I am assuming you are a female. I'll try to help explain, but I know I'll probably just end up causing more confusion. I have done an extensive amount of research on my own time in regards to acne pathology.
First thing and possibly most important!
Why are you taking Adderall? Is it a prescription? You said this situation was reproduced before from Adderall consumption?
Only thing I can think of that makes sense is that being a stimulant in the phenethylamine class it exhibits similarities to other popular stimulants/psychostimulants. CNS stimulants often stimulate adrenal gland activity as well. Over secretion of adrenal hormones may exacerbate the root issue that is giving you cystic acne. I have read about cystic acne coming from Adderall protocols, but the conscientious agreement is that genetic predisposition is largely to blame for that specific physiological response.
Another idea is that the adderall is disrupting healthy sleep cycles and you are actually in a sleep deprived state, but the adderall's stimulant properties mask the markers you recognize.. (
irregular sleep/unhealthy sleep patterns can increase cytokines inflammatory activities thus exacerbating your acne)
Or....you can just visit your doctor. The propoganda about Accutane and increasing acne, suicidal thoughts, depression, G.I aggravation etc.etc. has conflicting studies on every topic. The claims majority read are based on anecdotal evidence so make sure you do some research yourself and evaluate all sides of the argument.
1.
Antibiotics and acne! Why this isn't the long-term choice!
*just my two cents from research...it makes sense*
Minocycline- it is a antibiotic in the family of tetracyclines which is generally considered a broad-spectrum antibotic in reference to the wide variety of ailments its used in (in conjunction with other pharmaceuticals). It helps destroy a big culprit of acne called, propionibacterium acnes. Usually it can be readily treated and mitigated as it
generally is generally susceptible to the traditional protocol, but from my personal reading endeavors have displayed that their is a recognition that an antibiotic resistant strain of P. acnes has been encountered and shows resistance to the tetracycline family (
monocycline, doxycycline, tetracycline), the macrolides (
erythromycin, telithromycin), and lincosamides (
clindamycin is one i've read about quite often..)
Its honestly impossible to say what bacteria you have without legitimate testing, but the presence of antibotic resistant bacterium is becoming increasingly common among the world. Also its worth noting that when antibiotics are used for the treatment of acne it is generally a temporary fix. It may hastily clear up your skin and improve your mood, but it treats the superficial symptoms and does not nullify any effect associated with the root issue. So always try to remember pharmaceutical intervention in regards to antibiotics should not be the first avenue of attack in my personal opinion/experiences.
**Regardless of everything said.. Always consult a dermatologist with anything you do** Sometimes it doesn't hurt to have a consultation with a few. I get different responses all the time from medical professionals and thus collectively craft the appropriate approach from there.
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Lessons from Europe. Antibiotic-resistant acne
2.
Spironolactone for the treatment of acne! (Only covering its pharmacokinetics related to acne)
***Generally for hormonal based acne
I've read on this one extensively and its honestly quite intriguing on how it eventually helps hormonal acne. Spironolactone is technically a steroidal antimineralocorticoid, but also exhibits antiandrogen and antiestrogen activities. (very complex pharmacokinetics, but I mentioned those two because they are relative) the antagonist properties associated with inhibiting estrogen/androgen production is very minor, but the mode at which it illustrates its receptor location selectivity almost fits the category of SARM (selective androgen receptor modulator). Spiro does this by binding to your SHBG (sex hormone binding globulin) at an exceedingly higher affinity than other compounds. This inherently interacts with androgens and estrogens attempting to couple with SHBG and displaces the hormones. (oestrogenic hormones are displaced to a higher rate due to their lower affinity for receptor binding/activation)
Now why is this SHBG activity relevant? Androgens and estrogens bind to SHBG in the bloodstream as a transporter, but SHBG also mediates the bioavailability of sex hormones. Technically a sex hormone can freely circulate the blood stream and be considered "free" and thus able to enter a cell, but SHBG actively controls these actions. So by competing for SHBG against other sex hormones it is theoretically reducing the bioavailability of circulating hormones. Also being an anti-androgen/anti-gonadotropin its an antagonist to testosterone production. Disruption of natural HPTA function lowers concentration of all sex hormones. (androgen/estrogen/progestin) Also its activity with estrogens causes inhibition in regards to conversion of estradiol (E2) into estrone (E1). (estrone is a weak form of estrogen, estradiol is the number one estrogen in highest concentration and the most potent as well, estriol is just the metabolite and general waste of estradiol. Still has minor affinity for ER activation)
In case of confusion- Men and women have gonadotropins secreted by their pituitary gland. Human's are born with gonads regardless of sex. They eventually transform into either testicles or ovaries, but either sex shares a fundamental nature of mechanics in the system and even secrete similar hormones.
Best bet would be to see dermatologist who can help solidify the notion to consult an endocrinologist. Remember that treating issues caused by hormones can be very bizarre. Sometimes its within a few days you begin noticing improvements or other times it takes a least 6-8 weeks for the protocol to show any results! Also as you age the activity of your endocrine system changes as well. From what I can gather is that you are still pretty young (early 20's?) and our hormone system is still in the midst of establishing its final little tweaks before pubertal growth finally stops. (puberty is generally considered to occur in your teenage years, but the HPTA/HPOA is still working out kinks past 18 and is generally considered stable around 25 years of age...Generally speaking)
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My collection of Spironolactone information and studies....
Spiro acts on the following proteins..
-Androgen Receptor
-Progesterone Receptor
-Glucocorticoid Receptor
-Cytochrome P450 11B2 (mitochondrial activity)
-17 Alpha-Hydroxylase
-17,20-desmolase
-3-oxo-5-alpha-steroid-4-dehydrogenase
-sex hormone binding globulin (the antiestrogen activites are heavily involved here)
-voltage-dependant calcium channel
-dihydrotestosterone (DHT)
- Spironolactone Indentification/pharmacology
- http://www.ncbi.nlm.nih.gov/pubmed/20510769
- http://www.dermnetnz.org/treatments/antiandrogens.html
- http://www.ncbi.nlm.nih.gov/pubmed/23619437
- http://www.sciencedirect.com/science/article/pii/S0960076002001541
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1869626/