'digestive symptoms just downstream'. Is this even possible?

Hi mates,
I’ve read now multiple times on here people claiming digestive symptoms to be just an downstream effect of dysfunctional AR receptor.
But afaik digestive stuff are at least not common symptoms in diseases like Hypogonadism, Androgeninsensitivity syndrome or 5-ar deficiency.
So can you please prove me wrong?

Anyone?

There are multiple reasons why androgen insensitivity could be the culprit here
I think the biggest reason would be chronic stress caused by neurosteroid dysfunction/ sleep disturbance. if you’re stressed out constantly it will effect your digestion

I forgot to get back to this one.
I cant speak for Finasteride, but coming from Accutane, there are more probable direct causes.
Being that Ive just been talking about this, here’s one of them.
Epigenetic changes in immunity could lead to numerous bowel disorders.
There’s also long term multiple studies post Accutane to back up this notion.

Retinoic Acid and Immune Homeostasis: A Balancing Act


RA is instrumental to the function of tolerogenic dendritic cells during immune homeostasis.

RA has a role in balancing Th17 and Treg responses, and is also essential for proper T helper cell responses.

The outcome of RA signaling is determined by the microenvironment in which the signal is received.

RA deficiency can result in the development of a broad spectrum of autoimmune diseases.

RA has therapeutic potential for autoimmune diseases.

In the immune system, the vitamin A metabolite retinoic acid (RA) is known for its role in inducing gut-homing molecules in T and B cells, inducing regulatory T cells (Tregs), and promoting tolerance. However, it was suggested that RA can have a broad spectrum of effector functions depending on the local microenvironment. Under specific conditions, RA can also promote an inflammatory environment. We discuss the dual role of RA in immune responses and how this might be regulated. Furthermore, we focus on the role of RA in autoimmune diseases and whether RA might be used as a therapeutic agent.

Effects of Isotretinoin Treatment on Epigenetic Programming in T Cells
Eugenia Becker, Claudia Stanzel, Kirstin Atrott, Gerhard Rogler, Isabelle Frey-Wagner
Background Retinoids are essential nutrients involved in the maturation of the immune
system. The majority of in vitro and in vivo studies provided evidence that retinoid treatment
exhibits anti-inflammatory properties and is effective acne therapy. However, there is a
controversial discussion about a causal relationship between isotretinoin treatment and the
onset of inflammatory bowel disease (IBD). Some patients have claimed that they developed
acute intestinal inflammation during isotretinoin treatment or had an onset of IBD weeks
or even years after cessation of the medication. We have previously shown that isotretinoin
treatment has no adverse effects in two mouse models of inflammatory bowel disease. Here
we investigated the influence of isotretinoin treatment on genetic imprinting in two T cells
subsets as a potential mediator of long-term effects of isotretinoin treatment on the immune
system. Methods Balb/c mice were treated with isotretinoin (30 mg/kg bodyweight) or vehicle
orally for 2 weeks and kept for further 4 weeks to study potential direct and long-term
effects. Naive T cells and regulatory T cells were isolated directly after the treatment period
and at the end of the study by magnetic cell sorting. After isolation of genomic DNA,
microRNA and mRNA, samples were sequenced with the Illumina® technique to study
changes in methylation patterns, microRNA and mRNA expression. For predicting target
genes of determined microRNAs the software Target Scan and Traget Scan Custom were
used. For identification of pathways significantly affected by isotretinoin treatment the
software Meta Core® was applied. Results Analysis of epigenetic modifications in naive and
regulatory T cells revealed potential long-term effects in both T cells subsets. In regulatory
T cells mainly the methylation pattern was altered in T cells isolated four weeks after cessation
of treatment. In naive T cells on the other hand predominantly microRNA expression was
altered in T cells isolated after four weeks without treatment. Pathway analysis by Meta
Core® revealed that pathways of immune responses, concerning antigen presentation and
T helper cell differentiation were affected. Further functional analysis of affected pathways
is currently under investigation. Conclusions Preliminary results identified changes in methylation pattern and microRNA expression in naive and regulatory T cells which might mediate
potential long-term effects after isotretinoin treatment, yet differences between the different
T cell subsets were far more pronounced than differences induced by isotretinoin treatment.

Page 122

1 Like

[deleted]

I could take what I just posted here a few steps further.

Commensals Suppress Intestinal Epithelial Cell Retinoic Acid Synthesis to Regulate Interleukin-22 Activity and Prevent Microbial Dysbiosis

Retinoic acid (RA), a vitamin A metabolite, regulates transcriptional programs that drive protective or pathogenic immune responses in the intestine, in a manner dependent on RA concentration. Vitamin A is obtained from diet and is metabolized by intestinal epithelial cells (IECs), which operate in intimate association with microbes and immune cells. Here we found that commensal bacteria belonging to class Clostridia modulate RA concentration in the gut by suppressing the expression of retinol dehydrogenase 7 ( Rdh7 ) in IECs. Rdh7 expression and associated RA amounts were lower in the intestinal tissue of conventional mice, as compared to germ-free mice. Deletion of Rdh7 in IECs diminished RA signaling in immune cells, reduced the IL-22-dependent antimicrobial response, and enhanced resistance to colonization by Salmonella Typhimurium. Our findings define a regulatory circuit wherein bacterial regulation of IEC-intrinsic RA synthesis protects microbial communities in the gut from excessive immune activity, achieving a balance that prevents colonization by enteric pathogens.

20 years later.
Its important to note the following study only included females.

Severe Acne in Female Patients Treated with Isotretinoin is associated with
Dysbiosis and its Consequences

The study included only female patients. The conclusions are
therefore only relevant for females. Isotretinoin is associated with
dysbiosis, malabsorption (with visceral fat decrease) and signs of
dysimmunity. Symptoms develop more than 20 years after the intake
of the medication taken at usual range and duration. A facilitating role
of Propionibacterium acnes cannot be excluded. Isotretinoin is known
to impair stem cells renewal and TLR2 expression in the mucosa of the
small gut. These pharmacological effects, explaining the efficacy of the
medication on acne (“the metabolic syndrome of the pilosebaceous
gland”) may induce the progressive atrophy of the jejunal mucosa
and its long-lasting consequences. No therapy is available yet.
Patients, prescribers and authorities should be aware of this adverse
event which incidence is high (2.6% of outward gastroenterological
consultations) especially when multi-annual surveillance for several
years are expected.