SIBO (Small Bacterial Overgrowth) Stomach Acid, Bile Flow, MMC Dysfunction and more

I found this article interesting. It talks about a whole bunch of things that can cause SIBO. I noticed that many of the causes alot of people on this website are dealing with. Such as:

celiac disease

  • chrons*
  • lyme disease*
    *ehlers danlos *
    hypothyroidism
    low stomach acid
    bile flow and enzyme deficiency
    diverticuli
    IgA deficiency

As we can see from this list, although SIBO can lead to many wide-ranging symptoms throughout the body, it is also the result of specific health concerns. SIBO itself is not the disease; it is the end result. If we simply treat SIBO, we are not addressing the root conditions that allowed SIBO to thrive.

A full treatment plan must address the bacterial overgrowth of the small intestine while also working on the root cause(s) to ensure a complete eradication of SIBO and decrease the chances of recurrence.

Why?

Earlier in your post you recognise any bacterial overgrowth that may or may not be occurring as being a downstream problem.

Surely the correct answer is that we must find the root cause rather than wasting our time talking about this stuff.

Well I think that it’s the cause of our on going suffering and inability to return to “homeostasis”.

Why? It seems like common sense to go after the root cause of something in order to eradicate it “permanently” We have seen many people here get better when focussing on their diet/gut health. I believe once we develop something like sibo for whatever reason. Things can go south pretty quickly and in different directions for each individual. I have found gut dysbiosis-> inflammation causing leaky gut, then for example one gets autoimmune problems. The thyroid and adrenals get stressed over time and “wear out”. Viruses can reactivate and thrive in these conditions as well.

Well, I just posted this elsewhere. Here the cause for SIBO is Accutane.
They also chose only female patients to rule out the following,

Exclusion criteria: Male patients were not included because gender
may influence small gut absorption, dysbiosis, tobacco and alcohol
abuse, immunity and Body Mass Index.

Severe acne is mainly caused by Propionibacterium acnes (PA) and is sometime treated with isotretinoin. Propionibacterium species may alter
intestinal mucosa and isotretinoin may induce mucosal side-effects. We investigated whether severe acne (treated or not with isotretinoin) is
associated with dysbiosis and its consequences.

^So right here I am looking at this differently based on what I have posted in my other thread.
Maybe propionate and or propionibacterium as an intestinal regulator.
Then you could maybe take this a step further looking at immunity and fat metabolism.

Btw, I have never been able to put on body weight or fat since Accutane.

Group 2 (isotretinoin) has a lower body weight (56.9 ± 9.9 versus 61.1 ± 15 kg; p<0.05) and Body Mass Index (20.84 ± 3.8 versus 22.85 ± 5.2; p<0.05)
than the control group (despite being younger (40 ± 10 years versus 50 ± 16; p<0.05).

Small Intestinal Bowel Overgrowth (SIBO) is due to bacterial
proliferation in the jejunum. These bacteria are consuming unabsorbed
disaccharides because of mucosal enzymatic deficiencies or excessive
intakes of sweetened food. Drug-induced mucosal atrophy belongs to the long list of possible etiologies. SIBO is associated with non-severe
complains like diarrhoea or constipation, bloating, abdominal pain
and sometimes with severe malabsorption and its consequences (e.g.
anaemia, Vitamin D or unsaturated lipid acids deficiency, fatigue,
decreased immunity) [1-3].

Propionibacterium
species may adhere to intestinal mucosa [31]. They secrete
hyaluronidase and can alter intestinal mucosa

^just like on the skin, Accutane may create an environment to eradicate propionibacterium to a degree that it doesn’t come back.

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Wanted to add to this, once again im already quickly having doubts about propionibacterium as a probiotic. It has taken cycling or coming off and going back on this a few times to realize this. Im going to turn my sole attention on retinoic acid metabolism now. Like the vitamin d study I recently posted, its metabolism to its active form could be predicated by select bacterial colonization.

Vitamin A and Retinoic Acid Exhibit Protective Effects on Necrotizing Enterocolitis by Regulating Intestinal Flora and Enhancing the Intestinal Epithelial Barrier

These results suggest that VA may regulate intestinal flora, alleviate inflammatory reactions, and enhance the intestinal epithelial barrier in NEC. Thus, VA may be an effective drug for providing protection against NEC in newborns.

Keywords: Inflammatory factors; Microbial communities; Necrotizing enterocolitis; Retinoic acid; Tight junction proteins; Vitamin A.

Retinoic Acid Improves Incidence and Severity of Necrotizing Enterocolitis by Lymphocyte Balance Restitution and Repopulation of Lgr5+ Intestinal Stem Cells


These findings raise the exciting possibility that dietary manipulations could prevent and treat NEC by modulating lymphocyte balance and the ISC pool within the newborn small intestine.

Keywords: necrotizing enterocolitis, intestinal stem cells, T lymphocyte, retinoic acid, regulatory T cells, Th17 cells

I use NEC as an example because its complications can become SIBO, short bowel syndrome, stricture like gastrointestinal dysmotility, and a slew of other serious issues that could also lead to systemic inflammation and even affect blood flow.