Diet alone WILL NOT lower cholesterol. Many are not aware of a sub-type of cholesterol called apo a. That are at best only transiently responsive to diet.
This type of cholesterol needs a medication, and no amount of dieting or exercise will lower this type of cholesterol.
Now, Iam going to go into the mechanism of action for this type of cholesterol.I will try to make this simple and not go into the long terms associated with this genetic cholesterol.
An independent risk factor for artery clogging cholesterol(atherosclerosis).
Lipoprotein a(LPa. This type of cholesterol carries a another sub type of cholesterol called apo B (When apo B is elevated it is considered a risk factor for heart disease)there is a molecular bridge that forms between apo a apo B and this leads to cholesterol build up on the arteries.
To explain, Mechanism of Action it is
Just the way things work.
Signing off for now
This site deals with cholesterol and it's sub-types and when it is necessary to test for the sub-types of cholesterol.There are also postings of recipes to lower dietary cholesterol. You will also find the different apolipoproteins that contribute to athersclerosis.
Wednesday, December 2, 2009
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Hi Laura
ReplyDeleteGlad to find your blog. Members of my family have FH.
Marilyn
Hi Marilyn,
ReplyDeleteHope all is well with you and yours. Iam sure you read my story. I don't want to pry and I will understand if you wish to be confidential on your family history,but Iam interested in how they were diagnosed.
Laura
Laura
ReplyDeleteMy 16-year-old daughter had her total cholesterol checked at her pediatrician's office when she was 8. It was very high, so they sent her for a fasting lipid profile. Her total cholesterol was 389. Her LDL was very high, I don't remember the exact number. At that point, we were referred to a pediatric cardiologist. When changing her diet did not bring her LDL down to normal levels, they said she probably had FH. My husband is a carrier but his LDL is only moderately elevated. My late mother-in-law had FH, although I was never able to find out her exact lipid numbers.
My husband's family history is as follows:
mother: nonfatal MIs at 58 and 82.
maternal uncle: fatal MI at 40
maternal grandfather: fatal MI at 35
My husband (age 54) has no symptoms, but he had a coronary artery calcium scan in 2007 and his score was 488 (93d percentile). So we know he has extensive atherosclerosis, and his cardiologist has him on 80 mg atorvastatin plus 1500 Niaspan. He also has elevated lipoprotein(a), although the Niaspan has lowered it (from 57 to 37).
So, basically, we know my husband must have the mutation, or our daughter would not have inherited it. We would not know he had FH simply from his lipid profile, because his LDL is not that high. I'm told that 10-15 percent of people who have an FH mutation have "incomplete penetrance," which means their LDL is only moderately elevated.
My daughter is lucky because 20 mg atorvastatin has brought her LDL down to normal levels. When not on medication her LDL is about 250-270.
My mother-in-law was on statins ever since they came on the market. That undoubtedly helped keep her alive, but she developed heart failure, peripheral artery disease and atrial fibrillation. This summer she fell and broke her hip and she was gone three days later. The stress to her system of the injury and surgery was just too much, given everything she had wrong with her.