Posts Tagged ‘medicine’

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More Biology

Friday, November 30th, 2018

I have posted a few times on Biology and should really do more. Here is one.

In a previous post, I stated that mitochondria are not present in sperm.

The “African Eve” theory is derived from the fact that all mitochondria are inherited from the mother. There are no mitochondria in the sperm.

That was a mistake as, someone pointed out, sperm have motile flagellae and that requires Mitochondria. However, my second comment was also, perhaps, incorrect.

An astute reader pointed out that my statement above is incorrect. Actually, it is a sign of how old I am as this was the previous understanding. However, sperm do have mitochondria but they are tagged for destruction and do not survive in the egg. Why this is, is not explained although the paternal mitochondria may be harmful in some fashion.

Now, I might still have been wrong.

But new research suggests that in some cases, mitochondrial DNA can be inherited from fathers, too. A group of researchers found three unrelated families where individuals had mitochondrial DNA from both parents. A total of 17 people across these three families were affected, suggesting that mitochondria aren’t as exclusively maternal as scientists believed.

In nearly all mammals, this mitochondrial genome is inherited exclusively from the mother, and transmission of paternal mitochondria or mitochondrial DNA (mtDNA) has not been convincingly demonstrated in humans. In this paper, we have uncovered multiple instances of biparental inheritance of mtDNA spanning three unrelated multiple generation families, a result confirmed by independent sequencing across multiple unrelated laboratories with different methodologies. Surprisingly, this pattern of inheritance appears to be determined in an autosomal dominantlike manner. This paper profoundly alters a widespread belief about mitochondrial inheritance and potentially opens a novel field in mitochondrial medicine.

There are lots of new developments in biology, such as studies of dental specimens in archeology.

An example is the use of plants in the diet of Neanderthals.

The most popular idea is that the disappearance of the Neanderthals was caused by the greater competition of the ancestors of modern humans, Homo Sapiens, who appeared more or less at the same time as the Neanderthals disappeared from Europe, and one of the explanations as to how that happened could be their diet. The Neanderthals are thought to have had more limited diets, while our ancestors had more flexible, adaptive diets that included seafood and a variety of plants.

Yet even though archaeological science has advanced considerably over the last few decades and has come up with new theories about the diets of the Neanderthals, today we still only have a patchy image of their dietary ecology given that we lack full, environmentally representative information about how they used plants and other foods.

This new piece of research into the fragments of dental calculus or tartar shows that the use of plants was a widespread, deeply-rooted subsistence strategy of the Neanderthals.

More detail is coming as dental tartar is beginning to be analyzed.

Archaeological tooth tartar has previously been shown to preserve milk proteins, but the international study, led by researchers at the University of York and the Max Planck Institute for the Science of Human History, has proved for the first time that it can also reveal more precise information about a wider range of food proteins, including those from plants.

And

Analysing 100 archaeological samples from across Britain, as well as 14 samples from living dental patients and recently deceased individuals, the research team found that potential dietary proteins could be found in about one third of the analysed samples.

Dr Speller added: “In the teeth we look at from individuals who lived around the Victorian era we identified proteins related to plant foods, including oats, peas and vegetables in the cabbage family. Occasionally, we find evidence of milk and oats in the same mouth — I like to think it’s from eating porridge!”

We know quite a bit about the diet of “Otzi,” the Iceman found in the glacier in 1991. His remains are a unique treasure for anthropology.

More recent analysis of Ötzi’s stomach and intestines has resolved this contradiction: the contents of his intestines have revealed fragments of bones from an ibex, alongside various remains of plant origin. A detailed genetic analysis of his intestinal contents also showed that he had consumed venison. The latest study conducted on his stomach contents revealed that his last meal consisted largely of ibex and venison with a high percentage of fat. Studies have also shown that the Iceman – and, indeed, the entire population of present-day South Tyrol – had a very balanced diet. Early types of grain – such as einkorn and emmer – were probably consumed in the form of porridge or bread. The diet also included a large number of other plant products, including various vegetables, fruits and wild berries, as well as dried wild fruits.

We knew this by 1998 when I wrote my medical history book. Here is a 1998 article on his diet, which was known at the time./


But at the top of the colon, Zur Nedden made out a slight bulge, which the radiologist suspected was a clump of half-processed food. The progress of the food indicated that the Iceman had last eaten about eight hours before he died, possibly of hypothermia, on the Hauslabjoch pass, which cuts over the main Alpine ridge dividing Austria from Italy at 10,500 feet above sea level.

Not until several years after the discovery did the Innsbruck scientists finally cut a hole into the mummy, insert an endoscope, and snip out about .004 ounces from the colon. Dr. Werner Platzer, the University of Innsbruck anatomist then in charge of research on the corpse, gave .0016 ounces milligrams of the material to Oeggl, who had already been studying the rich botanical finds from the site.

Pollen provided a snapshot of the environment the Iceman was exposed to in the hours before his death
Oeggl’s sample was barely the size of his little fingernail. Under the microscope, he quickly identified the flake-like, semi-digested material that made up the bulk of the sample as einkorn, the most important wheat of the Neolithic, the period of prehistory in which people lived in semi-permanent settlements and survived by agriculture and keeping animals. The discovery of einkorn, which does not occur naturally in Europe, in the Iceman’s intestinal tract suggested that he had contact with an agricultural community. The dominance of bran in the sample led Oeggl to believe that the wheat had been finely ground into meal and made into bread, rather than eaten as a porridge, where the grains would have been eaten whole and found in larger pieces in the colon. But the bread would have been little like modern breads. In order to get bread to rise when yeast is added, the wheat grains must contain a high level of gluten, which lends the dough a durable elasticity and therefore holds the pockets of air. Einkorn has low levels of gluten, so the bread made with it was probably hard, somewhat like a cracker, and rather tough on the teeth.

That is interesting.

There are even suggestions of medical therapy in dental calculus from Neanderthals.

The international team analysed and compared dental plaque samples from four Neandertals found at the cave sites of Spy in Belgium and El Sidrón in Spain. These four samples range from 42,000 to around 50,000 years old and are the oldest dental plaque ever to be genetically analysed.

“We found that the Neandertals from Spy Cave consumed woolly rhinoceros and European wild sheep, supplemented with wild mushrooms,” says Professor Alan Cooper, Director of ACAD. “Those from El Sidrón Cave on the other hand showed no evidence for meat consumption, but appeared instead to have a largely vegetarian diet, comprising pine nuts, moss, mushrooms and tree bark — showing quite different lifestyles between the two groups.”

“One of the most surprising finds, however, was in a Neandertal from El Sidrón, who suffered from a dental abscess visible on the jawbone. The plaque showed that he also had an intestinal parasite that causes acute diarrhoea, so clearly he was quite sick. He was eating poplar, which contains the pain killer salicylic acid (the active ingredient of aspirin), and we could also detect a natural antibiotic mould (Penicillium) not seen in the other specimens.”

“Apparently, Neandertals possessed a good knowledge of medicinal plants and their various anti-inflammatory and pain-relieving properties, and seem to be self-medicating. The use of antibiotics would be very surprising, as this is more than 40,000 years before we developed penicillin. Certainly our findings contrast markedly with the rather simplistic view of our ancient relatives in popular imagination.”

The “Iceman” also had some evidence of medical treatment, although probably ineffective.

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The story of language gets more interesting.

Sunday, February 25th, 2018

I’m tired of politics.

I’ve been interested in autism for some years.

Some of autism is involved in language. Now we are starting to learn about the genetics of language.

It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 “the language gene” or the “grammar gene”. Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited – the discovery sparked a frenzy of research aiming to uncover the gene’s role.

Several years on, and it is clear that talk of a “language gene” was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. “When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language,” recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours.

This gene has many roles, some of which are involved in language. However, it is not that simplae.

All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed “area X”, which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches’ levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.

So what would happen to a bird’s songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component “syllables” as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.

What is next ? How about Neanderthals ?

The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo’s group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us – mutations accrued since our lineage split from chimps between 6 and 5 million years ago.

Pääbo admits that he “struggled” to interpret the finding: the Neanderthal DNA suggests that the modern human’s version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.

“We believe there were two things that happened in the evolution of human FOXP2,” says Pääbo. “The two amino acid changes – which happened before the Neanderthal-human split – and some other change which we don’t know about that caused the selective sweep more recently.”

Language and autism are somehow connected.

Some of this is pretty primitive as yet.

Moreover, the striking conservation of both FoxP2 sequence and neural expression in different vertebrates facilitates the use of animal models to study ancestral pathways that have been recruited towards human speech and language. Intriguingly, reduced FoxP2 dosage yields abnormal synaptic plasticity and impaired motor-skill learning in mice, and disrupts vocal learning in songbirds. Converging data indicate that Foxp2 is important for modulating the plasticity of relevant neural circuits. This body of research represents the first functional genetic forays into neural mechanisms contributing to human spoken language.

This has got to be important if we can figure it out.

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2015 is gone, thank God.

Friday, January 1st, 2016

2015-a-maes-Marty_thumb

I am content to see the year 2015 gone. I can remember as a college student thinking that 1960 would never come. That was a good year. I didn’t graduate from USC as planned but I did get married and I did get accepted to medical school.

Some of the story is here in my short biography. More of it is here in my “stream of consciousness.” The next installment is here as I describe Basic Training.

When I got back from Basic Training in December 1959, I had my first date with Irene Lynch. A year later to the day, we were married and a week later, I got a letter from SC Medical School telling I had been accepted to the class beginning in September 1961. So, 1960 was a pretty good year.

In 2015 I spent what I think will be my last year teaching medical students at what is now named “Keck School of Medicine of USC” and is where I attended from 1962 to 1966. I went back to teaching there in 1998 in a program called Introduction to Clinical Medicine, which seems to be disappearing into the “Family Medicine” Department which is a shame.

I now have a book of memoirs called “War Stories: 50 years in Medicine” and which is a Kindle book only so far. Much of my medical school experience is included along with stories from my years as a surgeon. It started to be “40 years a surgeon” but I decided to include the rest and changed to 50. In June 2016, it will 50 years since I graduated from Medical School and that seemed a appropriate.

I enjoyed my time with students and I am quitting only because of frustrations with the Electronic Medical Record, about which I used to be enthusiastic, and with changes in the County Hospital which used to be a wonderful teaching institution. The Electronic Medical Record, now more often called The Electronic Health Record, probably because much of it is not about medicine, is a big problem.

The EHR, as it is called, has acquired a bad reputation.

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The Medical History of the American Civil War III

Friday, September 4th, 2015

This continues the series from a lecture I have given a few times.

Slide23

William W Keen was a student when he first served as an Army surgeon at Bull Run. That experience changed the Army medical services and gave a great deal of power to the volunteer organizations.

Slide24

William Hammond quickly replaced the incompetent surgeons who had been in place when the war began. He was competent but argumentative and clashed with Stanton who became Secretary of War.

Hammond met Jonathan Letterman. Hammond worked with Letterman and Rosecrans on the design of a new ambulance wagon.

The atmosphere in the upper levels of medical services was then one of internal strife and personal conflicts. Hammond—a tall and imposing young man[12]—was no man of intrigue, nor even, according to all accounts, a very flexible person. However, the situation offered him the possibility for advancement. When Finley, the 10th Surgeon General, was fired after an argument with Secretary of War Edwin M. Stanton, Abraham Lincoln, against Stanton’s advice and the normal rules of promotion, named the 34-year-old Hammond to succeed him with the rank of brigadier general. Hammond became Surgeon General of the Army on 25 April 1862, less than a year after rejoining the army.

Lincoln liked “Men who fight” and defended his choices but Hammond was just too hard headed.

On his initiative, Letterman’s ambulance system was thoroughly tested before being extended to the whole Union. Mortality decreased significantly. Efficiency increased, as Hammond promoted people on the basis of competence, not rank or connections, and his initiatives were positive and timely.

On 4 May 1863 Hammond banned the mercury compound calomel from army supplies, as he believed it to be neither safe nor effective (he was later proved correct). He thought it dangerous to make an already debilitated patient vomit. A “Calomel Rebellion” ensued, as many of his colleagues had no alternative treatments and resented the move as an infringement on their liberty of practice. Hammond’s arrogant nature did not help him solve the problem, and his relations with Secretary of War Stanton became strained. On 3 September 1863 he was sent on a protracted “inspection tour” to the South, which effectively removed him from office. Joseph Barnes, a friend of Stanton’s and his personal physician, became acting Surgeon General

Stanton later died of an asthma attack so his “personal physician” was important to him. Calomel was “The Blue Pill” that had been advocated by Benjamin Rush. It was an ancient remedy based on the success of mercury in the treatment of syphilis dating back to Paracelsus in the 14th century. Medicine until the 20th century was quite primitive and many remedies were tried for wildly inappropriate indications.

van gogh

For example, a Van Gogh painting of his doctor shows evidence of digitalis intoxication which might have caused his death. Yellow vision is one indication of overdose of digitalis (sudden death is another) and a Van Gogh painting, Portrait of Dr. Gachet shows the characteristic yellow tint plus an example of the plant held by the doctor.

Anyway, Hammond was replaced after some of his innovations including evacuating the wounded from the Peninsula Campaign of McClellan. They were taken by ship back to large hospitals near DC.

Slide25

Slide26

Treatment of the wounded early in the war was primitive and would soon improve under Hammond’s reforms.

Slide27

The volunteer organizations began to make their influence felt and the Army was unable to resist the reforms.

Slide28

Tripler, for whom the great Army hospital in Hawaii is named, was chosen by McClellan to be the chief surgeon for the Army of the Potomac. His great innovation was the “Ambulance Corps.”

Slide29

The “Ambulance Corps” restored the invention of Baron Larrey and began the reforms of the Union

To be continued

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The Coming Shortage of Doctors.

Monday, August 3rd, 2015

33 - Lister

This Brietbart article discusses the looming doctor shortage.

Lieb notes, that the U.S. is only seeing 350 new general surgeons a year. That is not even a replacement rate, she observed.

A few years ago, I was talking to a woman general surgeon in San Francisco who told me that she did not know a general surgeon under 50 years old. The “reformers” who designed Obamacare and the other new developments in medicine are, if they are MDs, not in practice and they are almost all in primary care specialties in academic settings. They know nothing about surgical specialties.

They assume that primary care will be delivered by nurse practitioners and physician assistants. They are probably correct as we see with the new Wal Mart primary care clinics.

The company has opened five primary care locations in South Carolina and Texas, and plans to open a sixth clinic in Palestine, Tex., on Friday and another six by the end of the year. The clinics, it says, can offer a broader range of services, like chronic disease management, than the 100 or so acute care clinics leased by hospital operators at Walmarts across the country. Unlike CVS or Walgreens, which also offer some similar services, or Costco, which offers eye care, Walmart is marketing itself as a primary medical provider.

This is all well and good. What happens when a patient comes in with a serious condition ?

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Expensive babies.

Sunday, July 5th, 2015

Mila

There is a post on Instapundit today about expensive babies.

It references a new book about a premature baby and is named “Girl in Glass.”

That baby was referred to by the CEO of AOL in a speech to employees explaining why he was cutting benefits for all employees. Her care cost 1 million dollars. The Guardian article goes on to complain about US healthcare (of course) and the cost of premature baby care.

I have a somewhat similar story in my own new book, War Stories. My story is not about a premature baby, although I have one of those too, but a little boy who was born with a heart defect that caused an 18 month hospital stay at Childrens’ Hospital in Los Angeles.

Here it is:

Following my general surgical residency training, I spent an additional year training in pediatric heart surgery at Children’s Hospital. During this time I learned more about the amazing resiliency of children and their recovery from terrible illness. I was also reminded of the constant possibility of catastrophic error in medicine. One young patient named Chris was the best example of the tremendous recuperative powers of children. He was coming in for open-heart surgery to repair a large ventricular septal defect. The ventricles are separated by a muscular wall called the septum, which forms during early fetal development of the heart. The heart has four chambers, two atria and two ventricles, which are separated by walls called “septa,” plural of septum. There are a number of major cardiac anomalies associated with the development of the atrial and ventricular septa and also with the rotation of the heart and the connection of the great arteries to the ventricles from which they arise. Chris was born with a very large defect in the septum between the right and left ventricle. In this situation, the newborn goes into congestive heart failure very shortly after birth. The defect causes no trouble before birth because the lungs are not inflated and the blood flow through the lungs is very small. The cardiac circulation in utero consists of oxygenated blood returning from the placenta through the umbilical veins, passing in a shunt through the liver and then entering the right atrium, which also receives the non-oxygenated venous blood from the body. The oxygenated blood returning from the placenta enters the right atrium and passes through a normal atrial septal opening called “the foramen ovale,” which shunts it directly to the left atrium and left ventricle for circulation out to the body. This bypasses the lungs. The venous blood, and the umbilical vein oxygenated blood that does not go through the foramen ovale, enters the right ventricle where it is pumped into the pulmonary artery. There, because of the high pulmonary resistance it goes through another shunt, the ductus arteriosus, a connection between the pulmonary artery and the aorta, to bypass the lungs and circulate to the body. Minimal flow goes beyond the ductus into the pulmonary arteries until birth. During fetal life, the presence of a ventricular septal defect merely eases the task of shunting the oxygenated blood from the right side of the heart to the left and then out to the general circulation.

When the infant is delivered into the world from its mother’s uterus, it inflates its lungs and very rapidly major circulatory changes occur in the heart and lungs. The pulmonary arteries to the lungs, which during intrauterine life carry almost no blood because of a very high resistance to flow in the collapsed lungs, suddenly become a low resistance circuit with the inflation. The foramen ovale, which has a flap valve as a part of its normal structure, begins to close very quickly and the ductus arteriosus, connecting the pulmonary artery and the aorta, also closes within a matter of several hours. These two shunt closures are accomplished by hormonal changes associated with the changing physiology of the newborn. In very low birth weight preemies, that have low blood oxygen concentration due to immature lungs, the ductus often does not close. In the child with a ventricular septal defect, the sudden drop in resistance to flow in the pulmonary circulation together with the closing of the ductus arteriosus causes the shunt, which was directed from the right to the left heart in utero, to switch to a left to right shunt after birth. The pulmonary circulation is now the low resistance circuit and the systemic circulation; that is, the aorta going out to the arms, legs, and organs is now a relatively high resistance circuit. The flow in the pulmonary circuit goes up tremendously, a short circuit in effect, taxing the ability of the right ventricle to handle the load. At the same time circulation to the organs, the brain and the extremities, drops because of the shunt. This combination of circumstances produces acute congestive heart failure in a newborn. Cardiac output is huge but the flow is going around in a circle through the lungs and then back to the lungs.

Chris had a huge ventricular septal defect and as soon as his lungs inflated and the pulmonary circulation began to assume the normal low resistance of the newborn, he developed an enormous left to right shunt and went into heart failure. The venous return from the body entered his right atrium, passed into the right ventricle and on into the pulmonary artery to circulate through the lungs. Once the oxygenated blood returned to the left atrium on its way to the body, it was shunted back to the lungs because the pressure in the aorta and left ventricle was much higher than that in the right ventricle and pulmonary artery. The short circuit in the heart diverted almost all blood flow to the lungs and little went to the body. The right ventricle, which is thin walled and flat like a wallet, cannot handle the load and quickly fails. The treatment of an infant with a large ventricular septal defect and heart failure is to perform a temporary correction by placing a band around the pulmonary artery above the heart. This accomplishes two purposes. One, it artificially creates a high resistance and equalizes the pressure in the right and left ventricles so that the flow across the ventricular septal defect is minimized. The right ventricular pressure is as high as the left ventricular pressure and little or no shunt occurs. This stops the huge shunt and, with the smaller flow, the ventricle can handle the pressure. It also protects the lungs from high blood flow that damages the pulmonary circulation.

In a related anomaly called “Tetralogy of Fallot” a partial shunt occurs but it is the other way, right to left, since the pulmonary artery is severely narrowed at its origin as part of the anomaly. These children do not go into heart failure, but they are blue because of the mixture of venous blood from the right side and arterial blood from the left. Some patients with ventricular septal defect (VSD) do not go into heart failure because the shunt is not that large but if treatment is delayed and a continued high flow through the lungs persists, in later life they develop irreversible changes in the lungs from the damage to the pulmonary circulation by high flow rates. They become blue later as the increasing pulmonary resistance in the lungs reverses the shunt from left to right to right to left as in Tetrology of Fallot. This condition is called “Eisenmenger’s Complex” and, once it occurs, cannot be corrected. Once this reversal occurs they do not benefit from correction and require heart and lung transplantation. Some VSDs are small and do not produce enough flow to cause trouble, at least in childhood.

Chris had a pulmonary artery banding procedure at about two or three days of life and an extremely stormy course for a very long time postop. He was in the Intensive Care Unit at Children’s Hospital for over a year. He had a tracheostomy for much of that time as he was unable to breathe without a respirator for a year. He had intravenous feeding for well over a year. During this time he had several cardiac arrests and the staff became convinced that he would be brain damaged if he survived. Finally, after 18 months in Children’s Hospital, he went home. This had all occurred before my time. Now, 3 years later, he was being admitted for the definitive repair of his heart defect. The pulmonary band is Teflon tape and does not grow so the pulmonary stenosis, which had saved his life, was now a threat, as it did not permit adequate flow to his growing lungs. He was five years old and was joyously normal. His intellectual development, in spite of everything, was normal and he was a very calm and self-confident little kid. He was not afraid of the hospital or of us, the white coat brigade. Most nurses and staff in children’s hospitals and pediatric clinics avoid white coats preferring colorful smocks to reassure kids that we are all regular folks. The kids are not fooled but it does seem to defuse the tension, especially at first. When we would make rounds on the ward for the few days Chris was in the hospital for pre-op checks, he would go around with us. He wore his little bathrobe and sometimes carried charts for us. He was completely unafraid. I don’t know if it was because he remembered his previous experience; I didn’t think that memory would be very reassuring.

Anyway, the day of surgery came. His mother was a nervous wreck because she had come so close to losing him and here they were risking him again. I did not see much of the family on the day of surgery. His grandfather was a famous movie star, one of the biggest box office leaders of all time, and the hospital had thrown a big luncheon bash for the family as they waited. We heard about it and grumbled that they could have spent the money on a better blood bank (we were having trouble getting blood for elective cases), but no doubt they hoped for a big donation. The surgery, itself, was almost an anticlimax. The data from the original heart cath, when he was a newborn, suggested that he had almost no interventricular septum and we anticipated trouble reconstructing a new septum. As it turned out, his heart, in its growth during the past five years, had developed a good septum with a modest sized defect in the usual place. It was easy to patch and the surgery went well. The other worry with VSDs is the conduction system, the Bundle of His, which carries the electrical stimulation to the ventricles, and runs right along the edge of the defect but this was not a problem. There was no sign of heart block after the sutures were placed and tied. Postop we always took the kids straight to the Heart Room, a combination recovery room and ICU. The nurses there knew more about cardiology than I did and probably more than anyone else at Children’s below the rank of associate professor. His mother came in and stood at his bedside for a while just thankful to have him. I never saw the rest of the family although I did meet his father before he went home. He recovered quickly and completely. I had one more encounter with him about a year later.

After his recovery from the heart surgery he had another operation, this time on his leg. He had been in the hospital for so long as a baby with an IV line in his groin that his hip would not straighten out completely. A few months after the heart surgery he had another operation to release that contracture, the scar that had formed limiting his hip movement. It also went well but had been postponed until his heart was fixed. A couple of months after that procedure he was well enough to climb trees. I know that because he fell out of one of them and cut his forehead requiring several stitches. I removed the stitches in the office a couple of months after I started practice in Burbank. He recovered completely and is now an executive in the entertainment business. I have not seen him since 1972.

I don’t know what Chris’s care cost but I think it was worth it. AOL was foolish to self-insure and not buy reinsurance for catastrophic cases like Chris and Mila’s. There are ways to reform health care and to cut costs but they are not what AOL did or what Obamacare did.

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The book is now on Amazon.

Wednesday, June 17th, 2015

cover.

I have a new book out on Kindle that is now published. It is called “War Stories: 50 Years in Medicine.”

I’ve been working on this for 20 years and kept having to revise it as I would put it down and then go back to it after ten years. I finally decided to rework it and publish it two years ago. My students were reading the draft on my laptop while I was editing so maybe it will be interesting.

It is a memoir of patients. They are all patients’ stories that I have tried to describe accurately and to describe what we did then. Sometimes I screwed up and I tell those stories, too. Sometimes we did the best we could and we now know better. Some of these cases are still hard to explain.

Two of them, in the chapter on Melanoma, are about young women who developed major melanoma metastases years after the primary was excised but when they had become pregnant. The melanoma went wild in pregnancy, in one case ten years later. In the other, three years after I had removed the primary, she developed extensive metastases while pregnant. She refused abortion and I thought it would cost her her life. In both cases the melanoma vanished after pregnancy ended. In one case, the woman, last I heard, was free of melanoma 25 years later. The other was free ten years later. The medical literature says pregnancy has no effect on melanoma. Neither ever became pregnant again.

Another case is an example of the only supernatural near-death experience I have ever heard.

The book starts when I began medical school in 1961 and describes experiences with patients, including my summer working with schizophrenic men in 1962. I have a series of stories about patients I saw as a student and sometimes intersperse stories from later that are about similar cases and events. One that is amusing, I guess, is about my very first pelvic exam, on a 40 year old prostitute who had just gotten out of prison and enjoyed it thoroughly. I had a dozen student nurses as witnesses. I do have some biography in it but try to keep it to minimum.

After the first eight chapters, I go on to residency and then finally to private practice. I continued to teach and there are a few of those stories. There is a chapter on ethics including my thoughts on euthanasia and “benign neglect.” Toward the end of my career, I started and ran a trauma center in our community hospital. I also did a fair amount of testifying in court in both trauma cases and some civil cases where I testified for plaintiffs and for defense. I consider it a compliment that Kaiser Permanente had me testify for their defense even though I had also testified against them.

Anyway, the book is on Kindle and I hope somebody is interested. It has some similarity to my medical history book, which I plan to do a Kindle version of once this one is launched. In this one, I spend some time explaining the diseases in a way that I used to explain to patients and I still do to students. Without some basic understanding, most of these stories would not make sense and I hope the explanations are not too dull. If so, all comments are welcome. If anyone likes it, feel free to post a review on Amazon. Two reviewers from the first book in 2004 told me to let them know if I did another one and I have contacted them.

If anyone wants to discuss the book here, feel free to add comments. I guess I should add a link to my medical history book, A Brief History of Disease, Science and Medicine.

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Obamacare = Medicaid

Friday, May 8th, 2015

emergency

I have been interested in health care reform for some time and have proposed a plan for reform. It is now too late for such a reform as Obamacare has engaged the political apparatus and sides have been taken. The Obamacare rollout was worse than anticipated and it was hoped that the Supreme Court would have mercy on the country, but that didn’t happen and it has been the law for two years.

What has it accomplished ? Well, the forecast drop in ER visits hasn’t happened. It also didn’t happen in Massachusetts when that plan took effect.

Wasn’t Obamacare supposed to solve the problem of people going to the ER for routine medical problems? We were told that if everyone had “healthcare” — either through the ACA exchanges or through Medicaid expansion — people would be able to go to their family doctors for routine care and emergency rooms would no longer be overrun by individuals who aren’t actually experiencing emergencies.

As it turns out, Medicaid patients can’t get appointments with physicians.

“America has severe primary care physician shortages, and many physicians will not accept Medicaid patients because Medicaid pays so inadequately,” said Michael Gerardi, MD, FAAP, FACEP, president of the ACEP.

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Myopia

Friday, April 24th, 2015

myopia

A couple of interesting articles about the increasing incidence of myopia in children.

Myopia isn’t an infectious disease, but it has reached nearly epidemic proportions in parts of Asia. In Taiwan, for example, the percentage of 7-year-old children suffering from nearsightedness increased from 5.8 percent in 1983 to 21 percent in 2000. An incredible 81 percent of Taiwanese 15-year-olds are myopic.

The first thought is that this is an Asian genetic thing. It isn’t.

In 2008 orthoptics professor Kathryn Rose found that only 3.3 percent of 6- and 7-year-olds of Chinese descent living in Sydney, Australia, suffered myopia, compared with 29.1 percent of those living in Singapore. The usual suspects, reading and time in front of an electronic screen, couldn’t account for the discrepancy. The Australian cohort read a few more books and spent slightly more time in front of the computer, but the Singaporean children watched a little more television. On the whole, the differences were small and probably canceled each other out. The most glaring difference between the groups was that the Australian kids spent 13.75 hours per week outdoors compared with a rather sad 3.05 hours for the children in Singapore.

This week the Wall Street Journal had more. There are some attempts to deal with the natural light effect.

Children in this small southern Chinese city sit and recite their vocabulary words in an experimental cube of a classroom built with translucent walls and ceilings. Sunlight lights up the room from all directions.

The goal of this unusual learning space: to test whether natural, bright light can help prevent nearsightedness, a problem for growing numbers of children, especially in Asia.

The schools have tried to get Chinese parents to send the kids outdoors more but it doesn’t seem to work.

And it isn’t limited to Asians.

In the U.S., the rate of nearsightedness in people 12 to 54 years old increased by nearly two-thirds between studies nearly three decades apart ending in 2004, to an estimated 41.6%, according to a National Eye Institute study.

But Asians with their focus on education are the most effected.

A full 80% of 4,798 Beijing teenagers tested as nearsighted in a study published in the journal PLOS One in March. Similar numbers plague teens in Singapore and Taiwan. In one 2012 survey in Seoul, nearly all of the 24,000 teenage males surveyed were nearsighted.

So, what to do ?

Though glasses can correct vision in most myopic children, many aren’t getting them. Sometimes this is because parents don’t know their children need glasses or don’t understand how important they are for education. Other times, cultural beliefs lead parents to discourage their children from wearing them, according to Nathan Congdon, professor at Queen’s University Belfast and senior adviser to Orbis International, a nonprofit focused on preventing blindness. Many parents believe glasses weaken the eyes—they don’t.

Getting kids to spend even small amounts of time outdoors makes a difference.

Why myopia rates have soared isn’t entirely clear, but one factor that keeps cropping up in research is how much time children spend outdoors. The longer they’re outside, the less likely they are to become nearsighted, according to more than a dozen studies in various countries world-wide.

One preliminary study of 2,000 children under review for publication showed a 23% reduction in myopia in the group of Chinese children who spent an additional 40 minutes more outside each day, according to Ian Morgan, one of the researchers involved in the study and a retired professor at Australian National University in Canberra. (He still conducts research with Sun Yat-sen University in the Chinese city of Guangzhou.)

That is a very significant effect of small changes in behavior. Now the researchers are trying something new.

Dr. Morgan, Dr. Congdon and a team from Sun Yat-sen are now testing, as reported recently in the science magazine Nature, a so-called bright-light classroom made of translucent plastic walls in Yangjiang to see if the children can focus and sit comfortably in the classroom. So far it appears the answer is yes.

In 2007, Donald Mutti and his colleagues at the Ohio State University College of Optometry in Columbus reported the results of a study that tracked more than 500 eight- and nine-year-olds in California who started out with healthy vision6. The team examined how the children spent their days, and “sort of as an afterthought at the time, we asked about sports and outdoorsy stuff”, says Mutti.

It was a good thing they did. After five years, one in five of the children had developed myopia, and the only environmental factor that was strongly associated with risk was time spent outdoors6. “We thought it was an odd finding,” recalls Mutti, “but it just kept coming up as we did the analyses.” A year later, Rose and her colleagues arrived at much the same conclusion in Australia7. After studying more than 4,000 children at Sydney primary and secondary schools for three years, they found that children who spent less time outside were at greater risk of developing myopia.

What is the mechanism ? Maybe it is this.

The leading hypothesis is that light stimulates the release of dopamine in the retina, and this neurotransmitter in turn blocks the elongation of the eye during development. The best evidence for the ‘light–dopamine’ hypothesis comes — again — from chicks. In 2010, Ashby and Schaeffel showed that injecting a dopamine-inhibiting drug called spiperone into chicks’ eyes could abolish the protective effect of bright light11.

Retinal dopamine is normally produced on a diurnal cycle — ramping up during the day — and it tells the eye to switch from rod-based, nighttime vision to cone-based, daytime vision. Researchers now suspect that under dim (typically indoor) lighting, the cycle is disrupted, with consequences for eye growth. “If our system does not get a strong enough diurnal rhythm, things go out of control,” says Ashby, who is now at the University of Canberra. “The system starts to get a bit noisy and noisy means that it just grows in its own irregular fashion.”

Another possible treatment is the use of atropine drops in the eye.

Atropine, a drug used for decades to dilate the pupils, appears to slow the progression of myopia once it has started, according to several randomized, controlled trials. But used daily at the typical concentration of 1%, there are side effects, most notably sensitivity to light, as well as difficulty focusing on up-close images.

In recent years, studies in Singapore and Taiwan found that a lower dose of atropine reduces myopia progression by 50% to 60% in children without those side effects, says Donald Tan, professor of ophthalmology at the Singapore National Eye Centre. He has spearheaded many of the studies. Large-scale trials on low-dose atropine are expected to start soon in Japan and in Europe, he says.

More than a century ago, Henry Edward Juler, a renowned British eye surgeon, offered similar advice. In 1904, he wrote in A Handbook of Ophthalmic Science and Practice that when “the myopia had become stationary, change of air — a sea voyage if possible — should be prescribed”.

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Medicine is coming to be a government benefit.

Sunday, August 3rd, 2014

Obamacare is having serious trouble as I have discussed. The success stories, like California, are an example of what I have called Medicaid for All.

“It’s a total contradiction in terms to spend your public time castigating Medicaid as something that never should have been expanded for poor people and as a broken, problem-riddled system, and then turn around and complain about the length of time to enroll people,” said Sara Rosenbaum, a member of the Medicaid and CHIP Payment and Access Commission, which advises Congress.

Most of the new enrollees are Medicaid members and those enrolled in “private insurance” learn that they have severely restricted choice of doctor or hospital.

Now we have a new development.

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