The following excerpts are from the E-mail discussion of the committee on chronic mountain sickness, prior to

The 3rd World Congress on Mountain Medicine and High Altitude Physiology and  The 18th Japanese Symposium on Mountain Medicine carried out in Matsumoto, Japan (May 20th - 24th, 1998).

---

From:         "GUSTAVO ZUBIETA M.D. * IPPA *" <IPPA_0/ZUBIETA>

Date:         20 Mar 98 16:16:43

Subject:      Re: CMS Symposium

X-mailer:     Pegasus Mail v2.3 (R5).

 To:   "John Reeves" <John.Reeves@UCHSC.edu>

Dear Jack:

 

Thank you for your E-mail of march 15. We were out of town and

just returned yesterday.

 

You wrote:

> I have the abstract "Incidence of Disease at High Altitude in La Paz

> Bolivia".  Will that be the subject of your presentation in the CMS session?

 

Yes, we consider this to be more adequate to our field than in

the high altitude population in the world symposium. In fact we

meant to deal more with CMS in this presentation.

 

> How long are you planning to talk?

Would 20 minutes be fine?

 

> Keep in mind that we are hoping for as much

> time as possible for discussion.

> One of the main question that will require discussion is that

> of the definition of CMS, so that we can all play from the same

> sheet music. In your case, do you include or exclude persons with

> chronic lung disease in the CMS group?

 

Following is the summary of the modest opinion of my father and

myself, from many years of observations in the bowl-shaped city

of La Paz to El Alto (between 3100m and 4100m), with much CMS in

a population above 1.2 million:

1) In our concept, CMS or Monge's disease are adequate

denominations for a disease present only in hypoxic conditions

due mainly to respiratory and ventilatory alterations of

different etiopathogenesis, some complicated by other alterations

such as kidney disease, arterial hypertension, and so on.

 

2) CMS at high altitude is expressed as cyanosis and low arterial

saturation which gives rise to pulmonary hypertension and

increased polycythemia, as compensatory mechanisms of adaptation

to the disease under hypoxic conditions.

 

3) CMS is irreversible in diseases like pulmonary fibrosis, and

reversible in chronic bronchitis, for example. If the arterial

blood is completely saturated at 98%, as such is the case when

the subject descends to sea level, there is a regression of the

symptoms and signs. Giving continuous oxygen administration to a

patient with COPD at sea level, will achieve similar results.

 

4) Respiratory diseases are the same at high altitude, in

etiopathogenesis as those of sea level; but the impaired

respiratory function, with low oxygen saturation, below the

plateau of the saturation curve (in the steep part), shows

us what we know as CMS or Monge's disease.

 

5) Since CMS is a common denominator of diverse diseases of the

respiratory system, each case should be diagnosed and treated

according to the etiopathogenesis. It seems also evident that

some subjects are more prone to suffer pulmonary diseases.

Similarly, men have a greater tendency to develop pulmonary

disease, than women and consequently are more susceptible to

develop CMS.

So, hoping to answer your question:

The confusion arrives because the classical description of

Monge's disease in 1928, expressed that there is no pulmonary

anatomical or functional alterations, not able to become evident at the time,

due to the lack of modern technology that we have nowadays.

Not all patients with respiratory disease at high altitude

develop CMS. Some pulmonary diseases alter as a sequelae

the pulmonary function, like impaired diffusion, uneven

ventilation, increased shunt, or hypoventilation. These lead to

low saturations in hypoxic conditions and to CMS.

 

Please read our article New Concepts on Chronic Mountain Sickness

We enjoyed preparing these comments, and if you should have any

doubts, questions or comments please feel free to send us an E-

mail.

We were hoping to meet you in Cuzco, and inquired about you but

they said you were in Russia. We were supposed to go the meeting

in Ukraine invited by Beloshitsky. We ran into many problems. We

couldn't get to Ukraine from Moscow. We will tell you more when

we meet in Japan.

Gustavo Sr.      &      Gustavo Jr.

 

 

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

                    Gustavo Zubieta, M.D.

            HIGH ALTITUDE PATHOLOGY INSTITUTE * IPPA *

Av. Saavedra 2302                       Tel:    591-2-368734

P.O. BOX 2852                           Fax:    591-2-229504

La Paz, Bolivia                         E-mail: zubieta@oxygen.bo

-------------------------------------------------------------------------

 3/31/98            8:20 AM
 

Thank you so much for the thoughtful remarks.  They are extremely useful for

the purpose of initiating discussion.  As a bystander who does not see CMS

patients,  but who is interested in consensus, I do see differences of opinion

that could and should be laid out on the table for friendly discussion, where

everyone benefits.  Getting these diverse opinions in ahead of the meeting

should make people aware of the differences, and allow them to think about the

problems. I hope you agree. Final answers may not come from the meeting, but

the process of discussion will have been initiated.  I am trying to keep Wu

informed by fax of these discussions, but am not sure the faxes are getting

through.  I have taken the liberty of sending your thoughtful comments around,

as I believe they deserve wide distribution. I hope that is O.K.

 

 

Jack

 

 

--------------------------------------

Date: 3/30/98 4:05 PM

To: John Reeves

From: GUSTAVO ZUBIETA, M.D. * IPPA *

Jack:

          Here goes the homework requested by you, Lorna Moore

and her colleagues.

 

 

We feel troubled by the subject of scoring CMS.  As you can read

from our publications, we are confident that there is no "loss of

adaptation of life at altitude", but rather an adaptation of

pulmonary, cardiac, renal or other disease to the hypoxia at high

altitude. (And to tell you the truth, CMS patients do remarkably

well, provided their basic disease is treated or looked after).

 

 

In general, patients with CMS are examined while attending a

regular consultation. Most often, after suffering the disease

during many years and only when they and their family become

aware of the change in the color of the skin, particularly in the

face. Also, when the consultation is for another kind of disease

and the routine laboratory tests report increased polycythemia.

At this time, the signs and symptoms can be present in different

degrees and are prominent or more evident in THS.

 

 

The score will only be valid for some patients with CMS and

exclude others. Gastrointestinal ulcers, are frequent findings.

Gastro-intestinal bleeding, will change the score. The same

happens with Gout. Several patients with CMS have increased uric

acid, and some with evident signs of Gout by deposits in the ear

helix. Gout can lead to well known pulmonary alterations.

 

 

Similarly, hypertension is also present in some of them. This

generally implies kidney disease. Finger clubbing is present in

some, even when they are very young. In broncho-pulmonary lesions

of smokers, for example, there can be severe cyanosis, low

saturation, increased polycythemia and pulmonary hypertension. If

they stop smoking there is significant improvement. This is the

same as at sea level, but in chronic hypoxia they reach lower

saturation. Another example are some patients with asthma. This

shows that CMS patients have a different etiopathogenesis. If all

these examples are not included, are they going to be considered

a different kind of disease? It does not seem so.

 

 

At altitude, "cyanotic pulmonary diseases and asymptomatic high

altitude polycythemia" (as defined by Hultgren) are, in our

experience, CMS, and the later approaches more exactly CMS

present at moderate altitude.

 

 

If you use a score, you have to be aware that it will apply for

that moment only and it will most probably change even within the

next few days. Also, great differences in scoring will be found,

depending on the degree of compromise of lung or cardiac

function, the type of disease, and of course the altitude.

 

 

Why?  Because patients that have CMS are subject to viral

diseases, bronchitis, colds or even seasonal climate changes (we

have a CMS patient with allergies). This we described as triple

hypoxia syndrome (THS), an acute condition overimpossed on CMS

(please see further down and the article in our Web page below).

 

 

So, if the score pretends to be used to access the moments'

clinical state of the patient with CMS, that is fine.

 

 

About scoring CMS:

 

 

In the score used by Dr. Wu in CMS, the signs are present

particularly in AMS and the triple hypoxia syndrome, that we also

call "sorojche (AMS) in bed".  With the exception of hyperaemia

in conjunctivae and mucosae, which are chronic.

 

 

The scores 0, 1, 2 and 3 for none, mild, moderate and severe,

seem adequate.

 

 

We think that everybody agrees that the disorder regresses on

descent to sea level, in around one month. Patients who reascend

to high altitude, and are exposed again to hypoxia, develop CMS

once more. This is a mechanism of adaptation, to supply the

necessary oxygen to the tissues. The patients from low lands with

chronic pulmonary diseases commonly unnoticed at sea level,

develop CMS at altitude. Are we going to consider these cases as

a loss of adaptation?. Certainly not, it is hard to think in such

a way.

 

 

We agree that the most appropriate approach to score the disease,

are the laboratory findings: hemoglobin or hematocrit and oxygen

saturation, with or without carbon dioxide retention, depending

of the severity of the case. For over 15 years now, we have been

using a classification by number of red blood cells ("El mal de

monta$a cr"nico y los mineros", published in the magazine of the

Academia Nacional de Ciencias de Bolivia,1985;4:109-116), and it

has proved to be a good guide in our medical practice.

Originally, diagnosis was based on clinical examination, chest x-

rays film and hemogram only, due to the lack of equipment.

 

 

 

It is as follows:

 

 

moderate  6.5 to 7.5 million RBC/mm3

severe    7.5 to 8.5 million RBC/mm3

grave     > 8.5 million RBC/mm3

 

 

For 3600 m. of altitude only.

 

 

We feel now that it would have been better to name them as mild,

moderate and severe and to use the hematocrit or hemoglobin,

which amount to the same thing.

 

 

----------------------

 

 

With respect to your 7th question, (a very good one, indeed);

yes, there is an altitude at which everyone gets CMS.  Please see

the abstract "Pulmonary disease, CMS and gender differences at

high altitude" that we plan to present as a poster.  When the

respiratory frequency and ventilatory capacity are unable to

compensate the extreme hypoxia, the last resort for the human

being is to develop severe pulmonary hypertension (right heart

hypertrophy) and increase the number of the red cells. All

permanent residents will be sick with CMS at 5500 m, for example

at the mine of Chorolque located at 5562 m. Since not everyone

has equal capacity of adaptation, the CMS will be more severe in

some than in others, and still they will survive. Of course, in

miserable conditions.

 

 

In terms of genetic predisposition, CMS is most probable for some

individuals, over 40 years old, who have a tendency to gain

weight, but this is due to the predisposition to get sick from

respiratory disorders.

 

 

Also, about impairment of intelligence in these patients, and

intelligence itself in chronic hypoxia, we drop the subject for

the moment.

 

 

It is important to mention that chest X-rays films as a test of

diagnosis of CMS is mandatory, (and now CAT scan or NMR)  as is

the clinical history of pulmonary diseases, and the pulmonary

function tests.

 

 

-------------------------------

 

 

In summary, to answer the first question about Chronic Mountain

Sickness, "What is it?".

 

 

We feel that the most simple description of CMS, is going to be

the most adequate for the moment. In that respect we are closer

to John Weil's definition.

 

 

Our definition is:

 

 

"CMS or Monge's disease is found in residents at high altitude

with some abnormal pulmonary function (increased shunt, impaired

diffusion, uneven ventilation and/or hypoventilation), sequelae

of diseases of diverse etiopathogenesis. These lead to a

sustained (and variable) low oxygen saturation and cyanosis,

giving rise to pulmonary hypertension and increased polycythemia

as compensatory mechanisms of adaptation to the disease under

chronic hypoxic conditions. The symptoms and signs are reversible

by descent to sea level or by increasing the PIO2."

 

 

 

 

 

Both of us (Gustavo Sr. and Jr.) discuss this subject profoundly

and we only write down the subjects in which we are in full

agreement.

 

 

We are expectant of the discussion on the scoring system.

 

 

Gustavo Sr and Gustavo Jr.

 

 

----------------------------------------------------------------------

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          id 3382 ; Mon, 30 Mar 98 18:10:51

To: "John Reeves" <John.Reeves@UCHSC.edu>

From: ZUBIETA@oxygen.bo (GUSTAVO ZUBIETA, M.D. * IPPA *)

Date:         30 Mar 98 18:10:51

Subject:      CMS discussion

Priority: normal

X-mailer:     Pegasus Mail v2.3 (R5).

 

 

-------------------------------------------------------------

 

 

Date: 10 Apr 1998 16:47:23 +0100

From: "John Reeves" <John.Reeves@UCHSC.edu>

Subject: FWD>Comments, please

To: "Inder Anand" <anand001@maroon.tc.umn.edu>,

        "Ingrid Asmus" <ivasmus@ouray.cudenver.edu>,

        "Peter Bartsch" <Peter_Bartsch@ukl.uni-heidelberg.de>,

        "Buddha Basnyat" <BASNYAT@NPL.HEALTHNET.org>,

        "Linda Curran" <lcurran@castle.cudenver.edu>,

        "Marlowe Eldridge" <mweldridge@ucdavis.edu>,

        "Bob Grover" <rgrover@polylog1.cpunix.calpoly.edu>,

        "Peter Hackett" <75543.465@compuserve.com>,

        "Toshio Kobayashi" <toshi39@gipac.shinshu-u.ac.jp>,

        "Fabiola Leon-Velarde" <106435.1365@compuserve.com>,

        "Shigeru Masuyama" <masuyama@med.m.chiba-u.ac.jp>,

        "Professor Mirrakhimov" <cardio@imfiko.bishkek.su>,

        "Carlos Monge" <cmonge@upch.edu.pe>,

        "Susan Niermeyer" <Susan.Niermeyer@UCHSC.edu>,

        "Hideki Ohno" <eisei@ndmc.ac.jp>,

        "Akio Sakai" <sakaiak@gipac.shinshu-u.ac.jp>,

        "Tatiana Serebrovskaya" <sereb@physiology.kiev.ua>,

        "Peter Wagner" <pdwagner@ucsd.edu>,

        "Gustavo Zubieta" <zubieta@oxygen.bo>,

        "Lorna G. Moore" <moore_lg@defiance.uchsc.edu>

 

 

Mail*Link(r) SMTP               FWD>Comments, please

 

 

Very interesting and important comments from the Zubieta's.  Dr. Leon-Velarde

and myself, the Zubieta's  and others would like to hear some comments on

these points.

 

 

Jack Reeves

 

 

--------------------------------------

Date: 4/10/98 8:59 AM

From: GUSTAVO ZUBIETA, M.D. * IPPA *

Dear Jack:

 

 

We completely agree  with you, that we should be aware of the

differences in opinions and also of the similarity in the

approach to clarify some aspects in CMS.

 

 

The paramount point of this forthcoming congress, I am sure

(Gustavo Sr.), is that the assistants, while enjoying the

friendship, try to find out some clues that will benefit

thousands of people, who live, get sick and are treated at high

altitude, all around the world. We are sure that everything you

are doing is OK and please feel free and confident to make us

notice any illogical digression of our part.

 

 

Regarding the difficulty in making sure lungs are normal in CMS,

because severe polycythemia itself alters gas exchange, Dr. West

points out:

 

 

"I would like to add a small point. Jack Reeves stated that

'severe polycythemia itself alters [pulmonary] gas exchange'. I

do not think this issue is settled. We induced severe

normovolemic polycythemia in dogs (hematocrits up to 76%) and

found no broadening of the distribution of ventilation perfusion

ratios (J. Appl Physiol. 65:1686-1692, 1988). In the introduction

to that article we reviewed the published studies on whether

polycythemia impairs pulmonary gas exchange and no clear message

emerged."

 

These interesting remarks, show us that many people think that

polycythemia (of unknown etiopathogenesis), affects pulmonary

function in CMS. According to Dr. West's research, this would not

be so.

 

 Gustavo Sr, believes that those experiments resemble more what

would happen in polycythemia Vera (Vaquez-Osler disease), where,

according to the scarce bibliography, he has, there are no

cardio-pulmonary alterations. If these experiments were repeated

at high altitude, probably the results would be the same: No

broadening of the distribution of ventilation-perfusion ratios.

 

 

Some authors found that in polycythemia Vera, the pulmonary

diffusing capacity was greater than in normals, attributed to

increased hemoglobin concentrations (Journal of Clinical

Investigation, Vol 4, NO. 7, 1963). Polycythemia increases the

total surface of red blood cells exposed to oxygen, which is

another advantage.

 

 

In Monge Medrano's original paper, he thought that he found

polycythemia Vera of high altitude (1928). Then he realized that

it was not exactly the same so he changed his point of view to

"loss of adaptation" and CMS (1937 & 1943). The clinical

description and observation of increased polycythemia was an

important contribution to high altitude pathology, made 70 years

ago. We look forward to the presentation by Carlos Monge and

Fabiola Leon Velarde, our distinguished friends, on the history

of how CMS was discovered .

 

 

If the disease exists at high altitude, with the original

description, Gustavo Sr. has not been able to see it in over 40

years of medical practice (and we were always looking for it). As

you know there are thousands of people with increased

polycythemia, in the Bolivian high plateau (abnormal), that can

be easily diagnosed by simple observation in the streets, when

there is the experience.

 

Some of the participants in the CMS discussion affirm that they

have found people with CMS but with no anatomical or functional

alterations. It seems to us that we are observing a different

kind of pathology. By the way, we have neither seen one case of

Polycythemia Vera. When one of us was in USA, nobody gave an

adequate explanation about this last disease. The only thing I

know for sure is that polycythemia vera is accompanied by

leucocytosis, increased platelet count and can evolve to a very

severe hematological disease.

 

 

As we previously pointed out, AFTER PROVING THAT THESE PEOPLE

HAVE CARDIO-PULMONARY PATHOLOGY, ARE WE GOING TO EXCLUDE THEM FROM CMS OR MONGE'S DISEASE?

 

 

For this reason, our point of view is that pulmonary diseases,

that leave sequelae, give rise to low saturation and consequently

CMS.

 

 

Lets suppose that 3 individuals, apparently normal, one 20 years

old, and two 40 years old, move from the lower part of the city

of La Paz, at 3000 m. They remain 3 months at 3500 m, and 3

months at 4100 m (in the city of El Alto, the highest part). The

blood tests will show that the 20 years old and one of the 40

years old have their hemoglobin and hematocrit normal, for each

 altitude. The other has increased his hemoglobin to around 20

gm%. Can we say that this last one has "lost his adaptation"? and

that the other two have adapted?. The last one has developed

chronic mountain sickness. Do we call this: "adaptation"  or

"loss of adaptation" ?. This is not a hypothesis, it is a fact of

common observation. Furthermore, if he has "lost his adaptation",

is he unable to live there any longer ?.

 

 

Here, we are in the most critical point, in health problems.

Should this man go to the lowlands, even though he feels well in

the intellectual and physical conditions? When he becomes aware

that he has CMS, it turns into a big economical and social

problem. Of course, he will, from time to time, suffer from colds

with headaches, lassitude, sleep disturbance and so on (as any

healthy subject with a cold) that will be diagnosed by physicians

as the CMS alteration, but in reality it is the triple hypoxia

syndrome in CMS, that is transitory and treatable.

 

 

Since the participants are unable to go to discuss the cases in

the different hospitals, clinics or laboratories, of each

country, may we suggest that you ask each participant in the

liberal discussion on CMS (if feasible), bring a color photograph

of the patient, the clinical history, the laboratory findings,

the cardio-pulmonary function tests or any additional data, to

the meeting so that we can all see the differences and discuss

them, in a friendly way. These results will show us more than a

thousand words.

 

 

Gustavo Zubieta Sr.   &    Gustavo Zubieta Jr.

 

 

----------------------------------------------------------------

To: "John Reeves" <John.Reeves@UCHSC.edu>

From: ZUBIETA@oxygen.bo (GUSTAVO ZUBIETA, M.D. * IPPA *)

Date:         10 Apr 98 10:12:34

Subject:      CMS discussion

Priority: normal

X-mailer:     Pegasus Mail v2.3 (R5).

 

-----------------------------------------------------------

 

Date: 20 Apr 1998 08:47:15 -0600

From: "Lorna G. Moore" <Lorna.G.Moore@UCHSC.edu>

Subject: Re: Lorna's questions on "adaptation"

To: "GUSTAVO ZUBIETA, M.D. * IPPA *" <ZUBIETA@oxygen.bo>

Cc: john.reeves@UCHSC.edu

 

 

        Reply to:   RE>Lorna's questions on "adaptation"

 

 

Thank you for your interesting reply.  If I interpret your remarks correctly,

you are asking if the effects of CMS on life expectancy (mortality) are

similiar to those of COPD at sea level (or at altitude).  That might be an

interesting way to get at the seeming confusion over the uniqueness of CMS as

a high-altitude condition.  Looking forward to seeing you in Japan!

 

 

Lorna

 

 

--------------------------------------

Date: 4/19/98 7:28 PM

To: Lorna G. Moore

From: GUSTAVO ZUBIETA, M.D. * IPPA *

Dear Lorna:

 

 

Your fundamental points regarding the term "adaptation",

stimulated and gave an electrifying boost to everyone's thoughts.

Thank you for letting us know the interesting definition of

"adaptation" by Theodosious Dobzhansky. We had not heard it

previously.

 

First of all, I (Gustavo Sr) am compelled to explain the

importance of the term "adaptation", which concerns me very

strongly. Any term in medicine implies a concept (knowledge) of

the diseases  which will set the rules for prevention and

treatment (CMS in this case). I include in CMS many kinds of

pulmonary disease in chronic hypoxia.

 

 By associating CMS with the term "loss of adaptation", attention

has been focused only in the increase of the number of red blood

cells. This, mislead many studies. With such a concept, many

people with pulmonary disorders have been sent to the lowlands in

order to reduce their hematocrit and they die very soon. Due to

the hot, humid and oxygen rich environment (an optimum medium for

bacteria) there is worsening of infectious diseases

(tuberculosis, for example). Some remain living their life as

anyone in the lowlands in any part of the world, with unnoticed

mild respiratory or ventilatory impairment.

 

Another form of treatment was targeted to decrease the

hematocrit, by using radioactive compounds (such as phosphorous)

or cytolytic drugs (such as fenilhidrazine). Nowadays, the

pharmaceutical market is full of "medicines" announcing that they

can "reduce" the number of red blood cells. Phlebotomy has to be

revised, in lieu of the advance of knowledge in hypoxia, but we

will not deal with this subject in this letter.

 

 

In relation to impaired fertility:

 

We don't know of any specific studies, however it is a common

observation that the fastest growing city (over 600,000

inhabitants) in Bolivia happens to be El Alto "the high plateau"

(4100 m). There, according to a presentation we will give in

Matsumoto, about 52% of the males and 28 % of females that

receive medical attention in all diseases,  have a hematocrit

 above 58 %.

 

 The people of the city of El Alto, reproduce even in the most

disadvantageous conditions of poverty, lack of adequate housing,

lack of hygiene and so on.

 

On the other hand, I (Gustavo Sr.) have studied sick miners of

high altitude mining centers in Bolivia, who had increased

polycythemia with pulmonary diseases and several of them had over

8 children. Many of the children died, because of bad sanitary,

nutritional and infectious conditions in the mines. They only

stopped having children when the women reached menopause.

 

Incidentally, it is well known that human fetuses live in hypoxic

conditions (and that they are polycythemic! ). That is probably

why they don't die, and can tolerate very long apneas and extreme

hypoxia during delivery. At high altitude, it surprises us more.

By the way, breath-holding in CMS is one of our subjects of

presentation in Matsumoto.

 

In dealing with hypoxia, environmental factors should never be

overlooked. For example, impotence that has to do with fertility,

is not a common complaint at high altitude, as it happens in

developed countries (paradoxical?)

 

 

About life expectancy:

 

 There are no great differences between disease at sea level and

at high altitude, in the course of life. Again, we know of no

studies on life expectancy in respiratory disease at high

altitude. For example, at sea level, chronic obstructive

pulmonary disease (COPD) and emphysema affect 20-30 % of the

adult population, with more than 60,000 deaths/year. The

predominant age is over 40 and the predominant sex is male. This

is strongly similar to our clinical observations here (except the

death incidence per year, that is not quantified).

 

If patients with CMS, have reduced life expectancies, it will

probably be due to a reduced life expectancy of chronic lung

disease, just as at sea level. Depending on the severity of the

cases, naturally.

 

We have followed patients with CMS, for over 14 years,  into

their 80's and we have never looked after one, the moment he

died. No one has reported, up to date, an autopsy of CMS.

Probably, because when the pathological alterations were

discovered, they were classified as cardio-pulmonary disease.

 

By the way, malnutrition, cor-pulmonale, hypercapnia and a pulse

> 100 are all poor prognostic indicators in COPD at sea level.

The same happens at high altitude. Furthermore, cor-pulmonale in

patients with CMS is probably an advanced and untreated

consequence of respiratory disease. Increased polycythemia can't

be absent in many cases.

 

At sea level, supplemental oxygen, has been shown to increase

survival. This is conflictive for us. It would imply that there

is a shorter life expectancy for high altitude residents, but

that does not seem to be so. Ever since the use of penicillin,

life expectancy has expanded also at high altitude. Previously,

many people died of pneumonia in their forties. With better

 

nutrition, improved health care, and more hygiene, we are seeing

people, more and more, that live well into their nineties. We are

not saying that altitude is the best place to live in, but just

that we live here.

We are aware of how easy it is to make a mistake or fall into

speculation, but what you just read comes from our on-site

experience, a lot of hypoxia and its interpretation....

 

 

Gustavo Sr. &  Gustavo Jr.

 

 

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From: ZUBIETA@oxygen.bo (GUSTAVO ZUBIETA, M.D. * IPPA *)

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