Can you get Mad Cow Disease or Chronic Wasting Disease from a tattoo?
by Rev. Dr. Gregory Lowrey (2008)

[Let’s just save some time and say NO! This is just another attempt at fear mongering in an attempt to one-up the (ignorant) competition. But for the actual scientific research and evidence that there is no danger – read on.

My introduction to the horrible threat of PRIONS in tattooing:

I received a phone call the other day at the studio from a very nice lady who told me that she and her husband had recently received their first tattoos at the COMICON (comic book convention) in San Diego, California and that they are now “hooked” on tattoos and wanted to get some from our studio.

In spite of us being recommended to her as “the best tattoo studio in Utah” (of course, I agree), she was worried because we use stainless steel tubes (the handle part of the tattoo machine that the needle bar passes through), which we clean, autoclave sterilize and reuse.

The artist who tattooed her and her husband told them that any tattooist who uses stainless steel tubes is irresponsible and that only artists who use plastic disposable tubes are safe to go to.

It is an unfortunate but standard practice in the tattoo world for tattooists to invent or pass on false pseudo-science regarding the industry to try to scare clients into not patronizing their competition because the competitor fails to take (unnecessary) precautions against the invented (fake) health threat.

So in this case, the tattooist was saying that there were disease causing elements called prions that autoclaves can’t kill but than can kill you and that it is a big threat in the tattoo world, and that anyone who doesn’t know about it or perform preventative procedures is ignorant and unsafe.

In researching claims that tattooing can pass on prions I could only find one person in the industry, Pat Fish from Santa Barbara, California who is promoting the idea.]

[My Comments will be in these nice little Brackets]

From Pat Fish’s Webpage:
“In any responsible tattoo studio most of the set-up is disposable, and until recently it was enough that the machine equipment was autoclave sterilized between uses. That's what I did for the first 20 years of my tattoo career. But now we have PRION diseases.”

“Prions cause diseases like Mad Cow, and because they are misfolded proteins, they are not alive and cannot be killed by autoclaving. So if a tattoo artist uses a metal tube in their machine and carefully cleans it in an ultrasonic and then autoclaves it, they are still not able to get rid of this class of diseases.”

“You might think they only have mad cow in the UK, but Alzheimer's is also caused by a prion, and leaves the same sort of holes in your brain. The main difference is that it is slow-moving and usually affects old people while mad cow strikes the young also. It is something that can be passed with blood contaminated equipment, and is a new risk factor with tattoos.”

[Pat has done the world further disservice by putting her “Dangerous Tattoos” videos on Google. Since Pat is very active in the tattoo world, especially in California and has been around long enough to be able to get press, especially when she has new dangers to expose, her misleading claims regarding prions are especially repugnant.]

The Truth About Prion Diseases
[If you want to know the truth about disease – go to the United States Center For Disease Control – the CDC headquartered in Atlanta, Georgia. Every reported transmission of any disease from any doctor or hospital worldwide is reported, catalogued and analyzed by the CDC. If you don’t want to bother going there yourself – lucky you – I did it for you – so read on and wonder!]

So, from the CDC:
[If you don’t understand some of the scientific language, don’t worry, I’ll give some simpler explanations as we go along. I just want to be fair and give the actual report that my statements are based on.]

Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.
The causative agent of TSEs is believed to be a prion. A prion is an abnormal, transmissible agent that is able to induce abnormal folding of normal cellular prion proteins in the brain, leading to brain damage and the characteristics signs and symptoms of the disease. Prion diseases are usually rapidly progressive and always fatal.

A List of Prion Diseases
Listed below are the prion diseases identified to date.

Human Prion Diseases
Creutzfeldt-Jakob Disease (CJD)
Variant Creutzfeldt-Jakob Disease (vCJD)
Gerstmann-Straussler-Scheinker Syndrome
Fatal Familial Insomnia

Animal Prion Diseases
Bovine Spongiform Encephalopathy (BSE) - (Mad Cow Disease)
Chronic Wasting Disease (CWD)
Transmissible mink encephalopathy
Feline spongiform encephalopathy
Ungulate spongiform encephalopathy (1)

Several prion disease–related human health risks from an exogenous
source can be identified in the United States, including the iatrogenic transmission of
Creutzfeldt-Jakob disease (CJD), the possible occurrence of variant CJD (vCJD), and
potential zoonotic transmission of chronic wasting disease (CWD). Although crossspecies transmission of prion diseases seems to be limited by an apparent “species
barrier,” the occurrence of bovine spongiform encephalopathy (BSE) and its transmission
to humans indicate that animal prion diseases can pose a significant public health risk. Recent reports of secondary person-to-person spread of vCJD via blood products…

[So here, the CDC is saying that generally (but not always) there is a cross species barrier that prevents this animal disease from infecting humans. The CDC is always very careful to say things like “can pose a significant health risk” even though there is no proof that such a health risk exists – they are just covering their butts. “Can pose a risk” does not equal “Does pose a risk” – it just leaves open the potential that some risk could possibly occur – like the potential risk of the Earth spinning out of it's orbit.]

Prion diseases, also known as transmissible spongiform encephalopathies (TSEs),
are a group of animal and human brain diseases that are uniformly fatal and often
characterized by a long incubation period and a multifocal neuropathologic picture
of neuronal loss, spongiform changes, and astrogliosis. Investigators believe
the etiologic agents of TSEs are abnormal conformers of a host-encoded cellular
protein known as the prion protein. Prion diseases do not characteristically elicit
an immune response by the host, and the mechanism of brain damage is poorly
understood. However, progressive neuronal accumulation of the disease-associated
prions may damage neurons directly, and diminished availability of the normal
prion protein may interfere with the presumed neuroprotective effect of the normal prion protein, contributing to the underlying neurodegenerative process.

Prion diseases attracted much attention and public concern after an outbreak of
bovine spongiform encephalopathy (BSE) occurred among cattle in many European
countries and scientific evidence indicated the foodborne transmission of BSE
to humans. Variant Creutzfeldt-Jakob disease (vCJD), the new form of
human disease resulting from BSE transmission, is distinguished from the classic
form of CJD by the much younger median age of affected patients, its clinical and
neuropathologic features, and the biochemical properties of the protease-resistant
prion protein. The classic form of CJD was first reported in the 1920s,
decades before the first BSE cases were identified in the mid-1980s. About
10%–15% of CJD cases occur as a familial disease associated with pathogenic
mutations of the prion protein gene, and about 85% of classic CJD cases occur as a
sporadic disease with no recognizable pattern of transmission. The stable, almost
predictable, occurrence of the disease in many areas of the world, primarily in the
elderly, led to the speculation that sporadic CJD may occur from de novo spontaneous
generation of the self-replicating prions, presumably facilitated by somatic
random mutations. Beginning in the 1970s, iatrogenic person-to-person transmission
of the CJD agent was reported in a small percentage of CJD patients.
This iatrogenic spread involved the use of contaminated corneal and dura mater
grafts, neurosurgical equipment, and cadaver-derived human growth hormone. At
present, the number of iatrogenic CJD cases is on the decline as a result of public
health preventive measures implemented as the various modes of transmission
were identified.

[So, contrary to Ms. Fish’s proclamation of a NEW DANGER, prions were discovered in the 1920’s, 10-15 percent are caused by a family related genetic disorder that you can’t do anything about and the other 85 percent have no recognizable pattern of transmission. This means that they just don’t know exactly how the disease is transmitted –BUT tattooing is certainly not implicated at all.

In fact the few cases (less than 50 worldwide since 1920) are on the decline due to the better cleaning of surgical instruments that were exposed to cutting up the brains and eyes of dead people who died from the disease and then using those same contaminated surgical instruments to do brain surgery on other people. So the allegation that this is a new danger and on the rise is just hogwash!]

Soon after the discovery of prions, their similarity with a normal cellular protein,
which is a structural component of cell membranes, was identified. This
cellular protein was given the name prion protein. In humans, the prion protein is
encoded by genes located on the short arm of chromosome 20. Although the exact
function of this protein is unknown, a protein found in such abundance in mammals,
particularly in neurons, could have multiple functional roles. Several putative
functions of the prion protein have been proposed, including supporting neuronal
synaptic activity, binding copper, and interacting with other cell-surface proteins
to provide neuroprotective functions. Prions are primarily distinguished from
the cellular prion protein by their three-dimensional structure. The cellular prion
protein is predominantly composed of the α-helix structure and is almost devoid
of β-sheet, whereas about 43% of scrapie prions are composed of β-sheet.
Other distinguishing characteristics of prions include their resistance to inactivation
by proteolytic enzymes, conventional disinfectants, and standard sterilization
methods . Prions are abnormal conformers of the cellular prion protein, the
presence of which appears to be a prerequisite for the replication and propagation
of prions . Although the exact mechanism of prion replication remains unclear,
the agent is believed to promote the conversion of the cellular prion protein into
the abnormal conformer by an autocatalytic or other unidentified process

The iatrogenic transmission of CJD was first reported by Duffy et al. in 1974
(33) in a 55-year-old patient who developed autopsy-confirmed CJD 18 months
after receipt of a corneal graft. Autopsy confirmed that the donor of the corneal
graft also died as a result of CJD. Since then, one patient each with a probable
and a possible risk of CJD transmission via corneal graft has been reported from
Germany and Japan, respectively (40, 48). The German patient died at 46 years of
age, 30 years after receipt of the corneal graft. The CJD transmission in this patient
was considered probable primarily because her CJD illness, although, typical for
the disease, it was not confirmed by neuropathologic testing. The donor of the
cornea, however, died as a result of autopsy-confirmed CJD. In the Japanese case,
the recipient died of confirmed CJD, but no information was available on the donor
of the corneal graft.

Three additional cases of CJD (two from the United States and one from Japan)
in corneal graft recipients have been reported but not published. All three cases
occurred independently of each other, and investigations indicated no evidence of
CJD in the cornea donors. Because of the large number of corneal transplantations
carried out each year, particularly among the elderly, it is expected that sporadic
CJD, not causally linked with the corneal grafts, will occur among this population.

[So, here are 6 cases worldwide since 1920 – not exactly a pandemic! Also, the " resistance to inactivation by proteolytic enzymes, conventional disinfectants, and standard sterilization
methods did not at the time (as shown later) include autoclave sterilization which Ms. Fish correctly claims does not kill Prions (since they are a protein and not alive) BUT the CDC reports that contrary to Ms. Fish's implication, autoclave sterilization does in fact "inactivate" the misfolded prions.]

Creutzfeldt-Jakob Disease Associated with
Neurosurgical Equipment
In 1977, two unusually young patients aged 17 and 23 years were reported to have
acquired CJD 16–20 months after having a stereotactic electroencephalographic
(EEG) procedure in which depth electrodes were used that had been implanted
2–3 months earlier on a patient who subsequently died of autopsy-confirmed CJD
(8). The heat-sensitive EEG electrodes were cleaned with benzene and disinfected
with 70% ethanol and formaldehyde vapor between uses. Contamination of the
EEG electrodes was demonstrated >2 years after their original use by experimentally
implanting the electrodes into a brain of a chimpanzee who became ill 18
months after implantation (36).
Worldwide, four CJD patients causally linked with exposure to contaminated
neurosurgical instruments have been identified (72, 75). Three of these cases occurred
in the 1950s in the United Kingdom, and the patients’ CJD illnesses were
confirmed by neuropathology testing of autopsy brain tissues. Their neurosurgical
procedures were performed within one month of craniotomy procedures in other patients who subsequently died of CJD. The fourth patient was reported in
1980 from France. The absence of recent CJD cases associated with a neurosurgical
procedure was believed to be due to advances in standard hospital instrument
sterilization procedures. Although these advances well may have prevented
CJD transmission via contaminated neurosurgical instruments, several laboratory
studies indicated that current standard sterilization procedures may not completely
inactivate the CJD agent.

[Now we see that in the 1970’s 4 more people (in the whole world) were infected by using surgical implants that were used on a chimpanzee that had CJD (brain wasting disease). While they said in the 1970’s that “current” standard sterilization procedures (they fail to say what those procedures were) “may” not completely inactivate the CJD agent, they go on to say on page 197 that (apparently modern) “standard autoclaving procedures seem to be superior to conventional chemical disinfection”. So it appears that the “standard” referred to that didn’t work so well, was soaking in a chemical solution and did not involve autoclaving at all. This stands in stark contrast to Ms. Fish’s claim that autoclaving does not kill the prions. In fact, according to the CDC autoclaving is the most effective method of inactivating prions. Additionally, consider that it would be very rare for a tattoo artist to dip his/her needle into CJD infected brain tissue prior to applying that needle to the skin of their client. If your artist is into that, I’d recommend finding a different artist to work with.]

Human Growth Hormone–Associated
Creutzfeldt-Jakob Disease
In 1985, three U.S. patients aged 20–34 years were reported to have developed
CJD after receipt of pituitary-derived human growth hormone (hGH) through
the National Hormone and Pituitary Program (NHPP) (17, 37, 46). The patients
received the hormone between 1963 and 1980 for growth failure secondary to
hGH deficiency, and their identification led to the discontinuation of hGH use in
the NHPP. A follow-up study was initiated of 6272 of the estimated total of 7700
patients who had received hGH as part of the NHPP (56). As of April 2004, 26 of
the total estimated NHPP patients, including 21 of the originally identified study
cohort, developed CJD. All 26 patients began their hormone treatment before a
size exclusion chromatography purifying step was introduced in the extraction
process in 1977.

[ This report explains that the growth hormone was extracted from the brains of corpses, and again, corpse-brain human growth hormone is not a typical ingredient in the tattoo process. In 1977 a preventive process was introduced so that what happened to these 26 patients of the 7,700 who received the hormone does not happen anymore to anyone. Certainly, this is not a NEW DANGER for the tattoo community.]

Annu. Rev. Public. Health. 2005.26:191-212.
Downloaded from arjournals.annualreviews.org
by IRMO/Information Center on 03/14/05.

[Dura Matter is a medical term for brain tissue. This report deals with the grafting of brain tissue from dead people to the brains of living people – again not a typical component of the tattoo process]

DuraMater Graft-Associated Creutzfeldt-Jakob Disease
Transmission of CJD via dura mater grafts was first reported in 1987 in a 28-yearold
woman from the United States who developed the disease 19 months after a craniotomy procedure involving implantation of Lyodura, a brand of dura mater graft processed by B. Braun Melsungen AG of Germany (18, 69).

In contrast to the processing procedures used by this German company, U.S. dura processors
avoided commingling of dural grafts from different donors and kept records to
facilitate identification and tracing of donors of each dural graft (19). The unusually
young age of the 1987 U.S. case-patient, the previous association of CJD
transmission with nervous tissue exposure, and the differences in processing of
Lyodura compared with other dural grafts convinced public health investigators
about the probable causal link of the patient’s CJD illness with the Lyodura graft.
In May 1987, because of this probable causal link, the Lyodura manufacturer revised
its procedures for collecting and processing dura mater grafts to reduce the
risk of CJD transmission.

After Japan announced the identification of 43 dural graft–associatedCJDcases,
Canada, Japan, and some European countries banned the use of human dura mater
grafts in neurosurgical procedures

[So, there was in the 1980’s one case in the United States and 43 cases in Japan of the commingling (mixing) of brain tissues (some apparently containing CJD contaminated tissue) which were then used to treat the brains of the 44 people who developed CJD issues. In 1987 the manufacturer revised it’s procedures to insure that CJD contaminated brain tissue no longer made it into the mix. And surprise - after excluding contaminated tissue - no more cases!
Again – application of brain graft matter is generally not part of the tattoo procedure]

United Kingdom
BSE was first recognized in the United Kingdom in 1986, where it caused a large
outbreak among cattle (28, 67). The leading hypothesis for the origin of BSE
is cross-species transmission of scrapie to cattle via the feeding of meat-andbone
meal that was contaminated by the inclusion of scrapie-infected sheep parts.
Spontaneous occurrence of the disease in cattle, much like sporadicCJDin humans,
has also been hypothesized. Although the origin of BSE remains controversial, it
is widely accepted that the practice of using rendered BSE-infected carcasses for
cattle feed had amplified the outbreak until a ruminant feed ban was instituted in
1988 (7, 28, 67). Because of concerns about cross-contamination of cattle feed
with prohibited material intended for other species, a specified bovine offal ban
(also known as specified risk material ban) was introduced in 1990 to remove the
known infectious parts of cattle from all animal feed. A dramatic decline in the
BSE outbreak was registered in response to these feed bans.

As the U.K. BSE outbreak progressed, several important public health preventive
measures were implemented before and after evidence of BSE transmission to
humans surfaced in 1996. These measures included a 1989 specified risk material
ban for human food, a 1996 prohibition of the processing of cattle ≥30 months old
for human food, and total ban on the feeding of mammalian protein to any farmed
animals (67). The measures introduced in 1996 were intended to contain the BSE
outbreak aggressively by keeping potentially BSE-contaminated feed off the farms
and to remove as many BSE-infected materials as possible from the human food
supply system.

Exposure to residual BSE-contaminated
feed is the most favored hypothesis because as little as 10 mg of infected material
has been shown to be infectious in experimental animal models.

On December 23, 2003, seven months after the identification of indigenous BSE
in Canada, the U.S. Department of Agriculture (USDA) announced the preliminary
diagnosis of BSE in a 6.5-year-old nonambulatory cow that was slaughtered
for human food on December 9th of that year (25). On December 25th, the BSE
diagnosis was confirmed by an international reference laboratory in Weybridge,
England. The USDA’s investigation traced the birth of the cow to a farm in Alberta,
Canada. DNA testing later confirmed the Canadian origin of the cow. At the
time of slaughter, meat from the BSE-positive cow had been released for human
consumption, but tissues considered to be at high risk for BSE transmission (e.g.,
brain, spinal cord, and small intestine) were considered unfit for human consumption
and, thus, sent to be rendered for other uses (e.g., to produce nonruminant
animal feed)

[Here is a single case of one cow who contracted BSE (mad cow disease), but the contamination was discovered before any meat was released to the human population, though I was disappointed to see that they released it to be used for dog and cat food – yet there were no reports – since December 2003 – of any BSE transmission – and of course it had nothing to do with humans and again, even though the pet food produced in 2003 likely has already been consumed, I would caution against getting tattoo services from “artists” who mix pet food in with their inks or dip their needles, tubes etc. into pet food products.]

The cross-species
transmission of BSE was heralded by the identification in the United Kingdom of
a BSE-like disease in zoo animals beginning in the late 1980s and in domestic cats
beginning in 1990 (28). This resulted in the institution of national CJD surveillance
in the United Kingdom, which detected an unusual clustering of ten young patients
(median age, 28 years) with a unique clinical and neuropathologic profile (74). The
unusually young age of the patients and their clinicopathologic homogeneity led
U.K. researchers to suspect that the cases may represent an emergence of a new
form of CJD resulting from BSE transmission to humans. The occurrence of this
variant form of CJD (vCJD) was announced in 1996, approximately nine years
after the identification of BSE in the United Kingdom. Absence of similar cases in
other countries with comparable surveillance programs, their continued occurrence
almost exclusively in the United Kingdom, and additional laboratory studies further
strengthened the causal link between vCJD and BSE. As of November 1, 2004,
a total of 151 vCJD cases had been reported from the United Kingdom (30).
In addition, three cases (one each from Canada, Ireland, and the United States)
among persons with potential BSE exposure in the United Kingdom because of
their past U.K. residence, 8 vCJD cases from France, and 1 case from Italy have
been identified

[151 people, (one from the USA) appear to have gotten the variant form vCJD and BSE (basically different names for the same disease) from their cats. Now, how they got it from their cats was not determined, but it seemed to be a short term, contained problem and I would suggest that because it was short term and related to a certain geographic region (UK) and that no more cases have occurred that my best guess would be that people ate cat food from a batch contaminated with BSE, etc. since all the diseased, non-edible parts of “food” animals are sold to pet food companies. This seems to be a one time occurrence, that again has nothing to do with tattoos. However, if your tattoo artist has an open can of cat food at his station that he is dipping his tattoo needle into, be sure to check the manufacture date to ensure the cat food was not made between 1980 and 1990 - and then - still run like hell!]

Bloodborne Transmission
A highly probable bloodborne, person-to-person transmission of vCJD was reported
in the United Kingdom in a 69-year-old man who had vCJD onset in late
2002, 6.5 years after receipt of 5 units of packed red blood cells (51). One of the
red blood cell units was obtained from a 24-year-old donor who developed vCJD
>3 years after donation. Both the donor and recipient died of pathologically confirmed
vCJD. The unusually older age of the recipient, appropriate latency period,
and the remote likelihood that confirmed vCJD in a donor and recipient pair would
have occurred by chance alone indicates that this episode represents a highly probable
bloodborne transmission of vCJD. The patient was identified as part of a
cohort study of 48 patients who received blood components during 1980–2003
from 15 donors who subsequently died of vCJD.

[Now – here, we finally have a “bloodborne” transmission of vCJD, but it affected 17 people who all received blood transfusions from people who were highly suspect of already having vCJD in their blood. This all happened in the UK with blood donated between 1980 and 2003 (not a current problem) and has not recurred. Also, this was a problem that was again isolated to the medical community and had nothing to do with tattooing. Certainly there is an obvious difference between a cleaned and sterilized tube through with the needle simply travels as used in tattooing and an actual intravenous blood transfusion where quantities of contaminated blood are forced into the patient (victim). If your tattoo artist is offering you a blood transfusion as an additional service - well, I advise you check the blood source (newer than 2003) and then - run like hell!]

The bloodborne transmission of vCJD had long been suspected as possible because
of some unusual features of the disease. These features included the ease
by which the vCJD agent was detected in lymphoid tissues, raising the possibility
that it could also be found in circulating lymphocytes, and the existence of a possible
blood phase, or prionemia, of the agent as it travels from the original site of
infection in the gut to the brain (71). The FDA, on recommendation from its Transmissible
Spongiform Encephalopathy Advisory Committee and with support from
the CDC and the National Institutes of Health, had recommended a blood donor
deferral policy to exclude donors who have spent specific periods of time in the
United Kingdom and other European countries

[I do not know of any tattoo artist who dips their needle into a persons gut (intestines) and then uses that needle to tattoo the clients brain. Therefore this method of transmission also is likely to not have any relationship to the tattoo procedure.]

[So the medical community has determined that a sufficient deterrent to this type transmission is to exclude blood donation from people who have spent time in the UK or other European countries. Again, tattoo artists generally do not mix blood from previous clients into the ink used to tattoo. Also, we must remember that it is not the ink that is being claimed to be an issue but the tube which is cleaned and sterilized in a manner that the Medical community and CDC consider most effective at inactivating these prions.]

[And they conclude on page 206 “No scientific evidence exists to causally link any form of BSE with a sporadic CJD-like illness in humans.” How much more do we need to hear beyond “NO SCIENTIFIC EVIDENCE EXISTS TO CAUSALLY LINK ANY FORM OF BSE WITH…CJD-LIKE ILLNESS IN HUMANS.” Really! Can the CDC make it any clearer?]

Chronic Wasting Disease
The increasing spread of CWD in the United States and the zoonotic transmission
of BSE raised concerns about the possible transmission of CWD to humans
(6). Several CJD cases or apparent CJD clusters with suspect CWD transmission
have been reported in the United States (4, 6, 23). Epidemiologic and laboratory
investigations of these isolated cases and clusters did not provide convincing evidence
for a link between CWD and the patients’ illnesses.

[So again, there was a suspicion that turned out to not have any demonstrable connection. Zoonotic means "from animals".]

Three distinct prion disease–related human health risks from environmental sources
of infection can be identified in the United States. These include the iatrogenic
transmission of CJD, occurrence of vCJD from exposure to BSE-contaminated
cattle products in the United States or other countries with BSE, and possible
transmission of CWD to humans. The iatrogenic transmission of CJD appears to
be on the decline following appropriate preventive measures that were instituted
as the different iatrogenic modes of spread were identified. Additional iatrogenic
CJD cases, however, can be anticipated primarily because of the long incubation
period associated with prion diseases.

[Again, the medical authorities only conclude that there is a “possible” transmission, but admit that THERE HAVE BEEN NO DOCUMENTED TRANSMISSIONS except for their suspicions based on circumstantial evidence as in diseased brain tissue from a cadaver who died from the disease being grafted into the brain of another person or tools, improperly cleaned that were used on dead brains of people who died from the disease being used on live people’s brains who later contracted the disease, and that since there is a long incubation period, there is anticipation that some potential may exist for additional cases to turn up, not because there is an ongoing problem, but because some of the people who were treated in the 1970’s and 1980’s, primarily in England will eventually develop symptoms AND that preventive measures have been put in place that has shown a decline (actually they don’t note any additional cases – that is quite a decline) in transmission. However, no medical authority anticipates additional cases due to current transmission and certainly not through tattooing.]

To date, only one vCJD patient has been identified as a resident of the United
States (25). This patient is believed to have contracted the disease while growing
up in her native country of Britain during the height of human exposure to
the BSE outbreak.

Although the public health preventive measures recently instituted
by the USDA should further reduce the risk of BSE exposure to the U.S.
population, the possibility that domestically acquired vCJD may appear in the United States cannot be totally dismissed.

[Can ANYTHING ever be totally dismissed - zombies, winning the lottery...?]

However, this possibility is probably much smaller than the risk of contracting vCJD as a result of BSE exposure during any previous travel or residence in countries where a much higher rate of BSE has been documented.

[Hmmmm……no mention of tattooing.]

Recent reports of vCJD transmission via blood products
obtained from donors who were incubating the disease are of concern because
of a potentially large number of blood donors who might have been exposed to
BSE and are incubating the disease. Theoretically, these persons might transmit
the vCJD agent if they donate blood while they are clinically asymptomatic.

The blood donor deferral policy instituted by the FDA is expected to greatly minimize
this possible risk of bloodborne transmission of vCJD in the United States. The
findings of vCJD transmission in a patient who was heterozygous at codon 129
may have implications for the eventual size of the vCJD outbreak. Heterozygous
patients may develop vCJD after a longer incubation period and at an older age
than methionine homozygous patients, potentially resulting in a more protracted
course for the vCJD outbreak.

To date, no convincing evidence of CWD transmission to humans has been
reported. (2)


1. Department of Health and Human Services, Centers For Disease Control and Prevention, http://www.cdc.gov/ncidod/dvrd/prions/
2. Annu. Rev. Public Health 2005. 26:191–212, doi: 10.1146/annurev.publhealth.26.021304.144536,THE PUBLIC HEALTH IMPACT OF PRION DISEASES, Ermias D. Belay and Lawrence B. Schonberger, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases,Centers for Disease Control and Prevention, Atlanta, Georgia 30333;

[And as far as Ms. Fish's claim that prion disease also causes Alzheimer, nothing could be further from the truth. Current research actually shows that normal prions prevent Alzheimer and no mention of misfolded prions or any prion contributing to Alzheimer exists at all - this is simply an invention of Ms. Fish - (shame on you).]

Prions key in Alzheimer's disease

Alzheimer's cell engineered to reproduce amyloid protein
Alzheimer's disease is characterised by 'plaques' in the brain
Proteins which cause mad cow disease may also protect against Alzheimer's disease, UK researchers say.

Prions naturally present in the brain appear to prevent the build up of a key protein associated with the condition.

In laboratory tests, beta amyloid, the building block of Alzheimer's "plaques", did not accumulate if high levels of the prions were present.

The findings could lead to new treatments, the Proceedings of the National Academy of Sciences reported.

Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don't know yet

Professor Nigel Hooper

In variant Creutzfeldt-Jakob disease (vCJD), the human version of mad cow disease, the normal version of the prion protein present in brain cells is corrupted by infectious prions causing it to change shape, resulting in brain damage and death.

But little is known about purpose of the normal prion proteins.

Due to the similarities between Alzheimer's and diseases such as variant CJD, researchers at the University of Leeds, looked for a link.

Plaque formation

They found that in cells in the laboratory, high levels of the prions reduced the build-up of beta-amyloid protein, which is found in the brains of people with Alzheimer's disease.

In comparison, when the level of the prions was low or absent, beta amyloid formation was found to go back up again, suggesting they have a preventive effect on the development of the condition.

The researchers also looked at mice who had been genetically engineered to lack the prion proteins and again found that the harmful beta-amyloid proteins were able to form.

Study leader Professor Nigel Hooper said they now needed to look at whether ageing had an affect on the ability of the prion proteins to protect against Alzheimer's.

"Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer's plaques.

"Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don't know yet."

He said although they needed to learn more, theoretically if a treatment could be designed to mimic the effect of the prions it could halt the progression of the disease.

Professor Clive Ballard, director of research at the Alzheimer's Society said this was the first time a link had been made between prions and Alzheimer's.

"These are early findings, which suggest prion proteins may have a regulatory effect on the development of beta amyloid."
He added: "This provides the foundations for a novel approach to finding new therapeutic targets in Alzheimer's disease."

[So, my research shows that there is no relationship between tattooing and PRION transmission and that the claim of some tattooists that autoclave sterilization does not "kill" prions is simply a play on the public's ignorance, since it is obvious that you cannot "kill" something that is not "alive" to begin with, but the we should pay attention to the claims of legitimate Medical Researchers which support autoclave sterilization as the best method of eliminating the danger of potential transmission by "inactivating" the prion.

At the same time, let's not forget that we are all "full of prions" and that it is only a certain type of abnormal prion that is found in the brains of people or animals that already have "mad cow disease" that is harvested and transmitted to the brains of other people that have caused any problems at all - not likely in the recieveing of a tattoo.

It is my opinion that this is just another example of tattooists playing on the ignorance of the public and the ignorance of other tattooists and the willingness of the community at large to make tattooing out to be a dangerous practice and profession.

To me, it is disgusting when tattooists will use fear mongering campaigns to make themselves look safer than their competition, and to imply or outright claim that other tattooists are unprofessional and a danger to their clients if they don’t subscribe to the misrepresented, invented and otherwise fake pseudo-science they use to try to make themselves look superior.

My conclusion is that after a survey of all available studies on so called PRION DISEASE that no such thing even exists. Plastic tubes are a convenience that many traveling artists take advantage of (even though I have yet to see a plastic tip that performs as well as a steel tip) and that there is no danger in a clean, autoclaved steel tube.

I have surveyed every article made available by the CDC relating to tattooing and have not found one single instance where the transmission of any disease has been proved to be a result of the tattoo procedure.

While it may be true that some diseases have been passed from tattooists to their clients, generally they are airborne viruses and are not a result of the tattoo equipment or procedure of tattooing. The same virus could just as easily be contracted from your grocery clerk, day-care worker, postman or politician.

Our industry needs to educate itself and quit buying into the scare tactics of unscrupulous competitors and politicians looking to win an election on a “save the children” campaign, which is what we saw a rash of in the late 1990’s.

Tattooing has been around for at least 14,000 years (some anthropologists claim over 30,000 years) and has been performed in some of the most unsanitary conditions imaginable without any reported health problems.

It’s time we get educated and stand up for our rights and the truth.

Tattooing is not a threat to public health and safety.
Unscrupulous, ignorant and untrained tattooists are simply a threat - period and a disgrace to an industry that like it or not performs a very personal and historically spiritual service to the public.

Dr. Lowrey (Doc) has been tattooing for 20 years, apprenticed under his wife Katrina (Kita Kazoo) who apprenticed in Yuma, Arizona under world famous Beverly Hills tattoo artist Dan Brown who apprenticed under world famous San Francisco tattoo artist Lyle Tuttle.
Dr. Lowrey has been practicing wholistic healing since 1978 and has operated two number one studios with his wife Katrina; Royal Oak Tattoo in Greater Detroit, Michigan and Happy Valley Tattoo (Voted #1 since 2002 and Best of Utah in 2008) in American Fork, Utah. He also is CEO of UBU Ministries which considers tattoos and piercings as spiritual practices and are promoted in their ministry as optional emblems of individual spiritual expression.
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