There’s Silver in Them There Pills

December 25th, 2013

Like most medically-trained people (and hopefully many of the rest of us), I’ve been highly concerned about the rise of drug-resistant microorganisms, bacteria that can’t be treated with our standard antibiotics. A recent article in The Wall Street Journal with the intriguing title “Antibiotics of the Future” offered considerable hope, but let look at some background on the subject first.

The WSJ article said that two million patients each year in the United States develop infections that doctors can’t combat with our normal antibiotics; earlier in the year, the CDC in a report titled “Antibiotic Resistance Threats in the United States 2013” estimated that at least 23,000 of them die. They divide the microorganisms, all bacteria except for Candida (a fungus), into three groups: those whose threat levels are considered urgent, serious or concerning. The three in the urgent category include Clostridium difficile, which causes severe, life-threatening diarrhea, often in patients who have been hospitalized and are already on antibiotics, and leads to a quarter-million infections, 14,000 deaths and a billion dollars in medical expenses yearly. Then there are the carbapenem-resistant Enterobacteriaceae,  abbreviated as CRE (the carbapenems are powerful antibiotics considered the “drugs of last resort,” used when all other old and modern antimicrobials fail or are thought to be likely to fail; Eneterobacteriaceae are bacteria that are part of the normal gut flora.)

CRE infections most often happen in patients getting treatment for other serious conditions. They may be on a respirator, have a long-term catheter in their bladder or have been on other antibiotics. One estimate says there are 9,000 CRE infections a year and they cause at least 600 deaths. Patients in intensive care units not infrequently have IV catheters placed in large veins in the neck, chest or groin to allow hospital personnel to give medications and draw blood sample for a prolonged period of time. If these get infected they can cause a bloodstream infection (sepsis is the medical term). About half of all hospital patients who get CRE that goes on to cause a bloodstream infection die.

The third infectious urgent threat level is the bacteria, Neisseria gonorrhoeae, that causes the STD gonorrhea. The CDC estimates more than 800,000 cases occur yearly in the United States and 30% of these are resistant to some antibiotic, but almost all can be treated, at this time, with a two-drug cocktail. Gonorrhea causes severe reproductive system complications and the CDC says it “disproportionally affects sexual, racial and ethnic minorities.”

Then there is MRSA, methicillin-resistant Staphylococcus aureus. This bug is classified as serious, not urgent, yet there are roughly 80,000 severe MRSA cases a year and over 11,000 of these patients die. Most major MRSA cases are seen in healthcare setting among patients with weakened immune systems (e.g., those on hemodialysis or receiving cancer therapy) but less serious MRSA  can case problems in otherwise healthy people, including athletes who share towels or razors, children in day-care and members of the military in cramped quarters. Some of these infections, usually of the skin, can become severe and life-threatening.

The CDC piece, except for Candida, excludes non-bacterial diseases, but I received a reader comment a while back from a person whose website (Mphonline.org) has a post on Deadly Viruses.  Like parasitic diseases, e.g., malaria, viruses through the ages have killed simply enormous numbers of people. Now we’re facing a future when bacterial illnesses could overtake their status as the prime infectious threats to mankind.

An article in the December 23, 2013 online version of the New York Times described an increased death rate among dolphins, with many dying of viral disease. A number of them also showed evidence of antibiotic resistant bacteria, presumably from environmental contamination. Dolphins have been termed the modern equivalent of the canary in the coal mine, a biological early warning system analogous to the times when miners used to carry caged canaries while at work; if there was any methane or carbon monoxide in the mine, the canary would die before the levels of the gas reached those hazardous to humans.

The New England Journal of Medicine in January, 2013published an article titled “The Future of Antibiotics and Resistance.” The lead author, Dr. Brad Spelberg, works where I did my research fellowship. He and two colleagues mention that antibiotic-resistant bacteria are considered, in a major yearly publication by the World Economic Forum  (WEF), to be a leading risk to human health.

The World Economic Forum’s (WEF) 2013 publication on Global Risks analyzed fifty possibilities (e.g., economic disparity, religious fanaticism, rising greenhouse gas emissions, terrorism, water supply crises), examining their likelihood over the next decade, the impact if they actually happen and how interconnected they were to each other.  It used those to generate analyses of three major risk cases: one was on the threats to economic/environmental systems, a second on so-called ‘digital wildfires” from misinformation, and  The Dangers of Hubris on Human Health, devoted to antibiotic-resistant bacteria.

In a study done in Europe, 50% of French patients experiencing a flu-like syndrome (FLS) expected their physician to prescribe an antibiotic; FLS may be caused by influenza virus or other viruses and antibiotics are not of any use against these viral diseases. The WEF piece mentioned an article reporting 98% of Chinese children seen in a Beijing pediatric hospital for common colds were given antibiotics.

Huge quantities of antibiotics are being used for animals as well.  Animals being raised for their meat are often given antibiotics as growth promoters. A 1950 article in Science News announced results from Lederle Laboratories that lacing the hog feed with trace amounts of an antibiotic could increase the yield of meat by a half. Then in 1977 the FDA sent out a notice that it would withdraw approval of non-medical use of penicillin and tetracyclines, but no hearings on the subject followed that non-binding pronouncement.

A Federal District judge finally ordered those FDA hearings in 2012, but an article online less than two weeks ago said only suggestions to the animal-growing industry have resulted. In 2009, more than 3,000,000 kilograms of antibiotics were given to US patients; in 2010, 13,000,000 kilograms were used for animals.

Back to the Wall Street Journal article: it mentions four new approaches to treatment of these deadly bugs. The two I found most intriguing were research to befuddle the bacteria by working against the signaling chemicals they use to become infectious and using silver to increase the ease with which antibiotics enter the microbes.

There’s a way to go before these concepts are translated into bedside medicine, but there is more than a glimmer of hope on the horizon.

 

Noise-Induced Hearing Loss and Acoustic Trauma

December 14th, 2013

I was in the gym recently and, after riding a recumbent bike for a little over an hour, went to the mats to do some stretches. There’s usually a class in the room on the other side of a wall and I could see young women exercising in a karate-like manner. But what immediately caught my attention was their background “music,” vaguely familiar and incredibly loud. That wasn’t the first time I’d heard an ear-threatening sound level coming from that room, but it clearly was the worst. It reminded me off a rock concert I went to many years ago.

I wondered how many of the class members had been exposed to that intensity of sound repeatedly and if it had caused them problems. Then I thought about the instructor who must hear the noise many times a week. I couldn’t tell if she was wearing any ear protection, but doubted it.

Later in the day I mentioned the episode to my wife Lynnette who wears hearing aids and is at the gym for Pilates at least three times a week. Sometimes her class has music, playing at a much lower decibel level, but when it does she has mentioned difficulty in hearing the leader’s voice calling out what move comes next. She said the women’s locker room, again a wall away from the class exercise area, almost shakes when that  other group is in session.

When I thought about the noise levels I sometimes hear (noise is defined as “unwanted sound”); one of the loudest forms is often coming from a car next to me at a stop light with a youngster listening to music while leaving the windows of their vehicle open. I guess that’s so we can all listen to their choice of music.

I went back to the basics, trying to understand just how loud that studio must be compared to other environments where noise levels can be dangerous to our hearing and our brains.

Noise is measured in decibels (dB), named after Alexander Graham Bell who invented the “electrical speech machine’ we now know as the telephone. The subject took me back to the physics of sound and its perception.When you hear a sound, anything from a whisper to a gunshot, your ears and brain are involved in a complex process that begins with an object, let’s say a gong, vibrating in something. That something could be solid, liquid or gaseous, but to simplify even a bit, we’ll assume it’s ordinary air (I’ve never heard of anyone hitting a gong underwater, so that’s a reasonable assumption.)

The anatomy of the middle and inner ear.

The anatomy of the middle and inner ear.

The frequency of the vibrations (in this case how rapidly the metal moves back and forth) is the determining factor in the pitch of the sound, but the energy of the vibration determines its loudness. So if you strike a gong hard, it emits a louder sound than if you barely touch it. The vibrations move tiny particles toward your ear which acts as a funnel to bring the sound energy to your eardrum, through a series of tiny bony connections to your inner ear.

The minuscule bones, technically the malleus, incus and stapes, but usually called the hammer, anvil and stirrup, amplify the pressure the sound exerts on your ear drum, enabling the next step in the hearing process, motion of fluid in a structure called the cochlea. This is a snail-like spiral with three tubes separated by membranes and tiny hair cells that transmit the sound as electrical impulses to your brain.Which hair cells are moved lets your brain know the pitch of the sound; how many hair cells are moved allows the brain to know how loud the sound was.

Here’s a link to a loudness comparison chart. The softest sounds we can hear (e.g., rubbing one finger over another next to an ear) are said to be zero dB, but if you whisper to someone a few feet away, the sound is somewhere between 15 and 30 dB. The scale in logarithmic, so 10 dB is 10 times as loud a zero, 20 dB is 100 times as loud and 30 dB is 1,000 times as loud. Talking  at a normal volume to a friend who is three feet away generates a 60 dB sound, a million times as loud as zero dB. Yes, that amazes me too.

Don't sit in the front row.

Don’t sit in the front row.

So the next time you (or your kids or grandkids) want to buy front row tickets to a rock concert, remember the sound level will be 115-120 dB. I had recently  seen an article on the subject of noise-induced harm in The New York Times. Its title was “Fighting Hearing Loss from the Crowd’s Roar.” Fans at several professional football games had broken a Guinness World record for the loudest crowd noise level. The first game’s crowd screamed at a measured 136.6 dB; a short time later, another team’s fans registered a 137.5 dB roar.

I found a 2001 ENT grand rounds presentation on “Noise-Induced Hearing Loss” from UTMB, the University of Texas Medical Branch. Nearly one-third of Americans with hearing loss, roughly 10 million total, had impaired hearing due to noise. It is the most common preventable cause of permanent hearing loss. Other, more recent comments, mention associated tinnitus (ringing in the ear) and hyperacusis, sensitivity or intolerance to sound, as associated effects from excessive noise.

If your ears are exposed to even less intense sounds over a period of time, the hair cells and their blood vessels, supporting structures and even nerves can be damaged. The loudest recommended exposure with hearing protection is 140 dB and OSHA, The Occupational Safety & Health Administration sets legal limits for sound intensity in workplaces at 90 dB average over an eight-hour day. If the sound is even louder, the permissible time exposure is shorter; it’s cut in half for every 5 dB increase in noise level. So if you work in an environment where the sound intensity averages 100 dB, OSHA would say you should have a two-hour shift.

Another federal group, the National Institute for Occupational Safety and Health (NIOSH) sets its eight-hour cutoff at 85 dB and halves that time for every 3 dB increase. So at 100 dB, NIOSH recommends your shift should only last 15 minutes!

This old cannon might explode if it were fired. Don't be nearby!

This old cannon might explode if it were fired. Don’t be nearby!

A sudden, exceeding loud noise can also cause a long-term hearing deficit; this form of noise-induced hearing loss is often called acoustic trauma. An explosion or a cannon going off  near to you might be examples, but other noises in the 130-140 dB range can be responsible for this form of damage to your hair cells.

For the past thirty-two years OSHA has mandated a Hearing Conservation Program to protect every worker in general industry who is exposed to 85 dB or more over an eight-hour shift. It includes baseline and yearly free hearing exams, free hearing protectors, training in their use and evaluation of their adequacy.

But a discotheque may have a 110 dB sound level and even using the OSHA limits, much less the NIOSH levels, you shouldn’t be exposed to that level of noise for more than a half hour.

So it’s wise to stay away from very intense noise levels, especially outside of your work environment, in places where those OSHA rules don’t protect you.

I’m afraid that many of our younger generations will lose their hearing as they are exposed to noise levels we once would have thought to be rare.

 

 

Medical Marijuana 2: immingrants to Colorado

December 8th, 2013
Smokeable pot or marijuana  brownies is what most officials feared.

Smokeable pot or marijuana brownies is what most officials feared.

This morning’s edition of The New York Times had an interesting article on marijuana migrants to Colorado. These aren’t people looking for recreational pot, they’re parents of kids with intractable seizures. In August, Dr. Sanjay Gupta, a neurosurgeon who was President Obama’s initial choice as U.S. Surgeon General in 2009 (he’s now CNN’s chief medical correspondent), published a bombshell article in CNN Health with the title, “Why I changed my mind on weed.” Gupta had previously published a 2009 Time magazine article, “Why I would vote No on Pot”, but then undertook an extensive review of past efforts pro and con marijuana. He discovered that the 1970 decision to make the drug a Schedule 1 substance was not based on solid evidence of addictive properties and lack of medical efficacy, but rather on the absence of studies and, presumably therefore, was a political choice, not a scientific one.

The problem, of course, is by making pot Schedule 1, those studies could not be easily done, if at all.

Gupta refers back to a 1943 study in New York City under Mayor LaGuardia. The medical arm of that research concluded smoking pot neither led to addiction nor was it a “gateway drug,”

Gupta also reviewed a huge number of relatively recent U.S. studies of the drug; interestingly, 94% of them were designed to show the dangers of marijuana and only 6% looked at its benefits.

I did find a 2009 article in The Journal of Clinical Investigation, a premier research journal, with the arcane title “Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells,” Like most JCI articles it was quite complex, but the bottom line was the scientists involved (from Spain and from Harvard) concluded THC, one of the major chemicals in marijuana, may be useful in fighting cancer. They did not suggest cancer patients should smoke pot!!!! Rather, a chemical pathway uncovered in the study could lead eventually to anti-tumor therapies.

A recent review of research studies on the use of cannabinoids (marijuana contains over 500 of these chemicals with THC and CBD being the most significant) for seizure disorders was titled “Slim Evidence for Cannabinoids for Epilepsy.” It noted that marijuana appears to have an anti-epileptic effect in animal studies, but we don’t know yet if that’s true in people. The extensive literature review only found four human studies, none of high quality, and concluded no reliable conclusions could be drawn at the present time. But CBD appeared to be safe for the relatively short time it was given in these projects.

High quality studies clearly need to be done in this arena.

So why did Dr. Gupta change his mind?

In the first place he felt Americans had been misled by the 1970 decision to classify marijuana as a Schedule 1 drug. And then there is Charlotte’s Web, an oil said to be low in THC (the chemical which leads to a pot “high’) and chock-filled with CBD which has no psychotropic effects, but appears to have a variety of positive medical effects.

In 2006 a Colorado woman gave birth to twins, one of each gender. When they were only 3 months old, the girl started having seizures, first one, then many. The doctors said her scans and blood tests were normal, but eventually, when she was two and a half, a neurologist at Denver Children’s Hospital she had found a rare genetic mutation associated with an intractable type of epilepsy. Another specialist put the child, Charlotte, on a special diet sometimes useful in drug-resistant epilepsy.

A plethora of side effects and, two years later, the return of multiple seizures, drove her parents to a relentless hunt for something that could stop her convulsions. Eventually they heard of a California boy being treated with a cannabis product for the same rare syndrome as their child.

Colorado law demanded two doctors approve her application for a medical marijuana card. Charlotte’s mom found a Stanford-trained MD, PhD and a Harvard-trained internist who had significant reservations because of Charlotte’s age, but felt all other treatment options had been tried. Both signed the card.

An initial dose of a low-THC, high-CBD product in oil form from a Denver dispensary gave incredible results…no seizures for the first week of treatment. But the oil was in short supply and expensive.

And it's not the optimal form for medical use.

This is not the optimal form for medical use; the high CBD oil may be.

Enter the Stanley brothers, six men who owned a large marijuana dispensary and grew their own plants. They had developed another marijuana-derived oil that was low in THC, while containing lots of CBD. They had also started a nonprofit, the Realm of Caring Foundation, to provide cannabis and its derivatives to those who had major diseases (cancer, MS, seizures, Parkinson’s), but were unable to pay market prices for the substances.

Fast forward to Charlotte at age six, having seizures in her sleep only two to three times a month (versus up to 300 a week). Her neurologic status has markedly improved and the oil she takes has been named after her. Dr. Gupta visited her and other patients who have had similar results.

Not all find their panacea in Colorado medical marijuana derivatives, but one of the two physicians who signed Charlotte’s card, working with Dr. Edward Maa, an assistant professor of neurology at the University of Colorado School of Medicine, has accumulated a series of eleven such children with drug-resistant major seizure disorders and eight had a decline in seizure frequency of 98-100%. The data is about to be presented at an American Epilepsy Society meeting.

There’s another side to the Colorado story, a familiar and sordid one. An August, 2013 article in The Denver Post was titled “Oversight of Colorado medical marijuana doctors remains spotty.” It detailed a sting operation which led to a conviction of a Loveland physician who prescribed marijuana for an ankle sprain ten years past and for back pain even the patient said wasn’t present. The two state governmental agencies who should be providing oversight of those doctors who provide medical marijuana prescriptions have largely been inactive.

The Colorado State Health Department has referred the names to the board of medicine of a very small number of physicians who account for an inordinate percentage of medical marijuana recommendations . They say these are the outliers, implying the vast majority who prescribe the drug are doing in an ethical and appropriate manner. I’m not so sure that is true and a law enforcement officer has been quoted as saying, “Very little has occurred to any of these physicians until now.”

To complicate matters, Colorado voters (and those in the state of Washington) in November, 2012, approved the use of recreational marijuana for anyone over 21 years old. The Justice Department response is captured in an online article “Tolerating Pot With a Frown.”

I think medical marijuana is here to stay; we’ll see how many careful studies get done to determine who should get actually it.

 

 

 

 

 

 

 

Medical Marijuana: Politics versus Science

November 27th, 2013
Marijuana in its raw form.

Marijuana in its raw form.

I recently read a New York Times article by Jane Brody titled “Tapping Medical Marijuana’s Potential” in which she notes the long history of medical, spiritual and recreational use of the drug and mentions it contains  a multitude of chemicals (400 plus) in its raw form.  She confirmed my thought that if people are to use the drug for medical reasons, a joint or a pipe certainly isn’t the optimal modality for administering it, When smoked, the number of compounds released multiplies by a factor of five (over 2,000 chemicals) and some are felt to lead to risks similar to those of tobacco.

As of November, 2013, twenty states and the District of Columbia have medical marijuana clinics; two states have even legalized its recreational use and a Gallup poll in October reported fifty-eight percent of Americans support legalizing marijuana for non-medical purposes. That’s way up from the 12% in 1969 and roughly a third at the start of the 2000s who favored changing the laws concerning marijuana. Subgroups in this survey that still opposed legalization were those sixty-five and older and those who identified themselves as Republicans ( 62% of Democrats and 65% of Independents {up 12% since 2011} favored the change). Even the over sixty-five group had a considerable (+14%) increase in the last two years of those who are in favor of loosening the laws on the drug.

I’m going to stick to comments on medical marijuana, and not get into a discussion of recreational use.

Cornell University Law School’s Legal Information Institute website details 21 USC § 812 Schedules of Controlled Substances. There are five levels of these drugs (or substances) and the most tightly controlled is Schedule I, drugs/substances (D/S) with a high potential for abuse and no currently accepted medical use in treatment in the United States. Additionally there is a lack of accepted safety for those D/S even if they are given under medical supervision. There’s a long list of  Schedule I drugs including heroin, LSD, mescaline and GHB (the date rape drug). But marijuana is right alongside those, mostly for political, as opposed to scientific reasons.

Schedule II D/S  have a high potential for abuse, but do have a currently accepted  medical use in this country, some with and others without severe restrictions. Abuse can lead to severe psychological or physical dependence. Opium and cocaine are in Schedule II. Schedule III D/Ss have less potential for abuse, a currently accepted medical use and abuse can lead to moderate or low dependence. Amphetamine and its derivatives are in Schedule III. As you would expect, Schedule IV and V D/S have lower potential for abuse and habituation.

In 2005, the U.S. Supreme Court, discussing California’s medical marijuana regulation (voted in under the 1996 Proposition 215) in  a case titled Gonzales v. Raich, issued a majority opinion that Congress had the power to prohibit local cultivation and use of marijuana in that state. They did so by case precedent under the Commerce Clause referring back to a 1942 decision about wheat farming. Justice O’Connor, Chief Justice Rehnquist and Justice Thomas dissented with Justice O’Connor writing that the Court’s decision was sweeping overreach. She noted the two women who had sued the US Attorney General and the DEA were, in one case, raising a very small number of marijuana plants and, in the other case, relying on locally grown plants. Neither one was engaged in interstate commerce nor even conceivably had enough of the drug to substantially affect such. Both were acting in accordance with California law.

In 2008, an article in CMAJ, the Canadian equivalent of JAMA, reviewed safety studies on marijuana used medically and noted that short-term usage of the then existing forms of medical cannabinoids “appeared to increase the risk of non-serious adverse effects (the most common being dizziness), but not serious ones. The problem was the risks in longer-term use weren’t well defined, even in that country which had been the pioneer in 2001 by legalizing medical usage of the drug.

2009 Department of Justice memorandum, directed at “Selected United States Attorneys,” discussed “Investigations and Prosecutions in States Authorizing the Medical Use Of Marijuana.” It firmly held to the DOJ being committed to enforcing the Controlled Substances Act (CSA) in all states, saying Congress still felt marijuana was a dangerous drug; its illegal distribution and sale was a serious crime and its sale provided gangs and cartels with oodles of money. While adhering to the CSA was still a clear priority, DOJ felt federal resources should not be expended in the pursuit of individuals who use marijuana medically in compliance of state laws.

An April, 2010 article in NEJM, written by two attorneys from the University of Maryland School of Law, mentions that the American Medical Association had recently voted for reviewing marijuana’s status as a Schedule I drug. At that time, fourteen states had passed laws to allow the medical uses of the drug and over a dozen more were considering the idea. But there was very little if anything being done to “advance the development of standards” concerning dosing, packaging, potency, quality or purity issues. Experts in this country had urged reclassification to Schedule II as a means to allow rigorous testing of possible benefits, dosing and delivery means.

In early 2012, Mayo Clinic Proceedings published two articles and an editorial on Cannabis. The first article reported a case series of 98 patients with “Cannabinoid Hyperemesis.” The first term meant chemicals found in marijuana and the second implies severe, persistent vomiting. The more common use of the medical term refers to the one to two percent of women who have continued, severe, nausea and vomiting during pregnancy…a condition termed hyperemesis gravidarum (gravid means pregnant).

How much THC is in this joint? Who knows?

How much THC is in this joint? Who knows?

A superb, long and detailed review by J. Michael Bostwick, MD of Mayo’s Department of Psychiatry and Psychology has the intriguing title, “Blurred Boundaries: The Therapeutics and Politics of Medical Marijuana.” and is available on an NIH website. It is well balanced and covers many facets of the history and pharmacology of the drug with caveats on its use in young individuals, an association with psychosis (marijuana may or may not be causative, but its use appears to have a distinctly negative effect on those already psychotic), the pros and cons of using it medically, and the currently available pharmaceutical cannabinoids.

The New York Daily News, on January 22, 2012, had an article titled “Marijuana-based drug Sativex may get FDA approval.” A followup published August 14, 2013 in an industry online news source, Fierce Pharma, said the European pharmaceutical firm GW now had an American partner company working with the FDA on a Phase III trial for the drug in treating cancer pain and spasticity in multiple sclerosis patients. The oral spray has already been approved for patient use in the U.K., Canada, Denmark, Poland, Austria and Sweden. It has a mixture of THC, the psychoactive component, and cannabidiol, a non-psychoactive cannabinoid that can lessen the negative effects of THC while, potentially, offering reduced anxiety and anti-seizure effects of its own.

An October 3, 2013 article in Time Magazine’s World section was titled “Canada Rolls Out a ‘$1 Billion” Privatized Medical Marijuana Industry.” Medical marijuana has been legal in Canada for more than a decade but was strictly regulated. In a country whose population as of July, 2013, was estimated to be just over thirty-five million (versus the United States’s November, 2013 estimate of 317 million), there are almost 40,000 registered medical marijuana users. The Canadian government thinks that there will be over eleven times that number by 2024 and has recently voted to shift to private companies, as opposed to Health Canada, controlling the drug’s distribution by mail-order, but still under tight restrictions.

What next in the sweeping changes concerning marijuana? I’d like to see well-controlled prospective medical studies, but those can’t happen until (and unless) it becomes a Schedule II drug.

 

 

 

 

STARI or a Lyme Disease variant?

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

Here’s the spirochete you definitely don’t want to have..it 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.

Macular disease, cataracts and art

October 24th, 2013

My wife and I are supporters of two art museums, one locally and the other in Denver. I also have a personal interest in eye problems, especially cataracts and macular disease, as my father had lost an eye as an intern (a paper cut led to an infection and, in those days, before antibiotics, there was concern about the other eye developing problems, a medical issue called sympathetic ophthalmia). In his late 80s he had a cataract in his remaining eye and, when he was examined by an ophthalmologist at the Cleveland Clinic, was found to have macular degeneration, a chronic eye disease  usually seen in people over 50.

Someday my visions may deteriorate to this point.

Someday my visions may deteriorate to this point.

I became aware, as I read about Dad’s problem, that one day it might become mine as well; one of the risk factors for macular degeneration is a family history of the disease.

I’ve pasted in a list of symptoms from this condition (copied from a Mayo Clinic website).

  • The need for brighter light when reading or doing close work
  • Increasing difficulty adapting to low light levels, such as when entering a dimly lit restaurant
  • Increasing blurriness of printed words
  • A decrease in the intensity or brightness of colors
  • Difficulty recognizing faces
  • A gradual increase in the haziness of your central or overall vision
  • Crooked central vision
  • A blurred or blind spot in the center of your field of vision
  • Hallucinations of geometric shapes or people, in case of advanced macular degeneration

The National Eye Institute, a branch of the NIH, has a fact sheet on age-related macular degeneration (AMD) that’s worth looking at if you or someone in your family develops this problem. I’ll mention a few things from that website as AMD is a major cause of vision loss in older adults. To begin with the macula is the part of your eyes that gives you the sharpest, most detailed vision. It’s the extremely sensitive part of the retina, the layer of tissue  at the back of your eye that responds to light, converting images, focused by the eye’s lens on this equivalent of camera film, into electrical signals that travel via the optic nerve to the brain. If the macula is damaged, fine points of these images become less clear.

If this happens to a non-artist, someone who doesn’t make their living through images they put into a form that others can enjoy, it still leads to less sharp vision. You may have problems reading, driving or recognizing an image such as a face. Since your peripheral vision isn’t affected, you’ll probably be able to walk around without major difficulty.

But image that you’re an artist. You gradually realize your vision is becoming less clear. You used to be able to read an eye chart at the 20/20 level, meaning you can read the same row of small letters on the chart at 20 feet which those with normal vision can. Now your visual acuity, measured when you see your eye specialist, is slipping and you worry that it will affect your ability to paint as well as you once did.

Having 20/20 eyesight does not necessarily mean perfect vision. 20/20 vision only indicates the sharpness or clarity of vision at a distance. There are other important vision skills, including peripheral awareness or side vision, eye coordination, depth perception, focusing ability and color vision that contribute to your overall visual ability.

Some people can see well at a distance, but are unable to bring nearer objects into focus. This condition can be caused by hyperopia (farsightedness) or presbyopia (loss of focusing ability). Others can see items that are close, but cannot see those far away. This condition may be caused by myopia (nearsightedness).

I’ve written about these medical problems before, but was riveted by a pair of articles I found in two AMA publications yesterday. A Stanford eye surgeon, Dr. Michael F. Marmor, just published a supurb article on Edgar Degas’ progressive loss of vision in his later years. Degas was born in Paris in 1834 and died there in 1917. His painting altered from 1860 , when he had essentially normal vision, to 1870 and beyond  when first one eye, then the other progressively lost visual acuity. By 1897 he was seeing at a 20/200 level; that means he could would have to be twenty feet away from an eye chart to read the letters that someone with normal vision could read from 200 feet away.

The style and details of his paintings, especially his pastels, have been shown to change as Degas’ eye problems progressed, but Dr. Marmor’s article calls our attention to one oil painting, Scene from the Steeplechase: The Fallen Jockey. Here’s a link to the painting in the National Gallery of Art; it was originally painted in 1866 and reworked by the artist in 1880-81 and again in 1896 with considerable changes made which Dr. Marmor shows can be linked to Degas’ declining visual acuity.

A number of other significant artists have demonstrated visual loss in their work. An April, 2007 article in ScienceDaily focuses on Dr. Marmor’s work, mentioning he’s authored two books on art and eye sight: Degas Through His Own Eyes and The Artists’s Eye (I’ve ordered a copy of the latter book through Amazon).

The Blind with Camera School of Photography website mentions a number of other famous figures from the art world who struggled with visual issues. Among those were El Greco, Rembrandt, Van Gogh, Paul Cezanne, Claude Monet, Mary Cassatt, Camille Pissarro and Auguste Renoir. Georgia O’Keeffe, who lived to the age of 98, also suffered with significant eye disease in her later years; her almost complete loss of eyesight and ill health during the last fifteen years of her life significantly curtailed her artistic productivity. Her eye problems began in 1968, and by 1971 macular degeneration caused her to lose all her central vision.

How is this honeybee similar to Monet?

How is this honeybee similar to Monet?

Monet had cataracts which not only diminished his visual acuity, but also affected his perception of colors. He resisted having surgery, but eventually decided to have one cataract removed. After the operation, according to science writer Carl Zimmer’s review of the San Francisco Exploratorium’s free  publication, Color Uncovered, Monet, like honeybees, was able to see ultraviolet light (normally filtered out by the lens of your eye) and painted water lilies a pale blue. Bees are guided to pollen by light signals we are unable to perceive; Monet had lost a lens to surgery, but gained a spectrum of light perception the rest of us lack.

I have zero talent as a visual artist, but after bilateral cataract surgery my vision is correctable to 20/20…for now.

 

 

 

Nut allergies et al

October 8th, 2013
Warning, may contain some of these.

Warning, may contain some of these.

I recently heard from Kevin Thompson, a Colorado blogger who read one of my posts and wondered if I’d include a link to one of his on my website. I knew of tree nut allergies only in the most general terms, but found his post gripping and, for parents of a child with nut allergies, potentially life-saving.

But I wanted to do some reading on the subject myself and also needed to see what else Kevin had posted on his blog.

Before I move on to his recent ideas on nut allergies, I’d like to mention (and give you a link to) another of Kevin’s posts, “10 of the Most Common Food Allergies in Kids.” In that one he discusses, in non-technical terms, children’s alleges to eggs, milk, soy, wheat, peanuts, tree nuts, fish, shellfish, strawberries and (amazingly) kiwi fruit.

The American Academy of Pediatrics website has a July, 2013 update on diagnosing food allergies in children. That post mentions the most common pediatric food allergies are to dairy products, egg whites, poultry, seafood, wheat, nuts, soy and chocolate. Like any kind of allergy, those to food happen when your immune system, reacting to a substance foreign to your body, produces antibodies, chemicals that usually help to protect you from infections, or as the Mayo Clinic website on allergies says, “unwanted invaders that could make you sick.”

The reaction from your immune system leads to inflammation, but the area affected and the seriousness of the reaction varies. What Kevin was talking about is the high end of the spectrum, those forms of allergic responses that can be life-threatening.

Some years back a nurse at the allergy clinic my wife goes to (fifty miles north of us in Cheyenne, Wyoming), asked if someone in the home could give Lynnette her allergy shots. That would mean she didn’t have to drive a hundred miles every other week. I was drafted although I had never given shots in my years as a practicing physician. I learned quickly; after all I had performed kidney biopsies and, in my early days in nephrology, stuck large needles into arteries when a patient had acute kidney failure and needed dialysis.

But I needed some onsite drugs in case Lynnette had a medium or, heaven forbid, a major reaction to the allergy shots.

Here's what an EpiPen looks like.

Here’s what an EpiPen looks like.

I purchased some over-the-counter Benadryl and our family practice physician wrote us a prescription for epinephrine in the form of an EpiPen (there are other brands). This is an auto-injector, something you slam into the outer thigh of a person having a really serious allergic response to a foreign substance (i.e., an allergen) or to exercise or for unknown reasons. It’s available in an adult form with 0.3 milligrams of epinephrine or in a half dose (EpiPen Jr)  and I purchased a two-pack that came with a training device.

I hadn’t tried that before today, so I just got it out of its box and followed the instructions. I removed the Blue Safety Release, swung the device against my outer thigh and pushed it, hearing a click that, with the actual EpiPen would have meant a needle had extended and, while I held it against my thigh for ten seconds, would have injected me with the (hopefully) life-saving medicine. I would have been comfortable using the actual EpiPen, but thought I should simulate a non-medically-trained person practicing how they would use the real thing.

I hadn’t mentioned it yet, but you don’t take the time to lower the trousers of the person (whether that’s you or someone else) having serious allergic problems  to use the EpiPen; it goes right through the cloth in the event of a life-threatening emergency. It does have a needle and it does contain the epinephrine to counteract a major allergic reaction.

The Trainer  doesn’t contain any medication and has no needle; it’s also reusable, so somebody can practice with it until they are comfortable with the procedure.

Why in the world would you do this to yourself or someone else? The website of the American Academy of Allergy Asthma and Immunology describes this condition, medically termed anaphylaxis, as a serious, life-threatening allergic reaction, mostly commonly seen with foods, insect stings, medications and latex exposure. The signs and symptoms typically involve more than one part of the body . They require an immediate injection of epinephrine and a trip to the emergency room (call 911, don’t drive the person yourself).

Most commonly, anaphylaxis starts within a few minutes (five to thirty) after exposure to the allergen (the substance to which the person is allergic). It can lead to any combination of: hives, swelling in the throat or elsewhere, wheezing, difficulty swallowing, trouble breathing, a feeling of tightness in the chest, syncope (fainting), vomiting and/or diarrhea with cramps, a feeling of impending doom and/or paleness or redness of the body or face.

Occasionally it can have a delayed start, so I had my wife practice with the EpiPen Trainer also just in case I’ve left the house after I’d given her the shots, waited fifteen minutes to check the areas where they went in (one on each arm), and recorded the local reaction or lack thereof.

So let’s go back to Kevin Thompson’s blog post, “How to Keep a Child With Nut Allergies Safe at School.”It walks you, as a parent, step by step, through the means to safeguard your child’s health after they have been diagnosed with an allergy to nuts (tree nuts or peanuts). I think it’s well worth reading if you have a youngster with those kinds of potentially fatal allergic problems. From approaching the school’s personnel, to helping the child her- or himself be knowledgable, to ensuring the teachers and others at the school are prepared to deal with an anaphylactic reaction, to considering other options, the post is something I’d recommend you print multiple copies of and pursue with due diligence.

It’s best to be prepared and even over-prepared for a life-threatening situation.

 

 

Lyme Disease Redux

September 23rd, 2013

Yesterday’s edition of The New York Times had an article by an experienced academic physician that called for a new Lyme disease vaccine, Dr. Stanley A. Plotkin, a professor of pediatrics at the University of Pennsylvania said new CDC data had been released showing a ten-fold greater incidence of the disease than was previously thought. He explored the history of the vaccine put on the market in 1998 by a major US pharmaceutical company, then called SmithKlineBeecham (now it’s become GlaxoSmithKline).

I looked for that news release from the CDC and found their old numbers in an August, 2013 online site (30,000 cases a year reported by state and DC health departments) had been superseded by new preliminary figures coming from three different databases. So instead of the numbers we’ve thought represented human cases, 96% of which occur in thirteen states in the Northeast and upper Midwest, we have 300,000 cases a year, still heavily concentrated in those regions.

The white-footed mouse is the main reservoir for Lyme disease.

The white-footed mouse is the main reservoir for Lyme disease.

In 2011 Richard Ostfeld, a senior disease ecologist working at the Cary Institute in New York published an excellent book, Lyme Disease: The Ecology of a Complex System, aimed at a mixed readership of scientists and nonscientists. I’ve mentioned this before but should reiterate his finding that white-footed mice were a highly significant reservoir (host animal) for the bacteria that is then transmitted to humans by, in this country, one particular insect-like species, the black-legged tick.It’s actually an arachnid, cousin to spiders and scorpions. There are other host species and a variety of predators, weather/climate conditions and habitat factors also play a role.

His work predicted a surge in cases of Lyme disease in the spring of 2012, based on an acorn crop boom-and-bust cycle. The town of Whitman, MA, published an online summary of this prediction quoting the Cary Institute’s press release. In brief that mouse species’ population soars in a year with an abundant acorn crop and falls markedly when acorns are scarce. The organism that causes Lyme disease is a bacterial species called Borrelia burgdoferi, The white-footed mouse is a superb host for that bug; the mouse doesn’t get sick; the bacteria multiplies and there is an abundant supply of B. burgdorferi waiting to spread to other animals. Those mice are also frequently bitten by the tick in question, especially around their ears.

In the seasons of acorn abundance the mouse population soars and the ticks, which need a blood meal three times in their life span (once in the larval storage, once as a nymph and once as an adult), have plenty of mice to feed on.

But then comes a lean crop year for the acorns and the B. burgdorferi infected ticks have to find other blood sources for their next meal. Any mammal will do, but humans are certainly among those available. If we are camping or hiking through an area where the tiny tick nymphs or abound, we may never notice the bite. We may not even be wearing any  bug spray or perhaps have more skin exposed than is safest. The nymphs are cold-blooded, so the countryside has to warm up from Winter’s blasts before they are ready to feed. If it’s a milder cold season (and with global warming that may be the case), the nymphs may be out looking for a meal as early as April.

Forest ecologists from the Cary Institute noted 2010’s crop of acorns was very heavy;  mouse population numbers rose appropriately. Then, in the fall of 2011, their research site had a marked acorn scarcity. Mouse numbers plummeted leading to a prediction from the group of at least 20% more human cases of Lyme disease.

Let’s return to Dr. Plotkin’s article in the New York Times. Eight years ago he almost lost an adult son to a cardiac complication of a Lyme infection. Alec D. Plotkin was walking his dog on an August day in Pennsylvania when he abruptly lost consciousness and collapsed. In 2011 his father (Dr. Plotkin) published an article, “Correcting a Public health Fiasco: The Need for a New Vaccine against Lyme Disease,” in the Journal Clinical Infectious Diseases. At that time the yearly US case estimate was (reported cases only) roughly 20,000, but as Dr. Plotkin noted, “the extent of underreporting is unknown.” He mentioned that the state of Connecticut’s statistics would imply that 1% of its entire population could develop the ailment over a ten-year stretch and that nine of sixteen countries in Europe, where Lyme disease is caused by a different variant of B. burgdorferi, had data showing an increased case incidence over time.

But you may or may not have the pathognomonic rash.

But you may or may not have the pathognomonic rash.

On Septmeber 19, The New York Times published the obit of Dr. Stephen E. Malawista, who, as chief of rheumatology at Yale School of Medicine had, with his postdoctoral student, Allen C. Steere, defined Lyme disease. In the fall of 1975 two women from Lyme, CT and Old Lyme had developed joint swelling, peculiar rashes and neurological complaints undiagnosable by their local physicians. Each went to Yale seeking answers.

Researchers there noted that the clinical picture, which was originally felt to be juvenile rheumatoid arthritis, had occurred in clusters and at a rate 100 times that expected for JRA. It also was clustered in warm-weather months. Dr. Malawista suggested the name Lyme arthritis and he and his team made the eventual linkage with tick bites. In 1982 Dr. Willy Burgdorfer found the bacterium responsible and Yale scientists wnet to work to develop a vaccine.

It was finally licensed in 1998, but a series of events, detailed by Dr. Plotkin in his medical article, led to it being removed from the market four years later. In brief: the CDC’s Advisorty Committee on Immunization Practices (ACIP) gave greater emphasis to protective clothing, tick repellants and, in the event of an infection, consistent early diagnosis and antibiotic treatment, than to the vaccine, even for those at high risk. Then it was only tested in adults and more in the group who got the vaccine than in the control group experienced some transient joint soreness…but not actual arthritis (typically red,hot, swollen, painful joints. The marketing of the drug was inappropriately directed at a lay, not a medical audience. A class action suit was brought against Glaxo, the drug company which produced the vaccine and, in spite of later studies showing no increase in Lyme-related joint disease, was settled by Glaxo for $1 million in 2003. Only the lawyers involved got any money.

By then the vaccine was off the market.

It’s clearly time for it to come back, perhaps in a new version, perhaps developed by a different company, but, in any case a human Lyme disease vaccine is needed.

 

Ditch fad diets; use common sense instead

September 16th, 2013

When I returned home on September ninth from a twenty-eight-day trip, I found stacks of mail, magazines and newspapers plus about 650 emails to wade through. Most got short shrift and the old papers were pitched. But then I found four editions of JAMA and started reading selected articles. Over the years I’ve deplored the menagerie of fad diets that have been described, advertised and exploited for profit.

You don't have to weigh and measure each time you eat a pea

You don’t have to weigh and measure each time you eat a pea

So coming upon a Viewpoint piece in the Aug 21, 2013 edition, I read with intense interest  “A Call for an end to the Diet Debates.” The pair of PhDs who authored the two-page discussion, Sherry L. Pagoto and Bradley M. Appelhans, are both academics, serving on the faculty of major medical schools. They commented on the host of studies and four recent meta-analyses that have reviewed the results of a variety of diets varying the amount of protein, carbohydrates and fats one is allowed.

Their conclusion is they don’t differ in their results in any significant way and that sticking to a diet and adding exercise is what counts.

There’s a second comment that was striking: in spite of markedly increased percentages of US adults being overweight or obese, the chances of their getting any counseling on the issue when they see their primary care physician have fallen. Researchers from the Penn State College of Medicine published an article in February of this year titled “A silent response to the obesity epidemic: decline in US physician weight counseling.” The National Center for Biotechnology, a National Library of Medicine section, published a short version of this study comparing outpatient visits in 1995-1996 to those in 2007-2008 (the most recent data available from an ongoing national ambulatory medical care survey).

What I think this means is that we still don’t pay physicians enough for preventive medicine interventions; we pay much more for procedures, what I think of as “Catch-up Medicine.”

Over the past forty-seven years, ever since I graduated from medical school in 1966, I’ve seen a host of fad diets come and go. The Rice Diet, invented at Duke where I served as an intern and resident, is still around, but was originally utilized as a very-low-protein approach for patents with severe kidney disease. Since then we’ve seen high protein, low protein, several that focus on carbohydrates, and, this year, in a blog from a Phoenix newspaper, an entertaining look at “5 Fad Diets to Avoid in 2013.”

Those include: a gluten-free diet (reasonable only for those who actually have been diagnosed, preferably by an experienced physician, as having gluten intolerance); the Dukan Diet (I’ll supply a link to the WebMD review of this French approach), essentially a high-protein and limited calorie approach that may work short-term, but doesn’t supply a balanced diet for the years to come; the alkaline diet (here’s another review from WebMD) which claims to alter your blood pH, which is nonsense, but basically is a fresh fruit and vegetable plus hydration approach which in itself isn’t unreasonable for those who don’t have kidney disease or severe diabetes. But the components of this diet can easily be purchased in your supermarket and therefore don’t need to be obtained through a website; the HCG diet, dangerously restrictive in calories and supplying a hormone that ought to be used only by a physician’s prescription, usually for fertility issues (here’s a Mayo Clinic review that says the diet dangerous); and finally, the beef tapeworm diet where some go over our southern border and actually pay to be infected with a parasitic disease. I don’t feel the need to even comment on the logic of that approach.

So what does make sense to me is, as always, eating less and doing more.

Of course that’s not as easy as it sounds. Some of my previous posts have alluded to the ways I’ve made this work for me, but you may or may not find them to fit your own lifestyle.

Use a good scale, but it doesn't have to be this fancy.

Use a good scale, but it doesn’t have to be this fancy.

So I’d suggest the following: 1). Don’t fall for the expensive fad diet ploy; eat in whatever pattern suits you (three meals a day is my habitual approach, but I sometimes eat two with a medium-sized brunch in anticipation of an evening event that includes food in abundance), but avoid snacking and late evening binges; 2) Eat balanced meals with more fruits and vegetables and less (or no) red meat than is typical for many Americans; 3). Find a form of exercise that you’re comfortable with and do it almost every day (We walk an hour a day and I spend another hour or often two in the gym six days a week; that may not work for you, especially if you have a full-time job.); 4). Don’t beat yourself up when you fall off your eating and exercise (figurative) bike, but get back on it ASAP. 5). Weigh yourself daily on a good scale, at the same time of day, wearing nothing (or as little as possible) and keep a record of your weight. 6). Don’t expect to lose twenty-five pounds in a few weeks. If you did that, my bet is you’d gain it all back in a year. Aim for a pound a week.

I took my eating plan, which I first decided on in 1996 or 1997, and really started using in early 2009, and wrote down all of the ideas and some recipes my wife added; I ended up with a 50,000 word book that I may eventually try to polish enough to publish. There are a number of specifics that I’ve added to the six basics concepts in the paragraph above, but I’ll mention those at another time.

I still occasionally struggle with one aspect of my eating plan; late-night reading can be a prelude to minor binging. And events with food are another potential minefield. But I’ve managed to get back to my diet whenever I’m above what I consider to be my acceptable range.

So I have four by six inch cards that tell me: “Don”t snack at events.”

I’ll bring one along tonight when I go to a writers’ meeting; there will be two speakers, but someone is bound to have lots of snacks for the group.

I don’t plan to eat them.

Cancer screening redux

August 12th, 2013

The JAMA article I’ve mentioned in my last two posts provided an interesting sequel. It mentioned lung and bronchus cancers in the group with breast cancer and prostate cancer, those whose incidence has gone up a fair amount, and death rates have gone down.

That confused me as the numbers showed only a smidge more being diagnosed (an 8% increase) and actually a death rate increase in the same ball park (eleven precent). The footnote said a National Lung Screening Trial looking at higher risk individuals concluded low-dose CT screening could reduce death rates by 20%. I had missed this article which was published in the New England Journal of Medicine in 2011 and had over 53,000 subjects who were randomly assigned to screening with either a single chest x-ray or low-dose CT. The point was CT scanning picked up early-stage cancers and their percentage was way up, while the proportion of later-stage cancers actually was less.

Lung cancer is the third most common in both genders in the United States and is the number one cause of cancer-related deaths. If you’re a heavy smoker, the chances of your dying from lung cancer go up immensely The CDC webpage on lung cancer risk factors calls cigarette smoking the major issue causing ~90% of all lung cancers in this country.

I’ve mentioned this before, but let me reiterate my Dad’s smoking cessation and mine. He had three rooms in his private practice office and one day realized he had put a lit cigarette in the ashtray of each room, He never smoked again and lived to ninety-four. I smoked as a youngster for four years, never heavily, and I quit as a senior in medical school when I saw one of my VA patients smoking through the trachesotomy he had had for cancer.

The August edition of the Annals of Internal Medicine, published one day after the piece in JAMA, has an article titled “Screening for Lung cancer with Low-Dose Computed Tomography” (AKA a CT scan). This one reviewed four trials of CT screening; only one was large and of good quality. It actually was the research reported in the NEJM article and the project was stopped at six and a half years when it was noted how much lung cancer mortality was reduced.

What’s interesting in this new review article is a series of comparisons: you need to screen 320 at-high-risk subjects by low-dose CT scanning to prevent one death from lung cancer and 219 to prevent one death from any cause. That wasn’t striking until I read you need to screen 1339 women aged 50 to 59 with mammography to prevent one breast cancer death and 817 people with flexible sigmoidoscopy (a shorter version of the colonoscope that can reach an estimated two of three colon polyps) to prevent one colon cancer death.

The third category of cancer screening focused on melanoma, the worst of the three common skin cancers (the others are squamous cell and basal cell cancers). In the time frame from 1975 to 2010 the incdence of melanoma went up 199% while the death rate from this tumor went up only 32%. I found a very recent online article on this cancer, reprinted from an April, 2011 publication, by US News and World Report. It focused on its warning signs and prevention as well as treatment.

We live at  an altitude of ~5,200 feet, so our exposure to damaging  UV rays from sunlight is considerable. My wife drives 55 miles to several times a year to see a dermatologist and the last few years I’ve gone with her on one of those visits and had a skin check,

Try to catch these very early

Try to catch these very early

Melanomas account for three quarters of all deaths from skin cancer and are felt to result from excessive exposure to UV light. We walk in the early morning and after dark, not during the middle of the day, don’t use tanning beds, my wife always wears sunscreen (I confess I don’t routinely do so, but I should), and neither of us has “fair or freckled skin’ or a family history of this disease.

The NCI says a change in the size or shape, color or texture of an existing mole, one of the black or brown patches that most of us, by adulthood have a number of (10-40 is common).I like the NCI’s ABCDE approach to look at moles: A stand for asymmetric, different parts of the skin lesion not looking the same; B means borders that are irregular, shaggy or ill formed (uneven or scalloped); C is for color that varies from part of the mole to another; D is for diameter (melanomas, while they may be smaller, usually are larger than a pencil eraser in size): and E is for evolving (changes in size, shape, color, elevation or even bleeding, crusting/scaling or itching).

Any of these signs should prompt a quick call to your doctor and perhaps a visit to a dermatologist.

Fortunately, the only skin cancer either of us has had thus far was a squamous cell and it was removed by the Mohs technique, in which a section of the lesion is surgically removed by a specially trained physician, and then immediately stained and examined under the microscope to make sure the borders are clear of any tumor. The process is repeated until safe borders are noted.

The last kind of cancer I want to mention is thyroid; during the thirty-five year period its incidence went up 185, but its death rate went down 7%.

Be sure your doc knows if you or your family member has had a thyroid problem

Be sure your doc knows if you or your family member has had a thyroid problem

In spite of having a first cousin who had this tumor, it was the one I knew the least about. So I went to the MD Anderson Cancer Hospital’s website on Thyroid Cancer Prevention and Screening. They mentioned on type that runs in families and is genetically linked, but for most of us, looking at our neck carefully twice a year, having our physician do a cancer-related exam yearly, making sure your salt has iodine, and knowing that most of these lesions occurs in women (3/4s), typically between age 20 and 55 is a good start. One other comment was exposure to radiation, especially in childhood is a significant risk factor.

There are other cancer screening procedures, but those are the common ones. Your physician may have a few more in mind.