catalyses the metabolism of both methanol and ethanol is saturated by relatively low concentrations of ethanol.

Our data also indicate that levels of blood methanol are related to the concentrations of blood ethanol with time.

At the present time it is not  possible to define any definitive relationship between the degree of intoxication observed during chronic ethanol ingestion and the accumulation of methanol in blood.

Similarly, it is difficult to determine the contrilbution of methanol catabolism to the alcohol withdrawal syndrome after cessation of alcohol ingestion.

This question can only be answered by careful correlative studies of clinical phenomena and methanol metabolism in alcoholics after a period of experimentally induced alcohol intake and withdrawal.

Such studies are  currently underway in our research ward and laboratory. 

Conclusion

Accumulation of methanol in the blood of alcoholics was detected during long-term voluntary consumption of both bourbon and grain alcohol.

Blood methanol levels are dependent upon time and dose-related concentrations of ethanol, suggesting that it accumulates as a result of competitive inhibition of alcohol dehydrogenase by ethanol.

In both groups of drinkers the blood methanol may be derived in part from endogenous sources.





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Rich Murray
http://rmforall.blogspot.com
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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 10 Jul 2013 at 11:23pm
skeptic Josh DeWald often sides with industry PR while finding flaws in many common anti aspartame claims in video "Sweet Misery", Cori Brackett: Rich Murray 2013.07.10

http://rmforall.blogspot.com/2013/07/skeptic-josh-dewald-often-sides-with.html



I support vigorous  civil debate by all points of view, based on reason and public evidence, so I am making many discussions more available here.



http://www.soundandfury.tv/  Cori Brackett


1 hour 34 minutes


interview 2013.01.28

My guest for this interview is Cori Brackett, creator of the powerful and thought-provoking documentaries Sweet Misery and Sweet Remedy.

Cori talks about her own experience of being diagnosed with multiple sclerosis and describes how, through her research, she came to believe that the artificial sweetener aspartame played a significant role in her illness. ]



MercolaWatch: The Sweet Misery documentary

7.5.2013 | by Josh DeWald

I have intentionally been trying to avoid posting about aspartame, but Joe Mercola recently posted a reference to the relatively old Sweet Misery anti-aspartame documentary which I have already seen more times that I would like and responded to. This documentary features interviews with the main players in the anti-aspartame movement, who make statements that simply are not supported by the evidence. On my other blog, I have a 2-part “fact check” (Part 1Part 2) of the documentary.

Sweet Misery Fact Check – Part 1

Posted on July 8, 2011 by Josh DeWald

There is an HTML version available at  http://tinyurl.com/sweetfact1

A PDF version is available at:


Sweet Misery Fact Check – Part 2

Posted on August 3, 2012 by Josh DeWald 



Aspartame and Formaldehyde (or not…)

Posted on June 13, 2010 by Josh DeWald

long detailed critique with vigorous debate by 162 Responses

A possibly easier to read version of this better for pinting is available at  http://40two.org/Aspartame_Formaldehyde.pdf

There is also a separate entry which is a response to a Joe Mercola article posted to the Huffington Post which repeated some of the claims refuted here, as well as some additional ones. ]


If you have seen the documentary and read the article I urge you to take a look at my existing responses, but here I will offer a quick rundown of some of the key claims and responess.

Sweet Misery includes many heartfelt conversations with aspartame victims….”

This line about summarizes the bulk of the documentary: anecdotes. It features virtually nothing in the way of science, but is filled with stories from people that believe that they have been harmed by aspartame or from “experts” that can explain why someone would be harmed from aspartame. But it generally amounts to conspiracy theories or hypotheses that have already been studied and rejected by the scientific community.

Multiple Sclerosis

While Mercola only briefly mentions it, the documentary spends a lot of time discussing the alleged link between aspartame and multiple sclerosis (as well as some other disorders for which scientists honestly do not know exactly what causes it or how to cure it, such as fibromalgia).

This is in my Part 1, but there is simply no evidence that would link MS with aspartame. The only mention of aspartame on the National Multiple Sclerosis Society’s is on their page “Old Theories That Have Been Disproved“. Suffice to say they do not support the association and do not advise their members against aspartame. The Multiple Sclerosis Foundation also has a page “Examining the Safety of Aspartame” where they essentially call it out as all starting with an internet hoax post from “Nancy Merkle” and note that “aspartame appears to be quite safe” (aside from possible mild side effects in some people).

As to the multiple claims in the documentary, and Internet-at-large, saying that when they stopped consuming aspartame their symptoms went away, it turns out that the most common form of MS, known as Relapsing-Remitting, is actually known to go into spontaneous remission for months, years, or even completely

Brain Tumors

The documentary spends some time discussing the famous study by JW Olney to the effect that there was a dramatic rise in brain tumors following the introduction of aspartame into general use. The National Cancer Institute and French Food Safety Authority both slammed the study. The National Cancer Institute notes that had Olney included more years from before the introduction of aspartame, the graphs would have clearly shown brain cancers rising “8 years prior” to the introduction of aspartame, and this mainly in older people 70 or older. The French authority echoes that, adding that brain cancers actually stabilised in the mid-80s when aspartame came out.

So deeper looks at the data just don’t support the link between aspartame and brain cancer.

Blood Cancer (Lymphoma)

I don’t recall it from the documentary, but Mercola mentions the recent lymphoma study which he says finds a “clear association” between aspartame and lymphoma. I wrote about this study when he originally cited it. I will simply requote the study author’s own conclusions:

Although our findings preserve the possibility of a detrimental effect of a constituent of diet soda, such as aspartame, on select cancers, the inconsistent sex effects and occurrence of an apparent cancer risk in individuals who consume regular soda do not permit the ruling out of chance as an explanation.

Brigham and Women’s Hospital, who’s PR department promoted the study actually essentially apologizedbefore it was even published:

It has come to our attention that the scientific leaders at Brigham and Women’s Hospital did not have an opportunity, prior to today, to review the findings of the paper,[...] Upon review of the findings, the consensus of our scientific leaders is that the data is weak, and that BWH Media Relations was premature in the promotion of this work. We apologize for the time you have invested in this story

“Clear association”? Hardly. But Mercola and others will likely continue to cite it as strong evidence, without any sort of caveat.

Methanol Toxicity

In Mercola’s notes, he discusses the claim that humans are incapable of properly processing methanol and, therefore, aspartame is dangerous. Amazingly, Mercola does not even do the typical anti-aspartame play that all the other foods that have methanol as a breakdown product (such as fruits, vegetables, wine) are “special”.

Methanol (methyl alcohol) is of course dangerous when taken in large acute doses. There does not appear to be any build-up whatsoever of formic acid in the body (Stegink 1978) (it is excreted in urine) for normal consumption of aspartame. Only someone with the inability to process the formic acid/formate out of their system would be reasonably expected to have issues with aspartame and products that breakdown into methanol. I discuss this in the “Part 1″ linked above as well as in another article (which was actually my first on aspartame, and now has quite a few comments on it of anti- and pro-aspartame folks battling it out which turns out to be quite interesting).

Thousands of complaints, 90+ symptoms

Another of the standard tactics of the anti-aspartame folks is to state that there are “more than 10,000 complaints” involving 90+ symptoms (usually it’s cited as 92, but Mercola says 91). As readers of this blog are probably now aware, filing a report with the Adverse Event Reporting System (AERS, with vaccine equivalent VAERS) is not even remotely equivalent to being evidence or proof of harm. They are merely data points. You can download them in fact (good luck finding aspartame listed, or on the “potential hazards” list), and have no use until properly analyzed and investigated. A 1992 investigation (making use of the actual patient data and their consumption patterns as well as direct “challenge tests”) into the seizure-related AERS data found no association with aspartame.

Walton’s list of “independent” studies against aspartame

I chuckle a little bit every time this list gets mentioned. The film has Walton himself mentioning it. If what he had found was in fact 97 studies against aspartame, that would be something. But he did not. Not even close. I classified the entries on a Google Spreadsheet and discussed in “Part 2″ of my look at the documentary before as well as in a prior article on aspartame and formaldehyde . At best, five — 2 on seizures, 1 on headaches, 1 a famous debunk’d study, and another was not able to be reproduced — of them could be considered both peer-reviewed and relevant to aspartame. The rest are about methanol generically, find no harm (not sure why he includes these) or are just letters to the editor and case studies. I urge anybody who takes the documentary at face value on this point to look at the full list to see if it really represents evidence against aspartame.

Shenanigans during approval process

  • “Covered up” Waisman monkey study – Waisman actually died before the study was completed , but Searle still submitted the data they had to the FDA (so certainly not “covered up”). Seizures occurred in the medium and high dose groups (100 and 120x maximum daily intake). However, same can be induced using equivalent amounts of phenylalanine (one of the components of aspartame).
  • FDA commissioner “illegally” overruled Board of Inquiry decision – Not illegal, the Board of Inquiry is not a legal body (Code of Federal Regulations Title 21, Subpart B, S. 13.30). The commissioner felt that there had been ample demonstration of safety. Additional details can be read in the Government Accounting Office’s 1987 report on the approval process of aspartame.
  • “Clear conflict of interest” when Searle paid for independent analysis – FDA required them to pay for the study by UAREP. It was in no way sponsored by Searle.
  • Reagan’s first executive order removed FDA’s ability to prevent marketing of aspartame – This never happened (Federal Register).

Conclusion

As popular as it is, Sweet Misery is not an accurate portrayal of the scientific evidence regarding aspartame. It is full of anecdotes that do not stand up to scrutiny. It presents a series of conspiracy theories about the approval process, but offers no substantiation. I would recommend only watching the movie if you want to see what a long string of anecdotal evidence looks like (sincerely believed though they may be, I have no doubt about the honesty of the people portrayed in the film). The main part of the film I have not covered is the claim that Diane Fleming was wrongly convicted of murdering her husband via methanol poisoning (the documentary, not surprisingly, alleges that he was killed from aspartame in has gatorade and diet drinks).

Tagged in aspartame / mercola

About Josh DeWald  ,

I am a software engineer, husband and parent of two. I have been involved in the Skeptical movement for a few years now, especially since having children and so needing to fight pseudoscience related to parenting (vaccines, homeopathy, etc). I've been fortunate to attend TAM twice with my wife (who is also of a Skeptical bent). I also have a blog known as "What Does the Science Say?" ( whatdoesthesciencesay.wordpress.com ), where I have an odd habit of writing a lot about aspartame.





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Post Options Post Options   Thanks (0) Thanks(0)   Quote RichMurray Quote  Post ReplyReply Direct Link To This Post Posted: 10 Jul 2013 at 6:13am
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
http://rmforall.blogspot.com/2012/03/methanolformaldehyde-paradigm-for.html
http://health.groups.yahoo.com/group/aspartameNM/message/1642


http://www.whilesciencesleeps.com/multiple-sclerosis-the-solution/

Multiple Sclerosis: The Cause and the Solution Uncovered -- at Last!

An exhaustive analysis of the medical and scientific literature,
authored by a uniquely qualified food scientist, persuasively reveals
the cause of MS and describes a path to recovery and prevention.

The symptoms of Multiple Sclerosis are identical to those of an
uncommon form of poisoning -- methanol poisoning.
Individuals who have been exposed to this poison over a long period of
time, in fact, develop MS.
This poison -- methanol -- is a major component of cigarette smoke,
which, until now, has been the only known cause of Multiple Sclerosis.

Dr. Monte's compelling work reveals that this poison is also contained
in certain foods that are canned and smoked or have had the insidious
sweetener, aspartame, added to them.
Unfortunately, the truth has been obscured due to the fact that
methanol is a poison only to humans and not to (laboratory) animals.

If you have MS, or love someone who does, you and your physician
should read what Dr. Monte has to say about methanol and its link to
MS.
To expedite the free exchange of what might be lifesaving information
about this disease, there is a file attached below to his website that
contains a full copy of Chapter 9 of his book, While Science Sleeps.
This chapter examines the cause of MS and posits the simple dietary
changes that can save your life.

Download a free copy of Chapter 9 and have a read
[ 99 pages, including list of all 740 full text online references for
book -- Chapter 9 has 146 references ]:

http://www.whilesciencesleeps.com/files/While%20Science%20Sleeps%20-%20Chapter%2\
09%20(Prepublication%20copy)%20Website%203-15-2012.pdf

The references are located on his website:

http://www.whilesciencesleeps.com/references/ ,

as are the simple dietary changes that you must follow because your
life may depend on it:

http://www.whilesciencesleeps.com/monte-diet/ .

Everything you need to know about MS is in Chapter 9.
If you are interested in knowing more about methanol poisoning and its
link to other diseases of civilization, you will want to read the
entire book, While Science Sleeps, by Woodrow C. Monte PHD, Emeritus
Professor of Nutrition and Food Science, Arizona State University.

Chapter 9:
Multiple Sclerosis

The Conflagration that is Multiple Sclerosis;
Listening to Nature’s Whispers;
The Scene of the Crime;
Location, Location, Location;
Details of Plaque Formation;
The Look, Touch, Taste and Smell of Multiple Sclerosis;
The Kitchen Autopsy;
The Cause of MS is within the Thickening Blood Vessels;
Symptoms Mean Little Unless They Are Identical in All Ways…Then They
Mean Everything!;
Learn a Little About Arginine;
Myelin Basic Protein (MBP);
Looking for the Shadow of Formaldehyde;
“Woody… They Have Done Our Experiment for Us.… But They Just Don’t Get It!”;
Finding the Shadow of Formaldehyde in the MS Brain: The Smoking Gun (a
Triple Blind Study);
Evidence That Methanol Causes MS;
The Etiology of Multiple Sclerosis -- Follow the Methanol;
A Food Scientist’s Nightmare Called Aspartame;
MS: a Disease of Colder Climates and Flush Toilets -- Before Aspartame;
A World Awash in MS after Aspartame;
Change in Frequency of MS by Sex:
the Methanol Source -- Food or Smoke -- Makes All the Difference;
Can Methanol Really Cause MS?;
MS Can Be Found in Some Places, but Cannot be Found in Others;
Industrial Exposure to Methanol -- Jobs that Can Last for an Eternity;
Teachers’ Paradigm;
MS Treatment -- Pharmaceutical Placeboes or Perhaps Worse;
Conclusion and Review;

Conclusion and Review

You can see for yourself now that the daily administration of methanol
to the human organism does not go unnoticed by the immune system.
The evidence is simply far too overwhelming for the pharmaceutical
industries to credibly justify ignoring it any longer.
As a scientist I can do little more than present a coherent molecular
theory, and then prove the hypothesis using three paradigms with two
distinct methods of methanol administration.
Viewing methanol toxicity as the etiologic cause of MS answers all of
the nagging questions and unexplained anomalies that have stalled the
search for the cause of this disease.
I realize that absolutely nothing can convince the pharmaceutical
giants, who are now heavily invested in developing their own useless
palliatives for MS, to give them up and rally around the methanol
hypothesis.
In the end, however, I believe that the truth will win out.
Henry Miller prophesied over 50 years ago:
It is possible that the cause of multiple sclerosis lies buried
somewhere in these lengthy protocols waiting to be found by someone
ingenious enough to unearth it.[#306]

Review

1. MS is a disease that begins around brain blood vessels, adjacent to
the exact locations where methanol converts to formaldehyde, very much
like Alzheimer’s Disease.

2. MS was first discovered long before formaldehyde, making the
determination of its cause impossible.

3. The vast majority of early researchers believed that the cause of
MS was a “toxic substance” that forms in and is distributed via the
blood vessels of the brain. “Whatever is being produced within the
vessel walls is the cause of the disease.”

4. All symptoms of MS can be found during the course of methanol
poisoning if the patient lives long enough.

5. Myelin Basic Protein (MBP) is the protein of the myelin sheath that
is removed during MS plaque development.
MBP contains a high percentage of arginine, which acts as a trap for
formaldehyde.
The MBP of MS patients has been shown to have reacted with
formaldehyde and cause a marked increase of the methylation of its
arginine.

6. The MBP of MS brain tissue has been shown to be severely deficient
in phosphorylation, which we know can be caused by formaldehyde.

7. The Smoking Paradigm: Cigarette smoke is high in methanol and is
the only etiological cause of MS that is generally accepted by the
scientific community.

8. Consistent circumstantial evidence links increases in
methanol-containing food consumption and in industrial use of methanol
to corresponding increases in MS incidence during the transition from
the 19th century into the 20th century.

9. The advent of aspartame, a methanol carrier, has introduced an
opportunity to quantify additional methanol in the food supply since
1981.

10. The Aspartame Paradigm: statistics show convincingly that as more
and more aspartame is consumed by the US population the incidence of
-- and perhaps more importantly the death rate from -- MS has also
increased dramatically.

11. The higher incidence of MS in colder climates was due to the
higher consumption levels of canned fruits and vegetables in temperate
climates.
This began reversing shortly after methanol-containing diet sodas and
other thirst quenching products became popular and inexpensive in the
tropics.

12. MS was at one time a disease of men when it was caused by
industrial contact.
It is increasingly more of a women’s disease.
When methanol is inhaled as a gas during cigarette smoking or
industrial contamination the distribution tends to be equal between
the sexes.
The stomach of the man, however, has 4 or 5 times more ADH in its
lining than that of a woman.
When methanol is consumed via diet soda, the ADH removes methanol
before it can get to the brain, so less of it reaches men’s brains
than women’s brains.
As more and more methanol has become a dietary poison, the shift from
male to female disease has followed.

13. The Faroe Islands are surrounded by countries with very high
incidence of MS, yet the country traditionally did not have the
disease represented in its population until after the occupation of
large numbers of British Troops during the Second World War.
Faroes have no trees or peat deposits and, therefore, developed
methods to salt and air dry fish and other meats for preservation,
unlike its neighbors, who dine on smoked foods at each meal.
The indigenous diet of the Faroans contains no methanol.

14. The Village of Wellington, Ohio experienced an epidemic of MS that
should have been traced to the escape of methanol fumes from a
foundry, affecting the populace located downwind of it.

15. Professions such as shoe making and papermaking that have been
shown to have high incidence of MS can also be shown to have exposed
their workers to levels of methanol.

16. The Teaching Paradigm:
The US teaching profession might just be the best profession to use to
link methanol exposure to increased incidence of MS.
Secondary school teachers suffer an incidence of MS almost twice as
high as their professional counterparts.
They also can be shown to have had consistent workday exposure to
methanol fumes by the ubiquitous use of Ditto machines that use high
concentrations of methanol as a print transfer agent.

It has been over 30 years since I heard my first unsolicited plea for
help from an aspartame consumer who had linked consumption of the
product to her suffering. My first thought after an hour’s listening
was that this courageous young woman would soon be diagnosed with
Multiple Sclerosis.
It is in her honor and in the memory of my friend from Wellington,
Colorado that I seek to explain the compelling link between methanol
and MS.


[ http://www.whilesciencesleeps.com/pdf/224.pdf

224. Kim J, Mastronardi F, Wood D, Lubman D, Zand R, Moscarello M.
Multiple Sclerosis: An important role for post-translational
modifications of myelin basic protein in pathogenesis.
Molecular & Cellular Proteomics 2003;2(7):453-62.

http://www.ncbi.nlm.nih.gov/pubmed/12832457 abstract

http://www.mcponline.org/content/2/7/453.full?sid=4999b20c-f767-4934-88e4-7a8cc4\
1ee4ca
free html rich full text version ]


The Monte methanol paradigm posits a simple, obvious major co-factor
for many novel diseases of civilization -- vastly increasing the
opportunity for extremely positive social service via avoiding all
methanol sources: Rich Murray 2012.02.06

Methanol from smoking and aspartame, in humans alone, is always made
into formaldehyde via the ADH enzyme inside the cells of blood vessels
and many tissues -- a little alcohol protects.

Many novel diseases of civilization result since 1800 -- heart,
stroke, Alzheimers, cancers, MS, autism, spina bifida -- increasing
rapidly with aspartame since 1981.


4 more positive reviews for While Science Sleeps, Prof. Woodrow C.
Monte, on Amazon.com: Rich Murray 2012.02.26
http://rmforall.blogspot.com/2012/02/4-more-positive-reviews-for-while.html
http://health.groups.yahoo.com/group/aspartameNM/message/1641


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 Amazon.com: Rich Murray
2012.01.26
http://rmforall.blogspot.com/2012/01/while-science-sleeps-methanol-from.html
http://health.groups.yahoo.com/group/aspartameNM/message/1636


new book, concise opus "While Science Sleeps" life saving facts re
aspartame (methanol, formaldehyde) -- 740 full text references are
free online -- Woodrow "Woody" C. Monte, retired Prof. of Nutrition,
Arizona State University: Rich Murray 2012.01.03
http://rmforall.blogspot.com/2012/01/new-book-concise-opus-while-science.html
http://health.groups.yahoo.com/group/aspartameNM/message/1631

www.WhileScienceSleeps.com

$ 37.98 text 236 pages -- 745 full text references free online --
Kindle electronic book, $ 9.80

http://www.amazon.com/review/RNGG3O7U33VCV


Rich Murray,
MA Boston University Graduate School 1967 psychology,
BS MIT 1964 history and physics,
254-A Donax Avenue, Imperial Beach, CA 91932-1918
rmforall@gmail.com
505-819-7388 cell
619-623-3468 home
http://RMForAll.blogspot.com

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