How I Practice Now

by Jacob Schor, ND, FABNO

I spent my first year of practice sucking on pellets of homeopathic Lycopodium, a remedy often prescribed for those who fall ill from the strain of keeping up pretenses, of struggling to maintain an image of self-assuredness when behind the façade they feel insecure.

Nothing in my four years of naturopathic school quite prepared me for the patients whom I began seeing immediately after opening our practice in an unlicensed state. None were those easy cases that I had come to expect in the school clinic; no kids with earaches, no women with yeast infections, no sore throats. Twenty years later, I still recall in detail the woman who presented with a chronic bladder infection. She questioned why I kept smiling at her and I had to confess that she was my first patient whom I knew how to treat.

I found a new mantra, a phrase that rarely left my workday consciousness: “They never taught this in school.”

A patient called those first months to ask if I could treat her sciatica: she described her pain as originating in her left piriformis, a condition that supposedly I had learned to deal with in a physical medicine class the year before. It wasn’t until she was on my table and I was about to jab my elbow into her posterior that she mentioned the massive tumor that was mashing her pelvis apart from the inside. My recollection is that she survived barely a week after seeing me.

Thinking back, it’s hard to believe we stuck it out and didn’t toss the towel in, so to speak. Perhaps it was the loans, the new baby, and the fact that patients would write a check as they were about to leave the office. Even if I didn’t know what to do.

Twenty years later and I still don’t know what to do much of the time, but I’m used to it. It’s part of the job. If it were easy, the patient’s “regular doctor” would have figured out what to do. Every workday there’s another surprise quiz. Somehow, I’ve found a rhythm, a routine for dealing with the unknown, a way to work that doesn’t involve pretending I know what I’m doing when I don’t.

Let me use a recent patient as an example. To hide his identity I’ll call him the kid. He’s 16 years old, and comes in to the office with his mom. He’s a swimmer, working the summer as a lifeguard, and his chief complaint is high blood pressure. My assumption that it is just a little bit elevated is wrong.

“How high are we talking about?” I ask innocently enough as I fiddle in the cupboard to find my stethoscope and the sphygy thing.

“About 160 over 120” the mom responds. I sit down and get the full story.

Just after the kid was born, he was diagnosed with hydronephrosis. “It got better,” his mom tells me. When his hypertension was first detected a few months back, he had the benefit of a full medical work-up. Both kidneys were working but one at half throttle. … His left kidney was doing about 75% of the work and his right only 25%. The docs prescribed a beta blocker to the kid and sent him home. The kid tried the drug for a few weeks and couldn’t stand the way he felt so stopped taking it. The drug made activities like competitive swimming or lifeguarding difficult.

My immediate reaction in my first years in practice would have been to adopt a trout face, my mouth wide open, staring blankly at the patient and waiting for inspiration. Now I’ve learned to hide my ignorance; I turn to my computer, click my way to PubMed.gov, all the while chattering away that we “are going to the National Library of Medicine …” and chanting inside my head, “It’s an open-book test.” In this case also crossing my fingers that the current hypertension is somehow related to the earlier hydronephrosis. Step 1: this is an open-book test: learn what you can.

Indeed this seems to be the case. In 2010 Mattias Carlström described the “Causal link between neonatal hydronephrosis and later development of hypertension.”¹ Together, the three of us, mom, me, and the kid, read the big words of the Carlström’s abstract. Since 2000,“… the surgical management of non-symptomatic hydronephrosis in children has become more conservative, but the long-term physiological consequences of this new policy are unclear. … In … complete ureteral obstruction, tubular atrophy and interstitial inflammation occur rapidly.” But in “… chronic partial ureteral obstruction, …  hydronephrosis is associated with renal injuries and is causally related to hypertension. …”

In other words if the kid had had major nephrosis, his obstructed kidney would have atrophied, died, and been surgically removed. In his case, the kidney has been partially obstructed and this chronic injury led to his hypertension.

Thus often my first step in treating a patient is to see if modern medicine/science offers any suitable explanation for the patient’s situation. These days I lean heavily on PubMed to find this information. Kidney physiology was complicated when Dr. Anna Macintosh tried to teach it to me back in the 1980s. It hasn’t gotten any simpler. Still, to try and treat the kid, I want to understand the mechanisms by which his wayward kidney is raising blood pressure.

“The mechanisms underlying the development of hypertension in … hydronephrosis are complex and involve changes in both the renin-angiotensin system and renal sympathetic nerve activity. Furthermore, oxidative stress and nitric oxide deficiency in the diseased kidney, with consequent resetting of the tubuloglomerular feedback mechanism, appear to play a pivotal role in the development and maintenance of hyper-tension.” (Carlström)

“Oxidative stress” and “nitric oxide deficiency”; these words are familiar, something I kind of understand. And things we might control.

A 1999 paper by Chevalier et al. that used rats to model the long-term response to temporary hydronephrosis in rats is of interest as well. Rats were subjected to “temporary unilateral ureteral obstruction (UUO)” during the first two days of life. Removing the obstruction did not reverse kidney damaged that occurred while things were blocked and a 40% reduction in nephron number remained. There was a persistent reduction in tubular epidermal growth factor and an overexpression of transforming growth factor-beta 1 (TGFB-1).²

Basically, a few minutes’ reading tells us a lot. The kid’s kidney was damaged shortly after birth and the resultant reduced performance triggers elevated blood pressure. The original and continuing process of deterioration involves several underlying mechanisms that have a lot to do with nitric oxide, oxidative damage, and TGFB-1. We now have targets to aim our initial therapies at.

This is all about translation. We translate the near gibberish found in the scientific journals into clinical relevance, into supplement names and suggested doses. I guess this is what they mean by “translational medicine.” It certainly is what the process means to me.

Working with the kid and his mom, we create a quick list of possible interventions that act on these “target of action.”

We narrow the list looking to see which of these supplements have any published evidence that they affect kidney function and lower blood pressure. We debate possible compliance issues versus possible effectiveness. I hope the kid will buy in to what we are doing. Nothing will matter if he doesn’t work with me.

We end up with a short list that includes curcumin, L-arginine, and melatonin.^3–5 We work out a treatment plan to give these along with a plan for him to monitor his blood pressure to see if it improves.

My first step thus is to view anything I don’t know as an open-book exam, one in which I can take a few minutes to learn the subject and then translate the current scientific knowledge and translate it into clinical therapies. It is not the last step.

The second step is to ask for help. Not as some patients would want, by my getting on my knees and holding hands with them in prayer. That’s not my style. Instead I contact colleagues who know more than I do. In this case of hypertension secondary to hydronephrosis, I wrote the two naturopathic doctors who in my mind know the most about kidney health, Jenna Henderson and Eric Yarnell. I asked them for advice. Henderson responded that she often uses taurine in this situation, so that was added to our “to try” list.

I haven’t had a follow-up visit with the kid yet and I’m starting to feel curious whether he is actually taking the supplements and giving them an honest try. Are they helping?

While I wait to see them again, I am thinking about taking it to the next level.

These days I know that naturopathic students get trained in a philosophic approach to naturopathic treatment that has been formalized over the years by Jared Zeff and Pamela Snider, in which the determinants of health and all sorts of hierarchical approaches are considered. Having myself been a onetime recipient of the AANP’s Vis Award, I feel a certain obligation to take some sort of enlightened approach and adopt one of these strategies.

But I don’t. For me it’s more a process of elimination. Can I think of a homeopathic remedy that I think will fix this kidney? Not yet, so I don’t prescribe one. The kid is pleasant, nothing in our visit has given me a nudge toward a constitutional remedy, nothing in the details of the disease process have shouted out to me, “Give this remedy!” so I simply skip it. For the time being.

Same with botanical medicines. I’m keeping a list of herbs to consider in the kid’s chart but not rushing to tell him to take any of them. I’m not sure he will. Not unless I find one that tastes really good.

I keep wondering, though, if there is some way to localize the effect of the supplements he is taking that would direct their impact to where we want it, in this case to the damaged kidney. The pathology seems centered in that kidney.

When I play “fetch the ball” with our dog and she is searching the wrong area, I will whistle and point. Is there some way to whistle and point those supplements to the kid’s kidney, to where they are really needed?

I am debating using low level laser therapy. These “cold lasers” apparently stimulate release of NO in the tissues treated. This NO release and resultant increase in blood flow is often used to explain their benefit in healing injuries. Interestingly, with reperfusion injuries, the laser treatment also appears to protect other organs injured by hypoxia. In a 2012 study of reperfusion injuries in rat colons, laser treatment appeared to protect the rats’ lungs.⁶

There is slim chance that the kid will put up with this idea; making time for laser treatments at home, or coming to the office for treatments just doesn’t seem high on his teenage priority list. What if we experiment at the office and see if a single treatment lowers his blood pressure? He might change his mind if he sees immediate results. Perhaps if I had someone better-looking and younger to administer the treatments, someone not my gender, compliance might not be an issue.

After two decades of practice, as you can see, I still don’t know what I’m doing. Each patient comes in with a unique story. It’s still a rare day when I say to myself, I’ve seen this before. It doesn’t bother me the way it once did. Perhaps it was all the Lycopodium I took.

Notes

1. Carlström M. Causal link between neonatal hydronephrosis and later development of hypertension. Clin Exp Pharmacol Physiol. 2010 Feb;37(2):e14–23. Epub 2009 Aug 4.

2. Chevalier RL, Kim A, Thornhill BA, Wolstenholme JT. Recovery following relief of unilateral ureteral obstruction in the neonatal rat. Kidney Int. 1999 Mar;55(3):793–807.

3. Tapia E, Soto V, Ortiz-Vega KM, et al. Curcumin induces nrf2 nuclear translocation and prevents glomerular hypertension, hyperfiltration, oxidant stress, and the decrease in antioxidant enzymes in 5/6 nephrectomized rats. Oxid Med Cell Longev. 2012;2012:269039. Epub 2012 Aug 7.

4. Rajapakse NW, Kuruppu S, Hanchapola I, et al. Evidence that renal arginine transport is impaired in spontaneously hypertensive rats. Am J Physiol Renal Physiol. 2012 Jun 15;302(12):F1554–F1562. Epub 2012 Mar 21.

5. Erşahin M, Sehirli O, Toklu HZ, et al. Melatonin improves cardiovascular function and ameliorates renal, cardiac and cerebral damage in rats with renovascular hypertension. J Pineal Res. 2009 Aug;47(1):97–106. Epub 2009 Jun 22.

6. Kirkby KA, Freeman DE, Morton AJ, et al. The effects of low-level laser therapy in a rat model of intestinal ischemia-reperfusion injury. Lasers Surg Med. 2012 Sep;44(7):580-7. doi:10.1002/lsm.22060. Epub 2012 Aug 6.