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|ginger has a long tradition of being very effective in alleviating symptoms of gastrointestinal distress. In herbal medicine, ginger is regarded as an excellent carminative (a substance which promotes the elimination of intestinal gas) and intestinal spasmolytic (a substance which relaxes and soothes the intestinal tract). Modern scientific research has revealed that ginger possesses numerous therapeutic properties including antioxidant effects, an ability to inhibit the formation of inflammatory compounds, and direct anti-inflammatory effects.|
|Studies have also shown that Nigella sativa oil has anti-inflammatory property by inhibiting cyclooxygenase and lipoxygenase (18). An in vitro study demonstrated that nigellone, a constituent of the crude extract of Nigella sativa seeds, inhibited histamine release from rat peritoneal mast cells (10) and may reduce allergy symptoms in humans (12)|
I have a bunch of black seeds, I can send you some if you want to try them.
Lots of sea veggies are cross contaminated with shellfish - maybe that's the reaction?
And I'm with you on not hiding foods. Dd's got an amazing food intuition that I don't want to mess with - I've been working on developing my own food intuition for this entire journey.
I don't think you can have celiac without the gene. But are they saying that they test for celiac and gluten sensitivity as separate things? And that there's a gene for gluten sensitivity that's not celiac, and that's what she has? It's not the most straightforward test I've seen...
|Why are gene results so complicated, and which genes predispose to gluten sensitivity/celiac sprue?
Gene tests for gluten sensitivity, and other immune reactions are HLA (human leukocyte antigen), specifically HLA-DQ, and even more specifically, HLA-DQB1. The nomenclature for reporting HLA gene results has evolved over the last two decades as technology has advanced. Even though the latest technology (and the one we employ at EnteroLab for gene testing) involves sophisticated molecular analysis of the DNA itself, the commonly used terminology for these genes in the celiac literature (lay and medical) reflects past, less specific, blood cell-based (serologic) antigenic methodology. Thus, we report this older "serologic" type (represented by the numbers 1-4, e.g., DQ1, DQ2, DQ3, or DQ4), in addition to the integeric subtypes of these oldest integeric types (DQ5 or DQ6 as subtypes of DQ1; and DQ7, DQ8, and DQ9 as subtypes of DQ3). The molecular nomenclature employs 4 or more integers accounting together for a molecular allele indicated by the formula 0yxx, where y is 2 for DQ2, 3 for any subtype of DQ3, 4 for DQ4, 5 for DQ5, or 6 for DQ6. The x's (which commonly are indicated by 2 more numbers but can be subtyped further with more sophisticated DNA employed methods) are other numbers indicating the more specific sub-subtypes of DQ2, DQ3 (beyond 7, 8, and 9), DQ4, DQ5, and DQ6. It should be noted that although the older serologic nomenclature is less specific in the sense of defining fewer different types, in some ways it is the best expression of these genes because it is the protein structure on the cells (as determined by the serologic typing) that determines the gene's biologic action such that genes with the same serologic type function biologically almost identically. Thus, HLA-DQ3 subtype 8 (one of the main celiac genes) acts almost identically in the body as HLA-DQ3 subtype 7, 9, or other DQ3 sub-subtypes. Having said all this, it should be reiterated that gluten sensitivity underlies the development of celiac sprue. In this regard, it seems that in having DQ2 or DQ3 subtype 8 (or simply DQ8) are the two main HLA-DQ genes that account for the villous atrophy accompanying gluten sensitivity (in America, 90% of celiacs have DQ2 [a more Northern European Caucasian gene], and 9% have DQ8 [a more southern European/Mediterranean Caucasian gene], with only 1% or less usually having DQ1 or DQ3). However, it seems for gluten sensitivity to result in celiac sprue (i.e., result in villous atrophy of small intestine), it requires at least 2 other genes also. Thus, not everyone with DQ2 or DQ8 get the villous atrophy of celiac disease. However, my hypothesis is that everyone with these genes will present gluten to the immune system for reaction, i.e., will be gluten sensitive. My and other published research has shown that DQ1 and DQ3 also predispose to gluten sensitivity, and certain gluten-related diseases (microscopic colitis for DQ1,3 in my research and gluten ataxia for DQ1 by another researcher). And according to my more recent research, when DQ1,1 or DQ3,3 are present together, the reactions are even stronger than having one of these genes alone (like DQ2,2, DQ2,8, or DQ8,8 can portend a more severe form of celiac disease).
So you have A reaction to gluten, but it's not necessarily affecting the villi, which is THE reaction for celiacs. But either way, you have to avoid gluten completely, so what really is the difference?
I'll go read in my autism forum on OAT results for you when I can, but a couple of reactions based on my very incomplete knowledge:
1) Several readings are high around fat metabolism. Possibly an issue, but with your high fat, low carb diet, perhaps fairly normal.
2) Low citric acid would be one I'd want to explore - I'll see what I can find on that for you.
3) Vitamin b-6 deficiency - in theory, that can be fixed by you taking enough b6. Are you taking some/alot already? (Wondering if your DD is able to absorb it, in that case).
4) High oxalates - make it hard to absorb a lot of minerals (including zinc, which then makes it hard to digest a lot of food...). Do you have any gut feel for why her oxalates might be high? It looks like she didn't have a lot of fungal/yeast markers.
|Enteric hyperoxaluria accounts for approximately 5% of all cases of hyperoxaluria. It is due to a gastrointestinal problem usually associated with chronic diarrhea. Malabsorption from any cause, such as colitis or jejunoileal bypass surgery, can result in enteric hyperoxaluria.The chronic diarrhea results in smaller levels of intestinal calcium for oxalate binding. Without the calcium necessary to adequately bind oxalate in the intestinal tract, additional oxalate is absorbed and then excreted in the urinary tract. Exposure of the colonic mucosa to excess bile salts increases its oxalate permeability. Enteric hyperoxaluria is characterized by severe hyperoxaluria (usually >80 mg/d), low urinary volumes, hypocalciuria, and hypocitraturia.|
How much bone broth are you doing? It sounds like it could be really good for calcium, and general gut health.
eta: And what were you eating, carb-wise when you did the test? How much milk is she getting?
Yeah- I forgot to mention, out of 8 yeast/fungal markers, she was only slightly high in one- the rest were low. So I feel good about saying I don't think it's a yeast issue. At least that's one thing I can cross off the list.
I was taking the P5P for a couple weeks, then someone (you, maybe?) mentioned something about it possibly causing symptoms with high copper, so I stopped just in case that was adding to my craziness lately.
Yeah- 3 high markers in the fatty acid metabolism- obviously something I need to look into more. Need to look at the Krebs cycle stuff too, because I know nothing about it.
And obviously... she's crazy deficient in vitamin C, so I'll probably start a trial of the corn-based SA that I have (that guarantees it's ok for corn allergic folk ... but since she's only IgE and not IgG for corn, I figure it's worth a shot.)
According to some posts in the autism-mercury forum:
1) you can get high oxalates from metals toxicity
2) l-carnitine and coqQ10 are good antioxidants and help with oxalates
3) milk thistle is really high in oxalates (as I say uh oh, better go read about that) - don't know if you're taking it, but thought I'd mention it
4) apparently grainy poops can be a sign of high oxalates - wasn't someone asking about that recently?
5) oxalates deplete gluthianone (big for detox), increase inflammation, and mess with zinc utilization
6) can cause bedwetting (Shannon, relevant for you?)
7) ALA (which some people use as a chelator, reduces oxalates. (I know you're read Tanya's stuff on how strong ALA is).
8) Lots of parents report whining/clinginess as an oxalates symptom
9) Many people with oxalates issues can't tolerate much vitamin C
10) Some people find b6/mag helps with oxalates, and vitamin K
11) High oxalates often come out as rashes/spots/even sometimes hives
12) There's a probiotic called vsl#3 that has strain that is supposed to help process oxalates
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