Frederick M. (Frederick Madison) Allen.

Total dietary regulation in the treatment of diabetes online

. (page 58 of 76)
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so


80


950


34.3


4855





0.82


1.26








" 3


SO


80


950


33.8


3750





0.76


0.94"








" 4


so


80


950


33.8


3790





0.77


0.68








" 5


so


80


950


34.3


4690





0.92


0.94








" 6


so


86


1000


34.1


3840





0.87


0.66








" 7




Fast-day.


33.9


2985





0.62


0.97


0.19


21.3


62.0


" 8


so


86


1000


33.5


3645





0.75


1.09








" 9


so


90


1050


33.5


4100





0.86


1.39








" 10


so


90


lOSO


33.4


3795





0.97


1.10








« 11


50


90


1050


33.5


3850


+


0.92


0.69








" 12
" 13


50

so


90
97


1050
1100


33.9
33.2


4175
3470


+
+


0.95
0.91


0.75
0.75


0.29


17.4


76.0


" 14
" IS


so


Fast-da
97


ly.
1100


33.3
33.1


2330

,3275






0.69
0.74


0.44
1.11








" 16


so


102


1150


33.5


4375





1.00


2.32








" 17


so


102


1150


33.4


4680


+


1.09


2.06








" 18
" 19


so
so


102
102


1150
1150


33.1
33.6


3810
3810


+
++


1.09
0.89


2.02
1.18


0.25


21.6


76.0


" 20


50


107


1200


33.8


4400


++


0.90


1.10








" 21
" 22


50


Fast-day.
107 1200


33.8

33.7


3980
2950


+




0.74
0.71


1.35
1.05









523



524



CHAPTER VI



TABLE X — Concluded.





Diet.


Weight.


Urine.


Blood.


Date:


Pro-
tein.


Fat.


Calo-
ries.


Volume.


Su-
gar.


NHa-N


Total
acetone
bodies.


Sugar.


Total
acetone
bodies

in
plasma
(as ace-
tone)
per 100
cc.


Plasma


1917


gm.


em.




kg.


cc.


gm.


gm.


em.


per cent


m«.


ml.
per cenl


Jan. 23


50


112


1250


33.9


4170





0.97


1.00








" 24


50


112


1250


33.8


4575





1.07


1.66








" 25


50


112


1250


33.9


4390


+


1.07


0.71








" 26


50


112


12S0


34.0


4035


++


0.99


0.89


0.27


22.2


69.0


" 27


SO


117


1300


34.0


4780


++


0.93


0.91








" 28




Fast-day.


34.2


3140


+


0.49


0.53








" 29


50


117


1300


33.4


2960





0.49


0.86








« 30


SO


122


1350


33.4


4425





0.81


1.64








" 31


50


122


1350


34.0


5325


+


0.94


2.77








Feb. 1


50


123


1350


34.0


3640


+


0.83


1.38








" 2


50


123


1350


34.0


4360


+


0.99


2.44


0.29


23.4


67.0


" 3


SO


128


1400


34.4


4690


+


0.99


1.59








« 4




Fast-day.


34.3


3330


+


0.67


1.67








" 5


50


128


1400


33.6


3175





0.84


1.37








" 6


50


134


1450


34.0


3800





0.82


1.75


0.35


24.8


61.0


" 7


SO


134


1450


34.0


4S9S


+


1.43


2.57








" 8


SO


134


1450


33.9


4490


+


1.21


2.83








" 9


50


134


1450


33.9


4690


+


1.12


2.86








" 10


50


139


1500


34.0


4380


+


1.00


3. 85








" 11




Fast-day.


34.0


1980


+


0.59


1.23








" 12


SO


139


1500


33.5


2905


+


0.72


1.60








" 13


SO


144


1550


33.6


4670


+


0.97


3.41


0.24


25.4


65.


" 14


50


144


1550


33.0


4650


+


1.09


2.65








" IS


50


144


1550


32.8


3955


+


1.08


2.14








" 16


SO


144


ISSO


32.5


3735


+


1.37


3.78








« 17


SO


ISO


1600


32.6


4000


+


1.16


2.88








" 18




Fast-day.


32.8


1370


+


0.76


0.60








" 19


50


150


1600


32.2


3420


+


0.97


3.32








" 20


SO


85


999


32.2


4820


+


1.40




0.26


29.25


56.0


" 21


50


85


999


32.4


3791


+


1.12










" 22


50


85


999


32.7


3988


+


0.90










« 23


SO


86


1002


32.7


4645


+


0.90










" 24


50


85


999


33.0


3750


+


0.77




0.27




52.0


" 25




Fast-day.


33.3


3190


+


0.53










" 26


SO


85


999


32.9


3228





0.42










« 27


SO


85


999


32.4


4040





0.57




0.23






« 28


60


81


1000


33.3


4767





0.68











INFLUENCE OF FAT IN THE DIET 525

masked by a loss of water driven out by the fat feeding. There was
no improvement in strength or comfort. As a whole, the test
indicated distinct injury to the patient from the laboratory stand-
point by the cautious addition of fat in excess of the assimilative
power, with no compensating clinical benefit.

Beginning February 20, the fat was reduced to make a total diet of
1000 calories. Glycosuria gradually cleared up and the ammonia
excretion diminished.

On February 28 the protein was increased to 60 gm., keeping the
total calories at 1000. Faint traces of glycosuria appeared on some
days thereafter (see graphic chart). On March 14 the fat was in-
creased to make 1100 total calories, arid again on April 18 to make
1300 calories. On April 23 the fat was further increased to make
1500 calories, but then diminished on May 2 to 1300 and on May 7
to 1200 calories. During this whole period of 2 months the patient
was obviously just at the edge of her tolerance, showing faint sugar
and ferric chloride reactions very frequently, but never excreting a
titratable quantity of sugar or developing any marked acidosis. In
the first week shown in Table XI (May 14 to 20) the condition made
an evident change for the worse, for on the identical diet as much as
11 gm. sugar and 2.3 gm. acetone bodies were excreted on certain
days. The opportunity seemed favorable for testing whether this
change represented "spontaneous downward progress" on the part
of the patient, or whether it was merely the culmination of several
months of diet slightly overtaxing the tolerance. A sudden addition
of 100 gm. fat was made on May 21, with an additional 50 gm. on
May 22, thus raising the total diet to 2600 calories. Marked and
continuous glycosuria and ketonuria followed, as shown in Table XI
and in the graphic chart. Also the total acetone increased in
the blood plasma, and the alkah reserve fell as low as 42.3 per cent
on May 26 and 27. The patient, who had welcomed the opportunity to
eat more, quickly became unwell and unhappy. The daily adminis-
tration of 20 gm. sodium bicarbonate on May 28, 29, and 30 seemingly
lowered the blood sugar and urine on the first day, but had doubtful
eifect thereafter. It also raised the plasma bicarbonate temporarily,
but by May 30 this was again down to 43.7 per cent in spite of the
alkali dosage. It is also possible that this dosage may have been



TABLE XI.
Patient No. 43.





Diet.




Urine.


Blood plasma.




Date.


1


1


1


•3

8

<


u


2
1


B

I


^




i

1


o
o

vol.
ter
cent


mg.


Remarks.


1917


gm.


gm.


gm.


cc.




kg.


cc.


gm.


gm.


pit
cent




May 14


60


103.0








1202


33.0


3510





1.49








— ■




" 15


60


103.0








1202


33.4


5070


+


2.30


0.192


55.7


49.0




" 16


60


103.0








1202


32.9


5075


5.04


1.71













" 17


60


103.0








1202


33.8


5215


10.90


1.61













" 18


60


103.0








1202


34.0


5200


10.40


2.24













" 19


60


103.0








1202


34.3


5640


10.90


1.28













" 20


Fast-day.




34.1


1895


7.22


1.03


0.213


64.5


21.8




" 21


60


203.0








2132


34.8


3330


+


2.10


0.175





29.8




" 22


60


253.0








2597


34.9


5720


+


7.01













" 23


60


253.0








2597


34.6


4740


18.01


9.48













" 24


60


253.0








2597


33.9


3205-1-


18.99


10.63













" 25


60


253.0








2597


34.2


2680


18.52


9.58













" 26


60


253.0







2597


34.2


2280


13.80


9.57


0.298


42.3





5: 00 p.m.


« 27




30.0







279


34.6


2035


35.60


9.80


0.233


42.3





10:00 a.m.


" 28*


60


253.0







2597


33.7


1090


5.67


8.61


0.286
0.154


57.6
48.3


52.1
77.5


9:00 "
6:00 p.m.


" 29*


60


253.0








2597


35.6


2995


24.06


18.41













" 30*


60


253.0








2597


34.4


3475


24.84


17.25


0.222


43.7


99.0


5:00 "


« 31


60


10.0








332


35.4


5115


45.72


11.18


0.216


48.3


52.1


9:00 a.m.


June 1


60


10.0








332


34.9


5645


31.90


4.46













" 2


60


10.0








332


35.0


4845


24.23


1.55













" 3


Fast -day.





35.5


1575


8.80


1.31


0.228


57.9


40.8




" 4


(C





34.8


860


+


1.29


0.170


58. 9


42.3




" 5


60


4.0








282


34.4


4100


+


2.01













" 6


60


4.0








282


34.6


4900


+


0.88













" 7


60


3.0








275


35.4


5440


+


0.49













« 8


60


3.0








275


34.9


3570


+


0.51













" 9


60


3.0








275


34,5


4520


+


0.36


_










" 10


Fast- day.





34.1


1855


+


0.31


0.208


64.5


43.1


10:00 a.m.


« 11


59











249


34.4


4005


+


0.64


0.159


59.8


20.4


9:00 "


" 12


59











249


34.4


4660





0.42













" 13


59


1.0


1.0





255


33.0


4610





0.41













« 14


59


1.0


1.0





255


33.4


4820





0.29













" IS


59


1.0


1.0





255


33.8


4605





0.23













" 16


59


1.0


1.0





255


34.2


5250





0.47


0.128





13.4


5:00 p.m.


" 17


Fast- day.




34.3


2230





0.54


0.200


67.3





11:00 a.m.


" 18


59 1.01.0 40


535


33.8


3640





0.18


0.113





26.6


9:00 «



* 20 gm. sodium bicarbonate on this day.

526



INFLUENCE OF FAT IN THE DIET 527

partly responsible for the maximum of 99 mg. total acetone per 100 cc.
of blood plasma on May 30. Here also dyspnea was not present, but
on account of general malaise the patient was glad to discontinue the
fat ration.

Accordingly on May 31 fat was eliminated from the diet as far as
convenient, keeping the protein unchanged. The first effect was seen
upon acidosis, in the fall of acetone bodies in blood and urine, the
spontaneous rise of the plasma bicarbonate, and the reHef of the
clinical symptoms. The sugar excretion rapidly diminished. The
hyperglycemia was more stubborn, but there was a progressive di-
minution down to a normal level on June 18, following the fast-day
of June 17. Thereafter it proved possible, as in the preceding pa-
tient, to increase the protein to 84 gm. daily without glycosuria. In
another test, not included here, a similar return of diabetic symptoms
followed an increase of the total calories of the diet.> The s3Tnptoms
were again abolished by diminution of calories without change in
protein. It has also been possible to prolong the freedom from active
symptoms up to the present, so that "spontaneous downward
progress," if existent, has not as yet been manifest.

This question of downward progress has been investigated by long
as well as short feeding experiments on animals, but it is seldom that
circumstances permit a similar close comparison between individual
human patients treated on opposed principles. It has come about
that without experimental intent, treatment was carried out along
opposite Unes in two patients of the present series, so closely com-
parable as to afford the most exact comparison possible in clinical
observations. These are patients Nos. 37 and 66. It will be seen
from their histories that both represented juvenile diabetes of the
usual type. Both cases were controlled by treatment in such man-
ner as to restore normal conditions in both urine and blood as far as
determined by the routine tests'. The condition of the two appeared
equally favorable from the clinical standpoint. The treatments dif-
fered in respect to the total calories of the diet. After the prelimi-
nary fasting and undernutrition which cleared up symptoms, the
boy (No. 37) was treated along former orthodox lines. He was
allowed a high caloric ration supposedly suitable for his age, with the
idea of facilitating normal growth and development. Exercise was



528 CHAPTER VI

employed to build up his muscles and consume surplus food. He was
discharged from the hospital with nearly the same body weight as
at entrance, and, with his feeling and appearance of splendid health,
seemed to afford an example of the most successful treatment. He
followed the diet with absolute fidelity and for a short time enjoyed a
practically normal existence. 2 months after leaving the hospital,
and 7| months from the onset of the diabetes, marked hyperglycemia
was found without glycosuria or other sjonptoms. This plain warn-
ing was met only by diminution of carbohydrate, not of the total
diet or weight. The blood sugar continued to rise, and at the second
admission traces of sugar and ferric chloride reactions were present
in the urine and the carbohydrate tolerance was found markedly re-
duced. The patient was allowed to go home after only 2 weeks in
the hospital, on a' diet of 40 calories per kilogram, at an increased
weight, with hyperglycemia continuously present. After this dis-
charge the progress was rather rapidly downward, and at the third
admission, 1 1 months after the first, the patient was almost in coma.
Much lower diets were then necessary, but the condition was still
never adequately controlled, especially as respects hyperglycemia.
After further steady downward progress, death occurred two years
after the first onset of diabetes. The result of treatment was favor-
able only to the extent that life and comfort had been so greatly pro-
longed, in a patient threatened with death within a few weeks or
months under other conditions.

The girl (No. 66) received such a diet in the hospital that she was
dismissed weighing 5 kilograms less than at admission. The two
patients were closely similar in natural size and weight. The boy had
been discharged on an average ration of 2100 calories, or 43 calories
per kilogram at his elevated weight. The girl was discharged on
an average ration of 1630 calories, or 3'6 calories per kilogram at her
reduced weight. This diet was slightly too high; for 5 months after
discharge, or 14 months after the onset of diabetes, blood samples
taken for observation purposes on 3 successive mornings before
breakfast showed a slight hyperglycemia of 0.130 per cent. This
warning was heeded by reducing the total calories to a little over
1300 average, by diminishing fat, while the protein was kept the
same, and the carbohydrate actually increased by 5 gm. Along



INFLUENCE OF FAT IN THE DIET 529

with the hyperglycemia there had been a gain of 8 kilograms in
weight. The reduced diet diminished the weight to 50 kilograms,
which was identical with that at the first admission. Both blood
and urine then remained normal. Later it happened that the girl
was placed temporarily on the same treatment as the boy; that is,
the fat intake was inadvertently increased, and the beginning of glyco-
suria was met by a reduction of 15 gm. carbohydrate in the diet.
Fortunately the increase of body weight aroused suspicion. On re-
calling the patient to the hospital, marked hyperglycemia and strong
acetone reactions were found. The mistake was corrected by reduc-
tion of fat and total calories, while the carbohydrate was again
increased by 15 gm. Accordingly, in contrast to the boy's death
2 years after the onset of diabetes, the girl still has the feeling and
appearance of perfect health, normal conditions in blood and urine,
and full possession of her original carbohydrate tolerance. She has
grown and developed normally, apart from being kept slightly but
not noticeably below maximum weight. The boy on his unduly
high diet developed glycosuria frequently with colds, but the girl
passed through an appendix attack without showing sugar. If there
is any "spontaneous downward progress" in her case, it has not yet
made itself manifest.

The only objection to the comparison must be based on the as-
siunption that the diabetes was inherently more severe and progres-
sive in the boy, and that the girl represented one of the unusual
juvenile cases with little progressive tendency. In support of this
assumption is the fact that the boy was close to coma within 3 weeks
from the onset of known symptoms, whereas the girl entered the
hospital without alarming symptoms, 5 months after the first sus-
picious signs of diabetes. The justice of the comparison is supported
by several considerations.

1. It has been the experience with this series of diabetic patients
that the most accurate measure of severity is found in the tolerance
for carbohydrate and other foods. Coma is often merely an incident
depending upon the character of the diet, and is not a reliable index
of the true assimilative function or progressive tendency. The girl
was 1 year younger than the boy and not so robust. The actual
fact is that during her several months of diabetes she had progressed



530 CHAPTER VI

downward to such an extent that her assimilation was distinctly
lower than that of the boy. In the initial test with green vegetables
the limit of her tolerance was 140 gm. carbohydrate, as compared
with 175 to 200 gm. for the boy. Furthermore, the capacity for
improvement was far more evident in the boy, for after 4j months
in the hospital he was able to tolerate 400 gm. carbohydrate, whereas
it can be seen from the girl's graphic chart that she showed glyco-
suria on May 18 and 29 on a slight increase of diet which was far
below the regular tolerance of the boy.

2. The progressive tendency in the girl's case was further demon-
strated by the hyperglycemia and other threatening signs on two dif-
ferent occasions when she happened to be subjected temporarily to
the same unfortunate kind of treatment as the boy. The harmful-
ness of an unduly high fat ration was thus proved also in her case.
The development of these sjonptoms more quickly and on a lower diet
than in the boy's case confirms the assimiption that the diabetes was
actually more severe in the girl.

3. The claim that the result in the boy's case was due solely to an
inherent progressive tendency could be supported only on the as-
sumption that he was somehow immune to the injurious effects of
high caloric diets. Such effects have been easily and plainly demon-
strable in every case tested, and the rule is believed to be without
exception for all typical cases of diabetes. In the light of the plain
evidence of all the preceding experiments, it can only be concluded
that the excessive caloric ration was one important cause of the
downward progress in the case of this boy. Downward progress has
thus far been avoided in the girl's case by avoiding such overstrain
of the metaboHc power. It is strongly suggested that a similar result
might have been obtained by similar methods in the boy's case, and
that his death within 2 years was not due to any inherent and in-
evitable process in himself, but directly to the lack of proper treatment.

Though experimental results place the principle of total caloric
restriction for diabetes on a basis not affected by the many variables
which determine cUni'dal success or failure, yet the general results of
treatment under this method, in comparison with the results obtained
with such fat diets as have heretofore been employed in the man-
agement of diabetes, constitute the most important body of evidence



INFLUENCE OF FAT IN THE DIET 531

in support of the practical usefulness of this plan. A number of case
histories in this series show the diasters which have occurred when-
ever the principle of total caloric regulation has been violated. On
the other hand, as far as the treatment has been properly carried out,
it is believed that the method of restricting fat and total calories in
the same manner as carbohydrate and protein has proved vaHd in its
conception and beneficial in its application.



CHAPTER VII.

RESULTS— PROGNOSIS.
Severity of the Cases.

A standard of severity of diabetes is difl&cult to define. In an at-
tempt to classify cases according to the actual degree of the diabetic
disturbance and the problems offered in treatment, the judgment of
severity has been formed from three factors, (1) carbohydrate toler-
ance, (2) age, and (3) clinical course.

1. Accepted criteria in the past have been the assimilation of car-
bohydrate added to a protein-fat diet, the intensity of glycosuria on
a given diet, acidosis, and (with a few authors) changes in protein
metaboUsm and the degree of difl&culty in bringing the urinary ni-
trogen quantitatively and quaUtatively to normal. If diabetes is a
disorder of the total metaboUsm, these indices based upon carbohy-
drate, fat, and protein metabolism are equally valid and yield equiva-
lent information. The essential thing is the power of assipiilating
food. Diabetes is severe in proportion as this power is deficient.
The choice of a test comes down to a question of convenience of per-
formance, ease and reliability of interpretation, and safety for the
patient. In some severe cases, the injury from excess of protein or
fat is promptly evident. Generally, however, the manifestation is
slower, and the injury is correspondingly more lasting. Carbohy-
drate acts most rapidly in producing glycosuria. Standard condi-
tions for comparison are provided by testing with carbohydrate alone
with exclusion of other foods. Glycosuria and hyperglycemia pro-
duced by pure carbohydrate subside promptly on its withdrawal, in
contrast to the slower rise and fall when they result from protein-fat
excess. Such a carbohydrate period, with its attendant undernu-
trition, acts favorably upon acidosis and upon the diabetes itself, so
that with intelHgent management a thetapeutic as well as a diag-
nostic purpose may be served. Diet and other accidental factors in-

532



RESULTS — ^PROGNOSIS 533

troduce many elements of confusion in the untreated case. When
the rush of symptoms is checked by fasting and perhaps a subse-
quent undernutrition period, until the acute condition is well con-
trolled, a carbohydrate test has ?,lways proved a reliable index of the
general food tolerance. Other conditions, such as noted below, being
equal, the food tolerance has afforded the best basis of judgment con-
cerning the existing grade of severity of the diabetes, comparisons be-
tween patients, and the degree of difl&culty to be anticipated in treat-
ment. A patient received in or near coma may have far milder
diabetes and be much easier to keep in good condition subsequently
than one received with slight or no active symptoms but with a mini-
mal assimilative power. Later tests give indications of the progress
when modifying influences are properly considered. For example,
with therapeutic reduction of weight there may be an apparent gain
of assimilation, and with increase of weight there may be an apparent
loss of assimilation, while the actual functional capacity is unchanged.
Increased tolerance at the same or higher body weight shows genuine
improvement.

2. Age is no absolute guide, for mild diabetes in children and severe
diabetes in the aged are known. In general, however, it is recognized
that the danger from diabetes is in inverse proportion to the age.
Two reasons may be assigned for the difference : first, the higher me-
tabolism in children especially imposes a heavier burden upon a weak-
ened assimilative function; second, the more severe type of diabetes,
occurring generally in the young, is a specific disorder of the islands
of Langerhans, seemingly partly functional in most cases, but subject
to rapid aggravation and organic degeneration of islands due directly



Online LibraryFrederick M. (Frederick Madison) AllenTotal dietary regulation in the treatment of diabetes → online text (page 58 of 76)