Accutane FAQ

The gastrointestinal (GI) tract harbors a complex community of bacteria, fungi, viruses, archaea, and their genomes, which affect human health and disease [1]. Dysbiosis, or a disruption of the gut microbiota, refers to adverse changes in the microbiota associated with disturbed homeostasis and disease [2]. Gut dysbiosis has been associated with behavioral changes and impaired immune function characterized by increased proinflammatory biomarkers in both humans and rodents [3,4,5]. Cancer treatments, notably chemotherapy, while lifesaving, have been associated with gut microbial dysbiosis [6,7,8]. Moreover, gut microbial associated changes in psychological and cognitive function following chemotherapy treatment have also been found [6,9,10]. Notably, while some of the studies discussed herein used techniques such as PICRUSt to infer the metabolic capacity of the microbiome, we focused our discussion of the findings from these studies on the taxonomic characterization of the microbiota using 16S rRNA sequencing, and, therefore, refer to microbiota throughout the manuscript as opposed

The microbiota–gut–brain axis facilitates crosstalk between the microbiota and brain via neural, endocrine, immune and metabolic pathways [1,11], which are susceptible to chemotherapy-related toxicities. In a pre-clinical study with adult female mice, 6 cycles (i.e., one treatment per every other day) of paclitaxel chemotherapy altered gut microbiota composition, which was associated with changes in taxonomic relative abundance, colonic tissue integrity, and microglial activation [12]. In clinical studies, chemotherapy treatment has been shown to alter the gut microbiota. In a sample of 36 pediatric patients with acute lymphoblastic leukemia, stool samples collected at baseline and days 3 (mid-treatment) and 7 (immediately post-chemotherapy) showed that high-dose methotrexate chemotherapy significantly reduced the overall taxonomic abundance of the gut microbiota during treatment and relative to healthy controls [7]. Another study found that chemotherapy decreased abundance of microbes belonging to the Firmicutes phylum [8]. Moreover, chemotherapy-induced mucositis, a common GI symptom in patients undergoing chemotherapy, is associated with increased symptoms of pain, anxiety, and depression [13].

The microbiota–gut–brain axis influences immune function and behavior [14]. The epithelial layer that lines the GI tract is a fine-tuned interface between the host and the external environment. The epithelia’s paracellular permeability under healthy physiological conditions is tightly regulated by tight junction proteins that prevent passage of macromolecules [15]. Chemotherapy may compromise the protective epithelial layer in the gut [12]. Compromising this layer can lead to increased intestinal permeability (i.e., “leaky gut”), which will provide easy passage of bacteria and their byproducts, such as lipopolysaccharide (LPS), a bacterial endotoxin component of the cell wall of Gram-negative bacteria, from the gut lumen into the bloodstream [9,12,16]. A compromised gut can lead to an immune response, characterized by the expression of sickness behaviors (e.g., lethargy, anxiety, cognitive dysfunction)[17]. Chemotherapy has thus been implicated in increased intestinal wall permeability, mucositis, sickness behaviors, and changes in the gut microbiota [6,7,8,9,12]. However, it is unclear whether these adverse changes persist in the longer term after treatment has ended.

Chemotherapy is associated with acute and chronic adverse changes in psychosocial health, but potential underlying mechanisms require elucidation. Mental health, a dimension of psychosocial health (i.e., psychological, behavioral, emotional, and social factors), in this context, refers to one’s emotional, psychological, and social well-being [18]. A growing body of research implicates the gut microbiota in symptoms of anxiety and depression [16,19,20], post-traumatic stress disorder (PTSD) [21], fatigue [22,23], cognitive and social function, pain [1,24,25], and GI disturbance [26,27,28]. Moreover, changes in the gut microbiota have been associated with anxiety and depressive behaviors in animals and humans [16,29,30,31,32].Chemotherapy has been associated with cognitive and psychological impairments [9,33,34]. Many survivors of cancer have been treated with toxic anti-cancer therapies and face chronic physical and psychosocial challenges because of cancer and its treatments. During and after chemotherapy treatment, cognitive impairments (e.g., attention, concentration, processing speed) are reported [33]. Survivors also tend to report higher incidence of anxiety, depression, cancer-related fatigue, and other psychosocial symptoms compared to healthy peers [35,36]. However, potential underlying mechanisms that may contribute to the maintenance of psychosocial symptoms require clarification.

Although many cancer survivors face post-treatment challenges regardless of their age, young adults may face additional challenges and unmet needs [37,38]. Young adults may be particularly susceptible to psychosocial issues following a cancer experience due to the added stress of developmental challenges (e.g., finding a long-term partner, fertility concerns, career development, gaining financial stability) compared to older survivors [38,39]. Understanding potential chronic effects of cancer treatments on the gut microbiota, GI, and psychosocial outcomes, and how these factors may relate, is needed to improve cancer survivors’ wellbeing.

Source: https://www.mdpi.com/1718-7729/29/5/243/htm

As previously stated, Isotretinoin is a vitamin A derivative (13-cis-retinoic acid). Generally, signs of vitamin A toxicity are associated with long-term consumption of vitamin A in excess of 10 times the RDA (8,000-10,000 μg RAE/day or 25,000-33,000 IU/day). [1]

10 times the maximum RDA is 250,000 to 330,000 IUs.

The dosage of isotretinoin for acne treatment can start as low as 0.5 mg per kg of body weight per day (0.5 mg/kg/day) and it can go up to a high dosage of 2 mg per kg of body weight per day. And intermediate dosage also exists for one mg per kg. [2]

Mg to IU converter >

The condition caused by vitamin A toxicity is called hypervitaminosis A. It is caused by overconsumption of preformed vitamin A, not carotenoids. Preformed vitamin A is rapidly absorbed and slowly cleared from the body. Therefore, toxicity from preformed vitamin A may result acutely from high-dose exposure over a short period of time or chronically from a much lower intake (2). Acute vitamin A toxicity is relatively rare, and symptoms include nausea, headache, fatigue, loss of appetite, dizziness, dry skin, desquamation, and cerebral edema. Signs of chronic toxicity include dry itchy skin, desquamation, anorexia, weight loss, headache, cerebral edema, enlarged liver, enlarged spleen, anemia, and bone and joint pain. Also, symptoms of vitamin A toxicity in infants include bulging fontanels. Severe cases of hypervitaminosis A may result in liver damage, hemorrhage, and coma. Generally, signs of toxicity are associated with long-term consumption of vitamin A in excess of 10 times the RDA (8,000-10,000 μg RAE/day or 25,000-33,000 IU/day). However, more research is necessary to determine if subclinical vitamin A toxicity is a concern in certain populations (89). There is evidence that some populations may be more susceptible to toxicity at lower doses, including the elderly, chronic alcohol users, and some people with a genetic predisposition to high cholesterol (90). In January 2001, the Food and Nutrition Board of the US Institute of Medicine set the tolerable upper intake level (UL) of vitamin A intake for adults at 3,000 μg RAE (10,000 IU)/day of preformed vitamin A (56).

Source: https://lpi.oregonstate.edu/mic/vitamins/vitamin-A