Posts Tagged ‘medical controversies’

STARI or a Lyme Disease variant?

Thursday, October 31st, 2013
Here's the spirochete you definitely don't want to causes syphilis.

Here's the spirochete you definitely don't want to causes syphilis.

There continues to be considerable controversy over the extent of Lyme Disease  in the United States. Its cause is a spirochete, a skinny, long bacteria that is coiled and looks like a microscopic spring. Historically this family of "bugs" was known to have a member that caused syphilis, a scourge of mankind for thousands of years. Then in 1975 a new disease made its first appearance with a cluster of cases in both children and adults in Lyme, Connecticut. Over fifty cases were reported in the first two years of the epidemic, the black-legged tick Ixodes scapularis was found to be the vector that transmits the disease to humans and  in 1982 the spirochete Borrelia burgdorferi was identified as the bacteria responsible for the rash, arthritis, cardiac and neurological manifestations of what was eventually termed Lyme disease. The World Health Organization calls the illness Lyme borreliosis and it is widely found in Europe from Turkey to Sweden with nearly 65,000 cases a year, some differences in signs and symptoms and another tick species as the transmitting agent.

Lyme disease has clearly spread from its origin in the northeast US and is now an illness that affects hundreds of thousands yearly. The Center for Disease Control and Prevention (CDC) has  a website with extensive information on Lyme Disease,  and links to frequently asked questions about the illness. Among those bits of information is the blunt statement that Lyme disease, to a great extent, only occurs in three endemic regions of this country. Those cases occur in the area from northeast Virginia to Maine and some north-central states, including Wisconsin and Minnesota.

But it also can be spread by another tick much further west, especially in California where a different black-legged tick, Ixodes pacificus is the vector. And the CDC's own interactive map of Lyme disease cases from 2001 through 2012 shows it has struck in Florida, Texas and a number of other states, albeit without the number of cases seen in the east and northeast portions of this country.

Humans aren't the only species affected; dogs can get Lyme disease also and the incidence of the illness has markedly increases. A canine vaccine is available. Horses, cattle and cats can also get Lyme, but much less commonly.

A major issue is whether Lyme disease or something quite similar occurs in the South. The debate on that started twenty-five years ago and continues to today.

In 1988, Dr. Edwin Masters, a family practice physician in Missouri and amateur forester, gave a talk on Lyme disease to a forestry association. He had extensively prepared for his lecture and subsequently began to see cases of what he thought was Lyme disease in his own practice. Many had a rash similar to Lyme victims elsewhere (erythema migrans, abbreviated as EM). Some had swollen joints, neurological signs and symptoms and positive blood tests for Lyme disease using the test most commonly available then. Masters reported his cases to the Missouri Department of Health, but found that his reports were ignored.

He didn't give up at that point, but carefully photographed the EM rashes his patients presented with and stored blood samples. In the North the CDC said just having the reach was diagnostic, but denied that was true in the South.

A 1999 paper published by scientists from Amsterdam and New York said that there are ten different species of the spirochete bacteria that is called Borrelia. At that time three were known to cause disease in humans.

A multi-part 2009 blog post in Psychology Today's Emerging Diseases series (written by Pamela Weintraub, the Executive Editor at Discover Magazine) was titled "Rebel with a Cause: The Incredible Dr. Masters." It details the last thirty years of the live of the physician who championed the cause of Southern Lyme disease.

The Lone Star tick appears to be the vector for Lyme-like diseases in the South.

The Lone Star tick appears to be the vector for Lyme-like diseases in the South.

A 2013 Discover Magazine In-Depth report Ticked: The battle over Lyme Disease in the South, tells the story well (I downloaded it for $1.99). In brief, many people who live in the South have had a Lyme-like illness that the Lyme and Tick-Borne Diseases Research Center at Columbia University calls STARI, Southern Tick-Associated Rash Illness. From the CDC's conservative viewpoint this is not Lyme Disease since it has never been clearly proven to be caused by the spirochete Borrelia burgdorferi sense stricto (that translates to "In the strict sense")  and, according to the CDC doesn't cause the major complications associated with that illness. Their 2011 webpage on STARI says patents bitten by the Lone Star tick can sometimes develop an EM rash like those of Lyme disease victims, but the skin manifestations of STARI are slightly different and arthritis, cardiac or neurological complications don't occur.

Kerry Clark, a PhD associate professor in the Department of Public Health at the University of South Florida, took up the cudgel for Southern Lyme disease after Masters' death. He is a medical entomologist at USF who had collected and studied ticks for years. After giving a Lyme disease talk in Georgia three years ago, he was approached by a woman from an Atlanta suburb who told him there were many similar cases in her town. Clark collected many ticks from the patchy woodland areas infiltrating the area; most were juvenile (nymph phase) or adult Lone Star ticks.

Several days later he found one engorged tick on his own scalp. Since he has had fatigue, intermittent mental "fuzziness," twitches and a strange recurrent pounding headache.

Clark recently published a major study in the International Journal of Medical Sciences (easily available on the National Library of Medicine website) with the title "Lyme Borreliosis in Human Patients in Florida and Georgia, USA." It gives demographic, clinical and lab data on ten such patients with suspected Lyme disease. Clark and his associates used a newly developed test developed specifically for the genospecies Borrelia burgdorferi. Worldwide this includes more than 20 different "bugs" with seven in North America, but in the past only one had been generally accepted as responsible for Lyme disease. With DNA confirmation, they reported finding other closely-related spirochetes in patients' blood and skin as well as in Lone Star ticks.

My first take was this was an impressive article, but I am aware of those who would treat many patients with a variety of symptoms for "chronic Lyme disease" over extended periods of time using repeated doses of expensive intravenous antibiotics. And there is another subset of physicians, including, unfortunately, one of Clark's co-authors, who use treatment modalities which I view with great skepticism.

If other academic laboratories confirm Clark's work, perhaps we can get to definitive answers and make available tests that help determine when and how to treat patients with atypical Lyme disease.

Having seen diagnoses come and go (e.g., the virus that supposedly caused chronic fatigue syndrome was eventually found to be a lab contaminant), I'm waiting for those confirmatory studies.








babesiosis, caused by the parasite Babesia microti —

a pathogen similar in type and impact to the one that causes

malaria. Ticks in the South also carry other diseases, including

Rocky Mountain Spotted Fever and ehrlichiosis, caused by two

kinds of related bacteria.



The Columbia University Lyme and Tick-borne Disease Research Center's website has a nicely balanced discussion of STARI, Southern Tick-Associated Rash Illness, sometimes called Masters Disease in honor of the now-deceased Missouri family physician who initially reported cases of what was felt to be a Lyme Disease-like illness.

Discover magazine, which I subscribe to, has an In-Depth publication available for $1.99 on the controversy concerning a Lyme disease-like illness in the south. It's well written by Wendy Orent, a PhD anthropologist/science writer who teaches at Emory University; she has also published a controversial book on plague.

Orent was also involved in a debate about the possibility of an H5N1 (bird flu) epidemic.  According to Orent, there was no legitimate basis to assume that any large-scale epidemic would ensue as a result of the H5N1 virus.

Marijuana and Schizophrenia: What's the association?

Saturday, July 6th, 2013

My wife called my attention to an editorial page piece in the July 2, 2013 edition of The Wall Street Journal linking marijuana use to schizophrenia. I at first wondered who the paper had chosen as a distinguished medical figure to write on his or her research study of the association between use of this drug and the most severe mental illness, but read the commentary and realized it was written, not by a professor, but by a Yale psychiatry resident in training.

Having been a Duke resident more than 45 years ago, I was aware that young physicians at major teaching centers might, as I did, see a particular spectrum of the general patient population, in many cases the most ill portion of it.  Therefore I was less than certain of the strength of the basis for his viewpoint, but felt it was a highly significant topic and it was well worth perusing the literature pro and con.

Does this cause mental illness?

Does this cause mental illness?

In 2010 Time magazine published a well-balanced article titled "The Link between Marijuana and Schizophrenia." That led me to several medical research reports, but the lay press article itself was interesting.

It commented that studies showed those who were diagnosed with schizophrenia were approximately twice as likely to be marijuana smokers than groups who didn't have this dire diagnosis. Some studies, viewing things prospectively, suggested (note the word, please) that pot smokers were at double the risk of developing schizophrenia as those who never smoked the drug.

But, as the Time article noted  the portion of our US population diagnosed with this debilitating illness has remained constant at roughly 1%, and the current National Institute of Mental Health (NIMH) web-based discussion of schizophrenia agrees with this figure. It mentions that some drug abusers exhibit symptoms like those of patents with schizophrenia, but NIMH states that most researchers do not think that drug abuse is the cause of this mental illness.

A short piece from the CDC on childhood mental disorders in JAMA  for July 3, 2013, confirmed that schizophrenia is way down the list of mental disorders in US children. On the other hand, ADHD, behavioral/conduct disorders, anxiety, depression, use of illicit drugs or alcohol or cigarette, autism spectrum disorders and even Tourette syndrome (a neurologic disorder characterized by tics {repetitive involuntary movements and vocalizations} are listed as affecting multitudes of our youth.

In any given year, according to the CDC article, up to one fifth of our kids and adolescents have a mental disorder, while inpatient admissions have sharply increased for both mental health and substance abuse problems, especially for "mood disorders," e.g., anxiety and depression.

But there may be a subset of marijuana-using/abusing youngsters that merits special attention.

A 2011 Harvard Health Publications (HHP) blog piece by the then editor of the series, a woman whose bachelors degree was not in a medical field, but had a brother who developed schizophrenia, is titled "Teens who smoke pot at risk for later schizophrenia, psychosis."

I was concerned that she might have a biased slant on the disease, but impressed, as I read her blog piece by the articles she cited.

But then I went back to the articles themselves, as I routinely do. The first was in the British Medical Journal in 20111 and was a population based cohort study, a comparison of two different groups. The outcome was the "incidence and persistence of sub-threshold psychotic symptoms after adolescence." The verbiage used was that the use (and especially the continued use) of cannabis was a risk factor for developing severe mental illness.

I'd read the study as showing kids who end up psychotic often have smoked (or otherwise used) marijuana.

The second article cited was from the Archives of General Psychiatry, again a 2011 publication and was a meta-analysis (a study of a number of articles). The authors reviewed a large number of published research studies, picked 83 of them which met their standards for inclusion and pooled the results for statistical purposes.

That's a common way to look at data in order to have enough of it to reach a significant conclusion, which in this case was that the age of onset of psychosis was 2.7 years younger in the group who used cannabis.

Once again, that's only an association, but not a proof of causation.

The third article came from Lancet (in 1987) and was the result of  long-term followup of 45,550 Swedish military conscripts. Those who had smoked pot more than fifty times had a much higher rate of developing serious mental illness.

I want to go back to the blog in Harvard Health Publication, because here's where I have to differ with the author. Her statement that, "So far, this research shows only an association between smoking pot and developing psychosis or schizophrenia later on" makes sense; she admits the data don't prove marijuana causes psychosis.

But in the very next paragraph, she compares this research to that on cigarette smoking first being noted to be associated with lung cancer and later found to be a major cause of that disease.

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Don't get me wrong; today's marijuana is reputed to be much stronger than that which was around when I was a young research fellow and volunteered time at the Long Beach Free Clinic. And some of the studies I've read in the last week would certainly make me want to caution a teenager with a family history of schizophrenia that pot smoking is really risky for them.

Maybe we're going to see an epidemic of the disease in those of our younger generation who smoke marijuana and don't any family history of schizophrenia or other major mental illness.

But I sure haven't see any data yet that convinces me that's going to happen.

Lyme disease: the battle continues

Wednesday, July 3rd, 2013
Stay away from ticks

Stay away from ticks

In April of 2012 I wrote a series of posts on tick-borne diseases. This is my 315th post so when the subject of chronic Lyme disease (called post-treatment Lyme Disease syndrome {PTLDS} by the CDC) came up in a well-balanced article in The New Yorker I needed to revisit what I had written 14+ months ago before I could determine if there was anything new on the subject.

It delineates the ongoing controversy which basically comes down to whether chronic Lyme disease actually occurs. Most academic physicians and organizations deny that this exists, but a large group of patents with a multitude of long-term symptoms have interacted with physicians who are willing to treat such an entity. They've formed an International Lyme and Associated Diseases Society who "argue that the traditional approach to diagnosis and treatment, put forth by most American physicians, all but guarantees failure."

A pamphlet from a group formed to fund-raise and increase awareness, the Lyme Action Network, is titled "It Might Be Lyme." The multitude of symptoms under this rubric is astounding as is the conclusion that years of (often intravenous and horrendously expensive) antibiotic therapy is needed to ensure a cure of the ailment.

The author of the New Yorker article was recently interviewed by Terry Gross on NPR. He comments that our current state of knowledge of the illness is incomplete, but notes that the symptoms of many of those who are said to have "chronic Lyme" are vague, commonplace and difficult to attribute to this disease when there are no positive tests and/or they don't live in region of the country known to have Lyme disease.

Let's start with a comment. I found only one medical article that shifted my point of view even a tad bit.

A research group headed by a Johns Hopkins-associated physician with infectious disease training published a study of patients with PTLDS symptoms in a journal I've never heard of before: Quality of Life Research.

His group enrolled 63 patients with the skin manifestation of Lyme disease and systemic symptoms (therefore people with pretty clear-cut diagnoses to fit the ailment) in a prospective cohort study. They followed this group and the control subjects for six months and saw each of them five times. After conventional treatment with a three week course of the antibiotic doxycycline all signs of Lyme disease went away, but after six months slightly over a third of the patents had new-onset fatigue, one fifth had widespread pain and 45% had neurocognitive problems (thinking issues that relate to a particular part of the brain).

This is the first article I've seen that prospectively followed patients with Lyme disease, but my caveats are: it was a small group (63 patients) with obvious Lyme disease and the followup period is relatively short.

I'd like to see a considerably longer prospective study of a much larger group.

Don't wait until the tick has finished its meal

Don't wait until the tick has finished its meal

The introduction to the article mentions that Lyme disease is caused by a spirochete bacteria (therefore a long, coiled member of the same family as the syphilis, but there hasn't been human to human spread that I'm aware of and of course, Lyme is not  a venereal disease). It is  the most common vector-borne (transmitted by a blood-sucking insect or arachnid (mites or ticks) infectious disease in North America. In 2009 nearly 40,000 cases were reported in this country, but most feel that there are likely at least 100,000 cases a year.

There are four other, less prevalent, illnesses that the deer tick vector can transmit, but funding for control of ticks is regarded as low especially when compared to that in Massachusetts for mosquito control in an effort to prevent other ailments, especially West Nile virus and eastern equine encephalitis.

Many academic physicians with infectious disease training feel strongly that Lyme disease should be treated with antibiotics for a month or less in most cases with an exception made for those who develop Lyme arthritis (who may require up to three months of treatment).

After realizing I hadn't done my due diligence, it was time to read lots of background material, including the article in The New Yorker. I downloaded the Kindle edition of Lyme Disease: The Ecology of a Complex System, a 2010 book written by Richard Ostfield, a Ph.D. field biologist.

This is a fascinating opus written from a different point of view, one of a scientist working at the Cary Institute of Ecosystem Studies, a private, not-for-profit in New York state with research focusing on the interactions among organisms that influence the risk of human exposure to vector-borne diseases.

Dr. Ostfeld outlines the natural history and ecology of LD and shows it is a much more convoluted ailment than I had realized. I had thought that the bacterium, the vector and the host were those I had read about, namely Borrelia burgdorferi, the black-legged tick and the white-footed mouse. But just focusing on the potential host species, chipmunks and shrews may carry the microorganism and the tick bites or tries to bite other animals, some of which are "less-efficient/competent reservoirs." So white-tailed deer and robins, depending on their abundance or lack thereof, may play a role in the likelihood of your catching LD, as may the terrain (e.g., densely forested versus subdivided into patches).

We had dinner recently with friends and one of the number was a physician who works for the CDC and has lectured extensively on Lyme disease. He feels quite strongly that the viewpoint of many of those who espouse long-term antibiotic therapy for LD is influenced by financial reward and that data is lacking to prove that this entity exists.

Allen Steele, the doctor who first discovered Lyme disease, now a rheumatologist at Massachusetts General Hospital, is the country's foremost Lyme disease researcher. These days he finds himself distrusted and sometimes harassed by those who feel Lyme disease often has chronic manifestations. A June 2, 2013 article in the Boston Globe highlighted the issue with its title "Drawing the lines in the Lyme disease battle."

I certainly don't agree with a fringe view  I found claiming that the LD bacterium was weaponized for bio-warfare.

At the end of my reading I side with the more traditional, academic view of Lyme disease. I think the other group has yet to prove its case.




Should I be taking aspirin?

Wednesday, January 30th, 2013

I take a dose equivalent to 1/4 tablet of aspirin

One of our friends recently told my wife she'd stopped taking aspirin after a news report linked regular use of the medication to macular degeneration. We've both taken 81 mg of aspirin a day and, after I'd heard that people may not absorb the enteric coated form well (and I couldn't find any other form in that size at the local drugstore), I'd ordered ten bottles of chewable orange-flavored aspirin online from Amazon.

Then I decided to read the medical reports that our friend's recommendation had been based on. She doesn't have a medical background and hadn't looked at the original data, but instead had seen a warning in a newspaper article. Let's start at The New York Times blog. On Dec 12, 2012 they published an article by Anahad O'Conner titled "Aspirin Tied To Rare Eye Disorder."

It's a very well-worded article written by a 31-year-old, Yale-educated Times reporter who writes a weekly science column and has published two books He notes the article he based his piece on was from JAMA with the lead author, Dr. Barbara Klein, being a professor of ophthalmology at the University of Wisconsin, Madison. Since I'm a UW graduate (BS 1963, MD 1966), I was particularly interested in her study.

It used data from the Beaver Dam Eye Study, started in 1988-1990 and concluded in 2010. O'Connor very appropriately noted this was an observational study, not a prospective, controlled research project. In other words a group of ~5,000, aged 43 to 84, agreed to have regular eye exams and reports were published after the 5-, 10-, 15- and 20-year followups.More than 300 publications have resulted from this project with data supporting a relationship of cataracts and age-related macular degeneration (AMD) to cigarette smoking.

Klein's paper stated that an estimated 19.3% of US adults take aspirin on a regular basis. It's commonly recommended for anyone who has had a heart attack (secondary prevention), but many   of us who've never had evidence of coronary vascular disease also take aspirin. This is primary prevention and is controversial with some data suggesting reduction of heart attacks in men over 45, but not women, although they may have a 17% reduction in stroke incidence.

A senior who has AMD may need a magnifying glass.

A January 21,2013 article from an Australian group reported a two-fold increase in AMD of a particular type, independent of smoking habits. Nearly a quarter of regular long-term aspirin users developed neovascular AMD, two and a half times the percentage of those who did not regularly take aspirin.

A 2001 paper in the Archives of Ophthalmology reported a randomized, double-masked, placebo-controlled study of low dose aspirin (one adult tablet every other day) plus 50 milligrams of beta carotene (a vitamin A precursor rated possibly effective in treating advanced AMD) among over 20,000 US male physicians aged 30 to 84 in 1982. The study was stopped after ~5 years due to a statistically extreme reduction (44%) in first heart attacks. There were fewer cases of AMD in those taking low-dose aspirin than in those who got the placebo.

There's also some data supporting aspirin's role in cancer prevention, especially in malignancies of the colon. Here the benefit was unrelated to aspirin dose (75 mg/day and up), but increased with age.

So let me look at my own risks: my dad had a large polyp in the earliest part of the colon, an area hard to see even on colonoscopy. It was initially felt to be benign, but later had some areas of low-grade malignancy. He also had macular degeneration in his remaining eye  diagnosed at age 90+ (the other eye having been removed nearly sixty years previously after a bad cut and a subsequent infection). My brother died of a heart attack at age 57 and my mother had a heart attack at age 74 with a cardiac arrest; (Dad resuscitated her and she lived to age 90).

The editorial that accompanied the recent JAMA article is thoughtful and impressive. Its title was "Relationship of Aspirin Use With Age-Related Macular Degeneration: Association or Causation?" and it concludes "From a purely science-of-medicine perspective, the strength of evidence is not sufficiently robust to be clinically directive." It then switches to a different viewpoint, the art-of-medicine perspective, saying maintaining the status quo is currently the most prudent approach, especially in secondary prevention (someone who has already had a cardiovascular event). For those of us who haven't, the risks versus benefits should be individualized based on our own medical history and value judgement.

I'm going to discuss this with my own physician but not stop taking a chewable 81 mg aspirin daily until I do.

Pain Pills and their ugly cousin: Part 1

Thursday, December 20th, 2012

I had a total knee replacement nearly twelve years ago. On the Orthopedic ward I was told I could have one or two strong pain pills every 4 to 12 hours depending on how much pain I was experiencing. Since I have a fairly high pain threshold I decided to take the minimum dose, one every twelve hours. I took the first pill, felt considerable relief from the pain, but also felt strange, so I stayed at that dose.

One way to flex & extend after a total knee replacement

Then I ran into a snag. My release from the hospital depended on the degree of flexion I could achieve in the leg with the new knee. Several times a day I was hooked up to a device that gradually bent my leg. It really hurt, but I toughed it out. The nurses and the physical therapists (PT) didn't seem to communicate with each other and I was a bit slow to catch on.

"You're not making enough progress," my surgeon said. "I think we'll have to extend your stay."

Something finally clicked in my mind. I was hurting enough so the ward staff hadn't set the machines degree of flexion higher. I decided to take two of the pain pills an hour or so before the PT appeared to check my ability to have the leg bent passively.

This time I was in no pain, although I did feel weird.

"You're doing much better today," she said. "I'll tell your doc you can go home tomorrow."

I had been given a strong pain pill, probably oxycodone and they were going to give me a prescription for several weeks worth to take at home. I asked, "Can I have extra strength Tylenol instead?" I repeated that request when I had low back surgery six months later.

Since that time there's been considerable controversy about strong pain medications. The initial question was whether physicians were under-prescribing for patients with severe pain, usually cancer-related, in fear of getting them "hooked" on the drug. Subsequently there have been at least two tidal shifts in how pain medicines are viewed, one urging more treatment of pain including giving the most potent meds for chronic non-malignant pain (CNMP) as well as for cancer patents (who clearly needed to have adequate pain control and weren't always getting it).

Very recently there's been a re-evaluation of the trend. I want to go back to the basics and then follow the timeline of expert opinion that's been expressed on the subject in the last two hundred years. But I'll begin much further back than that.

A 2008 article now available online and authored by staff from the National Development and Research Institutes and from the Department of Pain Medicine and Palliative Care at New York City's Beth Israel Hospital explored the treatment of chronic pain in depth. A few comments from that article surprised me.

a field of opium poppies

In Mesopotamia, nearly 5,500 years ago, Sumerian farmers cultivated a plant called Hul Gil which translates as the "joy plant." We call it the opium poppy. An August 2002 PBS special titled "Bitter Harvest" walks through how this plant is processed into the highly potent street drug, heroin, with at that time 13 million addicts worldwide The United Nations Office on Drugs and Crimes (UNODC) has a 2009 paper online estimating similar numbers. The major alklaloid (a usually colorless, complex and bitter organic chemical) in opium  was isolated in 1903 and named morphine (the Greek god of dreams was Morpheus). Then the Bayer company made a chemical from morphine and gave it the brand name Heroin.

Nowadays much of the world's crop of opium poppies is grown in Afghanistan. The 2009 estimate from UNODC was for $60 billion of the worldwide total of $68 billion.

But I've strayed away from my theme, which isn't street drugs, but prescription medications, so I'll stop here and get back to the synthetic opiods in my next post..


Prostate Cancer Controversies

Friday, September 7th, 2012

A prostate cancer awareness symbol

Prostate cancer is the most common cause of cancer death in older men. A few years ago most of us males over the age of forty (it seldom occurs before that) were periodically screened for the disease using the PSA test (a blood test for a prostate-specific antigen) and had digital rectal exams to check the size and consistency of our prostates whenever we had our yearly appointment for a physical and also had comprehensive lab work done.

Then things changed: the annual medical exam was discarded by most physicians in favor of a targeted examination, which in my case, with my history of high blood pressure, includes a nurse taking my BP and my doc listening to my heart and lungs. Not much else, unless I have a specific complaint. I'm 71 and haven't had a digital exam for five years. I had a PSA done when blood was drawn for other reasons and it was 0.7, well under the level that would have raised any concern about my prostate.

In October, 2011, the Harvard Health Blog provided two points of view on pending new recommendations for prostate-specific antigen (PSA) testing from the U.S. Preventive Services Task Force. A panel of experts after a thorough review of the literature on prostate cancer had concluded, that for men over 50, screening using the PSA test offered a low benefit to risk ratio. A huge controversy broke out with the American Urological Association arguing against the proposed new concept. Other physicians noted that an elevated PSA doesn't always mean cancer and, much more importantly, doesn't  distinguish which cancers of the gland are likely to be fast-growing and life threatening.

Oncologist, Dr. Marc Garnick, editor of Harvard's "Annual Report on Prostate Diseases," noted that the new testing recommendation was not a blanket statement fitting all men: those at higher risk (African-Americans and men with family history of cancer of the prostate) may still be suitable candidates for annual PSA testing. He later published an article in Scientific American mentioning that the use of regular PSA testing had led to over a million men having treatment for prostate cancer since 1985 and many thousands of men having complications of prostate surgery or radiation therapy (impotence, incontinence, rectal bleeding).

Dr. Garnick basically agreed with the task force's conclusions; felt the evidence supporting regular PSA testing was flimsy, but thought that the procedure gave important information after a cancer of the gland has been diagnosed.

Garnick was interviewed by a senior editor of the magazine and the resultant February 8, 2012, piece supplies audio comments from Dr. Garnick which detail some of the issues. One such concerns a man who has had his malignancy removed by a total (radical) prostatectomy. His PSA should plummet down to undetectable levels and, if it doesn't, either not all the cancer was excised or there has been spread beyond the local area (metastases).

I was reading my email a few days ago and noted one from my friend Rick with a link leading to an article from the Fred Hutchinson Cancer Research Center in Seattle titled "Prostate Cancer: 6 things men should know." There were six myths rebutted and I especially noted four conclusions: eating tomato-based foods and products doesn't prevent the malignancy; high testosterone levels don't correlate with risk of this tumor; omega-3s don't lower the risk (actually very high blood levels in one study were associated with higher risk); dietary supplements (selenium and vitamin E) don't prevent the disease.

At age 50 and above, this was on my schedule; at age 71 it's not

Another online publication from the Hutchinson Center gives background information on prostatic cancer. They note the frequency of the disease increases in men over 55, that obese men have a higher risk of developing an aggressive form of the disease, as do smokers. Those who drink red wine (four 4-ounce glasses a week) were noted to have a 60% lower incidence. Older men may receive unnecessary surgery; in this group the malignancy, often small and slow-growing, may not be life-shortening.

The need for screening in the general population of men is an ongoing medical controversy. We'll likely hear much more about PSA testing, but many would concede that a new type of evaluation needs to be developed.

I agree and for now I don't plan to have any more PSAs drawn.




DSM-5 on substance abuse

Monday, August 27th, 2012

Some take the pills; others use the rolled-up twenty to inhale illicit drugs

I'm home and working on my Mac laptop, so I can add a few links and photos to this post. Let's start with a New York Times article dated May 11, 2012 that caused a huge flap. Ian Urbina, a senior NYT reporter is no stranger to controversy, but his article titled, "Addiction Diagnoses May Rise Under Guideline Changes," prompted an unusually strong response from the American Psychiatric Association (APA), the group responsible for revisions to DSM.

Urbina interviewed a number of senior figures in the field and wrote that the new version by expanding the list of associated symptoms in alcohol and drug addiction, adding a new "gambling addiction" diagnosis, and possibly even pasting in an NOS (not otherwise specified) category for "behavioral addiction," could add as many as 20 to 30 million people to those fitting under DSM's umbrella of illnesses.

He quoted Dr. James H. Scully, Jr. the APA's Chief Executive Officer and Medical Director at American Psychiatric Association, as saying "The biggest problem in all of psychiatry is untreated illness and that has huge social (sic) costs."

Others with considerable stature in the mental health (MH) field had qualms. Dr. Allen Frances, head of the DSM-IV revision team, stated , "We'll see false epidemics and medicalization of everyday behavior". Researchers in Australia estimated 60% more people would be considered alcohol addicted under DSM-5's definitions, while a health writer at said the new manual could lead to 40% of college students being called alcoholics.

The APA responded with a bit by bit rebuttal of Urbina's article. They noted that DSM-5's terminology would be "substance abuse disorder," not addiction and expected early intervention could stop progression of the problems and therefore benefit society. The diagnosis itself would require more symptoms than in DSM-IV and those would have to produce clinically significant issues. They denied there would be a new NOS behavioral category other than gambling disorder and noted prior DSM versions had a variant of that diagnosis.

Referring back to the 2004 publication of the NESARC study (the National Epidemiologic Survey on Alcohol and Related Conditions) headed by NIH's Dr. Bridget Grant, PhD, PhD (she has a double PhD in psychology and epidemiology), the APA's Work Group noted their recent analysis of her 43,000-subject project  showed no significant change in prevalence. The APA feels it is our healthcare system, not our diagnostic criteria, that determines access to care. The new criteria would include gradations from mild to severe and their take is that this, not the distinction between abuse and dependence, is what is most crucial in improving both prevent and treatment. The APA feels the proposed new health legislation, not the changes to be seen in DSM-5, would expand quantity and quality of therapy.

Others have noted, however, that the APA makes ~$5 million a year from publishing the DSM and APA individual members could profit considerably from the increased number of patients the new guidelines could bring to their practices.

When does the cocktail-hour fan become the twenty-four-hour-a-day drunk?

The July 27, 2012 edition of Psychiatric Times had an article on "Substance Abuse in Aging and Elderly Adults." This arena is often overlooked or forgotten, but as of 2009 the "elderly" made up nearly 13% of the US population and a quarter of all prescription drugs sold in this country go to that group. When data from  a 2009 National Survey on Drug Use and Health performed by SAMHSA, the Substance Abuse and Mental Health Services Administration, were examined, there were marked increases in illicit drug use in older adults. For those over 50, alcohol is the most common substance abused, but opiates were the second ,while anti-anxiety drugs and skeletal muscle relaxants were also  on the commonly misused list.

The bottom line, I think, is that substance abuse is common, seen at all ages from youth to the elderly, and a significant problem in this country. There is considerable debate, even among experts in the field as to what criteria should be applied in diagnosing this problem and Dr, Allen's comments on the APA's role in crafting DSM should be taken seriously.

Mutating the deadly H5N1 flu virus

Saturday, May 5th, 2012

This ferret is healthy

There's been a recent controversy as to whether potentially dangerous medical information should be made available to the public. Now it's happened and I'm somewhat less concerned than I was a few weeks ago. The online version of Nature just published the work of the University of Wisconsin group on making the Highly Pathogenic Avian Influenza (HPAI) type A H5N1 virus transmissible from mammal to mammal, in this case ferrets.

This is potentially a terrible disease; it's killed 355 of the 602 humans (~59%) known to have contracted the HPAI A(H5N1) virus to date. None of those cases involved human to human spread of the flu bug involved. But that's roughly 600 times as lethal as an "ordinary" flu pandemic and more than 20 times as deadly as the 1918 flu.

So why am I less worried than I was?

When I read the article in Nature in detail (and it's tough slogging even for a physician), I realized that the virus, in the process of making it capable of airborne transmission, had also been made less virulent. None of the ferrets used as research subjects died of the disease . The new virus was also found to be preventable by a vaccine and treatable with one of the existing anti-flu medications.

The other thing I quickly understood is this is not a process that the average man (or woman) on the street or even the vast majority of scientists and/or physicians could duplicate. It involved an enormously complex set of laboratory procedures, many of which would demand long-term expertise and experience in the field. Theoretically a virology lab could be influenced by links to a terrorist group or have their own "ultra-green" agenda; neither possibility sounds at all likely to me.

The other paper, detailing the work done on HPAI A(H5N1) in Rotterdam, is yet to be published. That one has me more concerned, but I've just read a paper "Dangerous for ferrets: lethal for humans?" that carefully explores the question involved.

The authors reminded us that a previous paper had discussed the recreation of the so-called Spanish flu virus that killed 50 million worldwide in 1918. I'll write about that in detail some other time, but when that publication appeared, its authors were hailed as heroes, not as dolts.

The work of Ron Fouchier, a senior figure at the Erasmus Medical Center in Holland took the virology world by storm. He first announced his group's alteration of H5N1 at an international meeting in Malta in September, 2011. Initially his variant of the flu virus was thought to be much more deadly to ferrets than the UW bug. A May 3, 2012 paper in Time Healthland discusses the infighting among scientists that followed, but notes that Fouchier's paper should be out in the magazine Science in the near future.

Apparently Fouchier's mutated virus also turned out to be less of a ferret-killer than was initially thought.

There's the normal flu season and the other kind

But that's not the major issue here. Most of those working in the virology field feel a natural mutation of H5N1 or H1N1 or other flu strains is more to be feared than anything produced in a lab. Yet the relatively benign 1977 H1N1 flu pandemic, so-called Russian flu, may have escaped from deep freeze in a lab.

Every year has its flu season; some are much worse than others.



Tick-borne Disease part four: the chronic Lyme Disease controversy

Monday, April 30th, 2012

Sometimes you need an expert panel to resolve a controversy

A March 27, 2012, Wall Street Journal article, "This Season's Ticking Bomb,"predicted that the unusually warm weather most of the country has been experiencing meant we would also see many more cases of tick-borne diseases, If you click on the link, be sure to look at the section called "View Interactive" to get to a series of suggestions on reducing your family's risk of tick bites.

The article itself talked mainly about Lyme disease. There is an International Lyme and Associated Diseases Society (ILADS), but much of their Lyme disease website information was from 2006.  They are on one side of a major medical controversy, how to care for patients who have had Lyme disease and continue to have problems, especially with short-term memory, fatigue, or musculoskeletal issues, well after they have been appropriately treated with short-term antibiotics.

Two articles were published on this subject in 2007-8: the first one, "Chronic Lyme Disease: an appraisal"  is available online; the other, "A Critical Appraisal of Chronic Lyme Disease," appeared in the New England Journal of Medicine.

The real question is whether the bacteria involved, Borrelia burgdorferi, remains in the body of a patient after relatively short-term antibiotic therapy and if a considerably longer course of drug treatment is warranted. The ILADS says, "Yes" to both questions and refers back to a Harvard & Tufts study published in the Annals of Internal Medicine in 1994.

The most recent CDC online information states that 10 to 20% of those who receive standard therapy for Lyme disease will have some lingering symptoms. However they term this "Post-treatment Lyme disease Syndrome." I found that European cases of Lyme and similar diseases are usually caused by our Borrelia borgdorferi's cousins; data from that literature may not be relevant here.

In November 2006, the Attorney General of Connecticut (CAG) pushed the Infectious Disease Society of America (IDSA) into a detailed review of their Lyme Disease guidelines by starting an investigation to decide if they had violated existing antitrust laws. By April 2008, the IDSA and the CAG agreed to end the probe by convening a review panel, with members from Duke, the NIH, Dartmouth, the U.S. Navy, Baylor, Tulane and other centers, to decide if the original guidelines had been based on sound medical/scientific evidence and if they needed changes. An MD, PhD medical ethicist screened panel members for any conflict of interest. A public hearing was held to include other viewpoints. The Final Report of the Review Panel was published in April, 2010.

Some will think the decision ties their doc's hands.

It basically upheld the 2006 IDSA guidelines, but added 1). In some cases (non-pregnant adults or kids 8 or older who've had a tick of the Lyme-carrying species attached for 36+ hours in an area with high infectivity rate of ticks with B. burgdorferi), a single dose of doxycycline (if they have no allergy to this drug) may be given  if the tick was removed within 72 hours; 2). Antibiotics are appropriate for adults and children 8 or older with early, uncomplicated Lyme disease; 3).  "Reports purporting to show the persistence of viable B. burgdorferi organisms after treatment with recommended regimens for Lyme disease have not been conclusive or corroborated by controlled studies." and 4). "The risk/benefit ratio from prolonged antibiotic therapy strongly discourages prolonged antibiotic courses for Lyme disease.

And at the end of the report, they mentioned a disease I'd never heard of; I'll do some more reading and write about it later.





Medical Waste: Part two

Sunday, April 15th, 2012

this ECG is normal

In my last post, about trying to decrease the incredible expense of US health care, I gave a link to the ideas Dr. Donald Berwick had outlined in the April 11th edition of JAMA. He thinks we could save huge amounts in six areas: failure of care delivery; failure of care coordination; overtreatment; administrative complexity; pricing failures and fraud & abuse.

Now I'd like to look at a few specific examples.

The same JAMA edition had a research article titled "Association of Major and Minor ECG Abnormalities with Coronary Heart Disease Events" It detailed the followup of nearly 2,200 people in my age range and up (they were 70 to 79) who were in the Health, Aging and Body Composition Study. Thirteen percent had electrocardiograms with minor changes when the study started; twenty-three percent had more significant changes. Both kinds of ECG changes were associated with an increased likelihood of having coronary artery disease (CHD) during the subsequent years.

Now ECGs are relatively cheap and can be done in many settings. But the senior author, Dr. Reto Auer, said in an interview for a publication called heartwire "Our data do not permit one to say anything about clinical practice." The article itself concluded, "Whether ECG should be incorporated in routine screening of older adults should be evaluated in randomized, controlled trials."

In the same edition of JAMA a Northwestern University Preventive Medicine professor, Dr. Philip Greenland, commenting on Auer's research, mentioned a 1989 summary of the value of the "resting ECG," which said additional study was needed. Dr.Greenland said the major finding in Auer's work was a relatively new measurement called the net reclassification index (NRI). As opposed to diagnostic studies (e.g., does this patient have heart disease), this study hoped to be prognostic, telling what the chances were of a major heart event occurring in the future to a particular study subject. In this case the NRI helped most in reclassifying people into a lower CHD risk group, not a higher one.

All of that is fascinating and the Auer article is a superb example of carefully performed research. But, my fear is that many physicians won't read the caveats. If you ignore the last paragraph, skip the editorial and never get to "'s" take on the work, you may well decide that every older adult should have an ECG done on a regular basis.

What should we do if your cholesterol is high?

In the same edition of the journal is a pair of short articles deliberately set up to examine a medical controversy, in this case whether a middle-aged man with an elevated cholesterol, but no personal or family history of coronary heart disease should be given statin drugs to lower his cholesterol. This is a new feature of the journal, and the accompanying editorial, with the intriguing title, "The Debut of Dueling Viewpoints," explains this will be a continuing series of discussions and debates.

What a wonderful idea.





The the online publication, actually had a nice summary of the two pieces,