The Great Prednisone Experiment of 2026: Non-Classic Congenital Adrenal Hyperplasia and Quitting Prednisone
This post is a bit of a change of pace from the usual programming here at Life Among the Clouds. This blog is mostly about Multiple Sclerosis, the disease that barged into my life in 2021 and has provided me with hundreds of things to write about since then. However, MS isn't the only chronic disease that I've been living with. Long before I ever heard the words "you have Multiple Sclerosis," I was diagnosed with Congenital Adrenal Hyperplasia (CAH). Specifically, I have the non-classic form, which is a much milder form of the disease than classic CAH.
For most of my life, managing CAH has meant taking a small daily dose of prednisone. Five milligrams per day. That sounds like nothing when you compare it with the enormous doses of prednisone that those of us living with autoimmune diseases take to manage flairs. When I had my optic neuritis attack, I was prescribed 1250 mg per day for 5 days, and then an extensive tapering schedule. But here's the thing about prednisone: a small dose doesn't necessarily mean an inconsequential dose. I've been taking it for a very long time. I started on cortisone when I was 6 years-old, and transitioned to prednisone in my teenage years.
What is Congenital Adrenal Hyperplasia (CAH)?
If you've been reading this blog for a while, you probably know far more about MS than you ever wanted to know. But you may be wondering: What the heck is CAH?
CAH is a genetic disease that affects the adrenal glands. The adrenal glands sit on top of your kidneys and produce several important hormones, including cortisol, aldosterone, and adrenal androgens.
There are several different types of CAH. Mine is non-classic CAH, which is the milder form of the most common type of CAH: 21-hydroxylase deficiency. CAH is inherited in an autosomal recessive pattern, meaning that the condition involves inherited changes in both copies of a particular gene. In the most common form of CAH, that gene is called CYP21A2, which provides the instructions for making an enzyme called 21-hydroxylase.
Alright, that’s a little heavy on the science lingo, so let’s use an analogy to make this a bit easier to digest. Imagine your adrenal glands are a hormone factory. The raw material entering the factory is cholesterol. Through a series of chemical steps, the adrenal glands turn that raw material into different hormones. Cortisol is one of the major products. Aldosterone is another. Androgens are another branch of the production line. In CAH caused by 21-hydroxylase deficiency, one of the enzymes needed to make cortisol isn't working properly. Think of it as a factory where one of the machines on the assembly line is malfunctioning. The materials can't move efficiently through that part of the production process. The body doesn't simply shrug and say, "Well, I guess we'll stop trying." Instead, the pituitary gland at the base of the brain keeps sending the adrenal glands instructions to make more cortisol. But here’s another part of the problem, the adrenal gland can’t just make more cortisol. When it receives production orders from the pituitary gland, those instructions tell it to ramp up production of everything that the adrenal glands produce. The result is the rather bizarre biochemical situation that defines CAH. The adrenal glands can produce too little cortisol while simultaneously producing too much androgen. This usually presents as premature puberty, triggered by the high androgen levels. My parents had a watchful eye on me because my mom has CAH, so my CAH was caught quickly. In classic CAH, there can also be inadequate production of aldosterone, the hormone that helps regulate salt, fluid balance, and blood pressure. In non-classic CAH there is usually enough residual 21-hydroxylase activity to maintain adequate aldosterone production.
So why are the adrenal glands called "hyperplastic"? This is the part that always seemed counterintuitive to me. "Adrenal hyperplasia" sounds like the adrenal glands should be making more of everything, but that's not quite what is happening. The "hyperplasia" refers to the adrenal glands becoming enlarged because they're being chronically stimulated to work harder. The adrenal glands respond to that constant stimulation by growing and increasing their activity, even though they still can't efficiently complete the particular biochemical step that's missing.
The name tells us a lot about CAH:
"Congenital" because it's inherited.
"Adrenal" because it involves the adrenal glands.
"Hyperplasia" because the adrenal glands become over-stimulated and enlarged.
Now here's where my particular CAH story gets weird. My mom has CAH, but my dad isn't a carrier. Do you remember learning about Punnett squares back in Grade 11 biology? Those little boxes where you combine the genes from mom and dad and predict what genes their children will inherit. If mom and dad both have blue eyes, then their children will have blue eyes too. Well, according to a Punnett square, I shouldn’t have CAH.
CAH due to 21-hydroxylase deficiency is autosomal recessive, meaning that, in the usual situation, a person with CAH has pathogenic variants affecting both copies of CYP21A2. In the simplified version we learned back in high school, that means that you need two affected copies of the relevant recessive gene. But my dad doesn’t have that recessive gene to contribute.
I've actually had genetic testing completed at North York General Hospital to investigate this. That testing found that I have only one recessive gene variant associated with CAH. This should make me a carrier for CAH and not a patient, and yet, that’s not how it panned out. I do have CAH. Genetics gets considerably more complicated than the tidy little boxes we drew in biology class.
The usual explanation for autosomal recessive conditions is that a person needs disease-causing variants in both copies of the relevant gene to have the condition. That's certainly the basic model we were taught. But real human genetics doesn't always behave quite so neatly. There can be things like variants that aren't detected or fully characterized by a particular genetic test, differences in how particular variants affect enzyme function, and other genetic mechanisms that don't fit perfectly into the simple "one gene, one disease" model. My geneticist told me that my situation is a good example of how much we still have to learn about genetics.
Sometimes science says: "Based on what we currently understand, this shouldn't happen."
And your body replies: "That's cute."
It's one of the stranger pieces of my medical history, and honestly, I think it's pretty fascinating.
There is a spectrum of CAH. People with classic CAH have much more severe enzyme deficiency and can have significant cortisol and, in some cases, aldosterone deficiency. The most severe form can cause life-threatening adrenal crisis without treatment. Non-classic CAH is different. There is still some 21-hydroxylase activity, so the condition is much milder. People with non-classic CAH generally don't have the salt-wasting problems seen in classic CAH, and some people have few or no symptoms and don't require lifelong treatment. Others are treated with low-dose glucocorticoids to manage symptoms related to excess androgens.
This brings me back to prednisone.
Because prednisone is a glucocorticoid, it essentially supplies the body with the hormone that my adrenal glands have trouble producing adequately. It also helps tell the pituitary and adrenal glands: "Okay, we've got enough cortisol over here. You can turn down the production line." That reduction in stimulation can decrease the overproduction of adrenal androgens and other precursor hormones, which is why prednisone has been a useful treatment for me.
But after years and years of taking it, the question I'm now asking is:
Do I still need it?
And that's where this experiment begins.
The Problem with Prednisone
Why would I want to stop taking a medication that I've been taking for decades and which has successfully been managing my CAH? Long-term glucocorticoid use comes with a whole list of potential consequences. Even relatively low doses of prednisone are associated with increased risks of things like osteoporosis and fractures, hypertension, diabetes, cardiovascular disease, and serious infections. Long-term steroid exposure can also cause weight gain, changes in body composition, skin changes, mood and sleep problems, cataracts, and other complications. I think you’ll likely agree that there’s a lot of downsides to continuing to take prednisone forever.
So can I just decide to stop taking it? Unfortunately not. When you take prednisone every day, your body gets used to having glucocorticoid supplied from an outside source. The adrenal glands essentially get the message that they don't need to work quite so hard making their own cortisol. The result is adrenal suppression.
After long-term steroid use, the adrenal glands may not immediately be able to produce enough cortisol on their own. That's why prednisone generally can't just be stopped abruptly after prolonged use. The hypothalamic-pituitary-adrenal axis can take time to recover. In someone with CAH, there is an additional wrinkle: insufficient cortisol production is already part of the underlying problem.
So this isn't exactly a case of me casually deciding, "I don't like prednisone anymore. Bye!" There are real risks here.
The Impetus for the Experiment
Ironically, one of the things that got me thinking seriously about this was something that had absolutely nothing to do with my adrenal glands. It was my gastrointestinal hemorrhage.
Back on January 27, 2026, I had a catastrophic GI hemorrhage. I lost more than five units of blood, went into hypovolemic shock, and ended up in the hospital. It was terrifying. For more information about this experience, you can read my blog post titled, “Plot Twist: Surviving a Catastrophic Gastrointestinal Hemorrhage and Discovering my Immune System is at it Again”. This ultimately led to the discovery that my Disease Modifying Therapy (DMT) to treat my MS, Kesimpta, had caused drug-induced immune-mediated colitis. I switched to a new DMT, Mavenclad, and thankfully this medication side effect resolved.
This experience made me think about my health in a different way. It caused me to think about the long-term consequences of the medications that I take. It also caused me to think about things which I can do now that might make me healthier in the future. My research led me to the discovery that some people with non-classic CAH can successfully discontinue treatment with glucocorticoid therapy after their childbearing years. Why had no one ever told me about this?!?! I see my endocrinologist every 6-8 months and she never presented this as an option. My mom had also never heard that this might be possible.
At my last appointment with my endocrinologist, I brought it up. If I don't actually need lifelong daily glucocorticoid therapy for my particular form of CAH anymore, is it worth finding out whether my body can manage without it? Together, my endocrinologist and I decided that the answer was yes.
Which brings us to...
The Great Prednisone Experiment of 2026
The plan is wonderfully simple. I'm reducing my prednisone by 1 mg per day each month.
So:
5 mg → 4 mg (July) → 3 mg (August) → 2 mg (September) → 1 mg (October) → 0 mg (November)
Assuming that everything goes according to the plan, I'll take my last prednisone pill on Halloween and see what happens. Hopefully no tricks and just treats! However, I’m not just going to blindly follow the calendar. If my body starts telling me that it's not ready, I'll listen.
What could go wrong?
The biggest concern is adrenal insufficiency. In the worst-case scenario, adrenal insufficiency can progress to an adrenal crisis, which is a medical emergency.
Symptoms I'm watching for include things like:
unusual or profound fatigue
weakness
dizziness or lightheadedness, particularly when standing
nausea or vomiting
abdominal pain
loss of appetite
headaches
muscle or joint aches
low blood pressure
feeling unusually unwell during an illness or other physical stress
confusion or significant deterioration
Some of these symptoms are frustratingly nonspecific. And in my case, I already have several possible explanations for feeling tired, lightheaded, or generally crappy (MS, taking Mavenclad, recovering from drug-induced immune-mediated colitis). So I’m paying attention to patterns rather than assuming every bad day means adrenal insufficiency. However, more serious symptoms (severe vomiting, dehydration, profound weakness, confusion, collapse, or other signs of an adrenal crisis) are an entirely different matter and require urgent medical treatment. Adrenal crisis can be life-threatening.
Another important piece of this experiment is stress dosing. People with CAH who require glucocorticoid treatment often require increased glucocorticoid coverage during significant physical stress such as a high fever, gastroenteritis with dehydration, major surgery, or major trauma. So if I get sick, I will temporarily increase my dose in response, and then factor this into the taper.
This isn't simply going to be me crossing each month off a calendar until I reach zero. My endocrinologist and I are going to be watching what happens and adjusting the plan if necessary.
There are two possible outcomes to this experiment. The first is that my body handles the taper beautifully and I discover that I don't need daily prednisone anymore. Maybe I reduce some of the long-term risks associated with chronic steroid exposure. That would be fantastic. The second possibility is that I learn that my adrenal glands aren’t capable of taking over adequately and I have to return to my 5mg per day of prednisone for the rest of my life. The goal isn't "get off prednisone at all costs." The goal is to determine whether it is possible to get off prednisone in the hopes that, if successful, I manage to avoid some of the common side effects of long-term prednisone use.
My husband questioned why I would start this experiment right when I had also started a new DMT for MS. I understand his concern. However, with my medical history, there’s always something. I don’t want to delay doing something which could present a real upside for my health indefinitely because I so happen to have other medical drama happening at the same time. I may never try it if I let my other medical drama get in the way.
I started this experiment on July 1, 2026. So far it has been going well, but I’ve only just started the potentially “spicy” part of the experiment. Four mg per day and 3 mg per day is close enough to mimicking the body’s natural cortisol needs, but the drop to 2 mg per day and 1 mg per day requires my body to be producing some of its own cortisol too. Failing that, I could well see signs of adrenal insufficiency.
I'll be documenting what happens along the way, and I’m hoping that this doesn’t involve an adrenal crisis. I’ve had enough with medical emergencies this year. Wish me luck!
Now if you are reading this because you have CAH, please note that this is a medical experiment being overseen by my endocrinologist. This is not a DIY challenge. If you have read this and thought “maybe I’ll just stop taking prednisone too”, please don’t. Talk to your endocrinologist, form a plan, and only proceed with medical supervision.
