to Jean re Mark's cited article.....

[Guest guest]

HI Jean,

I only read the abstract as well as Mark's friends comments that Mark posted so

I

am not too familiar with all the details of the research that he is sharing with

us but

this is my take on it:

First of all, his research is exploring the association between disease states

caused

by calcium metabolism / deposition and therapy that can control that metabolism

/

deposition. As we know, excess calcium in the body can give rise to many

disorders...including atherosclerosis, kidney stones, crystals found in joints,

etc

(usually anything that has " stones " or " hardening " attached to it refers to

calcification) . In fact, calcium metabolism problems are a big cause of disease

processes (osteoporisis, parathyroid disease, certain forms of pancreatitis,

etc).

When you read calcification of the pancreas, this is deposition of excess

calcium

and goes hand in hand with atrophy (or dieing off of the pancreas). So, the

researcher may be speculating that if a CP patient could control this deposition

of

calcium in the ducts (pancreas stones in the ducts are often calcium containing)

as

well as that found in " dead " portions of the pancreas, this may be a way of

slowing

down the progression of the disease or preventing future occurences of ductal

obstruction. And, for those that suffer AP as a result of parathyroid disease,

this

may be a way to prevent this (?). In his example with blood vessels, he is

postulating, I think, that the harm is created by the interaction of excess

calcium

with the cells that line the vessel walls (endothelium), causing blood flow to

be

reduced which creates ischemia which then causes all sorts of cascading events

that just spiral into more and more damage. This could also be another

mechanism

to the pain generation found in CP: that is, the ischemia in the circulatory

system

that supplies the pancreas.

If that is a supposition that holds true, there may be benefit to treating CP

patients

with the medicine that he mentioned - sodium theosulfate. This medicine binds

any

excess calcium so that it reduces the chance that the calcium will precipitate

in

tissues and vessels and go on the cause the inflammation, ischemia and other

routes to pain generation. He also mentions that this is a safe medicine with a

history of treating other disease states that are associated with excess calcium

in

the system.

I hope that I explained this close the the idea that the researcher is

presenting. The

danger is that this is pure extrapolation, as far as CP / AP is concerned...that

what

looks promising for one disease state may not hold true for another....but at

the

least, there seems to be valid reason to suggest that this route may be

effective in

treating CP pain and progression that could be linked to calcium deposition in

blood

vessels, ducts and tissue of the pancreas. I do not think that the take home

lesson

is for patients to try this now....only that this may be a basis for future

research.

Laurie

[Guest guest]

I think you explained that perfectly and I think you are right..I don't

suggest that anyone just run out and give this a shot, but it is something

to keep on our minds.....who knows what may come of it...I am glad Pete told

me of this though..I hope this finds you and yours well

Mark

to Jean re Mark's cited article.....

>

>

> HI Jean,

>

> I only read the abstract as well as Mark's friends comments that Mark

> posted so I

> am not too familiar with all the details of the research that he is

> sharing with us but

> this is my take on it:

>

> First of all, his research is exploring the association between disease

> states caused

> by calcium metabolism / deposition and therapy that can control that

> metabolism /

> deposition. As we know, excess calcium in the body can give rise to many

> disorders...including atherosclerosis, kidney stones, crystals found in

> joints, etc

> (usually anything that has " stones " or " hardening " attached to it refers

> to

> calcification) . In fact, calcium metabolism problems are a big cause of

> disease

> processes (osteoporisis, parathyroid disease, certain forms of

> pancreatitis, etc).

> When you read calcification of the pancreas, this is deposition of excess

> calcium

> and goes hand in hand with atrophy (or dieing off of the pancreas). So,

> the

> researcher may be speculating that if a CP patient could control this

> deposition of

> calcium in the ducts (pancreas stones in the ducts are often calcium

> containing) as

> well as that found in " dead " portions of the pancreas, this may be a way

> of slowing

> down the progression of the disease or preventing future occurences of

> ductal

> obstruction. And, for those that suffer AP as a result of parathyroid

> disease, this

> may be a way to prevent this (?). In his example with blood vessels, he is

> postulating, I think, that the harm is created by the interaction of

> excess calcium

> with the cells that line the vessel walls (endothelium), causing blood

> flow to be

> reduced which creates ischemia which then causes all sorts of cascading

> events

> that just spiral into more and more damage. This could also be another

> mechanism

> to the pain generation found in CP: that is, the ischemia in the

> circulatory system

> that supplies the pancreas.

>

> If that is a supposition that holds true, there may be benefit to treating

> CP patients

> with the medicine that he mentioned - sodium theosulfate. This medicine

> binds any

> excess calcium so that it reduces the chance that the calcium will

> precipitate in

> tissues and vessels and go on the cause the inflammation, ischemia and

> other

> routes to pain generation. He also mentions that this is a safe medicine

> with a

> history of treating other disease states that are associated with excess

> calcium in

> the system.

>

> I hope that I explained this close the the idea that the researcher is

> presenting. The

> danger is that this is pure extrapolation, as far as CP / AP is

> concerned...that what

> looks promising for one disease state may not hold true for another....but

> at the

> least, there seems to be valid reason to suggest that this route may be

> effective in

> treating CP pain and progression that could be linked to calcium

> deposition in blood

> vessels, ducts and tissue of the pancreas. I do not think that the take

> home lesson

> is for patients to try this now....only that this may be a basis for

> future research.

>

> Laurie

>

>

>

>

>

>

>

>

>

>

>