1: I hope to see some specialists regarding my gut. But I don't know what kind of tests they'll be able to do. If you see a gut specialist within the medical system then it's not like they're going to test your gut-biota composition, are they?
2: And I have no idea what they'll prescribe for (e.g.) gut dysbiosis; not sure how that's treated. You can do probiotics and prebiotics but how often will they test your gut-biota composition in order to see how it responds to treatment?
3: What do you think about kefir? And about Pepto Bismol?
4: I had a weird incident recently where I took way too much of an iron supplement. Do you know if an incident like that could actually cause like permanent dysbiosis (or some other permanent gut issue)? Not sure how much damage you can do with a one-time incident. It wasn't 100% a one-time incident in the sense that I did ingest the iron supplement more than once. But it was only once that I took way too much. See below.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8159756/
Previous research studying the impact of iron on the gut microbiome has produced conflicting conclusions. Within bacteria iron can play a crucial role in growth and proliferation, for example iron can be required for the proper functioning of some bacterial proteins and enzymes. Additionally iron can modulate expression of some virulence factors.
162,
163,
164 Therefore, iron has been shown to be an important element required for the growth of some but not all gut bacteria including
Bacteroides spp.
165,
166 and
Enterobacteriaceae,
167 whilst
Lactobacilli species do not require iron for growth.
7,
8 Interestingly,
Lactobacillus plantarum 299v, and a probiotic (containing
Bifidobacterium bifidum W23,
B. lactis W51,
B. lactis W52,
Lactobacillus acidophilus W37,
L. brevis W63,
L. casei W56,
L. salivarius W24,
Lactococcus lactis W19, and
L. lactis W58) have been shown to increase host iron absorption.
168,
169 Various proteins and enzymes involved in bacterial replication and growth require iron as a cofactor to function. Iron is a cofactor involved in the synthesis of DNA (i.e., ribonucleotide diphosphate reductase),
170,
171,
172,
173 electron transfer and generation of ATP (i.e., cytochromes), and the neutralization of harmful oxidative species (i.e., superoxide dismutase). Iron deficiency can inhibit these bacterial cell processes, which can impair bacterial growth. Microbes that require iron for growth and survival have evolved processes to prevent nutrient deficient states. During iron deficiency, bacterial iron acquisition gene programs are de-repressed by the ferric uptake regulator family (FUR) proteins. FUR proteins act as an iron-dependent repressor that controls numerous iron-regulated genes by binding free ferrous (2+) iron to prevent transcription when bacteria are exposed to sufficient iron. During iron deficiency, FUR proteins de-repress gene programs that enhance iron acquisition from their hosts to promote growth.
164 Mechanisms to acquire iron include: (i) siderophores formation, (ii) cell surface ferric reductases to reduce free ferric (3+) iron to ferrous (2+) iron for bacterial utilization and (iii) production of cytotoxins and haemolysins to release iron stores from host cells.
174,
175,
176
...
Under normal conditions pathogenic bacteria must overcome resistance from commensal microbial communities in order to colonize. Commensal microorganisms activate immune responses which can lead to the elimination of pathogenic bacterial species. However, the level of immune activation is important, as instead of leading to elimination of pathogenic bacteria, alternatively intestinal inflammation can promote the colonization of pathogens.
179 One of the hallmarks of intestinal inflammation-induced dysbiosis (
Fig. 1) is that of increased abunance of enterobacteria species. Due to the differing microbial profile in the inflammed gut there is also an association with an altered siderophore profile. As siderophores are responsible for metal ion abundance, this altered profile can further influence the type of bacteria which survive and grow.
180 As such, because iron is an essential element for most bacteria to thrive, one key role of the intestinal immune response is to limit the availability of iron to pathogenic bacterial species.
181
https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click on image to zoom&p=PMC3&id=8159756_jla-10-160-g001.jpg
A previous study has shown that dietary iron inhibited growth of the enteric pathogen
Citrobacter and drove selection of asymptomatic
Citrobacter strains; these responses were associated with insulin resistance and increased glucose levels that suppressed pathogen virulence.
140 In addition to promoting insulin resistance dietary iron also increased intestinal glucose levels, a key gut environmental change that suppressed pathogen virulence, and drove selection of asymptomatic
Citrobacter strains.
140 However, in contrast, other studies have shown that decrease in iron availability is beneficial via reducing growth of potentially pathogenic gut bacteria.
182,
183 Dietary iron supplementation has adverse effects such as inducing higher levels of pathogenic gut bacteria and the occurance of intestinal injury.
111,
113,
182,
184,
185 Addionally a study investigating iron supplementation in African children found that there was an increase in the number of enterobacteria and a decrease in lactobacilli which correlated with gut inflammation.
186
...
The principal conclusions arising from this review article are summarized in the accompanying
Figs. 2 and
and3.3. Specifically, the illustration in
Fig. 2 highlights the main concept of iron-mediated modification of the gut microbiome being a potentially important determinant of metabolic consequences in the host.
Fig. 3 depicts the various ways in which iron overload or deficiency can occur and subsequently re-shape the gut microbiome and alter barrier function. The impact of these changes on the host is dictated via cross talk mediated by gut-derived factors as shown in the figure. Ultimately, the clinical manifestation of this is the syndrome of dysmetabolic iron overload.
https://academic.oup.com/ibdjournal/article/23/5/753/4561079
Iron is an important nutrient for both the host and colonizing bacteria. Oral iron supplementation may impact the composition of the microbiota and can be particularly damaging to patients suffering from inflammatory bowel disease (IBD). However, patients with IBD may require iron supplementation to treat their anemia.
