Just last week, I wrote about the poor outcomes from studies on a new minimally-invasive approach to gastric stapling, via the oral route. Now, I want to call your attention to an article published last week in the Archives of Surgery that raises questions about the safety and long-term success of current gastric banding procedures. The study, conducted in Belgium was headed by Dr. Jacques Himpens, looked at outcomes in patients who had laparoscopic gastric banding procedures performed between 1994-1997. The study results were alarming; in about 30% of patients, the bands eroded and 60% required additional surgery. Also, most patients were still quite overweight; patients had ended up losing well less than half of their excess weight. The investigators concluded that gastric banding procedures “result in relatively poor long-term outcomes.” The study was limited in that data were available on only about 60% of the total number of patients but it represents one of the few studies out there with long-term data on gastric banding procedures. Of course, one could take a positive approach to the data- most patients were quite a bit less heavy than they were before the procedure, and about 60% of the patients expressed satisfaction with the surgery. Anyway, these data illustrate a principle in medicine that I have often written about- one must weight risks vs. benefits for any treatment, be it growth hormone injections or gastric banding. It is the unknown risks that pose the greatest dilemma in trying to decide if a proposed therapy is a good idea.
Risk Of Exposure To Radioiodine From Japan
You probably know that a major earthquake and tidal wave hit Japan a few weeks ago. One of the many problems associated with this catastrophe was damage to several nuclear reactors with leakage of radioactive materials, including radioiodine (I-131). You may or may not know that exposure to radioiodine is associated with increased risk of developing thyroid cancer. The risk is directly related to the exposure (i.e., radiation dose) and is highest in young children and pregnant women. Much of what we know about the association between radio iodine and cancer risk comes from the experience at the Chernobyl power plant in Russia in 1984. We know that exposure from breathing contaminated air confers greatest risk, followed by ingestion of contaminated milk and fresh vegetables. Children under age 10 years are at greatest risk. Risks are also related to the distance from the radiation source- the damaged nuclear plants in Japan are more that 5000 miles from the west coast of the U.S.- that’s a long distance. Risk is also related to time. For radioiodine, the half-life is about a week, so that the exposure risks decrease rapidly over time.
What should people in the U.S. do to prevent/minimize risks for the development of thyroid cancer ?
Last week, the Pediatric Endocrine Society (formerly named in honor of Lawson Wilkins) published a letter summarizing the risk of exposure to radioiodine from Japan. The letter was written by Andrew Bauer, a pediatric endocrinologist at Walter Reed Army Medical Center in Washington, D.C. Dr. Bauer reviewed the situation and offered advice regarding the use of potassium iodine (KI) to high risk populations in the U.S. (i.e., young children and pregnant women). Oral KI is highly effective in preventing radioiodine from being taken up by the thyroid, thereby effectively eliminating the risk of developing thyroid cancer from the exposure. Dr. Bauer made clear in his letter, that at present, there is no reason to consider KI prophylaxis anywhere in the U.S. I think it would be worthwhile for both pediatric endocrinologists and primary care doctors to read Dr. Bauer’s letter, but I haven’t yet figured out how to provide a link to the letter, unless you are a member of the Pediatric Endocrine Society, but I will try to do so. Meanwhile, a number of other professional societies have published statements on-line (e.g., Radiation Risks to Health: a joint statement from the American Association of Clinical Endocrinologists, the American Thyroid Association, The Endocrine Society, and the Society of Nuclear Medicine, March 18, 2011). So far all the experts are saying we should stay cool and avoid the temptation to stock up on KI.
More About Weight-Loss Programs And An Apology
Three entries in three days! I must slow things down so that readers don’t expect a steady stream of entries. Anyway, I want to update my entry from yesterday and add a few new items.
First, the on-line article in the New York Times March 16, 2011 regarding the demise of Satiety Inc., the company that had promoted gastric stapling via the oral route, was published in the paper version of the newspaper yesterday (“Hoping to Avoid the Knife,” written by Andrew Pollack). The article is very well-written and is a good review of the entire field of bariatric surgery ( i.e., weight-loss surgery) and approaches that minimize the surgical aspects.
Second, there is another interesting article in the New York Times today about treating obesity. The article is entitled “Warmed-Over Atkins? Don’t Tell the French,” written by Elaine Sciolino. Why this article is in the Thursday Styles section of the paper and not the Business Section (where the Pollack article appeared) I haven’t a clue other than the subject is the very stylish French. Anyway, the article discusses Pierre Dukan, the so-called “French Dr. Atkins.” Dr. Dukan is not well known in the U.S., but in France he is a giant celebrity and there is even a term to describe his devotees, “Dukanistes.” What prompted the article is the news that Dr. Dukan’s diet plan will be published in a North American edition (presumably for the first time, and presumably in English) entitled “The Dukan Diet.” The article discusses the diet, which seems to me to be just about identical to the original Atkins Diet- high protein/high fat/low carbohydrate. I have no comments regarding the Dukan Diet except that as I have said in the past, almost every diet ever dreamed up, works just fine, but I am not aware of any diets that have shown consistent benefit over the long haul. Of course I know you will probably buy the book and try the diet. Whatever.
Finally, I have a bit more about hCG. I learned yesterday from a physician colleague of mine that hCG is available not only in drop form but also as an oral spray (e.g, KetoMist or ‘My Fat Cure’ Homeotherapeutic HCG Oral Spray). This physician has been taking a spray dose of the stuff every day for about a year (his wife bought it for him). He told me it is great stuff and that he lost 30 pounds over the past year. I told him I was impressed and asked if he did anything else besides taking the spray to achieve such good results. He smiled and told me that he cut way back on his calories and increased his exercise. I bit my tongue and didn’t say a word other than to tell him he looked great.
I almost forgot my apology. Yesterday I was trying to “clean up” my website and delete spam but keep the interesting reader comments. Well, I managed to delete all of the comments. Sorry.
An Addendum: Use Of Human Chorionic Gonadotropin (hCG) For Weight Loss
Yesterday I wrote an entry on the use of hCG for weight reduction. Here I want to add a few things about the post and tell you about 2 interesting articles on obesity. First, regarding my comments about the hCG craze, I want to make clear that I was not trying to be critical about “alternative” medicine, just quackery. I will be the first to admit that the scientific method has its limitations; many studies of this and that have either “proven” a benefit or lack of benefit for a particular treatment or procedure, where later studies have truly proven the opposite. So, all of us (health care professionals and consumers) must maintain both a healthy optimism and skepticism about medical procedures and therapies that seem on the fringe. Don’t get me wrong, I think use of hCG (either homeopathic drops or injections of the real stuff), is a really bad idea as a method to treat obesity.
Changing the subject a bit, I want to call your attention to two interesting articles. The first, published today in the New York Times on-line (I suspect it will make it into the hard-copy paper in the next day or so). The article was entitled “Hoping to Avoid the Knife,” and written by Andrew Pollack. The article reported that the “scar-less” weight loss surgery technique developed by Satiety, Inc., turned out to be a bust and venture capitalists who put $86 million dollars into the project have pulled out of the project. The idea was to avoid all the problems with general anesthesia and scars that come with traditional stomach shrinkage procedures used for weight reduction (e.g., gastric-bypass, lap-banding) and cut costs. Anyway, apparently, the study results were not so hot. What I found interesting about the article, other than the bad news for Satiety, Inc., was the long discussion about the current state of things with all types of surgical procedures for weight reduction.
The second article was published today the New England Journal of Medicine and is entitled “Obesity Prevalence in the United States- Up, Down, or Sideways.” The article was written by Susan and Jack Yanovski and although it is an editorial, is a beautiful summary of the various recent data sets that have examined the prevalence of obesity in the U.S. There are some differences in the data among the various data sets; one can debate whether the prevalence of obesity has stabilized or is still increasing but two things are clear. First, the prevalence of obesity in the U.S. is astonishingly high and this poses a serious health threat. Second, even if the overall prevalence is not increasing, the percentage of people with extreme obesity (BMI equal or greater than 40) is climbing steadily. The authors offer a very interesting discussion about what we should do about the problem. I highly recommend that you read the article.
The Entrepreneurial Spirit Is Alive And Well In The US: Human Chorionic Gonadotropin Clinics
As an endocrinologist, I probably should know quite a bit about all the various hormones out there. But, somehow I fell down on the job. It is only in the past week or so that I learned about the hCG/weight loss craze. It’s all over the news and the internet. The other night I saw 3 hCG ads on TV. What is this all about?
Human Chorionic Gonadotropin or hCG for short, is a glycoprotein hormone that is produced mainly in the placenta (the fetus and various tumors can also make the hormone). As the name implies, the hormone stimulates the gonads, akin to the pituitary gonadotropins, luteinizing hormone (LH) and follicule-stimulating hormone (FSH). It was discovered in 1919 and within a few years it was found to be useful as a pregnancy test. The “A-Z test” (named for Asheim and Zondek) was based on the fact that the urine of pregnant women promoted ovarian follicular development, ovulation, and formation of the corpus luteum (the “scar” in the ovary formed after ovulation and the site of progesterone production). In the 1930s it was established that hCG was a placental hormone. In the 1940, the hormone was purified. We now know that the hormone consists of 2 subunits, alpha and beta. The alpha subunit is virtually identical to several other pituitary hormone alpha subunits including LH and FSH and thyroid-stimulating hormone (TSH). In addition, the beta subunit of hCG is very similar to that of LH and, as we will discuss, hCG works a lot like LH.
What does hCG do?
Although the function of hCG in pregnancy is not completely understood, most experts believe the hormone is critical to maintain the function of the corpus luteum ( i.e., adequate progesterone production) during early pregnancy. The hormone level in the blood (and urine) rises rapidly in early pregnancy, reaches a peak at about 10-12 weeks and then gradually declines to a steady but low level throughout the rest of pregnancy. Not surprisingly, the hormone level is higher in pregnancies with multiple fetuses. Levels are very high in cases of maternal isoimmunization (i.e., Rh factor disease) and in women with hydatidiform mole or choriocarcinoma.
Clinically, other than its use as a pregnancy test, hCG has been used mostly as a fertility drug, in women to stimulate ovulation, and in men, to stimulate sperm production. The hormone is also used by pediatric endocrinologists and urologists in an effort to coax undescended testes into the scrotum. I do not think it is used much these days for this purpose
The use of hCG for weight reduction
The idea of using hCG as a diet drug seems to have come from the work of a British endocrinologist named Albert Simeons. Don’t ask me why, but Simeons studied the use of hCG injections for weight reduction in pregnant women and overweight boys in India. He found that treating these patients with extremely low-calorie diets (500 kcal/d) for several months at a time and low-dose hCG injections resulted in impressive weight loss that was mostly fat tissue, not lean body mass (i,e, muscle). Apparently, the idea caught on and for quite a number of years, hCG has been widely used (but below my radar) as a weight-loss drug. As best I can tell, there are no convincing scientific data to show any weight loss benefit from hCG (a very good reference on the subject is Lijesen GK et al: Br J Clin Pharmacol 1995;40:237-43). Various medical professional organizations have issued warnings about the ineffectiveness of hCG for weight loss.
Homeopathic hCG
Perhaps, the most interesting development has been the rapid rise in the popularity of oral hCG, so-called “homeopathic hCG.” This product comes in the form of drops and can be purchased from numerous sites on the internet. The sites typically consist of pages and pages of testimonials and how to purchase the product. I do not know if it is true, but an article in Wikipedia states that the U.S. Food and Drug Administration has deemed homeopathic hCG an illegal substance and it is not protected as a homeopathic drug. I am not aware of any credible scientific studies showing any health benefit from these oral products. One would not expect any benefit since “real” hCG is only biologically active when taken by injection. As you might expect, homeopathic hCG drops are very expensive, with typical treatment courses costing many hundreds of dollars.
Injectable hCG
What about hCG injections? There is no question that injected hCG is biologically active and has legitimate medical uses in the treatment of infertility. In men, hCG acts about like LH to stimulate testis testosterone production. In fact, hCG has been used by drug doping athletes to normalize testis size after they have taken high dose testosterone injections to enhance athletic performance; the testosterone injections inhibit LH secretion, resulting in shrinkage of the testes. In women, the effects of hCG are complex. The hormone can promote ovulation, and as discussed earlier, it can help support the corpus luteum and progesterone production. The hormone can also lead to increases in estrogen production by first stimulating synthesis of testosterone in the ovary which is then converted into estrogen by enzymes in the ovarian granulosa cells. Unfortunately, in some patients, hCG injections can result in the ovarian hyperstimulation syndrome in which very large increases in testosterone occur. The condition can be life-threatening with the development of massive edema and vascular thromboses. Many other hCG side effects have been reported. Of course, when used as fertility drug, hCG injections can greatly increase a woman’s chances of having a multiple pregnancy. Anyway, if hCG doesn’t really help promote weight loss, it is my opinion that the possible therapeutic risks (many) outweigh any possible benefits (none proven).
What is most amazing to me is that apparently many insurers will cover the cost of hCG injections for weight loss if prescribed by a physician . The hormone is marketed by several pharmaceutical companies (e.g., brand names include Chorex, Novarel, Pregnyl, and Profasi). Even without insurance coverage, the cost of injectable hCG is quite low, about $2.00/injection (a good summary of the costs and side effects can be found at eHow.com).
Who said our health care system is broken?
FYI: Nice Review About Vitamin D
I this afternoon’s mail, I got this week’s New England Journal of Medicine. To my surprise and pleasure, there was a review article about vitamin D written by Clifford Rosen (Rosen CJ: Vitamin D insufficiency. New Engl J Med 2011;364:248-54). The article does a far better job than I did in my last entry to discuss the vitamin D/calcium controversies. I strongly suggest you check it out.
What’s All The Excitment About Vitamin D and Calcium?
Recently quite a bit has been written about the apparent epidemic of vitamin D deficiency in the U.S. There have been many newspaper articles written about the need to increase vitamin D and calcium intake to prevent weak bones and fractures. As best I can tell, it is now the standard of care to measure vitamin D levels (as serum 25-hydroxy vitamin D or 25-OH vitamin D)) in all middle-age women and in elderly men and women. It seems that DEXA scans (a way to quantify bone mineralization) have become almost as common as blood glucose measurements. I have spoken to quite a number of people, mostly women, whose doctors (primary care docs and OB/GYN docs) have measured their vitamin D levels, found them to be “dangerously low,” and have prescribed supplemental calcium and vitamin D. So, do we really have an epidemic of vitamin D deficiency? I would submit that it’s mostly nonsense. I will try to explain.
First, there is no question that, weak bones (osteoporosis) are a problem in the elderly, particularly women. The prevalence of pathological fractures (those resulting from only minor trauma), particularly of the hips and spine are significantly increased in seniors and are very serious indeed. For the most part, osteoporosis in the elderly is the result of a number of factors including poor nutrition resulting in insufficient intake of vitamin D and calcium, decreased physical activity, and low levels of the sex hormones estrogen and testosterone.
Many people now take vitamin D and calcium supplements in an effort to keep their bones strong. Widespread use of these supplements led to a recent consensus statement by medical experts regarding recommendations for calcium and vitamin D supplementation- really an effort to clarify just what calcium and vitamin D requirements are at different ages (see “Extra vitamin D and calcium aren’t necessary, report says,” written by Gina Kolata, NYT November 30, 2010, page 1, A20). We will come back to the report later in my entry.
Vitamin D and Calcium absorption
Calcium absorption from the gut is different than for minerals such as sodium and potassium which are almost entirely absorbed; the absorption of calcium is incomplete and dependent on the body’s “need” for calcium. It is a good thing that calcium absorption is regulated since, unlike sodium and potassium, the kidneys cannot excrete excess calcium very well; large calcium loads can cause serious damage to the kidneys. Thus, the body normally absorbs just the right amount of calcium regardless of the dietary intake. The rate of calcium absorption is controlled by vitamin D, primarily 1,25-diOH vitamin D, the active component (25-OH vitamin D and related compounds can also modulate calcium absorption somewhat). The way this all works is that when the blood calcium drops even a slight amount, the parathyroid glands secrete parathyroid hormone which, in turn, stimulates formation of 1,25-diOH vitamin D, which in turn, stimulates intestinal calcium absorption. The process is modulated by other hormones such as growth hormone and estrogens, which have direct effects on the secretion of 1,25-diOH vitamin D. Glucocorticoids (e.g., hydrocortisone) in high doses can inhibit calcium absorption but this effect can be overcome by increasing intake of vitamin D.
Calcium absorption can be decreased in conditions that decrease fat absorption which decreases vitamin D absorption. Also, diarrheal states or any other conditions that increase intestinal motility, decrease calcium absorption. Some intestinal conditions such as celiac disease directly inhibit absorption of calcium. High fiber foods, particularly certain cereals can inhibit calcium absorption; high fiber foods contain large amounts of phosphates (specifically, an organic phosphate, phytic acid, which contains inositol hexaphosphate) which blocks calcium absorption. It is interesting that whole wheat flour contains large amounts of phytic acid but fortunately, the leavening process (adding yeast to bread), breaks down the phytic acid.
Absorption of calcium in dietary supplements (e.g., vitamins) can be affected by the chemical form of the calcium. Calcium supplements are generally either calcium carbonate or calcium citrate. Calcium carbonate, the most common form of supplemental calcium, requires an acid environment for optimal calcium absorption. Thus, diseases or drugs that decrease stomach acid inhibit calcium absorption. The citrate form of calcium is soluble and does not require an acid environment for absorption. So, if one is taking supplemental calcium that is in the carbonate form, it is usually recommended that the medication be taken along with or immediately after eating, which stimulates stomach acid production. I have not seen any good data showing just how different absorption of supplemental calcium is when taken with food or on an empty stomach. I doubt it matters much but just to be on the safe side, I suppose people should take calcium carbonate-containing supplements with meals.
Vitamin D is essential for normal growth and development. Both deficiency and excess of the nutrient can have serious consequences. Deficiency of vitamin D causes rickets, while excess can cause hypercalcemia and injury to many tissues, particularly the kidneys. Vitamin D is formed from 7-dehydrolcholesterol, a cholesterol precursor found in the skin. Ultraviolet light converts the precursor to vitamin D. Vitamin D2 (called ergo-calciferol) is formed from irradiation of the plant sterol ergosterol while vitamin D3 (called cholecalciferol) is formed from irradiation of 7-dehydrocholesterol. Both vitamin D2 and D3 are as potent as vitamin D in treatment of rickets.
Vitamin D (and vitamin D2 and D3) is not metabolically active. Rather, it is activated by first being converted to 25-OH vitamin D and then to 1,25-dihydroxy vitamin D. The first conversion takes place in the liver and the second in the kidneys. Both 25-OH vitamin D and 1,25-diOH vitamin D are metabolically active but the latter much more so (about 1000X more active). Vitamin D is a fat soluble vitamin which can be stored in the body fat for many months and be slowly converted into the active metabolites. This is a big problem in cases of vitamin D over dosage. As a fat soluble vitamin (just like vitamins A, E, and K), vitamin D anbsorption is affected by conditions that inhibit fat absorption, such as certain intestinal diseases and deficiencies in the intestinal enzymes responsible for fat absorption. Thus, it is important to consider the possibility of vitamin D deficiency in all patients who have fat malabsorption. Likewise, people who ingest very low fat diets, may have somewhat decreased dietary or supplemental vitamin D absorption. Of course, adequate exposure to sunlight, results in synthesis of all the vitamin D normally required. Some drugs do affect conversion of vitamin D to 25-OH vitamin D (e.g., cimetidine, some anticonvulsants) and as one would expect, liver disease can affect synthesis of 25-OH vitamin D as well. Kidney disease can affect synthesis of 1,25-diOH vitamin D.
For people taking vitamin D supplements, it is generally recommended that they be taken with food. One recent study showed that vitamin D absorption was significantly increased when taken with the biggest meal of the day (Mulligan GB, Licata A: Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D. J Bone Min Res 2010;4:928-30). I am not sure how to interpret the results of the study. There were only 17 study subjects and all had normal 25-hydroxyvitamin D levels at baseline. I don’t doubt the fact that taking vitamin D supplements with meals, particularly high fat meals, increases vitamin D absorption. What I question is whether it matters much for most people? If levels of 25-OH vitamin D levels are normal, is higher better? I have not seen any data to show any health benefits. In fact, recent studies show no relationship between serum 25-hydroxy vitamin D levels and mortality rate. Anyway, I suppose that for both calcium and vitamin D supplements, it makes sense to take them with food.
The Expert Committee Report
So, back to the recent expert report on vitamin D and calcium supplements. The bottom line is that most people do not need vitamin D and calcium supplements and they may, in fact be harmful. There are data to suggest that extra calcium can increase the risk of heart disease and compelling data to show that extra calcium increases risks for kidney stones and permanent kidney damage. The Institute of Medicine convened an expert committee to examine the available data to determine just how much vitamin D and calcium people really need. Much of the “push” to treat with calcium and vitamin D supplements was based on the misguided notion that levels of serum 25-OH vitamin D below 30 ng/ml were low. Based on this standard 80+% of people in the U.S. were vitamin D deficient. In fact, the committee concluded that levels between 20-30 ng/ml were just fine (in the “old days” the lower limit of normal for serum 25-OH vitamin D was about 15 ng/ml and I suspect that has not changed at all). Note: breast-fed babies DO need supplemental vitamin D.
What did change was the availability of new drugs called bisphosphonates to treat osteoporosis. The pharmaceutical companies, perhaps aided by the endocrinologists, pushed and pushed for more aggressive treatment of patients with weak bones. A new disease entity was created- osteopenia. This was defined as a condition in which the DEXA scan results showed normal but below average bone mineralization. To be sure, people with osteopenia are more likely to develop osteoporosis than those with higher bone mineral densities, but there was no scientific justification for treating large numbers of patients with bisphosphonates (and supplemental calcium and vitamin D) to improve their bone health. We certainly had the opportunity to learn about the complications that can develop with use of bisphsphonates (e.g., jaw necrosis).
The expert committee updated the recommended dietary allowance (RDA) for calcium and vitamin D emphasizing that most people in the U.S. already receive enough of both nutrients to manage just fine without supplements. For example, in women ages 51-70 years, the committee recommended calcium RDA of 1200 mg/d with a maximum of 2000 mg/d; the recommended vitamin D RDA for people 9-70 years was 600 IU with a maximum of 4000 IU. I know many people whose physicians have recommended that they take 20,000 IU or more of vitamin D daily to treat either their osteopenia or “low” 25-OH vitamin D levels. Crazy stuff
In summary, osteoporosis is a serious medical condition that can be caused in part by low calcium and/or vitamin D levels and that can predispose people to bone fractures. Most people in the U.S. are not deficient in either calcium or vitamin D and can maintain normal levels just by eating well and maybe, getting sun exposure now and then. If a person has a legitimate need for calcium and/or vitamin D supplementation, taking the supplements with food results in better absorption than if taken on an empty stomach. Physicians would do well to read the recent Institute of Medicine report on vitamin D and calcium supplementation.
Weight-loss Strategies: Some New Data
FYI: There was an interesting article in the New York Times the other day about the eternal struggle for weight loss. The article was published October 25, 2010, written by Nicholas Bakalar, and entitled “Approach may matter in advice on weight.“ The study, conducted by Nicholas Rodondi and colleagues at the University of Lausanne in Switzerland, looked at the relationship between the way doctors talked to their patients about weight reduction and results. The investigators found that “motivational talk” was more successful than “non-motivational talk” in resulting in weight loss after 3 months. The investigators defined motivational talk as an approach that enlists the patients’ desire for change and is not judgmental or confrontational. Anyway, it’s an interesting study and the approach makes sense but 3 months follow-up is clearly not long enough to determine if not fussing at overweight patients works best.
Who Invented Tanner Sexual Staging?
Every pediatric endocrinologist knows what “Tanner staging” is and how to do it but I am amazed that many of my younger colleagues do not know who or what the word “Tanner” stands for. In fact, Tanner staging is named after James Mourilyan Tanner, a distinguished English pediatrician who died on August 11, 2010 at the ripe old age of 90 years. I had the honor and pleasure of having knowing Dr. Tanner whose contributions to pediatric endocrinology were enormous. Tanner staging is a method developed by Dr. Tanner to describe in a series of steps, the progression of sexual maturation in males and females from pre-pubertal (Tanner stage 1), to full adult sexual maturation (Tanner stage 5). Thus, Dr. Tanner developed a method to grade the level of sexual maturation for breasts in girls, pubic and axillary hair in boys and girls, and genitalia (testes, scrotum, and penis) in males on a scale of 1-5. Of course, to develop such a scale, Dr. Tanner first had to study the course of adolescent sexual development in a large number of girls and boys. Dr. Tanner did this as part of his work in overseeing a long-term study of malnutrition in a large group of British children living in an orphanage in Harpenden England. Not only did his work result in a method for characterizing a child’s level of sexual maturation, his work also led to the development of modern-day growth charts, so indispensable to growth assessment.
So, when you see a clinic note on a 10 year old girl in which the physician has written “breast development was early T2 while pubic hair was T 3″ you can be sure every pediatric endocrinologist (and pediatrician) knows just what that patient’s pubertal status is. None of this would have been possible without Dr Tanner’s meticulous data collection month after month and year after year in the Harpenden orphans.
Dr. Tanner was one of the first pediatric endocrinologists to use human growth hormone and I remember well a lecture he gave many years ago, long before recombinant DNA-derived growth hormone was available. He lamented just how difficult it was to be certain that a patient did or did not have growth hormone deficiency; at the time, he estimated that even in “classic” cases, we over-diagnosed growth hormone deficiency about 30-40% of the time. Personally, I don’t think we do even that well these days despite all the fancy new growth factor tests (e.g, IGF-1, IGFBP3)!
I also remember how he used to talk about the importance of careful measurements. He lectured and wrote extensively on the proper way to measure children. Along with another Englishman, Reginald Whitehouse, he promoted the use of stadiometers for quantifying height in children.(a stadiometer is a fancy yardstick, perhaps more properly called a meterstick, with a counterweighted head board and a counter for direct reading of the height. A well-made stadiometer is expensive, but essential if one is to obtain reliable height measurements).
Anyway, for you younger pediatric endocrinologists out there, next time you carry out a physical examination in a child or adolescent and you do Tanner staging (which of course is a routine part of most every physical examination performed by a pediatric endocrinologist) , remember who to thank for the sexual staging system.
The Doctor-Patient Relationship: What Should Patients Be Looking For?
The other day, I mentioned that I would be writing about my experiences in dealing with my mother’s recent death. Early in my medical career, when I was a resident physician, much of the time I treated patients in an acute care setting, and not surprisingly, quite a number of them died from the assorted problems that got them to the hospital. If it was not a motor vehicle accident, then it was a myocardial infarction, meningitis, and so forth. In none of the patients did I have a long-term relationship preceding the acute event that brought them to the hospital, and my focus was primarily on the disease itself rather than on the disease, the patient and family. Over the past 35 years I have been a medical specialist and have had only a few patient die (mostly from motor vehicle accidents or drug overdoses) and with none was I serving as a primary care physician. So, it was mostly uncharted territory that I ventured into when my own mother became ill and was diagnosed with terminal cancer early in May of this year.
A brief medical history
My mother lived in Columbia, Missouri, not far from me. She was born in 1919 and had been generally quite healthy. A few years earlier, she developed a peripheral neuropathy (etiology unknown) and had to use a walker to get around. She stayed active, swimming 2-3 times a week. She had a primary care doctor, a general internist,who was on the faculty at the University of Missouri and whose office was only a few blocks from her home. She had a good relationship with the doctor and the nurse who worked with him and everything was fine and dandy. Then, all of a sudden, the doctor closed his practice and my mother did not have a primary care doctor. The doctor she had been seeing contacted my mother and told her that he was leaving the clinic, wished her well, and and he suggested another physician who he had taken the liberty of speaking with, and who had agreed to accept my mother into her practice. So far so good.
In January of this year (just after her original doctor left the clinic), my mother developed some vascular problems with her legs. She was seen in the internal medicine clinic by the “new” physician who took a brief medical history and referred my mother to a vascular surgeon for a consultation. From the time of the first visit with the new physician, my mother was not pleased. I felt the problem was mostly that my mother had gotten used to the previous doctor and that over time she would warm to the new doctor. Oh was I wrong.
As it turned out, my mother had an arterial thrombosis in her right leg and had vascular surgery at the end of January of this year. The surgery was not easy for her (at age 90 years, I don’t think any surgery is easy); she spent a week in the surgical intensive care unit but things improved steadily. Once out of intensive care, she was transferred to a medical/surgical ward and was cared for by the vascular surgeons and by the internal medicine hospitalists. Every day she was seen by a different internal medicine doctor and not once did she see or even hear from her new primary care doctor.
After discharge from hospital, my mother was scheduled to be seen by her primary care doctor. As it turned out, after the appointment was made, the doctor’s schedule changed and my mother was seen by an internist who was just “covering.” The clinic had known for a week that the primary care doctor would not be in clinic for my mother’s appointment, but did not inform my mother. The “covering doctor” knew nothing about my mother’s case history and I would describe the clinic visit as a disaster. My mother swore that she would never go back to that clinic again and she didn’t. She insisted that I find her a new doctor, someone like her previous doctor. I decided that my mother might do better with a family practice doctor. I twisted a few arms and the Chairman of the Department of Family and Community Medicine, and also a geriatrics expert, said he would be pleased to see my mother. An appointment was made for late April of this year.
Is it gall-bladder disease?
In mid-April, my mother developed intense itching and then her urine turned dark. Remember, my mother was in-between primary care doctors at this time. I ordered some basic lab tests (I was forced to order the tests since my mother did not have a doctor) and had the results sent to the new primary care doctor explaining in an e-mail that he was to see my mother for the first time in about a week for what was to be routine clinic visit. The test results were consistent with biliary obstruction but there was also anemia and the platelet count was very high. I as a pediatric endocrinologist was way out of my comfort zone. Within an hour after I e-mailed the lab test results to the new doctor, he called me and told me that he wanted to see my mother the next day if she was willing. She reluctantly agreed to the clinic visit (by this time she was tired of all doctors, nurses, hospitals, and clinics).
The first clinic visit with the new doctor
The next day, I drove my mother to the new doctor’s office and from the beginning, I knew things were going to be different. Starting with the receptionist then the nurse, and finally the doctor, it was a completely different atmosphere than at the internal medicine clinic where it was “all business.” First, all of the personnel acted as if they were actually happy to see my mother and made her feel comfortable. The doctor had already reviewed my mother’s chart (we have excellent electronic medical records at my university medical center ) and the visit didn’t start out as if the doctor didn’t know anything about my mother, which had been the case every time at the internal medicine clinic after my mother’s first doctor left the clinic. The new doctor’s demeanor was excellent. He spoke to my mother, not to me as had been the case previously and made her think she was his only patient. He didn’t rush and he explained things to my mother and told her what he wanted to do, why, and asked her it she was willing. When we left the clinic my mother was the happiest woman on earth- she had found a doctor just like her first one and she had complete faith in his recommendations.
The bad news
Unfortunately, as it turned out, my mother did have biliary obstruction, not from a gall-stone but from inoperable pancreatic cancer, diagnosed in mid-May of this year. To make a long story, a bit shorter, every step of the way from the work-up to the diagnosis and until my mother’s death on August 20, her primary care doctor “ran the show.” He took charge and made sure she saw whatever specialists she needed to see (e.g., oncological surgeon) but he maintained control of the treatment plan. He arranged for hospice care and was able to persuade her to do it even though I hadn’t been able to. He worked closely with the hospice team throughout.
At the very end of April, the new doctor went out of town for 2 weeks (on a cruise with his wife), but he had informed my mother of his upcoming trip and made arrangements for another colleague to manage her case while he was away, and called her immediately on his return. He even made a house call the afternoon before my mother died. Remember, this is the Chairman of the Department, a very, very busy man. But, once he agreed to see my mother, he made clear in everything he said and did that he had taken “ownership, ” something her previous doctor had not. For me it was a wonderful experience, considering the circumstances.
My mother certainly had enough to deal with given her diagnosis and the last thing she needed was to have a lack of confidence in her health care provider. But, my mother had complete faith in her doctor and it made all the difference in the world. Her doctor was not an expert in pancreatic cancer and maybe not expert in anything except the most important thing, expertise in knowing what it means to be a patient’s doctor.
Ownership and Medical Homes
These days there is considerable discussion about the need for each patient to have a “medical home.” The idea is that all patients, particularly those with chronic diseases, need to be part of a medical care system that can meet all of the patient’s care needs and that the patient care is provided in a organized and efficient fashion. Who can argue with such a concept? With my mother’s illness, I learned that having a medical home is not enough; it is also necessary that one person, be it a physician, nurse, social worker or whomever, needs to take ownership of the patient and do everything possible to be certain the patient’s medical care needs are being met within the medical home. For my mother, getting excellent health care could not keep her cancer from taking her life, but it made the final days and weeks of her life far better than they would have otherwise been. There is a lesson here for all of us.
One last thing. For those of you who are particularly interested in end-of-life issues, I highly recommend a recent article in the New Yorker, entitled “Letting Go. Rethinking end-of-life treatment,” written by our old friend, Atul Gwande. I warn you in advance- the article is long- but very well done.