Cardiologist: Owen, come back and see me in 20 years

The discussion of the Linus Pauling vitamin C/lysine invention for chronic scurvy

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Ralph Lotz
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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#31  Post by Ralph Lotz » Mon Feb 22, 2010 3:20 pm

If this is the case, then I wonder why Abbott hasn't done any head-to-head studies with Lipitor or Crestor. A positive result would be a goldmine for them.


There are no if's about it.
Many cardiologists give their patients the niacin and CRESTOR or LIPITOR together. At least that might keep the Lp(a) from killing them. Then they can concentrate on the other deadly side effects.

A goldmine?

Slo-Niacin 500 Mg, 100 Tablets is $12.74 at CVS online.
NOW 500mg TR/250 Tablets, $7.99
"Unless we put medical freedom into the constitution...medicine will organize into an undercover dictatorship..force people who wish doctors and treatment of their own choice to submit to only what..dictating outfit offers." Dr. Benjamin Rush

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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#32  Post by godsilove » Mon Feb 22, 2010 5:01 pm

Ralph Lotz wrote:A goldmine?

Slo-Niacin 500 Mg, 100 Tablets is $12.74 at CVS online.
NOW 500mg TR/250 Tablets, $7.99


Despite this, Niaspan sales are roughly $200 million every quarter and prescriptions rose following the ARBITER-HALTS study (vs. ezetimibe). Not bad for a drug that competes with generic niacin! What makes you think Abbott wouldn't stand to benefit from a head-to-head trial with one of the blockbuster statins, especially if the superiority of niacin is so obvious?

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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#33  Post by ofonorow » Tue Feb 23, 2010 4:20 am

rmb60 wrote:I understand that Cardiologists refer to the Angiogram as the Gold Standard for detecting blockages in the heart, how does your test compare to this ?....The only reason I ask is that I had a Nuclear tracer Stress test of my heart which also showed no problems but an Angiogram was offered to be certain, I declined but remain curious.


I don't understand either. An angiogram seems to make sense if some darkness (poor blood flow) was uncovered, but if the test showed good circulation, I personally do not see much value in the angiogram. I suppose they may be looking for the type of plaque, e.g. unstable. Sounds like they don't trust their own testing.
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American Scientist's Invention Could Prevent 350,000 Heart Bypass Operations a year

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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#34  Post by Johnwen » Tue Feb 23, 2010 5:36 am

Cells increase expression of LDL receptors in response to decreased intracellular levels. It's a homeostatic response, so there's no excess cholesterol winding up in the bile duct.

So what your saying here is that statins increase the cells response to ldl thus taking more inside the cells which causes lower serum cholestrol levels. Then what your saying is the liver plays no part in the cholesterol lowering process. I think you need to go back to the basics and learn what role the liver actually plays and quit confusing yourself with bias and misleading studies.
But I'll ask you again: even if you are going to be prejudiced and ignore all the studies showing no increased risk with statins, then what exactly are you basing your assertions on - other than your own opinion?

It’s called Education you should try it. I have my beliefs and I’m entitled to them and if they are not inline with what others believe they have a problem, because they will not change my beliefs
To steal ideas from one person is plagiarism. To steal from many is
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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#35  Post by godsilove » Tue Feb 23, 2010 4:59 pm

Johnwen wrote:
Cells increase expression of LDL receptors in response to decreased intracellular levels. It's a homeostatic response, so there's no excess cholesterol winding up in the bile duct.

So what your saying here is that statins increase the cells response to ldl thus taking more inside the cells which causes lower serum cholestrol levels. Then what your saying is the liver plays no part in the cholesterol lowering process. I think you need to go back to the basics and learn what role the liver actually plays and quit confusing yourself with bias and misleading studies.


:?:

I don't recall saying that the liver plays no part. The reason why LDL receptor expression is upregulated is because statins inhibit the HMG-CoA reductase enzyme, thus lowering intracellular levels of cholesterol. In doing so, the cells will increase absorption from the bloodstream and the net effect is not an increase in intracellular levels. Since you're "educated", I'm sure you understand what homeostasis is.

It’s called Education you should try it. I have my beliefs and I’m entitled to them and if they are not inline with what others believe they have a problem, because they will not change my beliefs


Well, you're certainly entitled to your opinions, but not your own facts. But thank you for admitting that you are unlikely to change your beliefs - there's no point in further derailing this thread.

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Re: Cardiologist: Owen, come back and see me in 20 years

Post Number:#36  Post by Johnwen » Wed Feb 24, 2010 3:55 pm

I don't recall saying that the liver plays no part. The reason why LDL receptor expression is upregulated is because statins inhibit the HMG-CoA reductase enzyme, thus lowering intracellular levels of cholesterol. In doing so, the cells will increase absorption from the bloodstream and the net effect is not an increase in intracellular levels. Since you're "educated", I'm sure you understand what homeostasis is.



Your close with you observations but the liver is what controls the serum levels not the cells ability to uptake it. In this case an enzyme affects both. Homeostasis is only present when there is no outside interference. If the cells need more of any essential product and the producer or storage supply is being suppressed medically then cell death and complete death will soon follow.

Statins inhibit an enzyme called HMG-CoA reductase, which controls cholesterol production in the liver and in the cells which export more ldl receptors to the cells surface to make sure that there is sufficient uptake of cholesterol from the blood.
The statins actually act to replace the HMG-CoA that exists in the liver, thereby slowing down the cholesterol production process. Additional enzymes in the liver cell sense that cholesterol production has decreased and respond by creating a protein that leads to an increase in the production of ldl receptors in the liver. These receptors relocate to the liver cell membranes and bind to passing ldl and vldl . The ldl and vldl then enter the liver and are combined and broken down to their simplest form by the bile and processed out to the common duct and stored in the gallbladder. If the bile is not capable of breaking down the ldl and vldl completely, due to an imbalance or the discharge of cholesterol is in excess of bile capabilities. It is conceivable that the unreduced ldl and vldl can solidify within the gallbladder. More often it will pass to the intestines for elimination. However due to the decreased levels of ldl and vldl in the body. There will be an increase in the protein NPC1L1 which transports dietary and intestinal cholesterol from the digestive tract an into the blood and back into the process.

When there’s something that the body needs to exist there is redundant systems to insure that levels needed by the body are maintained. This is especially true if the item is used extensively and daily. When modern medicine tries to alter what’s needed it is usually met with substantial resistance and side effects. You can see above that the body is capable of circumventing and literally slipping it back in thru the backdoor!
To steal ideas from one person is plagiarism. To steal from many is
research!


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