Hypo glycemia
Hi Everyone,
Since way before my WLS I have had episodes where if I dont eat I get the following symtoms....cold sweats, very shaky, weak, a fog like feeling in my head, sometimes I even get the feeling that I want to cry or am very irritable, and I can not concentrate. I have mentioned it my Dr's in the past and have had labs done but have always been told that I am fine. Now I am know that I dont make up the feelings, since WLS I have had it happen a few times, it happens less than before WLS. It happened again yesterday and I can not seem to pin point what triggers it now. I dont dump and do eat sugar, but only in moderation. When I got these feelings before WLS I had a strong urge to eat sugar and would along with other stuff but I always with sugar like orange soda. Now I get the urge to eat protien and that works, I want nothing to do with sugar.
So I guess my question here is.....what do you all think. Dr's say that my blood sugar levels are always with in normal range. So what gives?
Any thoughts are appreciated.
Melissa
Often post-ops find themselves having episodes of hypoglycemia... sometimes from going too long without eating and others have it after eating. When it happens after eating it is an overreaction of the body to carbohydrates. The body will give off more insulin then needed driving blood sugars down.
I think that being obese are bodies are used to carbs being ingested in large quantities and they are used to giving off large doses of insulin in response. Plus we have an overabundance of pancreatic cells (islet cells) that produce insulin.
The best way to control it and keep it in check is to avoid simple carbs and to never eat carbohydrates by themselves. Watch quantities of carbs and make sure that if you are going to eat them that you eat them along with protein and fat. The mix of protein and fat along with the carbs changes how the body processes them and will reduce the insulin response.
Kathy
guess what! You do dump and this is how you do it. there are a lot of misunderstandings as to what dumping is. for some people it is cramps, diahrhea etc shortly after eating that is early dumping. others get reactive or alimentary hypoglycemia - late dumping, a couple hours after the food. it can be more difficult to connect the events because they are separated in time, and then the person thinkds it is unrelated. Only one way to stop it, no refined sugar and natural sugar only in combination with protein.
your blood sugar probably is in the normal range when you are at the Dr, but I'll bet if you were checked while you were symptomatic you would be low.
reactive, or alimentary hypoglycemia is an effect of wls - it is dumping.
2104 The American Journal of Clinical Nutrition 32: OCTOBER 1979, pp. 2104-2114. Printed in U.S.A.
editor: Norton S. Rosensweig, M.D.
comments in gastroenterology
Alimentary hypoglycemia: a new appraisal1
Steven B. Leichter, M.D.
ABSTRACT The clinical evaluation and the results of oral glucose tolerance tests in patients
with alimentary hypoglycemia, reported previously or studied as part of our group of 24 patients
with this disorder, suggest that alimentary hypoglycemia may differ from other reactive hypoglycemias
in clinical presentation and importance. Unlike other reactive hypoglycemias, alimentary
hypoglycemia may be associated with severe or permanent neuropsychiatric complications. Subtle,
"neuroglycopenic" symptoms of hypoglycemia may occur, instead of "typical," "adrenergic"
symptoms. Glucose ingestion, by causing early hyperglycemia and provoking the release of
insulinotropic enteric hormones appears responsible for this disorder. Therefore, therapy with diets
low in simple sugar, but unrestricted in complex carbohydrate and fiber are now advocated. Am.
I Clin. Nutr. 32: 2104-2114, 1979.
Alimentary hypoglycemia, as an accepted
form of reactive hypoglycemia, is generally
believed to have the same mild clinical characteristics
and favorable prognosis as other
reactive hypoglycemias (1-5). Common dinical
features are said to include a similar
pattern of symptoms, a comparable and low
incidence of neuropsychiatric complications,
and a responsiveness to therapy with lowcarbohydrate
diets. These assumptions may
not be completely warranted. The results of
a number of studies have now suggested that
important differences may exist between the
clinical features of alimentary hypoglycemia
and other reactive hypoglycemias, although
these differences have not been documented
clearly (6). In our studies of patients with
alimentary hypoglycemia, we have noted discrepancies
between the syndrome, as it presented
in our patients, and as it is often
described. Therefore, this review was compiled
to define the characteristics of alimentary
hypoglycemia, and to delineate differences,
which may exist between alimentary
and other reactive hypoglycemias.
Methods
The methods used in evaluating the patients cited in
this review, and details about most of the patients included
in our study group have been reported previously
(7-9). All patients were studied 2 or more years after
gastric surgery. No patient was obese. Every patient gave
informed consent or was studied as part of a diagnostic
evaluation for dumping syndrome.
Subjects were given an initial history, physical cxamination
and a 5-hr. oral glucose tolerance test
(OGTT), using 75 g of glucose (10). The patients were
fasted overnight before each test, and were kept in a
sitting position to minimize variations in the results ( I 1).
Some patients, who had given informed consent, were
given repeat OGTT's with the prior oral administration
of propranolol, 10 mg, 30 mm before the administration
of glucose. All subjects were observed by a nurse or
physician during each test, and any symptoms that occurred
during these tests, and their time of occurrence,
were noted. Samples of venous blood for measurement
of plasma glucose and serum insulin levels were obtained
before and at 30-mm intervals after the glucose ingestion,
as described by Permutt et al. (12).
Plasma glucose concentrations were determined using
the Auto Analyzer (Technicon, Ardsley, N.Y.). Serum
insulin levels were measured by radioimmunoassay (13,
14). Serum vitamin B12 concentrations were assayed by
the method of Raben and Robson (IS). Serum gastrin
concentrations were measured by a commercial radioimmuno-
assay kit (E. R. Squibb & Sons, Princeton, N.J.).
All statistics were analyzed with Wang 2200B calculator,
using programs supplied by the manufacturer (Wang,
Inc., Tewksbury, Mass.). Tests of statistical significance
included nonpaired t test and x2 analysis.
The diagnosis of alimentary hypoglycemia
Alimentary hypoglycemia is a postprandial
phenomenon, which is an accepted cornpli-
From the Department of Medicine, University of
Kentucky College of Medicine, Lexington, Kentucky
40536.
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ALIMENTARY HYPOGLYCEMIA 2105
cation of gastric surgery, and is usually associated
with the broad diagnosis of "dumping
syndrome." The other disturbances that are
usually grouped in the "dumping syndrome"
are: enteric symptoms of diarrhea and abdominal
cramping, which occur within 30 to
60 mm after eating; and vasomotor symptoms
of flushing, nausea, fatigue, palpitations, and
diaphoresis, which occur within 60 min after
eating (16, 17). Some investigators appear to
include alimentary hypoglycemia as one of
the dysfunctions of dumping syndrome itseLf
(16), whereas others imply that it is associated
but separate complication of gastric surgery
(17).
The criteria currently used to diagnose alirnentary
hypoglycemia are the criteria for
diagnosing all forms of reactive hypoglycemia.
They are based on both symptornatology
and plasma glucose levels noted by history
and during 5-hr OGTT's (5, 6, 1 1, 12, 18, 19).
To establish the diagnosis, there should be a
history of symptoms, "typical" for hypoglycernia.
In addition, a plasma glucose level
:s50 mg/dl and the typical symptoms, as
described by history, must be documented
during OGTT. These criteria have been suggested
because slight, asymptomatic nadirs in
plasma glucose levels, s50 rng/dl, may occur
in a significant minority of persons during
OGTT's (20), and because the symptoms,
considered typical for reactive hypoglycemia,
may also occur in other disorders, such as
anxiety.
To most reviewers (1-5, 21), typical symptoms
of reactive hypoglycemia refer to the
"adrenergic" symptoms of hypoglycemia (4,
5). Adrenergic symptoms and "neuroglycopenic"
symptoms are the two sets of symptoms
associated with hypoglycemia (6). Not
only do they differ in their presentation
(Table 1), but also in their potential risks to
TABLE 1
Adrenergic and neuroglycopenic
symptoms of hypoglycemia
Adrenergic symptoms Neuroglycopenic symptoms
Nervousness Somnolence
Anxiety Lethargy
Hunger Confusion
Palpitations Transient sensory or
motor defects
Diaphoresis Irritability
Headache Headache
the patient. Whereas adrenergic symptoms
are dramatic in onset, easily recognized, and,
by inducing hunger, often remedied by the
patient quickly, neuroglycopenic symptoms
may be insidious and subtle in presentation,
not recognized as symptoms of hypoglycemia,
and, therefore, not alleviated quickly. Thus,
persons who suffer from neuroglycopenic
symptoms are considered to have a greater
risk of severe or permanent neuropsychiatric
complications of hypoglycemia than persons
with adrenergic symptoms. Neuroglycopenic
symptoms are not thought to occur in reactive
hypoglycemia (1-5, 21).
Because the symptoms of alimentary hypoglycemia,
as other reactive hypoglycemias,
are said to be adrenergic symptoms, the diagnostic
criteria for alimentary hypoglycemia
imply that patients have adrenergic symptoms
as their typical symptoms. This may not
be invariably true. There is no prior description
of symptoms patterns in a large series of
patients with alimentary hypoglycemia available
in the literature. In our group of 31
patients, studied for postprandial phenomena
after gastric surgery, 24 had symptoms and
biochemical abnormalities, which fulfilled
the diagnostic criteria for alimentary hypoglycemia;
however, 13 of these 24 patients
had symptoms by history and during the
hypoglycemic phase of their OGTT's, which
resembled neuroglycopenic, rather than adrenergic
symptoms. All of these subjects had
low plasma glucose levels ı50 mg/dl, during
their OGTT's, and the mean lowest plasma
glucose level observed in the 24 hypoglycemic
patients during the OGTT's, 41 ± 2 mg/dl,
was significantly lower than that in the seven
normoglycemic patients, 74 ± 6 mg/dl (P <
0.001). Both by history, and at the time these
patients had chemical hypoglycemia, they
noted headache, lethargy, irritability, confusion,
somolence, dysarthria (one patient), and
grand mal seizure (one patient). Thus, typical
symptoms may include both neuroglycopenic
and adrenergic symptoms in alimentary hypoglycemia,
and clinically important cases of
alimentary hypoglycemia may be overlooked
by assuming that adrenergic symptoms alone
occur in this form of hypoglycemia.
Another, possible source of confusion in
establishing the diagnosis of alimentary hypoglycemia
by the history of symptoms may
be similarities between the symptoms of ali-
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2106 LEICHTER
mentary hypoglycemia and those of early,
postprandial, vasomotor phenomena. Overall,
vasomotor phenomena occurred in 2 1 of
our 3 1 study patients (67.7%), during the
control OGTT. Ofthese subjects, 14 had both
vasomotor phenomena and adrenergic or
neuroglycopenic symptoms after ingesting
glucose and, also, by history. Since there are
a number of symptoms common to vasomotor
phenomena and hypoglycemia (Table 2),
some difficulty may be encountered in establishing
by history alone which group(s) of
symptoms is present in every case. Defining
the interval between eating or glucose ingestion
and the onset of symptoms may often be
useful in distinguishing vasomotor phenornena
from alimentary hypoglycemia. Whereas
all 14 patients had the onset of vasomotor
symptoms within 30 to 60 mm after eating,
according to the history, no patient had the
onset ofhypoglycemia symptoms sooner than
90 mm after eating. Additionally, no patient
had chemical hypoglycemia (Table 3) or hypoglycemic
symptoms before 90 mm after
ingesting glucose during the control glucose
tolerance test. This experience is similar to
TABLE 2
Symptoms" of vasomotor phenomena
and alimentary hypoglycemia
Symptom
Vasomotor
phenomena
Hypoglycemia
Weakness
Flushing
Palpitations
Fatigue
Hunger
Nausea
Somnolence
+
+
+
+
+
+
+
+
+
+
+h
+"
a A "+" indicates occurrence of the symptom; a "-"
indicates that the symptom does not occur. bHunger
is usually associated with adrenergic symptoms of hypoglycemia;
nausea may rarely occur with neuroglycopenia.
Somnolence may occur in neuroglycopenia. (See
text for references).
TABLE 3
that reported by other investigators (1 1, 19,
22-25).
Another means ofconfirming the diagnosis
of alimentary hypoglycemia, that has been
advocated by Hofeldt and his colleagues (11,
19, 25), is to assess changes in counter-regulatory
hormone secretion when presumed
hypoglycemia occurs during oral glucose tolerance
tests. This suggestion is based on previous
observations that hyperglycemic hormones,
including catecholamines (26, 27, 30),
glucagon (28), cortisol (29-33), and growth
hormone (29, 32, 34, 37), are released in
response to hypoglycemia. As important as
such criteria may be, the validity of their use
to exclude the diagnosis of alimentary hypoglycemia
may not be established clearly; however,
the demonstration that counter-regulatory
hormones have been released in a patient
being evaluated for this hypoglycemia may
suggest or confirm the diagnosis. Of the
known counter-regulatory hormones studied
in detail, cortisol may be one reliable index
of physiological hypoglycemia. Many studies
have shown that hypoglycemia, associated
with the administration of exogenous insulin,
will consistently induce a significant increase
in plasma cortisol levels (29-33, 38-40). In
contrast, plasma glucagon levels may not always
increase when hypoglycemia is induced
in normal subjects (41), patients with reactive
hypoglycemia (42), or patients with diabetes
mellitus and autonomic neuropathy (43). The
degree of hypoglycemia appears to determine
whether counter-regulatory hormone secretion
may occur, rather than the rate of decline
in plasma glucose concentrations (44). Other
hormones, such as vasopressin (45), and pancreatic
polypeptide (46) may also participate
in the homeostatic response to hypoglycemia,
although their exact role in the counter-regulation
of hypoglycemia is unclear. At present,
none of these counter-regulatory hormones
have been studied in detail in patients
Interval between glucose ingestion and occurrence of peak serum insulin or
lowest plasma glucose in 22 subjects with previous gastric surgery and
alimentary hypoglycemia
Parameter Percenta ge of patients
Time (mm) 30 60 90 120 ISO 180 210 240 270 300
Peak serum insulin 9 64 18 9
Lowest plasma glucose 4.5 18 18 50 4.5 4.5
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ALIMENTARY HYPOGLYCEMIA 2107
with alimentary hypoglycemia. Until the assessment
of counter-regulatory hormone secretion
may be more specifically used to define
alimentary hypoglycemia, the absence of
counter-regulatory hormone secretion may
not necessarily exclude this diagnosis in an
individual patient. Nevertheless, validation of
the diagnosis by demonstrating an increase in
plasma levels of a counter-regulatory hormone,
which is released consistently with alimentary
hypoglycemia, appears desirable.
The clinical importance of alimentary
hypoglycemia
Presumptions about the prevalence, severity,
and risks of neuropsychiatric complications
have discouraged concern and interest
in alimentary hypoglycemia (1-5, 16, 17, 19).
Alimentary hypoglycemia is believed to be
an infrequent complication of gastric surgery,
affecting only 2 to 7% of patients after such
surgery, whereas other forms ofdumping syndrome
may affect 4 to 25% of patients (47).
As other reactive hypoglycemias, alimentary
hypoglycemia is not believed to cause serious
or permanent neuropsychiatric injury (1-5).
Patients have been described with neuropsychiatric
dysfunction after gastric surgery;
however these problems have been ascribed
to preexisting personality disorder (48-50), or
to the neuropsychiatric effects of hypovitaminosis
12 (5 1, 52). These associations may or
may not reflect all neuropsychiatric problems
in patients with prior gastric surgery and
alimentary hypoglycemia. Estimates of the
prevalence of alimentary hypoglycemia may
be low, because the criteria for diagnosing
this hypoglycemia were not stated in most
large series (53-55), and patients may not
have had oral glucose tolerance tests as part
of their evaluation. Similarly, patients with
neuropsychiatric dysfunction and prior gastric
surgery, who were noted to have hypovitaminosis
B12, did not have OGTTs as part
of their work-up (51, 52), and in most, there
was no improvement in their neuropsychiatnc
disorder with vitamin B12 therapy. Personality
disorders and reactive hypoglycemia
may be more common in persons with peptic
ulcer disease, but neurological dysfunction
cannot be explained by this association.
An association may exist between alimentary
hypoglycemia and neuropsychiatric dysfunction.
As we have briefly reviewed elsewhere
(7), at least nine cases, including two
cases from our series have now been reported
in which serious neuropsychiatric dysfunction
was documented in persons with alimentary
hypoglycemia. These disturbances included
coma, seizures, and presenile dementia.
Proving a direct, casual link between the
presence of alimentary hypoglycemia and
neuropsychiatric dysfunction is difficult,
since hypoglycemia causes no specifically
characteristic injury to the brain or other
tissues (1-3, 21); however, the possibility that
such an association might exist led us to
examine all subjects in our group of 3 1 patients
carefully for the presence of neuropsychiatric
dysfunction. In addition, because hypovitaminosis
B12 has been suggested as a
cause of neuropsychiatnic injury in patients
with prior gastric surgery (5 1, 52), we measured
serum levels of vitamin B12, in every
patient with neuropsychiatric dysfunction. Of
24 patients with alimentary hypoglycemia, 10
had serious neuropsychiatric dysfunction
(Table 4). These complications included personality
change with unusual irritability and
diminished ability to think, memory lapses,
presenile dementia, dysarthria, and seizures.
At least six patients were initially referred for
study by neurologists or psychiatrists. In cvcry
case, except the patient with seizure disorder,
the neuropsychiatric dysfunction either
occurred or worsened during the hypoglycemic
phase of an oral glucose tolerance test,
as noted in Table 4 and, by history, occurred
more than I hr after eating. The patient with
seizure disorder was noted to have a plasma
glucose concentration of 36 mg/dljust before
grand mal seizure. This prevalence of alimentary
hypoglycemia and neuropsychiatric dysfunction
in our group of patients with prior
gastric surgery should increase concern about
the association of these two problems.
The glucose tolerance in alimentary
hypoglycemia
A rapid and often excessive increase in
plasma glucose levels occurs soon after glucose
ingestion in patients with prior gastric
surgery (8, 9, 11, 22-25, 56-59). In prior
studies, peak plasma glucose levels have usually
been noted 30 to 60 mm after glucose
ingestion. Among the 31 patients we have
evaluated after gastric surgery by glucose tolerance
tests, the peak plasma glucose level
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2108 LEICHTER
TABLE 4
Neuropsychiatric dysfunction in study patients
Age
and
sex
Type
of
,,
surgery
Symptoms
Lowest , glucose
' Vitamin
Bı
mg/di pg/mi
60 M V & P Decreased concentration 43 970
62 F V & P Memory lapses 45 440
49 F V & P Irritability 50 490
49 F V & P Dysarthria, memory lapses 27 410
45 M V & P Irritability, unconsciousness
39 460
45 M BI Seizure disorder 44 380
65 M BII Presenile dementia 50 700
53 M BII Presenile dementia 47 330
54 M BlI Irritability 46 480
59 M BIl Memory lapses 27 250
"The lowest a V & P represents vagotomy and pyloroplast; BI represents Billroth I; BII represents Billroth II.
plasma glucose level noted during the control OG1'T. cSerum vitamin B12 concentration.
occurred 30 mm after glucose ingestion in 11
patients (35.5%), and 60 mm after ingesting
glucose in 19 (6 1.2%). A peak level was observed
more than 60 mm after glucose ingestion
in only 1 patient, at 90 miii. Based on
available criteria (10), hyperglycemia was
common in our group ofpatients (9), as it has
been in other series (24, 57). After glucose
ingestion, 26 of our 3 1 patients had plasma
glucose levels, which exceeded "normal" values
according to the criteria of the United
States Public Health Service Consultants
( 10). However, none of our subjects had fasting
hyperglycemia, and diagnostic criteria for
diabetes mellitus were fulfilled on only one
case. As we have reported (9), the peak
plasma glucose level, during a glucose tolerance
test, tended to be higher in patients with
a Billroth gastrectomy than in patients with
vagotomy and pyloroplasty. This observation
has been made by other investigators (24).
Moreover, the rate at which plasma glucose
rose in our patients after ingesting glucose
was somewhat greater in those with gastrectomy,
3.63 ± 0.7 mg glucose/dl/min than in
those with vagotomy and pyloroplasty, 2.68
± 0.3 mg glucose/dl/min, although this diffenence
was not statistically significant.
Insulin secretion during the control
OGTT's was also abnormal in most patients.
As reported in other studies (8, 9, 24, 25, 56-
59), glucose ingestion provoked a significant
and excessive increase in serum insulin levels
in most subjects. Of our 3 1 patients in this
study, 94% of the hypoglycemic subjects, had
serum insulin levels exceeding 100 zU/ml,
and 61% had serum insulin levels exceeding
150 ı.tU/ml. Peak serum insulin levels in normal
subjects are usually less than 100 ıtU/ml
after glucose ingestion (60-62). In addition,
the interval between glucose ingestion and
the peak serum insulin levels may be longer
in patients with gastric surgery than in normal
subjects. Whereas peak serum insulin levels
in normal subjects usually occur 30 to 60 min
after glucose ingestion (60-62), the peak serum
insulin levels occurred 60 to 120 min
after glucose ingestion in the majority of our
patients (Table 3).
Intravenous glucose tolerance tests of endogenous
glucose utilization (63), may also
be abnormal in postgastric surgery patients.
Of the available studies on endogenous glucose
utilization in these patients, two of three
have noted that glucose utilization appears to
be diminished (9, 64, 65); however, the intravenous
glucose tolerance tests did not predict
the occurrence of any abnormalities in oral
glucose tolerance tests. Thus, what derangements
are indicated by intravenous glucose
tests in patients after gastric surgery are unknown.
Etiology of alimentary hypoglycemia
The rapid "dumping" ofcarbohydrate into
the upper small intestine of patients with
prior gastric surgery, the rapid absorption of
glucose, and the consequent (early) hyperglycemia
have been assumed to cause reactive
hyperinsulinemia and alimentary hypoglycemia
(2, 4, 14, 17, 22, 66, 67). Prior studies
have shown that gastric emptying is more
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ALIMENTARY HYPOGLYCEMIA 2109
rapid in these patients (22, 66, 67), that glucose
absorption may be more rapid (9), and
that hyperglycemia after glucose ingestion is
common (8, 9, 1 1, 22-25, 56-59). A correlation
between the degree of hyperglycemia,
the degree of hyperinsulinemia, and the severity
of alimentary hypoglycemia has been
suggested (59).
More recent studies have suggested that
these relationships may be more complex
than previously supposed. The role of glucose
in stimulating insulin secretion in these subjects
is well-accepted, but glucose may not be
the only physiologically important stimulus
of insulin secretion. No correlations between
early hyperglycemia and either hyperinsulinemia
or late hypoglycemia in patients with
alimentary hypoglycemia have been observed
(9, 24), although, correlations between early
hyperinsulinemia and late hypoglycemia may
be demonstrated (9). Not all subjects who
have early hyperglycemia have late hypoglycemia
after glucose ingestion (56, 58). Patients
with Billroth gastrectorny, who tend to have
more severe early hyperglycemia than patients
with vagotorny and pyloroplasty do not
have a higher prevalence of alimentary hypoglycemia
(24). The same concentration of
glucose, infused intrajejunally to either normal
persons or patients with previous gastric
surgery causes a greater release of insulin
than with intravenous infusion, although
plasma glucose levels are higher after the
glucose load is infused intravenously (58).
These data, and similar results in other studies
(12), have suggested that factors released
by the intestine after glucose ingestion act,
with glucose, to stimulate insulin secretion.
At least some of these insulinotrophic factons
have now been identified, and an insulinotrophic
role has been proposed for still
others, but not confirmed. Interest has focused
on glucagon-like, gastrointestinal hormones,
such as gastric inhabitory polypeptide
(GIP) (68, 69), enteroglucagon (GLI) (68, 69),
and secretin (70). In addition, insulinotrophic
activity has been proposed for cholecystokinm
(71). GIP has been studied extensively
(72). It is released in normal subjects after
glucose (72, 73) or fat ingestion (72, 74). It
appears to be hypersecreted in patients after
gastric surgery, given oral glucose (75). The
possible hypersecretion of GIP after glucose
ingestion in patients with prior gastric surgery
may be related to the specificity of glucose
versus other sugars as a stimulus for GIP
release (76), and to the greater secretory capacity
for GIP of the upper versus the lower
small intestine (77). Thus, ingested glucose
may be dumped into the disrupted, GIP-nich
upper small intestine more rapidly in persons
with prior gastric surgery than in normal
subjects. The hypersecretion ofGIP may participate
in stimulating the hyper-release of
insulin that follows glucose ingestion in these
patients. In the presence of hyperglycemia,
GIP stimulates insulin release (78-8 1) and
may partly account for insulin secretion after
glucose ingestion in various subjects (72). Essentially
the same schema may be proposed
for GLI innormal subjects or in patients with
previous gastric surgery (82-85), although
GLI has not been studied in as much detail
as GIP. The insulinotrophic actions of other
gastrointestinal hormones, such as secretin
(70, 86-90), cholecystokinin (7 1), or gastrin
(91, 92) are not well established, and the
secretory patterns of these hormones with the
ingestion ofvarious nutrients by patients after
gastric surgery are unclear. Additionally,
there are some gastrointestinal factors, such
as neurotensin (93), substance-P (93), or somatostatin
(94) which may inhibit insulin
release in normal subjects. The secretion of
these factors in postgastric surgery patients is
unknown. Thus, enteric hormones appear to
participate, with glucose, in the hyperstimulation
of insulin release after glucose ingestion
by patients with previous gastric surgery.
GIP and GLI have already ben implicated in
these enteropancreatic events. The list of gastnointestinal
hormones involved in alimentary
hypoglycemia will probably enlarge.
Dietary therapy of alimentary hypoglycemia
Concepts about the therapy of alimentary
hypoglycemia may be changing. The mainstay
of therapy for this hypoglycemia continues
to be dietary. Until recently, low carbohydrate
diets were uniformly advocated (1-5,
95). Concern about the efficacy of these diets
was first raised by investigators, who noted
that patients often failed to adhere to them
(96, 97). However, many investigators have
now demonstrated that diets high in complex
carbohydrates and dietary fiber may improve
rather than worsen glucose tolerance in various
disorders including alimentary hypogly-
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2110 LEICHTER
cemia (98), reactive hypoglycemia (99), and
diabetes mellitus (100-102). They may also
improve glucose tolerance in normal subjects
(100). The mechanism(s) for this therapeutic
effect of diets high in fiber and complex
carbohydrates in patients with alimentary hypoglycemia
is unclear, but may involve the
"trapping" of low molecular weight carbohydrates
in a viscous gel formed by the fiber
and complex carbohydrate (103). Significant
biochemical and symptomatic improvement
may also be due to a decrease in the simple
sugar content in this diet, with an associated
decrease in the postprandial release of insulinotrophic
enteric hormones. We have
treated 21 ofour patients with a diet, designed
to eliminate concentrated simple sugars, but
with 50 to 55% complex carbohydrate. This
diet is somewhat similar to diets high in fiber
and complex carbohydrate, but it does cxdude
certain foods, as fruits, which are not
restricted in the high-fiber diets, and the fiber
content is not purposefully increased. Of our
21 patients, with alimentary hypoglycemia,
15 had been following a low-carbohydrate
diet, with 40% or less of their calories as
carbohydrates, before our evaluation. We estimated
the effects of each diet on the frequency
of symptomatic episodes of hypoglycemia
experienced by the patients during a 1-
week period. By these subjective criteria, the
diet low in simple sugar was superior to the
low-carbohydrate (Table 5). In addition, we
were able to reproducibly provoke episodes
of alimentary hypoglycemia in some of our
patients by feeding them one of the foods
restricted by the diet, such as sweets, oranges,
or commercial peanut butter with a high
sugar content. These observations, which
may have been influenced by patient or investigator
bias, were nevertheless dramatic in
many cases. Future studies on diet and alimentary
hypoglycemia may wish to distinguish
whether restriction of simple sugar, increase
in fiber or in complex carbohydrate or
combinations of these factors mediate the
beneficial effects, which have now been ascribed
to the dietary fiber in high fiber-high
complex carbohydrate diets.
Drug therapy for alimentary hypoglycemia
An accepted drug therapy for alimentary
hypoglycemia has not been established, although
the use of a number of pharmacological
agents has been suggested. Sulfonylureas
(57, 104, 105), cyproheptadine ( 104), phenformin
( 12, 106), diphenylhydantoin (106),
and propranolol (8) have all been tested in
small groups of patients. Phenformin is now
unavailable, and cyproheptadine, which has
been used to control postprandial diarrhea,
has never been tested specifically for treatment
of alimentary hypoglycemia. As an inhibitor
of cortisol secretion (33), cyproheptadine
may not have beneficial effects in alimentary
hypoglycemia. Diphenyihydantoin
may be a useful therapeutic agent, but it has
been tested in only a few patients. Some
improvements in alimentary hypoglycemia
has been noted in small groups of patients
treated with sulfonylureas, but the mechanisms
by which these drugs act in alimentary
hypoglycemia are unknown, and concern
about their safety (107), may have limited
more detailed clinical investigation of their
use. We previously reported biochemical and
symptomatic improvement in 10 patients
treated with propranolol before glucose
ingestion (8), and have now studied a total of
20 subjects by the same methods (8). We
continue to note a significant increase in the
lowest plasma glucose observed after glucose
ingestion (Table 6). However, the mechanism
for this effect of propranolol is unclear. No
TABLE 5
Subjective response of symptomatic patients to a
low-carbohydrate diet or a diet fr cc of concentrated sugars"
Diet No improvement
Subjective response
partial improvement
Adequate improvement
Low-carbohydrate 13 2 0
Low-concentrated 2 8 11
sugar
x2 = 22.29 P < 0.005
a Responses were graded as: "no improvement"-an equal number of symptomatic episodes on each diet; partial
improvement-the frequency of symptomatic episodes decreased by at least 50% with institution of the diet;
"adequate improvement"-no symptomatic episodes were noted by the patient.
Downloaded from www.ajcn.org by on November 16, 2006
Parameter Control OG1'T OGTT + propanolol P
Lowest plasma glucose" 47.6 ± 4.8 60.9 ± 3.7
Thanks Wil ... I have an appt with the endocrinologist on the 11th ... my OGTT showed my BS level at 36 after the first hour and 64 the second, plus my insulin levels were high ... this test was done a month or so after I had a seizure, and the paramedics measured my blood sugar at 23.
I've been collecting as much as I can on this, and I plan to bring all this to him when I see him.
Karyn
I don't think it's dumping because I get it when I don't eat. I have tested my sugars when I feel this way and they're really low.
I especially notice this in the mid morning if I ate cereal or oatmeal (and not protein) for breakfast. If I drink a protein shake or eat a protein bar or just protein, I'm fine. If not, I feel like I'm going to pass out.
I have a protein snack ready for mid-afternoon and later evening as well.
My doctor is experimenting with this surgery on non-obese people who are diabetic because it seems to cure diabetes. I didn't have diabetes before hand, so I just figure it makes our sugars go even lower.
Your sugars may be normal when you get tested, but test them sometime when you feel this way. Mine were in the 40s and 50s, but after eating protein, they go back to normal.
Take care
Joni
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