John_Yudkin_-_Pure_White_and_Deadly_revised_1986_OCR

Pure, White and Deadry
carried out at King's College Hospital in London. Physicians and
surgeons were asked to send us anyone coming to them complaining
of severe dyspepsia that had lasted, though perhaps not continuously,
for more than six months. Many had had symptoms for five
years or more. The only patients not included in our experiment
were those who were going to have an operation for their condition.
Each patient was carefully questioned and examined by a physician,
and than sent on to a nutritionist. Alternate patients were
instructed either in the conventional dietary treatment commonly
used then, or in the low-carbohydrate diet. The conventional treatment
consists of telling the patients to avoid fried foods and irritants
such as pickles or foods containing spices, to take frequent small
meals, and to avoid alcohol, especially on an empty stomach. At intervals
each patient came back to the physician for assessment of the progress
of his condition, and to the nutritionist to check the diet that he
was following. The physician did not know which diet each patient
was on; the nutritionist did not know how the patients were progressing.
Mter three months, the diets of the patients were reversed, so
that those taking the conventional diet were transferred to the lowcarbohydrate
diet, and those taking the low-carbohydrate diet transferred
to the conventional diet. The experiment then continued for
a further three months.
Having made the conditions of the experiment so stringent, we
were not surprised that it took us more than two years to get together
information on 41 patients who had reported regularly for six
months, and had, as best we could judge, adhered to our instructions.
From the detailed records kept by the physician, he and I
then separately assessed their total progress and classified them as
having shown no change, or having reported various degrees of
improvement or deterioration at the end of each three-month period.
Our assessment differed in only one or two instances as to the degree
of change, but not once did we disagree as to whether the patient reported
that he was better or worse or just the same. It was only after
the clinical assessment that we looked to see whether the patient had
begun with the low-carbohydrate diet or with the alternative diet.
In summary, the results are pretty clear. Of the 41 patients in our
trial, two said that they were worse on the low-carbohydrate diet,
eleven said that they were no different on either diet, ,but a decided
majority - 28 - said that they were very much better on the lowcarbohydrate
diet. Some of these were quite certain that the
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A pain in the middle
improvement was so great that nothing on earth was going to make
them give up the low-carbohydrate diet. One said, 'I feel better than
I have been for five years.' Another was even more enthusiastic: 'I
have never felt better round my stomach in all my life.' The patients
included men and women, some with gastric or duodenal ulcers,
some with hiatus hernia, and some who probably had ulcers which,
as so often happens, had not been revealed by X-ray examination.
These results, of course, pleased us a great deal. They suggested
that chronic and severe indigestion, from several causes, could be
greatly relieved by diet alone in something like 70 per cent of
patients. This result was especially pleasing because there had been
increasing disappointment in the last few years about the results of
dietary treatment of these conditions. Several research workers had
put patients on fairly strict 'gastric diets' - steamed fish, white meat,
mashed potatoes, milk puddings - or on the more liberal but still
fairly conventional diet I described earlier. All these investigators had
concluded that the diets did not seem to relieve the severe dyspepsia
of their patients, whether or not they had a definite ulcer. Now it can
no longer be said that diet does not relieve severe dyspepsia. The right
diet may well do so; but of course the wrong diet will not.
The low-carbohydrate diet we had used in our study was limited
in both starch and sugar. For a variety of reasons we suspected that
it was the reduction in sugar that was chiefly responsible for the
improvement we saw, so we carried out a further experiment to look
at the effect of sugar in a normal diet. Working with young men,
we managed to persuade seven of them to swallow a gastric tube
first thing in the morning. They did this before and again after two
weeks of a high-sugar diet. Through this tube we obtained samples
of their gastric juices at rest, and then further samples were taken
at Is-minute intervals after they had swallowed a bland 'test meal'
consisting mainly of pectin. Each sample was analysed in the standard
ways, most importantly by measuring the degree of acidity and
digestive activity.
The results showed that two weeks of a sugar-rich diet causes an
increase in both acidity and digestive activity of the gastric juice,
the sort of change you often find in people with such conditions as
gastric or duodenal ulcer. The sugar-rich diet increased the acidity
by 20 per cent or so; the enzyme activity was increased nearly threefold.
And let us remember that these effects were seen early in the
morning, before breakfast - two weeks on the high-sugar diet had
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