VeinEase (60 Veggie Caps) AOR

Background Information

Another
theory on the progression of CVI is that tissues surrounding the veins
and even the inner lining (endothelium) of the veins themselves become
oxygen-deprived. This leads to increased blood vessel permeability and
an inflammatory response that can cause adhesion sites to develop on the
inner lining of the veins where leukocytes can attach themselves and
secrete even more inflammatory factors; this damages the vessel lining.
Fibrin also often accumulates. All of these inflammatory factors, when
leached out of the vessels into the surrounding tissues, can damage the
tissues, causing damage to the fat layer under the skin, or the skin
itself, producing itchy or painful lesions.

What Causes CVI?
CVI can result from genetic weakness of the vein walls, from
hormonal changes during pregnancy, or from damage to the valves. Other
factors that can contribute to CVI include a sedentary lifestyle, low
blood pressure or high blood pressure. Venous walls are not as elastic
as arteries, so when high blood pressure constantly applies outward
force against the walls of the veins, the veins become distended or
stretched. This stretching changes the shape of the veins and makes it
impossible for the valves to close properly, allowing blood to flow
backward, or venous reflux. Venous reflux is associated with more severe
CVI.

Understanding Venous Insufficiency
Venous insufficiency can occur in the superficial veins or in the deep
veins. Most varicose veins are related to superficial venous
insufficiency that usually begins in high-pressure areas either at the
top of the thigh and produces a varicose vein growing downward or in the calf and growing upward.
Deep venous insufficiency is much more serious since the primary cause is a blood clot (deep venous thromboembolism, DVT), and half of DVT patients end up with a pulmonary embolism (blood clot in the lungs), where morbidity jumps to 1 in 3 cases. However, even just with superficial CVI the risk of DVT is 3 times higher, so it’s
important to manage even minor CVI properly.

Anatomy of the Venous System
Blood in the arteries gets pushed through the body by the
forceful pumping of the heart; since there is no risk of backflow,
arteries do not need valves. The blood flows from the larger arteries
into arterioles, smaller vessels, and then capillaries, which are tiny
vessels that allow the exchange of oxygen, CO2, nutrients and cellular
waste products between the tissues and the bloodstream. This exchange
process happens by diffusion.

The used blood then flows into venules and then veins, through which
the blood returns to the heart to be reoxygenated. At this point, there
is very little pumping force from the heart pushing the blood through
the veins. In addition, venous blood generally has to work against
gravity, moving up from the limbs to get back to the heart. So since
there is little pumping force moving the blood, and since the force of
gravity is strong, how does the blood get back to the heart?

Moving Muscles Pump Blood
The pumping force does help a little. However, muscle
contractions from leg movement contribute quite a bit to this process.
That’s why some people experience swelling of the legs after long
periods of sitting, or why others might faint after a hard workout if
they don’t cool down properly by continuing to move rather than just
stopping cold-turkey.

Veins Need One-Way Valves
The little, if any, force from the heart and the force of
muscle contractions aren’t enough to keep the blood moving against
gravity and toward the heart. Therefore, veins have one-way valves that
stop blood from flowing back down the extremities with gravity in
between pumps. If any of the three pumping mechanisms fail (heart
pumping, muscle contractions and one-way valves), blood may begin to
pool in the legs.