Replacing oatmeal

I agree with FlowersGal and enjoy listening to new ideas that make sense to me:

FlowersGal said...
Connor,

I don't want to further hijack the thread, just wanted to say I enjoy reading various theories and taking what I want from them, so I hope you don't refrain from posting your info. Beave, no need to get judgmental about someone posting research. Everyone is trying to be helpful and give advice that the questioner can decide what to do with.

People are welcome to share their opinions, and pose ideas. When they pretend/claim to be experts, others are entitled to probe a little deeper.

Sad to see someone claiming to be an expert pushing their opinions as if they were facts.

(I guess you refer to the failed Selby trial. Selby no longer has any interest in MAP.)

Connor77 said...
You didn't really understand my meaning when I explained it a second time, and you still don't. Epigenetics explains IBD way better than genetics, unless we are talking about obvious defects in things like mucosal barrier formation. In such individuals, their mucosa from stem to stern is hypersensitive no matter which treatment is involved. Another good example is those with alpha-1 anti-trypsin deficiency whose inflammatory response is disproportionate to the immune event, which not only affects their lungs but their bowels.

Ooh, alpha-1-antitrypsin. Which by complete coincidence just happens to be the same molecule that I posted a link about a few days ago. It's used as a marker of intestinal protein loss, which is useful for diagnosing protein losing enteropathy. As for alpha-1-antitrypsin deficiency, it's a rare inherited condition which causes lung and liver issues:
/www.blf.org.uk/support-for-you/alpha-1-antitrypsin-deficiency/what-is-it

Alpha-1-antitrypsin deficiency does apparently lead to a higher prevalence of UC. Out of 651 patients 10 had a confirmed diagnosis of UC: that's 1.5% of the AATD population.
/www.ncbi.nlm.nih.gov/pubmed/24176989

Around 146,000 people in the UK have a diagnosis of UC compared to 5000 patients worldwide who have been diagnosed with AATD:
www.alpha1.uk/links/publications/diagnosis-treatment/

In a nutshell, AATD is vastly more rare than UC and is going to explain very, very few cases of UC. It's also a hereditary condition, so it's not a good example of epigenetics.

Connor77 said...
In such individuals, their mucosa from stem to stern is hypersensitive no matter which treatment is involved.

This relates to UC how?

Connor77 said...
The genetics proposed for IBD don't explain the rates of increase in developed countries whatsoever. Genetics may tell us which genes get activated during an epigenetic (environmental) event but they are not predictive of disease formation in this instance. They just aren't.

Well, this goes back to multifactorial or complex diseases, which I mentioned in the last thread and which you also ignored. Some diseases are caused by a combination of genes and environment. They've pinpointed many of the genes involved; what's far harder to nail down are the environmental factors.

Connor77 said...
Impressing you is not on my list of things to accomplish, so I'm not bothered. The ER thing I said was about statistics, which you are again misinterpreting either willingly or not. People are claiming that the rate of IBD diagnosis is increasing because we have better monitoring, and I am saying that's not the reason because even 40 years ago most cases of pro-longed or severe UC ended up in front of a doctor for diagnosis. Maybe their technology wasn't as good but the disease was still around. Even if you account for a marginal rate of misdiagnosis between then and now, the rate of IBD is still increasing in the west. We're not talking small numbers here.

An estimated 15% of UC patients are hospitalised with severe disease; most mild to moderate cases 40 years ago would probably have gone undiagnosed. Also, most cases of UC don't get worse over time.
/emedicine.medscape.com/article/183084-clinical
journals.lww.com/ibdjournal/Abstract/2012/03000/Review_of_the_disease_course_among_adult.20.aspx

Connor77 said...
Again, "better monitoring" does not explain the increases in UC rates.

It almost certainly partly, if not wholly, does.

Connor77 said...
There already was a study on MAP and IBD, it's called the Shelby study. It's the biggest cohort study to date. The study has since been criticized for using antibiotic dosages well below what doctors are supposed to use, resulting in lower remission rates than are actually being achieved in clinical practice right now. Even so, the study showed higher remission rates than the next leading IBD medication. It's not a pet theory, it's real science. I'm on the AMAT protocol now after MAP was cultured from my blood. If you want to put your head in the sand that's your business, but a simple Google search or read up on HumanPara will give you more info.

The chances of MAP being the sole cause of Crohn's, let alone UC, are remote to say the least. I guess you don't see how being totally wedded to your MAP theory makes you a biased observer.

Connor77 said...
I don't welcome discourteous discourse from anyone, especially since my time and effort here is 100% voluntary. Thank you.

Yes, because the rest of us get paid for our time and effort.

In all fairness, I don't think there has been out-right-attacking going on. At most, rudeness and requests for backing claims. As some statements are outside of the normal realm of what the majority of us would consider to be "layman's knowledge of UC", I don't think it is entirely unfair to ask. And I do feel there is a fair amount of inquisitiveness. We're all here to learn after all.

Everyone is welcome to share ideas and opinions, and everyone should also recognize that there will be questions and also some who just disagree as consequence thereof. It is just how it works, whether you're in the scientific-journal-world, or on the Internet. IMHO, it's pretty darn boring if everyone just instantly agrees and pats you on the back, and a bit idealistic to expect it (Nobody should have thin skin or get emotional about it). If a given user gets on your nerves then use the Thumbs Down icon to ignore/hide all future posts by that user, it's on the forum for a reason. That's better than being confrontational to them, which only serves to escalates things.

Myself, I'm no medical expert (professionally, I write software documentation/help as a technical writer). Just deal with UC day-to-day, using a lot of trial-and-error, and reading everything I can all with the hope of getting a few tidbits of information that'll make my QOL a little easier (like the majority of folks here). I feel I am knowledgeable about UC, have no ego about it, and am the first one to admit I might make misstatements or be wrong at times haha. I often get people questioning my statements or contradicting my statements (happens to everyone, really). Everyone here speaks based on their experience with a UC, and we all have had very different experiences. It just is what it is, and really makes HW interesting to get a variety of very different perspectives (different from our own and our GIs)

Huh, oatmeal? I'd forgotten all about that Well, while we're on the subject, I've always found oatmeal to be one of the best foods for my Crohn's. I recently tried using a nut milk (no carageenan), but it made no difference and I prefer the taste of cow's milk (particularly whole milk), so I switched back. But there's all kinds of oatmeal and milks you can try, so experiment with different types.

As for this:

Connor77 said...
The only thing I'll correct is that I never said MAP causes everyone's IBD. I've said on many occasions that if your IBD is refractory and you test positive for MAP then you should definitely consider AMAT. These are my criteria.

Fair do's, and I stand corrected on that particular point. I don't often admit I'm wrong, so it's a pity you've missed this rare event by putting me on ignore