Archive Page 93

Let Patients Lead – Explaining Addiction and Recovery to Families

We knew that the most powerful way to provide substance abuse treatment is in a group setting. Group members can offer support to each other and call out each other’s self deceptions and public excuses, oftentimes more effectively than the clinicians. They share stories and insights, car rides and job leads, and they form a community that stays connected between sessions.

Participants with more experience and life skills may say things in group that we clinicians might hesitate saying, like “Now you’re whining” and “Time to put on your big boy pants”. They can become role models by being further along in their recovery and by at the same time revealing their own fear or respect for the threat of relapse.

What has also happened in our clinic, entirely unplanned, was that after an informational meeting where we explained the group model and had a national expert physician speak about opioid recovery, several parents raised their hand and said there should be a group for families, too.

We listened and within a few months we started such a group and now, a year and a half into it, the group is co-led by a few of our patients, who naturally had become leaders of the patient group earlier.

There is magic in having these more experienced patients explain to our sometimes bewildered parents and family members how the addicted and recovering mind works, not from having seen it a hundred times, like the clinicians, but by actually having lived it.

The positive feedback and appreciation of this, our “Friends and Family” group has elevated these experienced patients to a mentor role now also for the families trying to be the most help for their loved ones in recovery.

Our biweekly conversations are turning the spotlight on the small and large victories that come with recovery and have put the challenges in perspective through stories of the ultimate successes these mentors have had themselves.

This week, my Tuesday patient group and the Friday Friends and Family group will be held without the two clinicians who usually run the groups and also without our medical assistant, who herself plays a crucial role as both confidant and voice of the program. A stand-in clinician and a covering medical assistant will be there and I will be there virtually as usual through video conferencing.

The glue that will hold everything together will be our informal peer counselors, and I have no doubt the groups will continue as if nothing had changed because of the momentum these folks have brought to our endeavors.

They know how much they mean to all of us. By sharing the experience of their own recovery, they have breathed irreplaceable life into these groups to sustain them even if some of the facilitators are on vacation.

We Have Lost Track of the Natural History of Disease

You almost never hear about diseases having a beginning and an end anymore. It is as if all diseases are viewed as either acutely life threatening or inevitably chronic and requiring lifelong treatment.

Voltaire is credited with saying “The art of medicine consists in amusing the patient while nature cures the disease”. There is a lot of truth to that.

Some of the most common acute infections we treat in primary care, for example, are actually self limited, resolving on their own in the vast majority of cases. This is the case with strep throat, ear infections, many cases of “walking pneumonia” and even uncomplicated urinary tract infections.

Untreated strep throat, for example, very rarely becomes acutely life threatening. The reason we always prescribe antibiotics is to prevent late complications like rheumatic fever and glomerolunephritis, a kidney injury that was so common even with treatment when I trained that we always checked the urine after treating someone for strep. Now we hardly ever see this problem anymore, as if the strains of streptococcus have changed or evolved. Antibiotics can also help prevent peritonsillar abscess formation, which is quite rare.

Some diseases that we now think of as chronic and always requiring treatment are of course the lifestyle related ones like type 2 diabetes, hypertension and gastroesophageal reflux. We all know they can often be reversed in motivated people through changes in habits. So often these days, though, we prescribe medications early on, because it requires less effort on our part than counseling and monitoring change of patients’ daily habits.

Psychiatric diseases that we think of as obviously chronic include anxiety, depression and bipolar disease and even schizophrenia. But that is not always the case, and in some cases we may actually be turning transient diseases into chronic ones by the very treatments we prescribe for them.

Again going back to my Swedish medical education, I was taught that there were two kinds of depression; reactive where there was an identifiable external trigger like a major life event or endogenous where no trigger could be found. We Swedes only treated the latter form, whereas in the United States even the reactive form that we knew to usually be transient was treated with antidepressants – back then usually the tricyclic amitriptylene.

The American thinking was apparently that reactive depression could become chronic if left untreated, but many studies have now suggested that the opposite is true.

Several disturbing examples of this phenomenon are illustrated by author and journalist Roger Whitaker. His work, including his bestseller “Mad in America”, plowing through the scientific literature and contrasting that with pharmaceutical marketing and common psychiatric prescribing practices, is quite thought provoking:

A 1983 paper he quotes said this:

“Without antidepressant therapy, episodes of clinical depression last from 2 months to several years, with an average of around 5 to 6 months. One-third of the patients recover within a year; probably one out of four untreated episodes may last more than 2 years….Age and culture seem to influence the course of depression. In addition to the classified clinical depressions, there is a considerable prevalence in the general population of depressive symptomatology and dysphoric states, apparently related to genetic factors, age, and stress. Little is known about the course and indications for treatment of these latter conditions, which should be the target for more systematic study and research in the ever widening fields of the phenomenology and therapy of depression.”

Whitaker points out the shockingly disappointing results of some of the studies done on treating depression or not. He points out that the modern antidepressants, the selective serotonin reuptake inhibitors (SSRIs) were shown to increase levels of available serotonin at synapses, and the assumption was made that depressed patients had a deficit of serotonin, but this was actually never proven. He goes on to make the case that treatment with SSRIs may instead cause permanent changes in brain chemistry that induce chronic depression.

He quotes many leading academics who openly question the serotonin theory as a cause of depression.

Ironically, in our daily work, we are mandated (by our Federal payers) to screen for and offer treatment for depression – and SSRIs are the first line treatment. This brings us to the fundamental principles of medicine and “First, Do No Harm”. We should always ask ourselves these two questions:

What happens if I do nothing? and What’s the worst complication the treatment could cause? What does the literature say? Maybe we should take a closer look.

Are we in the same situation as the physicians who started wondering if bloodletting was really such a good idea. But it seemed like a frightening proposition to withhold what might be a patient’s only hope. Now we know that bloodletting actually made things worse.

In the case of SSRIs I certainly don’t know what’s what, but I do know that in this country at this point in time we are very quick to prescribe them, and I do know that we are not at all talking about the natural history of depression. I also know of an awful lot of patients who have had difficulty coming off SSRIs, so I do know they cause powerful, long lasting changes in how our brains work.

Patients Are the Real Healers

The Swedish word for physician is läkare, which literally means healer. That seems a lot more glamorous than the American word physician, which is derived from physic, the old fashioned laxatives that were thought to rid the body of poisons and impurities. But we are actually the healers a lot less often than we think.

The more we learn about how the body works, the more we have to admit that rather than us doctors, it is each patient that heals themself with at most some guidance from us.

We may recommend a change in diet, but we aren’t there to watch what our patients make of the advice we give them. We may prescribe a medication, but we know that many of the standard treatments in our armamentarium are only marginally better than placebo, and we now understand a little bit about psychoneuroimmunology, so we have to admit that patient expectations greatly influence the efficacy of treatments, even surgical procedures. We have learned this from sham knee operations for meniscal problems, for example. Imagine that, placebo surgery, not just pills.

This goes all the way back to the words of Hippocrates: “Let food be thy medicine and medicine be thy food”, “Walking is man’s best medicine” and “The natural healing force within each of us is the greatest force in getting well”. These quotes seem especially relevant in our struggle with the chronic diseases of the times we now live and practice in – heart disease, diabetes, arthritis; all of them at least in part autoimmune in their pathophysiology. If he body can attack and destroy itself, it also has the potential to do the opposite, to heal.

Our job, then, is to provide basic medical care AND to inspire, empower or whatever one calls awakening the self healing potential that a good diet, physical activity, good sleep, healthy relationships, care of one’s emotional needs and a good measure of faith, trust and optimism can ultimately bring about.

Sickle Cell Disease and Phenylketonuria (PKU): You May Have the Genes, But Your Diet Determines Your Symptoms

Sickle cell trait is much more common among Africans in Africa than among African-Americans. But sickle cell anemia is more common here. How can that be?

The answer is very simple – EPIGENETICS, specifically your diet.

Not all people with sickle cell trait from both parents get sickle cell anemia. An environmental link had long been suspected and has been known for almost 90 years. I was unaware of it, having grown up and trained in Sweden and working in Maine, two corners of the world with almost no sickle cell anemia cases.

The reason for this difference is that the typical African diet includes cassava and African yam, foods with significant amounts of thiocyanate. Americans with sickle cell trait don’t typically eat these foods, and that’s why they develop symptoms more often.

In 1932 potassium thiocyanate (KSCN) was used to resolve sickle cell crisis. My reading suggest that this method never did become standard care, and was hardly mentioned at all until 50 years later, when it still didn’t become an accepted strategy. Potassium thiocyanate binds through a process called carbamylation to the site of error on the sickle hemoglobin molecule inside the red blood cell and corrects it. The shape and lifespan of the red blood cell are normalized by this reaction.

A 1986 article that tells the story from 1932 even proposed viewing sickle cell anemia as a thiocyanate deficiency anemia affecting people only if they are homozygous for sickle cell trait, rather than a genetically determined disease.

UptoDate mentions hydroxyuria treatment, which can be very toxic, but makes no mention of dietary modification of sickle cell disease at all.

This is an example of EPIGENETICS, factors that affect how our genes (GENOTYPE) may or may not cause disease or other visible attributes (PHENOTYPE). People who are homozygous for the sickle cell trait and still don’t get the disease because they eat cassava have the genotype but not the phenotype, if you will.

But it gets even more interesting. While sickle cells are more resistant to the malaria parasite, and cassava eating normalizes the shape and behavior of the red blood cell, this does not increase susceptibility to malaria. This is because cassava provides phytochemicals that weaken the plasmodium falciparum. This is an example of what has been called Human Plant Parasite Coevolution. This is explained in a talk by anthropologist Fatima Jackson. I highly recommend watching it.

So, as the saying goes, we are what we eat, or more accurately, what we eat determines or influences the environment of our genes and their tendency to manifest (express) their potential OR NOT.

All this came to my attention somewhat randomly, and I found it shocking that this isn’t more widely known. This knowledge puts Sickle Cell Disease in the same category as PKU, a genetic disease we routinely screen for and prevent by modifying the diet of patients with the PKU genotype. Having had two patients with this disease, born before routine testing started, I am particularly struck by the fact that this old discovery hasn’t become common knowledge 87 years after it was first published.

So there it is, PKU (or sickle cell) genotype causes the disease (phenotype) only if the genes are in a certain environment (epigenetics), for example with regards to diet.

Ordering Tests Without Using Words: Are ICD-10 and CPT Codes Bringing Precision or Dumbing Us Down?

The chest CT report was a bit worrisome. Henry had “pleural based masses” that had grown since his previous scan, which had been ordered by another doctor for unrelated reasons. But as Henry’s PCP, it had become my job to follow up on an emergency room doctor’s incidental finding. The radiologist recommended a PET scan to see if there was increased metabolic activity, which would mean the spots were likely cancerous.

So the head of radiology says this is needed. But I am the treating physician, so I have to put the order in. In my clunky EMR I search for an appropriate diagnostic code in situations like this. This software (Greenway) is not like Google; if you don’t search for exactly what the bureaucratic term is, but use clinical terms instead, it doesn’t suggest alternatives (unrelated everyday example – what a doctor calls a laceration is “open wound” in insurance speak but the computer doesn’t know they’re the same thing).

So here I am, trying to find the appropriate ICD-10 code to buy Henry a PET scan. Why can’t I find the diagnosis code I used to get the recent CT order in when I placed it, months ago? I cruise down the list of diagnoses in his EMR “chart”. There, I find every diagnosis that was ever entered. They are not listed alphabetically or chronologically. The list appears totally random, although perhaps the list is organized alphanumerically by ICD-10, although they are not not displayed in my search box, but that wouldn’t do me any good anyway since I don’t have more than five ICD-10 codes memorized.

Patients are waiting, I’m behind, the usual time pressure in healthcare.

Can’t find a previously used diagnosis. Search for “nonspecific finding on chest X-ray” and multiple variations thereof.

I see R93.89 – “abnormal finding on diagnostic imaging of other body structures”. Close enough, use it, type in exactly what the chief of radiology had said in his report. Move on. Next patient.

Several days later I get a printout of that order in my inbox with a memo that the diagnosis doesn’t justify payment for a PET scan. Attached to that is a multi page list of diagnoses that would work.

Frustrated, I go through the list. It’s another day, other patients are waiting. Eventually I come across R91.8 “other nonspecific finding of lung field” – not exactly pleura, but what the heck, close enough, let’s use that one.

Why is this – me hurriedly choosing the next best thing on a multipage printout, while my other patients are waiting – any more practical, accurate or fraud proof than having me describe in appropriate CLINICAL language what the patient needs and letting SOMEONE ELSE look for the darn code?

Here I am, trying to order what a radiologist told me to order, without having the tools to do it.

Next thing you know, Henry’s insurance will probably have some third party radiologist deny coverage because he disagrees with my radiologist, and I’ll be stuck in the middle…

Not quite what I thought I’d be doing. Who works for whom in healthcare?


I just realized none of the posts show on an iPad or a computer, but they do show on an iPhone. WordPress is working on this. In the meantime, please visit my Substack.

 

 

Osler said “Listen to your patient, he is telling you the diagnosis”. Duvefelt says “Listen to your patient, he is telling you what kind of doctor he needs you to be”.

 

BOOKS BY HANS DUVEFELT, MD

CONDITIONS, Chapter 1: An Old, New Diagnosis

Top 25 Doctor Blogs Award

Doctor Blogs

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

Mailbox

contact @ acountrydoctorwrites.com
Bookmark and Share
© A Country Doctor Writes, LLC 2008-2022 Unauthorized use and/or duplication of this material without express and written permission is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given.