trainedobserver
Paranormally Disenchanted
I forgot what this thread was about.
Is this the cheese thread? [wanders away]
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I forgot what this thread was about.
I figured that pointing out how outdated the arguments in the article you posted were had pretty much sealed it. I figured that's why you didn't post anything more recent that shows that vaccines cause autism, since you know, there isn't anything that shows that.
yes, Angelo and I are friends and communicate via PM regularly. I do respect his opinions and plan on changing 99% of them.
The funny thing is that most people would think that Pixel and I hate each other, but we don't. Do we annoy each other? Probably. And do we think we are both really wrong about stuff? Yup. But at the end of the day, we can take shots at each other and still get along.
...What's the alternative, to see how much farther I can piss than you? Excuse me, any ladies here, that was a bit over the line. ...
Good question: "Back in 1999-2000 I proposed that we would see a dramatic increase in dementia cases as a result of misdiagnosis of Cruetzfeld-Jacobs (mad-human) disease as Alzheimer's or the generic "dementia" diagnosis. Dementia deaths are not usually cause for an autopsy, so it stands to reason that many of these mad-human deaths could well be misidentified by the medical establishment. Transmissible Spongeform Encephalopathy (TSE) caused by the onset of misfolded proteins called "prions" can incubate for up to 40 years before the onset of full-blown symptoms. ---chris"I forgot what this thread was about.
TSE or CY disease is a damn serious disease, and it pisses me off to no end that the so-called "'authorities" are pretending to be so blaise about it. I LOVE a good steak, and pot roast, but I just don't enjoy them like I used to.
Hell, we could all be infected.
Mad cow would explain the way some skeptics think!(Arrr ).
Chronic Wasting Disease (CWD)
America's answer to mad cow disease
Definitions:
Chronic Wasting Disease (CWD): a spongiform encephalopathy (prion disease) in deer or elk that is closely related to mad cow disease, scrapie in sheep, and Creutzfeldt-Jakob disease in humans. CWD has been reported in mule deer, black-tailed deer, white-tailed deer, Rocky Mountain elk, and possibly one pronghorn antelope [9, 4]. CWD transmits efficiently to mink and then to hamster experimentally [6, 9]. Tens of thousands of hunters in the Ft. Collins area have eaten tainted game from game procesing facility pools [10]; efficiency of transmission to humans is unknown. The incubation period for kuru is 40 years (dated from cessation of exposure) and counting [9].
Origins of CWD: The first case of CWD was seen in 1967 in a captive mule deer at the Foothills Wildlife Research Station (operated by the Colorado Dept. of Wildlife) in Ft. Collins and was attributed then by station employees [10] to close confinement of deer to former (scrapie) sheep pasture or to horizontal transmission from sheep allowed [9] into the pens. The shortest known incubation time in deer is 17 months, dating the exposure back to 1965-66 or earlier. Surplus does were released back into the wild after fawning in the facility; the first case in free-ranging wild deer was seen in 1981. Other infected animals were shipped to zoos (Denver, Toronto, Laramie), game farms (see below), and similar research facilities in Colorado and Wyoming.
Alternate theories of CWD origin: These posit a naturally occurring prion genetic disease; possible but not supported by recent genotyping studies by O'Rourke [1]) or transmission at winter feeding stations via rendered downer cow protein (ie, a non-UK strain of bovine spongiform encephalopathy) or CWD deer or elk recycled as rendered road kill. CWD deer are commonly observed at a feeding station on Lexington Lane in Estes Park, Colorado [10].
Trace-back: A game farm, zoo, or research facility that sold an elk or deer to a second facility where CWD was later positively diagnosed for the first time. The trace-back farm is presumed to be contaminated even if it has never reported CWD. Examples: Colorado has numerous trace-back game farms among the 11 in the Ft. Collins disease epicenter; improbably, none of these have ever reported CWD. Ear tags had been discarded in the Oklahoma CWD elk case, causing uncertainty in trace-back (limited to Montana, Idaho, or Utah).
Trace-forward: A game farm, zoo, or research facility that bought an elk or deer from a contaminated facility (possibly in another state) where CWD was later positively diagnosed. Sometimes broadened to include animals imported from a state or region known to have CWD because under-reporting is rampant [the economic impacts are devastating]. Animals at the trace-forward facility must be closely monitored and not be allowed to furnish animals to still other game farms. Examples: Vermont has trace-forward elk from Colorado but does not require autopsy of adult elk deaths as recommended [1]. Trace-forward could not be conducted [1] on Nebraska elk sold at auction in Missouri and Colorado because records are not kept.
Exposed herds consist of trace-back plus trace-forward herds.
Ingress or egress: Deer and elk can escape or be released from game farm facilities and introduce the disease into wild cervids of that state. Alternately, deer or elk attracted to plentiful feed or captive members of their own species and enter the large fenced pastures, sometimes fawning there and contracting disease. [1,4, 9] Typical initiating events are a tree falling on a fenceline during a storm or erosion at a stream or gully crossing. Fenceline contact of wild animals with captive animals (possibly nose rubbing, urine, faeces,or hay mites) in facilities that are not double-fenced may also suffice to transmit CWD [1,9]. Example: wild deer on the same premises as a captive elk herd acquired CWD in South Dakota (see A, B).
Conflict of interest: A state fish and game department that derives most or all of its salary and program revenue from the sale of game tags jeopardizes this revenue by disclosure of CWD or by safety warnings to hunters. This revenue model is applicable to all 11 western states. Also includes departments of agriculture for different reasons. Conflicts of interest can affect the design of monitoring programs, choice of sampling techniques and pathology method, disclosure of results, and non-adherence to the precautionary principle. Diagnosis: public relation releases from the agency equate absence of evidence to evidence of absence. Example: Colorado fish and game officials held a news conference in 1998 stating they would continue to enjoy eating venison from untested deer and elk from epidemic strongholds because it had not been proven to transmit to human [10], a vacuous reassurance as no study has ever been conducted.
Elevated silver, barium and strontium in antlers, vegetation and soils sourced from CWD cluster areas: Do Ag/Ba/Sr piezoelectric crystals represent the transmissible pathogenic agent in TSEs? (This makes me concerned about nano-silver)
High levels of Silver (Ag), Barium (Ba) and Strontium (Sr) and low levels of copper (Cu) have been measured in the antlers, soils and pastures of the deer that are thriving in the chronic wasting disease (CWD) cluster zones in North America in relation to the areas where CWD and other transmissible spongiform encephalopathies (TSEs) have not been reported.
The elevations of Ag, Ba and Sr were thought to originate from both natural geochemical and artificial pollutant sources stemming from the common practise of aerial spraying with "cloud seeding" Ag or Ba crystal nuclei for rain making in these drought prone areas of North America, the atmospheric spraying with Ba based aerosols for enhancing/refracting radar and radio signal communications as well as the spreading of waste Ba drilling mud from the local oil/gas well industry across pastureland.
These metals have subsequently bioconcentrated up the foodchain and into the mammals who are dependent upon the local Cu deficient ecosystems. A dual eco-prerequisite theory is proposed on the aetiology of TSEs which is based upon an Ag, Ba, Sr or Mn replacement binding at the vacant Cu/Zn domains on the cellular prion protein (PrP)/sulphated proteoglycan molecules which impairs the capacities of the brain to protect itself against incoming shockbursts of sound and light energy.
Ag/Ba/Sr chelation of free sulphur within the biosystem inhibits the viable synthesis of the sulphur dependent proteoglycans, which results in the overall collapse of the Cu mediated conduction of electric signals along the PrP-proteoglycan signalling pathways; ultimately disrupting GABA type inhibitory currents at the synapses/end plates of the auditory/circadian regulated circuitry, as well as disrupting proteoglycan co-regulation of the growth factor signalling systems which maintain the structural integrity of the nervous system.
The resulting Ag, Ba, Sr or Mn based compounds seed piezoelectric crystals which incorporate PrP and ferritin into their structure. These ferrimagnetically ordered crystals multireplicate and choke up the PrP-proteoglycan conduits of electrical conduction throughout the CNS. The second stage of pathogenesis comes into play when the pressure energy from incoming shock bursts of low frequency acoustic waves from low fly jets, explosions, earthquakes, etc. (a key eco-characteristic of TSE cluster environments) are absorbed by the rogue "piezoelectric" crystals, which duly convert the mechanical pressure energy into an electrical energy which accumulates in the crystal-PrP-ferritin aggregates (the fibrils) until a point of "saturation polarization" is reached.
Magnetic fields are generated on the crystal surface, which initiate chain reactions of deleterious free radical mediated spongiform neurodegeneration in surrounding tissues. Since Ag, Ba, Sr or Mn based piezoelectric crystals are heat resistant and carry a magnetic field inducing pathogenic capacity, it is proposed that these ferroelectric crystal pollutants represent the transmissible, pathogenic agents that initiate TSE.