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TOXIC MOLD VICTIMS DONATIONAL FUND


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My MSH is 14 (at the time of the testing.. It might bee less than that now). This proves extreme mold exposure for a long duration. See the blood work listed below this MSH FAQ Section: 

http://www.moldwarriors.com/glossary.cfm

MSH FACT SHEET(Cited from: http://www.moldwarriors.com/msh-info.htm )

Q: What is alpha melanocyte stimulating hormone (MSH)?
A: MSH is an anti-inflammatory, regulatory hormone made in the hypothalamus. It controls production of hormones, modulates the immune system and controls nerve function, too. It is made when leptin is able to activate its receptor in the proopio- melanocortin (POMC) pathway. If the receptor is damaged by peripheral immune effects, such as the release of too many pro- inflammatory cytokines, then the receptor doesn’t work right and MSH isn’t made. Leptin controls storage of fatty acids as fat, so MSH and leptin are a major source of interest.
Q: Isn’t this damage to the leptin receptor just like what we see in insulin resistance?
A: Actually, the mechanism is almost identical. A lot of our obesity and diabetes is inappropriately blamed on overeating when the real problem is damage to these regulatory receptors.
Q: What does MSH do?
A: MSH sits as the central hub of a series of important effects. MSH controls hypothalamic production of melatonin and endor- phins. Without MSH, deficiency creates chronic non-restful sleep and chronic increased perception of pain, respectively. MSH deficiency causes chronic fatigue and chronic pain. MSH also controls many protective effects in the skin, gut and mucus membranes of the nose and lung. It also controls the peripheral release of cytokines; when there isn’t enough MSH, the peripheral inflammatory effects are multiplied. MSH also controls pituitary function, with 60% of MSH deficient patients not having enough antidiuretic hormone. These patients will be thirsty all the time, urinate frequently and often will have unusual sensitivity to static electrical shocks. 40% of MSH deficient patients won’t regulate male hormone production and another 40% won’t regulate pro- per control of ACTH and cortisol.
Q: What illnesses are associated with MSH deficiency?
A: Any illness that begins with excessive production of pro- inflammatory cytokines will usually cause MSH deficiency. This is the basic mechanism that underlies damage caused by exposure to biologically produced toxins neurotoxins (biotoxins) made by invertebrate organisms, including fungi (molds), dino- flagellates (ciguatera and Pfiesteria), spirochetes (Lyme disease), blue-green algae (Cylindrospermopsis in Florida and Microcystis all over the world) and bacteria, like anthrax. Nearly 100% of the patients who have Chronic Fatigue Syndrome (CFS) will have MSH deficiency. Do we know that all CFS is due to biotoxins? No.
Q: OK, if something is going on in the body that causes inflammation, like exposure to toxins made by mold in Sick Building Syndrome, and the immune system is cranking out these proteins, cytokines, that are great for our health when they are released in the right amount at the right time, but harmful when too many are made at the wrong time, why don’t we just fix the cytokine response and watch MSH get going again?
A: Good question. We are looking at an incredibly small area in the hypothalamus, one in which there is a real risk of permanent damage from cytokines to blood flow to this pathway. And who is to say that the vital receptors aren’t destroyed by too much attack for too long? Once MSH production is damaged too much, it is too late.
Q: So, if the toxin and cytokine illness goes undiagnosed, or someone says the illness doesn’t exist, like what we have seen for a long time with mold and in Lyme disease, there are going to be people whose MSH supply just dwindles down to nothing.
A: Right. These patients are miserable. They live, but there is no life. They are given Oxycontin or Neurontin or Elavil or Xanax, for example, but nothing really helps. Families are destroyed, careers are ruined, financial resources are poured into tests that mean nothing and therapies that hopefully won’t cause harm, because they never help. Even worse, because MSH levels are rarely measured, many doctors look at the MSH deficient patients as if they are making up the illness, making up the pain to get drugs or looking for disability. And lots of them end up on disability, costing our society not just the unnecessary expense but also costing us the lost productivity.
Q: What is the answer for those people who are MSH deficient? Why don’t we just give them MSH? It should be so simple, like giving insulin to a diabetic who needs it, right?
A: Should be, but it isn’t. The FDA is real particular about giving potent hormones like MSH to just anybody. Just look at cortisone. A little bit is necessary for life, but too much will kill you. MSH can’t be given to people until animal toxicity studies are done, showing safety, and that costs a lot of money, even if the paper work can be done.
Q: Why don’t all the big drug companies jump on this? If what you are telling me is that there are a large number of people who will need daily replacement of MSH, and by the way, it looks like our supply of Sick Buildings that will generate MSH deficient patients won’t dry up any time soon, then there should be a huge market for somebody.
A: No doubt about that. There are companies looking at MSH as we speak for weight loss, skin pigment changes and as an antidepressant, but no one is looking at MSH in chronic, fatiguing illnesses.
Q: So, if you can raise the money to prove MSH is safe, then what?
A: Researchers at the NIH, like Dr. Robert Star, would likely be willing to help with the experiments in humans. I’m sure there are other academic researchers who would come forward, but the problem is that the experience of physicians with MSH is so limited. Certain researchers, like Dr. James Lipton of Zengen and Dr. Star, who know MSH, know what a huge area of medicine is involved with MSH. But the average endocrinologist, for example, just doesn’t deal with MSH deficiency. We will use my database of nearly 2000 patients with illnesses associated with MSH deficiency to develop a double blind, placebo controlled, crossover clinical trial after we have done a titration study to prove how much MSH is needed, given in what route, for how long, with what side effects and with what adverse reactions over time. When our work demonstrates what I feel it will, then suddenly, there is hope for a large number of chronically suffering people.

MMP9

matrix metalloproteinases, including #9, are enzymes that effect the tissues underneath blood vessel walls (sub- intimal space). MMP9 is particularly adept at delivering inflammatory elements out of blood vessels and putting them where they shouldn’t be in brain, nerve, lung, muscle and joint. If you see high MMP9, look for toxins and cytokines.

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Pathology Report

Issued: 11/07/09 ID# MR00035017

Subject Name: HELFRICH, PETER

Specimen #: S-09-18590

Sex: M

Date Collected: 10/27/2009



Date Received: 11/05/2009



Attending Physician: Dr. Pollan,

PMFS Strong Memorial Hospital

601 Elm. Ave. Box 705

Rochester, NY 14642





Specimen Identification: Right Buccal Mucosa, lesion present for unknown period of time.



Clinical History: Peter Helfrich has been exposed to toxic fungi within his apartment.



Specimen Description: The specimen, labeled tissue for slide prep documentation only, consists of two tan-red fragments aggregating to 0.9 x 0.8 x 0.3 cm, completely submitted in one cassette for slide prep documentation only.



Microscopy: One Specimen

• There is a moderate amount of basket-weave fibrinous inflammation observed on the mucosal surface in a uniform application.

• There is thickening of the epidermis of between 8-16 cells thick. Normal thickness of epidermis is 1-3 cells.

• The Buccal biopsy does extend to the full depth of the muscle layer to reveal the full depth of the fibrin deposition.

• There is hyaline-appearing fibrinous inflammation just beneath the basement membrane and it continues well into the deep tissue including muscle, demonstrating the classic fingerprint of moderate chronic exposure of a year in duration to Trichothecene Mycotoxins.

• Several arteries are partially occluded with fibrinous inflammation or exudates, which is typical of all arteries of the body, and consistent with severe poisoning of the Trichothecene Mycotoxins. There are 30 microns of fibrin deposited within these arteries.

• The fibrinous inflammation is also indicative of ongoing ambient inhalation exposure to the highly poisonous Trichothecene Mycotoxins. The uniform reaction observed to the dermis is consistent with fungal vapors of Trichothecene Mycotoxins.

• Fibrinous inflammation is formed in the body when it is exposed to Trichothecene Mycotoxins. The fingerprint is highly specific and no other chemical exposure will cause this.

• The small arteries indicate a severe yeast infection within the systemic circulation. There is a severe infection of yeast observed within the small arteries.

• The buccal tissue reveals a strong positive reaction to Trichothecene Mycotoxins by filling the deep dermis with fibrin. There also is moderate amount of muscle necrosis observed. This confirms the fact that when Mycotoxins are present within the tissue, fibrin is also found.

• The stage of progression of this chemical poisoning of Trichothecene Mycotoxins is evaluated as Late Stage II.

• On examination of the buccal tissue no neoplastic cells were observed.





Diagnosis

The pathology clearly demonstrates severe chronic poisoning for a year in duration to Late Stage II from exposure to the highly irritating epoxides, Trichothecene Mycotoxins, via vapors, dermal contact and inhalation, which is consistent with the formation and progression of the disease called Trichothecene Mycotoxicosis. There are severe yeast organisms observed within the small arteries of the buccal tissue.



_________________________________________

William A. Croft, DVM, PhD, Medical Pathologist





Significance of Tissue Biopsy



Peter Helfrich clearly demonstrates cellular poisoning to the extent of Late Stage II in progression of the disease called Trichothecene Mycotoxicosis within his body. The severity of the fibrinous inflammation in the arteries observed within the buccal tissue, similar to skin is indicative of the state of the rest of the arteries within the body. The integumentary (skin) is of substantial importance and can be used for diagnostic purposes. ,



These highly poisonous epoxide chemicals react systemically, in other words, with all the body’s organs and systems in a generalized diffuse fashion in a stealth manner. By examination of arteries in one organ, a clear picture is available of what will be present in other arteries and other organs with the same extent of damage.

The biology, pathology, and the fingerprint of Trichothecene Mycotoxicosis resulting from consumption, dermal exposure, and inhalation has been well-established in humans and animals and has been widely reported , , , , in the available medical and scientific literature.



There is significant evidence that points to moderate loss of tissue cells and fibrinous inflammation of the other major organs and systems: brain, lung, heart, liver, spleen, kidneys, pancreas and the gastrointestinal, cardiovascular, skeletal, reproductive, lymphatic and immune systems in humans after exposure to Trichothecene Mycotoxins. In most cases, the necrosis, or dead tissue cells from these organs will not be regenerated or replaced.



The reduction and eventual removal of the Trichothecene Mycotoxins that caused fibrinous inflammation indicating Mycotoxin exposure is of the utmost importance in the therapeutic approach of patients with this level of progression of the disease. In cases of continued exposure to the Trichothecene Mycotoxins the intestinal mucosa cannot regenerate and will slough leading to the starvation of the patients. Patients should be made aware of this health condition and attempt to remove themselves from contaminated environments. At this stage in the disease, without treatment of the affected systems, the prognosis is poor, and with therapy the prognosis is guarded to good. Major efforts must also be made to control yeast infection within the body, which is consistent with Trichothecene Mycotoxin exposure.





THERAPY: Treatment of fibrinous inflammation can only be accomplished under a strict set of controlled conditions:

• Controlled environment that is totally free of Mycotoxins.

• Rehabilitative therapy using nutritive means.

• Monitor patient for fungal infection and yeast infection due to the severe immune depression.

• The patient should also be watched and monitored for development of cancer within the following organs: brain, spinal column, respiratory system, liver, spleen, kidney, urinary bladder, lymph nodes, thyroid, parathyroid, hormonal glands, including pituitary gland, gastrointestinal system, reproductive system including breast, pancreatic, skeletal, muscle and skin.

• Peter Helfrich is 33 years of age. The LD-50 (lethal dose at 50%) of Trichothecene Mycotoxins is 500 parts per billion/kg. The patient’s exposure can be computed by dividing the patient’s weight (138 lbs) by 2.2 pounds, will yield 62.7 kg, and multiply that times 90 ppb/kg will yield 5.6 mg, Daryl Stasky exposure to the highly poisonous epoxide chemicals, Trichothecene Mycotoxins, at minimum levels.

• In laboratory rats 500 parts per billion/kg deposited 20-21 microns of fibrin within the small arteries. Peter Helfrich expressed 30 microns of fibrin deposition or equal to 500 ppb/kg or 44.76, Peter Helfrich’s exposure to Trichothecene Mycotoxins on a pathological level. That amount of Trichothecene Mycotoxins is highly significant biologically1-8 and puts Peter Helfrich in Late Stage II of this disease.





Conclusion

It is my opinion to a reasonable degree of pathologic, scientific and medical certainty that the ingestion, dermal exposure and inhalation of Trichothecene Mycotoxins by Peter Helfrich has caused a high number of adverse health effects to the central nervous system, brain, spinal cord, peripheral nervous system, skeletal, respiratory, cardiovascular, digestive, hepatic, pancreatic, renal, reproductive, lymphatic and immune systems and remaining systems.



It is my opinion to a reasonable degree of scientific and pathologic certainty that the available scientific and medical peer-reviewed publications, research literature and studies relating to the adverse and toxic health effects caused by inhalation, dermal exposure and ingestion of Mycotoxins are reliable and widely accepted in their relevant scientific and medical communities.



The opinions I have expressed in this case conform to the current body of peer-reviewed scientific and medical literature, which is generally accepted as reliable in both the scientific and medical communities.



______________________________________________

William A. Croft, DVM, PhD, Medical Pathologist

WAC/kmg

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REPORT

COMPLETE: October 12, 2009
DATE OF ANALYSIS:
Peter Helfrich
35 Clinton St., Apt #10
Plattsburgh, NY 12901

REPORT ID:1118
SAMPLES RECEIVED: 1
Dear Peter,

This is a final report from MouldWorks for the single bulk sample we received October 5th, 2009, taken from your home at 35 Clinton St., Apt. #10, Plattsburgh, NY. Here are your results.

1118-1 tape (Bathroom - Behind Shower)
Microscope:

Penicillium sp./Aspergillus sp.
Stachybotrys sp.

Cultured

Aspergillus sydowii
Aspergillus versicolor
Oedocephalum glomerulosum
Stachybotrys sp.
Trichoderma harzianum
Actinomycetes
Dry-spored Acremonium sp.

General Comments

Our analysis of the above set of samples found abundant evidence of a mold infestation in the bathroom sampled in this home. The sample contained viable spores, vegetative cells and/or reproductive structures from a variety of fungal species, including many molds which require moderately high to extremely high levels of available moisture before they can colonize an indoor site. The presence of these microorganisms can be directly attributed to elevated levels of available moisture locally. Specifically, Stachybotrys requires a water activity of at least 0.94 before it can germinate and colonize indoor sites. Water activity is a measure of the proportion of moisture available to organisms growing on a semi-solid substrate. Finding molds indoors that require such high levels of moisture is a strong indication that this site has experienced flooding, leaks or other water intrusion events. I gather from the chain of custody form that the shower stall had been leaking for some time and this is almost certainly the source of the moisture that supports these colonies. Without first addressing the moisture problems behind the mold growth, molds will undoubtedly continue to plague this site.

Due to the presence of several toxigenic mold species, I'd strongly recommend having a professional come in and clean up the infestation properly to avoid stirring up spores and risking further personal exposure. A professional mold remediator will have the equipment and expertise needed to remove the colony safely, under containment, ensuring that any spores released during the work are removed from the building. It is important that any remediation job is guaranteed with third-party air sampling for mold spores following completion. Without this step, you have no way of knowing whether the project succeeds in improving the indoor air quality

Health Effects

Some of the molds found in this sample have the potential to adversely affect your health. In the paragraphs below, I'll detail some of the risks thought to be associated with exposure to each of the concerning molds that were identified. Let's start by looking at the most concerning mold found in this sample, Stachybotrys.

The whole issue of stachybotryosis and trichothecene mycotoxins is reviewed in a recent book by Nicholas Money (Carpet Monsters and Killer Spores, Oxford University Press). He concludes that Stachybotrys should be taken very seriously indeed. Here is what the findings of the last 5 years suggest:

Stachybotrys toxins include a very potent trichothecene, Satratoxin G, which may seriously damage lungs and internal organs. It is probably the agent responsible for the burning sensation when active strains are inhaled (not advised). In a study published just a little over a year ago, researchers at Michigan State University established a link between Satratoxin G and the death of nerve cells in the part of the brain responsible for the sense of smell in mice. Researchers allowed mice to sniff a single dose of Satratoxin G equivalent to that which a person without respiratory protection would be exposed to in a room contaminated with Stachybotrys chartarum. They then tracked the damage to the neurons lining the nasal passages of the mice at time intervals after exposure. Every mouse exposed to Satratoxin G developed a significant loss of these nerve cells through a process known as apoptosis within a day of exposure. In apoptosis, a type of programmed cell death, cells essentially commit suicide, in this case in response to exposure to Satratoxin G. Additionally, each exposed mouse developed inflammation of the nasal lining and the olfactory bulb, the part of the brain that relays sensory information from the nose to other parts of the brain. Significantly, this inflammation and loss of nerve cells were also triggered by exposing the mice to smaller doses over five consecutive days indicating a cumulative effect.

Although it isn't yet known how Satratoxin G affects human noses, it is known that the nerve cells damaged in the mouse study are similar in both species. Studies in the past have focused on the role very small mold spores or pieces of spores might play in irritating the lungs. However, this study conclusively shows that the nasal passages may be damaged as well. The nose acts as a "scrubber" removing significant amounts of both very large (>5 microns) and very small (nanoparticle-sized) constituents of aerosols. More work needs to be carried out on the effect these particles have once deposited.

In addition there are several other categories of nasty substances made by the fungus, including several which are immune system depressants and may account for vulnerability of people who are chronically exposed to the toxin to respiratory illness - colds, etc. The fungus also makes stachylysin, which causes leakage of blood from the small capillaries and breakdown of the red blood cells.

There are two species of Stachybotrys commonly recovered from interior habitats, S. chartarum and S. chlorohalonata (formally described just a few years ago). These two species can be distinguished on a special culture medium, and I did this routinely in the past. However, after discovering several instances in which both species were present in the same sample, I thought it prudent to consider any Stachybotrys infestation as potentially hazardous. Only about half of S. chartarum strains make trichothecenes, but they may make the other kinds of toxins mentioned above. S. chlorohalonata does not make trichothecenes, but it does make other mycotoxins known to be mutagenic.

It has been claimed that the spores of Stachybotrys are too large to get far into the respiratory passages. However, it is now known that the trichothecenes in Stachybotrys chartarum are localized in the spores and that tiny fragments of the spores (sub-micron sized) can become airborne. These observations suggest in turn that aerosols containing mycotoxins can be generated in environments where Stachybotrys infestations occur even if no spores are seen in air samples. Indeed, pure mycotoxins have been filtered from the air in buildings where Stachybotrys infestations are severe. Given this information, it would be prudent to regard any Stachybotrys infestation as a potential danger and treat the site with respect.

The two Aspergillus species observed in the cultures prepared from your sample are also of some concern. These molds can produce huge numbers of dry spores which are easily lofted into the air and are slow to settle. Spores from any species of Aspergillus should therefore be presumed allergenic. In addition, each of the species identified in this sample may present additional health risks worth discussing:

Aspergillus versicolor produces the mycotoxin sterigmatocystin. This compound is a chemical cousin to aflatoxin, one of the most mutagenic substances known. Fortunately, sterigmatocystin is much less mutagenic than aflatoxin, but sources I consult advise caution when dealing with this mold. Beyond this, it is now known that A. versicolor also produces aerosols of sub-micron particulates that could easily penetrate deep into the respiratory tract; these tiny particles can be mycotoxin-laden, creating a dangerous situation. Very recent work has shown that mycotoxin production in these fungi occurs only at relative humidities in excess of 90% when growing on wallboard and other building materials. The author (Kristian Nielson) concludes that sites which have experienced alternate cycles of wetting and drying are at most risk for mycotoxin contamination. Sites such as this, in which Aspergillus versicolor is mixed in with Trichoderma, Actinomycetes or other wet wall microorganisms, are at maximum risk for contamination by sterigmatocystin. Having said all of that, I must mention that sterigmatocystin does not become really mutagenic until it has been acted on by enzymes in the liver, and it is an open question whether inhaled mycotoxins ever get to the liver.

Aspergillus sydowii is a frequent agent of invasive aspergillosis. The fungus is able to enter the body through the epithelial cells of the lung and disseminate through the blood resulting in acute pneumonia. Although this sounds quite frightening, this condition requires the patient to have a previously existing severe loss of immunocompetence for the fungus to gain hold. Cases in otherwise healthy patients haven't been reported.

Lastly, the Actinomycetes found in this sample are not molds at all, but filamentous bacteria. They produce huge numbers of really minute dry spores which are probably allergenic, since their small size would allow them to penetrate respiratory passages efficiently. Actinomycetes typically grow in wet sites and are part of the wet wall syndrome. These bacteria are typically ignored in mold reports - but they should not be. Workers in Finland have reported that some Actinomycete spores, unlike most toxic mold spores, may actually trigger inflammatory responses in the lungs.


All samples have been processed and analyzed using MouldWorks SOP 1, SOP 2 and SOP 7.

All samples were inspected prior to processing to ascertain their condition. Unless expressly stated in the report, all samples were in adequate condition for analysis.
Sincerely,



Matt Visser
Mycologist and Lab Manager

MouldWorks, LLC
3190 Lakeview Drive
Beulah, MI 49617
541-844-6236