ValleyForge wrote:Greater blood flow has never been correlated with intimal hyperplasia. Turbulent yes, but not greater flow.
I presume you are referring to a lack of correlation between endurance athletes and IH.
Turbulent flow is associated with high flow, as well as whole blood viscosity changes related to hydration state.
It's most plausible that endurance athletes generally have a healthier diet with lower inflammation and oxidation; and this gives some protection against turbulent flow and IH.
But if you combine a few hundred thousand km's of cycling and a junky fast food diet....
The iliac artery and veins service pelvic, buttock, and lower limb fat which increase substantially in both sexes with a higher bodyfat %, so you still get stretching of these veins....and if they are already IH damaged, then what's the additional stretching going to do?
ValleyForge wrote:Can you explain what similarity you are referring to?
The similarity that varicosities are asymmetrical in cyclists.
ValleyForge wrote:This is not any recognised mechanism. In fact, intra-abdominal pressure is usually negative, not positive. Venous return from visceral fat is not via the iliac veins or vena cava. Can you explain how these vessels are implicated?
Research the relationship between central adiposity and IAP; and respiratory cycle and IAP.
Can you advise normative IAP values during the third trimester of pregnancy, and variation between standing and supine or sidelying?
IAP and venous return is adversely effected in pregnant obese women.
Can you advise if varicose veins during pregnancy are all hormonal.
ValleyForge wrote:Unless I am mistaken, veins down "supply" anything.
yes, you are right I should have said iliac veins to service blood return from greater mass.
ValleyForge wrote:This is not based on any recognised mechanism. Intra-abdominal pressure is usually negative; intra-thoracic pressure even more so.
refer to IAP and BMI relationship again.
review intra-thoracic pressure and venous return during the respiratory cycle, though I didn't raise that.
I was focusing on venous return from the lower limbs and the effect of increased bodyfat, especially central adiposity.
ValleyForge wrote:Mechanical stress yes. The systemic inflammatory markers that are elevated in several vascular conditions (Beurger's esp.) definitely.
Completely different systems. Systemic hypertension (high blood pressure) does not lead to increased venous blood pressure.
They have different pressures yes (physiology 101), but they both degenerate in the presence of systemic inflammation and oxidative stress, and no doubt are both adversely effected by extreme volumes of repetitive mechanical kinking.
ValleyForge wrote:Look, I agree that the human vascular system is fascinating and its embryology even more so. Not even NBNCo could have come up with something so convoluted.
Turbulent flow and some inflammatory processes cause intimal hyperplasia; turbulent flow from non-anatomical kinks in the vessel, loss of the original smooth endothelial lining and hyper-viscosity syndromes among others. There are a few band/obliteration syndromes too - 12th rib and arcuate ligament syndromes are amongst the best defined. There are several others purported, but lets leave them as minutae.
Turbulent flow in the arterial system is associated with hypertension; and whole blood viscosity which is associated with hydration state.
It's clincially irresponsible to dismiss factors that lead to greater bodyfat as being inconsequential to arteries AND veins.