Let He Who Has Not Sinned Cast the First Stone

Ripping Off the Genetic Bandaid:

This is how government and researchers provide themselves with an income.  Not only that, they lead breeder’s to believe that the health/genetic tests they use as a “guarantee” for puppy buyers are dependable tests causing problems for breeders when a puppy is returned for a genetic problem or the breeder is accused of selling “sick” puppies because of the genetic test.  A test is only as good as the research that provided basis for that test.  Before the argument of “that person is a purist” is approached, I am not against opening a stud book for genetic diversity reasons.

Almost all research for human diseases start with animals.  The Dalmatian is considered by researchers to be a “unique” dog because it processes uric acid in the same fashion as HUMANS.  Dr. Robert Schaible started the Dalmatian backcross experiment over thirty years ago.

The reason for investigation into the genetic uric acid process in Dalmatians was, according to Dr. Bannasch’s research grant from the National Institutes of Health (NIH) “The Dalmatian is unique among dogs in that it excretes uric acid rather than allantoin……..Uric acid levels are a contributing factor for many human diseases including gout, kidney stones, cardiovascular and renal disease. The elucidation of a novel gene function should provide new avenues of investigation for the treatment of the human condition.” [1]

If you can read through the verbal spaghetti, this is the beginning of Genetic Engineering.   Scarey Stuff when you know how the conclusions were brought about.

The actual way to give some proof as to whether or not an experiment works is through laboratory tests on an animal.  In my opinion, some proof would have been:

  1. Controlled Lab experiments in food; Backcross Dalmatians fed a high purine diet over a period   of time  (a low purine diet is suggested for Dalmatians that form urate stones)
  2. Controlled water experiments
  3.  A control group of “HUA” Dalmatians AKA Regular AKC Dalmatians that had not been backcrossed.
  4. Testing for stones, of any kind, in a group of Backcross Dalmatian’s lifetime. (Dalmatian stone disease does not generally appear until the dogs are at least five years old.)

None of the above suggestions, nor any others,  were used in any experiments on the Backcross line of Dalmatians and were refused based on the statement from a Backcross proponent that the IACUC would not approve tests.  This turned out to be a bit of a stretch of the truth.  While I am uncertain as to the actual truth of the matter, Dr. Irvin Krukenkamp had an email forwarded to the DCA email list that said “The CHF rejected the PRE proposal on the grounds that it does not fund research from Breed clubs (or individuals).”  Research would have been helpful to prove if those backcross Dalmatians produced a lower than rate of urate stones or infection stones than AKC Dalmatians and other dogs.

Dr. Danika Bannasch gave a lecture at the Dalmatian Club of America National Specialty in 2007 concerning genetics and uric acid in Dalmatians.  I was personally there and witnessed Dr. Bannasch say that the research was going slowly but tried to console those that were having doubts even though Dr. Bannasch’s and Dr. Robert Schaible’s research had been underway for years, over 30 years with Dr. Schaible.

Approximately eight months before a Dalmatian Club of America AKC Breed Club vote about registration for “a healthier Dalmatian”. Jan 9 2008 Denise Powell, reviver of the Backcross experiment (The Heritage Project),  sent a personal email to myself and Dr. Irv Krukenkamp: “I know very well, that Bob’s reports about the dogs in his breeding program cannot be considered scientific proof any more than any breeder’s claims about their dogs are proof” .  Dr. Robert Schaible, Geneticist and professor of Genetics as Purdue University,  is creator of the backcross Dalmatian breeding experiment over 30 YEARS AGO!

Another email from Denise Powell, Backcross Dalmatian experiment reviver :“I am relying not only on what Bob Schaible (who has a PhD and taught genetics at the medical school at Purdue) tells me about the descendants of the backcross project, but on the opinions of very knowledgeable people who have studied all the available science. People like  Irv Krukenkamp MD, Dr. Suzy Hughes DVM, Mary-Lynn Jensen, PhD, Jim Seltzer, PhD, Danika Bannasch, DVM, PhD” Denise Powell, Backcross Dalmatian “reviver”,  personal email.  Compare this with information that is thrown around on the internet by those paid by HSUS.

In May 2008, I found an article [3] that had been published in the National Institutes of Health PubMed website which appeared to prove what Tremble and Kempler [6] had already discovered back in 1938 about uric acid and Dalmatians.  This pubmed.com  information was published by a University Professor in the Dalmatian Club of America’s magazine, The Spotter.  Note that I was only giving information.  While I thought I knew what it was, I did not decide at the time whether or not it was right or wrong nor did I have it published in The Spotter but was asked permission, at the time I did not understand why my permission needed to be granted.  I am not a university educated medical researcher nor am I a doctor, Just the messenger.

Sometime around mid 2008, I received a phone call from my Dalmatian’s breeder (a DCA board member) asking me to agree to place a letter in front of the ID number of Backcross Dalmatians to approve AKC registration.  My reply “NO!”  The reasoning behind my personal refusal was the fact that the breeder’s that were promoting the experiment were touting “healthier” Dalmatians, a marketing ploy without any proof.  Notice the similarities to animal rights?!  Not even to mention the fact that the University of California Davis research, who was conducting the genetic research in Dalmatians, is heavily supported by the Morris Animal Foundation who has Andrew Rowan, Chief Science Officer of the Humane Society of the United States (HSUS/an animal rights group), on the Animal Welfare Advisory Board.  Animal Rights and Animal Welfare are NOT the same.  Animal Rights and Animal Welfare are a contradiction in terms.   One other downside to this “solution” was: the majority of people not familiar with AKC registration paperwork would not know what the “letter” in the ID number meant.  The dogs would be shuffled into the gene pool like a deck of cards.

Most people would not appreciate the full meaning of “shuffled into the gene pool like a deck of cards.”  To explain: Veterinarians automatically assume when presented with a Dalmatian patient with stone disease, that Dalmatian is treated for Urate Stones with a snap of a finger without checking to see what KIND of stone the Dalmatian has.  When changing the genetic makeup of a breed, and then shuffling them into the gene pool, dogs will be misdiagnosed with the incorrect type of stone because of the Veterinarian’s assumptions.  Dissolving different types of stones takes different kinds of medications.  Correct analysis of stones in veterinary offices is very low.

If the whole point to the Backcross Theory was to create healthier dogs, wouldn’t you want it stamped in big bold letters on their registration?!  Later on, a Backcross Dalmatian was registered in England and after registration, the owners request was to REMOVE the letter on the registration certificate. 

In another telephone conversation with my Dalmatian’s breeder in August of 2008, I was told that Dr. Danika Bannasch had submitted a final research paper on uric acid in Dalmatians but it had been rejected and resubmitted.

Received: August 12, 2008; Accepted: September 30, 2008; Published: November 7, 2008: “Mutations in SLC2A9 will likely have important consequences for a number of different disorders of uric acid homeostasis in people.” Plos Genetics: Bannasch D, Safra N, Young A, Karmi N, Schaible RS, G. V. Ling. (2008) Mutations in the SLC2A9 Gene Cause Hyperuricosuria and Hyperuricemia in the Dog. PLoS Genet 4(11): e1000246. doi:10.1371/journal.pgen.1000246 [7]

If you take the time to read the article referenced above, you will notice that there is absolutely no information on how many of these “Backcross Dalmatians” did or did not produce stones.  In fact, up until the time I had discontinued membership with the Dalmatian Club of America there was no information or research on how many or if any of these Backcross Dalmatians produced stones, the reason for the experiment to begin with over 30 years earlier.

The very same day the article referenced above was published in Plos Genetics, the following article was published in Veterinary Practice News: “Gene Responsible for Bladder Stones in Dalmatians Found”  Friday, November 7, 2008, 7:30 p.m., EDT. The study was supported, in part, by a fellowship from the Morris Animal Foundation and the National Institute of Diabetes and Digestive and Kidney Diseases within the National Institutes of Health”[8] The very same day the article was published in the National Institutes of Health pubmed.com website.

A tab on updates to the DCA website concerning the backcross theory was kept by Carroll Weiss, Former Director (1991-2002) DCA Study Group on Urinary Stones. “Disclaimers suddenly appearing on the 12 June 2008 **official LUA/Backcross website.**  :.

Disclaimers DCA LUA webpage ”

Pay very close attention to how animal rights transforms the word “breeders” into that dreaded nasty phrase “puppy mill” and then apply that method to how “Backcross Dogs” was transformed to “Normal Dalmatians” and “Uric Acid” to “Urate Stones” without any proof or scientific documentation of a “healthier Dalmatian.”   Note that in documentation, after being called out, the “medical records” and “numerous boxes of data” disappeared from the website and became “There is no formalized ‘project’, ‘study’ or ‘research’ that pertains to the breeding of LUA Dalmatians [backcross dogs].”  Then ask yourself, why would they want to call a “healthier Dalmatian” a “Normal Dalmatian” when normal is a high uric acid dog in Dalmatians?  Ever heard of the shell game?  Keep  your eye on the ribbon, urate stones not uric acid.

The following is an example of how they were changing the name of these dogs from “Backcross Dogs” and eventually all the way to “Normal Dalmatians (NUA)” without so much as a blink of an eye.  This is the exact same method animal rights groups use and change words to confuse : “For now we are using the term LUA descendants for the pups with the Uu or UU gene and HUA descendants for the pups with the uu gene. If you can suggest a term that can be applied to all pups from litters where some are LUA and some are HUA, please let the LUA committee know” Jan 9 2008 personal email from Denise Powell, owner of the “heritage project” and backcross Dalmatians.  Later in the year, an email was sent out by Dr. Irvin Krukenkamp about “nomenclature” (and knowledge of NIH Dr. Elaine Ostrander’s work) which is just a fancy word for definitions.  This was a way for someone with a fancy title to tell everyone that the words and definitions you once knew from Webster’s Dictionary were being changed in the middle of the show.  Sounding familiar yet?  Wayne Pacelle is excellent at this slight of hand.  Remember, “breeders” to “puppy mills” and “uric acid” to “urate stones”.

You might pay a little attention to the genetics being used but the most important issue, and the issue they claim to be addressing, is urate stone disease in Dalmatians.  Don’t take your eye off the ball, urate stones.  Big words and confusing genetics can distract the eye from the goal.  Look for proof of the backcross theory.  What is the Cause of urate stones in Dalmatians?”  Not “what are the symptoms” or “what is the identification of the urate transporter” but the actual Cause of urate stones.  You have to know if dogs do or do not have urate stones to know if they will ever produce or not produce urate stones.   On January 9, 2008 Denise Powell wrote in a personal email to myself and Dr. Irvin Krukenkamp; “But I feel confident that, in time, research will prove that the LUA Dals are free of risk of forming urate stones. “  Scientific Medical research does NOT depend on what someone Feels.

From the very moment that discussion broke out in the DCA about stone disease, emotional, not scientific, arguments with big words were being thrown around.  An example of this is “Hyperuricosuria occurs when excessive amounts of uric acid are found in the urine; the acid can form “stones” that block the urethra and require surgical removal.” [9]This is a quote from the University of California Davis (UC Davis) website.  A little truth can be found in most emotional arguments.  In the previous quote, “surgical removal” is the emotional heartstring.  This type of surgery is a very bloody and disturbing operation.  The problem with the UC Davis argument is urate stones are one of the easiest forms of stones to dissolve compared to other types of stones and rarely require surgery.  There are many types of stones and ALL dogs, and ALL humans for that matter, are capable of forming a bladder or kidney stone.   Note the similarities to animal rights propaganda, a little truth here and there with a pull of the heartstring at the end.

A personal email sent to myself from Joanne Nash, a prominent Dalmatian breeder and a Backcross Dalmatian (LUA) breeder wrote on August 20, 2008 “LUA dogs do not form urate stones. They may form other types of stones from infections, etc., just as other breeds do.”  Without proof of any kind, a well-respected Dalmatian breeder of many years, specifically told me, a novice Dalmatian enthusiast, that backcross Dalmatians (LUA) would not form urate stones.  So why would the Dalmatian Club of America Foundation hire Joe Bartges, a professor at the University of Tennessee, to conduct research as to why some Dalmatians form urate stones while most do not even though “ALL” Dalmatians are considered to be producers of high uric acid levels, just like humans?

Danika Bannasch, DVM, PhD, Professor of Genetics, Department of Population Health and Reproduction, nominated Powell for the El Blanco honor. “Denise revived an almost dead breeding experiment to produce ‘normal’ Dalmatians that will never develop urate bladder stones,” Bannasch explains. “We used these dogs to identify the gene and causative mutation for excretion of high levels of urate in Dalmatian urine.” [2] Notice the jump to conclusion without any proof.  The identified gene may or may not actually be the cause for excretion of high levels of urates but does not prove the cause of forming stones when only a small percentage of Dalmatians form urate stones but “all” Dalmatians are “fixed” for the recessive gene identified.   Another way to put this would be something like ALL Dalmatians/Humans have high uric acid levels but only a small percentage of them form urate stones.  High uric acid levels and urate stones are NOT interchangeable phrases.

On January 15, 2008, this article was posted to the DCA email list and the “showdal” list :“The high levels of uric acid in the blood serum, though precariously poised to form stones in the urinary tract, also help prevent cancer and contribute to long human life spans. For other mammals, the conversion of uric acid to more soluble forms before elimination deprives them of a key antioxidant and limits their life spans.” [4] Notice how one doctor’s viewpoint can completely contradict another.  You have to have proof, not just their word.  Please make sure to note that I am NOT saying that this article was correct.  I am showing an opposing viewpoint that would have to be proved.  Notice how I could persuade you to believe, without any proof, that uric acid in the blood serum could help prevent cancer.  There’s that heartstring.  Cancer and “limits their life span.”  See how animal rights groups have such an easy time convincing everyone that “breeders are bad” to “puppy mills are bad” to “hobby breeders are bad” and then to “hobby breeder puppy mills.”

The American Kennel Club (AKC) consideration of the registration of Backcross Dalmatians based solely on their genetic makeup, not a medical improvement, by National Institutes of Health Elaine Ostrander, Dr. Jarold Bell AKC Health and Welfare Advisory Panel and Tuft’s University, Dr. Patricia Olson Morris Animal Foundation President at the time and currently of the Humane Society of the United States Veterinary Association.  NOT ONE mention of anything conclusive, one way or the other, concerning urate stones in Dalmatians. Not one mention of how many dogs produced urate stones, stones of any kind, or whether they were clear of stones their entire lifetime.  However, the paper referenced above states “for molecular genetic studies that may assist the breed in resolution to this issue.”  [5] What “issue” are we talking about here????!~!!!!!!!  The actual issue is Dalmatian stone disease not the identity of a gene.  All cheek swab submissions for backcross Dalmatians were those submitted by Denise Powell on 27 Dalmatians without anyone checking to see if those cute little ribbons around the puppies’ necks fell off and were replaced or mixed up.  Remember, “There is no formalized ‘project’, ‘study’ or ‘research’ that pertains to the breeding of LUA Dalmatians [backcross dogs].”  Over 30 years of experimentation and only TWENTY SEVEN submissions? 

Mary Lynn Jensen PhD., a previous Dalmatian Club of America Foundation (DCAF) board member, an owner/breeder of backcross Dalmatians and extremely active in promoting the Backcross line of Dalmatians, was kind enough to answer questions on the DCA forum.  In 2008 during the backcross registration discussion in the DCA,  Mary Lynn Jensen replied to a question about high uric acid being the cause of urate stones.  She said that “Researchers *have* looked at this issue for many years from many different angles and have never been able to identify a *single* factor that causes this condition to occur.”  In essence,  Mary Lynn Jensen PHD said that high uric acid is NOT the cause of urate stones in Dalmatians.  Adding to the mystery of Ms. Jensen’s words was an email sent from her on November 13 2012 to a prospective puppy buyer “…yes it is possible to breed a Dalmatian that will not ever have urate stone problems.  The high uric acid levels found in most Dalmatians (and humans) are caused by a simple recessive gene and so by breeding carefully to a descendant from a one-time out cross to a Pointer more than 35 years ago, it is possible to produce Dalmatians who carry copies of the gene for normal levels of uric acid.” An EXACT quote from Ms. Jensen’s email.

Even I could be misled from the statement above after reading their writing for years. This is done intentionally to mislead.  High uric acid levels are like a warning ticket you might get from a police officer.  The officer notices that you are a “cute blonde” and thinks he might be able to get your phone number by issuing you a “warning” traffic citation.  This doesn’t mean that you were actually speeding although you could have been.  This just proves that you were driving a car.  The officer did not stop the driver because of a violation.  The same applies to urate Stones.

Dalmatians are capable of producing Urate Stones but only a small percentage of them actually do, just like humans.  2010 VETERINARY TEXTBOOK authors are the U. Minnesota Stone Center’s experts, Drs. Carl Osborne, Jody Lulich, and Joseph Bartges “Although all Dalmatian dogs excrete relatively high quantities of uric acid in their urine, apparently only a small percentage forms urate uroliths [stones].” [10] Raise your hand if you have every produced a Urate Stone.  A few hands raised out of Billions of people even though you are all capable of producing urate stones.

I practically begged the Dalmatian Club of America to stop the misinformation that was being spread around.  Their reply was almost an absolute refusal.  From the time that I spoke out wanting proof of claims that were being made, there were many direct and indirect threats to me personally and to others that were being vocal about their disbelief in the backcross theory.  This is one of the last messages that I sent to the DCA online list:

—– Forwarded Message —– From: Igignac <igignac@cox.net> To: Kimberly <dalmatianlane@yahoo.com>; DCA <members@thedca.info> Sent: Wednesday, March 17, 2010 8:37 PM Subject: Re: [DCA Members] APGAW (Health Quotes)
Kimberly,
These are wonderful rules that should benefit   all dogs.  Thank you for bringing them to our attention,  I think it   would be a great idea to bring such thoughts to A.K.C. and see  if we can   get them to embrace these  rules.
Ivan Gignac igignac@cox.net
 _____________________________________________
 Kimberly wrote>
http://www.labour.org.uk/animal_welfare_policy [accomplishments   of the labour party concerning animals]
http://www.worldanimalforum.org/about_member_en.php [heads   of RSPCA, HSUS, WSPA “having lunch”]
http://www.rspca.org.au/how-you-can-help/campaigns.html [campaigns   of the RSPCA, exactly those of HSUS]
http://www.wspa.org.uk/latestnews/2008/udaw_apgaw.aspx [WSPA   is a HSUS affiliate influencing the APGAW]
 Here’s some, and just some, of the APGAW’s suggestions on   laws to make about pedigreed purebred dogs.
1. Any person who breeds dogs (whether or not in the course of a business)   must follow good breeding practice. What is “good breeding practice” could be   set out in a code of practice drawn up by a suitable expert body. To fail to   follow good breeding practice could be an offence, perhaps similar in form to   s9 of the AWA 2006.
2. The regulation could include a prohibition on the showing of a dog   unless that dog has been certified by an independent body to have been bred in   accordance with good breeding practice.
3. A certificate of health would be a requirement for those that want to   purchase insurance for their pets.
4. An exemption of health tests for all dogs at a “re-homing”   center.
There’s more but those against animal rights groups do   not congregate with animal rights groups.
Kimberly Long dalmatianlane@yahoo.com

From: “TYRODAL1@aol.com”   <TYRODAL1@aol.com> To:   members@thedca.info Sent:   Wed, March 17, 2010 9:37:22 AM Subject: [DCA Members] APGAW (Health   Quotes)

The list of animal welfare organisations that contributed is endless   but if you go to the above link you can read for your selves. RSPCA being a   major animal charity was of cause one of them.
Membership of the inquiry was made up of 9 MP’s and 3 peers including   all political members of the associate parliamentary group for animal welfare   (APGAW) were sent a letter inviting them to participate and the resulting   members reflect the major political parties.
The members were as follows…
  • David Ames MP (Conservative)
  • Harry Cohen MP (Labour)
  • Baroness Gale (Labour)
  • Mike Hall MP (Labour)
  • Lord Hoyle (Labour)
  • Eric Martlew MP (Labour) Eric Martlew MP, Chairman of the Associate Parliamentary Group     for Animal Welfare (APGAW) invited the World Society for the Protection of     Animals (WSPA) [an HSUS company] to present a new initiative which     could improve animals’ lives all over the world to the Group today http://www.apgaw.org/news.asp?newsID=27
  • Baroness Masham (Crossbench)
  • Eliot Morley MP (Labour)
  • Mark Pritchard MP (Conservative)
  • Andrew Rosindell MP (Conservative)
  • Andrew Stunell MP (Lib Democrats)
  • Roger Williams MP ( Lib Democrats)
And this does not include input fom the science world! Further more   Kimberly, I have no idea were you got the idea that Labour is   an animal rights lobbyist party?
Are you trying to say that all these reports on Pedigree dog health   have some hidden agenda? other than saying health should be apart of pedigree   dog breeding.
What is the point in funding health projects if the results are   ignored by breeders because they think it will limit the genepool when infact   the more healthy dogs you have the bigger the genepool becomes. Do you realise   the only objection the clubs in the UK had against me importing my 2 NUA   Dals is the fact that the US as poorer hearing stats than the UK and Europe,   because you still breed from blue eyes and uni’s. The USA is the only country   in the world that readily excepts these dogs in a breeding program.
Health is as easy or difficult to breed for as we wish   to make it. there will always be those who will not see health to   be as important as they should, but the breed clubs should always be   setting goals to make sure that there members do.The DCA have done and paid   for more research than any other club, Why choose to ignore the   results.
Julie Evans
http://www.tyrodal.co.uk/ Breeder of show & working champion   Dalmatians and Knabstrupper Spotted Horses. Tel – 07786 148749. 01341   280805 Please check out – A healthier future for Dalmatians… nuadalseurope.co.uk  

Genetics can be confusing.  Pay attention to the common sense.  “Identification of the gene and mutation that cause high levels of uric acid in the Dalmatian dog will further establish it as a model system for the human condition. Uric acid levels are a contributing factor for many human diseases including gout, kidney stones, cardiovascular and renal disease. The elucidation of a novel gene function should provide new avenues of investigation for the treatment of the human condition.”  What “condition” are we talking about here?  ALL Dalmatians/Humans have high uric acid levels but only a small percentage of them form urate stones. If all humans have the “condition” of high uric acid levels, why is it considered a disease in humans and Dalmatians?  And notice, not one mention of the actual problem that was being addressed to begin with, Urate Stones.  And why would humans live approximately 75 years and Dalmatians only 11?  I understand that you may not fully appreciate the last question but Think About It!

Now think about animal/pet legislation.  Researchers need money to conduct research.  This is a business of rush, rush.  Hurry for the answer even if it isn’t the correct answer, just something that looks good to get to the next research project to get more money from the government/NIH.  Even when that research goes bad, generally no one knows why a dog/person became ill but it’s another reason for a poorly advised lobbyist to go back to the government to say “look at all these dogs/people that are dying, we need more laws to protect them and more money for research.”  See how “they” circle the wagon?!  Who thinks that a researcher is going to step in front of a firing squad to say to the group of people their “poor” research affected negatively, I DID IT.  That is not only a career pitfall but a complete financial ruin.

I make mistakes just like anyone else.  If anyone has any complaint about what I have written, please feel free to email me anytime.  dalmatianlane@yahoo.com

Kimberly Kraemer

Former member of the Dalmatian Club of America

P.S.  In the interest of Full Disclosure: I was member of the AKC Dalmatian Club of America (DCA) for about two years and personally handled a Dalmatian to Championship.  There are only a few people in the DCA that I know personally.  One of my AKC Dalmatians was bought from a person that bred Dalmatians on her farm who was accused of being a “backyard breeder” and that Dalmatian was accused of a lineage from a “puppy mill”.  Mr. Wipple, a Patches, died at the age of Eleven and 1/2 when he was medically misdiagnosed urinary tract problem.  The best dog I’ve ever owned.  A Dalmatian’s lifespan averages around Eleven years for those Dalmatian owners that have been surveyed, according to reports that I have read .

Young Wipple 001 - Copy

1. http://www.labome.org/grant/r21/dk/the/molecular/the-molecular-basis-for-an-animal-model-of-inherited-hyperuricosuria-7230143.html
2. http://www.vetmed.ucdavis.edu/whatsnew/article.cfm?id=2528
3. http://www.ncbi.nlm.nih.gov/pubmed/18327257
4. http://www.reasons.org/articles/kidney-stones–evidence-for-divine-design
5. http://www.thedca.org/LUA/MARSreport.pdf
6. http://www.jbc.org/content/125/2/445.full.pdf
7. http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000246
8. http://www.veterinarypracticenews.com/vet-breaking-news/2008/11/07/gene-responsible-for-bladder-stones-in-dalmatians-found.aspx
9. http://www.vetmed.ucdavis.edu/whatsnew/article.cfm?id=2528
10. 2010 VETERINARY TEXTBOOK authors are the U. Minnesota Stone Center’s experts, Drs. Carl Osborne, Jody Lulich, and Joseph Bartges

And for anyone that is interested,  It is not as though I do not believe in medical research.  In fact, here’s a theory….REMEMBER, I SAID THEORY!:

—– Forwarded Message —– From: Kimberly Long <dalmatianlane@yahoo.com> To: Jacki McGovern <tarbarr_dals@yahoo.com> Sent: Sunday, February 3, 2008 10:58 PM Subject: Theory

Here Jackie…..take a look.  I went on your female VS. male theory.  This is some of what I came up with.  I think some of the stone formers might be consuming high levels of minerals …zinc, lead and molybdenum.  Not enough to poison them completely but enough to elevated their uric acid level to form stones.  I have my own case study right here in front of me…..with my own Dal that passed away a couple of years ago.
Kim
P.S.  Tell me what you think.  Am I off my rocker? LOL
THEORY:Males Dalmatians have a higher chance of getting urate stones because they carry less copper in their body than females.  High intake levels in diet and water of Zinc, Lead  and Molybdenum can cause a copper deficiency along with the possibility of urate stones.  The copper deficiency may not be enough to cause copper toxicosis but, too much zinc,lead and molybdenum in the diet and water would cause URATE STONES.
 
Urate stones affect more males than females.
Difference:
Males have LESS COPPER in their bodies than females
Note: This is very important.  The reason is mainly because of estrogen and testosterone.(generic explanation)
 
Connection:
Male Minature Schnauzers, Male Bulldogs and Male Dalmatians, have four things in common.
Copper Toxicosis, Urate Stones, Gender, and Copper Levels
 
Copper is processed through the liver
(Note: Copper Toxicosis is the inability of the liver to process copper throughout the blood stream(generic explanation.)
 
Excessive intake of molybdenum causes a physiological copper deficiency, and conversely, in cases of inadequate dietary intake of copper, molybdenum toxicity may occur at lower exposure levels.
(note: this connects low copper levels with molybdenum toxicity)
 
Molybdenum is distributed throughout the body with the highest levels generally found in the liver, kidneys, spleen, and bones (Wennig and Kirsch, 1988). http://rais.ornl.gov/tox/profiles/molybdenum_f_V1.shtml
 
Molybdenum is needed to convert purine to uric acid, and excessive intake could, in rare cases, increase uric acid levels and potentially trigger gout
 
Molybdenum is necessary for the function of at least three
important enzymes in the body: 1) aldehyde oxidase for our bodies’
handling of aldehydes it produces and those encountered in the
environment; 2) xanthine oxidase for the conversion of purines into
uric acid; and 3) sulfite oxidase for the conversion of irritating
sulfites into harmless sulfates. In addition, molybdenum is found in
many biological processes in conjunction with iron and is found to
cause a response in AK indicators similar to that of iron. In addition, molybdenum is found in many biological processes in conjunction with iron and is found to
cause a response in AK indicators similar to that of iron. Also,
molybdenum is an antagonist to copper and vice versa. Considering
all of the above factors has led to our understanding of how
molybdenum is usually a necessary adjunct to the treatment of
Candida albicans allergy patients and has speeded the recovery of
most of these patients even above and beyond the effective natural
procedures which were described in a previous paper by Mowles and
this author5.
Considering the reported fact that Mo was found in high concentrations in urinary tract stones and our data that Mo was less in stone kidney, it is speculated that Mo may play some unexplained but significant role in certain stage(s) of the stone formation
 
Food Sources OF Molybdenum
Barley
Beef Kidney
Beef Liver
Buckwheat
Hot Cocoa
Eggs
Legumes
Milk
Yams
Oat Flakes
Potatoes
Rye Bread
Spinach
Sunflower Seeds
Wheat Germ
Green Leafy Vegetables
 
 (Note: Connects males, liver, copper , urinary tract, and   molybdenum)
MOLYBDENUM would be the reason for reduced incidences of cancer not uric acid!  In many studies it has been proven to reduce cancer.
 
Breed also has a role in susceptibility to copper deficiency.  Ward (242) reported that Simmental and Charolais cattle had a greater copper requirement than Angus.  Differences in biliary secretion may explain the differences among breeds (243). Regardless of dietary treatment, biliary copper excretion was twice as high in Simmental compared to Angus cattle.  http://www.saltinstitute.org/47o.html 
Sulfate enhances the excretion of molybdenum (Friberg and Lener, 1986; Jarrell et al., 1980; Stokinger, 1981; Vanoeteren et al., 1982; Venugopal and Luckey, 1978).
Molybdenum is necessary for the function of xanthine oxidase
enzyme. Iron is also necessary for the function of this enzyme.
Xanthine oxidase converts hypoxanthine into xanthine and then
converts xanthine on into uric acid. (See Figure 3.) These reactions
are essential in the metabolism of purines. It follows then, that
patients with low serum uric acid levels should be checked for a
((Note: Opposite would be true, patients with high serum uric acid levels should be checked for excess molybdenum(and/or iron).))(MINE)
High-protein foods contain high amounts of zinc. Beef, pork, and lamb contain more zinc than fish. The dark meat of a chicken has more zinc than the light meat.Other good sources of zinc are peanuts, peanut butter, and legumes.Fruits and vegetables are not good sources, because zinc in plant proteins is not as available for use by the body as the zinc from animal proteins. Therefore, low-protein diets and vegetarian diets tend to be low in zinc.http://www.nlm.nih.gov/medlineplus/ency/article/002416.htm
Note: Excess Zinc causes a copper deficiency.  I checked the Gov. website for Zinc levels in the water.  Zinc is the NUMBER 1 increasing pollutant  and increasing levels have been found in the past between  1970-2001.  Article by the gov. was published in 2005
What is the health risk of too much zinc? Zinc toxicity has been seen in both acute and chronic forms. Intakes of 150 to 450 mg of zinc per day have been associated with low copper status, altered iron function, reduced immune function, and reduced levels of high-density lipoproteins (the good cholesterol) (34). One case report cited severe nausea and vomiting within 30 minutes after the person ingested four grams of zinc gluconate (570 mg elemental zinc) (35). In 2001 the National Academy of Sciences established tolerable upper levels (UL), the highest intake associated with no adverse health effects, for zinc for infants, children, and adults (2). The ULs do not apply to individuals who are receiving zinc for medical treatment, but it is important for such individuals to be under the care of a medical doctor who will monitor for adverse health effects. The 2001 Upper Levels for infants, children and adults are (2):http://ods.od.nih.gov/factsheets/cc/zinc.html#risks
High levels / Overdose / Toxicity / Negative Side Effects – Symptoms and/or Risk Factors:
 
Vanadium: Molybdenum:
Arthritis, aching bones, jaw, teeth, tonsils, ears, Skin eruptions, itchy skin, inflammatory spinal /
weakened immune system, chronic colds, joint disease, trabecular bone loss (spine, end-
gastrointestinal problems, trabecular bone loss, part of bone), decreased growth in all species,
 
————————————————————————————————————
mo·lyb·de·num (1778 –  Carl W. Scheele A metallic element that resembles chromium and tungsten in many properties, is used especially in strengthening and hardening steel, and is a trace element in plant and animal metabolism. Molybdenum is derived from the Greek word “molybdaena”, meaning “lead“.
 
Symptomatic lead poisoning in childhood generally develops at blood lead levels exceeding 3.9 umol/L (80 ug/dL) and is characterized by abdominal pain and irritability followed by lethargy, anorexia, pallor (resulting from anemia), ataxia, and slurred speech.http://www.manbir-online.com/diseases/lead.htm
 
Please see the table at the end of the article
————————————————————————————————————
 
Animal data
Although non-ruminant animals will develop symptoms of toxicity when fed high molybdenum diets,
ruminants are much more sensitive. Thus the toxicity seen in these species cannot be related to the
effects that would be expected in man. The toxicity is primarily expressed as a copper deficiency and
the ambient sulphate level has a marked effect on the interaction between copper and molybdenum.
Molybdenum toxicity in animals is commonly referred to as molybdenosis or teart. In appearance it is
similar to the disease of copper deficiency. Signs of molybdenum toxicity in animals include anaemia,
anorexia, profound diarrhoea, joint abnormalities, osteoporosis, hair discoloration, reduced sexual
42. It is hypothesised that stimulation of xanthine oxidase by high molybdenum intake
can lead to elevated tissue levels of uric acid, which in turn, may predispose to the
onset of gout (Gusev, 1969). In one study a high incidence of a gout-like disease
was reported in an area of Armenia , with soil levels of 77 mg molybdenum/kg and
39 mg copper/kg (Kovalsky et al., 1961). Exposure was assessed in the main
settlement in this area, using the population of the smaller adjoining village to
provide control data. On the basis of copper and molybdenum levels in the
different food products, the intake in the main settlement was calculated to be 10 –
15 mg molybdenum and 5 – 10 mg copper, compared to 1 – 2 mg molybdenum
and 5 – 10 mg copper in the control village (presumably these intake data are per
person per day). It is reported that in this area more than 50 % of the diet was
based upon locally grown products. A medical survey in the two villages in the
molybdenum-rich area revealed a prevalence of symptoms similar to gout in 31 %
of adults in the main village and 18 % in the other, control settlement. The
average rate of similar symptoms is reported to be 1 – 4 %, however it is not stated
whether this refers to the general population. The symptoms included arthalgia in
the hand, feet and knee joints and were accompanied by elevated molybdenum
 
47. The effect on the animal of high dietary molybdenum intakes depends upon the
species and age of the animal; the amount and the chemical form of the ingested
molybdenum; the copper status and the copper intake of the animal; the inorganic
sulphate and sulphur content of the diet and its content of substances such as
protein, cysteine and methionine, capable of oxidation to sulphate in the body; and
the level of intake of some other metals, including zinc and lead. The data are
summarised in Table 1. (Annex 1)
 
59. It was shown that rats administered sodium molybdate by oral gavage at a dose
level of 10 mg/kg caused a decrease in the DNA content of the liver, lung and
brain. This was accompanied by a decrease in the mitotic index and an increase in
chromosomal gaps, breaks and stickiness (Giri et al., 1981).
 
Many of the genes involved in copper or iron transport are
transcriptionally regulated by copper or iron availability (4).
CTR1, CTR3, FRE1, and FRE7 are induced by copper starvation
and repressed by copper repletion. This regulation involves
cis-acting copper-responsive elements (CuREs),1 found in each
of these promoters, with the consensus sequence 59-TTTGC(T/
G)C(A/G)-39, and a copper-sensing transcription factor Mac1
(13, 28–30). In vivo footprinting has demonstrated that Mac1 is
bound to CuRE elements under conditions of copper scarcity
 
and is not bound under conditions of copper sufficiency (28).
Furthermore, Mac1 undergoes copper-responsive intra-molecular
interactions that modulate trans-activation function (31).
Mac1 has homology with the amino-terminal 40 amino acids of
the minor groove DNA binding domain found in the Ace1/Amt1
copper-activated DNA-binding proteins that activate metallothionein
gene expression, but little homology outside of this
region (32, 33). In the Mac1 carboxyl-terminal region reside
two cysteine-rich repeats, REP-I and REP-II, that have been
demonstrated to function in copper sensing (34, 35). The
MAC1up1 allele, one of several dominant alleles with mutations
in REP-I, encodes a protein unable to sense copper and, as a
consequence, is constitutively bound to CuREs and strongly
constitutively activates expression of CTR1, CTR3, and
FRE1/7 (13, 28). Like genes involved in copper transport,
FET3, FTR1, and many other iron homeostatic genes are regulated
as a function of iron availability through conserved
cis-acting promoter elements by the Aft1 iron-sensing transcription
factor (36, 37). Indeed, the interdependence of the iron
uptake pathway on copper availability is also underscored by
the observations that FRE1 is regulated by copper and iron and
the ATX1 and CCC2 genes, encoding copper trafficking proteins,
* This work was supported in part by National Institutes of Health
Grant RO1 GM41840 (to D. J. T.). The costs of publication of this article
were defrayed in part by the payment of page charges. This article must
therefore be hereby marked “advertisement” in accordance with 18
U.S.C. Section 1734 solely to indicate this fact.
The nucleotide sequence(s) reported in this paper has been submitted
to the GenBankTM/EBI Data Bank with accession number(s) AF175404
and AF175405.
§ Recipient of a Centennial fellowship from the Medical Research
Council of Canada .
¶ National Institutes of Health postdoctoral fellow; supported by
National Institutes of Health Grant F32 GM18089.
** Participant in an international thesis training program between
the United States and Portugal .
‡‡ Burroughs Wellcome Toxicology Scholar. To whom correspondence
should be addressed. Tel.: 734-763-5717; Fax: 734-763-4581; E-mail:
dthiele@umich.edu.
1 The abbreviations used are: CuRE, copper-response element; BCS,
bathocuproinedisulfonate; BPS, bathophenanthrolinedisulfonic acid;
bp, base pair(s); Ctr, copper transporter; Cuf1, copper factor 1; ORF,
open reading frame; SOD, superoxide dismutase; PCR, polymerase
chain reaction; GFP, green fluorescent protein; TEMED, N,N,N9,N9-
tetramethylethylenediamine.
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 274, No. 51, Issue of December 17, pp. 36252–36260, 1999
© 1999 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A.
36252 This paper is available on line at http://www.jbc.org
 
 
——————————————————————————————————
Could the answer be SULFUR, DISTILLED WATER? lol
 
Grant County Indiana-Kimberly Long
Eleven chemicals (Table 4) were detected in the leachate well samples at levels of a health concern. Three other chemicals (aluminum, calcium, and cobalt) were found at elevated levels and will be evaluated in subsequent sections of this document. Benzene was detected in both wells. Bis(2-ethylhexyl)phthalate was detected in only one of the two wells. With the exception of benzene and bis(2-ethylhexyl)phthalate, the presence of the other chemicals are likely the result of former on-site operations. It is not possible to determine at this time the degree to which benzene and bis(2-ethylhexyl)phthalate are related to site activities (3).
Table 4. Chemicals of Concern in On-Site Leachate Well Samples, Marion (Bragg) Dump, March 1986.
Chemical
Maximum Concentration (ppb)
Comparison Value 
 
ppb
Source
aluminum
186,000
*
 
antimony
61
4
RMEG
 
arsenic
524
3
EMEG
 
benzene
42
1
CREG
 
bis(2-ethylhexyl)phthalate
1,000
3
CREG
 
cadmium
626
7
EMEG
 
calcium
683,000
*
 
chromium
696
50
RMEG
 
cobalt
353
*
 
copper
4,730
1,300
MCL
 
lead
5,090
15
MCL
 
nickel
1,900
200
RMEG
 
vanadium
696
30
RMEG
 
zinc
10,100
3,000
RMEG
 
 
 
There is plenty more information where this all came from.  I just can’t put it all on one page and keep everyone interested.
Kimberly Long
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