Failed.

After a potassium crash, my doctor increased the eplerenone to 25mg twice a day. Guess what? My blood pressure went HIGHER.

So now we’re doing an experiment: no eplerenone, potassium 20 MEQ twice a day, see what happens.

This just doesn’t seem to get any easier. It’s tiresome. Really, really tiresome.

Drugged.

So it’s come to this: 25mg Eplerenone once a day, and for the time being, no potassium pills. I started on 12.5mg and could tell that that wasn’t enough – this time around, I’m getting a bilateral trapezius muscle spasm, cramps in my feet and legs, and some digestive symptoms when the potassium drops too low. “Too low” for me means below 4.0 – it does not mean “below the lab reference range” which for most labs I’ve encountered is 3.6-5.2. My sweet spot seems to be 4.5-4.8, and keeping it there is a bit of a challenge. When I sensed that it was dropping, my doctor had me up the Eplerenone dose to 25mg – still considered sub-therapeutic for most, but then based on size alone, “most” are not me.

I’ve been on 25mg for 6 days now. The low potassium symptoms have mostly gone away. The first 4 days I had a lot of stomach upset, the 4th day I felt like I was having an out-of-body experience all day – I was sooooooo spacey! Yesterday, the 5th day, I woke up feeling clear-headed and without any muscle cramps, but still had some stomach trouble. Today – so far I’m feeling pretty much like myself all around. Here’s hoping it lasts.

As for hard numbers – we’re not sure at this point why I have this pattern, but my BP is staying in the mid-130s/high-80s range during the day, then daily, as predictable as clockwork, drops to 120s/70s-low-80s after the sun goes down. I’m not checking potassium again until the 20th, unless my symptoms signify a drop – I’m really trying to see if I can rely on “listening to my body” for this rather than weekly or twice-weekly blood draws. I think I’ve lived with this beast long enough that I can sense when it’s approaching, and surprisingly, my doctor is on board with this experiment.

And as for my doctor – for now I’m letting my primary care doctor manage this. As mentioned before, I have little confidence in the endocrinologist’s familiarity with this disease. Not to mention I hate going to his office (grouchy staff, crowded waiting room, expensive parking, a downer all around). And there’s the fact that I just can’t afford him. He bills my insurance company $650 for ten minutes of his time, of which I’m on the line for $150 each visit. I’m not a rich person and this isn’t a designer disease; I need to find a not-rich-person’s way to manage it.

Comedy of Errors.

So this morning? I showed up at the endocrinologist’s office to find out my results from the sodium loading.

And… wait for it…

There aren’t any.

Somebody at UCLA’s Santa Monica Clinical Lab effed up, big time, with my 24 hour urine sample. They checked the metanephrines, of course (which were negative, of course), but…

THEY NEGLECTED TO CHECK THE ALDOSTERONE.

Yes, you read that right.

***bangs head against wall***

The endo wanted me to repeat the test. I told him, HELL NO – It’s been over a week since I completed it and I STILL have a horrendous headache and elevated BP and probably the worst trapezius muscle spasm I’ve had since… ever, really.

I am done. DONE with the testing and the clueless doctors and with being medically interesting. Enough already. As I’ve said for years – my body, my science experiment – and even if it kills me, I am determined to be in charge from here on out.

There are two options, really. It’s simple. First get my potassium back under control (feeding me giant doses of salt pills will do the exact opposite) and hope that takes care of the BP once again. If it does – problem solved. I have hypokalemia – easy peasy, there’s my diagnosis. If that fails, I start taking the dreaded eplerenone. If that works – easy peasy, I have a hypertension diagnosis on my record and nothing more.

And if neither of those solve the problem, then maybe I’ll be willing to revisit this testing stuff. But at this point, I’m ready to just let the damned disease have its way with me, even if it kills me.

Because really, I think the medical establishment’s incompetence is more likely to kill me than anything.

And the adventure begins. Again.

My BP remains erratic, enough so that my medical people are investigating several possibilities, including hyperparathyroidism and, yes, the possibility that my other adrenal is acting up. Unless something comes up sooner, the ride begins on June 3.

Meanwhile, some worthwhile reading for anybody who has or has had PA and is having problems even after adrenalectomy or other treatment:

Primary Hyperparathyroidism With Concurrent Primary Aldosteronism

Two key takeaways:

…this unique case and the related findings support the notion that undetected hyperfunctioning of the parathyroid gland can contribute to maintaining hyperaldosteronism in PA. It also suggests the existence of a bidirectional link between the adrenocortical zona glomerulosa and the parathyroid gland, which can be relevant for the regulation of calcium metabolism and blood pressure.

and

PA is held to be autonomous from the renin-angiotensin system, but the term “primary” only denotes our scant knowledge of the mechanisms underlying the hyperaldosteronism. This case is, therefore, of interest from several standpoints, because it highlights one possible such mechanism and also suggests a bifunctional link between the parathyroid gland and the adrenocortical zona glomerulosa.

Emphasis mine, of course. How little do we know.

Aldosterone and insulin resistance.

Via the Yahoo PA group, this really great article just came my way, addressing the relationship of aldosterone to insulin resistance. I’ve been saying this all along, but this is the first time I’ve found Actual! Scientific! Evidence!! to back it up.

The adverse effect of excess aldosterone on insulin metabolic signaling (Figure 1) has generated increasing interest in the role of hyperaldosteronism in the pathogenesis of insulin resistance and resistant hypertension. This association was initially described more than 4 decades ago in individuals with primary hyperaldosteronism and impaired glucose tolerance (34). Increased plasma aldosterone levels are associated with insulin resistance independent of other components of the metabolic syndrome (35-37). In patients with primary hyperaldosteronism, resection of aldosterone-producing tumors and pharmacologic treatment both decrease blood insulin and glucose levels, which indicates an improvement in insulin sensitivity (37,38).

I’m happy to be able to report that now, nearly a year and a half after my adrenalectomy, I continue to no longer show ANY signs of insulin resistance. When my illness first became apparent in my early 30s, I thought the sudden weight gain concentrated in my midsection was due to approaching middle-age. When this was followed by abnormal labs showing IR and borderline high fasting glucose, I thought I was not only doomed to a typical apple-shaped middle-aged body, but to the diabetes that runs in my maternal family. This all seemed terribly incongruous to the lifestyle I was living – unlike my maternal relatives, who smoked like chimneys, drank like sailors, and lived in the suburbs planted on their butts in front of the TV or in their cars, I lived in the city and walked everywhere, was (then) a vegetarian with a textbook-perfect diet, practiced yoga, went hiking, rarely drank, and had smoked a cigarette exactly once in my life. It didn’t seem fair. Hell, it wasn’t fair.
But. The tumor is gone, and so is the weight gain, the abdominal obesity, the worry that I will have to face diabetic foot in my lifetime (warning, extremely graphic Google image search). And I say this all the time, but I have to say it again – I am so, so incredibly grateful to everyone – the doctors, the hospital staff, the friends who saw me through this journey – that I have this second chance.
~ ~ ~
I get stupid thankful about this, just about every day of my life. After seeing a most amazing gig last night with a dear friend, I was already bordering on the stupid-emotional side. He asked me, as he does from time to time, how I was doing health-wise. I’m not a crier, but I came thisclose to bursting out in tears. That I am doing okay – that I am doing damn fine, even – that I have friends who remember what I’ve gone through and who care enough to check in about that, is just something that overwhelms me almost every single day. Sometimes that fact that I am here, and well, is the thing that doesn’t seem fair nowadays, since every day that I check into the Yahoo group it seems that there is yet another person who is NOT doing well at all. I realize life can be, in general, a matter of luck – I’m lucky to live five minutes from a research hospital, I’m lucky to be a trained researcher myself who can read articles like the one linked above, I’m lucky that my disease was caught before it did any real damage. And the fact that not everyone afflicted with this condition has equal access to the resources I do absolutely pains me.

Six months (!) post-adrenalectomy.

Yesterday – Friday the 13th! – marked the six-month mark since my surgery. Six months! I’m not sure how that happened. My memory of being in the hospital remains crazy-clear and so much more recent. I’m still pondering conversations I had with visiting friends. And wondering if I really *did* flash my scars to everyone who visited.

But. How am I doing? Just fine, thanks. I’m not really due for much in the way of bloodwork until the 1-year mark, but here are the numbers that seem to matter right now:

  • Blood pressure: averaging 122/79. I’m not checking it obsessively as I once did, but am happy to report that when I do, the numbers are nearly always in the 120s/70s. Except immediately after drinking coffee, which is something I’m trying to determine if I should be doing at all any more.
  • Weight: steady at 111, despite the fact that I’m eating rice pretty much daily. Or potatoes. Or hey, when I’m feeling really daring, sometimes both! Before the surgery, rice – the only grain I can eat, due to a miles-long list of food intolerances – made me pile on the pounds pretty easily, and gave me a bit more reactive hypoglycemia than I was comfortable with. Potatoes gave me really, really bad reactive hypoglycemia – full-on food coma, even in tiny amounts. Now neither one bothers me, which is my unscientific way of proving that (a) the tumor caused insulin resistance, and (b) now that the tumor is gone, so is the insulin resistance.

As I keep yammering on about over at the Yahoo board, I really, strongly believe that there is so much more to this disease than hypertension and low potassium. So. Much. More!!! I realize that those two things are the things that can kill, but so can insulin resistance/diabetes, which I am fully convinced goes hand in hand with this illness. And considering how common IR and T2 diabetes are in the U.S., I have to wonder if it’s really a “rare” disease. My mother, for example, is one of seven siblings – the only one not to develop T2 diabetes and die at a younger age than her mother (who lived to be close to 100; her mother’s mother made it to 103!). My mother’s father, on the other hand, died of a heart attack in his early 50s. My hypothesis: adrenal adenomas, all of them, passed down along the paternal line to all except for my mom, who seems to have won the genetic lottery in many ways. Perhaps it’s no coincidence that from a phenotypical point of view, she resembles her mother; I, on the other hand, am a carbon copy of her dad.

I’m also pretty certain that as long as this country’s health care system remains unchanged, this will remain a “rare” disease and people will continue to die young, of heart attacks and strokes and diabetic complications, or suffer compromised quality of life. There is so obscenely much profit in drugs for hypertension (none of which work in PA, but most doctors don’t know that), and even more profit in drugs for diabetes. If a relatively simple surgery like mine can fix the problem and eliminate the need for drugs entirely – imagine the losses the drug companies would suffer. As long as healthcare remains profit-oriented, this cycle is not going to end.

I’ve said all of this before, I know. And I’ve also stated my belief that I’m one of the lucky ones. Not a single day has passed in the last six months when I haven’t thought about this, how thankful I am for the circumstances that made me able to say this: the accident of where I live (5 minutes from a top medical school), the support of my friends (without whom I never would have had the balls to go through with a surgery that may or may not have worked), and my own darned stubbornness (if I don’t like the answer I am given, I keep asking until I do like it).

Moderation: just another word for “denial.”

In my last post, I briefly touched on the relationship between PA and insulin resistance – in short, that it can be caused by the potassium depletion from the PA. I’ve been thinking about this quite a bit lately – what it meant for me during the 10 years that I had untreated PA, what familial link there may be, and on a larger scale, where it might fit in to the nation’s diabetes epidemic.

In January 2003, when I was at my sickest (and my highest weight, a whopping 173 pounds), I was diagnosed with two of the three: insulin resistance and metabolic syndrome. With a strong maternal family history of diabetes and heart disease, this would have been enough to scare me into action, but I was lucky: I was also diagnosed with fructose intolerance at the same time. The end result of following a diet for fructose restriction was essentially a low-carbohydrate diet – no sugars, no grains, no fruits – which enabled me to lose 50 pounds in less than three months. I’m pretty certain that this saved my life – at the very least, it reversed many of the symptoms of metabolic syndrome – and thus, I am a big believer in carbohydrate restriction as a preferable treatment (over drugs) for insulin resistance.

My mother, age 86, is the middle child of seven siblings, and is the only surviving one except for the youngest. Of the five who have died, four of them have died from diabetic complications or heart disease (or a combination of both, as all were diabetic). All were obese. The youngest living sibling is also obese and diabetic. The only two of the seven not to become both obese and T2 diabetic are my mother and the one sister who died young (a suicide).

When one begins the diagnostic process for PA, there are a lot of questions about family history. I don’t have a lot of information, but based on what I was able to put together – mainly, the above paragraph – I came to two conclusions: first, while I have no proof of this and never will, I suspect that every one of the siblings above who died of diabetic complications had an adrenal tumor. And, second, if one becomes diabetic as an adult, the best things one can do are remove all sugar and grains, processed foods, and “eating for entertainment” from one’s diet; and get up off one’s butt and move. I am convinced that I reversed my insulin resistance early on because I refused to remain sick and fat (even if this could not reverse the tumor!), and I am convinced that my mother’s apparent immunity to these diseases is due to her lifelong habit of walking everywhere (she never learned to drive).

~ ~ ~

Even if my adrenalectomy has, at least for the time being, rescued me from the danger zone of developing diabetes, I remain extremely interested in the subject, and I have RSS feeds set up for news items about the disease. So even though I don’t watch television and could care less about celebrity chefs, the recent hubbub about Paula Deen’s diabetes diagnosis came across my radar. And I’m siding with Anthony Bourdain here – she really is the most dangerous woman in America.

Why? Not because she advocates eating bacon cheeseburgers sandwiched between two glazed donuts, but because she advocates moderation (WARNING: link with sound!). Loudly and emphatically. Sorry, Ms. Deen, but I’ve got news for you:

Moderation doesn’t work. And you are living proof of it.

First, moderation goes against human nature. We’re hardwired to survive, and survival, historically speaking, means beating famine. So, when presented with food, we eat. Simple enough.

And, second, as I noted above – when one has metabolic derangement, carbohydrate restriction can work wonders. And that means complete and total restriction of all processed foods, sugars, and grains. That doesn’t mean “once in a while,” that doesn’t mean “have a cheat day,” that doesn’t mean “a little bite won’t kill you.” Because it will. Maybe not today, but slowly and painfully, it will kill you. If you don’t believe me, do a Google image search for diabetic foot (WARNING: disgusting images!).

Moderation, in my opinion, is just another word for denial. The minute one is diagnosed with any form of metabolic derangement, be it insulin resistance, T2 diabetes, or metabolic syndrome, one’s life changes. Or perhaps more accurately, one has to change their life – that is, if one wants to take control of the situation and get healthy again. The choices are simple:

  • Stop “eating for fun” – that means no cupcakes, no ice cream, no fast food, no corporate chain restaurants serving plates of ConAgra with a side of Monsanto – and get up off your butt and move.

OR:

  • Practice “moderation” and expect to be feeling crappy, popping pills, and getting fatter and sicker for the rest of one’s life.

There are only two choices. It’s up to you.

~ ~ ~

If you have been diagnosed with insulin resistance, pre-diabetes, or metabolic syndrome, read this first. It’s a pretty decent overview of what each of the terms mean.

Once you have done that, head over to Blood Sugar 101 and read every word that Jenny has written. Chances are it will contradict everything your endocrinologist tells you. And, unlike what your endocrinologist tells you – moderation, lots of whole grains, and many expensive drugs – it will work and you will feel better. It’s worth a try, isn’t it?