128
of carbohydrate (120 kcal. per kg.) and proper
solutions of aminoacids, with high proportions of
those which provide substrate for branched-chain
fatty acid, should significantly modify the course of
R.D.S.
Our clinical experience supports this contention.
Fourteen babies weighing 1050-1600 g. at birth and
having gestational ages of 28-32 weeks were treated
with total parenteral nutrition starting at birth or
within hours of birth. One infant with mild R.D.S.
died on the second day of life, probably of intra-
cranial haemorrhage. Of the remaining thirteen
patients, three showed signs of mild to moderate
R.D.S. but fully recovered, while ten of these premature
infants never developed R.D.S. All the infants on
total parenteral nutrition started to gain weight on
the second or third day, and were more active than
controls on a conventional regimen. In five additional
patients, with birth-weights of 2210-2900 g. and
gestational ages of 32-34 weeks, total parenteral
nutrition was started within the first 3 days of life
in response to well-established respiratory distress.
In two, R.D.S. was moderate, and in three the disease
was severe, accompanied by grossly abnormal bio-
chemistry (i.e., pH 7.12, P02 25 mm. Hg, PC02
72 mm. Hg) while under 70 % oxygen. All of these
infants showed dramatic, overnight response to total
parenteral nutrition.
The mortality-rate of one out of nineteen patients
treated with total parenteral nutrition is strikingly
lower than the 48% mortality in controls treated by
10% glucose and bicarbonate, and compares favour-
ably with mortality-rates for R.D.s. in leading
institutions.
Requests for reprints should be addressed to H. G.
REFERENCES
1. Gluck, L. Pediat. Clins N. Am. 1972, 19, 325.
2. Shelley, J. J., Neligan, G. A. Br. med. Bull. 1966, 22, 34.
3. Widdowson, E. M. in Biology of Gestation (edited by N. S. Asaki);
vol. II. New York, 1968.
4. Ghadimi, H., Arulanantham, K., Rathi, M. Am. J. clin. Nutr. 1973,
26, 473.
5. Adibi, S. A. Am. J. Physiol. 1971, 221, 889.
6. Growth and Development of the Child: White House Conference
on Child Health and Protection; part II, p. 19. New York, 1933.
7. Widdowson, E. M. in Growth and Development of Mammals
(edited by G. A. Lodge and G. M. Lamming); p. 224. New York,
1968.
8. Widdowson, E. M., Spray, C. M. Archs Dis. Childh. 1951, 26, 205.
9. Friis-Hansen, B. Pediatrics, Springfield, 1971, 47, 264.
10. Schendel, H. E., Hansen, J. D. L., Brock, J. F. S. Afr. J. Lab. clin.
Med. 1962, 8, 23.
11. McCance, R. A., Strangeways, W. M. B. Br. J. Nutr. 1954, 8, 21.
12. Andres, R., Cader, G., Zierler, K. L. J. clin. Invest. 1956, 35, 671.
13. Baltzan, M. A., Andres, R., Cader, G., Zierler, K. L. ibid. 1962, 41,
116.
14. Pozefsky, T., Felig, P., Tobin, J. D., Soeldner, J. S., Cahill, G. F.
ibid. 1969, 48, 2273.
15. Liggwns, G. C., Howie, R. N. Pediatrics, Springfield, 1972, 50, 515.
16. deLemos, R., Shermeta, D. W., Knelson, J., Kotas, R., Avery,
M. E. Am. Rev. resp. Dis. 1970, 102, 459.
17. Kotas, R. V., Avery, M. E. J. appl. Physiol. 1971, 30, 358.
18. Carson, S. H., Taeusch, H. W., Jr., Avery, M. E. Fedn Proc. 1972,
31, 154.
19. Baden, M., Bauer, C., Colle, E., Klein, G., Taeusch, H. W.,
Stern, L. Pediatrics, Springfield, 1972, 50, 526.
20. Munro, H. N. in Mammalian Protein Metabolism (edited by H. N.
Munro); vol. IV, p. 299. New York, 1970.
21. Naeye, R. L., Harcke, H. T., Blanc, W. A. Pediatrics, Springfield,
1971, 47, 650.
LOW-RESIDUE DIETS AND HIATUS HERNIA
DENIS P. BURKITT
Medical Research Council External Scientific Staff,
London
PETER A. JAMES
Manchester
Wythenshawe Hospital,
studies indicate that
Epidemiological
Summary hiatus hernia is
a characteristically
" Western " disease. Its geographical distribution
renders most conventional hypotheses as to its
causation untenable. It is postulated that the
unnaturally raised intra-abdominal pressures that
are necessitated to evacuate the firm stools resulting
from consumption of low-residue diets are an
important ætiological factor. This hypothesis is con-
sistent with epidemiological evidence.
INTRODUCTION
HIATUS hernia is one of the most prevalent defects
in the gastrointestinal tract in the Western world.
It is usually symptomless, but is not uncommonly
associated with cesophageal reflux, which is a common
cause of upper-abdominal symptoms. The percent-
age of patients submitted to upper-gastrointestinal-
tract radiological examinations in whom hiatus
herniation can be detected depends on the methods
used to demonstrate the defect and the diagnostic
criteria accepted. Although published figures vary,
they demonstrate that the condition is common and
that prevalence steadily increases with age. Hiatus
herniations were demonstrated in 1 in 5 radio-
logical examinations of the upper gastrointestinal
tract in Miami, U.S.A.I Hafter2 found them in
12·5 % of 2402 barium meal examinations. Pridie,3
in a review, concluded that when intra-abdominal
pressure was increased during radiological investiga-
tion of the gastrocesophageal junction, hiatus hernia
could be demonstrated in between 2-1% and 11.8%
of patients. In 560 consecutive barium-meal
examinations on patients not suspected of having a
hiatus hernia, he found it in 29-6% of all patients,
21% of males and 39% of females. The frequency
rose with age, from 9% in those under forty to 69%
in patients over seventy. Pridie’s patients swallowed
their barium while lying prone over a firm bolster,
and a hiatus hernia was diagnosed only if a groove
could be identified in the oesophagus above the
diaphragm, after the oesophagus emptied as much as
it could.
Only since the 1939-45 war has this high frequency
been recognised, and it has been suggested that the
apparent increase is more the result of improved
diagnostic techniques than an actual rise in preva-
lence. Experience in developing countries described
below does not support this view.
Current Concepts of Causation
When first recognised the upward protrusion of the
stomach through the diaphragm was believed to bea
"
developmental abnormality, and the term congenital
short oesophagus" was used to describe the condition.
Subsequently, and largely because of its relative rarity
during the first three decades of life, it became recognised

that this was an acquired and not a congenital defect.
The factors responsible for the movement of the stomach
upwards from its normal subdiaphragmatic position must
be a push from below, a pull from above, failure of
the sphincteric mechanism in the diaphragm to hold the
gastrooesophageal junction in its correct position, or a
combination of these effects.
Smithershas aptly described this balance of forces
thus: "The normal subdiaphragmatic position of the
vestibule is maintained by a fine balance between opposing
forces at the level of the diaphragm. The anatomical
arrangements are normally sufficient to prevent the vari-
able lower pressures in the thorax and higher pressures
in the abdomen from displacing the vestibule upwards
through the hiatus ".
Hypotheses to explain the causation of herniation
suggest mechanisms whereby this balance may be upset.
A Pulling-up of the Stomach
As long ago as 1932, von Bergmann and Goldner 5 sug-
gested that hiatus herniation might be due to oesophageal
contraction in response to a vagovagal reflex. Johnstone 6,7
and Harringtonalso blamed oesophageal contraction,
but they postulated that this was the result of fibrosis
following ulceration caused by reflux. They considered that
oesophageal reflux preceded and was the cause of the
herniation.
A Pushing-up of the Stomach
This implies abnormally raised intra-abdominal pressures
which have most frequently been attributed to tumours,
pregnancy, obesity, and constrictive clothing.
A Failure of the Diaphragm to Retain a Normal Relation-
ship with the Gastroaesophagel Function
In view of the increasing prevalence of herniation with
FREQUENCY OF HIATUS HERNIA IN SOME COUNTRIES IN AFRICA AND
ASIA
*
Personal communication.
129
advancing age, it has been suggested that atrophy of the
muscle in the diaphragmatic sphincter may be primarily
responsible. It has also been postulated that deposits of
fat frequently found related to the hiatus may be re-
sponsible for incompetence of the sphincter.
The Combined Effect of Two or More of these Postulated
Factors
Smithers9 considered a lax hiatus to be responsible for
reflux which in turn led to ulceration in the lower
oesophagus, with consequent fibrous contracture and
pulling-up of the stomach.
Reappraisal in the Light of Epidemiological Evidence
Hiatus hernia seems to be rare in developing
countries and almost unknown in communities who
have departed little from their traditional way of life.
One of us (P. A. J.) did not see a single case of
hiatus hernia or oesophageal stricture due to reflux
oesophagitis in an African during seven years as
the sole thoracic surgeon in Uganda. Eventration
of the diaphragm, traumatic herniation through a
ruptured diaphragm, hernias through the foramen
of Morgagni, and patent pleuroperitoneal canal were
all encountered. Stricture of the oesophagus was seen
on many occasions. All but two (the result of swallow-
ing corrosive fluids) were due to malignant disease.
P. A. J., working as a radiologist in England, has
diagnosed 27 cases of significant hiatus hernia using
conservative criteria in his last 200 consecutive barium
meals. All but 7 of these had shown gastrocesopha-
geal reflux at the time of examination.
Reports indicating the rarity of this condition in
native populations in developing countries are sum-
marised in the table. The lower age structure
cannot account for the enormous disparity between
the incidence of hiatus hernia found there compared
with Western nations, any more than it can explain
the even greater disparity with regard to diverticular
disease of the colon.15
The high figure for Vellore contrasts with all
other reports and suggests that either the methods
used or diagnostic criteria may have differed. There
is urgent need for prospective studies in different
communities using the same techniques and diag-
nostic criteria.
Conversations with many American surgeons and
radiologists have not indicated any obvious disparity
between the prevalence of hiatus hernia in White
and Coloured Americans. Dr. Alvin Segel (Cuyahoga
County Hospital, Cleveland, Ohio) wrote: " Our
hospital’s population is approximately equally divided
between white and black patients, and I do not be-
lieve that there is any significant racial difference in
the incidence of hiatus hernia ".
The causative factor must therefore be environ-
mental rather than genetic.
The conventionally accepted causes listed above
must be tested in the light of epidemiological
evidence.
Pull-up " Theory
This demands an explanation for the occurrence of
reflux which is postulated to cause oesophageal con-
tracture. The only explanation consistent with the
geographical distribution is that of Cleave et al.,16 who
postulate that the reflux arises from abnormal gastric
130
behaviour resulting from overconsumption of refined
carbohydrate foods and that this predisposes to reflux.
It seems to us that any pathological changes in the
oesophagus are more likely to be secondary to, rather than
primary causes of, hiatus hernia.
<< Push-up" Theory
Raised intra-abdominal pressures are almost certainly a
major cause of hiatus hernia, but they are produced, as
will be suggested below, by factors other than those already
listed, which, we submit, are untenable for the following
reasons:
Tumours.-Abdominal tumours grow to a much larger
size in countries where surgical treatment is less readily
available, and it is in these countries that hiatus hernia
has its lowest prevalence.
Pregnancy.-Women have more, not fewer, pregnancies
in countries where hiatus hernia is rare. Moreover, it
would be strange, as Cleave 17 remarks, if the human
race had not adapted to such a physiologically normal
condition as pregnancy.
Obesity.-Obesity is certainly associated with hiatus
hernia. There is, however, no reason to believe that it
significantly raises intra-abdominal pressures, and reasons
suggesting that the association between these two con-
ditions could be better explained on the basis of a common
cause than on a cause-and-effect relationship will be
given below.
Constrictive Clothing.-If constrictive clothing were a
causative factor the incidence should have fallen rather
than risen during the past 20 years.
ROLE OF LOW-FIBRE DIET
In Western communities the time taken for transit
of ingested markers through the gastrointestinal
tract is approximately double that taken in African
villagers, while the average weight of stool passed
daily is approximately half that passed by the
Africans.
These contrasts in transit-times and stool weights
have been attributed to the difference between the
low-residue refined diet of the West and the high-
residue traditional diet of the less developed countries.
The transit-times and stool weights of communities
on diets somewhere between those with the lowest
and highest fibre content typical of the West and rural
Africa lie between these extremes.18-20
It is now generally accepted that fibre-depleted
diets are the major cause of constipation, 21 the major
hold-up being in the large bowel. The exaggerated
contractions necessary to propel through the bowel
the small firm fxcal content associated with a low
residue diet result in unnaturally raised intraluminal
pressures. These are now believed to be the funda-
mental cause of diverticular disease.15,22,23
Not only is fxcal arrest responsible for raised
intraluminal pressures, but it is the fundamental
cause of straining at stool, an activity that probably
raises intra-abdominal pressures more than almost
any other factor. These pressures often exceed
200 mg. Hg and, unlike coughing, can be sustained
for several seconds. It has been suggested that these
unnaturally raised pressures may be an important
cause of hiatus hernia.24,25
This hypothesis is not only entirely consistent
with the geographical distribution of hiatus hernia
and its relatively recent emergence as a major
clinical problem in the Western world, but it explains
the recognised relationship between hiatus hernia
and certain other conditions such as diverticular
disease and gallstones, the famous Saint’s triad.
Heaton 26 has provided abundant evidence that
cholesterol gallstones may be largely the result of
refined-carbohydrate diets, which can also be
assumed to be a potent cause of obesity.
Diverticular disease and hiatus hernia are closely
associated epidemiologically. Their distribution
appears to be almost identical; available evidence
suggests that they emerged as diseases of clinical
importance in Western countries at about the same
time; they are both rare in people under thirty years
of age and their incidence increases strikingly with
age; and both are more common in women than in
men. These similarities suggest some causative
factor common to each, which we suggest may be a
fibre-deficient diet.
We are aware of no other hypothesis apart from
Cleave’s that is consistent with the geographical distri-
bution of this disease or its association with certain
other diseases.
Requests for reprints should be addressed to D. P. B.,
M.R.C. External Staff, 172 Tottenham Court Road, London
WIP 9LG.
REFERENCES
1. Zeppa, R., Polk, H. C. J. Florida med. Ass. 1971, 58, 26.
2. Hafter, E. Am. J. dig. Dis. 1958, 3, 901.
3. Pridie, R. B. Gut, 1966, 7, 188.
4. Smithers, D. W. in Tumours of the &OElig;sophagus (edited by N. C.
Tanner and D. W. Smithers); p. 69. Edinburgh, 1961.
5. von Bergmann, G., Goldner, M. Funktionelle Pathologie: eine
klinische Sammlung von Ergebnissen und Anschauungen einer
Arbeitsrichtung; p. 70. Berlin, 1932.
6. Johnstone, A. S. Lancet, 1941, ii, 18.
7. Johnstone, A. S. Br. J. Radiol. 1943, 16, 357.
8. Harrington, S. W. Am. J. Surg. 1940, 50, 377.
9. Smithers, D. W. Br. J. Radiol. 1945, 18, 199.
10. Whittaker, L. R. E. Afr. med. J. 1966, 43, 336.
11. Grech, P. ibid. 1965, 42, 106.
12. Moore, E. W. ibid. 1967, 44, 513.
13. Johnson, A. C., Johnson, S. Aust. Radiol. 1964, 13, 287.
14. Kim, E. H. New Engl. J. Med. 1964, 271, 764.
15. Painter, N. S., Burkitt, D. P. Br. med. J. 1971, ii, 450.
16. Cleave, T. L., Campbell, G. D., Painter, N. S. Diabetes, Coronary
Thrombosis, and the Saccharine Disease. Bristol, 1969.
17. Cleave, T. L. Br. med. J. 1960, ii, 465.
18. Burkitt, D. P., Walker, A. R. P., Painter, N. S. Lancet, 1972, ii,
1408.
19. Walker, A. R. P. S. Afr. med. J. 1947, 21, 590.
20. Walker, A. R. P. ibid. 1961, 35, 114.
21. Avery Jones, F., Godding, E. W. Management of Constipation.
Oxford, 1972.
22. Painter, N. S. Ann. R. Coll. Surg. Eng. 1964, 34, 98.
23. Painter, N. S. Am. J. dig. Dis. 1967, 12, 222.
24. Burkitt, D. P. in Medical Annual; p. 5. Bristol, 1972.
25. Burkitt, D. P. Br. med. J. 1973, i, 274.
26. Heaton, K. W. Clins Gastroent. 1973, 2, 67.
"
Psychiatristsare in a peculiar position trying to be moralists.
There is an inevitable arbitrariness about terms like ill, respons-
ible, schizophrenia, treated, cured, etc. etc., and we are in part
always dealing with power struggles between human beings.
The tendency to ethicize rather than be ethical is also ubiquitous.
Soviet psychiatry is, therefore, not alone in requiring constant
scrutiny; we too can defend the status quo especially of family
power struggles. It is therefore unconvincing for would-be
scientists like myself to pretend that the ’ethic of objectivity’
can always be adhered to in the practical policies of psychiatry.
The notorious Soviet trials, however, tend to treat evidence
from a forensic psychiatrist as though it was technical hard
information demonstrating psychosis in a way ordinary men
cannot hope to understand. Of course, once we concede that
some can appropriately be treated as mad rather than bad, as
I believe we must, we all know we have to make many complex
judgements. However, I feel they should be explicable to
intelligent laymen, whose views are not irrelevant."-F. A.
JENNER, Br. y. Psychiat. 1973, 123, no. 572, suppl. (News and
Notes).