Our Cat Story – Help Us Find Permanent Homes for The Rescues!

We are suckers for cats. They seem to know this and have spread the news amongst each other.

In the beginning (2007 or so), it was my husband and I living in a temporary rental home before purchasing our first home and property outside of the city of Willcox, Arizona (quite rural). At the time, we already had three (3) adult cats that we had rescued as kittens from the hot, dry desert. As you can see, they are all fat and happy.

Perfecta

Perfecta

Axle

Axle

Eloo

Eloo

Then one day while I was outside, a stray female kitty came up to me talking up a storm. She looked a little porky, so I figured she must have a home and did not feed her. Instead I just talked back and petted her. We noticed her hanging around often and began calling her “Mina”. We also noticed that parts of the rental home were “open” underneath where animals and pests could get under the house. I later sat on a quiet evening and swore that I heard kittens, but thought that I must be crazy.

Momma Mina

Momma Mina

Not long afterwards, my husband began befriending Mina too and we ended up putting a box on the porch with food to keep her sheltered from the rains we were having. Both of us still assumed she was a house cat because of her friendliness and fat belly but we were still not sure. Then, before leaving one night, my husband and I were on the front porch and noticed Mina was acting very strange and frightened. Then we saw why. All of a sudden we saw four (4) kittens in the box! OMG! Apparently these are the babies I was hearing…

These kittens were terrified of people and just little bitty kitties a few weeks old (eyes open and rambunctious). AWWW! Because we were on the main road, I told hubby we needed to get them inside the garage immediately for safety. What a job that was! So this is where Tammy, Lulu, Toni and Haley enter the story.

Toni, Tammy, Lulu & Haley

Toni, Tammy, Lulu & Haley

All five cats (kittens and Momma Mina) lived in our garage for a few days, and then they were relocated inside the rental home into one of the spare/unused bedrooms. We had Mina spayed and when the kittens were old enough, they were spayed as well (all females). When we moved into our home, we introduced everyone (Axle, Perfecta, Eloo to the new arrivals). Our original plan was to provide a safe environment with love and spoils until we could adopt the new arrivals out. My husband even said to me, “you know that no one will take care of them like we will.” We figured that with time, everyone would settle in, but that things might be difficult at first.

This have not gone as planned.

Our original cats (Eloo, Axle and Perfecta) each had a different reaction to the new arrivals. Perfecta hates anything new, but she eventually became used to the new cats. She is our oldest cat and has developed some health issues over the years (she is over 10 years old).

Axle is my “Mommas Boy” that used to jump in my arms and hug me, but he has developed some pretty severe behavioral issues and our whole dynamic changed. I cannot even describe how unhappy my Axle is; I have never seen a cat so cranky and upset.

Him and Mina did not get along at all and would attack each other frequently. This (for some reason) caused animosity between Axle and Eloo (who were brothers and buddies). Then things went downhill quickly for Eloo even though he loved his new harem.

We noticed that Eloo had something in his eye and started taking him to the vet. After numerous treatments and medications with no success, I took him back in to see another vet. This vet saw right away that Eloo had a tumor growing that was cancerous. Eloo is now chasing butterflies at the Rainbow Bridge (RIP buddy, we miss you!). This was beyond devastating for my husband and I so I won’t dwell on that for too long, except to note that things became worse between Mina and Axle afterwards.

Eventually, we were able to adopt Mina out, which did help some to settle the crazy dynamic we had taking place in the home (hissing, cattitudes, etc.). But no matter how hard we have tried, things just got harder…

The kittens have now become adults and it has been such a challenge to adopt them out due to being in a rural area. As if this was not difficult enough, we noticed that as they matured, some of them began to exhibit symptoms of Feline Hyperesthesia Syndrome. We also remembered that Mina had seemed to have these same symptoms, so the disease may be genetic according to the vet. We thought that Mina had only been playing when we saw her “spooking” about the house, but with hindsight, it became obvious she had this issue as well.

Of these kitties, now adults, we would like to find homes for Toni, Lulu, Tammy and possibly Haley (We are pretty attached to Haley, but if we found the right person(s), we may adopt her out).

We have provided a safe home for these babies for approx. 3 years (including an outdoor enclosure for them to go in and out safe from predators). However, some changes have resulted in us not being able to carry this on much further (financially and emotionally) but neither one of us wants to take them to a shelter or have them euthanized.

We need some help! It is extremely difficult to organize pet adoptions when you live in a rural area so I will make a shout out to rescuers elsewhere.

We will ask questions to insure the cats go to the proper home with the proper adopted parents.

We will also ask for a $25 adoption fee since the cats have been well cared for and are spayed, but they may need updated shots.

Personalities/Behaviors

All four are Calico females, and are all indoor cats (with exception of enclosure which allows them to be outside, but away from predators!)

Tammy

Tammy

Tammy shows the least symptoms (some back rolling, but she is a very healthy cat otherwise and this does not seem to bother her at all). She purrs and is a happy, social, very vocal cat. I think Tammy would do well in a household without children. She does well with other pets (may be spooked at first). Once she is comfortable, her motor runs.

Lulu

Lulu

Lulu is similar to Tammy in that she has little symptoms of the syndrome, but every once in a great while, does appear to be bothered by a “back-roll” but not for long. Lulu does not purr, is somewhat anti-social, easily spooked but a funny cat. She is the one that will require a one-two person household with no other pets, no children and a nice quiet environment. She is very easily spooked and only comes to you when SHE wants to rub on you. If you try to pet her, she runs away and looks at you as if you are evil. She does let us pet her with our feet :) Lulu is funny because she likes to drag things away. If I give her a scarf or pillow case, she tries to drag it off somewhere and it is just hilarious. She does have personality, even if she is a spooky cat. She just needs a quieter household without other animals.

Toni

Toni

Toni exhibits symptoms of FHS the worst. There are medications for this, but having a calm environment seems to help more than anything (even the vet said she is better off without meds since she does not exhibit severe symptoms such as biting). Touching her while the back-roll is happening seems to make it worse. However, Toni is very sociable, very talkative, but does not purr. She loves to cuddle with Axle and follows him around. She will require a household without children. But she may do well in a household with other pets.

Haley

Haley

Haley also exhibits symptoms frequently and licks herself continually. The episodes seem to last for a few minutes and then dissipate. Haley purrs very softly, she is very sociable, lovable, vocal and just an all around sweet cat. She is the one we are the most attached to. She has also really attached herself to me (we call her TP, short for “Toilet Paper” as if stuck to your shoe because she follows me around). For some unknown reason, Tammy and Lulu like to pick on Haley (stalk and stare at her), so this causes some strife between them.

It took forever to figure out how to get these images in here (glitches left and right) so even though I meant to type more, I am totally exhausted and hope that someone can help us and our babies!

Fore more information, please contact:

marvin(at)powerc(dot)net
angelique(at)powerc(dot)net

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Arizona Wildfires (Wallow, Horseshoe Two, Monument), Victim Support

If anyone in Graham or Cochise Counties effected by these fires needs a place for animals, livestock etc., we have 10 acres just south of Willcox with corral and tack barn and would be happy to help in any way we can. We also have a Dodge cargo-van that could be used to transport whatever to a safe place (animals, people, house stuff). The Horseshoe Two fire is currently 65% contained and does not appear to threaten our area anymore and we would like to help others somehow.

Contact:
Marvin & Angelique Welch
520-384-6294
angelique(at)powerc(dot)net
marvin(at)powerc(dot)net

We have also left our contact information with the city and some other agencies helping victims.

Here are places to go for more help:

City of Sierra Vista: http://www.sierravistaaz.gov/
Relocation Facilities: http://www.sierravistaaz.gov/egov/docs/1308109108175.htm

Monument Fire on Facebook: https://www.facebook.com/pages/Monument-fire-az/152424388163732
Monument Fire Pets on Facebook: https://www.facebook.com/pages/Monument-Fire-Pets/137387109672500

Fire Information, updates, maps, images and more:

Wallow Fire: http://www.inciweb.org/incident/2262/
Monument Fire: http://inciweb.org/incident/2324/
Horseshoe Two Fire: http://www.inciweb.org/incident/2225/

InciWeb has a great list of links here: http://www.inciweb.org/links/

Fire Perimeter In Google Earth (.kmz file): http://www.geomac.gov/asp-bin/GeomacKML/GeoMAC.kmz

USDA Active Fire Mapping Program: http://activefiremaps.fs.fed.us/

GeoMAC Viewer: http://www.geomac.gov/index.shtml

These fires are effecting so much, friends, families, animals, forests, watershed, air quality…Devastating!

For those who pray, please pray for all those effected by these fires. I have a childhood friend that I have known since kindergarten who now lives in Sierra Vista and who may need to evacuate in the near future. Both of us are originally from across the U.S., and ended up in AZ, which we thought was pretty cool until AZ turned into the valley of the shadow of death!

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Horseshoe Two Wildfire, Chiricahua National Monument/Coronado National Forest, AZ

My previous post covers from approximately 5/15/2011 to 6/7/2011. This post will cover images from 6/8/2011 to the present (6/14/2011).

BTW, the trees in my image header are from the Chiricahua National Monument, taken from a visit in approx. 2008 with my little cousin. This fire feels so personal. Now there is another that has begun in Sierra Vista near a childhood friend of mine. She is closer to that fire, than I am to Horseshoe Two. We need RAIN!

This slideshow requires JavaScript.

Here is the updated spreadsheet, where you can see the progression of the fire (based upon Inciweb reports):
http://sheet.zoho.com/public/angeliquewelch/horseshoe-two-reports

DATE STARTED: 5/8/2011
DATE SIZE (Acres) ACREAGE BURNED CONTAINMENT
5/18/2011 AM 30758 25%
5/18/2011 PM 32892 2134 25%
5/19/2011 AM 32892 25%
5/19/2011 NO PM UPDATE
5/20/2011 AM 34451 1559 25%
5/21/2011 AM 35860 25%
5/21/2011 PM 37500 1640 25%
5/22/2011 AM 37500 25%
5/22/2011 PM 40180 2680 25%
5/23/2011 AM 40180 25%
5/23/2011 PM 43000 2820 30%
5/24/2011 AM 43000 30%
5/24/2011 PM 44600 1600 35%
5/25/2011 AM 44650 35%
5/25/2011 PM 47280 2630 35%
5/26/2011 AM 47280 35%
5/26/2011 PM 49760 2480 40%
5/27/2011 AM 49760 40%
5/27/2011 PM 55100 5340 40%
5/28/2011 AM 55100 40%
5/28/2011 PM 59560 4460 40%
5/29/2011 AM 59560 40%
5/29/2011 PM 64290 4730 45%
5/30/2011 AM 64290 45%
5/30/2011 PM 66290 2000 50%
5/31/2011 AM 66290 50%
5/31/2011 PM 72900 6610 75%
6/1/2011 AM 72900 75%
6/1/2011 PM 80500 7600 75%
6/2/2011 AM 80500 75%
6/2/2011 PM 86140 5640 50%
6/3/2011 AM 86140 50%
6/3/2011 PM 90200 4060 50%
6/4/2011 AM 90200 50%
6/4/2011 PM 100200 10000 55%
6/5/2011 AM 100200 55%
6/5/2011 PM 100075 -125 55%
6/6/2011 AM 100075 55%
6/6/2011 PM 104285 4210 55%
6/7/2011 AM 104285 55%
6/7/2011 PM 106661 2376 50%
6/8/2011 AM 106661 50%
6/8/2011 PM 116024 9363 50%
6/9/2011 AM 116024 40%
6/9/2011 PM 128652 12628 40%
6/10/2011 AM 128652 40%
6/10/2011 PM 134615 5963 45%
6/11/2011 AM 134615 45%
6/11/2011 PM 141301 6686 45%
6/12/2011 AM 141301 45%
6/12/2011 PM 148505 7204 48%
6/13/2011 AM 148505 48%
6/13/2011 PM 157254 8749 53%
6/14/2011 AM 171333 14079 53%

I won’t even comment on the inconsistencies.

UPDATE 6/15/2011

I’ve created a group for SE Arizona residents to join as a community:

Group Homepage: http://groups.yahoo.com/group/SEArizona/
Click to join below:

Click to join SEArizona

Click to join SEArizona

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Horseshoe Two Wildfire, SE Arizona/New Mexico

UPDATE 6/7/2011

I do not even know what to say about this fire anymore. Below is a slideshow of how the fire has progressed from our perspective. We have watched flames at night and smoke during the day. The winds have been extreme. The fire is burning an average of nearly 4000 acres per 24 hours and the estimated containment date is not until 6/22/2011.

Yesterday (6/6) was the worst day for smoke yet (see slideshow images and note somewhat clear blue skies before 6/6). The entire valley was smoky (as seen in the images). My husband actually went to the doctor due to breathing difficulties, coughing and sore throat.

For the latest updates on the Horseshoe Two fire, see InciWeb Incident Information System: http://www.inciweb.org/incident/2225/

Here is a public spreadsheet I created based upon the data from the above reports from InciWeb from 5/18 to 6/7. Notice that on 6/4/2011 the AM report claimed that 90,200 total acres had burned. By 6/4/2011 PM report, this changed dramatically to 100,200 total acres burned. Then by 6/5/2011 PM report, 100,075 acres total which is -125 from the previous report. How does a fire consume nearly 10,000 acres that fast and produce a DECREASED total amount of acreage burned in the same 24 hour period?

Additionally, on 5/31/2011 AM report claimed the current containment status was 50%. By the PM report on the same day it went up to 75% containment. However, by 6/2/2011 this was lowered back down to 50% and has again been raised to 55% on 6/4/2011.

Spreadsheet based upon reports from 5/18/2011 to today 6/7/2011

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Mad As A Hatter: Mercury, Porphyria & Porphyrins (Part 3)

I wish I could put this together in a more coherent fashion along side of my own story, but I am utterly retarded lately and can’t get a good writing mojo going. So, for now I’ll post the publications first, and then try to keep a steady pace adding other resources I have found along the way. This post deals with a lot of recent research that is targeted towards understanding more about genetic susceptibility to various chemicals (medications, heavy metals, etc.), which could change how we approach medicine completely.

Here goes…

Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity.
Authors: Godfrey ME, Wojcik DP, Krone CA.
Publication: Journal of Alzheimers Disease, 2003 Jun;5(3):189-95.

There were 400 patients included in this study, all determined beforehand to have histories or symptoms suggestive of mercury exposure. Here are some interesting statements:

“Dental amalgam has been identified as the largest source of mercury vapor in the non-industrially exposed population and this vapor easily penetrates the central nervous system. Amalgam is uniquely situated in the mouth with mercury having direct access to the olfactory lobes and the limbic brain, via the oro-nasal mucosa and via retrograde axonal transport of mercury, with subsequent preferential accumulation of mercury in those areas.” (p. 189)

The article mentions a study funded by the NIH of military personnel which concluded that,

“…amalgam was a major, if the the main, source of mercury found in the body.” (p. 189)

There is so much in this one paper, so please read the full text if possible. Here are a few more quotes and then onto the next…

"At present, there are no readily acceptable in vivo diagnostic criteria for chronic mercury toxicity; diagnosis is predominantly based on patient history and clinical findings. Long-term exposure to mercury results in central nervous system and other effects. These include: chronic fatigue, irritability, mood swings, poor concentration, mental confusion, chronic headaches, insomnia, and tremors. (p. 190)

“…many of the currently middle-aged people with 30 surfaces of dental amalgam, could potentially be at an increased risk of toxicity, including AD [Alzheimer Disease].(p. 192)

“Mercury is destructive at the mitochondrial level where catalase can demethylate organic mercury species into highly reactive inorganic mercury. Inorganic mercury is also an extremely potent enzyme inactivator.” (p. 193)

The conclusion of the study:

“Therefore, amalgam, as the largest source of mercury vapor in the general population, should be included in the differential diagnosis of patients being investigated for neuro-psychiatric problems and short-term memory loss. Apo-E genotyping…warrants further investigation as an in vivo biomarker that could support the clinical differential diagnosis in the primary health environment, and help identify those symptomatic patients who are at greater risk of mercury toxicity and of AD.” (p. 193)

This next paper details more about the Coproporphyrinogen Oxidase (CPO/CPOX) gene and how mutations within this gene predict either an acute or erythropoetic form of porphyria.

Mutations in human CPO gene predict clinical expression of either hepatic hereditary coproporphyria or erythropoietic harderoporphyria.
Authors: Schmitt C, Gouya L, Malonova E, Lamoril J, Camadro JM, Flamme M, Rose C, Lyoumi S, Da Silva V, Boileau C, Grandchamp B, Beaumont C, Deybach JC, Puy H.
Publication: Human Molecular Genetics, 2005 Oct 15;14(20):3089-98.

In Part II of this post the relationship between CPOX (Corpoporphyrinogen Oxidase) polymorphisms, mercury and porphyrins were first mentioned in a paper from 1994 (Homozygous hereditary coproporphyria caused by an arginine to tryptophane substitution in coproporphyrinogen oxidase and common intragenic polymorphisms). The next few papers discuss more recent findings on these topics.

The association between genetic polymorphisms of coproporphyrinogen oxidase and an atypical porphyrinogenic response to mercury exposure in humans.
Authors: Woods JS, Echeverria D, Heyer NJ, Simmonds PL, Wilkerson J, Farin FM.
Publication: Toxicology and Applied Pharmacology, 2005 Aug 7;206(2):113-20.

“Mercury (Hg) in its elemental (Hg0), inorganic (Hg2+), or organic (e.g., CH3Hg+) forms is one of the most predominant toxicants in the natural environment.” (p. 113)

“Two novel single nucleotide polymorphisms were identified in the CPOX gene. One SNP at exon 5 (rs1729995) encoded a G > A change. This substitution led to a synonymous mutation in amino acid 330 (E330E). A second SNP in the CPOX gene was an exon 4 (rs1131857) A> C change resulting in an asparagine-to-histidine change at amino acid 272 (N272H).” (p. 117)

“The present study extends these findings [from previous studies] in describing a N272H polymorphism in exon 4 of the human coproporphyrinogen oxidase gene that appears to specifically modify the effect of mercury on porphyrin metabolism in humans, resulting in excretion of unexpectedly high levels of the atypical porphyrin, KICP [keto-isocoproporphyrin], in the urine.” (p. 119)

“Of particular concern is the potential increased risk of neurotoxicity associated with Hg exposure among subjects with the CPOX4 polymorphism, inasmuch as the neuropsychiatric disturbances associated with prolonged Hg exposure are similar to those observed in the form of porphyria (hereditary coproporphyria) caused by an inherited CPOX deficiency.” (p. 119)

A cascade analysis of the interaction of mercury and coproporphyrinogen oxidase (CPOX) polymorphism on the heme biosynthetic pathway and porphyrin production.
Authors: Heyer NJ, Bittner AC Jr., Echeverria D, Woods JS.
Publication: Toxicology Letters, 2006 Feb 20;161(2):159-66.

This study was conducted between 2001-2002 using 80 male dentists and 98 female dental assistants with prolonged mercury exposure. The purpose was to determine the efficacy of a model for predicting porphyrin concentrations of those occupationally exposed to mercury.

“…an increase in the urinary concentration of specific porphyrins has been described as a biomarker of prolonged exposure to all forms of Hg based upon selective interference with the fifth (uroporphyrinogen decarboxylase, UROD) and sixth (coproporphyrinogen oxidase, CPOX) enzymes of the heme biosynthetic pathway in kidney cells, a principal target of Hg.” (p. 160)

…Hg induces a specific change in the urinary porphyrin excretion pattern characterized by increased concentrations of pentacarboxyporphyrin (5-CP) and coproporphyrin (4-CP), along with the appearance of an atypical porphyrin identified empirically as keto-isocoproporphyrin (KICP).” (p. 160)

“…approximately 15% of subjects from several population studies have been found to display an atypical response to Hg exposure, characterized by excretion of substantially higher concentrations of all three porphyrins, especially KICP, independent of Hg dose. This atypical porphyrinogenic response (APR) to Hg has been attributed to a specific single nucleotide polymorphism (SNP) on exon 4 of the CPOX gene…These findings represent…the first report of a polymorphism in a human gene that modifies the effect of Hg on a biological process and suggest that the APR, which occurs as a consequence of Hg exposure in subjects with the CPOX4 polymorphism, might serve as a biomarker of susceptibility to Hg toxicity.” (p. 160)

The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans.
Authors: Echeverria D, Woods JS, Heyer NJ, Rohlman D, Farin FM, Li T, Garabedian CE.
Publication: Neurotoxicology and Teratology, 2006 Jan-Feb;28(1):39-48.

There were numerous interesting facts and tables from this article. So again, I recommend reading the full text for more details.

“The central nervous system (CNS) is the critical target organ of elemental mercury (Hg0)…” (p. 39)

“These findings, though limited in scope, identify CPOX4 as a genetic factor that potentially could modify the effect of Hg0 on CNS function in humans, potentially increasing vulnerability to Hg0 neurotoxicity.” (p. 46)

“There was also some concordance between dentists and dental assistants that is consistant with the selective behavioral profile of effects characterizing cases of hereditary coproporphyria.” (p. 45)

“We also found that both dentists and dental assistants experienced a decline in neurobehavioral performance at urinary mercury concentrations below 4 ug/l” (p. 46)

“…these findings support existing evidence of genetic susceptibility to Hg toxicity in human subjects.” (p. 47)

Interview with Dr. Boyd E. Haley: Biomarkers supporting mercury toxicity as the major exacerbator of neurological illness, recent evidence via the urinary porphyrin tests.
Authors: Boyd E. Haley, PhD and Teri Small
Publication: Medical Veritas, 2006.

JAMA Papers Perpetuate Myth.
Authors: David Kennedy, DDS
Publication: International Academy of Oral Medicine & Toxicology, June 14, 2006.

A 30-year follow-up of residual effects on New Zealand School Dental Nurses, from occupational mercury exposure.
Authors: Jones L, Bunnell J, Stillman J.
Publication: Human & Experimental Toxicology, 2007 Apr;26(4):367-74.

“The principal finding of this study is that the sample of NZ School Dental Nurses, who were chronically exposed to high levels of mercury vapor from heating CuAm, and skin contact with elemental mercury when mising filling material, do not appear to be neurobehaviorally compromised by their early career choice, now that they are aged in their fifties. However, while the exposed group perceived themselves to be in very good health, there were seven symptoms from a list of 33 selected from a medical definition of mercury poisoning, that were reported to a significantly greater extent than the control group. Unfavorable reproductive outcomes for the exposed group were reported at more than twice the rate of controls. Hysterectomy experience was statistically significantly higher in the exposed group, making this is a topic that warrants further investigation.” (p. 373)

This next article will be of interest to those who have children with autism. I first started coming across these correlations a few years ago and know this provokes many questions from parents (why isn’t my child being tested for porphyrins? polymorphisms? mercury poisoning? or at least ruling out a porphyria!) Strange if you ask me.

The Frequency of Polymorphisms affecting Lead and Mercury Toxicity among Children with Autism.
Authors: Shannon Rose, Stepan Melnyk, Alena Savenka, Amanda Hubanks, Stefanie Jernigan, Mario Cleves and S. Jill James.
Publication: American Journal of Biochemistry and Biotechnology, 2008, 4(2):85-94.

“In summary, we have demonstrated that some autistic children have a significant increase in the frequency of the ALAD2 variant allele that may underlie differential susceptibility to lead toxicity in these children.” (p. 91)

“Based on the behavioral diagnosis of autism, the brain is a common target for investigation into the biologic basis of autism. Nonetheless, because glutathione and heme proteins are ubiquitously expressed in all cells beyond the brain, research into the broader systemic effects of oxidative stress and heavy metal toxicity in autistic children should be pursued.” (p. 91)

Cloning, Expression, and Biochemical Properties of CPOX4, a Genetic Variant of Coproporphyrinogen Oxidase that Affects Susceptibility to Mercury Toxicity in Humans.
Authors: Li T, Woods JS.
Publication: Toxicology Sciences, 2009 Jun;109(2):228-36.

“In conclusion, the present studies evaluated the biochemical and kinetic properties of CPOX4, the product of a polymorphism of the human CPOX gene that modifies the effects of mercury on neurobehavioral functions in humans. The findings suggest that CPOX4 may predispose to impaired heme biosynthesis, which is limited further by Hg exposure. These effects may underlie increased susceptibility to neurological deficits observed in Hg-exposed humans with CPOX4.” (p. 235)

A significant relationship between mercury exposure from dental amalgams and urinary porphyrins: a further assessment of the Casa Pia children’s dental amalgam trial.
Authors: Geier DA, Carmody T, Kern JK, King PG, Geier MR.
Publication: Biometals, 2010 Nov 5. [Epub ahead of print]

“our study…found that the characteristic pattern of porphyria associated with Hg body-burden, specifically, elevated 5cxP, PrcP, and cP were significantly correlated with dental amalgam exposure in a dose-dependant fashion. The higher level of Hg amalgams exposure resulted in higher levels of Hg-associated porphyrins.”

“…this study helps to further establish the utility of urinary porphyrins as a biomarker of low-level Hg body-burden.”

“In addition, the relative 5-10% increases in the Hg-associated porphyrins observed over the8 year course of the present study, suggest that dental amalgams for the average individual do not cause a significant acute exposure to Hg, but instead represent a significant life-long source of chronic exposure to Hg, with a continuing impact on increasing Hg body-burden.”

“…the contribution to Hg body-burden from dental amalgams may eventually result in elevations in urinary porphyrins similar to those observed in individuals with diagnosed neurological conditions associated with Hg intoxication, and hence result in Hg body-burden levels associated with Hg toxicity.”

Here is one more link for this part that has a bunch of other resources to read.

Scientific journal articles, sent to the FDA from the IAOMT
20 Years of funding Peer Scientific Research has produced a prodigious body of empirical evidence

And then, after all of this research (there is still loads of stuff out there!), there are still retard articles like this:

Mercury Fillings: They’re Not Risky: Mercury Vapors Not Easily Absorbed by Body.
Author: Jeanie Lerche Davis
Publication: WebMD Medical News, 9 December 2004.

Here is an extract:

“Mercury amalgam fillings “are 100% safe,” says cynthia Trajtenberg, DDS, professor of…” She goes on to state that once the mercury is combined with silver and copper it is “transformed into a stable metal material that is not easily released into the oral cavity. Therefore, it is not harmful.”

I beg to differ…

Anyhoo, I really want to hear from others who have been mercury poisoned! Please leave me your comments after reading. What do you think? I want to hear from YOU.

Posted in Medical, Mercury, My Rants & Feelings, Porphyria, Porphyrins | Tagged , , , , , , , , , , , , , | 8 Comments

Mad As A Hatter: Mercury, Porphyria & Porphyrins (Part 2)

Please refer to Part I if you are reading this for the first time.

Now that the acute porphyrias have been ruled out with DNA, I have had to re-wind and review prior medical records to try to figure out what the hell happened to me. Trying to obtain copies of my own medical records was just BIZARRE! I did eventually get some records. Well, not the records that “accidentally” BURNED in a FIRE or the records from the diagnosing physician which were “accidentally” destroyed in a FLOOD. I wish I was kidding. After reviewing the records I did get (which oddly enough went back to the year I was born, begging the question of exactly what records in between were destroyed?), it now seems glaringly obvious that the other abnormal test results along with the elevated porphyrins (that were never conclusive for type of porphyria anyway) indicated heavy metal poisoning. This happened to me in 1995, after physicians supposedly should have known that non-specific elevated porphyrins and proteinuria might have indicated mercury exposure and not a genetic porphyria.

I left off in Part I with research that was being conducted and published in the late eighties regarding mercury and porphyrins. Now I will continue into some of the later studies. I always recommend reading the full text of these articles if possible because I do not fully comprehend all of this data and only extract what I feel is relevant to my topic and what I can understand at this time.

Experimental study of proteinuria caused by chronic exposure to mercury.
Authors: Zhao JY, Wang SJ
Publication: Biomedical and Environmental Sciences, 1988 Oct; 1(3): 235-246

Rats were used in this study to determine the relationship between mercury and kidney damage. Here are some extracts:

Although urinary mercury is an indicator of a kidney with a high mercury content, it does not reflect the status of mercury accumulated in kidney (as cited in Friberg et al., 1979[1]). Therefore, urinary mercury cannot be used as an index to monitor kidney damage.” (p. 235)

“The amount of mercury in the urine [of exposed rats] fell quickly after exposure, by 85-90% in 2 weeks. Thus urinary mercury can only be an index of recent [emphasis mine] exposure to mercury.” (p. 238)

“…the increasing excretion of low molecular-weight proteins was the first change induced by chronic exposure to mercury. With continued exposure, the excretion of albumin also gradually increased. These facts suggest that the proximal tubule was the primary site of damage by mercury, and the glomerulus eventually became involved.” (p. 238)

“Proteinuria is one of the most characteristic early manifestations of kidney disease (as cited in Beeson et al., 1979[2]).” (p. 241)

“By concentrating and isolating mercury in lysosomes, the tubular cells can accumulate much more Hg2+ without injury (as cited in Hook, 1981[3]), suggesting that the lysosomes have the strongest protective mechanism against mercury…this protective mechanism with the lysosome as the mercury detoxication center of the kidney had a close relationship with the occurrence of proteinuria and the excretion of urinary mercury…Therefore, proteinuria is a direct consequence of the failing physiobiochemical functions of the cell caused by a shattering of the lysosomes’ protective mechanism against mercury overdose.” (p. 242)

Urinary porphyrin profiles as a biomarker of mercury exposure: studies on dentists with occupational exposure to mercury vapor.
Authors: Woods JS, Martin MD, Naleway CA, Echeverria D.
Publication: Journal Toxicology and Environmental Health, 1993 Oct-Nov;40(2-3):235-46.

This study analyzed the urinary porphyrin concentrations of participating dentists in 1991-1992.

“Mercury selectively alters porphyrin metabolism in kidney proximal tubule cells, leading to an altered urinary porphyrin excretion pattern (p. 235).”

“In terms of specificity, the unique change in the porphyrin excretion pattern, characterized by elevated levels of five and four-carboxyl porphyrins, as well as by the expression of the atypical porphyrin, precoproporphyrin, is, to our knowledge, unique to mercury exposure. This pattern is different from that which characterized any of the known forms of inherited porphyria, and also differs distinctly from those elicited by exposure to other heavy metals…” (p. 242-3)

“Since these properties of mercury may ultimately underlie cell injury and toxicity during prolong mercury exposure, a mechanistic association between mercury-induced porphyria and toxicity involving oxidative stress reactions is suggested (p.243).”

Lastly, the article lists some of the applications of the “Porphyrin Profile Method as a Biomarker of Human Mercury Exposure.” I find #4 the most interesting:

“5. Confirm past [emphasis mine] mercury exposure in clinical and epidemiologic studies and identify susceptible subgroups.”

In my opinion, these studies verify that proteinuria is an indicator of possible mercury damage to the kidneys and that porphyrins can be used as biomarkers to determine past exposures. Why won’t my physicians look at this?

The last article mentions, “susceptible subgroups” which brings up the next study from 1994 discussing the human coproporphrinogen oxidase (CPOX) gene and Hereditary Coproporphyria (HCP). I definitely want to cover more on these topics, but for now it is important to understand that there is a relationship between mercury, and defects in the gene that cause Hereditary Coproporphyria (HCP).

Homozygous hereditary coproporphyria caused by an arginine to tryptophane substitution in coproporphyrinogen oxidase and common intragenic polymorphisms.
Authors: Martasek P, Nordmann Y, Grandchamp B.
Publication: Human Molecular Genetics, 1994 March; 3(3): 477.

The results are thus:

“…we found a point mutation resulted in an arginine to tryptophane substitution (R231W)…Furthermore, three common polymorphisms within the coproporphyrinogen oxidase gene were detected. Two DNA polymorphisms resulted in amino acids changes (H172N and V193l) and the third one was silent (E230E).”

I received the above publication from Pavel Martasek (one of the authors). The full story is for another day, but ultimately Hereditary Coproporphyria was the type of porphyria most physicians believed I suffered from, so my blood was sent to Pavel Martasek in Prague to test for HCP specifically through DNA. The rest I am about to share is confidential, but in the name of information and seeking truth I will share it. No mutation was found, but the silent polymorphism (he calls it E330E, not E230E, in all of my paperwork) was. Supposedly this polymorphism is “silent” but I will go into more about this topic another time. For now I want to note the polymorphisms associated with this gene and continue on to the next paper, also from 1994. (See The Role of Genetic Polymorphisms in Environmental Health. Authors: Lelada SN, Eaton DL, Wang SS, Rothman NR, Khoury MJ. Publication: Environmental Health Perspectives, 2003 June;111(8):1055-1064)

The effect of occupational exposure to mercury vapour on the fertility of female dental assistants.
Authors: Rowland AS, Baird DD, Weinberg CR, Shore DL, Shy CM, Wilcox AJ.
Publication: Occupational and Environmental Medicine, 1994 Jan;51(1):28-34.

Here are some extracts:

“Little is known about the reproductive toxicity of mercury vapour in humans. Six studies, mostly conducted in Eastern Europe, have reported abnormalities of the menstrual cycle including painful menstruation and changes in bleeding patterns and menstrual cycle duration among workers exposed to mercury; two of these studies involved dental workers.” (p. 28)

“The dissolved [mercury] vapour remains in the blood long enough to cross the blood brain barrier where it is oxidised [sic] and eliminated only very slowly. Necropsy studies of occupationally exposed subjects have found high concentrations of mercury in the pituitary, thyroid, and brain and there is evidence that mercury persists in these tissues for many years.” (p. 28)

“As a group, dental assistants have urinary mercury concentrations higher than the general population or other dental personnel, and cases of mercury poisoning have occasionally been reported.” (p. 28)

“We found reduced fertility among the two groups of women in our study with the highest estimated exposure to mercury vapour…” (p. 32)

I was diagnosed with endometriosis (through laparoscopy) in 2002 which does cause infertility, HORRIBLE menstrual periods and abnormal bleeding. In my opinion, mercury exposure may have contributed to this change in my reproductive system.

On further down the research time-line to 1996…

Altered porphyrin metabolism as a biomarker of mercury exposure and toxicity.
Authors: Woods JS.
Publication: Canadian Journal of Physiology and Pharmacology, 1996 Feb;74(2):210-5.

“In summary, we have developed and characterized a test for mercury exposure and potential toxicity based on a readily performed measurement of changes in urinary porphyrin excretion profiles. Initial studies attest to the potential efficacy of this test as a sensitive and specific biomarker of mercury exposure and toxicity among human sugject with low level exposure to mercury from occupation sources.” (p. 214)

That was from 1996! So here it is 2011 and numerous physicians are not aware of this and look at me like I am a retard when I mention porphyrins and mercury?

Continuing down the rabbit hole…

Urine mercury in micromercurialism: bimodal distribution and diagnostic implications.
Authors: Ely JT, Fudenberg HH, Muirhead RJ, LaMarche MG, Krone CA, Buscher D, Stern EA.
Publication: Bulletin of Environmental and Contamination and Toxicology, 1999 Nov;63(5):533-9.

The porphyrias: genetic and acquired aspects.
Authors: Sassa S.
Publication: Rinsho Ketsueki, The Japanese Journal of Clinical Hematology, 2001 Apr;42(4):237-41.

Porphyrinurias induced by mercury and other metals.
Author: Bruce A. Fowler
Publication: Toxicological Sciences, 2001, June;61(2):197-198.

“The heme pathway is also highly sensitive to inhibition by a number of inorganic agents such as lead, mercury, and arsenicals as well as organic agents such as the chlorinated benzenes and alcohol. There is also a high degree of correlation between excretion of specific porphyrins in the urine and other ultrastructural/biochemical alterations in organelles, such as the mitochondria, which contain a numbers of enzymes in the heme biosynthetic pathway. This indicates the utility of porphyrinurias in detecting early stages of cell injury.” (p. 197)

“In summary, the results of this paper provide further evidence of the utility of chemical-induced alterations in the heme biosynthetic pathway as a reliable class of biomarker for delineating both the total tissue burden of a toxic substance such as methyl mercury and the intracellular bioavailability of reactive chemical species of this toxic agent.” (p. 198)

I will cut off here with this last article from Dr. Boyd Haley. I still have more to share, so look for Part 3.

Leading Mercury Scientist, Dr. Haley, Refutes ADA in Congressional Testimony.
Author: Boyd. E. Haley
Publication: unknown original source

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[1] Friberg, L., Nordberg, G.F., and Vouk, V.B. (1979). Handbook on the Toxicology of Metals. pp. 355-369, 503-523. Elsevier/North Holland Biochemical Press, Amsterdam.

[2] Beeson, P.B., McDermott, W., and Wyngaarden, J.D. (1979). Cecil’s Textbook of Medicine, 15th ed., pp. 1331-1332. Saunders, Philadelphia.

[3] Hook, J.B. (1981). Mechanisms of renal toxicity. In Proceedings of the Symposium on Chemical Indices and Mechanisms of Organ-Directed Toxicity (S.S. Brown and D.S. Davies, Eds.) pp. 69-73. Pergamon, Barcelona, Spain.

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Mad As A Hatter: Mercury, Porphyria & Porphyrins (Part 1)

This topic is important to me, but also extremely difficult to write about due to my own experience and anxieties. I have this persistent urge to ask questions and gather information, but then wonder what the heck to do with what I have gathered when it becomes overwhelming. I’ll probably split this topic up into various blog posts instead of trying to fit everything into one. Maybe give some background on my experience and then delve into some of the information that I found. Rather than present everything in the disoriented fragmented fashion in which it happened, or how I found it. I’ll try to provide earlier research first and move forward toward more recent topics or references in later posts. I have a lot to share about mercury and porphyrins. It might end up being my autobiography in the end, but maybe that is what I am supposed to do. I just wish there was a purpose for all that I have been though. Here goes…

When I was eighteen years old I was diagnosed with a rare genetic disease called “acute porphyria” after a severe illness that completely changed my entire life (this is a gross understatement). However, even though I had told myself long ago that nothing I would ever endure in the future could ever be as bad as the first illness and original diagnosis was, I was dead wrong.

I just had some recent DNA studies completed and apparently I was misdiagnosed, well partially (genetic porphyria/likely wrong, acquired porphyrinuria/missed completely). For over fifteen years I have believed that I had a fatal, genetic illness that could cause mental illness and a whole strain of other lovelies. I also made life decisions based upon porphyria being genetic and autosomal dominant (50% chance of passing it on, not to mention an all around horrid illness you don’t want to pass on). However, porphyria or porphyrinurias can also be acquired through environmental exposure.

How could so many different physicians overlook my work environment? These are questions I will never be able to answer. I won’t go into too many details of my own medical case/records/symptoms etc. (interested verifiable physicians email me) except to note two things that might have provided a clue that genetic porphyria was not the answer, even though I was excreting abnormal amounts of porphyrins.

1) Elevated porphyrins were found in my urine and fecal samples. However, no PBG (porphobilinogen) testing was done during the time that I was urinating “strawberry”/”amber” urine in the hospital, which would have helped IMMENSELY when ruling out acute porphyria for sure. The initial porphyria tests were ran four months after the initial illness with discolored urine, vomiting, etc. The proud physician saw the elevated porphyrins and called it porphyria. Because proper testing was not performed while I was in the hospital (porphyrins and PBG during symptoms), and the initial porphyria tests were non-conclusive for a specific TYPE of porphyria, this “gray area” provoked me to ask questions for YEARS.

2) The reason I was kept overnight at the hospital to begin with was an initial urine test showing severe proteinuria (aside from the fact that I was peeing strawberries, puking myself inside out and felt like death) and some other abnormal test results (super high WBC count, high SGOT, rashes, etc.). It was noted in my records that I was a full time dental assistant (I had just started full time that year, after graduating from high school). Since the porphyrin testing was not done until four months after the initial hospital visit, they just called it a “virus” until then, apparently ignoring the proteinuria, other abnormal lab results and symptoms that might have led to what I now know, half my life later.

It was mercury. Not the planet, the Hg kind of mercury. It seems simple to me now, but why did it take so long to figure this out? I could be wrong, but I think it is because I am not the one with the PhD, yet I asked all the questions, did all the research, learned, and basically irritated a thousand different medical “professionals” by persisting they order further tests. If it were not for my persistence and bugging them to know exactly what type of porphyria I had, I would still think I had a horrid genetic disease!

What I was told: Elevated porphyrins = porphyria. Don’t drink, don’t go in the sun and watch the movie, “Madness of King George”. Oh yeah, we call this the “vampire disease”. Oh that’s freaking great! Anything else that may destroy me completely? That was it.

What I learned: Porphyrins are part of the heme biosynthetic pathway/porphyrin metabolism. If this pathway is disturbed, illness can occur. Naturally, I learned only about the porphyrias and how disturbances in the pathway caused porphyria. But I was not aware of the other things that could disturb this pathway causing illnesses that were similar to porphyria, but instead of being genetic, they are acquired.

Porphyrins LOVE binding to metals and they necessary for life, but in excess they can cause damage. Maybe I’ll delve into porphyrins in another post one fine day, but I just want to outline that they are IMPORTANT.

    porphyrin + magnesium = chlorophyll in plants
    porphyrin + iron = heme in humans

Here are some articles from various medical or dental journals. Some are available in free full text online, others can be ordered through PubMed.

Fatal mercury intoxication in a dental surgery assistant.
Authors: TA Cook, PO Yates
Publication: The British Dental Surgery Assistant, 1969 Dec 16;127(12):553-5.
See also, British Dental Journal 1970 Apr;28(9):167

In the article, a 42 year old woman (dental surgery assistant) with approximately 20 years of work exposure to mercury died as a result of that exposure. The high levels of mercury in her kidneys resulted in fatal nephrotic syndrome.

This woman’s symptoms mirror what I experienced while I was dental assisting and became ill, only I did not have nearly the long term exposure that she did. According to the case report the woman became,

“suddenly ill with vomiting, pain the the right lumbar region of the abdomen, adema of the face and legs, and the passing of dark urine.”

WOW, no way, me too! I was lucky though, she ended up going into renal failure, convulsions, cardiac arrest and then passed away. The report concludes with,

“Little doubt can remain that the rapidly fatal renal failure in this case was the result of mercury intoxication.”

Systemic mercury levels caused by inhaling mist during high-speed amalgam grinding.
Authors: Cutright DE, Miller RA, Battistone GC, Milikan LJ.
Publication: Journal of Oral Medicine, 1973 Oct-Dec;28(4):100-4.

Within this article is a list of conclusions from a book titled, Mercury in the Environment (Lars Friberg and J.J. Vosral):

8. Data from studies in both the U.S. and U.S.S.R. indicate that exposure to metallic mercury may give rise to effects at considerably lower concentrations than have been recognized before.
9. Despite the fact that exposure to, for example, metallic mercury has occurred for very long times; the biological half-life and accumulation risk in human beings in different organs are not known in any detail.
10. It is obvious that mercury compounds have various effects on the genetic material. Apparently all compounds are active as c-mitotic agents.

At the time this article was published (1973) there were apparently no references or previous studies to refer to regarding the mist created by high speed amalgam removal. This study used rats and exposed them to amalgam mist, concluding the following:

1. The dust [amalgam dust from removal] is almost immediately absorbed into the bloodstream as shown by immediate increases detected by measuring the blood mercury content.
2. The heart receives extremely high levels of mercury within minutes after exposure. Eighty-one times higher than the control level.
3. The brain and liver reach their very highest levels of mercury at 16 hours post exposure. Both these levels were approximately 7 times higher than controls.
4. The heart, liver, brain and kidney concentrate mercury from the blood.

“The authors cannot at this time state how much is absorbed by a patient under varying conditions or positively state that this rat study is comparable to humans. However, the authors wish to point out the possible dangers of exposure to mercury even in minute quantities that might occur in the dental practice.

U.S. Army Institute of Dental Research
Walter Reed Army-Medical Center

Embedded Sentinels of Toxicity.
Author: Janet Raloff
Publication: Science News, 1987 Feb 21;131(8):123-125.

This article jumped out at me while performing a search during a college course and using their “EBSCO” system for retrieving published articles. There are numerous important points made in this article, so I recommend reading the full article above.

Apparently researchers have KNOWN that porphyrins can be used as biomarkers for toxic exposure since 1987! (maybe one day I will explain why this comes as such a shock). For example, one quote states,

…enzymes that convert one porphyrin into the next during the synthesis of heme “are quite sensitive, as a group, to chemically induced disturbances,” explains toxicologist Bruce Fowler of the National Institute of Environmental Health Sciences…As soon as the action of one enzyme in the process is blocked, the porphyrin on which it was to have acted begins accumulating in the urine or blood…Identifying a relative excess of one or more porphyrins and a shortage of succeeding ones in the heme-building process “sort of points the finger at which enzymes are being inhibited by a toxic chemical,” Fowler says.

Additionally, a well known incident that occurred in Turkey in the late 1950’s was discussed in which three to four thousand people developed a porphyria after eating wheat that had been treated with hexachlorobenzene (HCB). This is one of the earliest examples of the use of porphyrins as a biomarker for a toxic chemical exposure. Until this huge porphyria epidemic, it was believed that all of the porphyrias were genetic.

Porphyrinurias and occupational disease
Authors: MO Doss
Publication: Annals of the New York Academy of Sciences, 1987;514:204-18.

The author cites a Goldberg and Rimington report from 1962,[1]

In the past the term ‘porphyria’ was reserved for those diseases of porphyrin metabolism caused by an “inborn error of metabolism,” that is, a genetic defect. “Porphyrinuria” was the term used to describe minor disorders of porphyrin metabolism induced by other diseases, or certain drugs or chemicals….The term “porphyrinuria” should be confined to those minor disorders or porphyrin metabolism caused by another disease, or certain drugs or chemicals, in which the clinical features are not directly attributable to the porphyrin abnormality.

This article came out the same year as the article above it (1987). Both differentiate between the genetic and acquired porphyrias by calling the acquired or non-specific porphyrin abnormalities “porphyrinurias” or “porphyrinopathies”.

I have not even produced 99% of the resources I have compiled and I believe that anyone with an IQ could review my records from 1995, and determine mercury was the likely cause. However today, even from well known toxicologists in my area (rural), I am told that they are not sure what could have caused the porphyrin abnormalities and do not care to seek out what may have caused them or my current disability. However the irritating/conflicting things I have been told are for another day.

That wraps up Part 1 of this post. In my next part, I will provide more articles from PubMed moving later into further research (1990’s) where porphyrins are being used as biomarkers to detect occupational exposure to mercury in dentists and more.

I will always feel like I am forgetting something or that there is some detail that will help someone understand where I am coming from and what this means to me. All well. My emotions and feelings are here for everyone to see, errors and all.

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[1] Goldberg, A. & C. Rimington. 1962. Diseases of Porphyrin Metabolism. C.C. Thomas. Springfield, IL. BACK

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