It seems to make a kind of sense. There are many culprits in HD. I would say oxygenation of blood and inflammation could be two of them. Choleresteremic HD is often characterized as an inflammatory disease.
How inflammation of the lung lining leads to inflammation of the arterial lining is not easily seen, but it is known that blocked lung linings does, for instance, in silicosis, lead to susceptibility to blood infections including tuberculosis and others.
It could also be that aerobic exercise is related to a clearing of the lungs. It is known that runners suffer far less lung damage than sedentary people, even given the same exposure to atmospheric pollutants. Deep breathing does much to clear the lungs out, more than it would seem it should do in bringing pollutants in. Particulate matter, it appears, is cleared by the spasmodic action of breathing deeper.
Another related thing is the beneficial effect of Vitamin E on HD. Vitamin E is known as the lung vitamin and it has been observed in medical studies that ingestion of vitamin E reduces the likelihood of lung disease (including cancer) in smokers. Could the observed benefit of a reduced incidence of CVD amongst people taking vitamin E (5000 man Finnish study) be related to its benefit to the lungs? Could well oxygenated blood be less turbulent, its red corpuscles more flexible and less likely to clot? Does oxygen influence LDL particle size?
Are cholesterol, calcium or histamine reactions which influence calcium release and plaque formation affected by better oxygenated blood in some way?
Oxygenation of blood may impair bacteria.)
Vitamin C here may play a therapeutic role here being an effective anti-histamine. I cannot make a connection between lung particulates, which may be allergenic and histamine in the blood but there may be one.
Persistent low level infections of pneumonia chlamydia for instance, (unrelated to the similarly named venereal infection) are suggested by some medical researcher to cause, perhaps 40% of all hypercholesteremic conditions! If this is true, it would appear that a normal test where indications of a compromised vascular system is evident, would be to trace the presence of these and related bacteria. I know this is not routinely done, but given the prevalence of the causative effect it seems strange that this sort of investigation is not often suggested.
(Linus Pauling's observation of the role of Vitamin C in reducing arterial plaque could have been related to its known effect in reducing histamine which sometimes seen when calcium in the present in the arteries in the "calcium channels", and a precursor to the formation of plaque. Pauling also promoted the dosing of L-Lysine as a decoy that would precent the arterial lysine receptors from acting to absorb LDL or Lipoprotein B. This may work but the L-Lysine-L-arginine balance according to Braverman must be respected. If it gets out of whack it may be more harm than good in the area of CVD. However increasing L-arginine could cause a decrease in zinc, which would impair vitamin B absorption, which could influence red corpuscles not to disaggregate as well, increasing blood turbulence.
It would appear that the B vitamins play a role in decreasing arterial blood turbulence, therefore clotting which is related. This perhaps explains why arteries experience plaque deposition and not veins. The designers of the first artificial hearts found a marked increase in blood turbulence in artificial hearts, because they were not flexible and adaptive in response to flow, thereby causing laminar decoupling and subsequent turbulence and blood aggregation or clotting. The vitamins folic acid and B12 make blood corpuscles slipperier and more flexible, thus reducing aggregation, clotting and turbulence. Ditto vitamin E, aspirin and coumadin.
Arteries, when they get plaque get into a vicious cycle of plaque and clot formation because of the increased shear in high velocity blood and the subsequent lack of adaptiveness of the arterial walls leading to fluid laminar decoupling. This also explains why high BP is so dangerous vis a vis thrombotic stroke and HA, as the blood has more of a tendency to form clots under its higher velocity accompanying smaller and less adaptive arterial cross section. The thing that makes sharks move fast in water au verso in the vascular system, prevents blood to moving fast and smoothly thru the arteries. The shark skin prevents laminar flow, and also adapts to the flow of water over it by changing shape. Healthy arteries do this when flexible, but cannot when they get compromised thus increasing the rate of plaque formation. (It would appear that blood pressure drugs by themselves should be beneficial, but they are not long term, which raises many questions. )
Exercise and perhaps good oxygenation do increase HDL, a potent CVD reducer. As well, it may be that oxygen increases flexibility of corpuscles. Certainly alcohol does not, which explains why alcoholics are more often stroke victims. The dried out blood corpuscles induce peripheral vascular breakage, exspecially among those whose diets are bioflavonoid, pro-xanthocyanicin and anti-oxidant poor. The vascular integrity of these diet compromised individuals is also poor due in part to alcohol's propensity to leach the body of vitamins. (Lack of Bioflavonoids and vitamin C caused British sailors on long sea voyages to get scurvy, a disease that expresses itself in weakened bleeding capillaries. Limes/lemons that were provided as a therapy provide a potent bioflavonoid cocktail, and a small amount of vitamin C.
The message to potential stroke victims, is to increase your bioflavonoid and vitamin C intake. Interestingly the vitamin that most strengthens capillaries in jig time is niacin which was observed by Hoffman in 1955. He found that niacin cured bleeding gums faster and more effectively than the traditional vitamin C cure. This discovery led him to theorize it could be a therapy where arterial lining was damaged causing cholesterol plaque formation. This turned out to be true, and niacin became the preferred treatment for hypercholesteremia, or hardening of the arteries, for 30 years. )
The message to drinkers is to increase their B12, folic acid, vitamin C, niacin, grape seed, unsweetened chocolated and n-acetyle cysteine intake. The resulting more fexible and less dried-out blood platelets are far less likely to clot, and being far more supple would have a much easier time of getting through the tiny capillaries of the brain. Often the blood platelets are larger than the capillaries, which explains why they need to be flexible. The major elements which make blood platelets flexible are B12 and folic acid. The pro-xantho cyanidins in dark chocolate and the n-acetyl cysteine reduce the dry out effect of the alcohol on the cells to a degree.
One of my grandfathers had his lungs damaged in a gas attack in the first world war. Although fit and otherwise seemingly healthy, he could not stand exposure to even very low levels of CO2 or CO. He could not also stand very much aerobic exercise. He had a marked tendency to "hardening of the arteries" and died of a HA in his early seventies.
EC<:-} |
