Quavergirl
New Blood
- Joined
- Aug 21, 2005
- Messages
- 16
Statins--the Country Doc view
I'm a cardiologist and use statins daily. There is a tremenous amount of data supporting their use (i.e. less dead bodies) and good documentation of their known side effects and therapeutic limitations (which I respect). More about that later if you are interested. Personally, I tailor the use of these drugs to each and every different patient sitting in front of me. A doc has to "adapt" guidelines--that is, be a "doctor", not just parrot the party line.*
I find the the development of statins fascinating. There was a little girl named Stormy Jones. She developed throat pain at age 8--thought to be a sore throat initially. Turns out she was having a heart attack. She was missing both copies of her LDL receptor gene in her liver; she had homozygous familial hyperlipidemia (about 1:1,000,000 incidence). Total cholesterol in these cases run in the 600-800 (sorry--US units) range and the patients develop physical signs of the cholesterol burden in their bodies. She was studied by some guys from Texas (Brown and Goldstein) They later won a Nobel Prize for ID'ing the LDL receptor. Stormy, however, died. Her doctors reasoned that a liver transplant would "cure" her LDL receptor problem, but they also needed to transplant her heart which had been destroyed by multiple heart attacks. They tried a heart-liver transplant but she did not survive.
Statins were thus created to force the liver to create more LDL receptors. They work great on heterozygous familial hyperlipidemia (missing one LDL receptor gene, incidence about 1:500 !!, LDLs run about 180-220) because there is at least one allele present to make more LDL receptors.
You can just wave a statin in front of those people and drop their LDLs in half. Patients with different genetic and non-genetic contributors to elevated LDL respond in a variable fashion--hence the need to customize therapy.
LDL reduction is not the entire story of why people die less as well as have fewer heart attacks and strokes while on statins. There are pleotropic effects of these drugs (anti-inflammatory perhaps?) that come into play and reduce "hard" events (We cardiologists are simple folk--we count the hard events like death, heart attack and stroke. Other fields are too soft--for example, an oncologist claiming that a cancer has a 30% "response" rate to a drug--what does that mean?? Does the patient live one day longer??) Anyway, LDL reduction alone does not account for the rapid drops in hard events seen in the big trials (tens of thousands of patients).
Q
*I also have a kid with autism, so my "faith" in popular medical science interpretation has been deeply shaken--more than every before I review the medical literature with the intent of weeding out the politics. Medicine is as subject to fads and mistaken "consensus" as is every other field (remember low-fat diets?)
I'm a cardiologist and use statins daily. There is a tremenous amount of data supporting their use (i.e. less dead bodies) and good documentation of their known side effects and therapeutic limitations (which I respect). More about that later if you are interested. Personally, I tailor the use of these drugs to each and every different patient sitting in front of me. A doc has to "adapt" guidelines--that is, be a "doctor", not just parrot the party line.*
I find the the development of statins fascinating. There was a little girl named Stormy Jones. She developed throat pain at age 8--thought to be a sore throat initially. Turns out she was having a heart attack. She was missing both copies of her LDL receptor gene in her liver; she had homozygous familial hyperlipidemia (about 1:1,000,000 incidence). Total cholesterol in these cases run in the 600-800 (sorry--US units) range and the patients develop physical signs of the cholesterol burden in their bodies. She was studied by some guys from Texas (Brown and Goldstein) They later won a Nobel Prize for ID'ing the LDL receptor. Stormy, however, died. Her doctors reasoned that a liver transplant would "cure" her LDL receptor problem, but they also needed to transplant her heart which had been destroyed by multiple heart attacks. They tried a heart-liver transplant but she did not survive.
Statins were thus created to force the liver to create more LDL receptors. They work great on heterozygous familial hyperlipidemia (missing one LDL receptor gene, incidence about 1:500 !!, LDLs run about 180-220) because there is at least one allele present to make more LDL receptors.
You can just wave a statin in front of those people and drop their LDLs in half. Patients with different genetic and non-genetic contributors to elevated LDL respond in a variable fashion--hence the need to customize therapy.
LDL reduction is not the entire story of why people die less as well as have fewer heart attacks and strokes while on statins. There are pleotropic effects of these drugs (anti-inflammatory perhaps?) that come into play and reduce "hard" events (We cardiologists are simple folk--we count the hard events like death, heart attack and stroke. Other fields are too soft--for example, an oncologist claiming that a cancer has a 30% "response" rate to a drug--what does that mean?? Does the patient live one day longer??) Anyway, LDL reduction alone does not account for the rapid drops in hard events seen in the big trials (tens of thousands of patients).
Q
*I also have a kid with autism, so my "faith" in popular medical science interpretation has been deeply shaken--more than every before I review the medical literature with the intent of weeding out the politics. Medicine is as subject to fads and mistaken "consensus" as is every other field (remember low-fat diets?)
)