C-reactive protein is better than LDL for predicting heart disease!
- 02-08-2003, 09:54 AM
C-reactive protein is better than LDL for predicting heart disease!
<P class=text><SPAN class=text>More very important reasons to be consuming Omega 3's. WW7 </SPAN>
<P class=text><SPAN class=text>------------------------------------------------------------------------------------</SPAN>
<P class=text><SPAN class=text>The full C-reactive protein story</SPAN>
<P class=text><SPAN class=text>By Dr. Phil Maffetone</SPAN>
<P class=text>A study published in the Nov. 14, 2002, issue of the <I>New England Journal of Medicine</I> made news headlines in recent weeks. Researchers measured C-reactive protein and LDL cholesterol in more than 27,000 healthy American women and then tracked them for eight years, finding that elevated C-reactive protein was a better predictor of cardiovascular problems than LDL.
<P class=text>While this caught the attention of many in the medical community and the media, it shouldn't be too big a surprise since other studies recently have indicated C-reactive protein may be a better indicator of heart disease than cholesterol assessments.
<P class=text>What's more disappointing is that the medical establishment and the media don't do more to explain what C-reactive protein is, what high levels indicate, and what can be done to remedy the condition. I can only assume they are waiting for a new drug that lowers C-reactive protein.
<P class=text>For those who don't wish to wait for that drug, here's a short-course. C-reactive protein levels are elevated in the presence of chronic inflammation, a condition many people unknowingly have. Chronic inflammation can be the result of many factors, ranging from physical activity to diet to stress.
<P class=text>In a large number of people, chronic inflammation may be an indicator of an imbalance of chemicals in the body called eicosanoids. Eicosanoid balance is disrupted by dietary factors including high levels of omega-6 vegetable oils, hydrogenated oils and saturated fats, and low levels of omega-3 fatty acids.
<P class=text>In addition to making certain dietary adjustments, consuming omega-3 oils may help balance eicosanoid levels and lower inflammation in some people. Other foods may also help thwart chronic inflammation. These include, garlic, ginger, citrus-peel oil, sesame-seed oil and turmeric.
<SPAN class=text>For more information about the connection between C-reactive protein, chronic inflammation and disease, including not only cardiovascular disease but also cancer, Alzheimer's, osteoporosis and diabetes, check out my booklet ttp://mafgroup.securedata.net/catalog/books/abc_inflam.shtml"><I>The ABCs of Inflammation</I> and also my book, ttp://mafgroup.securedata.net/catalog/books/fitness_health.shtml"><I>In Fitness and In Health</I>.</SPAN>
- 02-08-2003, 03:52 PM
- 02-08-2003, 03:54 PM
As do I. Sounds like new drugs are in the works and once the pharm. company is poised to make billions off of it they will then announce this "new" breakthrough.
Last edited by windwords7; 02-08-2003 at 05:35 PM.
I believe this is the only testosterone/c-reactive protein study available
The effects of varying doses of T on insulin sensitivity, plasma lipids, apolipoproteins, and C-reactive protein in healthy young men.
Singh AB, Hsia S, Alaupovic P, Sinha-Hikim I, Woodhouse L, Buchanan TA, Shen R, Bross R, Berman N, Bhasin S.
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059, USA.
The effects of T supplementation on insulin sensitivity, inflammation-sensitive markers, and apolipoproteins remain poorly understood. We do not know whether T's effects on plasma lipids, apolipoproteins, and insulin sensitivity are dose dependent, or whether significant anabolic effects can be achieved at T doses that do not adversely affect these cardiovascular risk factors. To determine the effects of different doses of T, 61 eugonadal men, 18-35 yr of age, were randomly assigned to 1 of 5 groups to receive monthly injections of long-acting GnRH agonist to suppress endogenous T secretion and weekly injections of 25, 50, 125, 300, or 600 mg T enanthate for 20 wk. Dietary energy and protein intakes were standardized. Combined administration of GnRH agonist and graded doses of T enanthate resulted in nadir T concentrations of 253, 306, 542, 1345, and 2370 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Plasma high density lipoprotein cholesterol and apolipoprotein A-I concentrations were inversely correlated with total and free T concentrations and were significantly decreased only in the 600 mg/wk group (change in high density lipoprotein cholesterol: -8 +/- 2 mg/dl; P = 0.0005; change in apolipoprotein A-I: -16 +/- 2 mg/dl; P = 0.0001). Serum total cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, triglycerides, apolipoprotein B, and apolipoprotein C-III were not significantly correlated with T dose or concentration. There was no significant change in total cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, triglycerides, apolipoprotein B, or apolipoprotein C-III levels at any dose. The insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose, derived from the insulin-modified, frequently sampled, iv glucose tolerance test using the Bergman minimal model, did not change significantly at any dose. Circulating levels of C-reactive protein were not correlated with T concentrations and did not change with treatment in any group. Significant increments in fat-free mass, muscle size, and strength were observed at doses that did not affect cardiovascular risk factors. Over a wide range of doses, including those associated with significant gains in fat-free mass and muscle size, T had no adverse effect on insulin sensitivity, plasma lipids, apolipoproteins, or C-reactive protein. Only the highest dose of T (600 mg/wk) was associated with a reduction in plasma high density lipoprotein cholesterol and apolipoprotein A-I. Long-term studies are needed to determine whether T supplementation of older men with low T levels affects atherosclerosis progression.
Randomized Controlled Trial
PMID: 11788637 [PubMed - indexed for MEDLINE]
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