Seasonal Patterns of onset in LC

[harvest_table]

This is interesting ....... the conclusions are as follows.

Conclusions: To our knowledge, this is the first study to examine systematically and report a significant seasonal incidence pattern of lymphocytic colitis. Our observations may support a potential link to an infectious source in lymphocytic colitis.

I'm unable to provide a link to the abstract however you can google about for it under the subject line in this thread under (JOCG)

Love,
Joanna

[mle_ii]

Here's a link:
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16208113

Here's the specific info that tells us the when:

RESULTS: The distribution of month of onset of symptoms showed a statistically significant (chi test of homogeneity, P = 0.0008) temporal variability and seasonal incidence pattern with excess cases during summer and fall and a paucity of cases during colder months.

There are a few reasons running through my head as to why this might be happening.

What things change seasonally?
Temperature (hotter during summer and colder during winter)
Sunlight (more sun during summer and less during winter)
Colds/Flu (more colds/flu during fall/winter, flu shots)
Diet/Foods (seasonal foods - fruits, vegetables)
Being indoors/outdoors (indoors more during winter less during summer)
Being in closer proximity to more people (indoors and closer to people during the winter, more visitors during winter-holidays)
Traveling/vacation (tend to do more traveling and camping during summer)
Seasonal allergies (pollen, molds, mildews, etc)
Sleep (we probably get more sleep during winter and less during summer)

I can think of reasons why each of these things would play into the majority of cases being during the summer fall.

What might be some other related reasons that don't have a seasonal cause of the disease?
Perhaps during the summer our plans (which there might be more of than during the winter) were stopped many times due to illness and finally we decide to go see the dr and then we get diagnosed.

The thing that's looking to me to be the most obvious is Vitamin D levels. Why is that since Summer would be when we're getting the most? Because I would venture to guess that it takes a bit of time for the illness to manifest to the level that it does. Perhaps we didn't do as much traveling one summer or spent more time indoors or our vitamin D levels were depleted. So we go into fall, winter and spring, all the while our vitamin levels are going down, our immune system isn't being regulated as well, some bacteria/virus or drug or food, caused us to have a leaky gut. Our immune systems get triggered towards a TH1 response, it isn't being regulated well because of Vitamin D levels being low. So TH1 causes inflmation, that isn't being regulated, this inflamation brings more immune response, still no regulation, a vicious cycle and in the end we get what we have. How do we get out of this cycle? Well we need some form of regulation and we need to reduce inflamation. And this is exactly what glucocorticoids (the steroids some take) or some of the other drugs we take does to bring down inflamation and regulate the immune system. And now we know what else can do this, Vitamin D.

Even while writing this I can think of various causes of Vitamin D being low.
Not enough Vitamin D in our diets - cholecalciferol (D3), don't consume supplemented foods (milk), no fish in diet (salmon, tuna, mackerel, sardines, eel), no eggs, no fish oil, or wrong kind (ergocalciferol or D2 is not as effective as D3)
Not enough cholesterol in our bodies
Not enough sunlight - time spent outside, length of time, angle of sun, polution, sunscreen usage
Skin issues - dark skin, skin damage disease/cancer/burns, age - this is where 7-Dehydrocholesterol is converted to Cholecalciferol via UVB light
Liver damage/disease - this is where one form of Vitamin D (Cholecalciferol) is converted to the stored version of Vitamin D (calcidiol or 25-hydroxy-vitamin D).
Kidney damage/disease - this is where calcidiol is converted to the active form of vitamin D (calcitriol or 1,25 dihydroxy vitamin D3)

So here's the path to calcitriol (vitamin D3).
????? -> 7-Dehydrocholesterol (NOT SURE OF THE EXACT PATH HERE)
7-Dehydrocholesterol (in the skin) + UVB (sunlight) -> cholecalciferol
cholecalciferol (hydroxylated in the liver) -> calcidiol
calcidiol (in the kidney) -> calcitriol

Mike

[mle_ii]

Ok it seems I got one part wrong.

Cholesterol -> 7-Dehydrocholesterol is not correct. In fact it goes the other way around.

So it is either:
7-Dehydrocholesterol + 7-dehydrocholesterol reductase -> Cholesterol
or
7-Dehydrocholesterol (in skin) + UVB -> cholecalciferol

Might this explain higher cholesterol levels in some folks here if we don't convert enough of it to cholecalciferol?

[tex]

Mike,

I'm not trying to say that vitamin D doesn't play a part in this issue, because it certainly might, but remember, they adjusted the criteria to reflect the onset of symptoms, not the time of diagnosis, nor even the time of the initial doctor visit. If the period of highest incidence of onset of symptoms occurs in summer and fall, I can't easily rationalize how a vitamin D deficiency could be causing the problem. After all, that's the part of the annual cycle when vitamin D is not only most available, but most people are also most likely to take advantage of it's availability. And, vitamin D levels in the body can change in a matter of hours, (even minutes), with exposure to sunlight. It's not like it takes months to build up a supply in the body. Furthermore, it's not likely that the additional chemical reactions that must take place to utilize it, would require a significant amount of time - probably hours or days, not weeks or months.

Also, the report suggests an infectious agent,

Our observations may support a potential link to an infectious source in lymphocytic colitis.

but like you, I fail to visualize where an infectious agent might be more likely to have a more significant effect in summer and fall, than in winter and spring - unless it might possibly be related to internal parasites, that we are more likely to encounter during those seasons. All things being equal, it would seem intuitive that there should be significantly less opportunity for infections in general, in the spring and summer, compared with the other seasons.

Since this is generally classified as an autoimmune issue, if there is indeed a seasonal link, I would tend to be suspicious of things like histamines, of possibility other products of seasonal allergies that might serve to act as an antagonist which provokes subsequent reactions in some susceptable individuals. Maybe something of this sort is initially causing those lymphocytes to accumulate between the epithelial cells in the colon. We've discussed the possible effects of histamines in the digestive tract before, I believe.

The 26% of otherwise normal individuals who showed the markers of LC in the research project that Joanna posted about in another topic, suggests to me that a lot of people may be latent LC patients, just waiting for the right trigger, or combination of triggers, to complete the reaction that changes them from asymptomatic to symptomatic patients.

Consider this: none of us with LC has any way of knowing how long we might have been asymptomatic, before we became symptomatic. It's possible that a significant percentage of the general populatiion has LC, but only a tiny percentage will ever become symptomatic. I'm not saying that this is the case - I'm just thinking out loud here.

Tex

[mle_ii]

Actually all of what you said still fits in with Vitamin D. Especially the last bit.

Here are my thoughts:
This isn't an overnight process, so folks were symptomatic during the summer and fall. What lead to that? When did the process of getting to be symptomatic begin? Looking at that recent study it appears we don't really know when it could have all begun.

Also, I agree that the levels of D that change within minutes/hours of being in the sun, but that isn't the form that is stored in the body for future use. The form that is stored is synthesized in the liver by conversion of the one created by sunlight or in your diet. Without enough stored throughout the year we become deficient. So if we were very low from the previous year and depleted even more during the fall/winter/spring then we're going to have sufficient time for the damage to occur when the immune system isn't regulated. And indeed some of the forms are instant, but other forms require storage for use year around. This is after all a vitamin (sterol) stored in the fat.

Also I find interesting that you mention parasites. It has been shown, in fact in a recent study I looked at, that worms can cause inflamitory bowel diseases to be brought down or even reversed. And why is this? It is part of the regulatory process; with more of a TH2 immune response (the one that fights parasite/worm infections) the TH1 response (what MC is) is regulated. This is part of the theory of why developed nations tend to have higher rates of IBD, we are cleaner and thus have fewer parasite infections.

What has me wondering about that study (yes I still need to read it) is perhaps I was asymptomatic and what actually brought me to the Dr was sugar malabsorption (whatever the cause of that is). What they found was the signs of MC/LC, but yet I wasn't really sypmptomatic. And what I mean by symptomatic is that I never really suffered the symptoms that others here have had. I never had water diarrhea many times a day for days and days on end. It was only here and there that I had similar symptoms.

Mike

[harvest_table]

I really enjoy you two thinking out loud.

Good discussion. Thank you.

Love,
Joanna

[mle_ii]

Well, here's a wrench thrown in the works... perhaps. Got back some test results one of which was my vitamin D levels. All within range, and what's even stranger is disregarding the lab range and using the ranges found via my readings on vitamin D I'm still within range.

Ok, so perhaps once again I'm a strange version of the MC/LC diagnosed. Like I've said I've never had the extreem symptoms that the majority of folks here have. Perhaps I was asymptomatic and on my way to full blown MC/LC and I caught it before hand, perhaps my Vitamin D levels have made a recovery, perhaps my symptoms/diagnosis of MC/LC is really a symptom of something else entirely and I never really had MC/LC. Very strange indeed.

[tex]

Well, if you had lymphocytic infiltration in the epithelial layer of the mucosa of your colon, then you met the definition of LC. There has been a lot of water under the bridge, since your diagnosis, (and a lot of stuff through your gut), so it's certainly not unreasonable to assume that nutritional conditions, and/or chemical balances may have been significantly different back at that point in your life.

I remember you mentioning the lack of certain symptoms before, but it didn't dawn on me until you just memtioned it again, that you might indeed be an example of an asymptomatic LC victim. (Hell, I didn't even know that there was such a thing, until Joanna found that abstract).

Hey, it's an honor to have you with us. If we keep researching, and comparing notes, one of these days we're liable to come up with something truly worthwhile. This is fascinating stuff.

Tex

P S Incidentally, if I recall correctly, the pig whip worm treatment has been shown to be highly effective, so long as the patient is willing to down those worm eggs every month or so, to keep the population thriving. LOL.