There are few more exciting things in life than when someone completely redefines our whole understanding of a common problem. History is littered with such eureka moments - for example when Albert Einstein predicted that light could be bent by gravity. When this happened during an eclipse it led to his international fame.
Although varicose veins don't interest as many people as the discoveries of Albert Einstein, they do affect around 40% of the population during the course of their life.
We have always been taught that varicose veins are caused by the valves in the veins failing, allowing blood to fall the one wrong way down the vein. Instead of being pumped back from the feet to the heart, blood falls back down the veins, causing varicose veins and worse. If the problem is not corrected, blood clots, ankle swelling, skin damage and even leg ulcers can ensue.
So why do these valves fail? And why do some people suffer with the condition and not others?
The valves are pairs of "pockets" on the inside of the veins, with the open part facing upwards. When the foot moves, muscular action pumps the blood up towards the heart and the valve "pockets" close, allowing blood to rush past upwards. When the leg rests, gravity exerts its effect and blood tries to fall back down the same vein. The blood gets caught inside these "pockets" opening the valve and preventing this backward flow. In this way, the valves make a one-way system for venous blood.
When people suffer from varicose veins, these valves do not close and the blood is able to fall back down the veins, either stretching the vein walls (making the visible bulging varicose veins) or causing inflammation in the surrounding tissues (leading to the problems of "hidden varicose veins" such as ankle swelling, venous eczema and venous leg ulcers).
Over the last hundred years or so, surgeons and scientists have been arguing about why these valves fail in some people. It can't just be simple "genetics" in the way that hair colour, eye colour or blood groups are defined. If it were, varicose veins would always occur in both legs and also in every vein in the legs rather than only in one leg or only affecting certain veins and not others. There are clearly many factors involved and hence the term "familial", showing it runs in families but not by simple genetic coding.
As with everything, to get to the bottom of a scientific problem, scientists look at the fundamental questions - in this case the valve itself. When we are children, our valves work. As we age, some of us will have valves that fail. We used to think this was due to pressure from above. However research carried out by my team has shown that the first valves to fail tend to be lower in the leg, with the valves higher in the leg failing later - the so-called "ascending" pattern of disease progression.
So if it isn't pressure, then what is it that makes these valves fail?
Vein experts have fallen into two groups. The first think it is the valve leaflets themselves that fail, preventing the "pockets" from opening and stopping blood from falling down the veins. These doctors look to repairing the valves as their holy grail. The second group think it is dilation of the vein wall that supports the valve leaflets, so that the leaflets become unable to meet and blood is able to fall down the vein. These doctors look to supporting the vein wall either by an external cuff or by tightening the wall itself, hoping that by reversing the dilatation the valve leaflets will be able to meet again restoring valve function.
With such a seemingly simple structure, it is not surprising that experts in the field have concentrated either on the valve itself and the structure holding the valve together (the wall) and have not seriously considered an alternative mechanism.
Enter one very bright young surgical researcher, Oliver Lyons, working under Professor Alberto Smith of Kings College London who has given us a completely new understanding of venous (and probably lymphatic) disease.
Research suggests that there are a series of genes that cause venous valves to develop properly. Missing one or more of these genes results in abnormal valve development. This is interesting - but not mind-blowing.
However what is mind blowing is the concept that once the valve is fully formed, it appears to require the genes to continue to be expressed to stay healthy. This is a major change in our understanding of genes and development. We do not expect that if you switch off those genes, the development would reverse and it would shrink away again. However Oliver and Professor Alberto Smith appear to have shown that when the venous valve has fully grown, the structure can reverse and shrink away again if the genes are "switched off". Even more fascinating, one of the causes they have identified that might do this is a change in the normal flow of blood through the valve.
The ramifications of this project are immense. We can now see why valves might fail around one that has already failed. Once one valve fails, and the flow reverses, this may be sufficient enough to affect the valves above and below the affected segment. Moreover, there would appear to be little point in trying to repair the valves or the vein wall if the valve itself is regressing due to a genetic signal (or at least absence of a genetic signal). Furthermore, this might even lead to a drug that can either prevent or improve varicose veins!
Sometimes clinical doctors and the general public ignore basic scientific research performed in universities, thinking there is little direct relevance to them. This fascinating work is one of those wonderful insights to show how basic scientific research actually changes the world and can have effects on millions of us in the future.