"Cystic Fibrosis" by Dr. Joel Wallach (excerpt from "Lets Play Doctor")

I copied this from a PDF document from Dr. Joel Wallach's book "lets play doctor" published in 1998. This section was found in Chapter 10. Sorry if some of it is jumbled. I can send you the original PDF if you would like, just email me at chooselife828@gmail.com.

CYSTIC FIBROSIS (mucoviscidosis): is the "crime" of

the century second only to diabetes (and that is only be-

cause diabetes affects millions and CF "only affects thou-

sands each year") in that it is preventable, 100% curable

in the early stages and can be far better managed in

chronic cases than it is currently managed by "orthodox"

medicine. Cystic fibrosis is an important fatal disease of

humans. CF was originally thought to be limited to white

populations of central European origin: today, CF has

been diagnosed in all peoples of the earth.

CF is thought to be genetically transmitted by the "or-

thodox" pediatricians, yet "they" have failed to prove

their theory despite multimillions of dollars spent in re-

search. Classically, the diagnosis is made when any two

of four criteria are present (Table 10-1), yet most "ortho-

dox" pediatricians will not diagnose CF without a posi-

tive "sweat test" (elevated level of sodium, chloride and

potassium in the sweat - greater than 65 mEq/L.

The "sweat test" has been elevated by dogma to "the

diagnostic test" for CF yet there are at least 17 known

diseases and syndromes that can give a positive sweat

test (Table 10-2), leading at least one group of investiga-

tors to refer to CF as a syndrome rather than a disease.

Initially described in 1933, CF was first thought to be the

result of a vitamin A deficiency in children dying with

celiac disease. In 1938, the term "cystic fibrosis" was

coined because the pathologist mistakenly thought the

changes in the pancreas were true cysts (fluid filled spaces

lined with normal tissue). It is well known today that

the "cysts" of CF are, in fact, a dilation of the pancreatic

functional unit (acini) with atrophy (shrinking) of the lin-

ing tissue. In 1952, the fact that congenital CF occurred

in a significant number of CF patients was established.

The foundation of the genetic theory of CF transmission

is based on the frequent congenital appearance and two

very poor papers, one published in 1913 which claimed

that two children with diarrhea had an "inborn error in

fat metabolism" and one in 1965 that did an epidemio-

logical study of a group of 232 Australian families with

CF - despite six sets of twins, the study failed to shed

clear light on the proposed genetic theory. These papers

were so poor they would not get past the letter opener at

any "orthodox" medical journal today. We have spent an inordinate amount of time on CF because this syn-

dromeagaindemonstratesveryclearlythatifanymedi-

cal specialty will be eliminated by discovery, that dis-

covery will never be given to the public by the "ortho-

dox" doctors!!!

In 1978, the first .universally accepted diagnosis of CF in

a laboratory ammal was made by one of us (Dr. Joel

changes in the pancreas and liver in baby monkeys and

were confirmed by CF experts from Johns Hopkins

Wallach). ThediagnosiswasbasedoncharacteristicCF

School of Medicine, Emory University and the Univer-

sity of Chicago! Experts from NIH and the CF Founda-

tion were overjoyed - that is until they learned that one

of us (Wallach) could reproduce the CF changes with a

congenital selenium deficiency in almost any animal spe-

cies. With this revelation, Wallach was fired with 24 hours

notice and "blackballed" from research (to show you how

ruthless they are, Wallach was fired ten days after his

wife died of cancer).

"

It has been learned recently that the positive "sweat test"

is the result of an essential fatty acid deficiency that

causes a secondary deficiency of "prostaglandin" (very

short lived hormones) that control the sodium, chlorides

and potassium levels of the sweat!!! Remember the talk

by the distinguished

anthropologist,

Dr. Johnathon

Leaky, Sr. who said "the more facts you have, the better

the truth you have."

The prevention of CF has been accomplished in pet, farm

and laboratory animals by the veterinary profession by

assuring adequate levels of selenium and essential fatty

acid nutriture to the preconception, pregnant and nurs-

ing mother. This is not as easy as it sounds because of

malabsorption problems (Le., celiac diseases and Crohn's

Disease) in a percentage of women!!! All things being

normal a supplementation of 200 mcg selenium per day and 5 gm of flaxseed oil t.i.d. would be adequate to pre-

vent CF.

Treatment of CF is very basic - treat the infant as early

as possible with selenium 1Mat 10-25 mcg per day. Plant

derived colloidal minerals may be used orally thereaf-

ter. Provide 5 gm of flaxseed oil orally t.i.d. Most impor-

tantly YOU MUST DETERMINE IF THE INFANT ISAL-

LERGIC TO WHEAT, COW'S MILK OR SOY!!! If you

do not correct the malabsorption problem, treatment will

only be minimally effective. In the case of older CF pa-

tients, IV essential fatty acids and 1M selenium provide

excellent management leading to a normal life expect-

ancy of 75 years!!! Compare this approach to the heart

and lung transplant offered by the "orthodox" pediatri-

cians!!! If the proper treatment is carried out, the "typi-

cal CF lung disease" will not develop. The lungs of CF

patients

are normal at birth and only develop

bronchiectasis after chronic essential fatty acid and cop-

per deficiencies have taken their toll. Don't forget the

base line nutritional supplementation here!

We went to China in 1988 to study Keshan Disease, a

known selenium deficiency disease of Chinese children.

We studied 1,700 autopsies and found 595 cases or 35%

had pancreatic CF (remember CF is supposed to be "ge-

netic disease of children of middle European extract" -

to justify this finding the proponents of the genetic theory

will no doubt claim that a very virile English missionary

impregnated 125,000 Chinese girls and, unfortunately,

he was "carrying the gene for CF."

Table 10-1. Four Criteria For The Diagnosis

of Cystic Fibrosis

1. Exocrine Pancreatic Insufficiency

2. Bronchiectasis

3. Positive Sweat Test

4. Family History of the Disease

Table 10-2. Diseases and Symptoms That Have

Reported Positive Sweat Test (1, 3, 9, 68, 72)

1. Adrenal Insufficiency

2. Ectodermal Dysplasia

3. Nephrogenic Diabetes Insipidus

4. Glucose-6 Phosphate Deficiency

5. Pupillatonia / Autonomic Dysfunction

6. Allergies

7. Calcifying Pancreatitis

8. Anorexia Nervosa

9. Cystic Fibrosis

10. Focal Hepatic Cirrhosis

11. Derangement of Prostaglandin Metabolism

12. Hypothyroidism

13, Fucosidosis

14. Malnutrition

15. Kwashiorkor

16. Diabetes

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