I have seen on the internet that prolonged steriod treatment can result in the development of steroid drug tolerance leading to decreased hormone secretion. In turn this may lead to drug dependence, as you need to keep taking that drug to keep your body to function normally.

Can steroid treatment lead to drug dependency, and if yes, how?

  • $\begingroup$ I have made an edit to specify your question as your original question was unfortunately too broad for Biology SE to be acceptable as a valid question. Feel free to roll back if these edits are inappropriate $\endgroup$ – AliceD Jan 5 '15 at 0:29
  • $\begingroup$ Your question on probiotic dependence, although unlikely to happen, could make a new separate question. $\endgroup$ – AliceD Jan 5 '15 at 2:24

All classes of drugs react differently in the body. Some bind to receptors, some clean receptors, some drugs cause re-uptake inhibition in the brain, and others destroy viral and bacterial infections. Classifying drugs and how the human body would develop a tolerance to them in a post on this website would take pages upon pages to answer. When you say steroids, i'm assuming you are talking about anabolic steroids. That is the male sex hormone testosterone and its multitudes of derivatives. (DHT and non-DHT). Your body does not in fact develop a "dependance" on the drugs, rather it is a checks and balances system that your endocrine system establishes. Lets say you take a dosage of Testosterone Cypionate at 200mg a week for a 20 week interval from your G.P (common treatment for andropause). In laymans terms, your body senses the increase of testosterone and tells your Leydig Cells in the testes to stop signaling LH (responsible for testosterone production). Because it sees that there is already an abundance of the hormone. Now, once treatment stops, there are a series of protocols one could take to stimulate the natural production of testosterone again. Other forms of AAS are much harder on the HPTA than others however. (Trenbolone Acetate)

  • $\begingroup$ I edited and specified the question and it still fits your answer I think (it's not my area of expertise). Please check. If the OP doesn't roll back you could adapt your answer since the first part ("...would take pages to answer") is pretty much redundant then - thanks! $\endgroup$ – AliceD Jan 5 '15 at 0:08
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    $\begingroup$ Yea it was definitely a needed edit. The title of his original question didn't really fit the breadth of what he was actually asking. Your edits are completely necessary in my opinion. As answering distinct drug dependencies would be outlandish here. $\endgroup$ – Macedon93 Jan 5 '15 at 0:21

Steroid treatment with glucocorticoid drugs such as dexamethasone, prednisolone, hydrocortisone, etc. can lead to drug dependence, that is, an adaptive state formed after long-term administration. Drug dependence may cause withdrawal syndrome after stopping the drug abruptly.

Glucocorticoids are used to treat inflammatory, allergic, immune and malignant diseases. In the insufficiency of the adrenal cortex, the dose of glucocorticoid should mimic the physiological concentration and circadian rhythm of cortisol secretion to compensate for the inadequate production of natural cortisol. Even in the case of relatively low exposure to glucocorticoid therapy, long-term excessive replacement can lead to weight gain, glucose intolerance and abnormal bone metabolism, which can lead to osteoporosis.

In various conditions such as congenital adrenal hyperplasia, polycystic ovary syndrome and certain types of tumors, the body may produce too much androgens, male hormones. Such patients may not show signs of glucocorticoid deficiency. Women may experience symptoms such as hirsutism, oligomenorrhea, acne, infertility, and male pattern baldness. Men are usually asymptomatic, but acne, early baldness, and testicular adrenal gland resting tumors may occur. In this case, the use of glucocorticoids is prescribed to suppress excessive androgen production, rather than to compensate for the lack of cortisol. Here, the prescribed glucocorticoid acts in the following way through the hypothalamic-pituitary-adrenal (HPA) axis feedback loop: increased glucocorticoids suppress the release of adrenocorticotropic hormone (ACTH), thereby inhibiting the biosynthesis of pregnenolone from cholesterol. Pregnenolone is a steroid and the precursor of all other steroids, including glucocorticoids, mineralocorticoids, androgens and estrogens. Therefore, glucocorticoid drugs suppress excessive androgen production, but at a cost of suppressing all other steroid hormones as well.

The type of glucocorticoid drug prescribed depends on whether the goal is to compensate cortisol insufficiency or to suppress excessive androgen production. Hydrocortisone suppresses HPA least and dexamethasone most, with prednisolone in the middle.

When glucocorticoids are used in doses exceeding equivalent physiological production by a healthy organism, and the glucocorticoid treatment is suddenly stopped, HPA suppression prevents the adrenal glands from producing enough cortisol. Even lower but close to physiological doses of glucocorticoid drugs for long time may cause problems. Over a period of several weeks to several months or years, this may result in the gradual atrophy of cortisol producing cells in the adrenal glands, unable to respond to ACTH stimulation the HPA axis, leading to secondary adrenal insufficiency, i.e. the inability to produce normal levels of cortisol. Therefore, glucocorticoid withdrawal must not happen suddenly. Generally, patients taking glucocorticoid doses for less than two weeks are less likely to develop HPA axis suppression, and can stop treatment suddenly without gradual reduction, except patients receiving frequent "short-term" steroid therapy, such as in asthma.

In the case of chronic treatment that has been carried out for months or years, the goal is to gradually reduce the therapeutic dose to a physiological level, such as by reducing the dose step-by-step every 3-4 days for a few weeks, and then slowly withdrawing the drug for several months, to restore the HPA axis. Importantly, the adrenal suppression effect may last for a period of time, so after stopping glucocorticoid treatment, it may take more than a year for the HPA axis to fully recover.

Further reading:

  1. Paragliola RM, Papi G, Pontecorvi A, Corsello SM. Treatment with Synthetic Glucocorticoids and the Hypothalamus-Pituitary-Adrenal Axis. Int J Mol Sci. 2017 Oct 20;18(10):2201. doi: 10.3390/ijms18102201. PMID: 29053578; PMCID: PMC5666882
  2. Nicolaides NC, Pavlaki AN, Maria Alexandra MA, Chrousos GP. Glucocorticoid Therapy and Adrenal Suppression. 2018 Oct 19. In: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K, Grossman A, Hershman JM, Hofland HJ, Kaltsas G, Koch C, Kopp P, Korbonits M, McLachlan R, Morley JE, New M, Purnell J, Singer F, Stratakis CA, Trence DL, Wilson DP, editors. Endotext Internet. South Dartmouth (MA): MDText.com, Inc.; 2000–. PMID: 25905379

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