Some people believe that BSE could be the cause of vJCD in human?!
There is pretty good evidence for that — though hard to know for
sure.
The more likely answer is that in our modern environment where
industrial chemicals, especially to the food supply of herbicides and
pesticides, have created “modern diseases” of Alzheimers, Parkinsons,
and Prion. They all take long periods of time to develop coinciding
with accumulation buildup in the body.
They all affect the brain which is the most sensitive portion of the
body to Metallic Ions.
The place where the pesticide Phosmet is most dense is England and
England has the most severe sheep scrapie plus BSE. I do not know if
England has the most dense population of Alzheimers and or Parkinsons.
Then again, I do not know if phosmet is responsible for Alzheimers and
Parkinsons.
I do know that the Midwest farm states in the USA has the highest USA
concentration of Parkinsons. I am thus guided into thinking that the
reason is because of the higher concentration of herbicide and
pesticide in the air and in the water and in the food. Some scientists
and politicians and commercial people have tried to hide this
Parkinson density under the quiet rug. And when they cannot hide it,
they then make the absurd claim that the genetical background of most
people in the Midwest USA are Scandinavian origin who are more prone
to Parkinson which is a hogwash argument.
but they also say that incubation period of vJCD is /much / shorter than
in the case of the ‘classical’ JCD. which could be about 10 to 20 years.
question: why haven’t we got an epidemic vJCD in great britain, for
instance?
Well, that is a very interesting question. In fact, we do not know two
key things. We do not really know how long the incubation period is,
and we do not know how transmissible it is (that is, what is the
probability that a human who eats a BSE prion will get the human
disease). In general, there is a barrier of transmitting prions from
one species to another, but there is no way to know how big the
barrier is. People have computer models for the vCJD epidemic — but
the models give widely varying predictions because of the unknowns.
Some people think there will be a big epidemic later, allowing for a
long incubation time. And some people are beginning to back away from
the more pessimistic predictions.
From what I remember in my readings of prion disease is that vCJD is
equally susceptible by all age groups not just the young. Only that
CJD seems to attack only the old. The vCJD attacks young equally as it
attacks old. I suspect the reason is because metal-ions cannot
differentiate whether a human is young of age or old of age. And that
if the dosage of metal-ions is big enough it matters not whether the
person is young or old. CJD maybe a different ion of say copper or
manganese or iron from vCJD. Not only do we have the various different
ions to cause prion disease but we also have the two variables of
whether the metals are excess in the body or a deficency in the body.
If a disease is caused by excess then it maybe a fast attacking
disease whereas if the disease is caused by deficiency it is slow
acting.
and again: why should be we -people over 55-60/y – immune against vJCD?
From my readings, old people are susceptible to both CJD and vCJD, but
young people are susceptible to vCJD. A possible chemical answer is
that young people often are more susceptible to a chemical in the
environment more so then old people whose body mass is larger and
whose cells are hardened by age. When you spray phosmet over human
populations the young are usually the first to see symptoms.
I’m not sure what the data is. I have heard that vCJD strikes younger
people. Do you know whether that means it strikes all ages “equally”
(which would be very different from “natural” CJD), or whether it
occurs _mainly_ in younger people?
If the former, it could be due to it being to an infection. The
infectious vCJD could hit all ages “equally”. In contrast, the regular
CJD requires some odd event to initiate in the body, and so the older
one is, the more likely.
If the latter is true… Hm, I wonder whether that initial uptake of
the protein from the digestive system works better in younger people??
But take that as speculation from me, not knowledge.
Granted many of my questions or trial experiments are
“irrelevant”, which is usually the norm for research in explorative
mode. But I also must lay a “irrelevancy” on your thinking regards to
yeast prions. In that yeast prion research is irrelevant for Prion
disease because yeast prions are not disease forming. To talk about
yeast prions in prion disease is like talking about apples compared to
golf balls. And if the science journals deleted or cut out all
articles on yeast prion then they would cut out 99/100 of all the
research related to prion disease.
If it turns out that Prion disease is a chemical disease caused by
metal-ions, then the time period of the 1980 to 2004 will have been
seen as years in which the biology community had wandered astray. And
that they had filled NATURE and SCIENCE and the literature full of the
yeast research that was utterly irrelevant as regards to the disease.
Bob, if I take my clothes out to dry in the sun, then the wrinkles are
altered. Likewise, if I take a protein from one solution into a
different solution and because the geometry is altered, does not allow
for a scientific conclusion that some misfolding had taken place. In
this sense the decade of the 1980s and 1990s or yeast prion misfolding
or of animal prion misfolding is no more of science merit then to
think that clothes drying in the Sun is “misfolding”.
To say that yeast prions do or do not cause disease could get to be a
semantic argument. The original discovery of prions in yeast was
focused on an unusual phenotype of yeast, one that could easily be
called a disease.
But more importantly, so what? Disease is simply an effect. The
question is, effect of what? What the yeast prion story does for us is
to establish an existence theorem of sorts. All parts of the basic
prion model can be shown to work.
The yeast work has the advantage of being experimentally accessible.
Much of our understanding of molecular biology started with simple
microbial systems. As we go into more complex organisms, we tend to
find that what we learned from microbes still holds, and there are
additional complexities. That is sort of where we are with prions.
Yeast tells us that the simple prion story works fine. Now, what
happens in mammals? That is harder to deal with, and undoubtedly more
complex. Factor X? Hsp 104? Or ??
The prion story is no more dependent on “disease” than is the story of
viruses or of bacteria. We may have some interest in them because of
cases where they cause disease, but it is not fundamental that any of
these cause disease. We understand that most bacteria do not cause
disease. Perhaps that is true also for viruses. Who knows whether it
is true for prions.