Friday, February 12, 2016

Forget electric or hybrid or mileage. There's only one thing that matters for your next car.

What are the worst things that happen to us directly? (i.e. not things that happen to our kids)

Death and extreme suffering of course. Unfortunately, one is inevitable — and the longer that is delayed the more likely the other. Don’t blame me, I didn’t make this world.

Then there’s accidentally killing someone with a car, most likely a cyclist or pedestrian. That’s got to be in the top 3, maybe top 1. Drive a lot and bad luck or bad judgment may have its way. It feels like something we want to avoid.

Historically we had to minimize driving and/or drive with care. Now though, there’s a third option. Cars are beginning to incorporate pedestrian-collision avoidance systems like Volvo’s Mobileye or Toyota’s Pre-Collision safety [1].

Forget electric or hybrid or mileage or CO2 emissions. What I want most is something to keep me from hurting unarmored people. Until we have fully autonomous cars these warning systems are my best option — especially when they work under low vision conditions like darkness, rain, snow and fog.

So when I buy our next vehicle in 3-5 years this technology will determine what I buy. Only then will I look at electric, hybrid and the rest. Maybe now you’re thinking the same thing — imagine how you’d feel in 2019 if you go without and do hurt or kill someone [3].

We will all have this choice to make in the next few years [2]. 

- fn -

[1] This ConsumerReports review mixes systems that protect drivers with things that protect pedestrians. One I care little about, the other I care a lot about. It’s hard for a car-centric culture to think about the unarmored.

[2] Government action would help greatly - another reason to vote Dem. So would insurance company discounts

[3] Easy to imagine the advertising.

See also

Deep Burning Butt Ache review: Piriformis syndrome, sciatica, deep gluteal syndrome, sacroiliac syndrome, deep buttock syndrome ...

One of the more interesting aspects of being an older physician is that we get to experience first hand problems we’ve treated (or mis-treated) in other people. We learn experiential subspecialties like cancer, pain management, arthritis (yay), hypertension, obesity, heart disease and the like.

My experiential subspecialty is sports medicine, particularly anything related to tendons and, most recently, joints. I owe my experience to a combination of bad genes (thanks Mom) and a need to move. 

Experiential specialties teach even new physicians that the medical knowledge base is weird. It’s not simply that textbook descriptions and treatment plans are incomplete, it’s also that they vary a great deal, both between references and within them. Even books that do some things well may cover other things poorly. If you hang around for a while you also see the same “thing” get new names and explanations, even if the treatments don’t change as much. Insider experience exposes some “well known” disorders as Potemkin villages — on closer inspection they kind of fall apart. (Osteoarthritis? We know almost nothing. There really is something wrong with how we explore disease).

Deep Burning Butt Ache (DBBA) is all of the above. Actually, that’s my term, not the scientific name. It’s sometimes known as “Piriformis syndrome”, “deep gluteal syndrome”, “sciatica” (older name, now obsolete), “sacroiliac syndrome” (less often), and “deep buttock syndrome”. PITA, inevitably.

I’ve had DBBA three times in my life. Once it was related to carrying a wallet in my hip pocket (today it would be a phone). That one cleared up when I moved the wallet, but it still took many months to completely resolve (also typical). A second time was related to inline skating, and only slowly resolved when the season ended. This time it seems to have come from playing ice hockey, but it is a bugger during my broken-arthritic-old-man CrossFit workouts —  especially running, rope jumping, and, weirdly, kipping pull-ups but not squats or box jumps. (There may be a new arthritic component to the problem, but I can’t tell that.)

Having lived with this a few times I think I’m in a good position to do an informed review of the accessible online literature. These references matched my insider experience:

I think with this set of references you know about as much as anyone does - except what the stretches actually look like (see below).  All of the references are pretty recent, that’s because until a few years ago DDBA didn’t “exist”. We used the term “sciatica” to include both disk and bone pressure on the sciatic nerve and what most now call “piriformis syndrome”. Two very different problems with different courses (disk problems often resolve in 6 weeks) and different management (esp. stretching).

The use of “Piriformis Syndrome” came out of the internet community; this may be the first crowd-sourced medical syndrome. In truth we really don’t know that the Piriformis muscle is the root problem; it gets blamed because in many people (muscle anatomy varies) the Piriformis lies on top of the sciatic nerve and the symptoms resemble those caused by known injury to the sciatic nerve. Unfortunately, the muscle is hard to study — there’s too much on top of it. For that reason I prefer terms like “Deep Gluteal Syndrome” or “Deep Buttock Syndrome” or “Deep Burning Butt Ache” (DBBA). Similarly I prefer “shoulder pain syndrome” to “rotator cuff tendonitis”. Humility is a good idea.

I particularly liked Dr. Pribut’s description of the problem (excerpt and emphases mine):

Dr. Pribut on Piriformis Syndrome

Piriformis syndrome is difficult to diagnose and resistant to therapy. The existence of piriformis syndrome has been doubted for years, but with the power of the Internet the reality of this syndrome has finally reached a tipping point. Previously, it was not even considered as a diagnosis, in others it was quickly ruled out. In others the symptoms are ascribed to "sciatica" or some other cause, even if the piriformis is considered as a possible cause. Often the patient has considered the possibility before the physicians, trainers, therapists and others have.

Piriformis syndrome may overlap with a variety of other problems including what McCrory et. al. have called a "deep buttock" syndrome. This includes pain in the buttock region, possibly pain in the hamstrings, occasionally pain in the back of the leg that is difficult to locate.

… Scant information is available on the piriformis syndrome in lay publications, and only a little more in scientific publications. The functioning of the muscle has not been clearly defined and examined in the literature. The location of the muscle does not allow for surface EMG (electromyographical) study. It is quite difficult, if not impossible to place a deep electrode in the muscle for study purposes also.

The anatomical position of the muscle leads one to conclude that it functions in some ways similar to that of the gluteus medius

The sciatic nerve passes immediately below the piriformis muscle

…Like Achilles tendonitis and iliopsoas tendonitis this is a very difficult problem to eliminate…

Dr Pribut, like most medical types, skips over the details of conservative management. We usually outsource that to physical therapy! It’s surprisingly hard to find good descriptions online, this is best I could do (don’t forget - nothing in back pocket!):

  • Roll sore butt over foam roller, can be combined with the cross-over sit stretch as in this picture. (The other exercises on this site don’t make as much sense to me.)
  • Rubber (lacrosse) ball over piriformis/sore spot, roll over it. I have no idea why this seems to help, it sounds crazy. Should make things worse.
  • Google Image Search: Piriformis stretch: I gave up and outsourced to the Google AI. Pretty good set, lots of examples of variations on sitting with one ankle on other knee and leaning forward/pushing down. That’s the fundamental external rotation stretch.
  • ”External” Rotation banded Hip Driver - CrossFit St Paul: this is an aggressive version of the classic sitting leg external rotation piriformis stretch; it’s one of a series of stretches in a single YouTube “lower body mobility” set.

For my personal flavor of DBBA I’m doing several versions of hamstring stretches, seated and freestanding “chair sit" external rotation stretches, leg over leg to chest stretches, foam roller, lacrosse ball, and, my personal favorite, the banded ”External” RotationHip Driver - CrossFit St Paul. After 6-8 weeks of this I’m improved, but a few hours of hockey or running/jumping will set me right back.

Oh, I’m supposed to not do things that make it worse? Well, yes. There will be at time. For now though I’m trying something counter-intuitive that I learned from my pretty-much-fixed long-term bad back problem (another experiential subspecialty of mine). I do the problem activity to produce mild to moderate burning discomfort, then I stretch it out, then I go back to the work. After I rest and recover I stretch some more. Experimenting, because we really don’t know much. Anyway, only 8 more hockey games left before it’s mountain biking (knee pain) season …

- fn -

[1]  Filler AG, Haynes J, Jordan SE, et al. Sciatica of non disc origin and piriformis syndrome: diagnosis by magnetic resonance neurography and interventional magnetic resonance imaging with outcome study of resulting treatment. J Neurosurg Spine 2005; 2:99–115.

I haven’t read the article, but looking the tumors they found (very rare in real world) I think they are a referral center …

“Piriformis syndrome: 68%

No diagnosis: 4%

Sciatic tumor: 1.7% (that’s 4 people in 239. I’m surprised it was so high, sample size small enough it’s likely random)

Lumbar stenosis: 0.8% (2 people)

Sacroiliac joint inflammation: 0.8% (2 people, surprised no sacroiliac arthritis)

Tumor in lumbosacral plexus: 0.4% (1 person, suspect referral bias.) 

Tuesday, February 09, 2016

Medical knowledge diffusion: The osteoarthritis example

For personal reasons I’ve been doing a deep dive into current medical knowledge of osteoarthritis — particularly the relatively early and aggressive diffuse joint condition i’m enjoying.

It’s given me an opportunity to compare what’s in a current Internal Medicine textbook (Harrison’s 18th edition, 2012) vs. a current Rheumatology text (Hochberg, 6th ed, 2015) vs. the medical literature. 

There’s a relatively clear trend. Harrison’s has vestiges of the 1980s and 1990s view of OA, which focused on injury and “wear and tear” and treats OA as thought it is a single disorder. It is cautious about exercise and joint use. There’s no way to slow, much less reverse, disease progression.

Hochberg, the specialist text, deprecates “wear and tear” and focuses on genetics, but inflammation is mostly a secondary response to some relatively unspecified joint process. In this text OA is a “heterogenous disorder”, which is a pedantic way of saying it’s a whole bunch of things that need to be divided up better. Hochberg is keener on exercise. There’s still no way to slow, much less reverse, disease progression.

The literature, of course, is all over the place, but there’s a consensus for dividing OA up into more useful diagnostic categories. In general exercise is encouraged with little caution. There’s a movement to treat some kinds of OA as a primary disorder of the pre-vertebrate ancient innate immune system (vertebrates also have an adaptive immune system). There are experiments now with medications which act on the innate immune system, like H3 blockers. Of course to be effective these would need to start early in what feels to some like a fast moving disease.

Future versions of Hochberg may or may not incorporate the medical literature. Some quite nice studies have sown that the medical research literature is usually misleading or flat out wrong; most physicians are wise to avoid it. I am, however, a bit disappointed that Harrison’s seems to lag behind Hochberg — the authors are drawn from a similar pool of researchers. Maybe it’s simply that Harrison’s 19th edition is due out shortly, the one I read was probably written five years ago.

For a family physician, internist or geriatrician one lesson might be to stop reading the “generalist” textbooks and skip to the specialist textbooks. Harrison’s is famously unreadable, Hochberg is actually an easier slog. This assumes one has online access to both of course, these are very expensive references.

See also

Monday, February 08, 2016

Google deprecated 'security questions' - in May of 2015.

How the heck did I miss this? Why wasn’t it all over my feeds? It’s sad Google actually had write a paper to prove the self-evident, but I guess even within Google there were executives who couldn’t get their head around this (emphases mine)…

Google Online Security Blog: New Research: Some Tough Questions for ‘Security Questions’

… we analyzed hundreds of millions of secret questions and answers that had been used for millions of account recovery claims at Google. We then worked to measure the likelihood that hackers could guess the answers.

Our findings, summarized in a paper that we recently presented at WWW 2015, led us to conclude that secret questions are neither secure nor reliable enough to be used as a standalone account recovery mechanism. That’s because they suffer from a fundamental flaw: their answers are either somewhat secure or easy to remember—but rarely both…

…  37% of people intentionally provide false answers to their questions thinking this will make them harder to guess. However, this ends up backfiring because people choose the same (false) answers, and actually increase the likelihood that an attacker can break in ….

.. the ‘easiest’ question and answer is "What city were you born in?"—users recall this answer more than 79% of the time. The second easiest example is “What is your father’s middle name?”, remembered by users 74% of the time …

… probability that an attacker could get both answers in ten guesses is 1%, but users will recall both answers only 59% of the time … Piling on more secret questions makes it more difficult for users to recover their accounts and is not a good solution …

We’ve only been saying this for 10 years. Yeah, Schneier of course, but really everyone else. Shame on Apple for persisting with this dumbass approach. (FWIW my security question ‘Fake Answers’ are basically unique random passwords - secure but a royal pain to manage.)

For all the flack I give Google, they’ve been doing better over the past 1-2 years. When it comes to security and usability of online resources they are without peer.

Thursday, February 04, 2016

Google and RSS: Not unfolding as anticipated

Google Reader died just 3 years ago. It feels a lot longer, I’m probably thinking of when Google burned Reader Social in favor of their G+ initiative. That was 5 years ago; eons by our reckoning, but things have changed less than we expected.

2013 was a truly bad year, but then Google ran into some G+ problems. Namely we hated it. They’ve since cut G+ into pieces, burned each piece, and scattered the ashes deep beneath the continental plates.

Meanwhile, despite a Feed 101 page that’s unchanged since 2004, Google’s Feedburner still lives. Google’s ancient Blogger Buzz blog is active, indeed blogs continue to be Google’s primary way of talking to the world.

Consider Google Fiber — one of their most critical projects. Today’s public housing announcement has a blogspot.com URL. More — take a look at the sidebar:

 Screen Shot 2016 02 04 at 9 58 43 AM

Ok, so it still has the obsolete G+ link, and Twitter and Facebook get colorful links, but note the old “Feed” link. Still there.

That’s not what we expected three years ago.

There’s more. Gmail has 1 billion active accounts. That’s big, but Google wants to replace it with Inbox. So Inbox is a good guide to Google’s current thinking. Inbox has an RSS (Atom) Feed.

RSS survived the great fire of 2013Media gurus are shocked to learn that RSS still rules the news. RSS is still the only standard for two essential net functions: notification and subscription. RSS is going to last (Feedbin and Reeder.app are my personal clients).

I wonder when Google will incorporate Feed subscription into Inbox.

See also: 

Thursday, January 21, 2016

Inflammatory osteoarthritis treatments: is there anything to watch for?

See also: Arthritis - the feeds and queries (reference post).

There’s something problematic about human tendons and cartilage. A wide range of infectious, auto-immune and idiopathic disorders land on them. I think dogs are no better, I can’t speak for other mammals.

We’ve tried to put boundaries around these disorders, to name them and attach treatments to the names. Some of our boundaries are better than others. Rheumatoid arthritis isn’t a bad tag. Osteoarthritis though, that label kind of sucks. It includes a wide range of clinical presentations at varied ages with diverse and poorly understood contributions of genetics, auto-immune activity, injury and healing, tendon and cartilage, inflammation and age. The one thing all of the diverse forms of osteoarthritis have in common is that there’s no useful treatment. We might as well call them the idiopathic untreatable arthritides (IUA).

Over the past 20 years or so IUA, or osteoarthritis, has had a few partitions. The biggest one so far was to carve out psoriatic arthritis; a history article claims it spun off in the 1960s (I thought 1980s, but maybe it took a while to make it into textbooks.) There have been efforts to split out “inflammatory osteoarthritis” (sometimes also called erosive osteoarthritis), but since there are no treatments (NSAIDs don’t count) IOA hasn’t quite launched.

I have something between psoriatic arthritis and inflammatory osteoarthritis, so I did a recent search of the UK’s Clinical Trials database for osteoarthritis + inflammatory, trials in UK, US, Canada and Germany and a similar search on the NIH ClinicalTrails.gov. The UK database draws on data from the WHO’s International Clinical Trails Registry Platform, but most of the trials were in the US. Of the two the UK database had the more interesting results.

These are the investigations for slowing disease progression that looked slightly interesting

The innate immune system connection is new to me, but a search in Google had an auto-complete….

Screen Shot 2016 01 21 at 10 01 04 AM

Spooky AI world indeed. Here’s the PubMed abstract for the article The Goog is suggesting, emphases mine:

Innate immune system activation in osteoarthritis: is osteoarthritis a chronic wound?
Curr Opin Rheumatol. 2008 Sep;20(5):565-72. Scanzello CR1, Plaas A, Crow MK.

PURPOSE OF REVIEW:
Synovial inflammation is increasingly recognized as an important pathophysiologic process in osteoarthritis, but the stimuli and downstream pathways activated are not well defined. Innate immune system activation, best documented in responses to pathogens, likely plays a role in induction of inflammatory mediators and the specific cellular infiltrate seen in osteoarthritis. Thus, the Toll-like receptors (TLRs) and their signaling pathways are of particular interest. These innate pattern-recognition receptors are activated not only by pathogens but by endogenous 'danger signals'. In this report, we review evidence that certain extracellular matrix components of joint tissues (hyaluronan and fibronectin) may act as TLR stimuli, and summarize recent literature implicating TLR activation in osteoarthritis.
RECENT FINDINGS:
Convincing evidence exists that hyaluronan/TLR interactions drive responses to tissue injury. Evidence of a similar role for fibronectin is growing. TLRs are expressed and functional in the joint, and many proteases and cytokines that promote cartilage catabolism are dependent on nuclear factor-kappaB, a TLR-activated transcription factor.
SUMMARY:
Activation of TLR pathways seems likely in osteoarthritis and may play a central role in disease development and progression. A model of osteoarthritis as a chronic wound, in which the innate immune response is triggered by molecular signals of tissue damage, is presented as a framework for future study of inflammation in this prevalent joint disease.

Well, well, well. That feels like me. I particularly liked this followup article from 2 years later, note the reference to dividing “osteoarthritis" into subsets:

The role of innate immunity in osteoarthritis: when our first line of defense goes on the offensive
J Rheumatol. 2015 Mar;42(3):363-71. doi: 10.3899/jrheum.140382. Epub 2015 Jan 15.

Although osteoarthritis (OA) has existed since the dawn of humanity, its pathogenesis remains poorly understood. OA is no longer considered a "wear and tear" condition but rather one driven by proteases where chronic low-grade inflammation may play a role in perpetuating proteolytic activity. While multiple factors are likely active in this process, recent evidence has implicated the innate immune system, the older or more primitive part of the body's immune defense mechanisms. The roles of some of the components of the innate immune system have been tested in OA models in vivo including the roles of synovial macrophages and the complement system. This review is a selective overview of a large and evolving field. Insights into these mechanisms might inform our ability to identify patient subsets and give hope for the advent of novel OA therapies.

So now I need to research currently FDA approved medications that are thought to be TLR antagonists, like H3 receptor antagonistsCiproxifan could be ordered from suspicious Chinese suppliers. Ok, Am I feeling lucky?

Probably not.

Exploring the “similar articles” and “citing articles” streams for the 2008 Scanzello et al article is quite interesting. Maybe we’ll make some progress. I’ve added some of those articles to my Pinboard arthritis stream, quite a few have free full text and are PubReader viewable. (yay NLM — the only good thing GWB ever did). I have some reading to do.

PS. As of Jan 2016 there are no interesting hits on “Heberden’s Nodes” and “Innate Immunity”. 

Update 1/21/2016

While discussing this with post with Emily something she said led us to a discussion of the curious history of the “H2 blockers”, particularly cimetidine (Tagamet). We remember when those drugs were introduced for gastric mucosa injury, as was common in OA patients taking NSAIDs.

The H2 blockers have an odd history with immune disorders. I recall eosiniphilic fasciitis had a curious response to cimetidine. Cimetidine is a physician-folk remedy for recurrent “cold sores” (usually ascribed to herpes simplex infection), which are now considered to be an innate immune response disorder. Cimetidine and ranitidine are also sometimes used to treat warts. As long ago as 1989 it was considered an immune response modifier, but researchers lost interest in the 00s. I did find a 2003 Japanese publication on cimetidine activity in suppressing rat adjuvant-induced experimental arthritis and a 2011 article suggesting sedating first-generation antihistamines and H2 blockers (cimetidine) impair innate immune responses to bacterial infection in mice.

On the other hand, there are some studies suggesting Cimetidine increases NK cell activity. I could easily see how shifting H2/3 balances would worsen osteoarthritis. I’m not quite ready to start taking a nightly cocktail of over-the-counter cimetidine and chlorpheniramine.

Update 1/21/2016

If you Google on Cimetidine and Osteoarthritis you’ll find a factmed page titled “Is Osteoarthritis a side-effect of cimetidine?” It says “Between January 2004 and October 2012, 78 individuals taking CIMETIDINE reported OSTEOARTHRITIS to the FDA…. of 2258 CIMETIDINE drug adverse event reaction reports”

I think what this group does is to dump the FDA FAERS files into Microsoft Access, then they generate web pages for each Drug - Condition pair and they sell ads off the pages. It’s a not-quite-criminal but not-quite-wonderful enterprise.

I doubt this is a meaningful finding, but if cimetidine truly does act on histamine receptors associated with NK activity and/or innate immunity it would not be surprising if it made some diseases worse as well as some better!

Update 1/23/2016

My intuition is not misplaced…

Antihistamines as treatments for autoimmune disease?
http://www.nature.com/nrrheum/journal/v9/n12/pdf/nrrheum.2013.169.pdf?WT.ec_id=NRRHEUM-201312
Jenny Buckland
Nature Reviews Rheumatology 9, 696 (2013) doi:10.1038/nrrheum.2013.169
Published online 29 October 2013

I’ve found articles on immune modulation activity of H1 and H2 antagonists, like chlorpheniramine, cimetidine and ranitidine dating back to the 1980s, including speculation on H1 and H2 receptor activity on human chondrocytes. Many starts and stops, but now we have innate immune system and the H3 and H4 receptors…

Update 1/24/2016

The Buckland article merely recapitulated an H4 blocker review — not worth paying Nature $8.

Meanwhile, I’ve started my own quixotic trial - Cimetidine 400mg/daily. A true shot in the dark, but it’s not like there are any alternatives. I’ll report out an ’n of 1’ observational result in 4-6 weeks one way or another. I reserve the right to terminate the trial if things go abruptly downhill but I’ll report out regardless.

Update 1/26/2016

Prion Disease and the Innate Immune System - mast cells in the brain play a role - of some kind. So what does cimetidine do there?

Upregulation of H2 receptors after cimetidine use - a risk of rebound with this experiment.

Update 2/1/2016

Cimetidine for chronic calcifying tendinitis of the shoulder, 2003.

Cimetidine decreases calcium levels and improves symptoms in patients with hyperparathyroidism… Cimetidine, 200 mg twice daily, was given orally for 3 months in 16 patients who did not respond to more than 6 months of conservative treatment… Calcium deposits disappeared in 9 patients (56%), decreased in 4 patients (25%), and did not change in 3 patients (19%) . Our results indicate that cimetidine is effective in treating chronic calcifying tendinitis of the shoulder; however, the mechanism by which cimetidine improves the symptoms is unknown.

Weird. I do have a long history of intermittent calcific tendinitis of the shoulders, though I’ve always managed it conservatively. There is only one article citing this study…The H2 blocker famotidine suppresses progression of ossification of the posterior longitudinal ligament in a mouse model. - PubMed - NCBI

Friday, January 15, 2016

Smartphone Calendaring: survey results

Our family loves our Google Calendars. Today, looking at Calendars 5.app on my iPhone, I see that our 5 (human) family members own 8 calendars and I’m currently subscribed to 7 organizational calendars and 3 or so related to weather, holidays and the like. We’ve been doing this kind of coordinated calendaring since I got our family (free then!) Google Apps about 9 (!) years ago. The early days were painful, but now it’s smooth — Google hasn’t done any recent damage.

So I was looking forward to talking about Calendaring in my special needs smartphone book (working title: Smartphones for all: Supporting independence with iPhone and Android.). Then I started writing … and ran into a wall. What we did works, but it’s far too geeky. I needed “The Apple Way” (iPhone) and “The Google Way” (Android and iPhone) to be understandable. 

The first step to that was learning what normal people do. So I wrote up a Google Form 2.0 survey (now closed) and promoted it on app.net (mostly geeky) and Facebook (not geeky) and my blogs (sort of geeky). Today I dug through it.

I received 74 responses, about half from experts and half from my target group.

 Screen Shot 2016 01 15 at 11 58 46 AM

Of this group of 74 about 1/6 didn’t use any personal calendars on their smartphone. I didn’t ask this group any further questions, so my survey data is about smartphone users who have personal calendars - about 5/6 in this case.

Among the 5/6 who did calendaring the iPhone was more common than I’d expected - 87%!

Screen Shot 2016 01 15 at 12 01 55 PM

Since most smartphones in the US are Android devices, that’s an unexpected result. I suspect some of that is an app.net effect (it’s pretty Apple-centric), but I wonder if many Android users don’t do calendaring. I did notice in the survey that Android users were disproportionately “expert users”, maybe Android users fall into an expert group and a web/messaging/youtube only group. I’m speculating there, but I think the non-expert responders to my survey are a lot like my book audience.

I looked briefly at my 33 expert respondents. Almost half had both personal and employer calendars, most had Google Calendars (many had both), and many viewed and edited multiple calendars. The only surprise was how many iPhone using experts made do with the native iPhone Calendar.app - 2/3 of them! Since most view multiple calendars they must be using Google’s obscure calendar sync web page.

Of my 28 non-expert Calendar few used an employer’s calendar and only 3/28 used Android. Of the 25 that used iPhones about 1/3 were using either Google’s Calendar.app or some other Google Calendar client (Calendars 5.app, etc) and 2/3 used iOS Calendar.app. Most of the iPhone users of Google’s Calendar service used multiple calendars and sent event invitations. iPhone non-experts who didn’t use Google Calendar also didn’t access more than one calendar and most had never sent an invitation. Many were unsure if their iPhone Calendars sync’d to iCloud (the default setup).

Despite obvious limitations with my sample I came away with some useful working conclusions for my book:

  • I can’t assume my readers have ever looked at the Calendar app.
  • I need to explain the relationship between the phone calendar and the “web” calendar and that changes made to one will show up in the other.
  • Many iPhone Calendar users are not aware that they sync their Calendars with iCloud and that there’s a web view of their iCloud calendar. Many use their iPhone Calendar like a paper datebook or the original PalmPilot Calendar.
  • Calendar sharing is effectively limited to Google Calendar users. It’s not only that subscribing to public calendars is basically a Google-only thing, it’s that most iPhone/iCloud users never make use of Apple’s relatively obscure iCloud shared Calendar overlays.
  • I need to explain what sending an invitation does.
  • Calendaring is not an Apple strength.

Monday, January 11, 2016

How to probe medical knowledge gaps -- and get a useful pub

I researched alcoholic myopathy the other day. The results were appalling. There’s been very little research in the past 25-30 years, fundamental questions are unanswered, repeated references are made to the same old prevalence numbers, etc.

It reminded me again of the big gaps in our medical knowledge base. Some topics get a lot of research, others seem to be forgotten. So I wondered about a way to characterize the gaps.

I think this would work, and it would be a nice paper for someone:

  1. From medicare data get list of most often used 1,500 ICD-9 codes (still 9 for US).
  2. For the “other” codes map them to the parent level in hierarchy.
  3. For this set obtain ICD long names (optionally, use the better structured SNOMED names using ICD to SNOMED maps).
  4. For each string run a pubmed query using the NLM’s API.
  5. For each results count which are reviews, randomized controlled studies etc. (standard NLM metadata).
  6. Analyze the results for outliers with few reviews, studies, etc. I’d expect 50-100 would be neglected.
  7. Publish.

Sunday, January 10, 2016

Medical history: What CT did to neurology, MRI has done to sports medicine

Few remember this now, but once neurologists were proud of their ability to localize brain injuries based on complex and detailed examinations. They could, for example, find a tumor or a stroke based on an examination.

Then CT scans came along, and we discovered that those exams didn’t, actually, work.

More or less the same things happened with cardiac auscultation and cardiac anatomy. I remember our cardiology teachers and my fellow medical students could hear “S4s” that somehow I could never hear.  I assumed it was because I was tone deaf. Then cardiac ultrasound took over…

I think the same thing happened with sports medicine. Once we had all kinds of specific shoulder tendon diagnoses we made based on examination. Then MRI showed things were messier. We used to talk about various hip soft tissue disorders like “piriformis” syndrome, not it’s just “deep gluteal pain syndrome”.

There’s a lesson in this somewhere.

Wednesday, December 30, 2015

Aetna's unethical cost savings are enabled by the "arbitration" laws purchased by large corporations

The New York Times did a superb series this fall on how large corporations changed American law to neutralize a major consumer protection — the class action lawsuit. Arbitration clauses mean a single consumer goes up against multi-million dollar legal teams, a hopelessly mismatched battle.

I realize that’s why Aetna can get away with cutting health insurance costs through strategic incompetence. Ten years ago if they were routinely evading their contractual obligations they’d be subject to a multi-million dollar suit. Sure, any penalties would be too small to truly impact Aetna, but a potential payoff would be big enough to fund a suit. More importantly, once a judgment was made, Aetna would need to wind the scam down — a recurring judgment might eventually amount to real money.

Today there’s really no downside for them. I’m certainly not going to take them to arbitration. So, yes, the Feds should block Aetna and Anthem’s acquisitions, but this is just one facet of a much bigger problem. The modern mega-corp has damaged our political and commercial landscape — from secular stagnation to political corruption. It may take the second coming of Theodore Roosevelt to set things right.

Monday, December 28, 2015

Why DOJ should block Aetna and Anthem acquisitions: A story of strategic pre-authorization delays

The health insurance industry is consolidating. Aetna acquired Humana and Anthem bought Cigna. That leaves UnitedHealth, Aetna and Anthem as the mega-corporate rulers of US healthcare. Unless, of course, the US Justice Department blocks these mergers. 

Like most people who pay attention to healthcare policy I very much hope the DOJ does its job properly. I’m glad we have the Obama DOJ to stand up for us, at least now we have a fighting chance. That’s not why I’m writing this blog post though, and it’s not the reason why I’ll be writing Senator Klobuchar to ask her to work against these mergers.

I’m writing this because, of course, I’m personally mad at Aetna. I think I know why Aetna and Anthem are in a position to do the acquiring, and it’s not because they’re better at delivering health care. I think they’re winning because they excel at both strategic incompetence supported by a tobacco-industry class executive culture.

In my case a physician ordered a radiology procedure for me that requires pre-authorization by my insurance company - Aetna. The order, alas, was placed in early December — perilously close to the end-of-year period. A period where cost can shift, depending on deductibles, from the insurance company to the insured, or from one carrier to another.

Aetna could decline the authorization. That might have been a reasonable act — not every physician recommended procedure is a good idea, particularly when the physician owns the imaging process. I’m guessing they don’t have grounds for denial, so instead they simply stall. Information is provided … and Aetna can’t find it. They ask for the same information several times. They will succeed in running out the clock. My physician’s staff tell me Aetna excels at this game, even by industry standards they’re good at not delivering what we pay for. Which is usually considered theft.

Aetna’s executives don’t have to write up a formalize this profitable process. They don’t need to put anything in writing. All they have to do is underfund their pre-authorization process (a “cost center”), or provide financial incentives to delay payments, or not staff for the holidays, or promote executives who are good at cost control. Most likely they do all four. 

I suspect Anthem has the same skill set, but Humana and Cigna probably aren’t quite as good at being evil. There are so many ways in healthcare to do well by doing wrong; it’s a rough rule of thumb that the more profitable a healthcare operation is the less good it’s doing.

Aetna is going to win their little battle with me. The best I can do to get even is write Senator Klobluchar (I know Senator Franken will oppose) and complete their legally mandated complaint form.

And I can write a blog post.

See also

Update 12/30/2015

After completing the official complaint form, and separately posting a public message to Twitter @aetnahelp and follow-up email to socialmediacustomerservice@aetna.com, I received this message on the morning of 12/30:

Screen Shot 2015 12 30 at 3 08 06 PM

Of course it’s too late now, Aetna ran out the clock. As we knew they would. Even though the bad guys won this one, I would try public Twitter messages and email to socialmediacustomerservice@aetna.com in future. A kind of special service track for the geek elite. 

Sunday, December 20, 2015

Growing old grudgingly: The CrossFit Inversion

Mature audiences only.

Under 45 not admitted.

You have been warned.

I was 53 when I started my CrossFit hobby. That was almost 3 years ago. I knew then, given the shape of 83, that there was a cliff ahead. I didn’t need my older friends to remind me of that, but they have. Faithfully.

Back then my gym had us post our “personal bests”, like best time for a mile, or best back squat. Since I’d never done olympic weightlifting, or even serious training, it was fun to rack up my lifetime personal bests as an old man. The gym stopped doing that, probably for a good reason, but I kept my own records. Six months ago I had another one in the deadlift.

It was the deadlift that did my latest injury. Lower back of course. Not a bad one, I’ve done this before, but aggravating. It’s the context that’s the real problem, this injury follows the knee and the shoulder. 

I get the message. My cliff started at 55; the arthritis probably moved it up a few years. Now I’m in post-cliff hang gliding mode.

I’m good at taking clearly delivered feedback like this. So I’m updating my list of personal bests and filing it away. Been there, done that. In its place I’m making up a list of personal “safe limits”. For my deadlift I’m afraid that will be low even for a little guy like me — something like 235. Safe limits go up very carefully.

Personal best replaced by personal max. That’s my CrossFit inversion. Now I’ll see how far that gets me…

Tuesday, December 15, 2015

Smartphone calendaring: a brief survey

i’m collecting some data on how people do calendaring on their smartphones to support my special needs smartphone for independent living book project. If you’re reading this before December 20th 2015, can you please fill out this 2-3 min, 3-7 question survey? Thanks!

Calendaring in iOS, OS X, Outlook 2010 and Google Android/Chrome are all very different.

If you’ve ever wondered why healthcare institutions can’t easily share data between computer systems, just take a look at Calendaring in iOS, OS X, Outlook 2010 and Google Android/Chrome.

Google went down the road of calendar overlays. You can have as many calendars as you like and you can share them across a Google Apps domain or between Google users. Public calendars are available for subscription. My current Google Calendar calendar list holds twenty distinct calendars of which 8 belong to my family. (One for each family member, one for entire family, a couple of parent-only calendars that the kids don’t see.) In Google’s world, which is consistent across Chrome and Android, shared calendars can be read-only or read-write. Google supports invitations by messaging.

I love how Google does this, but I’m a geek.

I’ve not used any modern versions of Outlook, but Outlook 2010 also supported Calendar subscription. They didn’t do overlays though, every Calendar stood alone. I never found this very useful.

Apple did things differently. Not only differently from everyone else, but also differently between iOS, OS X, and iCloud.  OS X supports calendar overlays and subscriptions, but the support of Google Calendar subscriptions is  weird (there are two ways to view them and both are poorly documented). iOS has a very obscure calendar subscription feature that I suspect nobody has ever used, but it does support “family sharing” for up to 6 people/calendars (also barely documented). There’s an even more obscure way to see multiple overlay Google calendars on iOS, but really you should just buy Calendars 5.app.

iCloud’s web calendar view doesn’t have any UI support for Calendar sharing, I’ve not tested what it actually does. Apple is proof that a dysfunctional corporation can be insanely profitable.

All three corporations (four if you treat Apple as a split personality) more-or-less implement the (inevitably) quirky CalDAV standard and can share invitations. Of course Microsoft’s definition of “all-day” doesn’t match Apple or Google’s definition, and each implements unique calendar “fields” (attributes) that can’t be shared.

Google comes out of this looking pretty good — until you try to find documentation for your Android phone and its apps. Some kind of reference, like Google’s Android and Nexus user guides. As of Dec 2015 that link eventually leads to a lonely PDF published almost five years ago. That’s about it.

I don’t think modern IT’s productivity failure is a great mystery. 

Saturday, December 05, 2015

Arthritis - the feeds and queries (reference post)

I feel like I’m tied to a railroad track, and see the light of the train approaching. And I don’t know if it’s one mile away, or 500. 
Anonymous, a patient three years into leukemia remission.

Cancer will give many of us that oncoming train feeling, but of course the light is always there. We’re just good at denial. When we’re young and healthy the train is probably far away. When we’re 93 it’s pretty close. In between we try not to look.

There’s only one “train”, but there are lots of smaller hits along the way. Bicycles and cars maybe. One of them ran into me recently, so I’ve renewed an old interest in the so-called “rheumatic disorders” (misleadingly named after bodily fluid flow).

It really is an old interest. Before I figured out how to do medical school [1], I closely read the 1982 version of the Arthritis Foundation’s “Primer on the Rheumatic Diseases”. Within the broad bounds of unreliable memory I recall that osteoarthritis was a “wear and tear” disorder of aging, rheumatoid arthritis and a handful of other disorders were “auto-immune” diseases, gout and non-gout crystal deposition were relatively well understood, and many viral and non-viral diseases (Gonorrhea and, a bit later, Lyme) caused arthritis. Steroids (not the androgen variety!) worked very well on the auto-immune disorders, but the long term side-effects were horrible and inevitable. We had reasonable drugs for Gout, gold for Rheumatoid arthritis (some value [7]), and nothing for osteoarthritis. Okay, so we had NSAIDs like ibuprofen, but we already suspected they were a mixed blessing. We’ve kind of given up on them.

Things aren’t that much different 33 years later. Relatively recently we’ve realized that “osteoarthritis” covers a multitude of evils, some or all of which, like “psoriatic” arthritis, are more than “wear and tear”. We still don’t have any great treatments for Systemic Lupus Erythematosis, though we now do less harm with the treatments we have. Rheumatoid arthritis has seen the most care improvements, but, amazingly, we can’t actually cure it or any other auto-immune arthritis [3]. We still wonder about the role of infectious agents in creating or sustaining auto-immune disorders but we have few leads [2][6]. The most recent (2005) edition of the Primer on Rheumatic disease says of Osteoarthritis “It is clear that this … includes a variety of different conditions, but we have made less progress …”.

More recent publications have even undone old certainties; we’re no longer confident that the various flavors of psoriatic and osteoarthritis are primarily “arthritic” (greek: Arthron, joint). Disorders along the osteoarthritis - psoriatic arthritis spectrum may begin as diseases of the tendons. Some of them may be lifelong disorders of tissue healing; small injuries accumulate due to a healing defect, perhaps with later onset of an auto-immune component reacting to disordered tissues.

My medical school interest became personal as I watched my mother go through the arthritis experience for about 35 years, ending as “rheumatoid arthritis” (our classifications are imprecise). It wasn’t pretty.

Which is all by way of introducing this “reference post”; a blog post that I’m going to be revising and extending. It’s a post supporting my surveillance of our historically limited knowledge base. I’ll revise it periodically over the next year or two. Sometimes I’ll post/tweet about updates to this reference post, but most of the interesting results will appear in a pinboard RSS stream tagged “arthritis” [4].  

My surveillance relies on PubMed [5] (National Library of Medicine) RSS feeds. Anyone can create these, but I’ve never seen anyone but me write about them. I’ll list them by topic below, but first I’ll describe what I’m not monitoring.

I’m not monitoring care guidelines or the cutting edge of rheumatologic practice. I see a rheumatologist for that; that’s his job. If I want an update on current practices I’ll take a look at FP Notebook’s Rheumatology Book. I’m not interested in alternative or complementary therapies — that way lies madness. I’m only mildly curious about lifestyle factors; mostly because we know so little and very little research is going to get funded.

I am curious about tolerance induction — the Holy Grail of the rheumatic disorder treatment. We’ve been hammering on this decades, but we have new tools now. This is what we really want - a cure for at least some of these diseases. I’m looking for articles on disordered healing and secondary arthritic conditions, but I’ve yet to figure out a good search for that one. Likewise I’m looking for articles that relate loss of self-tolerance to a dysfunctional pseudo-neoplastic component of the immune system (yeah, this is definitely fuzzy). More concretely anything about the role of infections organisms in precipitating or maintaining arthritis.

Here are the RSS feeds and “similar articles” queries I’m revising and using for each of these topics. I wish there were RSS feeds for the “similar to” queries, as I learn the topics i’ll put create RSS feeds with similar results.

tolerance induction

tendon injury (enthesitis) and arthritis

microbiome and role of infection in creating and maintaining arthritis
Immune system and neural networks (because I figure the immune system is a form of neural network)
other

- fn -  

[1] The way to do the didactic portion medical school is to maintain a relentless focus on examinations. If you’re doing well you may then indulge your passion and curiosity. 
[2] As a still distractible student I read the first speculative article written on an association between bugs living in the high acid stomach and gastric ulcer disease. Before then we thought the stomach was sterile; nothing could live in such a disagreeable environment. That probably contributed to my extremophiles and auto-immune disease post.
[3] Juvenile Rheumatoid Arthritis does resolve about half the time. Which is curious.
[4] Like all things Pinboard it has an RSS Feed: http://feeds.pinboard.in/rss/secret:c6ea18730310000211dc/u:jgordon/t:arthritis/. Sadly there are no RSS feeds for “similar article” queries and “My NCBI” doesn’t show feeds.
[5] My medical informatics career began in Family Medicine residence as a beta tester of the “Grateful Med” software. I believe the product manager, Rose Marie Woodsmall, was a dead head. I was among the last generation of medical students to use the paper Index Medicus to do journal research.
[6] I’d wondered years ago why we weren’t mining synovial fluid for foreign DNA. Turns out this was done in 2001 with interesting results, but the follow-up was limited until “microbiome” became a funding source.
[7] Gold was used to treat Rheumatoid arthritis from at least 1945 through the early 1990s. I seem to remember it was sometimes associated with extended remissions. I can find almost nothing on it written after 1965 or so, and nothing at all on how it worked. There’s very little on long term outcomes. Which is, you know, profoundly weird.

Update 12/18/2015

I have a hunch that whatever is afflicting me now is the end-stage of a congenital defect with soft tissue/tendon formation. I’ve always been prone to calcium deposits along tendons and to overuse tendonopathies. It would not be surprising that as I’ve aged my body’s ability to manage this problem, and heal from injury, has declined. That in turn could lead to some secondary auto-immune issues (prolonged inflammatory/antigen spill issues). I haven’t come up with a search criteria yet to explore this idea; it would probably show up in whole genome analyses. I would need to look for discovery of a gene associated with auto-immune arthritis/osteoarthritis that was important for tendon formation.