Until 1952, the most prominent experts in coeliac disease - a wasting
condition associated with the severe malabsorption of food - agreed
that it was caused by carbohydrate intolerance, the inability to digest
certain types of carbohydrate. A diet avoiding these carbohydrates
was
found to treat the condition effectively. Then an article in the
Lancet
started the current fashion that coeliacs are merely allergic to
gluten.
The success of a gluten-free diet, however, required the diagnosis
of
coeliac disease to be thenceforth restricted only to those patients
who
benefited from such a diet. Author and researcher Elaine Gottschall
explains that this change has left thousands of people with severe
symptoms which are going undiagnosed and untreated.
By Elaine Gottschall
Nutritional Therapy Today, Vol 7, No 1, 1997, page 8-11
The last time anyone counted, there were 15,000 named diseases
of man, and cures for 5,000 of them. Yet it remains
the dream of every young
doctor to discover a new disease. That is the fastest and surest
way to gain prominence within the medical profession.
Practically speaking, it is much better to discover a
new disease than to find a cure for an old one; your cure
will be tested, disputed and argued over for years, while a new disease is readily and rapidly accepted.
(Michael Crichton)
[1].
Coeliac disease appears to have always existed. Because its numerous
symptoms mimic those of several other conditions and because an obvious cause
has been elusive throughout the years, its recognition as a distinct
disorder and one which physicians could readily diagnose has been fraught with disagreement.
One of the first descriptions of this disorder was given in the
early
years of the Roman Empire by the physicial Aretaeus, who refers to
"
coeliac disease" as a chronic diarrhoea condition consisting
of
undigested food, lasting an extended period, and a debilitation of
the
whole body. [2] Arataeus described the diarrhoea as being light in
colour, offensive in odour, and accompanied by flatulence. Additionally
the patient is described as "emaciated and atrophied, pale,
feeble,
incapable of performing any of his accustomed works."
In 1855, Dr Gull writing in Guy's Hospital Reports [3] outlined
the
symptoms found in a 13 year-old boy that clearly suggest coeliac
disease as we understand it today: enlarged abdomen, frequent
and voluminous stools of a dull, chalky colour.
A few years later, in 1888, Dr Samuel Gee laid the foundation for
not
only describing the condition, but also establishing criteria for
diagnosis. Additionally, he established guidelines for successfully
treating the condition with a dietary approach. In his classic report "On
the Coeliac Affection", he wrote There is a kind of chronic
indigestion
which is met with in persons of all ages, yet is especially apt to
affect
children between one and five years old Signs of the disease are
yielded by the faeces; being loose, not formed, but not
watery; more bulky than the food taken would seem to account
for; pale in colour, as if devoid of bile, yeasty, frothy,
an appearance due to fermentation; stench often very great,
the food having undergone putrefaction rather than concoction.
The causes of the disease are obscure. Children who suffer from
it are not all weak in constitution. Errors in diet may perhaps be
a cause, but what error? [4]
Despite the meagreness of Gee's information about coeliac disease,
he saw clearly several important facts that escaped many
later investigations: (1) If the patient can be cured at all, it
must be by means of diet and
that cow's milk is the least suited kind of food, that highly starchy food, rice, sago, corn flour, are unfit.
(2) We must never forget that what the patient takes beyond his
power of digestion does harm. (Gee implied that unfit
foods played more than a negative role and actually produced
a pathologic condition in the digestive tract.)
Intestinal Fermentation
For many years there were numerous reports on the cause as well
as the treatment for what appeared to be coeliac. While
these inconsistent and inconclusive reports appeared in
Europe, there was much less interest in North America.
Shortly after the turn of the century, however, Drs L
Emmett Holt Sr, Director of Children's Medicine at Bellevue Hospital,
and Christian Herter of Columbia University worked together
for over seven
years on the clinical as well as the theoretical aspects of this disorder.
Their conclusions, published in 1908, entitled On Infantilism from
Chronic Intestinal Infection included the following main points:
(3) There is a pathological state of childhood marked by a striking
retardation in growth of the skeleton, the muscles and the various
organs and associated with a chronic intestinal infection
characterised by the overgrowth and persistence of bacterial
flora
belonging normally to the nursling period.
(4) The chief manifestations of this intestinal infantilism are
arrest in
the development of the body but maintenance of good mental powers
and a fair development of the brain; marked abdominal distention; a
slight or moderate or considerable degree of simple anaemia; the
rapid onset of physical and mental fatigue; irregularities of
intestinal digestion resulting in frequent diarrhoeal seizures. [5]
Drs Holt and Herter continued in their monograph to describe the
dominant bacteria found in the stools as well as some
of the byproducts of intestinal fermentation and putrefaction.
They noted that fat appeared in the stool and attributed
this to impaired fat absorption. Also, note was made of
increased mucus in the stool along with evidence of abnormal shedding
of intestinal cells. They continued to stress that two leading features
of this intestinal infantilism must be further investigated:
(5) The retardation of growth;
(6) The chronic intoxication.
They commented that retardation in growth could be attributed to
malabsorption of nutrients and the malabsorption could probably be
due to a chronic inflammation located in the ileum and
colon associated with the presence of abnormal forms
of bacteria. The chronic intoxication, they were certain,
resulted from the action of products of bacterial origin
with the toxins having as their main target the nervous system and muscles.
They concluded their treatise by stating: Temporary relapses are
very
common in the course of this disease, even when great care is being
taken to prevent them. The most frequent cause of such
relapses is the attempt to encourage growth by the use
of increased amounts of carbohydrates.
Disordered Carbohydrate Digestion
Although Herter's conclusions failed to gain acceptance, his observations were
so perceptive that further researchers "stood on his shoulders" in pursuing
the most effective dietary treatment. He saw that in every case proteins
were very well handled, fats were handled moderately well, while carbohydrates
were badly tolerated, almost invariably causing relapse or a
return of diarrhoea after a period of improvement. He said, "It
has
been already mentioned that the carbohydrates are the obvious and fruitful
cause of derangements of digestion that are clinically determinable, especially diarrhoea and flatulence."
Meanwhile, the interest shown by Drs Holt and Herter had been
transmitted to Dr Holt's two younger assistants at the
Vanderbilt Clinic, Dr John Howland and Dr Sidney V Haas.
In 1921, Howland, in his presidential address before
the American Pediatric Society, read a paper on "Prolonged Intolerance
to Carbohydrates"[6]. Although Howland did not use
the term coeliac disease (the condition was still known
by a great variety of names) he described his cases vividly:
There are loose stools from time to time with loss of
weight. The condition improves between the attacks somewhat, but
sooner or later a relapse occurs and there is a renewed loss
of weight. The relapses are increasingly severe. Eventually, there is
a condition of marked malnutrition in a peevish, fretful, but often
precocious child. The abdomen is distended at first intermittently,
and then almost constantly. The stools are never normal Even between
attacks
of diarrhea they are large, light gray in color, often frothy, and
usually very foul.. Growth suffers in proportion to the length of
time
that the symptoms persist, and many children are greatly below the
average in height. From clinical experience, it has been found that
of
all the elements of food, carbohydrate is the one which must be excluded rigorously;
that with this greatly reduced, the protein and fat are almost
always well digested even though the absorption of fat may not be as satisfactory as in health.
Dr Howland warned that after initial improvement occurs with the
elimination of carbohydrates, the stage where carbohydrates are added
is the most difficult. He explained that although the initial phase
may
be time consuming, "these patients well repay the efforts expended
on
them. They do not remain semi-invalids, many become vigorous and
strong, some even with no trace of dietary idiosyncrasies... Halfway
measures are quite unavailing and cause only loss of time.' Other
doctors confirmed Howland's treatment as achieving greater success
than any previous one, but the need for some tolerable
carbohydrate in the coeliac diet remained.
Specific Carbohydrate Diet™
Despite the remarkable success of Dr Howland's treatment with
emphasis on carbohydrate restriction, other doctors,
distracted by the occurrence of fatty stools continued
to believe that dietary facts were at fault. But although
there was some confusion resulting from this belief, there was
a steadily increasing recognition of the primary role of disordered carbohydrate
metabolism and digestion in causing coeliac disease.
Dr Sidney Valentine Haas, working with Dr Howland, was in full
agreement with Dr Howland's work but was interested
in learning if some form of carbohydrate could be added
to the diet to hasten recovery and provide a more varied
and nutritious diet. He had noted reports throughout the years
whereby children with severe diarrhoea had done very well on banana flour
(made of 70 per cent ripe banana) and plantain meal. It was at
the Home for Hebrew Infants that Dr Haas first experimented
with banana feeding [7]. One of his patients was an
infant who had difficulty in eating. The baby refused
all food. Dr Haas offered the baby a banana. At that
time, banana was considered completely indigestible by a sick child. Everybody
was horrified at the idea of feeding it to an infant everybody, that
is, except the infant, who not only took it but asked for more.
He was given more and thus Dr Haas discovered the banana
could be well tolerated.
He then decided to experiment with the banana, as the sought after
carbohydrate source, in the dietary treatment for coeliac. He soon
discovered that coeliacs could tolerate this carbohydrate, and, more
than that, the banana could be fed in large quantities with beneficial
effects. He further experimented with carbohydrate containing fruits
and some vegetables and found that they, too, could be tolerated
and
the coeliac could regain health on a far more varied diet than just
protein and fat.
During the next few years, Dr Haas treated over 600 cases of coeliac
disease with his Specific Carbohydrate Diet™, maintaining his patients
on it for at least 12 months, and found that the prognosis of coeliac
disease was excellent. "There is complete recovery with no relapses,
no deaths, no crisis, no pulmonary involvement and no stunting of
growth." [8]
By 1949, Dr Sidney Haas's reputation was known throughout the
world and on April 5th of that year, more than 100 leading
physicians met at the New York Academy of Medicine to
pay him tribute. The New York Times
reported: Today, on the occasion of the fiftieth anniversary of his entrance into the medical profession, one of America's great
pediatricians, Dr Sidney V Haas, is being honored for his pioneer
work in the field of pediatrics. Among Dr Haas's most
important accomplishments was in the treatment of celiac
disease, a digestive disturbance in which
the child is intolerant of starchy food, and which was generally
fatal at the time of his original work. Following his
discovery that the carbohydrate in bananas could be tolerated
by celiac patients, Dr Haas developed an accepted routine
therapy which laid the basis for later research and basic treatment in this field. [9,10]
In 1951, Dr Haas, together with his son, Dr Merrill P Haas, published
The Management Of Celiac Disease, the most comprehensive medical
text that had ever been written on coeliac disease [11].
With 670 references to published reports, the book described
coeliac disease more completely than had ever been done
before. The Drs Haas presented their success
with the Specific Carbohydrate Diet™ and offered their hypothesis
in the last chapter of their book as to why the diet was
effective. After decades of searching, it appeared that
not only was an effective and lasting dietary treatment
found, but that the Haas Specific Carbohydrate Diet™ was accepted by medical colleagues throughout the world as a
cure
for coeliac disease.
Protein vs. Carbohydrate Battle
But as Michael Crichton has written, "the battle" continued.
Within one
year after the publication of the Drs Haas's book, a singular report
appeared in the English medical journal Lancet [12]. A group of six
faculty members of the Departments of Pharmacology, Paediatrics and
Child Health of the University of Birmingham, after testing only
10
children, decided that it was not the starch (carbohydrate) in the
grains that so many had reported as being deleterious, but it was
the
protein gluten in wheat and rye flour that was causing coeliac symptoms.
They
concluded their Lancet report by stating in their summary:
Gastro-intestinal function was investigated in 10 children with;
coeliac
disease. The changes were very similar to those in adult idiopathic
steatorrhoea. The removal of wheat flour from the diet resulted in
rapid
improvement, both clinically and biochemically. Deterioration followed
the reintroduction into the diet of wheat flour or wheat gluten,
but
wheat starch had no harmful effect. Did you know? If you thought
that
sweetcorn was a gluten-free food, think again! Gluten is one of the
most
important byproducts of maize, and bags of corn are sold as animal
feed.
In the making of cornflour, the hardest part is separating the gluten from the starch.
They contradicted all previous work by stating that there was
no need to restrict carbohydrates and, therefore, an
unlimited choice of food could be ingested, provided
that wheat and rye gluten were excluded. Further, 'a
high caloric diet may be given throughout with biscuits made from cornflour, soya flour, or wheat starch instead of wheat flour."
They maintained that it was not the starch in grains that was the
culprit but that it was the protein gluten and that when the gluten
was
'washed out" of the flour, the remaining starch was perfectly
fme. And
overnight, the hypothesis gained ready acceptance. No need now for
doctors to worry about adherence to a diet which eliminated specific
carbohydrates found in many foods; only one dietary exclusion would
have to be made: the gluten in wheat and rye flour. No
need to delve into food biochemistry and ask why gluten-containing
foods such as corn would be considered permissible; it
was to be a "black and white" remedy
with no shades of grey.
Some patients showed remarkable clinical improvement in their general
well-being after following a "gluten-free" diet. However,
biopsy samples, as viewed under the microscope, showed
intestinal cells that were still markedly abnormal 13.
In addition, some patients who started eating
gluten suffered no ill effects at one time but became extremely ill
at
other times. Thus, not only do different coeliac patients vary in
their response to a gluten-free diet but the same patient
may vary from time to
time [14]. When the all too common relapse occurs, the patient is
most
often told that he/she must have inadvertently consumed gluten, and
it is
common for patients to become so nervous about making a mistake that
they
assume that anything on a product that begins with 'glut" must
be gluten:
glutamic acid, glutamine, monosodium glutamate, etc. Or that gluten
had somehow crept into the food in spite of the fact that
it did not appear on the label.
It soon became apparent that grains which contained proteins other
than gluten were having deleterious effects on the digestive
tract. Some patients suffered relapses and exhibited damaged intestinal cells
(microscopically) upon eating soy products (15, 16). Oats and barley
were found to contain gluten-like proteins which offended many coeliac
sufferers [17].additional reports implicated rice as well as other
grains
as being harmful to intestinal cells (18, 19).
Restricted Diagnosis
But the diet to manage coeliac disease had been simplified and
there now remained the problem simplifying the diagnosis.
It was decided that the new diagnostic tool, the intestinal
biopsy instrument, would be used to
identify coeliac. In spite of the symptoms the patient manifested,
the
patient would not be diagnosed as a true coeliac until other criteria were
met. A series of intestinal biopsies would be done: one tissue sample
would be taken from the small intestine before gluten was removed
from the diet; a second sample would be taken after the patient had
been
on a "gluten-free" diet. The biopsy samples would have
to reflect the changes in the diet. When viewed under
the microscope, the intestinal surface would have to appear
flattened or blunted while the patient ingested gluten.
After gluten withdrawal, the intestinal surface would have
to revert to its normal architecture of "hills and valleys".
If a patient fulfilled these established criteria, his
condition would then be given the name 'gluten-induced
enteropathy cocliac disease".
Thus, only a small number of persons exhibiting the clinical
symptoms of malabsorption
including diarrhoea, bloated belly, and failure to thrive could now
be classified as coeliacs. The others, an even larger
group, suffering with the same symptoms (but who did not
pass the required test using the intestinal biopsy criteria)
would be diagnosed as suffering from diarrhoea from an
unknown cause, steatoffhoea (fatty stools), malabsorption,
sprue, etc. Therefore, if a physician applied the strict definition
for diagnosing coeliac disease, the number of "true" coeliacs would
remain very small while there would remain a large group of patients
with assorted diagnoses or no diagnosis of any kind [7].
In a recent review of coeliac disease, the gastroenterologist writing
the article referred to this method of diagnosis as "the current gold standard for diagnosis" [26].
However, this method of diagnosis has been seriously questioned
by a
number of specialists. The flattened or blunted intestinal surface
has
been reported in innumerable disease states: infectious hepatitis,
ulcerative colitis, parasitic infections of the intestine including
various types of worms and single-cell parasites, kwashiorkor [21],
soy
protein intolerance, intolerance to cow's milk protein, intractable
diarrhoea of infancy, Crohn's disease [22] and bacterial overgrowth
of
the small intestine [23]. Just about all conditions associated with
diarrhoea seem to result in the same appearance of the small intestine
as is seen in the so-called "true coeliac" [24, 25].
Exceptions
And in spite of increasing numbers of sophisticated tests developed
to
confirm the diagnosis of coeliac disease, including antibody tests,
genetic testing involving HLA (histocompatibility antigens) markers,
and twin studies, there appear to be more exceptions to
the rule than those who follow the rule. The reality is that thousands of patients are
suffering and have never been given a diagnosis other than to see
a
psychiatrist, and thousands of patients are following gluten-free
diets
and are getting minimal relief, if any. The following is part of
an
unsolicited letter to the author, and her story is unfortunately
only too
common: After eight years of mysterious symptoms, dozens of doctors,
gruelling and often humiliating tests and general misery, no-one
could
decide what was wrong with me. I discovered that because my two sisters
and my daughter had been diagnosed as celiacs that I too should go
on the
gluten-free diet. Unfortunately for both my daughter, another sister
and
I, the gluten free diet did not work. Some symptoms were arrested
but none of us were thriving and we just weren't absorbing
food. We eventually found the Specific Carbohydrate Diet™
and it has been a godsend. I have never been healthier.
My daughter, once a sickly (often whiney), withdrawn child
with thin hair and dark circles under her eyes is outgoing,
rosy-cheeked and happy. Everyone has noticed her thick, shiny
hair. In fact she ran a marathon this year and placed 15th out of
79 children. Last year she ran the same race (before the diet) and
placed
53rd, arrived weepy and slept all the way home in the car. [27]
The Specific Carbohydrate Diet™ has been shown to completely cure
most cases of coeliac disease if followed for at least
one year. It is truly a gluten-free diet, eliminating all grains which contain gluten or
gluten-like proteins while also recognising the limitations of the
injured intestinal surface. For those people who are not satisfied
with
their progress on the gluten-free diet, the specific carbohydrate
diet
offers them the opportunity to become healthy. In the concluding
words of the writer of the above letter: I have been on
the specific carbohydrate diet for less than a year and
still have a way to go but my life has changed drastically
in this short time. I have more energy, virtually no pain
anywhere (before, my list of symptoms was endless) and no longer spend
half my life in the bathroom where my life was literally going down the
drain. I was underweight, had dry pale skin, dull looking eyes, suffered
from hair loss and was generally miserable. Now I am actively pursuing
my art interest - something I always had inside me, but didn't
have the energy or drive to tackle.
Elaine Gottschall has spent four years at the University of Western
Ontario researching the effects of various sugars on the digestive
tract
at cellular level, and one year researching the changes that occur
in the
bowel wall in inflammatory bowel disease. The results of her work
are
published in the journal Acta Anatomica
21:178
(22).The details of the specific carbohydrate diet can be found in
her
book Breaking the Vicious Cycle: Intestinal Health through Diet
available from SPNT Books,
P.O.Box 47, Heathfield East Sussex TN21 8ZX at Pound Sterling 13.95
including P&P. Elaine Gottschall will be speaking at SPNT's annual
conference on 8th March 1997 in London.
References
1. Crichton M: A case of need, p 84. Penguin Books, New York, 1968.
2. Aretaeus the Cappadocian: On the causes and symptoms of chronic
disease. The Sydenham Society, London, 1856.
3. Gull W: Fatty stools from disease of the mesenteric glands. Guy's
Hospital Report 1:369, 1853.
4. Gee S: On the coeliac affection. St Bartholomew's Hospital Report
4:17,1888.
5. Herter C: On infantilism from chronic intestinal infection.
MacMillan, New York, 1908.
6. Newland J: Prolonged intolerance to carbohydrates. Transactions
of
American Pediatric Society 44:11, 1921.
7. Golden Jubilee World Tribute to Dr Sidney V Haas. The Storv of
Dr
Sidney V Haas. New York Academy of Medicine, New York, 1949.
8. Haas SV and Haas MP: Management of celiac disease, p x. J B
Lippincott Company, Philadelphia, 1951.
9. Editorial. New York Times p 28, col 2, April 5th 1949.
10.Physicians Honor Pediatric Pioneer: New York Times p 34, col 2,
1
11.Haas SV and Haas MP: Management of celiac disease. J B Lippincott
Company, Philadelphia, 1949.
12.Anderson CM, French JM et al: Coeliac disease: gastrointestinal
studies and the effect of dietary wheat flour. Lancet:836-842, 1952.
13. Congdon P, Mason MK et a[: Small bowel mucosa in asymptomatic
children with celiac disease. Am J Dis Child 135:118-122,1981.
14. Rubin CE, Brandborg LL et al: Studies of celiac sprue. 111. The
effect of repeated wheat instillation into the proximal ileum of
patients on a gluten free diet. Gastroenteroigy 43:621-641, 1962.
15. Bleumink E: Allergens and toxic protein in food. In Eds Hekkens
WTJMand Pe6a AS: Coeliac Disease. Stenfert Kroese, Leiden, 1974.
16. Weiser MM: An alternative mechanism for gluten toxicity in coeliac
disease. Lancet 1:567-569,1976.
17.Baker PG, Read AE: Oats and barley toxicity in celiac patients.
Postgrad Med J 52:264-268,1976.
18.Strunk RC, Pinnas JL et al: Rice hypersensitivity associated with
serum complement depression. Clin Allergy 8:51-58,1978.
19.Vitoria JC, Camarero C et al: Enteropathy related to fish, ric6
and
chicken. Arch Dis Child 57:44-48, 1982.
20.Cluysenaer OJJ and van Tongeren HMM: Malabsorption in coellac
sprue. Martinus Nijoff Medical Division, Hague, 1977.
21.Creamer B: Coeliac thoughts. Gut 7:569-571, 1966.
22.Poley JR: Ultrastructural topography of small bowel mucosa in
chronic diarrhea in infants and children: Investigations with the
scanning electron microscope. In Ed Lebenthal E: Chronic
diarrhea in children. Nestit, Vevey/Raven Press, New York, 1984.
23.King CE and Toskes PP: Small intestine bacterial overgrowth.
Gastroenterology 76:1035-1055, 1979.
24.Araya M and Walker-Smith JA: Specificity of ultrastructural changes
of small intestinal epithelium in early childhood. Arch Dis Child
28:844855,1975.
25.Brunser 0 and Araya M: Damage and repair of small intestinal mucosa
in acute and chronic diarrhea. In Ed Lebenthal E: Chronic diarrhea
in children. Nestlt, Vevey/Raven Press, New York, 1984.
26.Kagnoff MF: Celiac disease. In Eds Yamada T et al: Texbook of
gastroenterology 2:1644. Lippincott Company, Philadelphia, 1995.
27.Personal correspondence from Jennifer Stenberg of RA1, Holstein,
Ontario, Canada NOG 2AO, to the author, 6th November 1996.
© Elaine Gottschall.
Originally printed in Nutritional Therapy
Today, Vol 7, No 1, 1997, page 8-11
