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About Cardiovascular Health
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 Back
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Heart disease is the #1 killer of both men and women in America.
According to the American Heart Association, one in every five deaths in America is the result of a heart attack.
However, a heart attack is the manifestation of vascular disease in only one tiny portion of the vascular system, namely the arteries that feed the heart itself. In other words, it is only the tip of the iceberg of vascular disease. Atherosclerosis, the hardening and scarring of plaque-ridden arteries, happens throughout the vascular system. If it results in a rupture and a blot clot blocks blood flow (thrombosis) in any one of an arteries feeding the brain, a stroke (the #3 cause of death in the US) occurs and the neurons downstream die from lack of oxygen. But even more far-reaching and sinister, is the fact that vascular disease causes compromised blood flow throughout the body. According to Michael Fossel, a Medical Doctor and PhD and prominent member of the anti-aging research community, this is ultimately the cause of most deaths in old age. He says:
Although other disease processes contribute to morbidity and mortality in the aged, the overwhelming cause of organ failure is an inadequate arterial supply; the overwhelming cause of this in turn is atherosclerosis.1
Which is why he makes the claim that "most deaths worldwide are the result of vascular aging".2
Compromised blood flow to the brain from an aging vascular system has also been implicated as a possible culprit in age-related cognitive decline and even in Alzheimer's Disease.3
So in the war against mortality, both in old age and early death, Atherosclerosis is public enemy #1. In its manifestation in heart attack alone, it is responsible for more deaths than all cancers combined, and more than any other cause of death period. But its manifestations go far beyond heart attacks. The good news is that there is so much we know about it today that we had no idea about only 30 years ago, and although diet and lifestyle habits are as bad as ever, the tools are out there in ways they never were before for a dedicated individual to maintain a healthy cardiovascular profile late into life.
It is now known that cholesterol is only part of the picture. In fact, fifty percent of heart attack victims have normal cholesterol levels. Your risk of a heart attack (and of vascular disease generally) is also dramatically influenced by silent inflammations as measured by levels of C-reactive protein (hs-CRP), homocysteine levels, blood sugar levels, propensity for coagulation as measured by fibrogen, ferritin (iron) levels, blood pressure, stress, weight and exercise.
If you are committed, you can attack heart disease 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 |
|
LDL |
80 |
|
HDL |
60 or more |
|
Total/HDL ratio |
2.5 or less |
|
Triglycerides |
100 or less |
| Homocysteine |
|
7.5 or less |
| hs-CRP (Silent Inflammation) |
|
1.3 |
| Fasting Glucose |
|
60-80 |
| Insulin |
|
2-3 |
| Fibrogen |
|
<300 |
| 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.
Supplementation
There are a number of supplements that can help to maintain your markers within those optimal ranges.
Cholesterol:
- Policosanol (studies, articles)
- Gugulipid (studies, articles)
- Vitamin E (studies, articles)
- Garlic (studies, articles)
- Curcumin (studies, articles)
- No-flush Niacin (studies, articles) (periodic liver monitoring recommended)
- Phosphatidylcholine (studies, articles)
- Vitamin E (studies, articles)
- Soluble Fiber [Psyllium (studies, articles), Grapefruit Powder (studies, articles)]
- Curcumin (studies, articles)
Vessel Health:
Blood pressure:
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.
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