Archive for the ‘Toluene’ Category

“It sort of blew our minds,” Robinson said.

For the record I am not posting this as Chemtrail article, that is something that I consider on the “fringe” but don’t let that offend you, we all have to make our own choices. I try to keep this site rooted in the believable so as to lend credibility to our effort. That being said I often notice the skies clear in the morning and then totally clouded over by jet contrails by evening and wonder “Just how much polution we are being exposed to?” I know it wasn’t like this when I was a child.

Interestingly, our friend Toluene shows up here yet again.

PITTSBURGH – A ground breaking study from a U.S. university has shed light on how the sun transforms jet engine exhaust, potentially creating toxic particles, reported Friday.

Researchers have discovered that drops of oil created by idling aircraft engines can over time turn into tiny particles that can easily penetrate the lungs and brain.

The surprising discovery has been detailed in the latest edition of the Atmospheric Chemistry and Physics Journal.

In the first study of its kind, experts from the Carnegie Mellon University in Pittsburgh, Pa., collected pollution from an idling commercial plane as it operated at different loads.

When the jet operated at full power the emissions were composed of mainly solid particles, however when it idled on the runway they took on a different form—microscopic droplets.

When the exhaust was exposed to sunlight in a “smog chamber” a chemical reaction took place that saw the formation of toxic particles from the interaction between the oil and gases.

It was found that sunlight can generate 35 times more particles than were originally emitted from the jet’s engine and 10 times what had typically been predicted.

These particles can include compounds such as benzene and toluene, which are known to impact health.

“Smog chamber experiments indicate that photo-oxidation of aircraft emissions produces significant amounts of secondary PM [particulate matter], which, under typical summertime conditions, exceed the primary emissions within minutes of the exhaust leaving the engine.

Allen Robinson of Carnegie Mellon University said the results were “unbelievable.”

“It sort of blew our minds,” Robinson said.

The research is a step further in understanding how aircraft emissions can impact air quality.


Gulf Disaster, “Natural Barrier of Our Skin is Gone”

I think you’ll find this very interesting and can give you some insight on what is the cause of our condition. Watch the video …

The Intel Hub
Alex Thomas

We have heavily documented the sickness that has been caused by BP and their use of the toxic dispersant known as Corexit. We have produced photographs, eye witness accounts [See the June/July archives of our radio show], and multiple blood tests. The problem is that every time we receive more evidence it doesn’t indicate that the crisis is beginning to get better, rather it indicates that it is much worse.

Kindra Arnesen has battled BP and their toxic spraying from the beginning and has been a ray of hope for all. She has helped to expose the many cover ups perpetrated by BP and their puppets within the American government.

Last week, a radio broadcast by The Coastal Heritage Society of Louisiana, complete with a radio host broadcasting live from the hospital, created a tremendous uproar throughout the internet. Florida Oil Spill Law posted the audio which was subsequently picked up The Intel Hub and as well as many others. The audio indicated that all the members of the CHSL radio show were sickened, with health problems ranging from a staph infection to neurotoxin poisoning.

Naturally the radio broadcast left many unanswered questions and Project Gulf Impact has attempted to answer at least some of them. Gulf Impact has worked diligently to expose the disaster and this video is one of the most important they have ever produced.

This video really speaks for itself. Kindra, along with many other gulf coast residents have had their natural skin barrier DESTROYED.

Doctors in the area will not deal with these clear medical problems. Have they been bribed or do they simply not want to put their livelihood on the line for the sake of someone else s health? Some have tried to help while others have seemingly misdiagnosed people on purpose.




Who would allow such a sickening chemical to be used so close to the human population? Why are the people of the gulf being used as guinea pigs in an experiment sanctioned by elements of our own government?

Please Spread this article to everyone you know. This is extremely important information. The Gulf disaster is NOT over, in fact, the actual spraying of Corexit hasn’t even stopped.

Another Theory for Sufferers to Consider

Crawling Sensations, Fibers and Other Noted Morgellons Syndrome Symptoms: Another Theory for Sufferers to Consider

by Joseph Keleher

I am not a medical professional. Let me repeat that. I am not, never have been and have no desire to ever become a medical professional. I might best be labeled a reluctant participant, as I suffered from Morgellons Syndrome Symptoms.

I have done my best to document what I went through (see Keleher 2008 “Hell and Back Again”). I wrote about connections to mercury and these horrific symptoms. I’ve angered medical professionals and sufferers. I’ve lost some old friends. I’ve found some new friends. I’ve written, emailed, and spoke on the phone with others who suffer. I’ve cried a bunch and still do (I don’t exactly know why).

I know it is possible to get well. I know what I suffered from and what I think most are suffering from is mercury as a neurotoxin. It is treatable with chelation and changes in lifestyle.

What I share are my thoughts. Yes, it is speculation. It is theory related to symptoms I had and you may still have. In reading be warned there are many “I think”s and “I believe”s. It’s all theory; it may be right or it may be wrong. Still, I feel compelled to share.

The Cause

I believe the recent growing numbers of those suffering from Morgellons symptoms is due to two ingredients- toluene and mercury.

Toluene is found in glues, methamphetamines and cocaine. I believe the toluene found in dental adhesives, and connected to symptoms by Dr. Omar Amin, correlate with a surge of sufferers of these symptoms (and possibly via prenatal passage the exponentially growing number of children with autism, ADD and ADHD).

I think toulene interacts with mercury to allow passage of this toxin into the nervous system. Toluene may dissipate after carrying mercury into the system leaving deposits of mercury. The primary source of mercury in the mouth (though there are other sources causing mercury increases including some skin creams, coal burning power plants, and historic mining activities) decreases as secondary deposits in the nerves increase.

The associated symptoms of this neurotoxin can be viewed as occurring in stages with new symptoms added as secondary deposits increase. The stages, based partly on my own experience, but also drawing from the experience of many others, might look like: 1) depression and panic attacks (typical symptoms of neurotransmitter blockage), 2) bloating, heart palpitations, and exhaustion, 3) crawling sensations, 4) fibers and skin lesions….and so on.

All of the symptoms noted with Morgellons, except crawling sensations and fibers, have been shown to be associated with mercury poisoning; because of this, I want to share how I think these two symptoms form.

Crawling Sensations

In the earliest onset of the “bugs”, I had faint flea-like zips across my scalp. I believe this was mercury pathways forming within the nerve cell network under my skin.

As the secondary levels of mercury increased, the sensations of crawling began. My crawling always started each night at the rear, right occipital area of my scalp (in journaling, at that time, I referred to the spot on my scalp as the “Mother Ship”); this area correlates with the low spot of my skull when resting (I have a preference for sleeping on my right with my head cocked back). The extreme density of mercury I believe was pooling.

Crawling typically began as the sun was setting and there was a change in temperature. Within weeks, the crawling expanded to my groin and bottom of my feet. Eventually my whole body had the sensations. It was during this time that I was diagnosed with sheet mites and scabies (and found out about something called Morgellons).

I believe as levels of mercury further increased, the crawling became more pronounced and expanded throughout my body. The sensation was especially disturbing when it began in my ear canals and nostrils.

I think the crawling is due to the expansion and contracting of mercury within the network of nerves. I picture it as one spider-shaped cell after another filling and twitching as mercury moves through (causing a kind of “cartoon effect” movement); one sufferer described this observed movement as certain proof of parasitic infestation. I still get a faint twitch occasionally at the base of my feet (but it feels different and I suspect it relates to nerve repairs and not mercurial movement).

If the Morgellons symptoms occur in stages related to increases in mercury, then I arrived at one of the middle stages. I never found fibers projecting from my skin or had any lesions. I’m thankful for this.


I think the fibers are the result of repeated cell damage repairs from mercury expansion and contrasting through the nerve system. A weak spot may have mercury break through and this will “scab” over. The fibers eventually poke through as they have nowhere else to go.

Final Words

I know there are many theories out there. Mine is one among many. Take it as such.

Morgellons is an especially cruel condition. In addition to the symptoms, the medical community has not been especially kind. The sensationalism of the media doesn’t help. Isolation and lose of connections to other people is difficult. There is one thing though that especially irritates me; I cannot stand that there are people taking advantage of the vulnerability of many sufferers. For those snake oil sales people making money off this condition, someday you will get yours; it is true what we do to others we do to ourselves.

For those suffering, be careful of the sharks, keep faith that answers will come soon, and always, always keep an “attitude of gratitude” for all you have. You are not alone and things will get better! I wish each and ever one of you a clear path towards health.

Thank you so much Joseph for another excellent and thought provoking article. Your thoughts really make me wonder if the NAC I take is a major player in my feeling better? Here are two other excellent articles written by Joseph that the reader might also want to examine.

Morgellons Disease – A Patient’s Perspective

Keleher 2008 “Hell and Back Again”

Neurocutaneous Syndrome (NCS)

I received permission from Dr. Omar M. Amin to republish this article. In some of my future blog posts I will be revisiting the subject of toxicity again. I have made reference to NCS in several posts in the past especially in connection with Toluene and other compounds.


On the Diagnosis and Management of Neurocutaneous Syndrome (NCS)
A toxicity disorder from dental sealants

Omar M. Amin, B.Sc., M.Sc., Ph.D.*
*Parasitology Center, Inc., 11445 E. Via Linda, # 2-419, Scottsdale, AZ 85259-2638  USA
Phone: 480-767-2522; Fax: 480-767-5855;  E-mail:
Web address:



Neurocutaneous syndrome (NCS), a newly discovered toxicity disorder, is characterized by neurological sensations, pain, depleted energy and memory loss as well as itchy cutaneous lesions which may invite various opportunistic infections. Components in the calcium hydroxide dental sealants Dycal, Life and Sealapex have been identified as sources of the observed symptoms. Sulfonamide and neurological toxicity issues are discussed and three case histories are presented. Additional notes on zinc oxide, Fynal, IRM and Sultan U/P sealers are also included. Diagnostic and management protocols at the Parasitology Center, Inc. (PCI) are proposed.


The original description of the neurocutaneous syndrome (NCS)1 was introductory in nature.1 Examination of many NCS patients and a careful study of their symptoms, exposures, clinical conditions and histories made it possible to identify the underlying cause of the syndrome and proceed with its management.


Materials and Methods

Patients were personally evaluated and their clinical history, records, symptomology and exposures carefully examined. Specimens provided or collected at the Parasitology Center, Inc. (PCI) were studied. An NCS status was only determined based on symptoms and determination that one or more of the suspect sealers have been used on prior dates. Sensitivity to sulfa and elevated levels of sulfa in the blood were used as a confirmation of sulfonamide toxicity. Continuing patients follow our recommendations for dental rehabilitation, extraction of suspect liner(s), and replacement with ethyltoluene sulfonomide (ETS) and zinc oxide free sealants. A list of vitamin/mineral supplements for patient use during the transitional period and another list of substitute sealants are provided.  Patients are followed up to monitor and insure the resolution of  symptoms.


Results and Discussion


The Neurocutaneous Syndrome

The disorder is double faceted with dermatological and neurological symptoms compatible with classical sulfa toxicity. The latter is characterized by changes in blood values, photosensitive reactions, allergic vasculitis sores, bacterial flora changes, and redness of the skin, which may lead to liver and kidney failure.2 The neurological aspects are characterized by pin-prick and/or creeping, painful and irritating movement sensations, often interpreted as parasite movements in various body tissues and/or cavities.. Movement sensations are either unipolar or bipolar and may proceed horizontally or vertically. They may manifest as variably shaped bruises or waves of elevated ripples or channels. In no case was the movement sensation related to parasites1. Neurological symptoms may also include loss of memory, brain fog, lack of concentration and control of voluntary movements.


Fig. 1. Early NCS sores on the thigh of KM. She was born in 1964, treated with Dycal in two teeth in 1982 and in one tooth in 2002. Neurological symptoms in upper quadrant started in 1997. Cutaneous symptoms began in Spring 2002 preceded by extensive treatment with topical sulfa preparations for possible mite infestation. Dycal was removed in December, 2002 and recovery is in progress.

The cutaneous aspects include small itchy sores (Fig.1), inflamed often elevated pimples (Figs.2,3), and fully inflamed and painful open/amorphous mucoid lesions that often enlarge and coalese (Fig.4). Histopathological sections of lesions (Fig.5) show superficial and deep perivascular infiltrate of lymphocytes, accompanied by interstitial deposits of granular mucin material. Eosonophils are usually present within the inflammatory infiltrate and foci of epidermolytic hyporkeratosis are often identified within the epidermis (Fig.5). Lesions may also be on the scalp where they may be associated with infestation of springtails (Collembola). 1 In many cases, lesions are associated with edematous reaction usually in the arms and legs (Fig.6). Blood vessels may also become enlarged and elevated, and head may become hot and turn red. The gum tissue and the teeth and oral mucoid secretions may turn gray and become compromised first and stay compromised the longest. The above creeping sensation is clearly distinguished from these caused by nematodes such as Toxocara canis3 or Dioctophyme sp.4

General symptoms usually include fatigue, compromised immune system, psychological trauma and loss of self- esteem. The depressed immune status in most patients appears to pre-empt them for opportunistic infections.


Compounding Factors


Fig. 2. Elevated sores on the forehead of KM (Fig.1); note the hot red color of the skin.


Fig. 3. Diffuse NCS sores covering the whole body that was treated with Dycal in 1985 (Case no. 1)

While NCS itself is not a contagious condition, superimposed opportunistic infections on open sores may be. Initial infection with fungus or bacteria appear to attract subsequent infestations with many arthropod species, especially springtails (Collembola: Insecta).1,5,6,7 Black specks associated with such infections appear to be metabolic waste (fecal elements) of these organisms or mycelial masses of certain fungal species. Staphylococcus aureus, S. haemolyticus,  Streptomyces spp., Candida albicans and Madurella spp. among others, have been identified from cultured swabs taken from sores of various NCS patients. These opportunistic infections have been shown to aggravate the cutaneous symptoms of NCS patients. The Madurella infections are usually associated with black grains of mycelial masses that may be related to the black specks and fibers observed by some NCS patients. The healing of certain patients lesions9 was observed to be proportional to the exit of remaining fibers from lesions.3 Patients experiencing complete remission remain susceptible to fungal promoting conditions in damp, shaded, moldy places.

Arthropods identified from sores include fleas, caterpillars, wasps, ants, beetles, winged flies, midges, thrips, ticks, mites, spiders, and springtails.1,4 Springtails may have close association with sores in many NCS patients but they, and other opportunistic infections, are not causal factors of NCS sores.


The Sealants

The three major calcium hydroxide sealants causing NCS (Dycal, Life and Sealapex) considered 9 include only about 50% calcium hydroxide in the catalyst (Table1). Of the components common to all three sealants, ethyltoluene sulfonamide as well as zinc oxide are considered most toxic. Toluene is a known potent nerve toxin.10 The sulfonamide component of this compound causes a sensitivity allergic- toxic reaction ultimately manifesting as the vascular mucoid sores characteristic of the NCS, especially in sulfa sensitive patients.




Fig. 4. Mucoid NCS/lesions on the face of MM.  She was born in 1950, poisoned with Fynal in six teeth in 1981 and in one tooth in 1986 as well as with Life in two teeth in 1985 and 1988.

Fig. 5. Histopathological section of one of the roughly 300 sores covering the body of SK. She was born in 1956 and reacted with typical NCS symptoms to a  zinc oxide cement (combined with Durelon) underneath a total veneer job in 1982. The section shows hyperkeratosis like perivascular dermatitis with eosinophils.

Fig. 6. Cutaneous sores and swelling in the right hand and arm of DB. Born in 1965, DB had 10 amalgam restorations in 1982 and 1983 using Life. She started experiencing symptoms including ulcerated rash all over the body, unilateral edema and pin-prick and subcutaneous movement sensations in 2001-2002. Life is being removed and recovery is in progress.

Zinc oxide was shown to be genotoxic11, cytotoxic12,13, killing microphages14, and causing chronic and fibrous inflammatory reaction15,16 ulcerations16 and osteosclerosis.17 Additionally, the toxic effects of zinc oxide and calcium hydroxide were shown to be similar.18,19 Calcium hydroxide was shown to cause periapical inflammation, typical granuloma and partial lack of healing.20 Titanium dioxide and Barium ions (Table 1) were also shown to provoke strong foreign body and bio-incompatible reactions in live tissue.21,22

Cytotoxicity of Dycal, Life and Sealapex was clearly demonstrated invivo and invitro in various tissues.23 Sealapex was shown to cause severe inflammatory infiltration15,24,25 and edema25 accompanied by subcutaneous tissue necrosis15,26 and progressive differentiation and reaction of monocytes, macrophages and epithelial cells27. The final phase of the inflammation is characterized by an intense granulomatus reaction especially in epithelial cells causing various intensities of irritation.28The cytotoxicity29,30 and neurotoxicity31 of Sealapex was well demonstrated in various mammalian systems.

As with Sealapex, Dycal was also shown to cause hemorrhage and acute to consistent inflammatory cells16,32,33 necrosis,16,32,33 tissue loss,33 karyorrhexis,16 neurotoxicity.34 and formation of serous exudates.16 Life has been the least researched sealant. It, however, has the same toxic ingredients, i.e., ethyltoleune sulfonamide and zinc oxide, as Sealapex and Dycal and has been associated with classical NCS symptoms in some of our patients, e.g., DB (Fig.6) and MM (Fig.4).

Sealants not containing ethyltoluene sulfonamide but including zinc oxide and eugenol have also been associated with NCS cases.These include Fynal(>75% zinc oxide), IRM and Sultan U/P (<50% zinc oxide). Fynal was associated with the cases of MM (Fig.4).  Similarly, IRM (by Dentsply caulk) and Sultan U/P (by Sultan Chemists) were associated with classical NCS symptoms in some of our patients.



Case Histories

Case #1.

    A white female born in 1951. In 1985 she underwent dental repairs, which included the use of Dycal in 20 teeth. The lady is allergic to sulfonomides, with IGE values reaching 5000. Every dental treatment was followed by aggressive skin reactions of allergic and toxicological nature (Fig.3). All tests for parasites were negative. Her symptoms fulminated into full blown typical sulfa toxicity reactions including oozing skin and nasal sores with bloody scabs and smelly discharge and an infection with S. aureus ( Fig.7). Other symptoms included loss of memory, kidney pain and urgency, sensitivity to light and electricity fields, pin-prick and moving sensations under the skin, and swelling. After each treatment, the white female felt totally knocked out with breathing and talking difficulties. She subsequently developed intestinal problems and her skin sores flared up with unbearable and unresolved itching. Photosensitive reactions presented as blotchy skin ( Fig.7) with severe burning sensations in the face, throat and chest.

       Dycal was removed in 1991-1992 and initially replaced with Harvard cement. The lady was confined to bed with whole body musculo-skeletal system pain, bowel disturbances and signs of polyneuropathy. Shortly after the removal of the Dycal in February 1992, most of her sores and rashes disappeared and she could tolerate sunlight (Fig.8).



Fig. 7. Case no. 1 before treatment; note the hot red face.

Fig. 8. after recovery.


Case # 2.

       Born in Chicago in 1965, JM was a healthy active Caucasian woman until she started experiencing her first symptoms in 1991. By then, she already had 17 fillings. No sealants were used in one filling; Dycal was used in the other 16. Her earliest symptoms appeared as skin break outs on the face and neck, which was recurrent over the following 9 years, accompanied by body tremors, sleeplessness and joint pain with occasional vomiting of black bile. Thrush appeared in the mouth and around the lips. Pain at the teeth roots persisted throughout the nineties associated with rapid major decay. A sensation of prickling pain with a pressure and movement under the skin, urticaria and skin ulcerations would last for weeks or months. JMs body showed random swelling with red marks in serpentine-like shapes. The swellings eventually bottlenecked at the knees and ankles. The chest burned and hurt with strange fits of coughing. JM then started losing hair as she experienced night fevers and sweats, and peeling of the skin.

       During the early 1990s JM was medicated with various antibiotics, antiparasitics and herbal remedies. She experienced some anti-inflammatory relief and occasional temporary clearing of ulcers after which ulcers returned and lasted longer. In 1998, massive ulcers appeared on JMs face at the nasiolobial area and on the skin ( Fig.9). A CBC in 1999 was unremarkable except for a high level of Alpha 1- Globulin of 0.5 (Normal range 0.2-0.4) and low levels of IgA of 99 (normal range 60-400) and IgG of 724(normal range 700-1500). The right ocular cavity was severely painful and JM was beginning to lose her eyesight.

     A major dental repair was completed in 2001 when Dycal was removed from all 16 teeth. Initially, JM experienced a few episodes of sickness, sweats, and vomiting. After the fourth visit, her eyebrow area had a dramatic reduction in swelling, sensation of movement and in the red-hot congestion of her face. JMs teeth were subsequently rebuilt with gold onlays section by section. By the end of the total repair, Nov.2001, JM has regained her normal skin (Fig.10) with no movement sensations or pain anywhere in her body. This state of total resolution has lasted to date without regression or relapses.



Fig. 9. Case no. 2 (JM) before treatment; note the lesion
on the right cheek and the hot red face.

Fig. 10. JM after recovery.

Case #3

       LG, a medium- built white American born in 1957, was in perfect health until September 18, 1998 when she had a filling in her tooth no. 18 using Dycal as a liner. She experienced severe headache within 2 hours. By 6:00 pm she was vomiting and delirious with the headache persisting. Her blood pressure then was monitored at 169/108 and remained high for the following three years despite repeated attempts to control it with Atenenol and Diazide. LG never experienced high blood pressure or headaches before. An MRI scan was negative. In 1999 LGs health deteriorated progressively with arthritis- like symptoms in her back, heart palpitations, mitral valve prolapse, fatigue, abnormal pap-smears including pre-cancerous cell abnormalities, night sweats, missed periods, and severe depression.  By March 2001, LG, who normally weighed 120 lbs has lost 20 lbs.

       In April 2001 lesions started appearing on LGs face, which quickly became red-hot.  Her legs became swollen and painfully burning. By May 2001, LG had several open lesions (6 mm to 2 cm in diameter) with some surrounding erythema, on her face and scalp. Her cheek pulsated as the facial lesions seemed to track to the chin (Fig.11) where the most fulminating lesion was; nearest to her teeth. The face was burning hot. Springtails (Collembola) and fibers were recovered from these sites. At that time, she showed low lymphocytes of 15.0% (normal 20-43%), high granulocytes of 77.1% (normal 51-74%) and high rheumatoid factor of 22.6 (normal <20 IU/ml). She also tested negative for all communicable diseases then. Her weight dropped to 92 lbs as she started experiencing movement sensations under the skin of her arms, face and scalp. Grayish pustular secretions oozed and moved down from the bloody lesions on the scalp and face. The lesion then extended to her legs.

       In January 2002, LG was diagnosed with NCS by OMA. She was allergic to sulfa and sulfonamide compounds. Following our protocol, LG had the filling and the Dycal liner removed from tooth #18 in April 2002. These were replaced with Starflow and Aria (a combination of Bisgma, Tegdma, Lidma and catalysts). Our recommended vitamin supplementation program was initiated then. By May 2002, all symptoms were resolved (Fig.12). Constitutional and neurological functions as well as psychological, emotional and energy levels were restored to normalcy.



Fig. 11. Case no. 3 (LG) before treatment.

Fig. 12. LG after recovery; note the return of the natural
baby skin back after healing of all facial lesions.



The toxicity of Dycal, Life and Sealapex has been well demonstrated in invivo and invitro studies of various animal and human models by many workers. The toxicity assumed cytotoxic, genotoxic, neurotoxic, phototoxic, necrotic, and inflammatory manifestations compatible with the pathology and symptoms observed in NCS patients. Ethyltoluene sulfonamide, common to all three sealants, is considered the primary cause of the NCS. The toluene component, a known nerve toxin, is believed to be responsible, at least in part, for the neurological symptoms. Neurological abnormalities are related to nerve damage associated with vasomotoric reactions due to a direct influence on the peripheral nerve endings.35 The sulfonamide component is the cause of the cutaneous symptoms, especially in sulfa-sensitive patients who usually had elevated sulfonamide/sulfa levels in blood tests and allergy to sulfa in skin sensitivity tests. The relationship between sulfonamide and phototoxicity has been well established.29 Resolving the symptoms (effect) by removing the sealants (cause) in patients undergoing treatments, confirms this cause-effect relationship.

The nature of causation of NCS precludes contagious transmission. Any similarities of symptoms among partners within the same household are traceable to the transmission of opportunistic infections, especially fungi.

It is recommended not to rehabilitate more than two or three teeth per month. The patient is given a list of vitamins and other supplements to take during the procedure and for the following few weeks until symptoms are completely resolved. After reaching the state of normalcy, the patient may still retain some sensitivity to moldy places lacking sun and fresh air circulation.

After additional test results become available and a satisfactory diagnosis of an NCS case is made at the Parasitology Center, Inc. (PCI), arrangements for dental rehabilitation are made and patient prognosis is monitored.


      I am grateful to Marie Erixon, Nordea, Sweden for her contributions to the better understanding of issues related to NCS.


1. Amin OM. Neuro-cutaneous Syndrome (NCS); a new disorder. Explore 2001; 10: 55-56.
2. Ockert K. Filling caused serious reactions. Trandlakartidningen 1994; 86: 470. (in Swedish).
3. Garcia LS. Diagnostic Medical Parasitology. Wash, DC: Am Soc Microbiol Press, 2001.
4. Urano Z, Hasegawa H, Katsumata T, Toriyama K, Aoki Y. Dioctophymatid nematode larva found from human skin with creeping eruption. J Parasitol 2001;87: 462-465.
5. Amin OM. Facial cutaneous dermatitis associated with arthropod presence. Explore 1996; 7: 62-64.
6. Frye FL. In search for the haphazardly elusive: a follow-up report on an investigation into the possible role of collembolans in human dermatitis. Vet Invert Soc Newsletter 1997; 13: 10-13.
7. Janssens F. Checklist of the Collembola: Collembola in association with man. http// 1999-2003; 10pp, and per comm..
8. Mahon CR, Manuselis G Jr. Diagnostic Microbiology. Philadelphia: WB Saunders Co, 1995.
9. Draheim RN, Murray AJ. Compressive strength of two calcium hydroxide bases. J Prothet Dent 1985; 54: 365-366.
10. Burry MB. Neurodevelopmental toxicity of toluene.M. Sc. Thesis: Seattle, Univ Wash, 2001.
11. Tai KW, Huang FM, Huang MS, Chang YC. Assessment of the genotoxicity of resin and zinc-oxide eugenol-based root canal sealers, using an in vitro mammalian test system. J Biomed Mater Res 2002; 59: 73-77.
12. Wright KJ, Barbosa SV, Araki K, Spangberg LS. In vitro antimicrobial cytotoxic effects of Kri 1 paste and zinc oxide eugenol used in primary tooth pulpectomies. Pediatr Dent 1994; 16: 102-106.
13. Pissiotis E, Spangberg LS. Toxicity of pulpisad using four different cell types. Int Endod J 1991; 24: 249-257.
14. Sadeghein A, Bolhari B, Sarafnejad A. A comparison of the effects of three endodontic sealers on adherence of mouse peritoneal macrophages. J Calif Den Assoc 2001; 29: 673-677.
15. Soares I, Goldberg F, Massone EJ, Soares IM. Periapical tissue response to two calcium hydroxide-containing endodontic sealers. J Endod 1990; 16: 166-169.
16. McShane CJ, Stimson PG, Bugg JL, Jennings RE. Tissue reactions to Dycal. J Dent Childr 1970; 37: 466-474.
17. Erausquin J. Periapical tissue reaction to root canal fillings with zinc, titanium, lead, and aluminum oxides. Oral Surg Oral Med Oral Pathol 1970; 30: 545-554.
18. Berman DS. Pulpal healing following experimental pulpotomy. Brit Dent J 1958; 105: 7-16.
19. Berman DS, Massler M. Experimental pulpotomies in rat molars. J Dent Res 1958; 37: 229-242.
20. Weinstein R, Goldman M. Apical hard-tissue deposition in adult teeth of monkeys with use of calcium hydroxide. Oral Surg Oral Med Oral Pathol 1977; 43: 627-630.
21. Bennatti-netto C, Bramante CM, Ber-Bert A, Lia RCC. Reacao do tecido conjuntivo subcutaneo de rato ante a implantacao dos materials components do cimento AH-26. Rev Bras Odontol 1982; 39: 11-20.
22. Smith JW, Leeb IJ, Torney DL. A comparison of calcium hydroxide and barium hydroxide as agents for inducing apical closure. J Endod 1984; 10: 64-70.
23. Topalian M. Effecto Citotoxico de los cementos selladores utilizados en endodoncia sobre et Tejido periapical. Endodocia-Caracas 2002,; 48pp, and per comm.
24. Buntak-Kobler D, Prpic-Mehicic, Najzar-Fleger D, Katunaric M, Talan-Hranilovic J, Suman L. Cytotoxicity of Ca(OH)2 endodontic sealers on connective, muscle and bone tissues. Acta Stomatol Croat 1993; 27: 175-180.
25. Sonat B, Dalat D, Gunhan O. Periapical tissue reaction to root fillings with Sealapex. Intern Endod J 1990; 23: 46-52.
26. Bezerra LA, Leonardo MR, Faccioli MR, Faccioli LH, Figueiredo F. Inflammatory response to calcium hydroxide based root canal sealers. J Endod 1997; 23: 86-90.
27. Tronstad L, Barnett F, Flax M. Solubility and biocompatibility of calcium hydroxide-containing root canal sealers. Endod Dent Traumatol 1988; 4: 152-159.
28. Zmener O, Guglielmotti MB, Cabrini RL. Biocompatibility of two calcium hydroxide-based endodontic sealers: a quantitative study in the subcutaneous connective tissue of the rat. J Endod 1988; 14: 229-232.
29. Beltes B, Koulaouzidou E, Kotoula V, Kortsaris AH. In vitro evaluation of the cytotoxicity of calcium hydroxide-based root canal sealers. Endod Dent Traumatol 1995; 11: 245-249.
30. Guertsen W, Leinenbach F, Krage T, Leyhausen G. Cytotoxicity of four root canal sealers in permanent 3T3 cells and primary human periodontal ligament fibroblast cultures. Oral Surg Oral Med Oral Pathol Oral Radiol 1998; 85: 592-597.
31. Serper A, Ucer O, Onur R, Etikan I. Comparative neurotoxic effects of root canal filling materials on rat sciatic nerve. J Endod 1998; 24: 592-594.
32. Good DL. Effects of materials used in pediatric dentistry on the pulp: a review of the literature. J Calif Dent Assoc 1999; 27: 861-867.
33. Heys DR, Heys RJ, Cox CF, Avery JK. The response of four calcium hydroxides on monkey pulp. J Oral Pathol 1980; 9: 372-379.
34. Norrsells N. Aven svenska tandlakare tillats nu sedan EU-intradet att anvanda den effektiva N2-metoden for rotfyllig. Med denna metod kan 500 miljoner kr sparas arligen at patientena och lidandet minskas. Endod Sverige 2002; 5p.
35. Hensten-Pettersen A. Skin and mucosal reactions associated with dental materials. Eur J Oral Sci 1998; 106: 707-712.   


See also: Amin, O. M. 2004. Dental Sealant Toxicity:  Neurocutaneous Syndrome (NCS), a dermatological and neurological disorder.  Holistic Dental Association Journal (No. 1, Jan.):  1-15

See also: Amin, O. M. 2004. On the diagnosis and management of neurocutaneous syndrome, a toxicity disorder from dental sealants. California Dental Association Journal 32 (9): 657-663.

Morgellons and More Cases of Collembola Infesting Man

I really do feel that Collembola do play a role in our itching and crawling sensations. In fact, I believe they are responsible for the majority of my crawling and biting sensations at this point. If I am correct, and I’m not sure I am, are they here to feed on fungi and or bacteria in my body? As I stated in  my very first post “It would seem the skin and body of the Morgellons sufferer has become like a rotting log, or the very least as favorable a home to both soil bacteria and soil based pests that they are both perfectly at home living in us”. However, not covered in this post are the fungi and bacteria that are found in the gut of the Collembola, could they set this whole thing in motion in us? Some are quite pathogenic. Just thinking out loud here.

I have a FIR (Far Infrared) heating pad that I purchased through Dr. Staninger and when I break out in these red pimple like things the FIR heatpad makes them go away and my skin returns to healthy looking very quickly, but it wasn’t cheap, around $350.00 if I recall. I don’t urge you to run out and buy one as it might not do the same for you and I know how much so many of you have already spent on things that haven’t worked. I have been considering lately as to whether or not the heating pad is killing them.

This post is a follow up to my first post regarding Collembola titled “Collembola – A Major Role in Morgellons Despite the Disinformation” and I hope you find this post interesting as well. I have found even more interesting information regarding Collembola. Here is a quote from

They are generally small and some species of Neelidae (Collembola) are among the smallest hexapods in the world at just over 0.2 mm long (about the same size of the period at the end of this sentence) while the largest Collembola are in the family Uchidanuridae which can reach 10 mm in length. Most species live for a year or less, however some live considerably longer and the record for long life in the laboratory is 67 months for a specimen of Pseudosinella decipiens.

Most Collembola feed on the fungi and bacteria found in rotting organic matter but many arboreal (living in trees) and epidaphic (living on the surface of the soil) species also feed on algae. Some feed on other plant materials and in some places particularly Australia Sminthurus viridus is a pest of lucerne crops. A few other species are carnivorous feeding on Nematodes and other Collembola.

Note that above text mentions that some species of Collembola can be as small as .2 mm.  Just so we are clear on things .2 mm is very small, .2 mm = 0.000787 of an inch !!!!! There are an estimated 30,000 to 100,000 undiscovered species of Collembola.



So How Small Can Insects Be Anyway?

fly The smallest insects are fairy flies, which are insects that parasitize other insects’ eggs by laying their eggs inside them. Fairy flies are only 1/5 of a millimeter in length. Many beetles are less than one millimetre in length, and the North American Feather-winged Beetle Nanosella fungi, at 0.25mm, is a serious contender for the title of smallest insect in the world. Other insect orders which contain extremely small members are the Diptera (True Flies) and the Collembola (Springtails). The “feather-winged” beetles and the “battledore-wing fairy flies” are smaller than some species of protozoa (single cell creatures). Megaphragma caribea a hymenopteran parasite from Guadeloupe, measuring out at a huge 0.17 mm long is in contention for the smallest insect.

See for more information. We are talking about flies here that you probably couldn’t see with your naked eye, amazing.


Okay, Back to Collembola

My first post talked about the National Pediculosis Association’s (NPA) study where they identified Collembola in 18 of 20 individuals studied, and also the 1955 cases is Sweden (there were many), and finally the 80 year old Woman in Romania. I would like to thank Sidney, one of our fellow readers and somebody that knows a lot about this subject. She pointed out to me that there were some mistakes in the identification in the samples of the 80 year old woman. She has first hand knowledge of this case.


rotifersSidney stated:


When Neculai removed the Collembola and Rotifers from the body of the 80 year old Romanian woman please bear in mind Neculai was not an entomologist, but a veterinarian pathologist and head of the department of veterinary medicine at his university. This was not a case of “sample contamination.” The Collembola was removed from the Romanian woman’s tissue by a needle aspiration biopsy. The corrections I mentioned in my email refer to the PUPA and LARVAL stage which Collembola do not have. Rotifers were also found within the Romanian woman’s skin (actual photos shown left), along with bundles of fibers.


I didn’t include the pictures of the fibers that Sidney sent to me but suffice it to say they look like our typical fiber bundles. So, some of the images that were put forth as various stages of the adult Collembola on my first post were actually found to be Rotifers.  If you really want to know more about Rotifers see this article “Epizoic and parasitic rotifers”. There is a interesting quote from the parasitic rotifer article (but you should click on the link and read the entire abstract).


There appear to be few records of epizoic or parasitic rotifers among vertebrates, apart from Encentrum kozminskii on carp, Limnias ceratophylli on the Amazonian crocodile, Melanosuchus niger, and an unidentified Bdelloid apparently living as a pathogenic rotifer in Man.

So, I’ll bet you can sense yet another blog post coming on Rotifers in the future and you would be correct, but for this post we are going to stay on the topic of Collembola.


More Cases of Human Collembola Infestation

collembola1 Let’s start with Dr. Omar, M. Amin, Ph.D., founder of PCI, who is a Professor of Parasitology and who works with something he calls Neuro-cutaneous Syndrome (NCS) which to me at least, seems to be exactly the same thing as Morgellons, though he might differ with me on that. The photo shown on the left is of a springtial (Collembola) that was taken from an actual patient. If you really want to dive into some of Dr. Amin’s information see this PAGE and follow the links on NCS. And if you hit this PAGE look at Table #2 and notice how many were documented to have springtails (another name for Collembola).

Here is a quote regarding the Collembola shown above from Dr. Amin’s site.


Scalp lesions also occur in patients with neurological symptoms and are usually associated with arthropod infestation.  JH (a tall, healthy, well-nourished, middle aged white American female from Arizona) had a number of such lesions (Fig. 4) from which springtails (Collembola: Insecta: Arthropoda) (Fig. 5) were collected by myself in December, 1995.  There is only two other published reports of springtails from humans (Hunter et al., 1960; Scott et al., 1962).


Very interesting. Dr. Amin mentions that there are only two other published reports of springtails in humans. However, he doesn’t mention any of the cases in my first blog post, nor did I mention the cases he is referring to (Hunter et al., 1960; Scott et al., 1962). But as you are about to find out, we are just getting started. We are very grateful for your work Dr. Amin, you provide an amazing amount of information to aid in our search on your site.


Collembola causing itching, biting, irritation, and papules …

Pescott, R.T.M. (1942:68-69) Australia:
“In 1939, specimens of springtails were received from a Melbourne specialist who stated that they were causing skin troubles on a female patient. The insect in question was the species Entomobrya multifasciata Tull., a European species originally described in 1871, but which is now cosmopolitan in its distribution. Womersley (3) records it as being common in cultivated areas in the Australian States. The symptoms of this case were as follows : the patient experienced a sharp biting sensation, followed by intolerable itching. There were few marks on the body with an occasional excoriated papule, while the irritation was distributed fairly generally over the trunk and limbs, but was most marked around the waist. Several specimens of the insect responsible for the condition were found on the patient’s body. She received no active treatment, but her clothes and bedclothes were sterilised and this was sufficient to destroy the insect and thereby remove the irritation.
On considering the origin of this infection, it appeared that the patient had recently moved into a new house where the garden was in the process of being made. The insects had apparently migrated to the patient when the grass, weeds and soil outside were disturbed.”

“In 1941, specimens of another springtail were received from a military hospital in Victoria, where skin irritations were occuring among the nursing staff. The species concerned was Entomobrya tenuicauda Schott., a native insect originally described in 1917 from Queensland, later recorded by Womersley (3) from Western Australia and Tasmania, and now from Victoria. In this instance, the presence of the insect produced on several nurses raised lumps very similar to mosquito bites, and which later were very irritable. In one instance there was also a good deal of reddening of the calf of the leg. These conditions lasted for somewhat less than twenty-four hours in each case, but reoccurred the next day, probably from more ‘bites’. On analyzing this case, it appears certain that the insects were introduced into the hospital with flowers, and from there moved on the affected nurses during their normal routine duties.”

Womersley suggested that the easily detached, long ciliated hairs of Entomobrya species undoubtedly would cause skin irritations.  Pescott concludes that severe skin irritation can be caused by certain species of Collembola: “Typical symptoms are a biting sensation, followed by intense irritation and the production of small pimple-like bodies.

Mackie, T.T., Hunter, G.W. & Brooke Worth, C. (1945:541-542) Australia:
“The Collembola are primarily phytophagous and are not usually thought of as medically important insects. Two Australian species, however, Entomobrya multifasciata Tullb. and E. tenuicauda Schott have recently been recorded as attacking man, the patients complaining of a sharp, biting sensation followed by irritation and papules similar to mosquito bites, with pruritus.”

Cited from Scott, H.G., Wiseman, J.S. & Stojanovich, C.J. (1962:430):
Entomobrya nivalis (cosmopolitan) and Entomobrya tenuicauda (Australasian) have been reported as causing a pruritic dermatitis in man.”

Cited from Ebeling, W. (1975):
“They [Collembola] have never been incriminated in the transmission of any human disease, but Entomobrya nivalis L., a cosmopolitan species, has been reported to cause an itching type of dermatitis in man, …”

Martini, M. (1952:354) cited from Bryk, F. (1955:1824) :
“Very discomforting mosquito-like skin irritations attributable to collembolans of the genus Entomobrya attempting to bite. ”

Mertens, J. in Christiansen, K. (1998 in 2001:in litt.) Belgium:
” Several years ago our Faculty of Medicine once offered me ‘strange small insects’, which were considered as being responsible for causing allergic reactions on the skin of a woman. Those insects were Seira domestica. I could prove that the scales of Seira on the cushioned seats caused the allergy. As you know, Lepidocyrtus, has scales too. ”

Mertens, J. (2004:in litt.) Belgium:
“In 1976 (or 1977), our Faculty of Medicine was puzzled by a rare case of skin allergy in a woman, living near Ghent. The allergy was caused by the scales of Seira domestica on a cushion of a rotan chair. Whenever the woman used the rotan chair, the allergic skin response occured (and only then). The chair was located in the veranda, which was quite moisty and where the temperature was enjoyable. It turned out that the hollow rotan branches of the chair hosted a population of Seira domestica. During the night, they left their hiding place and crawled all over the chair. The cushion collected many of the lost scales, causing as such the allergic reaction.”

Scott, H.G., Wiseman, J.S. & Stojanovich, C.J. (1962:430) Texas:
“Springtail insects (Orchesella albosa Guthrie, 1903, forma ainslieri Folsom, 1924) were found infesting the heads and pubic areas of a family in Buffalo, Leon County, Texas, in June 1961. No dermatitis was reported due to this infestation, and the source of the insects was not determined. Based upon known habits of this species, some moldy household item (perhaps bedding) was probably involved. Orchesella albosa has never before been reported infesting man or houses. Its chewing mouthparts are probably not capable of biting man.


At this point I’m going to stop referencing cases. There are many, many more on the following links at the end of this post that you will find extremely interesting. I wish I had time to do this post justice but I’m so busy just trying to be a dad, hold down a job, and stay well. However, if anyone is interested in finding out if Collembola can infest human beings the answer is on this post and in the following links.

One could make the argument, okay, so maybe you could dig up 30 or 40 cases of springtails in human tissue using the links below, but that’s not very many. And I would answer that with “Yes, but who is looking? We are told we are DOP without so much as an examination”


References (there is a wealth of case history on these links)

If you take the time to look at these links, especially the first two you will begin to realize there are a lot of references of human infestation of springtails (Collembola) in man. As as referred to above in the medical literature the patient experienced a sharp biting sensation, followed by intolerable itching. There were few marks on the body with an occasional excoriated papule, while the irritation was distributed fairly generally over the trunk and limbs it sure sounds a lot like us.


FOOTNOTE:  Dental Products Causing Neuro-Cutaneous Syndrome (NCS) Symptoms in NCS Patients


The toxic ingredients common to all belong in four major categories: Zinc Oxide, Ethyltoluene Sulfonamide (especially in patients with allergy to sulfa and toluene)

Dr. Amin feels strongly apparently that Toluene plays a major role in NCS and if you look at his site I don’t care what we call it, NCS and Morgellons exhibit the same exact symptoms. Most people when they think of removing fillings think of “Mercury Fillings” but the kind Dr. Amin is refers to here are the newer kind. You know, the new white ones that weren’t supposed to be bad for us, sigh …  I’ll be honest, I had quite a bit of dental work done before this all started, crowns and fillings and alike, all the new ceramic type too.

Grand Unification Theory – Sneak Peak

I haven’t had time to write up the entire “Grand Unification Theory” yet but I’ll give you a sneak peak. I happened to be doing more research when I stumbled upon something called the Toluene Pathway Map which shows how Toluene is broken down during biodegradation. Notice that Pseudomonas Putida is included in the map. Interestingly at the very bottom of the biodegradation map was something called Acetaldehyde which I immediately recognized from Jill’s post on BTEX. Toluene will eventually break down to Acetaldehyde . As I began to research Acetaldehyde it seemed to be linked to what I call the “Skin Crawling Family Tree”, that is, those that experience skin crawling sensations. Even more revealing the aldehydes were directly linked to some of the exact sensations that we feel, more on that later in this post.

The “Skin Crawling Family Tree”


All of the groups above suffer from Skin Crawling Sensations and the feeling of Bugs Crawling Under the Skin. What if we there was a common link between all of these groups? That is what this post is all about, I believe there is a common link, and that link is Acetaldehyde.

Meth Users

If you have been following my blog then you know how I have connected Morgellons to Toluene. If you haven’t read the previous posts click on the All Posts page and catch up, it should prove well worth your effort. In my Mr. Morgellons meet Mr. Meth, Your Distant Cousin I documented that Toluene is used in Meth production and they experience severe bug crawling sensations known as “Meth Bugs” or “Crank Bugs”. We know that Toluene breaks down into Acetaldehyde.

Cocaine Users

It turns out Cocaine users can also experience bug crawling sensations. From the article Cocaine and the Destruction of the Rainforests there is a quote

Annually, according to Peruvian forest engineer Marc J. Dourojeanni, coca growers dump 15 million gallons of kerosene, 8 million gallons of sulphuric acid, 1.6 million gallons of acetone, 1.6 million gallons of the solvent toluene, 16,000 tons of lime and 3,200 tons of carbide into the valley’s watershed.

For more on Cocaine and how it’s made see this DOCUMENT. We know that Toluene breaks down into Acetaldehyde.

Candida Sufferers

Acetaldehyde is the main waste product when Candida die-off occurs. For an interesting article see The Candida/Aldehyde detox pathway and the Molybdenum Connection for more information. The damage that Acetaldehyde causes to the body is tremendous and behind many other common diseases. Also, another good article is Candida Albicans and Acetaldehyde Toxin from which you will find this quote.

These effects of acetylaldehyde are multiplied many times over when candida die off occurs

Skin crawling sensations are common compliant for Candida sufferers. Also, this amazing quote:

The primary detoxification mechanism for scavenging unmetabolized acetaldehyde is sulfur-containing antioxidants [see Figure A]. The two most important are cysteine, a conditionally essential amino acid, and glutathione, a cysteine-containing tripeptide (a three-amino-acid polymer) [see Figure B]. Cysteine and glutathione are active against acetaldehyde (and formaldehyde) because they contain a reduced (unoxidized) form of sulfur called a sulfhydryl group, which contains a sulfur atom bonded to a hydrogen atom (abreviated SH).

Sulfhydryl groups interact with aldehydes to render tham incapable of forming cross links. This “mops up” or scavenges any stray acetaldehyde that is not properly metabolized into acetate (acetic acid) [see Figure A]. Although this is a powerful aldehyde detoxification mechanism, it is easily overwhelmed by the relatively large amounts of alcohol that are typically consumed with alcoholic beverages as compared to the amounts of alcohol and acetaldehyde that are produced through normal metabolism. Fortunately, sulfhydryl antioxidants can easily be fortified through dietary supplementation.

In one experiment with rodents [Sprince et al., 1974], a LD-90 dose of acetaldehyde (the dose that would normally kill 90% of the animals) was completely blocked by pretreatment of the animals with cysteine and vitamins B-1 and C. In other words, none of the cysteine-treated animals succumbed to the lethal dose of acetaldehyde! N-Acetylcysteine (NAC) protected almost as well as cysteine.

In another rodent experiment [Busnel & Lehman, 1980], alcohol’s ability to inhibit swimming after the alcohol had been completely metabolized was blocked by vitamin C. What this and the previous study suggests is that the pharmacologic and toxic effect of alcohol are different. The pharmacological effect (i.e., intoxication or drunkenness) is not inhibited by vitamin C or cysteine, but the toxic effect (e.g., the hangover, nervous irritability, swimming difficulty) is inhibited. This suggests that, with alcohol, you can “have your cake and eat it too.”

If that doesn’t sound exactly what we are going through with Morgellons I don’t know what does, notice how sulfur works so well.

Alcoholics going through DT’s

If you do some searching you will see that some alcoholics go through DTs so bad they experience the sensation of bugs crawling under their skin. It is my suggestion that this occurs when the massive Candida colonies they are maintaining go through die off 3 to 5 days after the alcohol flow is stopped. See Living with Alcohol for it’s link to Acetaldehyde.

Morgellons Sufferers

Like I have stated in previous blog posts many Morgellons patients have found high Toluene levels in their blood work and its metabolites such as Hippuric acid are found as well. Toluene will also biodegrade down the Benzoate path thus our glass crystals also (covered in another post). Much more can be said here. Of course, as this breaks down into the Acetaldehyde path and we suffer skin crawling just as the Candida sufferer does, it’s not the fungus in our case, it’s the Acetaldehyde being biodegraded from the Toluene in our bodies. I believe that Acetaldehyde causes the skin crawling sensation and not the actual fungus.


Formaldehyde (Tiny insects crawling over the eyes and nose?)

Let’s talk about a close cousin of Acetaldehyde and that is Formaldehyde. There is an amazing research paper out there on this, take a look at this quote:

Skin reactions: …chemical can be both irritating and allergy-causing…(EPA).  A slight sensation of tiny insects crawling over the eyes, nose and pharynx  (formication) is felt at 2-3 ppm.  (Zurlo N, via OSH, NZ.)  Contact with the vapour or solution causes skin to become white, rough, hard and anaesthetic due to superficial coagulation necrosis. With long exposure, dermatitis and hypersensitivity frequently result.  Prolonged exposure may also cause cracking of skin and ulceration, especially around the fingernails.

I wont bother to post all the links but I could find a thousand posts from Morgellons sufferers stating that they are sure they have bugs or worms crawling all over and in their eyes and around there nose, it’s a very, very common symptom. I too have felt that sensation on my eyes, like a bunch of mites crawling across the surface. Depending on what is laying around in our body I believe that Formaldehyde is often times created internally as well as Acetaldehyde.



This is just a very quick write up. I feel strongly that aldehydes such as Acetaldehyde  and Formaldehyde are the dominant causes of our symptoms. I’m glossing over a ton of evidence here such as the Putida and other things, I believe Toluene is being created in our bodies and am sure these are causing my symptoms.

Interestingly N-acetylcysteine (NAC) is great for binding to and ridding the body of Acetaldehyde  and so is Molybdenum, and Pantothenic Acid and Pantethine. However remember, I am no doctor. Also, cysteine is readily and abundantly found in human hair which is why I believe we suffer hair loss as the body is using all it can to bind to and rid us of the Acetaldehyde and I believe Formaldehyde is created also based on what chemicals we have laying around in our bodies at the time.

I think that all of the above groups in the “Skin Crawling Family Tree” suffer skin crawling due to the aldehydes being created in their bodies. I believe this could easily be proven. Something is creating Toluene in sufficient quantities in the human body to cause the Morgellons condition. We know Ps. Putida can create Toluene from glucose and that many alleviate their symptoms by cutting out most of the sugar from their diet. Is there a link here? There is a scientific paper out there which I will have to purchase to see the full text but I believe it links Acetaldehyde directly to skin crawling sensations in humans, we know it’s close cousin Formaldehyde already has been proven to do so.

Morgellons is an ongoing chemical reaction happening in our bodies with volatile organic compounds (VOC) such as Toluene. This is either being brought on by bioremediation bacteria which can create Toluene or the mere fact that Toluene is has now so thoroughly penetrated our environment. I hope this blog post spurs you on to do some research on Acetaldehyde and see if what I am saying is true. And if you find even more relevant information please post a comment on this thread.

Morgellons “Grand Unification Theory” Coming Soon …

Before we begin please remember that I could be wrong, do not get your hopes to high. Many have thought they too had this all figured out.

Who would have thought that when I asked Jill to make her guest post that she would lead me to the missing piece of information that would tie everything together? In fact, to her credit, Jill had this all gathered up, I am just going to take it to the next level and explain it all.

In my next post I am going present some information (following my current line of thinking) to you that is going to literally take your breath away when you read it. I believe the evidence I am about to present will make believers out of skeptics and cause those invested heavily in other theories to reconsider. The good news is if I’m correct, Morgellons isn’t some horrible hideous incredible disease (though the symptoms are) and even better news is that I believe there is a way out of this mess for all of us, and it will not take pharmaceuticals.

I’m terribly excited over what I have stumbled upon, or rather, been lead to. I’m sorry to post such a comment and know that many of you will be anxious to hear what I have to say, I promise you I will post the information as soon as I can. Also, the evidence I have isn’t conspiratorial or anything like that, it’s just something that ties Morgellons to all of our symptoms in such a way that it will be hard to ignore (and I believe this is an understatement).