Extended Release Niacin in Diabetics link
"Conclusions—In statin-treated men with type 2 diabetes mellitus, Extended Release Niacin decreased plasma Lp(a) concentrations by decreasing the production of apo(a) and Lp(a)-apoB-100.
Extended Release Niacin also decreased the concentrations of apoB-100–containing lipoproteins by decreasing VLDL production and the transport of these particles down the VLDL to LDL cascade.
Our study provides further mechanistic insights into the lipid-regulating effects of Extended Release Niacin."
- Received July 1, 2015.
- Accepted October 20, 2015.
- © 2015 American Heart Association, Inc.
LDLc treatment and its impact on mortality
Received: March 2, 2015 Article in press
Journal of Clinical Lipidology
- •Hypercholesterolemia is the highest population attributable risk factor for CHD.
- •LDL-C remains the primary treatment target for reduction of ischemic events.
- •Intensive statins and statin/ezetimibe are proven for secondary prevention.
- •Treatment of LDL-C to less tha 50 mg/dL are being tested with novel therapies.
AbstractCardiovascular (CV) disease is a leading cause of death worldwide, accounting for approximately 31.4% of deaths globally in 2012.
It is estimated that, from 1980 to 2000, reduction in total cholesterol accounted for a 33% decrease in coronary heart disease (CHD) deaths in the USA.
In other developed countries, similar decreases in CHD deaths (ranging from 19–46%) have been attributed to reduction in total cholesterol.
Low-density lipoprotein cholesterol (LDL-C) has now largely replaced total cholesterol as a risk marker and the primary treatment target for hyperlipidemia.
Reduction in LDL-C levels by statin-based therapies has been demonstrated to result in a reduction in the risk of nonfatal CV events and mortality in a continuous and graded manner over a wide range of baseline risk and LDL-C levels.
This article provides a review of:
1) the relationship between LDL-C and CV risk from a biologic, epidemiologic, and genetic standpoint;
2) evidence-based strategies for LDL-C lowering;
3) lipid management guidelines;
4) new strategies to further reduce CV risk through LDL-C lowering; and
5) population-level and health-system initiatives aimed at identifying, treating, and lowering lifetime LDL-C exposure.
I wrote Tubby Theory from Topeka in 2009, published it in 2010.
At that time I advised people with one risk factor to get a CAC and CIMT. If they had a plaque, they had subclinical atherosclerosis.
To get regression of the plaque, I advised low dose combination therapy with statin, niacin and Zetia.
Slowly add the drugs each month until the one of the following goals is reached:
non-HDLc less than 80
LDLp less than 75
apo B less than 60.
Low dose combination therapy is the way to avoid side effects especially since we need to treat atherosclerosis early to reduce the residual risk of treating late in the disease process and the patient will be on these drugs for a very long time.
Update and Validation of Tubby Theory link