Are bradyarrhythmias more common in long time endurance athletes?

 The relationship between the volume of aerobic exercise and health benefits has been described alternatively as curvilinear or U shaped with the current consensus favoring the former .

The curvilinear relationship between aerobic exercise volume and cardiovascular and all cause mortality is firmly founded in multiple large epidemiologic studies. The suggestion that the curve turns upward at some range of exercise volume and becomes U shaped  has not been actually  demonstrated in large epidemiologic studies. and is conjectural. 

.A reported increase in atrial fibrillation, foci of myocardial fibrosis and increased coronary artery calcification may  provide mechanisms for this proposed  ascending portion of the proposed U shaped curve which is the graphic representation of the "Extreme exercise hypothesis".

Is it possible or likely that  there may be other deleterious effects of too much of a good thing in regard to aerobic exercise.?Sinus node disease and cardiac conduction defects might also represent long term deleterious effects of long time aerobic exercise.I say "might" because there is suggestive but not conclusive data to that effect. 

 My personal experience ( 35 years of marathon running  and  development  of  a left bundle branch block (LBBB) and an exercise induced,high grade second degree AV block requiring a pacemaker) and  personal knowledge of two other long time, local runners also needing  a pacemaker) peaked my interest.

 But so much for numerator based reasoning what is the evidence for long time aerobic exercise contributing to the development of  clinically relevant bradycardia induced by sinus node  disease and/or A-V blocks. Case series and some epidemiologic studies provide some insight.

Andersen et al (1) published a  widely quoted cohort study of 52.755 cross  country skiers who participated in the Vasaloppet,a 90 kilometer cross country ski race,said to be the oldest and largest cross country event in the world. 

Outcomes of interest were hospitalizations for atrial fibrillation (AF) or bradyarrhythmias( BA) as documented in Swedish national registries. When comparison were made between those who skied the race more times ( five or more)  with those who skied only once there was a statistically significant  increase in the hazard ratios for both AF and BA.For AF the HR was 1.29 (1.04 -1.61,for BA the HR was 2.10 (1.28-3.47).

A similar trend for AF and BA was noted when the faster skiers were compared with slower skiers but failed to reach statistical significance.

The bradyarrhythmias were mainly second degree heart blocks but the hospital codes did not distinguish between type 1 and 2 which is an important distinction as type1 (Wenckeback) is recognized in endurance athletes and is not usually considered an indication for pace maker implantation.

This was very coarse grain study and such important data such as history of elevated blood pressure,diabetes,obesity,alcohol abuse,habitual level of exercise, etc were not available ..

 Baldesberger at al (2)  studied 62 former professional cyclists who had long since retired from competition . and compared them to 62 age matched golfers for controls. Two had pacemakers.None had bundle branch blocks or second degree AV blocks while six were said to have sinus node disease based on heart rates less than 40 per minute. A question that the authors wanted to answer was -does the slow heart rate , first degree heart block and type 1 second degree block said to be  common in competitive racers persist in later years after their period  of  heavy training has ended. Their persistence would suggest that vagal tone which is usually  the proposed mechanism for those cardiac finding is not correct and that electrical remodeling of the SA node and AV node might be responsible.  Though a small study these data suggesting increased risk of sinus node disease  seem to be the best evidence so far since a comparison was made with age matched controls 

The remaining data are simply case reports.

 Dr R Northcote (3)  published a study of the bradycardias seen in 20 long time, older endurance athletes in Scotland.Nine of the twenty had heart rates less than 35,six had a prolonged P-R interval and four had Mobitz type 2 heart block which disappeared with exercise..One of the 20 had a pacemaker implanted. A follow-up publication in 1999 (4) indicated that 2 more of the original group has been implanted with a pacemaker. 

Doutreleau et al (3) published a report of 2 active  endurance athletes with type 2 second degree heart block that occurred during exercise. The authors claimed erroneously that their publication was the first to report a high degree AV block either at rest or with  exercise, somehow  having missed Northcote 's2 reports. Exercise induced heart block is uncommon.

The athlete's bradycardia has traditionally been attributed to high vagal tone but an alternative proposed mechanism is electrical remodeling, specifically downregulation of the so called funny channel AKA HCN4. In older endurance athletes "fibrosis" of the SA noted is often proposed as the culprit but remodeling is an alternative explanation. The sparse data so far available suggest that SA node disease may be more common in endurance athletes while there is less compelling data implicating AV blocks. 

In a comprehensive review of the "extreme exercise hypothesis" by Eijsvogels in 2018 (6) there is no discussion of the issue of bradyarrhythmias but perhaps  clinically significant BA should at least be considered candidates for still another consequence of too much of a good thing. 

In 1964 writing in the same journal Dr. Lev and Dr. Lenegre  separately  described age related fibrosis of the conduction system as a cause of heart block in the elderly. In 1999 ,JJ Schott (7) identified two families with progressive cardiac conduction defects related to a mutation in the gene encoding for the sodium channel SCN5A.

How could one know given  for example an older endurance athlete  with a heart block if Lev/Lenegre disease  were responsible or if the block was somehow induced by excessive aerobic activity? 

1) Andersen K et al  Risk of arrhythmias in 52,755 long-distance cross-country skiers: a cohort study.Eur Heart J. 2013 3624 31, Dec 34 (47)

2)Baldesberger,S et al Sinus node disease and arrhythmias in the long term follow-up of former professional cyclists.Euro Heart Journal 2008, 29, 71-78

3)Northcote, R et al Electrocardiographic findings in male veteran endurance athletes. British Heart J. 1989,61,155-160

4)Hood,A and Northcote, R of Cardiac assessment of veteran endurance athletes, a 12 year follow up study. British J Sports Med. 1999, 33, 239-243

5)D'Souza, A,Cross talk opposing view: Bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. J Physiol 2015 Apr 15 593 (pt 8)1749-1741

(6) Eijsvogels T. et al The "extreme exercise  hypothesis":Recent findings and cardiovascular health implications Current Threat Options Cardio Med (2018)20:84

(7) Schott, JJ et al Cardiac conduction defects associated with mutations in  SCN5A .Nature Genetics 23:20-21 1999

Addendum : 12/12/20 In the original posting the section of Lev/Lenegre and SCN5A was inadvertently  omitted, 

Left Bundle Branch mediated cardiomyopathy- impressive results from His Bundle Pacing

 At least as early as 1989 CL Grines described significant functional abnormalities in patients with left bundle branch block (LBBB).

Blanc et al in 2005 and again Vaillant et al  in 2013  described patients with LBBB induced heart failure (HR) that was impressively improved  by cardiac resynchronization therapy (CRT) in the form of bi ventricular pacing.Blanc commented that this was a new concept of left ventricular dyssynchrony - induced cardiomyopathy.

In spite of the fact that it has been known for 30 years  that  left ventricular functional changes are caused by LBBB and it has been fifteen years since a LBBB induced cardiomyopathy was described we continue to find current journal articles that depict BBB without other cardiac disease as not a clinical problem.

R Singh et al (1) recently reported the results of His Bundle Pacing on 9 patients with LBBB-mediated cardiomyopathy. The left ventricular ejection fraction increased on average from 25% to 50% while the left ventricular end-diastolic volume decreased from 55 to 48mm., while the QRS duration decreased from 152 to 115 milliseconds. This represents another article indicating that His pacing gives results as  good or perhaps better than Bi ventricular pacing for CRT. 

1) Singh, R et al His-Bundle pacing: A novel treatment for left bundle branch-mediated cardiomyopathy.

J of Cardiovascular electrophysiology 2020 vol 31 no 10.

Habitual aerobic exercise and arterial stiffness

It has been known for at least 20 years or more than endurance exercise done over a  period of  time can mitigate the age related increase in central artery stiffness.Work published by Tanaka in 2000 and  data from the BLSA in 2003 established that relationship. refs 2 and 3 The duration and intensity of exercise are important determinates of that mitigation .

Sedentary aging is associated with changes in the left ventricle (LV) , including :
increase in wall thickness,increased mass and decreased diastolic function.The LV is stiffer and relaxes less well It has been suggested that the heart burdened by these accountments of aging are sitting ducks for a second hit  (High blood pressure,obesity,diabetes) which could lead to heart failure with preserved ejection fraction (HFpEF), a type of heart failure constituting about  one half of all HF cases and for which there is no good treatment.

Gates and colleges (1)from University of Colorado studied the question of whether  attenuation of age related increased in arterial stiffness by long term endurance exercise might help preserve LV structure and diastolic function. This was a reasonable hypothesis as it had ben the general party line  for years that the increased afterload imposed on the left ventricle from stiffening of the aorta with loss of its capacitance function would produce deleterious changes in the left ventricle and secondarily left atrium .

 In a cross sectional study  of 138 young,middle aged and older men who were sedentary, recreationally active or endurance trained ,Gates  found that regular endurance exercise did not"consistently modulate the changes in LV structure and function that occur with physiological aging in men" . Several publications from Ben Levine and the group from the Institute for Exercise and  Environmental Medicine in Dallas  have provided data that I believe provides refutation of that conclusion,their data demonstrating favorable remodeling of the Left Ventricle with maintenance of a more youthful left ventricular  compliance.


1)Gates,P E Left ventricular structure and diastolic function with human ageing. European Journal of Cardiology. 2003,24,2213-2220

2)Tanaka,H Aging habitual exercise and dynamic arterial compliance. Circ. 200 102, 1270

3)Havlik,R Association of physical activity and less vascular stiffness in 70-79 year old.The health ABC Study. J of Aging and Physical Activity. 2003, vol 11 , issue 2 156-166

Covid19, the Pareto Principle, super spreaders and value of testing backwards

 The Pareto Principle or the 80/20 rule states that a small number of events are  often responsible for a large numbers of consequences or outcomes.

Influenza spreads in a deterministic way, person to person .There is epidemiological evidence that points towards covid19 spreading in a more random fashion or stochastic mechanism in which randomness plays a major role in the form of super spreader events. It is believed that many, perhaps most persons infected by the Sars Cov 2 virus do not spread the disease to a  large number of people but rather to one or two at the most . Others , however, if the personal and situational  circumstances are right can spread the disease to hundreds of others .

The circumstances were right when "Patient 31" in Daegu South Korea was shown to be the index case in the covid19 infection of  5,000 cases in a megachurch super spreader incident;  Covid19 spreader events such as the Biogen Conference in Boston and the  choir spreader event in Washington are well known. Of course,person to person spread can then occurs in households or through close contacts in work settings  after the big event seeding.

The role of super spreader events opens the door to "backwards" testing in which a positive case 's previous attendance at event ripe for spread could be investigated .

See the excellent article by Zeynap Tufekci  in the Atlantic that discusses these concepts. 

(See https://www.theatlantic.com/health/archive/2020/09/k-overlooked-variable-driving-pandemic/616548/)

Exercise may prevent age related motor unit loss

Regular exercise may prevent-or at least  significantly slow down- motor unit loss  in the muscle groups exercised.  GA Powers et al demonstrated that there was significantly less loss of motor units in the tibialis anterior  muscles of long time runner as compared with older sedentary otherwise healthy subjects.   

The estimated number of motor units in the group of masters runner (average 65 years)was the same as those in young active runners (age average 25)

 

Interestingly the arm muscle of the runners did not show less motor unit loss, although one would think the arm movement during running would be helpful in that regard.

Muscle loss can be due motor unit loss ( remember the motor unit includes the anterior horn cell) or muscle atrophy or both. You have to think that once anterior horn cells die no amount of exercise will rejuvenate the muscle.

1) Power, GA et al  Motor unit number estimates in masters runners: use it or losse it?

Med Sci Sports Exerc 2010 Sept 42 (9) 1644-50

Population Medicine, The Baptists and Bootleggers and risk factor epidemiology.

 Goeffrey Rose in his 1985 book "Sick Individuals and Sick Populations" likely never intended to provide  intellectual grist for the mill of the major pharmaceutical industry but I argue he did just that...

His thesis is  that a large number of people at small risk for a given disease may give rise to more cases than the small number of those at high risk. Rose's population strategy was that there would be a large benefit to the population by treating the low risk people .Large benefit to the community may offer little to the each participating person and in some instances harm and bringing more benefit to an individual may have small impact on the population's health. This was labelled the Prevention Paradox. 

Interesting, this conception assumes that it makes logical sense to speak of the health of an aggregate which I argue is a category error. Is there a health of the community distinct from the health of its individual members?

Rose's imperative was to decrease the total disease burden of a population.What is important in this formulation is that the aggregate is more important that any of the individuals who make up the aggregate.Individual bees,except  for perhaps the queen, mater little , it is the health of the hive that must be promoted.

Next the idea of risk factor comes into play. This notion was brought into prominence and became part of the the jargon of medicine by the  authors of the Framingham study who set out to find the cause of coronary heart disease and concluded there is not one single cause but rather there are a number of factors, designated as risk factors,the possession of which by a person can be considered to increase  his risk of developing coronary heart disease. The field was ripe for the "treatment" of risk factors and "preventive" medicine would find  many new things to prevent.

The slippery notion of the nature of risk was given little attention in medical journals.- as the risk factor revolution of medicine burst forth, first with coronary heart disease and then for as many diseases whose risk factors the epidemiologists   ( and young general medicine department faculty members with recently minted MPH degrees) could generate with increasingly broad based and coarse grained data dredging .To name a few - osteoporosis,hypertension, diabetes,cancers, all have accumulated their own array of risk factors as have  alcoholic abuse, depression and internet addiction.With greatly increased access to computer statistics programs and processing and p value hacking it seemed that almost everything is a risk factor for something and making big deals over small differences ( relative risks less than 2) increased the risk that reading the daily news would makes the average reader think he was at a risk for something.

With Rose's population thesis and the epidemiologists' increasing supply of risk factors the opportunities for the drug companies burst forth.The idea that just about any disease can be described as a public health issue opening the door for "public health solutions" which typically involves governmental involvement if not governable coercion, at least in the form  nudges consisting of grants and public education campaigns. 

People were increasing treated for pre-diseases; pre-coronary heart disease, pre- hypertension,pre-diabetes, and even pre-bipolar treatment for moody,irritable ,grumpy kids .Cardiologist Tom Giles sarcastically talked about everyone  possessing the risk factors for  being "pre-dead".

Pre-patients ,after being informed of some risk factor for something,were advised to see their physician health care provider to "determine" their personal risk.This is of course an impossibility because all the provider can do is to parrot what the pre-patient has already read, namely that he is a member of a group   which has allegedly an increased risk, there being no technique learned in medical school  health care provider school that enables the provider to magically provide a personal risk, that concept making no logical sense. 

Note: This is a lightly edited version of a blog entry from five  year ago. It hits on several of the themes I have obsessed and ranted about for some time and thought it would be a good posting for my 1200 th blog entry since February 2005. 

In regard to the topic of population medicine I highly recommend the book 'Moving Mountains" by Dr. Michel Accad. In the book Accad discusses the emergence of population medicine as the results  of developments in economics,science and the ethics of healthcare much to the detriment of the physician patient relationship.

In regard to The Baptist and Bootleggers.I am referring to the concept popularized by Bruce Yandle . See "Bootleggers and Baptists. How Economic and moral Persuasion interact to shape regulatory Policy." Baptists and bootleggers both supported laws forbidding alcohol sales on Sundays , but for different reasons. 

Thoughts about the epidemiology of exercise volume and health effects

Considerable data exist that  allow reasonable estimates of the volume of exercise required to : 1) decrease cardiovascular disease (CVD) risk 2) decrease the risk of heart failure.

There are considerable coarse grain epidemiologic data that support the notion that regular aerobic exercise will decrease heart attack risk, reduce heart failure risk and reduce all-cause mortality.

The 2018 Physical activity guidelines for Americans recommended at a minimum of  approximately 8 metabolic-equivalent hours per week ( 8 met-hours or 500 met minutes per week.)

The recommendations translate to 150 minutes of moderate exercise (less than 7 Mets) or 75 minutes of vigorous  exercise per week.

 Arem et al ( 1) pooled data from 6 studies (661,137 men and women) and  demonstrated a 20% reduction in mortality among those who exercised at the recommended level with an HR of 0.8 (CI 0.78-0.82) and a 37% lower risk for those who exercised at 2-3 times the minimum level and the maximal benefit at 3-5 times the minimum (  0.61, CI 0.59-0,62)

Further no excess risk was evident even at exercise levels of 10 times the minimum.Here more did seem to be better and no definitive upper limit was apparent.

Wen et al (2) published all cause mortality  data similar  to Arem and  also found that the maximum  CVD mortality risk reduction (45%) ( HR 0.55 CI 0.46-0.66)  at an exercise level of 523 minutes per week, a level roughly 3.5  times the minimum recommendation.


These 2 articles are part of the evidence  regarding the safety of exercise levels higher than the 2018 recommendation. Drs Carl Lavie and James O'keefe have spoken ( TED) and warned  in print about the purported hazards of long bouts of  or too many years of aerobic exercise. In 2015,  perhaps in part reaction to the Arem article and commentary by Dr. Ben Levine,  Lavie and O'Keefe toned down their emphasis on the risk of long distant running.See here for a Runner's World article concerning that issue.

The conclusion to the Arem publication is refreshingly non-ambiguous and prescriptive ,quoting
Arem:

"In regard to mortality health care professionals should encourage inactive adults to perform leisure time physical time activity and do not need to discourage adults who already participate in high-activity levels."


Coarse grain epidemiological evidence strongly support the generally accepted notion that people who exercise none or very little have the highest risk and those who exercise the most have the lowest risk.

In a nutshell-the large coarse grain epidemiologic studies demonstrated that relativity low levels of exercise are better than none and further these studies were not able to demonstrate a upper level of exercise that is more risky than no exercise  though some data indicted that risk reduction at the highest level studied may have reached a plateau.

It is possible that there could  be some harmful or potentially harmful cardiac effects in a small number of long time and/or high volume endurance athletes that would not be detected by large data analysis such as that of Arem and Wen.

 That appears to be the case.

There are  three  conditions that  appear to be more common in high level exercisers. These are 1) atrial fibrillation 2) myocardial fibrosis and 3)coronary calcification.

While the current consensus view is that the relationship between exercise level and all-cause and cardiovascular mortality is curvilinear and not U shaped, the same cannot be said in regard to atrial fibrillation (AF) .

In a  2018 review (4) of the "extreme exercise hypothesis", which states that there is some level of exercise   that results in a harmful effects. Three conditions have been considered in that regard: 1) atrial fibrillation (AF), 2) myocardial fibrosis (detected by MR gadolenium scaning) and 3) acceleration of coronary artery calcification (CAC).


Eijsvogels,Thompson and Franklin (4) concluded in regard to AF :

 "that the relationship between physical activity and incident AF is best summarized by a reverse J shaped curve.Light to moderate  amounts of exercise decrease but large volumes of exercise potentially increasing the risk of AF."

Two of the studies mentioned are their review are  the Henry Ford study and Anderson's cross country ski study .

Even though a study from the Henry Ford Exercise testing project (5) demonstrated that higher cardiorespiratory fitness was associated with a graded reduction in AF (the higher the fitness level the lower the risk of AF),a large cohort study of cross-country skiers showed that those who finished more races and those who raced faster had higher risk of AF than those who did only one race and those who raced at a slower pace. In that study by Anderson  (6) of  52,755 long distance skiers those who finished five or more races versus those who finished only one race had a Hazard ratio for AF  of 1.29 95% CI 1.04-1.61.

The Henry Ford study looked at the relationship between fitness and incident AF and the Anderson study looked at volume of exercise and intensity of exercise and while  fitness and exercise level are correlated they are not the same. After the entry into the study when fitness level was determined there are no data on  the exercise history of the participants at Henry Ford.The Anderson study used number of races and speed of racing to give some broad measure of amount exercise which relates to the questions of exercise volume versus AF risk which is not directly addressed by the Henry Ford study.


The large mega data studies,such as those by Arem and by Wen , lack the statistical power to detect any mortality effect that might occur from AF,CAC and myocardial fibrosis in endurance athletes whose exercise volumes fall at the  extreme right end of the volume axis since there are relatively few subjects exercising at mega volumes.

Even though the relationship between exercise volume and/or intensity and CVD and all cause mortality is not U shaped, the relationship between exercise volume and AF is. 

The issue of the relationship between exercise volume and coronary calcification is less straight foward. Defina's(7) study presents data that high levels of exercise  (3,000 Met min  per week which is about 6 times the minimal 2018 recommendation) are associated with prevalent coronary artery calcification but not  increase in cardiovascular mortality. This apparent paradox might be resolved if it turns out that the increased in runner's calcium scores represent density and not extent of calcium and that the increased density is related to heavy calcified plaques which are made less vulnerable to rupture. 

1)  Arem H   et al. Leisure time activity and mortality: a detailed pooled analysis of the dose-response relationship. JAMA Int Med 2015 Jun 175 (6) 959  (full text is on line)

2)Wen,CP Minimum amount of physical activity for reduced mortality and extended life expectancy .A prospective cohort study. Lancet 2011,378 , 144.

3)Franklin, BA Exercise related acute cardiovascular events and potentially deleterious adaptations
following long term exercise training. Placing the risks into perspective-An update A scientific statement from the American Heart Association. Circ 2020 Feb 26 PMID 32100573

4) Eijsvogels, TMH et al The "extreme exercise hypothesis":Recent findings and cardiovascular health implications." Curr Treat Options cardio med 2018 20  84 

5)Querishi,WT Cardiorespiratory fitness and risk of incident atrial fibrillation:results from the Henry Ford Exercise (FIT) project Circ 2015: 131 ;1827

6) Anderson K et al Risk of arrhythmias in 52,. 755 long distance cross country skiers: a cohort study
 Eur Heart J 2013 Dec 34 (47)36

7) Defina,LF Association of all-cause mortality and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification . JAMA Cardiolog 2019, 42 (2) p 174

addendum 7/27/2020 Several changes made in the et to clarify meaning .8/14/20 and again minor changes to clarify meaning. also on 11/19/2020.3/21/21 Minor editing and typo corrections. 5/26/21 still more typos corrected.9/27/21 Comments regarding Defina's data added .

If high levels of exercise increase risk of coronary calcification does it also increase CV mortality

Do long time endurance athletes have an increased risk of coronary calcification? If so, does that correspond to an increase risk of cardiovascular events?


In this study (1)  the life long exercisers in the highest activity level (5-6 hours of vigorous activity per week) did show an 11% increase coronary artery calcification (CAC) of a score of 100 or higher but that group had an all cause and cardiovascular mortality risk lower than that in groups with a lower level of exercise.

The author conclusions:

"This study suggests there is evidence that high levels of physical activity (3,000 MET-min/week)are n iassociated with prevalent  CAC but are not associated with increased all-cause 0r CVD mortality after a decade of follow-up, even in the  presence of clinically significant CAC levels."

To the extent these results reflect reality,there may be some reassurance to folks who may have spent arguably too many hours running or cycling.

1) Defina, LF et al. Association of all-cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiology, 2019 42 (2) P174 (full free text available)


" a man hears what he want to hear and disregards the rest" The Boxer,, Simon and Garfunkel

Gain in life expectancy related to exercise not a U shaped curve phenomenon

Moore et al published an analysis of the effect of leisure time activity and the effect on life expectancy with data from over 650,000 individuals with a 10 year followup in persons aged 40 and over.

At the lowest exercise level which was 3.74 met-hr/week ( a MET level of 3 is described by the authors as a brisk walk and this level being equivalent to 75 minutes of brisk walking per week) there was a gain of 1.8 years.

150-300 minutes of a brisk walk per week yielded 3.4 years gained.

300- 449 minutes of brisk walking was associated with 4.2 year increase in life expectancy.

The lowest level at which they demonstrated a life expectancy gain was less than the minimal recommendation of WHO and of the US panel. Benefit seemed to plateau at around 300 mintues of brisk walking per week. Moore's data display was not U shaped.



1) Moore, SC Leisure time physical activity of moderate to vigorous intensity and mortality. Plos Med 2012 e1001 335

2) Aengevaeren,VL Exercise and coronary atherosclerosis. Circulation vol 141 no 16, 21 april 2020 p 1338 1350

Nicholas Taleb schools public health specialists,libertarians and pseudo-libertarians

Nicholas Taleb addresses pubic health "thought leaders", non-devout libertarians and pseudo-libertarians in this commentary regarding the issue of recommending masks for the public.

Some of the points he made include:

1)A significant and vocal and authoritative portion of the public health coterie (PHC) mistook or ignored the important distinction between "absence of evidence of efficacy" and "proof of lack of efficacy".The PHC did not have anything in the second category in their argument tool box. They mistook or ignored the distinction between  absence of evidence and  evidence of absence,something emphasized in epidemiology 101.

2) The PHC failed to recognize how effective the widespread use of mask would be.If A and B both wear masks, both protect the other This Taleb labelled the compounding effect. Witness the hair care business in which 2 stylists were infected and none of the 140 patrons exposed developed covid19. The secret was both the stylists and all of the customers used masks.

3)Libertarians and pseudo-libertarians are admonished by Taleb to remember the primary principle of libertarianism which is the non-aggression axiom. Exposing fellow humans to a serious illness  with whom a person comes in contract just might be considered an act of aggression.

On 6/15/2020 Dr. Fauci admitted that masks were not recommended earlier because there was a serious shortage of masks. Interestingly once masks or face coverings were recommended by the PHC masks of all sorts were available all over the internet. What if the public had been told earlier  that cloth face coverings could help, would there have not been the release of entrepreneurial energy (and charitable efforts) to get masks to people that we see now. Wonder how many deaths could have been prevented. 

Exercise and the aging heart versus aging in the sedentary heart

What are the arc (s?) of the normal aging heart ( the sedentary ageing heart and the exercising ageing heart).Are they different?

 Humans seem good at finding patterns-sometimes even from patternless noise.One of the stories told  by physiologists and cardiologists regarding the age related downhill course of cardiac function seems to go  something like this.

One way to simplify  cardiac function is to consider two parts of the cardiac cycle,1) contraction and ejection of blood and 2) relaxation and the refilling of the ventricle.

There are data indicating that the first signs of an impending problem are seen in the filling phase ie. diastole.From extensive echocardiographic and invasive physiologic measurements in humans the following sequence can be sketched out and penciled in.

First, there is impaired relaxation following by decreased elastic recoil and later diminished  compliance ( which is to say increased stiffness) and then -at least according to work from the IEEM group- remodeling of hearts with thicker walls and smaller ventricular volumes).Simply put- a sedentary ageing  lifestyle leads to a small stiff heart and long time endurance exercise leads to a larger more easily filled heart.The contractile function of the heart is well preserved with ageing , at least as indicated by measurement  of the resting ejection fraction.( increasing stroke volume with exercise is another matter as is left ventricular stress measured by speckle echo.)

This is largely consistent with the mainstream echocardiographic model which proposes a predictable,progressive process beginning with impaired relaxation,followed by decreased compliance and ultimately- as a compensation- elevated left side filling pressures.This model describes three phases of diastolic dysfunction indentifiable by combination of echo findings believed to reflect  how well or poorly blood flows into the ventricles from the atrium. This model recognizes that the various indices ( e.g E/A ratio, IVRT,maximal E wave velocity and the time constant of isovolumic pressure decay (Tau) change with age so that what would be abnormal in a 20 year old is normal in a 75 year old.It is thought that that filling pressure can be estimated by use of this model. NOTE-see end note 1 for reference to data that challenges the mainstream model by in part  providing data that cardiac cath measurements of left sided pressures do not regularly correspond with the three echo defined stages of diastolic dysfunction)

Next, I consider  what I have labelled as the "Dallas or IEEM theory" of cardiac ageing.

I do not know if Dr. Ben Levine would approve of my label or not. Maybe we could call it the Levine Theory.  see end note 2

A series of articles from the University of Texas Southwestern Medical School and the IEEM have provided extensive invasive and noninvasive data regarding cardiac function at various ages and the effect of longtime endurance exercise versus sedentary ageing on  cardiac structure and function.

Levine et al first demonstrated that lifelong endurance athletes ( 25 years or more of running a lot) had left ventricular compliance virtually identical to those of sedentary 20-30 years olds. Then they compared ventricular compliance in four groups of 25 each of people who exercised at various levels over a 25 years period. These were all subjects over the age of 64 and were screened to excluded pre-existing heart disease.Group 1 was sedentary people who exercised no more than one session per week. Group 2 were labelled "causal exercisers" and exercised 2-3 times per week. Group 3 (Labelled as committed exercisers}worked out 4-5 times per week and the "competitive" group trained 6-7 times per week and regularly raced.The racers had the most elastic  or compliant ventricles while group 3 was "very close" in terms of ventricular compliance while groups 1 and 2 has significantly stiffer hearts.Note: while exercise seemed to help maintain compliance , long time endurance exercise did not mitigate the age related loss of ventricular relaxation-as measured by the isovolumic relaxation time  (ivrt) which is the time from aortic valve closure to mitral value opening.

Next, Levine studied a group of 70 year old subjects  and an vigorous  exercise program was unsuccessful in improving the reduced compliance observed in that group. Next another study demonstrated that middle age subjects with a year long exercise program ( that involved in part high intensity interval training) were able to increase their ventricular compliance.This implies that past some point in time you cannot improve LV compliance with endurance training  with some interval training but middle age may not be too late.This does definitely not mean that exercise for those 70 years of age and older gain no benefit from aerobic exercise,,just that it looks like they will not  improve left ventricular compliance (at least withinthe time frame of Levine's subjects)

In another article Levine said that exercise in the range of that performed by the "committed exerciser" might be adequate.

My main question in this regard is "how much exercise "is sufficient to maintain a healthy compliant left ventricle." Levine's amazingly compliant  (pun intended) subjects not only stuck with program for a full year but after the first 6 months participated in a hig intensity interval program using the demanding 4X4 workout program that involves 4 minutes of exercise at 95% of maximal heart rate followed by 4 minutes of rest done four times.

End note 1. Grant et al (Grant A, Grading diastolic function by echocardiography:hemodynamic validation of existing guidelines.Cardiovascular Ultrasound 2015 513 :28) compared echocardiography results with  left heart catherization data in 460 patients.The data demonstrated that there were no differences in regard to left ventricular pressures between patients with normal diastolic function and those with grade 1 or 2 diastolic dysfunction but there were differences between normal and grade 3 diastolic dysfunction in patients with reduced ejection fraction.In those patients with preserved EF, there is no statistical difference between normal and any grade of diastolic dysfunction. (see figure 5 of their article which graphically illustrates the lack of the "predictable, progressive process "which characterizes the  current paradigm.)If the detection of elevated LV pressures which generally correlates with exertional shortness of breath is in part the goal of echo studies of diastolic function it appears to not be reached based on Grant's data.

end note 2. Dr Ben Levine is the director of the Institute for Exercise and Enviromental Medicine (IEEM) housed at the Texas Health Presbyterian Hospital Dallas and professor at University of Medicine Southwestern. His group have done a series of comprehensive physiological studies on subjects recruited from the Dallas Heart Study, a population based sample of 6100 subjects in Dallas .

In a nut shell the concept is that everyone with aging develops some degree of diastolic dysfunction related to impaired relaxation and loss of diastolic suction,Later aging (particularly sedentary ageing) is associated with loss of ventricular compliance ( AKA increased stiffness). A long term endurance exercise program is capable of mitigating the changes in compliance but not the decrement in relaxation and diastolic suction. IEEM's studies  further indicate that a sedentary lifestyle may lead to a small stiff heart which may be the precursor to heart failure with preserved ejection fraction (HFpEF) ) and the Dallas group suggest that an appropriate amount of endurance type exercise begun no later than early middle age may play an important role in the prevention of HFpEF.

"Humans are pattern-seeking story -telling animals and we are quite adept at telling stories about patterns, whether they exist or not".Michael Shermer.

End note 3:In 2008, Shermer coined the term "patternicity" -the tendency to find meaningful patterns in meaningless noise. I am not suggesting that the extensive,very carefully done research referenced above is meaningless noise.I just really like the quote but I certainty hope the "Dallas hypothesis" is a reasonably accurate approximation of the ways things  really are at least sometimes- having spent a lot of time running a lot over the last 40 plus  years.

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Has the issue of keep closed longer or open up quicker now a political non-debate?

The following is a quote from a commenter named Handle on Arnold Kling's blog from 4/25/2020 entitled Henderson-Wolfers Non-Debate.

"One of the most terrible things than can happen in our society is that some important and formerly neutral questions becomes politicized and the position one espouses become a strong signal of affiliation to a particular team....once there is a party line on the matter thinking ends all together."

Two  examples-Several members of the Republican party appear in Congress not wearing masks
presumably to make a point. ER Nurses stage a counter protest against a open things up protest,shouting matches break out.

Should Runners,walkers,cyclists beware the Coronavirus slipstream

The slipstream is the zone behind a person moving (walking, running,etc) which pulls the air along with the person.In the racing world it is known as drafting.

A recent news article about a study done by Belgian engineers has gone a bit viral itself.The wave of air flowing carrying respiratory droplets or drops  in the wake of a runners goes behind him   for distances greater than the magic 6 feet that we are admonished to respect as regards proximity to other humans in the world or preventive social distancing. At least the animations released by the researchers give that impression as do their data which at this writing has not yet been published in a peer reviewed journal.

See here for details.

If their  animations reflect the actual path  of exhaled particles,one might decide that even when you are out for a run to wear a mask at least some of the time.

See here for some questions and answers from one of the authors of the paper.

My personal take home is that when a runner passes me I should move to the side to avoid potential particles in his slipstream and ( with an abundance of caution) pull my mask up until the passer is 20 to 30 thirty feet  away. In the increasingly unlikely instance in which I actually overtake a runner and pass her I should move to the side and keep to the side to keep the passed person out of my slipstream.

Perhaps the equivalent of "My mask protects you,your mask protects me" for runners could be
"I'll keep you out of my slipscreen,you keep me out of yours"


According to the authors data a cyclist should stay 60 feet directly behind the bike in front or keep off to the side. Also they suggest that 16 feet behind a walker and 32 feet behind a runner to be approximations of the "aerodynamically equivalent social distance" which is six feet for stationary people.







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Role of masks for COVID prevention outside of hosptial use

The following is my opnion and not a medical recommendation.

 Public face mask use appears to be common in Asian countries and also is now required in 

the Czeck Republic where people wear masks as a civil duty with the  shared realization that "I protect you by wearing a mask and you protect me by wearing a mask."

Corona virus is spread by droplets by infected persons even if they are asymptomatic and both simple surgical type face masks and the more expensive and protective N 95 masks can significantly reduce spread of coronavirus.

Both type of masks have been scarce in the US as Covid 19 cases exploded. Expectations and then realization of actual mask shortages in medical care facilities lead public health officials to discourage the public from using masks in the hope that more would be available for health care workers

Sometimes it has been argued that the masks were not effective when used by the public while at the same time saying that the masks should be reserved for medical personnel use in whose hands they would somehow offer important protection to them. Of course, protection is not a function of one's profession.

It is likely that it was believed that  officially recommending masks would lead to a large public demand  , making it even more difficult for health facilities to obtain masks.

As Covid  19 cases continue to increase and the mask shortage worsened, the CDC  said that masks can be reused and ,that homemade masks and scarfs could be used as a last resort by health care workers. This was a major change in CDC recommendations.Home made masks and scarfs can be used to protect the public as well, although that was not said by CDC.

Jeremy Howard,a Deep Learning specialist from Stanford, has posted an excellent review of the use and value of face masks by the general public to decrease COVID spread and describes widespread use by the public in many countries.See here

https://www.youtube.com/results?search_query=jeremy+howard

He gives links to sites with important information on how to clean masks and how to make masks at home from towels, t shirts etc. Some may worry about being accused of taking masks away from doctors and nurses if they wear a mask in public. Home made masks hopefully defuse  that issue.

Summary:
Covid 19  is spread by droplets by asymptomatic as well as symptomatic persons
Various kinds of masks decrease risk of spread
Masks can be made at home and worn in public  without shame .A great DIY project
Masks  protect others perhaps even more than they protect the wearer
It has been suggested that it would be unpatriotic for the public to wear masks.I suggest the opposite.
wearing masks is patriotic.An asymptomatic covid 19  infected person being in public exposing others to the disease is certainly not patriotic.
I am not recommending  to bid up prices of masks,No one wants to take masks away from HCWs.
 But if you already have masks on hand ,wear them .If not they really can be made at home and will offer some important protection . Yes, less than the properly fitted and correctly worn N 95 and less than surgical masks but significant protection nevertheless.
Bottom line wear masks in crowds (including grocery shoping)

Finally, imagine for a moment if only 25% of subway riders in New York (8 million riders per day) wore masks for the last 2 -3 weeks what the results might have been. Also imagine the potential benefit after we all come out emerge from sheltering in place how potentially important wide spread use of mask might be in decreasing the risk and/or impact of a second wave.

The following quote is from Scott Alexander writing on his blog slatestarcodex.com on 3/23/20 giving a detailed analysis on the research of various masks and the protection they provide;

". So should you wear a mask?

Please don’t buy up masks while there is a shortage and healthcare workers don’t have enough.

If the shortage ends, and wearing a mask is cost-free, I agree with the guidelines from China, Hong Kong, and Japan – consider wearing a mask in high-risk situations like subways or crowded buildings. Wearing masks will not make you invincible, and if you risk compensate even a little it might do more harm than good. Realistically you should be avoiding high-risk situations like subways and crowded buildings as much as you possibly can. But if you have to go in them, yes, most likely a mask will help.

In low-risk situations, like being at home or taking a walk, I mean sure, a mask might make you 0.0001% (or whatever) less likely to get infected. If that’s worth it to you, consider the possibility that you might be freaking out a little too much about this whole pandemic thing. If it’s still worth it, go for it.

You are unlikely to be able to figure out how to use an N95 respirator correctly. I’m not saying it’s impossible, if you try really hard, but assume you’re going to fail unless you have some reason to think otherwise. The most likely outcome is that you have an overpriced surgical mask that might make you incorrectly risk-compensate.

If you are a surgeon performing surgery, bad news. It turns out surgical masks are not very useful for you (1, 2)! You should avoid buying them, since doing so may deplete the number available for people who want to wear them on the subway."

Here is a quote from a blog post by Tomas Pueyo entitled "Coronovirus:The Hammer and the Dance"which has attracted considerable interest.Here is the link.https://medium.com/@tomaspueyo/coronavirus-the-hammer-and-the-dance-be9337092b56

Pueyo considers masks part of the solution." (my bolding)

"the massive impact of policies like those of Singapore or South Korea:

• If people are massively tested, they can be identified even before they have symptoms. Quarantined, they can’t spread anything.
• If people are trained to identify their symptoms earlier, they reduce the number of days in blue, and hence their overall contagiousness
• If people are isolated as soon as they have symptoms, the contagions from the orange phase disappear.
• If people are educated about personal distance, mask-wearing, washing hands or disinfecting spaces, they spread less virus throughout the entire period."

(note the blue and orange wording references refer to charts in his article)

Maybe it is this simple: If asymptomatic patients are not contagious, the masks only for the symptomatic rule works, but if the  asymptomatic are contagious that rule does not work.

addendum: 4/11/20 Several glaring typos finally corrected. Also now the CDC has blessed the wearing of face masks by the general public, preferably of the home made variety.Two days ago at the grocery about 50% of the shoppers wore masks, most not of the DIY type.

Addendum 5/8/20 Today at Krogers only 2 of the approximately 40-50 person did not have masks.All of the store workers did and now they have erected plexiglass barriers shielding the checkers.

Do ARBs and ACEis make COVID 19 infection worse?

A recent article in the BMJ raised concern that drugs that inhibit parts of the RAAS system might be harmful to patients infected with the new novel corona virus  known as SARS-COV2 while the disease it produces is named COVID 19.

 Coarse grain epidemiologic data from the Wuhan outbreak indicated that one of the risk factors for bad outcomes was hypertension.It was then hypothesized that the increased mortality might be due to the subset of hypertension patients who were taking ARBs or ACEi as those may increase levels of ACE2 which has been shown in animals and possibly humans and ACE2 is the receptor for both SARS-CoV and SARS-COv2. So with more ACE2 would the results be a higher viral load?

On the other hand in an animal model of SARS-COV ARMS seems to reduce lung injury.

All this and a detailed recitation of the RAAS system as it relates to Corona viral infection can be found in the link found at the end of this post as can the citation for the BMJ article..That link is an article by Dr. GM Kuster et al published March 20 2020 in the European Heart Journal which reaches this conclusion:

In conclusion, based on currently available data and in view of the overwhelming evidence of mortality reduction in cardiovascular disease, ACE-I and ARB therapy should be maintained or initiated in patients with heart failure, hypertension, or myocardial infarction according to current guidelines as tolerated, irrespective of SARS-CoV2. Withdrawal of RAAS inhibition or preemptive switch to alternate drugs at this point seems not advisable, since it might even increase cardiovascular mortality in critically ill COVID-19 patients.

This is in agreement with a recent statement made by ACC/AHA.See herehttps://www.acc.org/latest-in-cardiology/articles/2020/03/17/08/59/hfsa-acc-aha-statement-addresses-concerns-re-using-raas-antagonists-in-covid-19



https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaa235/5810479?utm_medium=Email&utm_source=ESC&utm_campaign=ESC+-+Newstetter+-+week+13


addendum 4/620 clarification of the nomenclature for the virus and the disease caused by it

Can Asymptomatic persons positive for covid-19 transmit disease

I believe we need to act as if they can.

A report from the chief epidemiologist from China's CDC in early March seemed to be reassuring.
Dr. Z.Wu speaking on an online conference on March 6 told the audience that transmission from presymptomatic people is rare and indicated that the  rate was 1-5% among person in close contact with infected patients.

Subsequent reports and consideration of foci of  rapid spread, (e.g. the Boston Biogen conference,the ill- fated cruise of the Diamond princess) suggest presymptomatic transmission may not be rare.

Japanese researchers found 634 of the 3711 passengers on the Diamond Princess tested positive and estimated 17.9 percemt were asymptomatic .

Using data from Tiajin China  Dutch researchers used a mathematical model to estimate from Tiajin  that the proportion of pre-symptomatic transmission was 62% ( 95% CI 50-76 %)

Note- these two analyses give estimates  and not actual proven head counts of instances of spread from person without symptoms

Viral counts are higher in the nose and throat and peak earlier in covid 19 infections than was the case with SARS so that it seems very plausible that a pre-symptomatic person could transmit disease.

 Further, even if the outer bounds of these estimates are still overestimates  the likelihood of pre-symptomatic spread  raises  major questions regarding  some of the current guidelines and  advice from public health experts.

If exposed health care workers are allowed to return to work based on history of no symptoms and there is asymptomatic spread then other workers and patients are at risk.

Early on in the U.S, public health experts discouraged the use of masks by the general public at times with an apparently self contradicting argument that 1) masks don't really work and 2)masks should be reserved for doctors and nurses.

 Of course, Surgical masks are not as effective a N-95 units but since viruses spread by droplets , masks offer some protection. Telling the public  that masks don't work does not seem to be very good advice and that position seems to have largely walked back.

 Early on US public health spokespeople  downplayed possible pre-symptomatic transmission but now that has changed.In fact Dr. Scott Gottlieb said "We know there is asymptomatic spread".Further, in a 3/18/200 tweet he suggested that if the youth who are ignoring efforts to be socially distant they should be required to wear masks"

I believe also that high risk people who for good reason must venture into crowded areas  ( e.g. groceries) should wear masks. I know I am- being at high risk by reason of age.

What do Left bundle banch block and traditional right ventricular cardiac pacing have in common?

Although it was demonstrated at least as early as 1989 by CL Grines et al (1) that left bundle branch block (LBBB) could cause significant functional impairment of the left ventricule (LV), clinical description and  general recognition of a LBBB cardiomyopathy as a clinical entity would require a decade or more.

Pacing the apex of the right ventricule was the default method for cardiac pacemaker implantation for many years and  the path to recognition of a right venricular pacing induced cardiomyopathy and a better way to pace was neither short nor particularly straight.

In 2005 (Blanc et al ) and in 2013 (Vaillant) reports appears describing a dilated cardiomyopathy apparently induced by LBBB that in some instances were significantly reversed by cardiac resynchronization treatment (CRT).Blanc wrote "long standing LBBB may be a newly identified reversible cause of cardiomyopathy."

Further proof was offered by Barot et al (2017) in the form of a  retrospective followup report.Thirteen of 94 LBBB patients with normal cardiac function (normal ejection fraction (EF) and no evidence of coronary artery disease developed a significant reduction in LV function over a variable time.

Not only is LBBB dyssynchronopathy heart failure now recognized it has become apparent that the usual heart failure meds do not seem very effective. In 2015, NC Wang et al reported the lack of response  to medical therapy in 32 LBBB patients with new onset LBBB-associated idiopathic non-ischemic cardiomyopathy (NICM) and that "a high percentage were super-responders [to CRT]."

James Daubert and Edward Sze (3)argued in 2018 that the then current guidelines for implanting CRT require at least 3 months of guide-line directed therapy (GDMT) before implantation but there are no randomized clinical trials showing efficacy of medications and suggested that CRT should be  considered for first line therapy rather than GDMT as many  (most) symptomatic patients with LBBB do not respond to GDMT.

Since the early 1990s CRT has become an important treatment for heart failure  with reduced ejection fraction (HFrEF) and delayed intra-ventricular conduction with the greatest benefit in those patients with LBBB.CRT traditionally has meant right ventricular pacing plus pacing the left ventricle from a vein on the surface of the left ventricle accessed through the coronary sinus.This is referred to as Bi-V.  or biventricular pacing.More recently His Bundle pacing (HBP) has been suggested as being as good  and perhaps better than Bi-V or at least as an alternative in cases in which the coronary sinus lead could not be placed.In cases in which the mechanical dyssynchrony is caused by an electrical problem an electrical "fix" seems necessary.HBP would seem to be the best fix being more physiological than Bi_V pacing .


Placing a pacing lead in the apex of the right ventricle was standard procedure for bradycardia indications for many years before EP cardiologists raised the question and then gathered evidence and finally  concluded that in fact RV pacing could lead to significant loss of synchrony in the LV which   resulted in heart failure in a significant number of patients

The similarities of the EKG in right apical pacing and LBBB certainly suggested possible functional impairment from RV pacing.Cardiologists were interested in some alterenative pacing method to avoid the harm that was becoming evident in RV pacing but no good alternative presented itself, at least not until HBP.Reports of septal pacing in place of apical pacing gave conflicting results.

As effective as traditional CRT (i.e. Bi-v) is some 30 % plus of patients with HF do not response while some seem to be "super-responders".Patients with narrow QRS complexes do not respond and those with a LBBB pattern are more likely to respond but all patients with a similar LBBB EKG pattern do not all respond to the same degree nor do they necessarily have the identical patern of LV electrical activation.All patients with an EKG designation of LBBB are not created equal.

The typical pattern of LV contraction described in LBBB is the following:

The interventricular septum moves quickly to the left in early systole (in the isovolumic contraction phase, i.e before aortic valve opens).The LV lateral wall is pushed  outward and finally the electrical impulse traveling through myocytes reaches the lateral left wall area and it contracts pushing  the septum to the right.

The initial left shift of the septum is mainly  the result of the electrical impulse traveling from right to left (the opposite of the normal situation) and also from the pressure difference between the RV and LV as the RV contracts before the delayed LV contraction. This initial septal shift is called septal flash or septal beak and can be seen on M mode echo as well as on speckletracking echo.

Calle et al (2 ) have proposed that this septal flash may be the key to what "true LBBB" is- meaning the pattern of dyssynchrony that is responsible for the functional impairment and the pattern most "fixable" by CRT and by HBP as regards both LBBB and right apical pacing induced dysfunction.

Various other echo criteria have been proposed as the preferred measure to assess dyssynchrony and response to CRT without general agreement. About 50% of patients with the EKG pattern of LBBB are shown to have the septal flash and the associated dysfunctional out-of-sync LV contraction.

The septal flash indicates that the septum is activated from right to left initiating a sequence of dyssynchronous ventricular segmental contractions and relaxations that are deleterious to ventricular function and may result in remodeling and ultimately heart failure with reduced ejection fraction and is often reversible to varying degrees with CRT either by HBP or Bi-V.

So would CRT be expected to be useful in patients with RBBB since the septal  activation is from left to right.In theory- no but Sharma ( 3) et al have reported significant clinical improvement

 in some RBBB heart failure patients treated with HBP.Perhaps right to left septal activation ( as indicated by septal flash) is not a necessary condition for there to be improvement from CRT but I doubt one would see a super-response and the mechanism of benefit may relate more to improved atrial-ventricular synchrony improvement  and not correction of an abnormal septal activation.

1) Grines, Cl et al Functional abnormalities in isolated left bundle branch block.The effect of interventricular asynchrony. Circulation  1989 79 845-853

2)Calle,D et al, Septal Flash :At the heart of cardiac dyssynchrony. Trends in Cardiovacsular Medicine2019,14,9

3)Sze,E and Daubert,JP Left bundle blck induced left ventricular remodeling and its potential of reverse remodeling. J Intv Card Electrophysiol 52 (3) 343-352, 2018

How Will "medicare for alll" be like the military industrial complex?

The following quotes are from the blog "on health care technology" written by Margalit Gur-Arie:



"Go ask Northrup Grumman or Lockheed Martin or General Dynamics or even Boeing or Booz Allen or any other “beltway bandit” how getting money from the Feds really works. There are well-greased revolving doors between the Pentagon and its contractors. There are stock options and executive positions for high ranking Federal employees. There are 535 people in Congress responsible for allocating budgets, and all 535 are for sale. Most of this infrastructure is already in place for health care too and building the HHS Heptagon shouldn’t take very long. The American President has little to no power over Federal spending, and even less so when it comes to large procurement contracts, as the current occupant of the White House discovered the hard way, during the Lockheed F-35 kerfuffle....


Clearly large health systems will survive and thrive under a Medicare For All law, but how about private health insurance? Future President Bernie says they will all be banned. Is that so? Currently a full third of Medicare beneficiaries are insured and “managed” by a handful of large private health insurers. Medicare is paying those private contractors fixed amounts of money per head for their services. Medicaid is doing the same for most of its beneficiaries, and all military health insurance (TRICARE) is contracted out to the usual suspects. Basically, the vast majority of people covered by public insurance, are really insured by gigantic insurance corporations. Fact: under the hood, taxpayer funded health care is the bread and butter of private health insurance companies."

So her analysis suggests very little difference at all.

The well known revolving door in regard to government and the defense industry is paralleled by the what goes on in the health care and pharmaceutical industry.See here 

Important changes happening(and happened) in Med School Education what is it about?

Drs. Accad and Koka  discuss  major changes in Medical school education with Dr. Stanley Goldfarb.See here for the podcast.

Are the changes in the medical school curriculum designed to develop social and political advocates rather than well trained physicians?Dr. Goldfarb argues that it is.

The changes are all about population medicine,some thing I have blogged about often before see here.

Courses about climate and medical conditions are already on the curriculum of several medical schools ( see here ).One school mentioned in the linked article actually giving instructions on how to write op-eds about climate change supply a concrete example of Goldfarb's argument.Classes on
environmental justice are also appearing on the schedule.

The degree to which a progressive view point is often part of primary,high school and college education should make it no surprise that med school students are actually requesting courses
in social and environmental justice.

Should journals always report fragility index on a clinical trial.

Interesting article in December 2019 Circulation.(See here.) that discusses the "robustness" of a number of cardiovascular disease trials.

A  purported measure of robustness is the Fragility Index (FI) which is the number needed to move from the non-event group to the event group to turn a statistically significant finding into a non-significant one. A FI of 1 would mean that if one subject was moved from the event to the non event group there would no longer be a significant  difference.

A related concept is  the comparison of the FI to the number of subjects lost to follow up. The trial's results would be considered less robust if the number lost is greater than the FI.

Ridgeon et published a review of 56 RCTs in critical care treatment topics.The median FI was 2 and slightly greater that 40% of trials had a FI of one or less.So does that suggest that clinical guidelines based entirely or in part on those low FI studies are built on shifting sands?


But wait, listen to this criticism of the concept of FI by Dr. F.Perry Wilson before rushing to trash a RCT simply because the FI is too low. Wilson shifts the problem to one of having too much reliance on the p value in the first place.



1)Ridgean EE et al Crit. Care Med 2016,vol 44 ,1278

What could possibly go wrong when legislators think they know how to practice medicine

Here is another item from the file labelled "I'm so glad I don't practice medicine any longer"

A proposed bill from the Ohio legislature breaks new ground in the land of the  ignorant and absurd.

It would require a physician to transplant an embryo from the fallopian tubes to the uterus of the mother or face a charge of capital "abortion murder".See here