The missing 80%

80% of people with the potential to have UC, never get the condition triggered.

The obvious question is to then say that certain factors must increases the risk of trigger (not talking about the risk of having the gene - that's different).

But unless I've missed something this isn't true.

80% of all males and 80% of all females don't have their UC condition - > not sex related

80% of people living in "hot" climates and 80% of all people living in "cold" climates don't have their UC triggered -> not climate related

etc

In fact I've yet to read about a particular risk categoery that statisitcially is more likely to induce the disease. (Remember issues about Jewish ancestory etc refer to the potential to have the gene, not the trigger. There is still 80% of such people who don't have UC even though they have the potential)

So my proposition is this...that UC as we understand it today is not a condition, rather it is a collection of symptoms. In fact it is being treated as such by "modern" medicine. (the word modern being used here in the loosest possible sense!).

Last estimate gives 1,543 medical reasons for a person to have a headache. I wonder is UC similar in this repsect i.e. UC as we know it is a symptom not the underlying condition. This would go along way to explaining why people with UC have such varying symptoms.

But that's just a though, only a thought.

D

My thinking runs along these lines too. UC seems like more of a syndrome (the medical term for a group of symptoms commonly occurring together) than an single disease. It's just too different in it's minor aspects (food tolerances, response to meds, triggers for flares) in different people. While there probably aren't 1500 causes, I've long suspected there may be as many as 5 to 20.

I can't see how such an argument can be applied to most "standard" diseases where a cause and effect relationship exists. But no such cause - effect exsits for UC.

I've long found this an interesting way of thinking about UC. After all, there is some genetic susceptibility, an initial trigger, and a vast lot of possible environmental or developmental factors. How do all of these interact to produce the symptoms to which we refer as ulcerative colitis? How much does the organic pathology of UC differ between individual sufferers? Calling it a "syndrome" like Judilyn or a even a spectrum (in the same sense as "autistic spectrum disorder") rather than a specific disease might be more accurate. I strongly suspect that improvements in treatment will come not from new wonder drugs which are great for everyone, but from improved diagnostics which provide a more specific description of what an individual is experiencing (type XXIII ulcerative colitis, maybe!) - and who then can be treated by very specific agents (agents which may only work for a very small proportion of UD patients, but give this small proportion significant relief). Unfortunately this is both a form of medicine with a small target population - hence not well funded by drug company research - and expensive. Still, there does seem to be recent progress in identifying some of the biochemistry of UC, so I expect we'll start seeing more drugs like Remicade, though perhaps which will only be used after genetic or other testing to determine if the patient is in the correct target group, in the not-too-distant future.

Craig