Friday, August 18, 2017

1960-1990: The asthma institution

By the 1960s, the two asthma institutions in Denver that were opened to take care of tuberculosis patients were now mainly taking care of asthma patients, according to  And "by this time TB patients comprised only half of the patient population and asthma patients a third." (5)

It was in this decade that National Jewish Hospital opened a facility specifically for the increasing population of asthmatics with high risk asthma that was non responding to conventional therapy.  It was in 1969 that a fee for service based on a patients ability to pay was begun.

By 1976 Asthma was recognized as the most prominent chronic disease among children, affecting 1.5 million children in the United States, and this included myself.  It produced a lot of suffering for those afflicted, and it also accounted for about one-forth of all school days lost. (4, page 164)

It is a debilitating disease not only for the child who is suffering, but for parents who don't understand the disease, and fear their child might die.  Yet perhaps even worse than that for the parent is the helpless feeling that there's nothing you can do, and what you do do doesn't help. Probably because most of what they did back to was based on fallacies of the past, such as putting asthmatics in a steam filled bathroom hoping that would relieve an attack.

Yet for the child the suffering is even worse yet, and here I can allude to my own experience.  Many nights I would stay up late, many times all night long, my wrists firmly pressed on the window sill, by face up against the cold screen with the intend on sucking in cool air and oxygen.  Many nights I suffered in this way from an asthma attack.

When I was little I sat up on the bed, all frogged up, gasping for air.  I did this probably because I didn't know there was anything not normal about it.  When I was older I'd push open the window in secrecy in the middle of the night because I didn't want to bother my busy parents.  Another reason I suffered in secrecy like this was because I didn't want my parents to worry about me.

Another reason may have been because of a poor self esteem exacerbated by parents who disciplined me because I underachieved, even when I was probably underachieving because of my asthma.  Another reason for my low self esteem was because kids picked on me at school because I acted different from the "normal" kids.  I had a runny nose and they didn't.  I wasn't able to play baseball on teh dusty baseball diamond.  So they picked on me.  The same way my brothers sometimes picked on me when I didn't play baseball with them.  I was basically fodder for the other kids.

Now as I look back on all this I think I'm sometimes just saying this kind of stuff to justify why I was picked on as a kid, but based on my own medical records my counselors, my psychologist, and my medical physicians all believed this.  Asthma had taken a physical and psychological toll on me.  And to make matters worse my teachers and parents had no clue this was going on, and the end result was a shot self esteem and shot level of self confidence.

And then I had mood changes. And many children have mood changes, so my parents and physicians probably figured I was just one of those intractable children. I became stubborn sometimes at home, and I was emotionally distraught.  I remember being extremely depressed to the point my parents once grounded me from watching the news.  I remember pacing the living room for hours worrying about the death of a relative, or that I was going to get old and die.  Of course my parents and doctors had no clue I was depressed, or at least at the time they didn't associate it with the fact my asthma was poorly controlled. More recently my mom acknowledged to me she was aware of it, but I don't remember her ever doing anything to help me.

So, again, I can understand the theory that asthma was believed to be psychological.  Plus when a child is admitted to one of these hospitals the environment is controlled.  By the 1970s and 1980s air conditioning was added to both the children's ward and the gymnasiums where children exercised.  There was a focus on a good diet, and we were exercising all the time. Stuffed animals and items that collected dust were not allowed.  Clothing was washed regularly so it was allergen free, and furniture was made of leather or other solid material that was easy to wash and didn't harbor allergens.

By the 1970s there were two prominent asthma hospitals in Denver, one was National Asthma Center and the other was National Jewish Hospital at Denver.  By 1978 National Asthma Center admitted financial trouble, these two great hospitals merged to create National Jewish Hospital/ National Asthma Center.  The main campus was on Colfax Avenue, or the National Jewish Hospital campus.  The merger resulted in the "largest treatment center for pediatric and adult asthma," according to

Once admitted the children would under go an examination by a physician, and then spend the next several days undergoing a variety of tests.  I remember doing many pulmonary function tests, x-rays, electrocardiograms, sweat test (to rule out cystic fibrosis), and so many other tests I can't even recall all of them.  I just remember being exhausted by the end of it.

I met with a counselor on day one, and I think the main reason for my counselor was to help me deal with the day to day life at my new home, and also to help me learn to cope with life once I return home.  I saw my counselor once or twice a week, and once every two weeks I saw a psychologist.  I only saw a psychiatrist once that I remember, and he prescribed Xanax to help me relax. He actually prescribed an antidepressent before that, but I had an allergic reaction that gave me hives all over my body, so he must have decicded just to stick with xanax.  It seemed to work pretty well (I'll tell you the story about that later).

So I was admitted to the hospital in 1985, this was long after the psychosomatic theory of asthma had been proven to not be true.  But I'm certain the doctors trained to work there, and the psychologist, were still privy to these old theories.  I'm certain, especially after reading my medical records, that they believed much of my asthma was in my head.  They noted the anxiety.  They noted trouble when my mom visited, and how my asthma was exacerbated during these times.
Travis quotes one physician as saying that "once asthma has been established, acute attacks may be triggered by emotions.  There is a psychological basis for some emotionally precipitated attacks, particularly when the emotional upset is accompanied by shouting, crying and rapid breathing... it becomes impossible after a time to separate problems which are precipitating asthmatic attacks from those that are secondary to the asthma.  The secondary gain can be a significant problem."  (4, page 169)

This appears to be my proof that asthma was no longer believed to be psychological by the time I was admitted in 1985, although psychological factors can still trigger asthma. Most of the asthmatics admitted by this time were on systemic corticosteroids, and the fear of side effects was paramount.  Although, through the efforts of physicians at the hospital, I believe most patients went home on preventative asthma medicines, with controlled asthma, and off systemic steroids.  At least that was the case with me and the children I was admitted with.

It also must be noted that, even back in the 1940s I'm sure, occupational therapy was a major therapy given to asthmatic children admitted to the hospital.  Children with intractible asthma, and I can attest to this, do not develop many of the skills other kids do to cope with life.  This is the same for kids with other intractible diseases too.  They don't develop skills that most people take for granted, such as balancing a check book or searching for an apartment.  These types of basic skills that are worked on at the hospital, if the need is there.

And, again, there was a major focus on education and exercise.  These two were almost ingrained together at the asthma hospital.  You need to understand your disease and every part of it, and you needed to exercise.  Many times exercise was education, and education was exercise.  You need to know your medicine, and you need to be compliant with your medicine. And you need to now why you are exercising, and how it will make you better.

You need to know what aerobic exercise is, and if your legs weren't being kicked high enough in the air, you will be told this.  And unless you have a good excuse, like  your asthma was really acting up, you did as you were told.  And for the most part you did it because you wanted to, because you were just happy you were able to exercise at all, because most of use weren't able to prior to being admitted.

You will leave National Jewish educated, and if your physicians don't think you have a good grasp on your education, you will probably not be cleared for discharge.You need to take complete responsibility for your medicine, so that even if your parents back home aren't involved in your care, you know exactly what to do at all times.  You need to know why you are taking your medicines and why it's so important to take them every day. And you need to exercise.

You need to plan ahead on the first day of the week, and plan out what pills you will be taking and on what day and on what times during what day.  You need to plan before every trip out of your house to make sure you take your medicine before hand, and that you have all the medicine you will need on the trip, such as your rescue inhaler.  You cannot just take for granted someone else, even your parents, will remember your medicine when you leave the house.  It is solely your responsiblity.

You will have to also know when to take your rescue medicine, and when to wait.  You will also have to know your asthma triggers and how to avoid them.  You will also have to know what your symptoms of asthma are and what to do about them.  You have to know it all, and you have to be completely responsible for your own health.  That is essential, and it is engrained in your head over and over and over and over and over again until you are discharged.

And also you had to exercise every day.  The school I attended, the Kunsburg School, had a pool, and we swam two days a week during school.  And when we weren't swimming we had gym class.  Every evening after dinner we went to the gym in the school to do some form of aerobic activity.  We stretched, and then we moved for 20 minutes.  That was mandatory.  We did kickball.  We did basketball.  We did baseball.  We did dodge ball.  And if you weren't moving, you were pestered by the PE instructor until you did just that.

When you were first admitted you had a complete physical, followed by a series of tests.  Your asthma was stabilited one way or another, and then you were cleared within  You were then required to exercise, and you were required to attend school.

And then, during the evenings, and on the weekends, you had fun just like normal kids do. You go on field trips. You go to the mall shopping and you go to movie theaters to watch the best movies.  And you go to amusement parks, camping, and all sorts of fun things.  Sometimes you go to video stores and rend movies to watch at home.  You have parties with the other kids.  You have dances.  You have icecream socials.  You have dance and singing competitions.  You played games with the nurses and other kids.

In the winter there was a basketball team, and either you joined the team or you traveled with the team and you watched the team.  And in the spring there was a baseball team, and either you played or you watched.  And it was much more enjoyable to play than watch.  And you traveled to other institutions in the area, including those housing other sick kids, or otherwise sheltered kids.  The goal is to make the hospital as much like home as possible.  And, for the most part, they succeeded at this.  It was a really fun experience.  And all along you learned. Everything was a learning experience.

At one point during my stay I wrote in my journal:  "The only thing that makes this place seem like a hospital is the nurses wear stethoscopes over their shoulders."  For the most part that was true.  Although you were still thousands of miles away from your home, away from your parens, and you were chronically sick.  So most of the kids got homesick, and that was another issues the staff there had to deal with.  And, I'd assume, another reason for all the activities.

In 1985, while I was a patient at NJH/NAC, the name was changed to National Jewish Center for Immunology & Respiratory Medicine.  In 1995 the inpatient floors at the hospital were closed and a new pediatric outpatient program was added, and in 1997 the name was chanced again to

  1. Minton, Gregg, "Breathing Space,"
  2. Wamboldt, Fredrick S. "Asthma Theory and Practice: It's Not Too Simple," April 2, 2008,
  3. Jackson, Mark, "Asthma: A Biography,"
  4. Travis, George, "Chronic Illness in Children," 1976, California, Ford University Press
  5. "Clinical History,",, accessed 

Wednesday, August 16, 2017

1960s: Did rescue medicine cause a spike in asthma deaths?

A spike in asthma related deaths forced physicians to take a closer look at this disease. Upon review of the available data, they began to surmise that the very medicines meant to make life better for asthmatics was responsible.

The spike in asthma rates correlated with the releases and increased advertising of the new metered dose inhaler that was introduced to the market in 1957.  The first to be released to the market were the Medihaler Epi (epinephrine) and Medihaler Iso (isoprenaline).  As word got out there were devices asthmatics could carry in their pockets or purse that would give instant relief from asthma, sales of the device skyrocketed.  (5, page 11)

This followed a rise in the death rate.  According to Speizer, Doll and Heaf in 1968:
It is evident that an increase in mortality began to occur in about 1961 and that all ages between 5 and 64 years of age have been affected.  The greatest increase in mortality has taken place at ages 10 and 14 years, the ages the rate has increased eight times, from 0.3 to 2.5 per 100,000 persons.  The increase has, however, been substantial at all ages from 5 to 34 years, and at these ages the annual number of deaths increased by 308 and the death rate trebled from 0.7 to 2.2 per 100,000 persons.  (7, page 336)
They further noted that that for the purposes of their study, the investigated only data obtained for the age group of 5-34, mainly because as asthmatics get older "mortality from bronchitis begins to exceed that from asthma."  (7, page 336)

Initial studies involved questioning the attending physicians of the patients who died from asthma.  F.E. Speizer, Doll,  Heaf and Strang  in 1968 reported their findings.  (9, page 342)
Excessive use of pressurized aerosols was reported by 29 general practitioners without specific inquiry having been made.  The reports ranged from  a vague implication, such as "tended to use aerosols too frequently" or "suspicion of excess aerosol at death," to direct observation such as "died clutching aerosol" and a detailed account of the amount consumed.  In extreme cases the use of as many as two canisters per day or two in two hours was reported. (9, page 342)
Investigators speculated that, perhaps, such asthmatic were victim of the false sense of security provided by the inhalers.  Instead of seeking help, they continued to puff on their inhalers.  By the time they called for help it was too late.  (5, page 12-13)

Upon further review of the data, they learned that asthma death rates remained stable in most nations where asthma death statistics were available. However, there were significant spikes in six Western countries: England and Wales, Scotland, Ireland, New Zealand, Australia, and Norway. (1, page 15) (2, pages 15-19)

In England, in particular, the asthma death rate was stunningly high.  According to Speizer, Doll and Heaf in 1968, the asthma death rate in England "accounted for 5.7% of all deaths at ages 10 to 14 years, it ranked sixth in the list of causes of death." (7, page 336)

Since the sharpest rise in asthma deaths was limited to six nations, investigators searched for something that was particular to these regions.  What they learned was reported by Beasley, Pierce and Crane. They noted that isoprenaline forte... contained a concentration of isoprenaline two to eight times greater than the standard isoprenaline metered dose inhaler available in other countries. Epidemics occurred only in countries where the high-dose preparation of isoprenaline was available; and in the two countries which marketed the high dose preparation and had no increase in mortality, it was introduced late into their markets per-capita sales were low." (1, page 16)

When the product was later pulled from these markets and the death rate declined, this proved to many researchers that this was probably the cause.

References; ???
  1. "Asthma Statistics, ",, accessed 9/29/13
  2. Beasley, Charles Richard William, Neil Edward Pearce, and Julian Crane, "Worldwide Trends in Asthma Mortality During the Twentieth Century," chapter two in the book "Fatal Asthma," edited by Albert L. Shefer, 1998, New York, Marcel Dekker, pages 13-29
  3. Woolcock, Ann Janet, "Natural History of Fatal Asthma," chapter 14 of the book, "Fatal Asthma," edited by Albert L. Shefer, 1998, New York, Marcel Dekker, pages 179-196
  4. 1940s: Why did asthma morbidity and mortality increase
  5. Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11

References:  See "1940-1970:  Asthma morbidity and mortality spikes"

Monday, August 14, 2017

1950s: The first peak flow meter

Wrights original peak flow meters (circa 1950s)
If you're an asthmatic you may not be familiar with Dr. Martin Wright, but you probably are familiar with an instrument he invented:  the peak flow meter.  It was a convenient, inexpensive, hand held tool that could be used by the patient at home to assess the effects of bronchitis and asthma.  

It was first introduced in the 1950s by London physician, Dr. Martin Wright, of the Clinical Research Center at Northwick Park Hospital.  It was an instrument specifically designed to measure 'peak flow,' or the amount of air that can be forced out of a patient's lungs after a maximum inhalation.  

The original Wright was a large, heavy, clock shaped device and was too expensive for the common person to have at home.  It was generally used in hospitals to assess patients.  It worked by the patient blowing air into the meter, and this air rotated a pointer on a dial against the resistance of a spring.   The device gave the first accurate readings of a peak flow.

Mini Wrights Peak Flow Meters (circa 1970s)
In the 1970s Dr. Wright invented a new device that was inexpensive and portable.  It's basically just a "tube with a spring inside and a calibrated scale along the outside.  The puff from the patient under test pushes the spring back.  A pointer registers the furthest point reached.  The meter comes complete with a set of cardboard mouthpieces.  Doctors recon that the instrument could be useful in home treatment. Patient's could monitor their own lung power in a simple and cheap way of determining recovery from lung ailments."

This instrument was called a "Mini Wright," although ultimately it became known as the peak flow meter.  The devices were ultimately manufactured by various companies, and now you can get an array of different types.  The first ones were not disposable, although they were soon thereafter manufactured for single patient use only, and the separate cardboard mouthpieces are no longer needed  

Many peak flow meters available today
I remember the "Mini Wright" from when I was an asthma patient back in the late 1970s and throughout the 1980s.  I also remember having one at Shoreline when I first started working there.  I believe at some point it simply became lost.  Gone are the days of the Mini Wright, replaced by the even cheaper plastic models.

Can you guess how many peak flow meter brands are on the market?  I couldn't even fathom a guess, although I've had over 20 in my grasp at one point or another.

  1. "Hot Air Invention," New Scientist, March 1, 1979, page 675
Further reading and another picture:

Friday, August 11, 2017

1949-1969: The National Foundation for Asthmatic Children

One of the main reasons National Jewish Health was able to stay afloat through the years is that it recognized the changing health needs in America. While both National Jewish Hospital for Consumptives and Denver Sheltering Home for Jewish Children opened to provide opportunities for children and adults inflicted or affected by tuberculosis.

Between the 1940s and 1960s the number of tuberculosis patients declined, and the number of asthma patients increased. Plus there as a need for taking care of patients with other diseases, including emphysema, chronic bronchitis, cystic fibrosis, bronchiectasis, silicosis, sarcoidosis, and fungal infections (1)

Yet there was also an increased emphasis on research, hence the name change of the Sheltering home to Jewish National Home for Asthmatic Children at Denver in 1953, and in 1957 to Children's Asthma Research Institute & Hospital (CARIH). The hospital also performed research into immunity, and this was a major reason for the 1985 name change of National Jewish Hospital/ National Asthma Center to National Jewish Center for Immunology & Respiratory Medicine.

There was another institution in Tuscon, Ariona, that was similar to National Jewish. People with lung ailments flocked to Arizona due to its dry climate, which was perceived to better for adults and children with breathing difficulties. The National Foundation for Asthmatic Children (NFAC) was opened in Arizona in 1949. It was actually the first "diseased based organization to launch a national campaign on behalf of the asthmatic child. (2, page 115) During the 1950s National Jewish Home for Asthmatic Children started a similar educational campaign. (2, page 116)

Back then asthma was a little known disease, yet a massive advertising and public relations campaign by both National Jewish and NFAC increased awareness of the 2.5 million children in America with asthma. The campaigns increased awareness of the hospitals and research centers in both Denver and Tuscon. And the number of patients being referred to these hospitals increased. (2, page 116)

In 1973 CARIH changed its name to National Asthma Center, and admitted financial trouble by 1978, so it merged with National Jewish to create National Jewish Hospital/ National Asthma Center. This created the largest asthma hospital and research center in the world. Although there was an emphasis on patient care, the hospital continued to emphasize research.

While the school at NFAC closed in 1969, the hospital persisted. It was another option for children with hardluck asthma or other respiratory diseases. There was another such hospital in New York called Asthmatic Children's Foundation. In 1981 there were 15 similar residential treatment centers for asthmatics. (3)

In August of 2009 several former patients at NFAC met in Tuscon, Arizona to reminisce about their stay at the institution. The major emphasis back then about asthma was that medicine was used to treat acute symptoms, with included bronchospasm. Asthma was also a disease caused by a nervous disorder, or a suppressed cry for the mother. (4)

These kids were treated with a good course of education, exercise, and a good, healthy diet. They were also allowed to live a relatively normal life outside of that, by going on trips to town like normal kids, shopping, tours, amusement parks, parks, etc. They were also allowed to participate in games and other fun things kids do.

The kids "attend a boarding school for asthmatic children. These children can play out of doors year round and they become confident and competitive because they are competing with children on their own level," according A.B. Sieh, executive director for NFAC, in an article published in the Rotarian in August 1965. (5, page 51)

Boys and girls afflicted with bronchial asthma generally are admitted to the hospital for a one or two year stay, and this is at no charge, similar to the two asthma hospitals in Denver. The school the kids attend has a capacity of 72, and it's usually full (5, page 51)

Sieh notes that the "they come here pigeon chested with hollow eyes and sad faces... we have had children, who upon arrival, who could not walk up a single step without bringing on an asthma attack... the Arizona sun takes over and we have healthy looking children who can go home -- not cured, but rehabilitated to the point that they can cope with their asthma and live a normal life, attend public schools, and not be 'different.'

So while the main goal was to improve asthma, it wasn't like you were living in a hospital, at least not all the time. It allowed kids to get better, so they could go on to live normal lives.

  1. "Clinical History,",, accessed 11/7/12
  2. Mitman, Gregg, "Breathing Space," 2007
  3. Melvin, Tessa, "For 36 Children, Hope on Asthma," New York Times, September 26, 1982
  4. Beal, Tom, "Tuscon asthmatic kids of reunite, view latest research," Arizona Daily Star, August 3, 2009
  5. "These Rotarians: ABCs School," The Rotarian: An International Magazine, August, 1965

Monday, August 7, 2017

1960s: Spike in asthma death rate earns worldwide attention

A gradual rise in asthma deaths began during the 1940, although it gained little attention from the medical community, let along the general public.  However, a rising tide of asthma deaths in the 1960s not only gained the attention of the medical community, it resulted in an increase in research and studies into our disease.  This would have a significant impact on the millions of asthmatics around the world, and for the better.

The asthma death started to rise sharply in 1961.  Then, according to Beasly, Pearce and Crane:
In the mid-1960s, asthma mortality increased dramatically in at least six Western countries: England and Wales, Scotland, Ireland, New Zealand, Australia, and Norway.  In these countries, the mortality rates increased 2-10 fold within a 2-5 year period.  Other countries such as the United States, Denmark, Canada, and Germany did not experience epidemics, although in some countries such as Japan, significant increases in asthma mortality were noted within more narrowly defined age groups. (1, page 15)
It was the goal of researchers to discover the likely cause.  A variety of theories were postulated and investigated by the experts.

A.  Accuracy of physicians certifying the cause of death:  This was investigated and pretty much ruled out as a probable cause (7, page 337

B.   Changes in the way asthma was diagnosed:  While it was determined that asthma might be misdiagnosed or under diagnosed, this was ultimately ruled out as a likely cause in an increase in asthma fatalities (7, page 335)

C.  Increase in the number of cases of asthma:  This was actually considered as a likely cause noted by Speizer, Doll and Heaf in 1968.  They said, "In the absence of evidence t the contrary, it would seem that an increase in the case fatality rateis the most likely explanation of the increased mortality rate, and we have accepted this as a working hypothesis." ( 7, page 338),

D.  Environmental factors:  As noted by Speizer, Doll and Heaf in 1968:
"Certainly the increase could not be due to smoke pollution, which has decreased in English towns over the last decade, nor could it be attributed to pollution with sulphur gases, which has remained approximately constant (Ministry of Techology, 1967).  Motor traffic has increased considerably, and one of the constituents of motor fumes could perhaps have had a harmful effect.  If this were the case, however, a substantial difference in mortality would be expected between urban and rural areas, and we have failed to find any evidence of this in the national mortality data for 1966.  The death rate as 2.0 per 100,000 persons aged 5 to 34 in conurbations, 3.0 in urban areas of more than 100000 population, 2.2 in urban areas under 50,000 population, and 1.9 in rural districts. (7, page 338)
Similarly, Lawrence K. Altman said:
We often yearn for the "good old days." For instance, it is often said that there is more pollution today than before, but that statement i snot necessarily correct. Think back to those earlier eras.  Think of the stench from humans who found it dificult to keep clean when bathtubs were scarce. Imagine what it was like when horse manure constantly filled the streets.  It is said that in the 1920s asthma from horses was a common affliction. Dr. Sheffer told me about how a horse trotting along the street could trigger an asthma attack inDr. Robert Cook of Roosevelt Hospital in New York City.
Think also of the dust in the environment and pollution from wood-burning and coal-burning stoves.  Recall the inversions that caused so much sickness and death in Pennsylvania and London, England, a few decades ago. 
Many ofthe offending environmental hazards have been removed. Public health campaigns and legislation have reduced the amount of tobacco smoke and dangerous chemicals in the air.  Those changes have created a widespread impression that we live at a time when we breathe cleaner air (8, pages 5-6)
So, needless to say, environmental causes were ruled out as a factor. This is not to say that environmental factors are not likely factors in asthma morbidity in mortality.  It merely rules these out as likely culprits or the spike in morbidity and mortality during the 1940s and 1960s.

E.   Aging population:  This was not considered an adequate reason because a majority of the data collected by the experts is generally collected for asthmatics between the ages of 5 and 35 years of age, or some similar range.  The reason for this is because the older a person gets the greater the chance asthma will be complicated, or confused with, other medical conditions people normally get as they get older.  Asthma under the age of 5 is difficult to diagnose.  (1, page 13)

F.  Improved ability to recognize and diagnose asthma: This may result in an increase in the number of people diagnosed, but it would not explain the increase in morbidity and mortality.   (1, page 18)

G.  Change in mode of treatment.  There were actually two new modes of treatment on the market during the 1960.  They were:
  1. Systemic Corticosteroids
  2. Metered Dose Inhaler (MDI).  This was often referred to as pressurized aerosol (asthma rescue inhaler)
Systemic corticosteroids were never ruled out as a culprit.  However, Speizer, Doll and Heaf note the following: 
Corticosteroids were introduced into the management of the disease in 1952, but the increase in mortality did not begin until nine years later.  This discrepancy, however, is not sufficient to exculpate them entirely.  The frequent and prolonged use of corticosteroids spread slowly, and the risk of harmful effects may be at a maximum only after patients have been under treatment for several years.  
If patients were on a high dose of steroids and the patient suddenly stopped taking the medicine, this would result in adrenal gland suppression, which may result in death.

The asthma rescue inhaler was introduced between 1957 and 1960:  According to Speizer, Doll and Heaf:
These were introduced in England and Wales in 1960 and began to gain wide acceptance in 1961; and in the next five years their consumption is estimated to have increased more than fourfold (Ministry of Health, unpublished data).  The closeness of the correlation justifies inquiry into the possible harmful effect of the preparations, but a temporal correlatoin of this sort, taken by itself, is a poor basis for drawing conclusions about cause and effect." (7, page 335)
Ultimately, while there were many likely causes for the spike in asthma deaths during the 1940s and 1960s, the finger was pointing at beta adrenergic medicine as the likely culprit.  Whether this was the actual cause was never fully determined.

  1. Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century."
  2. Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma."
  3. Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc.  Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities."
  4. Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press
  5. Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc
  6. Mittman, Gregg, "Breathing Space," 
  7. Speizer, F.E., R. Doll, P. Heaf, "Observations on Recent Increase in Mortality from Asthma," British Medical Journal, February 10, 1968, 1, pages 335-339
  8. Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11
  9. Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," British Medical Journal, 1968, 1, 339-343Sheffer, Albert L, "Partner Asthma Center's Grand Rounds,",, accessed 10/5/13
  10. Bendy, Christine J., E.L-Fellah, R. Schneider, "Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration in vivo," 1975, British Journal of Pharmacology, 55, pages 547-554
  11. Yarbrough, J.,  L.E. Lansfield, and S. Ting, "Metered dose inhaler induced bronchospasm in asthma patients," , Annals of Allergy, Asthma and Immunology," July, 1985, (55)1, pages 25-27
  12. Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.

Friday, August 4, 2017

1940: Asthma death rate begins a gradual rise

The 1940's was a significant decade in the history of medicine, as advances in medicine resulted in declines of morbidity and mortality from some of histories deadliest diseases, such as consumption and influenza.  Our asthma history saw an opposite trend.  While asthma morbidity and mortality were negligible through the 1930, they started to gradually climb during the fourth decade of the 20th century.

Considering these other diseases were in the forefront of the general public, the spike in asthma deaths nearly went unnoticed. Some experts may have seen what was going on, although they had no way of even guessing at the cause.  The reason was because most of the public's attention remained on other diseases, with all public funds, therefore, not going for asthma research.  For this reason there was very limited data regarding asthma available to review.

That left researchers to reviewing death certificates.  However, many experts wondered if methods of certifying death certificates were even accurate.  There were probably times when asthma was misdiagnosed and under diagnosed.  A middle aged man with bronchitis may have been misdiagnosed with asthma.  A child with asthma may have been misdiagnosed with asthma. Likewise, a child with asthma may have gone unrecognized, and therefore un-diagnosed.

It actually wasn't until the 1960s when all eyes were opened to the rising death rates that death certificates were reviewed.  The experts decided to limit their research to asthmatics between the ages of 5 and 35.  The reason was that the likelihood of having pure asthma was greatest among this age group.  Those under five were hard to diagnose, and those over 35 had a a greater likelihood of having some other disease combined with asthma.  Figuring out which one resulted in death could sometimes be difficult to determine.

Data was collected from as far as 1900 for this age group.  According to Beasley, Pearce and Crane in 1968, here is what was learned:
Those Western countries in which relevant data have been published indicate that asthma mortality was uniformly low and relatively stable between 1900 and 1940.  The death rate began to increase gradually in the 1940s in a number of countries including New Zealand and Australia, in which a threefold increase over a 15-year period was observed.  Mortality declined again in the late 1950s in New Zealand, England, and Wales, but not Australia.  In contrast, little change in asthma mortality rates was observed in the United States during this period.  Although the interpretation of death rates over such an extended period is difficult, the historical data are likely to be acceptable accuracy in this age group." (1, page 14)
They also made one other observation:
It is interesting to note that isoprenaline was introduced in a nebulizer formulation during the 1940s when mortality began to increase, but whether this had a role in the increase in mortality was not examined in detail at the time. (1, page 14)
Trends in asthma related deaths were not significantly studied until the 1960s.  When this was done, one of the theories that arose for the rise of asthma deaths in the 1940s was the availability of nebulized isoprenaline at home.  Theorists sense this may have created a false sense of security among asthmatics, particularly children.  Where they once would have sought help, they now simply resorted to their rescue medicine.

Isoprenaline was a new line of sympaththeomimetic medicines, also known as beta adrenergic medicine, more recently as asthma rescue medicine.  Regardless of what it is called, it has the tendency to provide immediate relief from an asthma attack.  Having access to such medicine was a godsend for asthmatics, because it meant that they could get immediate relief in the convenience of their own homes.

While physicians were happy to provide such an opportunity to asthmatics, they were not ready for the potential consequences.  Allowing asthmatics to have quick access to such rescue medicine resulted in two things.
  1. Overuse of isoprenaline may have resulted in cardiac arrest. This would have resulted in suden death from isoprenaline overdose secondary to asthma. 
  2. Overuse of isoprenaline may have resulted in tolerence to the medicine. This would have made the asthma refractory to the isoprenaline, resulting in increased dosing. By the time the asthmatic gave up on the isoprenaline, it was too late. 
These were simply theories that were never proven.  It as impossible for researchers to question these asthmatics after they died, and therefore it was impossible to know how much isoprenaline they used, if any.  
However, in many instances, there were reports from family members and friends of these asthmatics using their rescue medicine prior to death.  

For these asthmatics, however, such theories were trivial and too late. Although data obtained from studying how they died may have resulted in safety precautions that saved the lives of many future asthmatics.  In this way, the experts made sure these asthmatics did not die in vane. 

Another good thing that came out of the rise in asthma deaths during the 1940s, and later in the 1960s, was better recognition of our disease by the medical community.  This ultimately resulted in better recognition by the public, and therefore better funding for future research.  

However, as morbidity and mortality from asthma still remained low in comparison to other diseases, the rise in public awareness continued to pale in comparison.  While it's sad to say, many asthmatics continued to suffer from their disease because the general public simply was not paying attention.  


  1. Beasley, Charles Richard William Beasley, Neil Edward Pearce, Julian Crane, authors of chapter two in the book "Fatal Asthma" edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc. Chapter two is titled "Worldwide trends in asthma mortality during the twentieth century." 
  2. Woolcock, Ann Janet, author of chapter 14 of the book, "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 14 is titled "Natural Histor of Fatal Asthma." 
  3. Sears, Malcolm R., "author of chapter 29 in the book "Fatal Asthma," edited by Albert L. Sheffer, 1998, New York and Hong Kong, Marcel Dekker, Inc. Chapter 29 is titled "Role of B-Agonists in Asthma Fatalities." 
  4. Jackson, Mark, "Asthma: The Biography," 2009, New York, Oxford University Press 
  5. Bisgaard, Hans, Chris O'Callaghan, Gerald S. Smaldone, editors, "Drug Delivery to the Lung," 2001, New York, Marcel Dekker, Inc 
  6. Mittman, Gregg, "Breathing Space," 
  7. Speizer, F.E., R. Doll, P. Heaf, "Observations on Recent Increase in Mortality from Asthma," British Medical Journal, February 10, 1968, 1, pages 335-339 
  8. Altman, Lawrence K., "The Public Perception of Asthma," Chapter one of the book "Fatal Asthma," edited by Albert L. Sheffer, New York, Marcel Dekker, Inc, pages 3 and 11 
  9. Speizer, F.E., R. Doll, P. Heaf, and B. Strang, "Investigation into use of drugs preceding death from asthma," British Medical Journal, 1968, 1, 339-343Sheffer, Albert L, "Partner Asthma Center's Grand Rounds,",, accessed 10/5/13 
  10. Bendy, Christine J., E.L-Fellah, R. Schneider, "Tolerance to sympathomimetic bronchodilators in guinea-pig isolated lungs following chronic administration in vivo," 1975, British Journal of Pharmacology, 55, pages 547-554 
  11. Yarbrough, J., L.E. Lansfield, and S. Ting, "Metered dose inhaler induced bronchospasm in asthma patients," , Annals of Allergy, Asthma and Immunology," July, 1985, (55)1, pages 25-27 
  12. Grant, Evalyn N., Kevin B. Weiss, "Socioeconomic risk factors for asthma mortality," chapter 17 of the book, Fatal Asthma," edited by Albert L. Sheffer, 1998, New York, Hong Kong, Marcel Dekker, Inc.

1913: Cauterize your nose, cure your asthma

Another interesting concept of Adams is that he denied that most asthmatics had allergies, although he associated abnormalities in the nasal cavity with asthma.  He noted that Henry Hyde Salter cursorily mentioned the relevance of the nose in cases of asthma, when such knowledge was known since 1844 when Herck of Freiburg noted the association of sneezing and asthma. (1, page 89)

Later, Adams noted, Voltolini, in 1872, claimed to have "relieved eleven cases of asthma by removal of nasal polypi.  This idea received further impetus when Lazarus, Brodie and Dixon and others showed that electrical stimulation of the nasal mucosa caused bronchial spasm."

Ernst Schmiegelow explained that Voltini noted that no other asthma physicians prior to him noted the link between nasal polypi and asthma.  And while polypi are not always associated with asthma, there are noted cases where, upon removal of the polypi, the asthma disappeared. Although, if asthma has existed long enough so that it is chronic, removal of the polypi will not make the asthma disappear. Schmiegelow notes that Voltini's opinions were confirmed by Hanisch. (2, page 14)

Schmiegelow notes that "Hanisch thinks that as not all nasal polypes cause asthma, there must be a certain debility of the whole organisation or at least of the organs of breathing. In the nasal polypes themselves he finds sufficient ground for the weakened state of the organisms and lungs, as the insufficient breathing, the restless sleep, the buccal respiration, etc., must be considered capable of causing the general weakness."  (2, page 14)

B. Frankel and Weber also confirmed the findings of Voltini, and they also believed that chronic catarrh could also cause asthma. They believed irritation of the nasal mucous membrane passed a message down the pneumogastric to the pulmonary fibres, causing asthma, and "the result of the reflex was always a bronchospasm.". (2, page 15) Henry Hyde Salter previously mentioned this, and referred to is as reflex asthma.  

Schmiegelow also mentions a Dr. Wilhelm Hack, who "supported by casuistic observations, considered a number of different nervous diseases from the same point of view. Hack's principal object was to show that in the swollen cavernous mucous membrane in the foremost end of the inferior turbinated bones, different nervous states of irritation originate, and these reflex neuroses can be caused experimentally, and they disappear entirely as soon as the places in question are operatively removed. The filling of the cavernous membrane is, according to Hack, the essential in the pathogenesis of these reflex neuroses."

Adams notes that other physicians were so focused on the other theories of asthma, particularly that asthma was neurotic, that they were overlooking the true cause: that there was a problem with the patient's nasal passage causing the asthma, or that there was a toxaemia in the blood causing asthma as I discussed in this post.

Adams emphasises the following: (1, page 89-90)
"I have seen patients with noses absolutely ruined, mere shells of what they should have been—their asthma remaining the same, but promptly clearing up on simple antitoxaemic treatment, except in the case of a poor woman who owed an opium habit to her doctor. Francis cauterises the septal tubercle of all asthmatics—sometimes a valuable temporary procedure; others would also cauterise the lower turbinals—an unnecessary addition. The value of proper nasal treatment cannot be gainsaid; but that it should be subsidiary and ancillary to treatment of the toxaemia I have, where mouth breathing was absent, occasionally and successfully proved by the experiment of carrying out the latter treatment and leaving the nose alone. Apart from the experimental and therapeutical evidence just mentioned, the importance of a nasal factor in asthma can be gauged from several considerations."
Some of the ailments he observed on asthmatics, were:

  • Nasal polypi
  • Deviated Septum
  • Hypertrophied areas in nasal passages
  • Pigeon chest (due to laboring for air so frequently)
  • Mouth breather
  • Expanded shoulders (due to years of laboring for air)
  • Expanded chest (due to emphysema if chronic)

Wednesday, August 2, 2017

1913: Adam: A perfect description of an asthma attack

Consider the following description of an asthma attack:
"In marked attacks not only is the struggle for breath so severe as to make the patient sit or kneel in bed, but he may even get out of bed and stand gasping at an open window, or clutching at any support that will aid the respiratory muscles of respiration. many will not go to bed at all, but sit in a chair all night, dozing when they can." (1, page 9)
If that doesn't describe one of my typical asthma attack when I was a kid I don't know what does. 

  1. Adam, James, "Asthma and it's radical treatment," 1913, London, Gasgow: Alexander Stenhouse

Monday, July 31, 2017

1913: Adam: Abnormalities Associated With Asthma

Dr. James Adam believed the most common cause of asthma was a toxin or poison in the blood.  The other cause of asthma was lesions in the respiratory tract (published 7/10/14).  While most physicians focused their attention on spasms in the lungs, he believed they should be focused more on one of these two causes of airway spasms.

He observed that many asthmatics, although not all, present with one or more of the following abnormalities along their respiratory tract or amid the chest and body:(1, page 12, 35-38)
  1. Polypi
  2. Septal deviations blocks air passage
  3. Turgid turbinals: blocks air passage
  4. Irritable turbinals (very sensitive to stimulus, causing coughing or sneezing)
  5. Congestion of mucus membrane (anywhere from nose, trachea or bronchi)
  6. Pigeon breast: from a lifetime of asthma the chest becomes deformed, where one sternum, or breastbone, is pushed outward
  7. Emphysema during asthma attacks, becomes chronic if asthma not cured 
  8. Barrel chest: rounded, bulging chest that shows little movementn with respiration.  It occus during a paroxysm, and becomes chronic if asthma not treated (sign of emphysema)
  9. Rounded, almost stooped shoulders (sign of emphysema)
  10. Unilateral nasal obstruction
  11. Sputum at the end of the attack
  12. Curschmann spirals in the sputum
  13. Eosinophile cells in sputum, with Charcot-Leyden crystals
  14. Heart Rate of 90-110
  15. Blood pressure within normal limits: paroxysm does not raise the blood pressure, but adrenalyn used to treat asthma may
  16. Blood pressure of 80-90 mmHg at end inspiration, and 120-130 at end expiration: decreased BP on inspiration may probably be due to impeded pulmonary circulation
  17. Flatulence during the paroxysm
  18. Asthmatics live long: In this, he agrees with other asthma physicians such as Salter and Berkart. (1, page 38) Adam notes this is true "so long as they don't become drug slaves)
While most other members of the medical community focused most of their attention on the spasmotic and nervous theories of asthma, Adam was focused on the Lesion Theory of Asthma and the Toxaemia theory of asthma, and for that reason his "radical treatment" would better help asthmatics as opposed to the more traditional treatment prescribed by other physicians.

  1. Adam, James, "Asthma and it's radical treatment," 1913, London, Gasgow: Alexander Stenhouse

Friday, July 28, 2017

1913: Two types of chronic asthmatics

James Adams explains that most cases of asthma are chronic before they are seen by a physician; that these cases are usually treated as bronchitis first (airway inflammation and increased sputum production).  Bronchitis "is really the form asthma commonly takes at first."  Only as time progresses, does asthma be come chronic. (1, page 31, 33)

He describes two types of chronic asthma: (1, page 30)
  1. Fat: Less common; overeating can lead to asthma; chronic bronchitis
  2. Lean: More common; usually as the disease becomes more chronic, a toxaemia in the blood will cause the asthmatic to become thin, with expanded shoulders and chest due to chronic laboring and emphysema.  
Adam writes that the most common sign of chronic asthma is "dusky, sallow skin with chloasms round the eyes, sure token of toxaemia. There is no mistaking this asthmatic chachexia (fatigue, weakness, as in wasting away) and the first sign of improvement resulting from correct treatment is the clearing of the skin; it looks as though it has been washed from the inside -- as it has been... it takes prolonged, repeated and severe paroxysms to develop the other (signs of chronic asthma). (1, page 31)

What causes the signs of chronic asthma, Adam notes, is the hyperaemia that is constantly ongoing and not treated (and it's usually not treated because most physicians don't respect the toxaemia theory of asthma.).  Toxaemia that is constant acts on the "skin and bronchial mucous membrane as well as on the tissues generally, producing the cachexia and bronchitis, the stress of the dyspnea, which is the main factor in producing the other thoracic changes, is intermittent.

Other signs of chronic asthma would be your distended chest and shoulders, pigeon chest, etc. These are signs that the person has a toxaemia, and that the person has been working hard to suck in air. (You can see more signs of the toxaemic effect on asthma in this post (1913: Lesions in respiratory tract cause asthma on 7/22/17)

Bronchitis is generally caused by a metabolic disorder, and therefore, the treatment generally revolves around decreasing carbohydrates (sugary foods), such as "sweets cakes." (1, page 33, 35)(also see chapter on atypical asthma)

  1. Adam, James, "Asthma and its radical treatment," 

Wednesday, July 26, 2017

1913: Adam Toxaemic Theory of Asthma

By the turn of the 20th century, the medical profession had readily accepted both the nervous theory of asthma and that spasmodic theory of asthma. The allergic theory of asthma was in its infancy, and the old toxaemic theory of asthma was no longer written about in new editions of asthma books.

Yet it was the old theory, the toxaemic theory of asthma, that Dr. James Adam proposed as the most valid explanation of asthma.  He understood that is was no longer accepted by the medical community, and he understood treatment based on this old theory was considered radical.  This, therefore, was the reason he referred to his asthma book as "Asthma and its Radical Treatment." (1, pages 1-3)

Dr. Adam said he continued to have much respect for Dr. Henry Hyde Salter who, during a series of articles published in the 1950s, articulated support for the nervous and spasmodic theories of asthma.  Yet Dr. Salter also articulated support for the toxaemic theory of asthma.  Of Dr. Salter, Adams wrote:
Hyde Salter’s book, written before most of us were born, must not be overlooked by anyone interested in the subject; he had probably a wider experience of asthma, and a better grip of the value of the dietetic treatment, than many twentieth-century authorities." 
Dr. Salter, from our own studies, was an ardent supporter of the idea that there was a direct correlation between what one puts into his body and asthma.  He wrote that many of his patients, including himself, observed that upon eating too much or eating the wrong foods, often lead to a paroxysm of asthma.  The prevention of asthma, therefore, was to eat healthily and eat light.  The remedy was emetics and enemas.

Salter believed the certain foods, or too much food, lead to some form of poison in the blood that leads to the nervous system causing bronchospasm.  Dr. Adam simply refined this theory as follows: (1, page 3)
Toxaemic theory of asthma:  Asthma is a disease of the nervous system, and "all neurosis are toxaemias."  A poison enters the body and this "hits the nerves of the respiratory tract."

Adam suggests that asthma is caused in this way:
This toxaemia arises partly in the bowel, partly in the tissues; it arises partly by absorption of nitrogenous poisons resulting from intestinal puttefaction under microbic action ; but mainly is due to an error in nitrogenous metabolism, the result of imperfect oxidation or enzyme action. In short, the poison arises from Proteid food or proteid tissue.
The error in proteid metabolism is closely connected with excess of carbohydrate in the diet.
The oxidation of the excess of the simpler carbohydrate molecule seems to interfere with proper oxidation of the more complex proteid molecule. In other words, the excess of energy food interferes with the metabolism of the tissues and tissue-foods; the imperfectly metabolised products so resulting set up asthma.
In other words, as Salter explained, the poison, or toxaemia, was the cause of some error in diet.  The result, according to Adams, was as followed
The toxaemia, whether arising in bowel or tissues or both, tends to show itself first as catarrh, later as spasm, in the respiratory tract. This toxaemia shows itself in conditions, catarrhal and spasmodic, other than, but closely related to, asthma.
He believed there were certain prodomata (early signs) of asthma that are often overlooked, and while these signs may not be present in all cases of asthma, if one is observed it can be a sign of an impending attack, such as:
  • Polyuria (excessive urine production)
  • Oliguria (diminished urine production)
  • Anuria (no urine production)
  • Constipation (unable to have a bowel movement)
  • Formication (sensation you have insects crawling under your skin)
  • Pruritus (sensation that results in urge to scratch; itchy sensation)
  • Urticaria (hives)
  • Erythema (redness of skin)
  • Cyanosis (Blueness of skin, representative of ischemia of tissues of hand, foot, lips, etc.)
  • Petechiae (red or purple spots on the skin caused by minor hemorrhage; local bleeding due to broken capillary vessels)
  • Embarrassed breathing (asthma)
The above will continue until something happens involving the elimination of something, which generally involves:
  • Vomiting (spitting up stomach contents)
  • Diarrhea (loose stools)
  • Polyuria (excessive urination)
  • Expectoration (sputum production)
Due to the toxaemic effect, the following are also associated with asthma (all are associated with increases of eosinophilia in sputum): (1, page 34-35)

  • Eczema: Commonest and most likely to occur in children with bronchitis. It usually shows up before asthma and disappears.  Although will continue to "dog" the patient if the asthma is not "cleared up." Cause is same as asthma, and treatment therefore same too (see treatment for both asthma and eczema is generally to restrict carbohydrates)
  • Ichthyosis: Probably caused by metabolic disorder
  • Psoriasis: Adams notes it's "said to be associated with asthma, but I have never seen the combination." Restricting carbohydrates generally doesn't work, but restricting "nitrogenous intake does." The difference in treatment may prove the non-association of psoriasis with asthma.
  • Dermatitis Herpetiformis:  Also associated with asthma. 
One of the reasons that he published his book was because he believed that "far too much attention has been paid (by the general practitioner) to the most striking feature of asthma, the asthmatic spasm; too little to the conditions that precede and cause the spasm, and those by which Nature cures it." Of course, the toxaemic theory of asthma provides the answer to why the spasm occurs, and thus its radical treatments would prevent and treat asthma.

Adams also noted that his theory came at a time when other theories were more readily accepted by the medical profession.  However, his idea are "put forward with the hope that it will be useful not only in the treatment of asthma but also in those other diseased states whose kinship with asthma is too."

  1. Adam, James, "Asthma and it's radical treatment," 1913, London, Glasgow: Alexander Stenhouse

Monday, July 24, 2017

1851-1913: The history of asthma sputum

Ernst Victor von Leyden (1832-1910 discovered
crystals in asthmatic sputum, and suspected these
to be the cause of asthma. During his era, he was
the closest supporter of Dr. Robert Bree's
bronchitic theory of asthma. (9, pages 14-15)
He believed these crystals somehow irritated the
"vagus in the mucus membrane of the bronchials,
and hereby caused by reflex action a spasm
of the muscles of the small bronchial tubes."
(10, page 8)
Most people find sputum disgusting, and so will have nothing to do with it. But as far back as 400 B.C. the medical significance of it was observed by ancient Greek physicians, and probably even earlier than that.

If you mention it at the dinner table your mother might smack your hand. But for the sake of gaining a complete grasp on the history of asthma and respiratory disease, we must delve into the topic of sputum.  Sorry, but we must.

It must have been observed at an early date in history that people with breathing issues produce sputum, sometimes consisting of a putrid smell, often consisting of many varied colors such as red, yellow, brown and white.

Yet rather than being petrified by the grossness of the substance, Greek philosophers became fascinated by it. They even gave it its own classification as one of the four humors that, along with determining ones personality, also determined whether was healthy or sick.

Prior to the philosophical medicine of the ancient Greeks, other ancient societies, and the primitive clans and families that roamed the lands before them, believed sputum was the production of some evil spirit, demon or god. When a person expectorated the substance, they were in essence expectorating an evil substance that caused the symptoms they were suffering from.

From the ancient world to the scientific revolution there were few changes in the way physicians viewed diseases and treated their patients.  In 1799 Dr. Robert Bree speculated that sputum contained a poison that it was trying to get out of the body, and asthma was the result.  This theory wasn't much different than any idea Hippocrates might have postulated.

Since the sputum preceded the asthmatic fit, Bree essentially speculated that asthma was essentially bronchitis, and thus created the bronchitic theory of asthma.  Others, without much more evidence, speculated sputum was the effect of asthma rather than the cause.

Such speculation gradually tapered off, but never really came to an end, during the scientific revolution, and mainly due to the inventions of the microscope, which allowed physicians to see that the human body was made up of substances too small to be seen by the unassisted eye, and the stethoscope, which allowed physicians to hear changes that occurred inside the chest and to diagnose diseases with accuracy prior to autopsy.

The microscope allowed physicians to learn that air passages were surrounded by smooth muscle, and that it was capable of spasming when stimulated.  The stethoscope allowed them to hear when sputum accumulated in the chest, and learn that it was the effect and not the cause of asthma.

So, pretty much, prior to the 1850s asthma was basically considered to be a disease of excess sputum, mainly because this was all physicians could observe with the unaided eye and ear.

Yet by the 1850s it was looking pretty clear that asthma was also a disease associated with spasms of the air passages, particularly by the wheezes heard by air flowing through narrowed air passages, and rhonchi heard as air flowed through sputum lined air passages.  (1, pages 592-595)

In 1851, Dr. Beau, along with his assistant Cozart, observed that fits of asthma usually ended with a wad of sputum being coughed up. Beau used this observation as evidence to support his theory that asthma was a disease of chronic catarrh, and that asthma was caused by increased sputum in the air passages.  (3, page 31)

When this sputum dried out mucus plugs formed that were capable of blocking the air passages, thus resulting in dyspnea and other symptoms of asthma, including the "sonorous and sibilant rhonchi -- their 'rales vibrants' heard upon auscultation with a stethoscope."  (3, page 31)

The fit, therefore, was resolved when mucus plugs were broken up with a fit of coughing.  (3, page 31)

Then, in 1878, at a time when most physicians had accepted the nervous and spasmotic theories,  J.B. Berkart used Beau's research as evidence of the bronchitic theory of asthma.

Berkart said:
With the displacement of the mucous plug into the larger bronchus, or on its expulsion by means of a fit of coughing, the dyspnea ceases, and with it also the rales disappear.  This form of bronchitis is, in their (Beau and Crozant's) opinion, due partly to an idiosyncrasy of the patient, partly to exciting causes, which greatly vary in different individuals."
Tiny crystals were first observed in sputum in 1851 by Jean Martin Charcot, but it wasn't until 1872 that these crystals were linked to asthma by Ernst Victor von Leyden. So history has given credit for this discovery to both men by calling the crystals Charcot-Leyden crystals.

Leyden, whose asthma theories were similar to Dr Bree's bronchitic theory, believed Charcot-Leyden crystals caused asthma by irritating...
...the peripheral extremities of the vagus nerve, and produce reflex spasm of the bronchial muscle."  
The asthma attack, as Bree and Beau observed, ended when a wad of sputum was coughed up during a fit of coughing. (4, page 14-15

However, it was the discovery of these Charcot-Leyden crystals that would ultimately put an end to the bronchitic theory of asthma.  This was noted by Dr. John Charles Thorowgood in 1878.  He said that these crystals were found in sputum obtained from patients with "ordinary catarrh and croupus bronchitis."  (4, page 15)

Thorowgood said:
The asthmatic patient while in a fit presents abundance of symptoms distressing enough to endure or to witness; and yet, when things seem to be at their worse, and the patient well-nigh at his last gasp, a remission comes on, the spasm yields, air enters the lungs, and the attack subsides, coincidentally often with access of cough and mucous expectoration." (4, page 16)(9, page 1,2)
In 1879, bacteriologist Paul Erlich discovered the eosinophil, and it was soon discovered that elevated levels of eosinophils (eosinophilia) was commonly found in asthmatics. (5)

In 1882 Heinrich Curshmann observed other spirals in asthma sputum and believed they were associated with causing asthma. He believed since Leyden's crystals didn't cause asthma, perhaps his crystals did. (5)

Later Curshmann's crystals were determined to be fragments of mucus plugs associated with asthma, and Leyden crystals were determined to be fragments of eosinophils. Eosinophils were later learned to be a type of white blood cell that, along with mast cells, are involved in the allergic reaction.

In 1911 Hermann Sahli described eosinophils in asthmatic sputum. Yet Sahli noted another author from 1891 who described eosinophils in asthmatic blood, and he concluded that these must be pathological with asthma. Yet he also noted that neither the cause of the eosinophils nor their origin was known. (7)

Sahli could isolate the area where the sputum came from based on epithelial cells in it, yet he did not understand the mechanisms of its production as we do today. (7)

Dr. James Adams describes asthma sputum in 1913: (8)
"Asthmatic sputum varies. Often there is none till the end of the attack; then it is in the typical form of small, tough pellets expelled by laborious coughing. The attack may then cease, or it may go on till a more free and profuse expectoration occurs."
He also wrote:  (8)
"The sputum does not readily decompose, and is said to be wonderfully free from microbes; but this is not always so, as I have occasionally found it teeming with them."
The true purpose of sputum is to ball up microbes inside the lungs and haul them out, and in this way the lungs stay sterile.  Surely asthma can be caused by inhaling a microbe, such as a bacteria, but it's also caused by asthma triggers (dust mites, smoke, fumes, chemicals, pollution, animal dander) that are innocuous to most people, and non infecting agents.

So this might explain why Adams most often found asthmatic sputum without an infecting agent, and sometimes "teeming with them."

Backing up a moment to 1906, Australian pediatrician Clemons van Pirquet coined the term allergy when he observed that some of his patients were hypersensitive to substances that did not bother other people (what we now refer to as allergens, or asthma triggers).  This was the first time asthma was linked with allergies.

By 1910 Histamine was discovered and found to be a major component in the allergic response.  So some went on to speculate that finding a way to block histamine would cure both allergies and asthma.

By 1946 antihystamines hit the market, and within a decade they were among the most commonly prescribed medicines.

Yet as time went by, it was learned that there was more to asthma and allergies than just histamine.  It was learned that asthmatic and allergic immune systems respond irrationally to allergens and asthma triggers by increasing production of eosinophils and this spearheads inflammation of the bronchial muscles.

Another weapon of the immune system is mast cells that line the respiratory tract and eyes, and these were discovered in 1953.  .

In 1967 Immunoglobulin E antibodies (IgE) were discovered.  It was later learned IgE has a significant role in the asthmatic and the allergic response.  The first time asthmatics are exposed to asthma triggers (allergens), say dust mites, their immune systems develop dust mite IgE antibodies that attach to mast cells that line the epithelial layer of the skin or respiratory tract.

The second time that person is exposed to that allergen (dust mites in this case), a mast cell that has a dust mite IgE antibody attached to it explodes and releases its contents:  the mediators of inflammation.  A mediator of inflammation called histamine was discovered in 1910, and others called cytokines and leukotrienes were discovered in the 1970s.

These mediators, when released into the blood stream, cause inflammation of the respiratory tract, thus causing the allergic and asthmatic responses.

In the allergic person, they can also cause inflammation of the upper respiratory tract, which includes the back of the throat and nose.  The offending substance (dust in our case) is recognized by the immune system, trapped in the mucus layer, absorbed by the mucus, balled up by the mucus, and sent on it's way up the respiratory track to be coughed up.

So this would explain what Dr. Bree, Beau, and Berkart observed. While hacking up a wad of sputum may have been related to the fit of asthma, it was not the cause, and had nothing to do with the cure.

Later it was learned that asthmatic lungs tended to produce an abnormal number of goblet cells, this results in an abnormal increase in mucus production during an asthma attack.  While some of this sputum may be coughed up, some becomes trapped in obstructed air passages, dries out to form mucus plugs, and this further blocks the air passages, thus compounding the asthma response.

When the fit ends, when the air passages relax and dilate, which may be a result of time or medications, the asthmatic will probably expectorate this sputum, which will usually be, if no bacteria or virus is balled up within it, white and sterile.  It will also have IgE and eosinophils in it, hence your Charcot-Leyden and Curshmann crystals.

So it's easy to understand how this production of sputum at the end of an attack could easily be misinterpreted as the cause, rather than the effect, of asthma.

  1. Lotval, J., "Contractility of Lungs and air tubes: experiments performed in 1840 by Charles J.B. Williams, European Respiratory Journal, 1994, (7) pages 592-595
  2. Bree, Robert, "A Practical Inquiry into Disordered Respiration Distinguishing the Species of Convulsive Asthma, their Causes and Indication for a Cure," 4th ed, 1810, London, page pages 117-118
  3. Berkart, J.B., "On Asthma: Its Pathology and Treatment," 1878
  4. Thorowgood, John C., "Asthma and Chronic Bronchitis: A New Edition of Notes on Asthma and Bronchial Asthma," 1894, London, Bailliere, Tyndall, & Cox
  5. Lipkowitz, Myron, Tova Navarra, "Encyclopedia of Allergies," 2001
  6. Brenner, Barry E, "Emergency Medicine, 1998, page 10
  7. Sahli, Hermann, "A treatise on diagnostic methods of examination," 1911
  8. Adams, James, Asthma and it's Radical Treatment, 1913
  9. Thorowgood, John C., "Notes on Asthma," 1878, 3rd edition, London, J & A Churchill
  10. Shmiegelow, Ernst, "Asthma, considered specially in relation to nasal disease," 1890, London, H.K. Lewis

Friday, July 21, 2017

1913: Speculation about asthma continues

My mom once said that house wives today probably know more than physicians in the 19th century. As I study the history of medicine and lung diseases, I have learned this is somewhat true to a certain extent, mainly because housewives like my mom had access to greater wisdom.

However, there are still an amalgamate of wive's tales, excuse the pun, that wives still use to treat their children when they are sick.  One of these was to place their asthmatic child in a hot and steamy bathroom.  We now know this may work to make breathing easier if the diagnosis was croup, but not asthma.  In fact, steam may make asthma worse because it makes the air thicker.  

Yet as the old saying goes: we do the best given the knowledge we know today, and as we learn better we do better. So by this saying, we cannot fault our parents for trying.  And as we have sick kids, we must do better.

So this brings me to the topic that caught my interest today, and that is that as I read case histories the various physicians wrote in old asthma books, I realize how much more knowledge I have as an asthmatic, asthma dad, respiratory therapist, and amateur historian.  

One of the neat things about reading an asthma history is I read a lot of case histories written by the various physicians knowing I know more than that doctor. A good example is here noted by Dr. James Adam in his 1913 book "Asthma and its radical treatment." (1, page 33-34)
'' A boy of 26 months was sent to me by Dr Alex. Morton. He had cured him of bad generalised eczema; but asthma occurred almost every night in spite of the fact that the dietetic regimen laid down by Dr Morton was what I myself would have set for the asthma. This boy was the subject of hay fever and ichthyosis; his urine showed persistent deposit of uric acid and increased indigogens. His maternal aunt had eczema in childhood, and now has asthma; his paternal aunt has eczema and asthma; there is a history of gout and uric acid on the mother's side. Treatment freed him fromasthma for a year. He then went to stay with his grandmother who coddled him, gave him the forbidden thing, sweets and cakes, and soon brought back both eczema and asthma. Not only so, but interesting etiologically is the fact that adenoids and chronic rhinitis have developed, for which treatment has been declined; but although this injures the prognosis, the asthma has never been so bad as at first. A boy, whose father was long asthmatic but has remained well for many years, was much troubled during the first two years of life with eczema, the result largely of overfeeding. He is now five, and during the last two years he has developed 'bronchitis,' which is now taking the more typical asthmatic form."
Adams further notes that: "The association, bad feeding, eczema, bronchitis, asthma, is too frequent and too plain for anyone to doubt that a metabolic error, or at least a toxic condition, is in play."

Given modern wisdom, I know that there was a major flaw in the analysis of Adam, and that was his decision to treat asthma and all the other maladies associated with it as a toxaemia. Surely it's a bad idea for a child to eat too many cakes, yet what might more likely cause the hay fever, asthma and eczema are allergies. The child was probably exposed to allergens near birth and at his paternal aunts. The remedy would be to not let the child go to his paternal aunts.  

The fact the parents were courageous enough, and perhaps wise enough, to decline treatment for adenoids and rhonitis, which may have involved surgical treatment, was impressive.Adam said himself that other asthma experts were so intent on focusing on the nervous theory of asthma and the spasmodic theory of asthma that they didn't see the true cause: toxaemia in the blood. He called his theory the toxaemic theory of asthma.

To his credit he did acknowledge his ideas would be seen as radical, of which they were. Plus, in a time when the trend was to generate theories about asthma based on science, Adam took the route of speculation.

As my asthma history continues, I will delve in later posts more into the theories and treatments of Adams that he describes himself as radical. They would not be radical if they were proposed 100 years earlier, but, given the era he was born in, yes he was quite radical.

  1. Adam, James, "Asthma and it's radical treatment," 1913, London, Gasgow: Alexander Stenhouse