Why don’t Veins develop atheromata ?

How arteries and veins are constructed

In this section, we start learning how problems occur. For it is their different construction (dictated by their different functions) that defines the nature of the things that can go wrong such as hardening of the arteries, high blood pressure, and blood clots.
Arteries

Arterial walls are composed of elastic tissue and smooth muscle. It is their elastic nature and the presence of substantial muscle tissue that allows them to expand and contract as the heart beats. This allows them to even out the increase in pressure caused by each beat. This is one of the primary reasons why hardening of the arteries (atherosclerosis) increases blood pressure. If you pump more fluid through the same sized tube, pressure must increase. On the other hand, if the tube is flexible and can widen, the increase is less. (We will talk more about this later.)
Veins

Veins are thinner walled than arteries and have less elastic tissue, and much, much less smooth muscle tissue. Instead, veins make use of valves and the muscle contraction of your body’s major skeletal muscles to squeeze blood along. This is the reason you’re asked to get up and walk around on a long plane flight—to prevent blood from pooling in your legs. As a side note, the lack of muscle in the walls of veins makes them more susceptible to bleeding when injured since there’s no muscle to clamp down.
Problems that can occur in arteries

There isn’t much mystery as to what the problem is—the build up of arterial plaque on the walls of the arteries and arterioles. There is, however, a great deal of mystery as to what causes it.
The basic problem is that arterial plaque (a combination of protein, calcium and cholesterol) starts building up on the walls of the arteries. This causes the arteries to both harden and narrow. So far so good! But what causes that buildup?
The cholesterol theory

The primary theory lays the blame on cholesterol—that as cholesterol levels climb in the blood, this causes plaque to form on the walls of the arteries. But this theory begins to collapse under even the most elementary scrutiny. As I mentioned in my newsletter, the Cholesterol Myth, one of my favorite questions to ask doctors is, "If cholesterol is the main culprit in heart disease, why don’t veins ever get narrowed and blocked?" And if you wanted to, you could throw capillaries into the equation too. Capillaries do not evidence the build up of arterial plaque. (They do, however, clog with amyloid plaque in the brain. But that’s a different problem that we’ll cover in a later newsletter.)
Think about this for a moment. If you have cholesterol circulating equally through the entire circulatory system, but it only causes plaque to build up in the arteries and arterioles, not the capillaries or veins, then how can cholesterol be the primary cause of the problem? If cholesterol caused plaque to form, wouldn’t it form everywhere? Since it only forms in the arteries, doesn’t the problem have to be something unique to those arteries?
The arterial wall theory

A more sophisticated version of the theory says that the build up of plaque is triggered by damage to the arterial wall—the endothelial lining. The lining consists of a thin layer of endothelial cells that performs two critical functions:
- It protects the "innards" of the artery from toxic substances in the blood.

- It helps regulate the expansion and contraction of the arteries by releasing a bio-chemical (cyclic GMP) into the cells of the smooth muscle in the arterial wall that change the tone or firmness of the artery.

- In an attempt to repair damage to the endothelium, your body will "patch" the damage with plaque.

- This produces one of two conditions—two sides of the same coin really.
Artherosclerosis (hardening of the arteries)

Damage to the endothelial lining is "managed" by the smooth muscle cells surrounding the lining. Smooth muscle cells respond to endothelial injury by rapidly multiplying and producing a fibrin/calcium/cholesterol patch. These patches, called plaques occur just inside the lining and thicken the artery’s inner wall. Over time, given multiple injuries, the wall of the artery begins to harden and become dysfunctional, no longer expanding and contracting to regulate blood pressure —and steadily narrowing the passageway through which blood flows.
Arteriosclerosis (plaque build up)

Another way of describing this process is that your body creates plaque to "paste over" any damaged areas—like a scab over a cut. Over time, given repeated injury, these plaques intrude more and more on the inner passage of the artery steadily compromising the ability of the artery to expand and contract and for blood to flow freely.
But it gets worse

The damage to the arterial wall also triggers an immune response with white blood cells flooding the area. This leads to a chronic inflammatory response in the blood vessel. Continued inflammation causes even more damage, which accelerates the process.
All of this, of course, brings up the $64,000 question: "Since the entire theory hinges on damage to the endothelial lining, what actually causes the damage to the lining, and why doesn’t it happen to the lining of the veins?"
Once again, oxidized fats and LDL cholesterol are named as the key culprits. Other suspected culprits include:

- Free radicals.

- High blood pressure (yes, high blood pressure begets more high blood pressure).

- Diabetes.

- High homocysteine levels.

- High C-Reactive Protein levels.

- Low levels of vitamin C (similar to scurvy).

- Low levels of nitric oxide.

- Heavy metals.

- Aging.

- Muscle matters
But once again, the question arises: "Are not all of these things present in the capillaries and veins too?" The answer, of course, is yes they are—which means there’s still a missing piece in the equation. The answer, according to the pH theory, lies not in what flows through the arteries and veins (which is identical), but in their construction (which is different). The key difference between arteries and veins is in the amount of muscle tissue surrounding the endothelial lining. In arteries and arterioles, the smooth muscle is extensive. In veins, it is minimal. And in capillaries, it is totally absent. Why does this matter?
It matters because when muscle tissue is used it produces lactic acid. If your body is healthy (in an alkaline state) and has ready access to an abundant source of oxygen rich blood, that lactic acid can clear quickly. But for those people who eat a high acid forming diet and are in an acidic state, the lactic acid cannot clear quickly. (Remember, blood vessels do not have direct access to the oxygen in the blood that flows through them. They are dependent on the vasa vasorum.) It is the lactic acid that provides the final trigger that causes damage to occur in arterial linings, but not so in veins. It is the presence of accumulated lactic acid in the smooth muscles surrounding arteries that ultimately causes plaques to form.
But even beyond lactic acid, there’s another area where muscle tissue matters: nitric oxide. The contraction of the muscles in the arterial walls is regulated by a signaling molecule that we referred to earlier called cyclic guanosine monophosphate (cyclic GMP) in the muscle cells. Cyclic GMP causes the arterial muscle to relax, in preparation for its next contraction. Cyclic GMP is triggered by nitric oxide, which is produced in the endothelial lining. The ability of the lining to manufacture enough nitric oxide to maintain artery dilation is one of its most crucial functions. As damage continues to build in the lining, it blocks nitric oxide-induced dilation, thus stiffening the arteries.
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