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BackAbout Cardiovascular Health

It is now known that cholesterol is only part of the picture of vascular health. If you are committed, you can attack circulatory health from all these angles. In a nutshell, to dramatically increase your chances of maintaining a healthy cardiovascular system, we recommend you keep your markers within these optimal ranges:



Smoking no
Cholesterol
Total 160-180 (mg/dL)
LDL 80 (mg/dL)
HDL 60 or more (mg/dL)
Total/HDL ratio 2.5 or less (mg/dL)
Triglycerides 100 or less (mg/dL)
Homocysteine 7.5 or less (umol/L)
hs-CRP (Silent Inflammation) 1.3 (mg/L)
Fasting Glucose 60-80 (mg/dL)
Insulin 2-3
Fibrogen <300 (mg/dL)
Ferratin <100
Blood Pressure
Systolic 120
Diastolic 80
Stress Not Type A with anger
Exercise yes :)


Diet

To keep overall cholesterol within a healthy range, the most effective thing you can do is to manage your intake of saturated fat. In our opinion, this can be done by avoiding dairy products all together (The dairy association has worked hard creating the Food Pyramid so that you might think that dairy is an essential food group, but don't buy it) and bringing your chicken and beef consumption into line with what we evolved around, which was probably once a week or less. For diet and lifestyle advice for keeping your other markers within optimal ranges, see our sections on blood sugar, silent inflammation, methylation, and stress.


Telomeres and Vascular Health

It is often an assumption about heart disease, and about aging diseases generally, that they happen with greater frequency to the elderly because they are decades in the making. While there is a sense in which this is true, advancements in the understanding of telomere biology are beginning to call the traditional understanding of this phenomenon into question.

Children with HGPS Progeria, a disease of premature aging, die tragically at a mean age of 12.7 years overwhelmingly of atherosclerosis. However, their cholesterol levels, as well as other risk factors mentioned in the above table, are normal.4 They pose a problem for the gradual damage theory of atherosclerosis and for any wear-and-tear theory of an aging disease. HGPS victims have a LMNA gene defect that compromises the structural integrity of the nucleus of most of the cells in their body, causing those cells to commit aptopsis (cell suicide) much more often and for other cells around them to hyperproliferate in an attempt to make up for the lost cells. As a result of this hyperproliferation, telomere lengths of the cells throughout the body of Progerics have been confirmed to be shorter than those of their peers,5 and their count of senescent cells higher.6 Reduced telomere lengths result in changed gene expression patterns, resulting in a less functional cell, and this is why many believe that atherosclerosis is the common pathology associated with HGPS. (more on Progerics and the telomere theory of aging) In atherosclerosis, we now know that as we age the arterial lining becomes comprised of cells whose gene expression has changed,7 becoming older, less functional cells8 unable to secrete the proper elastin and collagen proteins and senescent cells that are misshapen or dysfunctional.9

Under the telomere theory of vascular aging, the artery as a result can no longer maintain its smooth, healthy lining and begins to scar, crack, allow LDL particular into the membranes where they oxidize and begin the process of soft plaque formation.

LDL, smoking, high blood sugar, homocysteine and high blood pressure are statistical markers of atherosclerosis under this theory largely because they all damage endothelial cells lining the artery10, increasing cell division/turnover and shortening telomeres. Calvin Harley, the Chief Scientist at Geron, was able to show in 1995 that areas of high vascular stress showed telomere shortening prior to the onset of vascular disease11

If this theory is correct, telomere shortening is the 'true' cause of heart disease associated with aging in the sense that if you lived long enough and nothing else got you first, you would eventually contract atherosclerosis no matter what your diet and lifestyle by the simple fact that the telomeres in your arterial walls are shortening as they naturally divide.

It would also open the door to a potentially striking effect of telomere therapy in the future using a precisely controlled telomerase inducer for atherosclerosis and heart disease. Until that day, both theories predict that focusing on keeping your risk markers withing the optimal range laid out in the table above is the most effective form of maintaining a healthy cardiovascular system. See the following sections for managing:


More Information


References

1. Cells, Aging and Human Disease, ibid. Page 165.

2. Cells, Aging and Human Disease, ibid. Page 161.

3. Miano and Zlokovic, 2006 Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype
See also:
Briendl, Annette Paper recasts Alzheimer's as cariovascular disorder Bioworld Today. Jan 25, 2007

4. Fossel, Michael. Cells, Aging and Human Disease. 2004. Page 167

5. Allsopp et al. 1992. Telomere length predicts replicative capacity of human fibroblasts. Proc Natl Acad Sci USA 89:10114-10118.

6. Goldstein et al. 1983. Some aspects of cellular aging. J Chron Dis. 36:103-116.

7. Monagemi. Gene expression in athergenesis

Cooper. The vasculopathy of aging.

8. Britten M. The role of endothelial function of ischemic manifestations of coronary atherosclerosis

Kimura Y. Impaired endothelial function in hypertensive elderly patients evaluated by high..

9. In Cells, Aging and Human Disease, page 170, Michael Fossel writes:

In comparing young normal human aortic endothelial cells to senescent endothelial cells and endothelial cells imoortalized with hTERT, we find differences. Compared to young endothelial cells, senescent endothelial cells show a decreased production and activity of NO, changes critial in atherogenesis and hypertension. Similarly, senescent endothelial cells demonstrate increased monocyte adhesion, again implicated in atherogenesis. [..] In all cases, these differences are amerliorated or normalized by hTERT immortalization.

10. Xu D, Neville R, Finkel T. Homocysteine accelerates endothelial cell senescence. FEBS Lett. 2000;470:20–24.

11. Chang E, Harley CB. Telomere length and replicative aging in human vascular tissues.