Doctors Confirm 1st Law of Thermodynamics

February 25, 2009

A study just published in the New England Journal of Medicine concludes that reducing calories results in the same weight loss regardless of how the caloric reduction is realized. In other words a calorie lost from reducing fat, or carbohydrate, or protein has the same effect. “Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize,” is the study’s conclusion.

This study gets the tautology of the century award. How could these investigators have found otherwise without rewriting the law of conservation of energy and matter? The NY Times is duly impressed by the study’s importance. It’s featured in its Fitness and Health section. Lavoisier would have been delighted if he hadn’t already lost his head over something else.

Apparently, the state of science education has fallen so far that some further explanation is needed. If you burn 2400 calories a day (actually kilocalories) and eat a diet containing 2490 calories you’ll be 90 calories positive. It doesn’t matter what form these calories originally assumed; a calorie is a calorie. The extra 90 calories will be converted to fat and stored as flab. One gram of fat yields nine calories. Thus the 90 extra calories will result in 10 grams of fat. If this caloric excess keeps up for 45 days you’ll have an extra 450 grams of fat – about one pound. If you want to lose that pound you’ll have to burn 450 grams of fat to heat. This means that you’ll have to burn 4050 calories more than you consume. That’s a lot of calories just to lose one pound which is why weight loss is so hard.

Notice that no where does the source of the calories forsaken enter into this equation. If you want to lose a pound of fat you have to take in 4050 less calories than you metabolize. Thus the NEJM study which is getting a lot of press could not posssibly have been other than it is. No study was needed to discover this starling fact unless your initial premise was that the first law of thermodynamics was in question.


NY Times Execs Make Millions

February 23, 2009

The NY Times is waxing indignant about the high salaries paid to employees of universities. I predicted this 10 days ago. Of course I share their dudgeon as I don’t make that kind of money. Obviously these guys are paid too much. Of course, if I did make as much money as they do I would think I was appropriately paid and well worth a seven figure income.

The people listed in the Times article are all doing rather well at their jobs which may be an argument for their high salaries. I know this is lame, but I’m trying to be fair. Tamar Lewin who wrote the Times piece is doubtless a dandy reporter. She has a vastly larger audience than do I. She’s on to something and should pursue it.

The compensation packages for the NY Times’ top five executives are listed below. As you can see the information for the top two is N/A which could stand for not available, but not ashamed.

Mr. Arthur O. Sulzberger Jr., 57
Chairman and Publisher of The Times
Ms. Janet L. Robinson , 58
Chief Exec. Officer, Pres, Exec. Director and Member of Foundation Committee
Mr. Michael Golden , 59
Director, Publisher of the International Herald Tribune and Member of Foundation Committee
$1.10M $66K
Mr. P. Steven Ainsley , 56
Publisher of The Boston Globe and Head of New England Media Group
$814K N/A
Mr. John Geddes ,
Managing Editor

Mr Golden makes more than $1 million so it’s reasonable to assume that Mr Sulzberger makes considerably more. What kind of job has he been doing? Look at the chart of the Times’ stock price below and see what you think.


In one year under Mr Sulzberger’s leadership the share price has gone from about $20 to $4.  Five years ago a share of the Times sold for $50. And for this he gets millions! Why is he hiding his salary? Where’s the transparency? Ms Lewin needs to splash this across the front page. I bet she’s already on to the story. Good for her. There could be a Pulitzer here.

All this salary envy reminds me of Babe Ruth. In 1932 he was asked to explain why he earned more than President Hoover. His answer: “I had a better year.”

Life Expectancy, Medicare, and Preventable Death

February 21, 2009

I’ve recently read several articles dealing with the aging of our population. They all said that retired people have to confront the problem of a longer life expectancy. They have to husband their resources to last longer than did previous generations You’ve probably seen similar material. Everybody believes that old people are living a lot longer than did their forebears. The problem is that it isn’t true.

In 1850 the life expectancy for a white male at birth was 38.3 years. In 2006 it was 76 years – almost 40 years more. But that doesn’t tell us the fate of old people then or now. In 1850 a 70 year old white man had a life expectancy of a 10.2 years. In 2004 a 70 year white man could expect on average 13.7 more years of life. Only a three and a half year increase over more than a century and a half.

These observations have some fascinating explanations and important implications. In 1850 and well into the 20th century children died at an astounding rate. They died from an assortment of infectious diseases that are rarely seen today in the developed world. Deaths from these diseases virtually disappeared because of routine inoculations, antibiotics, and most important modern plumbing, sanitation and hygiene. The plumber by separating drinking water from sewerage has saved more lives than all the physicians who have lived or ever will live. So don’t complain the next time he charges you a couple of hundred dollars for a house call. He’s saved your kids’ lives.

People who don’t die young get the chance to grow old. We have more 80 year olds mainly because we have more 40 year olds. Put another way, there are more 80 year olds not because of better geriatric care, but because of better pediatric care. In 1850 20 year olds had a longer life expectancy than did newborns emphasizing how perilous childhood was back then.

Everyone is concerned about the financial train wreck that Medicare is or soon will become. This on top of the train wreck already here. The following question is inescapable. Is spending 10% or more of GDP to buy old people another three years of life a wise investment? The elderly undoubtedly would say yes. If you put a secret ballot on the question to their grandchildren I’m not sure what the answer would be.

Of course the question is more complicated than the way I posed it. Medical care for the elderly does more than prolong life. Much of it improves the quality of life. Cataract surgery does not lengthen life, but it really improves the quality of that remaining. The same is true for joint replacement surgery. I’m sure you can think of many other examples.

But what does the relatively small increase in life expectancy say about modern treatment for the main causes of death, cancer and heart disease? Cancer treatment has had almost no effect on mortality. The decrease in cancer deaths is almost entirely due to prevention, eg smoking cessation. We are regularly told that medical care needs to be refocused from treatment to prevention. The truth is we’ve already done this. Almost all preventable causes of premature death are being prevented. Children no longer die from infectious diseases. Nothing else we could conceivably do could have a fraction of the effect that this decrease in childhood mortality has had on overall human health.

Cardiovascular deaths have fallen in half over the last 35 years, yet old people don’t live that much longer. This suggests that when you are old if one thing doesn’t get you another will. There was a paper in Science around 1992 that suggested that if all deaths from cancer, heart disease, and diabetes were prevented life expectancy would only rise by about three years. A real but discouragingly small effect. The only way to dramatically increase human life span in the developed world is to arrest the aging process. Doing so would create a mammoth new set of social and political problems that you can work out yourself.

When a financial planner tries to sell you some instrument designed to cope with your longer post-retirment life span tell him to look at the life tables and come back latter. If your grandfather made it to retirement age he likely lived virtually as long as you will.

The Recordings of Enrico Caruso 1910

February 18, 2009

Caruso made 25 recording in 1910. Here’s a selection, Solo, profugo, reietto, from Flowtow’s Martha that’s not “M’appari”. It’s almost never played today. Caruso was in splendid voice and makes a fine case for this rarity. The bass in Marcel Journet. The number also shows the tenor’s liberal use of portamento; tenors today are a little more sparing in their use of this technique.

The highlight of Caruso’s 1910 recordings was the nine sides devoted to Gounod’s Faust. Together with “Salut demeure” (issues earlier) they contain most of the tenor’s music in this opera. Virtually the complete Garden Scene with Geraldine Farrar (he called her the “beautiful Geraldine”) was recorded on for sides. This excerpt give a hint of what Caruso sounded like in a compete performance. Heard in the first half of the scene are Gabrielle Gilbert and Marcel Journet.

Geraldine Farrar

Geraldine Farrar

Farrar appeared regularly with Caruso in this and other roles. We can only lament Victor’s failure to record the whole opera, though I don’t know if there would have been a market for such a gigantic undertaking in 1910.

Caruso again returned to Franchetti’s Germania.In Studenti! Udite! he was in such refulgent form that you almost want to hear a performance of that  forgotten (except for Caruso’s part in it) work. After two operations on his vocal chords  he sounds better than before the surgery. I’d love to know who his surgeon(s) was.

His recording of  No! Pagliaccio non son reminds the listener that he sang more of Pagliacci than the famous first act aria. It shows why this was his most popular role; he sang it 116 times with the company. His sound is very dark in this recording. There’s a tiny, almost unnoticeable, catch in the high note at the end. If you don’t listen carefully you’ll miss it, but still I wonder why he didn’t rerecord the number. You’d never have noticed it in the opera house.

Caruso never sang Verdi’s Otello on stage. He was thinking of doing it , but his premature death canceled that plan. Ora e per sempre addio shows what his audience missed. At the time of his death his voice was ideal for the most demanding tenor role in Italian opera.

If you listened to the Met’s broadcast of Il Trovatore (February 16) you heard how much this opera depends on great singers in all the major roles.  Unfortunately it was a negative lesson. Listen how effortlessly Caruso sings the tenor part of Mal reggendo. The mezzo is the great Louise Homer who is as equal to the task as Caruso.


Caruso's caricature of himself as Radames

Caruso and Homer are equally good in the Judgment Scene from Aida – Gia i sacerdoti adunansi. The power and excitement of their voices still resonates even after a century. If you want to give Verdi his due and you have pretensions to be the world’s greatest opera house you have to find singers who if not at this level are close.

He also recorded a song in English for the first time. The song is Tosti’s “Addio” (Goodbye) translated in English. Listen very carefully you will be able to understand a word her and there.

While Caruso was able to maintain this level of excellence he couldn’t have gotten any better. This as good as it can get.

More to come later.

Met’s New Il Trovatore Vocally Disappointing

February 17, 2009
Marcelo Álvarez

Marcelo Álvarez

Enrico Caruso declared that all one needed for a good performance of Verdi’s masterpiece of the id gone berserk – Il Trovatore – were the four greatest singers in the world. Unfortunately they did not show up last night at the Met’s first performance of it’s new production at least if you were listening on the radio. Alas they almost never show up for this opera.

On paper the listener had a good shot at three out of four. Marcelo Álvarez at his best never had the right sound for Manrico. Not anywhere near his best he barked his way through the role and gave a textbook example of how not to maintain a lyrical line in a less than provincial reading of “Ah, si ben mio.” His voice is dry and unpleasant and for this he gets opening night next season. He did a little better with “Di quella pira”. He omitted the first interpolated high C , but sang the second (down to a B). There’s not much left of his voice which was a pleasant, though not remarkable one when he first appeared.

Manrico needs a tenor with a firm and focused tone like that of Björling, Tucker, Corelli, or Domingo. If you have to transpose the Cs down a half tone fine. Even Caruso did it.

The 39 year old soprano, Sondra Radvanovsky, has an odd sounding voice that becomes fluttery the higher it goes. I think it’s because her voice is not well placed coming more from the throat than the mask. I suspect her voice will not age well.  Her rendition of Leonora was mixed. In the first act she mangled the high note she inserted near the end of “Tacea la notte placida”. It was a scream of indeterminate pitch. She ended the aria’s cabaletta with a low note. I don’t know if she intended to end the piece that way or if her nerves were shot after the earlier mishap. She did better in the fourth act. “D’amor sull’ali rosee” was well sung, but if you were expecting the lush sound of Milanov or Leontyne Price you were disappointed. There was a loud claque at the show – professional or amateur I don’t know – that sometimes carried the applause a little further than warranted.

Dolora Zajick has been one of the greatest of all Verdi mezzo-sopranos for the last two decades, but even she was not at her best. She got no applause after Stride la vampa – the claque was asleep. She attempted a high note near the end of her scena (“Ferma! Son io che parlo a te!”) with Manrico in the second act that while not a scream, was more an off pitch shriek. Her mid and low notes are still outstanding.

Dimitri Hvorostovsky should have taken on the Count at the Met 10 years ago. The best Verdi baritone of his generation hasn’t sung as much Verdi as he should have. At this stage in his career his voice is not as bright and beautiful as it was just a few years ago. His top is also not as free as formerly. There was nothing wrong with his portrayal it just wasn’t what was expected of it. He’s also starting to bellow – just a bit – at places were he used to sing suavely. “Il Balen” was ordinary. He didn’t even sound as good as he did when I heard him in Simon Boccanegra in San Francisco last year and then he was a little underpowered.

Bass Kwangchul Youn made little of a part (Ferrando) that is typically made little of. Gianandrea Noseda conducted. He followed the singers without incident. If the Met’s Lucia Di Lammermoor 10 days ago was a home run this 600th performance of Trovatore by the Met was a sacrifice fly. I’ve heard the opera sung at least as well in Sweden with a cast including no one you’ve ever heard of.

IRS Should Force Churches to Pray More

February 13, 2009

A new report by the IRS has documented that most not for profit hospitals don’t take care of poor people. The author of the report could have asked his mother and she’d have told him that hospitals only take care of non-payers at the point of a gun and she’d have done so at no cost to the government. An IRS report on whether a tax on love will increase federal revenues is due Valentine’s Day; the year has yet to be specified.

According to the Wall Street Journal, “Sen. Charles Grassley is considering introducing legislation that would hold nonprofit hospitals more accountable for their tax breaks, aides to the Iowa senator, who is the ranking Republican on the Senate Finance Committee, have said. The legislation would require them to spend a minimum amount on free care for the poor and set curbs on executive compensation and conflicts of interest, the aides have said.”  Some top level executives at not for profit hospitals are making (I’d never say earning) more than $1 million a year. I don’t know how many have corporate jets.

Sen. Grassley, the deep thinking republican from Iowa, has not thought deeply enough. This problem is worse than he realizes. Harvard is a not for profit corporation that has a 12 gazillion dollar endowment that used to generate tax free earning and likely will again sometime this century. It pays some of it’s faculty $500,000 a year and they have tenure allowing them to all hold the same opinions. Harvard’s president makes at least a million. Both these figures seem way too high to me. Grassley should haul some of these freeloaders before the finance committee and tell them about the real world.

After he gets finished with Harvard he can look closer to home. The University of Iowa probably pays its football coach $2 million or more a year. This is a real triple dip. The university is owned by the state, contributions to its athletic department are tax deductible, and it gets federal grants. I’m sure Grassley will be shocked and dismayed when he discovers these outrageous inequities. Even the team’s quarterback makes less than $2 million and he has to take hits by 300 pound linemen while the coach just needs a scowl and a clipboard. See list below. *

Grassley should also look at churches. They’re all tax exempt. They don’t even pay property taxes. This is grossly unfair to atheists. To belong to one of these tax exempt churches you have to be a member of its denomination. They refuse to admit people to membership because of their religion. Not only is this unfair it’s probably illegal. Some pastors are clearly paid too much. They get six figure salaries and plush benefits. The government should set limits on their compensation as a condition of their retaining their tax exemption. Furthermore, if churches want to keep their tax exemptions they should prove they are regularly praying for the souls of atheists. A certified prayer audit should be mandated. You don’t wanna pay you gotta pray.

Professional baseball enjoys an exemption from anti-trust laws. $27 million a year for a baseball player who uses performance enhancing drugs – I’ve already written about Viagra – outrageous. We need more of Grassley here too. The government should direct that no athlete who plays in a stadium that was given a tax break when it was built should get more than $500,000 a year, even if his sport doesn’t get a pass from anti-trust laws. Also no corporate jets for executives or players who’ve gotten any sort of help from government.

Talking about jets, Nancy Pelosi should have to fly on commercial flights just like the rest of us poor jerks. Joe Bidden should stay on Amtrak; he likes it and they need the business. Doing so would also spare the US embarrassment abroad. I’d let the president keep Air Force One as it would be mortifying if he got stuck on American Eagle in Lubbock when he was supposed to be in London.

When you come right done to it, everybody should work for minimum wage. The government should make up the rest with more benefits. What’s attractive about this plan is that no one will be making enough to pay income tax so the benefits will go further. Income tax receipts are now such a small fraction of our national expenditure that we won’t miss them.

As for Congress, their zeal for public service is obviously so great that they won’t mind working for nothing. Finally, if you need someone to blame about anything that’s going wrong don’t look in the mirror – blame George Bush. Bashing him should work for at least two more election cycles and it makes everyone feel so much better.

The following list has just been released – Feb 23, 2009

Top college salaries

Highest earners at private colleges (in millions, not including college presidents –  many president make more than $1 million):

1 Pete Carroll, head football coach, USC $4.4
2 David Silvers, clinical professor, dermatology, Columbia $4.3
3 Michael Johns, executive VP, health affairs, Emory $3.7
4 Arthur Rubenstein, executive VP and dean, School of Medicine, University of Pennsylvania $3.3
5 Zev Rosenwaks, professor, Center for Reproductive Medicine and Infertility, Cornell $3.1
6 David Swensen, chief investment officer, Yale $3.0
7 Harry Jacobson, vice chancellor health affairs, Vanderbilt $2.6
8 Jeffrey Moses, professor of medicine, Columbia $2.5
9 Norman B. Urmy, former executive vice president for clinical affairs, Vanderbilt $2.4
10 James Grifo, professor, obstetrics and gynecology, NYU $2.4

Erectile Dysfunction and Coronary Artery Disease

February 11, 2009

It’s not surprising that doctors have wondered whether erectile dysfunction (ED) is a marker of coronary artery disease (CAD). After all both disorders result from impaired blood flow to the two involved organs. Because the penile artery is about one third the diameter of the coronary artery, vascular disease affecting both these arteries might become symptomatic in the former before declaring itself in the latter. Thus ED might be a harbinger of heart disease. As ED and CAD have complicated pathophysiologies the association between them might be loose. But if the association could be documented interventions designed to arrest the progression of CAD could be started at an early stage thus preventing the disease from causing serious morbidity or premature mortality.

To this end a group of investigators studied a cohort of white men from Minnesota. The study is limited by the narrow group examined, that it partly based on a self report questionnaire, and examination of medical records. It’s authors are aware of these limitations and include them in their discussion. This study was published in the February 2009 issue of the Mayo Clinic Proceedings – (A Population-Based, Longitudinal Study of Erectile Dysfunction and Future Coronary Artery Disease).

The paper’s authors conclude: ED and CAD may be differing manifestations of a common underlying vascular pathology. When ED occurs in a younger man, it is associated with a marked increase in the risk of future cardiac events, whereas in older men, ED appears to be of little prognostic importance. Young men with ED may be ideal candidates for cardiovascular risk factor screening and medical intervention.

As I’ll show this conclusion, which may be correct, goes a lit bit beyond what the data allow. I’ll ignore any limitations of the study’s design and only concentrate on the data.


When all the subjects studied are lumped together those with ED are about twice as likely to get CAD as a similar group without ED. HR stands for hazard ratio while CI is the confidence interval. If the CI does not straddle 1 the HR is significantly different from the control group. The further away from 1 the CI the greater the significance (typically defined as a P value = or <0.05). If the HR is greater than 1 the ED group is more likely to have CAD. Were it less than1 the ED group would be less likely to have CAD. The comorbidity adjusted data account for the influence of other risk factors which predispose to CAD – smoking, hypertension, diabetes, high cholesterol, etc. The data support a link between ED and CAD.

Age stratified

These data were interpreted as showing that ED at a younger age was associated with CAD, but as you can see  (click on the table for a clearer image) the HR straddles 1 in all the groups. Thus while these data suggest an association with ED and CAD in subjects 40-49 they are not statistically significant and do not justify the conclusion reached by these investigators even if it turns out later to be correct. The comorbidity adjusted data are not even close to statistical significance. Just for kicks look at the HR for the subjects over 70. If you want to over interpret data you could say they suggest that ED is associated with a decreased likelihood of CAD.

So where are we? Just where we started. We need more information. If this association between ED and CAD  could be definitively established we could use ED in the relatively young as a risk factor for CAD and start treatment designed to prevent vascular disease. However, we would first require another study demonstrating the safety and efficacy of such a prophylactic regimen before we could confidently prescribe it. To be clear, I’m talking about whether we should us ED as a cardiovascular risk factor in patients who lack any other risk factor. And if so, should we treat these patients? If other risk factors were present we would already have reason to treat.

The same issue of the Mayo Clinic Proceedings has another article, Erectile Dysfunction and Cardiovascular Disease: Efficacy and Safety of Phosphodiesterase Type 5 Inhibitors in Men With Both Conditions, which examines both the evidence that ties ED with cardiovascular disease and the safety of phosphodiesterase 5 (PDE5) inhibitors in patients who have comorbid condition. This paper concludes that, Erectile dysfunction and cardiovascular disease, especially CAD, share the same risk factors: smoking, high blood pressure, high cholesterol, and diabetes. These 2 conditions also share the same pathophysiology, mediated by endothelial dysfunction. Thus, ED may be an important risk marker of silent vascular disease in men with no cardiac symptoms, providing physicians with a unique opportunity to uncover and address underlying CAD in patients who present with ED. It is recommended that physicians screen these patients for vascular disease. Because ED is often associated with comorbid conditions such as diabetes, hypertension, or dyslipidemia, screening should also include measurements of blood glucose, lipids, and blood pressure.

It doesn’t tell what the physician should do with a patient who has ED and high lipids, but who has no other cardiovascular risk factors. Primary treatment of hyperlipidemia (ie treatment of patients with high cholesterols without CV disease or other risk factors) has not been shown to be of value, though many physicians treat regardless. Is the combination of the two reason enough to prescribe a statin?

There are three PDE5 inhibitors currently available – sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra). They work by selective inhibition of PDE5 in the corpus cavernosum of the penis. This in turn reduces degradation of NO which increases cGMP which then results in vasodilatation, increased penile blood flow, and an erection.

So is it safe to give these drugs to patients who already have CV disease? The available evidence  which is well documented in this paper suggests it is. The safety profile of the three drugs available as well as that of their efficacy is the same.

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