Chris from Conditioning Research emailed this link to me, just before Troy asked about high fat eating after the surgical loss of your gall bladder. Many thanks Chris, immaculate timing. The main problem without a gall bladder is that there is no pulsatile release of bile acids to allow the formation of the lipid miceles needed for fat digestion and absorption. However, even without a gall bladder, there must be some on going bile secretion, even if there is no storage for a big release after a large meal. Is this enough? I commented that medium chain triglycerides might help, these are slowly absorbed without pancreatic lipase, but now I think about it, I'm not sure if this would work without bile acids to get the MCTs in to the enterocytes in the first place...
But there is a separate problem anyway. If you have coeliac disease you don't seem to produce cholecystokinin (CCK) when fat hits your small intestine. So under these circumstances, you may as well not have a gall bladder anyway!
There is obviously a trade off between the severity of the coeliac disease and the degree of cholestasis. The link above mentions active disease... I get the impression that villous atrophy is needed to get the blunted CCK response.
But then it's worth remembering that 1mg, that's one milligram, no typo, of gluten per day will sustain villous atrophy in unlucky individuals. They will be clinically and serologically normal under these conditions. I bet they don't make a lot of CCK though! Or get picked up by the average gastroenterologist.
So is subclinical coeliac disease any worse than having no gall bladder? Many many many people have sub clinical coeliac disease. Perhaps this is the wrong question. Maybe it would be better to ask whether THE reason you have had your gall bladder removed is that sub clinical coeliac disease was the underlying cause of your gall stone anyway. No CCK means no gall bladder contraction, which means no bile acid deposition, which means cholestasis, which means gall stones. Also means blunted fat absorption. Which means no CCK release... It's a chicken and egg situation.
Apart from coeliac disease and CCK, the other aspect which fascinates me is the effect of opioids on the sphincter of Oddi, at the end of the bile duct (includes the pancreatic duct in some individuals). Opioids spasm this sphincter. I know, I precipitated pancreatitis in a dog with a (big) dose of morphine once. It recovered.
So what does a continuous flow of gluten derived opioids through the gut do to the sphincter of Oddi? There's nothing I can find on pubmed directly related to this, but anyone with cholestasis problems or recurrent "idiopathic" pancreatitis wants to dump gluten big time. As if there weren't enough reasons to do this already.
So is anyone who is missing their gall bladder any worse off than someone eating to the food pyramid? Probably not. But who would want to be as dyspepsic as a food pyramid eater anyway???????? I guess the answer is dump the gluten, start with medium fat carried in real Food, dump the gluten, work up to higher fat loads, dump the gluten and try for 70% fat calories if any Olestra like effect allows, dumping the gluten. Whatever the outcome, sticking to Food and dumping gluten is the best you can do. Did I mention gluten?
PS at my time of peak gluten eating I was ultra sound scanned for gall stones. Negative, but that's just how it felt. Reading the celiac.com comments, it turns out you get that particular ache from gluten even after your gall bladder is removed! Maybe it's spasm in the sphincter of Oddi!
PPS When spell checking "Oddi" in google I found a host of support sites for people with dysfunction of this particular organ. Looks like it is coeliac disease rearing its head again.
And again, note the stupidity of ONLY biopsy sampling people who are anti endomysial antibody positive. Under diagnosis rules. As does 1mg per day of gluten induced, sero negative coeliac disease. Causing gall bladder disease. Or pancreatitis. You do not want pancreatitis. Honestly.