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I've pointed out before the occurrence of a small proportion of the population with the condition hypobetalipoproteinemia, whose genetic inheritance of natural very low LDL levels predisposes them to a condition known as a 'longevity syndrome' in which they do not suffer from atherosclerosis or the sequelae of cardiovascular disease.
As statin therapy is lowering LDL and C-reactive protein levels, attention is turning to molecules to raise HDL levels. A very high level of HDL is hyperalphalipoproteinemia
Hyperalphalipoproteinemia is also a genetic inheritance that is a 'longevity syndrome' which varies in incidence between women and men, between racial groups, and even between young and old. And in that, there is an interesting story. Let us call hyperalpha lipoproteinemia HALP. I am indebted to Dr. Vibhuti Singh, Dr. Elena Citkowitz and their colleague editors for their comprehensive review of HALP June 3, 2004. John Fahey
HALP has been described in most populations of the world but population-wide data for most countries is not yet available. What is known from population studies in the United States is suprising. For example, among randomly screened children and teenagers ages 6 to 19, this ' longevity syndrome' HALP is found to occur in 25% of black males, 17.2% of black females, 12.8% of white females and 7.8% of white males.
Ageing most certainly has an effect on the incidence of HALP since adults aged 20 to 79 were found to have an incidence of 13.3% for black men and women, 6.9% for white women, and 4% for white men.
A general population survey also shows incidence of HALP declining with age as shown by a prevalence of 15.8% in the 20 to 29 year age group, 8.4% in the 30 to 39 year age group, and 7.8% for those over 40 years of age.
The most important mechanism by which HDL protects against atherosclerosis is by removing excess cholesterol from peripheral cells and transporting it to the liver. This process is commonly termed the 'reverse cholesterol transport system'.
Familial HALP results in high plasma concentrations of HDL-C, lipoprotein A-1 and Apo-1. One metabolic cause is believed to be due to an elevated rate of production of Apo A-1.
This raises an interesting prospect. As defined by the US National Cholesterol Education Program Adult Treatment Panel III guidelines an HDL (HDL-C) level of 60 mg/dL (1.55 mmol/L) or greater has cardioprotective effects while the multi-center statin trials demonstrated that for coronary disease patients a level of LDL below 70 mg/dL (1.81 mmol/L) had reversal of atherosclerosis effects and therefore patients at severe cardiac risk are advised to bring their LDL below that level. Since further studies will unfold in the years to come defining preferable ranges and limits for maximal cardioprotection, it raises bold options for a healthy individual seeking optimal healthy longevity.
Since there is a wide variation in HDL and LDL levels among the general population as well as genetic differences in the levels of various enzymes involved in the reverse cholesterol transfer mechanism, it will take a long time before an individually tailored adjustment of lipoprotein levels will be feasible for the general population. At this stage I am willing to speculate that eventually medical opinion will advise levels trending toward 'longevity syndrome' levels with HDL 60 -100 mg/dL (1.55 - 3.6 mmol/L) and LDL 30-40 mg/dL (~0.8 - 1.0 mmol/L). Of course attention to triglyceride levels, VLDL, C-reactive protein, homocysteine and fibrinogen will need to be monitored and if necessary adjusted as stated in Erinpharm Central.
This web page is one of a number of ErinPharm web pages designed by me as a synopsis of topics that interest me. I have no affiliation of any kind to any pharmaceutical company or medical group. The opinions expressed are my own. I welcome communication and debate. I am an optimist. I look forward to the future with wonder.
John L. Fahey johnfahey2013@gmail.com
