This information will give you the power to make an informed decision about maintaining and improving your health. It is the result of decades of medical research that, in 2004, began an era in which we know the causes of chronic degenerative diseases such as atherosclerosis, realise they are maladaptions of our paleolithic genome, and know methods to re-adjust our cholesterol transport system. This is for those seeking optimal health (atherosclerosis can develop for decades before symptoms develop), for those starting to have difficulty walking, those developing claudication and peripheral vascular disease as well as for those learning to ward off heart attack, stroke, acute coronary syndromes, and death.
At the beginning of 2004 physicians were aware that patients at risk of stroke and heart attack should be treated with a statin to lower LDL-cholesterol levels below 100 mg/dL. (2.60 mmol/L) but many physicians and healthy patients alike were accustomed to regarding a total cholesterol in a blood test within limits of 100 - 199 mg/dL (2.60 mmol/L - 5.15 mmol/L) to be acceptable even when high in that range if the HDL-cholesterol level is high too. That is no longer true. Scientific excitement at new study results began circulating late in 2003 and reached general circulation April 8, 2004 in the New England Journal of Medicine when it was reported that high dose Lipitor unexpectedly showed not only a dramatic lowering of lipid levels but also a decrease in the marker for generalized inflammation, C-reactive protein, another indicator of cardiac risk. We now know all statins have this effect.
The findings indicate that in patients with acute coronary syndrome, drastically lowering LDL cholesterol to levels substantially below current target levels there is benefit, and that below 80 mg/dL (2.07 mmol/L) of LDL cholesterol, achieved with high dose Lipitor, plaque growth stops. This has profound implications for healthy individuals. These startling results indicate that monitoring otherwise healthy individuals and adjusting LDL and HDL and C-reactive protein to healthy levels will effectively prevent, halt progress, or reverse atherosclerosis and the many consequences of poor arterial flow.
These multi-center clinical trials are a remarkable advance for treatment of heart disease. The completed Prove-IT-TIMI 22, REVERSAL, IDEAL, SEARCH and TNT clinical trials are compelling evidence atherosclerosis can be placed into remission and reversed. Ongoing clinical trials are exploring how low to go with LDL-cholesterol while various companies are exploring raising HDL-cholesterol. Therefore a total cholesterol level is not fully informative. You need to know actual LDL-cholesterol and HDL-cholesterol levels as well as triglyceride levels. As yet medical scientists do not yet know how low to take LDL and how high to take HDL levels to achieve optimal plaque clearance. Studies are ongoing and indicate levels of LDL-cholesterol below 60 mg/dL (1.55 mmol/L) initiate erosion of coronary artery plaque. Aiming at these levels must be done under a physician's care since concomitant medications could cause serious adverse effects.
It is a powerful confirmation of many prior studies on the benefits of lowering blood cholesterol with lifestyle changes in nutrition, exercise, and vitamin supplements.
Since less than twenty five per cent of circulating cholesterol comes from the diet with seventy five per cent produced by the spleen, lungs, muscle cells, brain, and other tissues, this is an early alert for all healthy individuals with high cholesterol levels to take advantage of this information to ensure optimal healthy longevity.
For any individual seeking optimal healthy longevity that means taking the steps necessary to lower lipids, decrease C-reactive protein levels, and to develop a statin strategy to add to nutrition, exercise, and vitamins.
A medical treatment for reversal of atherosclerosis is also a treatment for the many degenerative diseases associated with early mortality, which have cut short the fullness of life to so many, with almost a million deaths alone in the United States last year.
ErinPharm advises that you consult with your personal physician, get blood drawn for a lipid panel, start a statin regimen if necessary, start to lower your LDL cholesterol to below 70 mg/dL ( 1.81 mmol/L), drop triglycerides to below 130 mg/dL (3.38 mmol/L) using omega-3 fish oils, take 100 - 200mg/day CoQ10 Ubiquinol to resolve statin side effects, increase HDL to over 60 mg/dL (1.55 mmol/L) or more with exercise (consult your physician). Monitor your homocysteine levels and fibrinogen levels, drink anti-oxidant fruit juices, and plan on a long life.
Updated August 16, 2011
New England Journal of Medicine, Volume 350: pp.1495-1504, April 8, 2004
C-reactive protein is a marker for generalized bodily inflammation and should be lowered to as near zero as possible since this is also a prime marker for cardiac risk. The American Heart Association has defined C-reactive protein (CRP) levels as low risk, average risk, and high risk with values of less than 1.0 mg/L, 1.0 to 3.0 mg/L, over 3.0 mg/L. Statins lower C-reactive protein levels and concomitant treatment with omega-3 fish oils will lower the level even further.
Omega-3 fish oils are of prime importance in lowering triglyceride levels as well as reducing inflammation, depression and mortality from numerous causes. Aim at achieving a triglyceride level of 130 mg/L (3.38 mmol/L) or less. Take care, omega-3 fish oils are also anti-coagulants.
For the bold and adventurous it may be instructive to reflect upon conditions known as 'longevity syndromes' in which LDL-cholesterol is extraordinary low or HDL-cholesterol is extraordinary high. Since the function of LDL-cholesterol is to deliver cholesterol to the tissues and HDL-cholesterol has the function of removing excess cholesterol then pharmacologic intervention to induce LDL-cholesterol lowering and raise HDL-cholesterol have led to the use of statins to lower LDL-cholesterol though net yet to the extent of levels found in those individuals.
According to the Merck Manual hypolipobetaproteinemia usually has no clinical manifestations, the individual has plasma total cholesterol (TC) levels ranging from 70 to 120 mg/dL (1.81 mmol/L - 3.10 mmol/L), HDL is normal to high, and LDL is 20 to 70 mg/dL 0.52 -1.81 mmol/L), usually below 60 mg/dL (1.56 mmol/L), normal food intake and fat absorption, are associated with a decreased incidence of coronary artery disease and other atherosclerotic sequelae and have been referred to as the 'longevity syndromes'. No treatment is required.
So your strategy should be frequent exercise, good nutrition, avoiding smoke, taking alcohol with prudence, following the information given on this web page and using, when necessary, a statin, omega-3 fish oils, and supplemental vitamins, maybe using niacin (consult with your physician), consuming anti-oxidant foods, juices (pomegranate juice), and vitamins to start raising your HDL level while following the literature on the race by pharmaceutical companies to come up with a safe medication to raise HDL-cholesterol levels.
Elevated homocysteine levels are a marker associated with cardiac risk. Ideally homocysteine should be below 9.0 micromol/L. Although folic acid, vitamin B6 and B12 have been used to lower homocysteine levels recent studies have shown that these supplements are not of benefit for ongoing cardiac problems. Fibrinogen levels should be monitored and maintained between 170 to 460 mg/dL (4.40 - 11.90 mmol/L).
Understand how to read your lipid panel. The lipoprotein particle levels measured in a lipid panel all contain cholesterol, protein, and triglycerides. HDL-cholesterol contains the most amount of protein, LDL-cholesterol the most amount of cholesterol, and VLDL-cholesterol the most amount of triglyceride. Total cholesterol levels are calculated according to the following equation:
Total cholesterol = HDL-cholesterol + LDL-cholesterol + (triglycerides divided by 5)
VLDL-cholesterol is mainly triglycerides so a VLDL value is recorded as one-fifth that of the triglyceride level.
Values given in mg/dL (USA) and mmol/L (UK).
The National Institutes of Health has already reported and is continuing research in growing new blood vessels in patients by inserting time-release capsules of basic fibroblast growth factor into the heart muscle of patients scheduled for bypass surgery.
For those at more advanced stages of cardiovascular disease surgical intervention is reaching more sophisticated levels to repair damage.
Clinical studies have proved that injecting the patient's own bone marrow cells into the calf muscle results in newly formed blood vessels for a person with peripheral artery disease, resulting in reversal of claudication in even the most severe cases.
We are about to enter an era in which replacement arteries made from our own cells become available as clinical trials are completed. This growth of knowledge on the research frontiers has come from a deeper understanding of Angiogenesis
The concept of pharmacological intervention to stimulate a rise in HDL-cholesterol has been the focus of major directed research studies since Pfizer's termination of their torcetrapib trials because of mortality data. They had been on the frontier running clinical trials to raise HDL-cholesterol by substantial amounts with a formulation called torcetrapib/lipitor. A major world-wide Phase III clinical study with 30,000 patients and 242 sites completed recruitment September 16, 2005. On completion of treatment these patients were placed into a one year mortality and morbidity study called ALLIANCE. Initial reports were that HDL levels rose up to 80% in some patients. This parallels reports with the ETC-216 Phase II clinical trial (torcetrapib is CP-529,414)
Devastatingly, Pfizer terminated these studies because of unacceptable cardiovascular events and mortality December 2, 2006.
Since the conceptual logic of raising HDL-cholesterol levels with a CETP inhibitor was intact other companies such as Merck with dalcetrapib and Roche with dalcetrapib are in the midst of major Phase III studies with promising results of substantial increases in levels of HDL-cholesterol. .
Debate arises over continuation of invasive angioplasty/bypass procedures for the most common kind of heart attack. N. Eng. J.Med 353;11, pp 1095-1104
John L. Fahey
To add to these remarkable studies is attention to the pomegranate fruit. I'm thankful to Dr. Isadore Rosenfeld (Fox News, Sunday, 10:30 am, June 19th, 2005) who pointed out that pomegranate juice in sufficient quantity is so packed with polyphenol antioxidants that reversal of coronary and carotid artery plaque has been observed.
If you smoke - stop. Smoking lowers HDL-cholesterol levels, oxidises LDL-cholesterol and promotes plaque accretion. Get a prescription for Chantix. (Champix in the UK).
Cytograft is on the verge of introducing into medical practice arteries to be produced for use as vascular grafts made from culturing fibroblasts taken from a skin biospy of the patient. This LfelineTM technology is in clinical trials in coronary bypass surgery, as a peripheral graft for the prevention of lower limb amputation, and as an arterio-venous shunt for hemodialysis access. At this stage of the clinical trials only patients with 'no option' critical limb ischemia are being screened to delay/avoid amputation. This is an actual real astounding turning point in medicine when such autologous vascular grafts are destined to become routine practice in surgery.
ErinPharm Cholesterol 01 Aiming at a healthy longevity.
I invite you to become a member of The Life Extension Foundation........John Fahey
