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Aspartame Creates Diabetic And Obesity |
From Dr. Betty Martini, D.Hum |
DIABETIC EPIDEMIC: Dr. Woodrow Monte in "While Science
Sleeps: A Sweetener Kills" said on
page 10, "Recently, during a study of over six thousand individuals
performed in six widely dispersed clinics in the United States, it was revealed
that the consumption of at least one 12 ounce can of diet soda a day for four
years was associated with a statistically significant sixty-seven percent
increased risk of type II diabetes." Diabetics abstaining from aspartame see so
many of their medical problems disappearing that were caused by this
poison. Then they say, "so what do I use now as a
sweetener?" I had this conversation with Mike Sylver many years ago
who grew herbs in the DIABETES MELLITUS Patients
with diabetes mellitus and "potential" diabetes currently consume
large amounts of aspartame products with the enthusiastic approval of their
physicians and dietitians. A popular aspartame tabletop sweetener containing
less than one gram of carbohydrate and four calories per packet is widely
recommended as a "free exchange." Multicolored ads for other
aspartame products focusing on diabetes appear in professional journals and lay
publications. Observations
involving 118 diabetic aspartame reactors (10 percent) in this series suggest the
need for caution. They indicate that aspartame
may adversely influence the control of diabetes, precipitate clinical diabetes,
and aggravate or simulate complications referable to the eyes, kidneys, and
peripheral nerves. Such
concern is reinforced by a report from The Centers for Disease Control
indicating a dramatic rise of diabetes among the adult population - from 6.5
percent in 1998 to 6.9 percent in 1999. Moreover, it involved almost every
demographic category (race; age groups). The CDC projected that the number of
Americans so afflicted will increase from 16 million to 22 million in 2025. The
initial 60 diabetics who completed the questionnaire fell into the following
categories (Roberts 1990). _____________________________________________________________________________________ Acronym Legend ACB
- aspartame cola beverage ASD
- aspartame soft drink ATS
- aspartame tabletop sweetener Group A
- 18 patients with untreated diabetes who developed high fasting blood glucose
concentrations (greater than 140 mg %) Group B
- 25 patients on insulin and diet Group C
- 17 patients on oral drugs and diet The
following clinical encounters deserve attention, and will be amplified in the
ensuing discussion. ·
Aspartame reactors
being treated with insulin or an oral drug sometimes could not decide if they
were experiencing a reaction to insulin or to aspartame. ·
Several
insulin-dependent diabetics seemed more prone to aspartame-induced convulsions-
both grand mal (see Case III-24) and petit mal (see Case III-25). ·
Insulin resistance and
diabetic control tended to improve promptly after avoiding aspartame products. ·
Questions arose about
missed or doubled dosages of insulin or oral drugs due to aspartame-induced
confusion (Chapter VI). ·
A few of my diabetic
patients (not included in this series) had abstained from aspartame before I
queried them about its use because they already had concluded that it
aggravated their condition. ·
Aspartame addiction
(Chapter VII - G) compounded the problem when diabetics used these products to
get their "sugar fix." A. PRECIPITATION OF CLINICAL DIABETES Several
patients whom the author had followed for years evidenced a prior diabetic
response ("decreased glucose tolerance") by glucose tolerance testing
- that is, their blood glucose concentrations after drinking a glucose load
exceeded 200 mg percent. On an appropriate diet, the fasting blood sugar (FBS)
concentrations remained normal (115 mg percent or less) or only slightly
elevated. Their subsequent elevated values (hyperglycemia), along with weakness
and other symptoms of diabetes, proved puzzling until it was ascertained they
used aspartame products. Clinical and biochemical improvements occurred when
such products were stopped. In
addition, some patients with longstanding reactive hypoglycemia were founded to
have fasting hyperglycemia for the first time after consuming aspartame (see
Case XIII-2 and XIII-3). Their FBS values then normalized after abstinence. Three
aspartame reactors developed diabetes after attacks of apparent aspartame
induced pancreatitis (Chapter IX-D). Case XIII-4 illustrates this sequence. Representative
Case Reports Case
XIII-1 A
47-year-old man with hemochromatosis or iron storage disease had been attended
several years. (This condition is also known as "bronze diabetes"
because iron deposits in the pancreas can damage the islet cells that produce
insulin.) When seen in July 1986, his FBS had risen to 159 mg percent. On
direct inquiry, he stated that he had been drinking considerable aspartame
sodas. The FBS declined to 97 mg percent three weeks after abstinence. Case
XIII-2 A
75-year-old woman had documented reactive hypoglycemia; her blood glucose
declined to 45 mg percent during a prior glucose tolerance test. She presented
in September 1986 with recurrent conjunctivitis over the past 1-1/2 years.
Three ophthalmologists prescribed local antibiotics without benefit. This
patient had been consuming large amounts of pudding and other products
containing aspartame. The FBS was now 143 mg percent. The hemoglobin A,C
concentration (an indicator of sustained blood glucose elevations) was 14.3
(normal 4-6). After stopping aspartame, her FBS progressively dropped to 119 mg
percent within one month. Concomitantly, the hemoglobin A,C decreased to 6.1. Case
XIII-3 A
78-year-old man had been treated since 1958 for reactive hypoglycemia
associated with a prior gastrectomy. He had developed an unexplained
arthoropathy involving the right elbow that was not gout. (The uric acid
concentration was normal.) This attack subsided within several days of
conservative therapy. His FBS was found to be repeatedly elevated - 156 mg
percent on 8/3/87, and 16 mg percent on 8/10/87. A mid afternoon blood glucose
concentration on 8/10/87, however, was only 65 mg percent. When asked about
aspartame use, he stated that he recently had been consuming large amounts of
diet root beer and diet cola. These were discontinued and replaced by his
customary interval snacks. A repeat FBS one week later was 118 mg percent. Case
XIII-4 A
62-year-old beautician began drinking aspartame soft drinks and pre-sweetened
tea to lose weight. She subsequently experienced severe abdominal pain
"under the rib cage on the left side." It became so intense that she
pressed both fists against the abdominal wall seeking relief. Bicarbonate of
soda afforded no benefit. There also was intense nausea, severe abdominal
bloat, and blood in the stools. Two
months after the onset of aspartame use, a physician found her FBS to be 435 mg
percent. It had been normal (100 mg percent) one year previously. She craved
sweet cider while consuming aspartame. A
diagnosis of pancreatitis was made. The patient continued to suffer these
symptoms while receiving cimetidine ("Tagamet") and an antacid in the
hospital. She then deduced that her problems might be related to aspartame in
her "diabetic diet," and demanded it be discontinued.
Thereafter, "my hurting left and my sugar was regulated." This
patient had a history of asthma, hypoglycemia attacks, and allergy to
penicillin. Her children also were aspartame reactors - a daughter suffering
abdominal distention and eye-ear problems, and her son aspartame-induced
headaches. B. LOSS OF DIABETES CONTROL WHILE ON
INSULIN THERAPY Twenty-three
diabetic patients among the first 551 aspartame reactors had been controlled
for considerable periods on diet and one or several doses of insulin daily.
Subsequently, they were found to have a persistent increase of the blood
glucose concentration (by home glucose monitoring) in the absence of
intercurrent infection or other problems conducive to loss of control.
Inquiries about aspartame revealed a moderate or large intake of diet sodas and
foods. Shortly after avoiding aspartame products, their glucose concentrations
generally declined, enabling a reduction in dosage of insulin. The
vicious cycle of poor diabetic control with superimposed aspartame-associated
infection and resistance to insulin was described in Chapter IX-H. The
experience of couples in whom both spouses were diabetic proved
impressive. Cases XIII-16 and XIII-17 illustrate such an "aspartame
diet." Comparable
problems in controlling diabetes surfaced in the form of questions sent
syndicated medical columnists. For example, a diabetic asked Dr. Neil Solomon
if there was a relationship between starting to drink diet soft drinks and
difficulty in controlling his blood sugar(The
Miami Herald October 8, 1986, p. D-2). Insulin-dependent
diabetic patients may have another superimposed problem of biotechnology: the
increase of side effects from genetically-engineered recombinant human insulin.
They include arthritic complaints, weight gain, and reduced hypoglycemia
awareness. Representative
Case Reports Case
XIII-5 A
61-year-old woman required hospitalization for readjustment of her insulin
dosage due to the loss of diabetes control even though she adhered carefully to
a "diabetic diet" and other measures. She also had been experiencing
intense dizziness, headache and progressive loss of memory. Considerable
aspartame product were being used as part of the recommended diet. The
patient then discovered her intolerance for aspartame products. "A
nurse told me about listening to you on radio station WWMR-FM, and gave me the
gist of your comments on aspartame
and its side effects. My diabetes is under better control since I have completely stopped using anything with
aspartame. I am feeling better. The dizziness is gone. The headaches are fewer, and I think my memory is
keener than it was even thought it has
only been three weeks." Case
XIII-6 A
think young woman with insulin-dependent diabetes described the severe
exacerbation of her visual and neuropathic symptoms, along with loss of
diabetes control, while consuming aspartame products. Her insulin requirement
had increased to 110 units daily. When she avoided aspartame, the visual and
neuropathic symptoms disappeared, and the insulin dosage could be decreased to
12 units daily. Case
XIII-7 A
59-year-old diabetic man had required 20 units of an intermediate-acting
insulin daily for many years. His insulin requirements more than doubled when
"my sugar ran out of control" after consuming three liters of diet
cola daily. Case
XIII-8 A
12-year-old diabetic boy required multiple hospitalizations while consuming
considerable aspartame. He was twice admitted in diabetic coma. The physicians
at a university hospital encountered considerable difficulty in stabilizing his
insulin dosage during the periods aspartame were taken. Case
XIII-9 A
46-year-old interior designer had maintained good control of insulin-dependent
diabetic for three decades. He then consumed several aspartame soft drinks and
up to five packets of an ATS daily. "At that point, my diabetes went
haywire, and I had terrible insulin reactions." Control of diabetes
reverted to its previous status within one week after stopping aspartame
products. Case XIII-10 A
45-year-old obese woman required hospitalization for uncontrolled diabetes. She
improved on an appropriate diet and split doses of insulin, with virtual
normalization of her fasting and random blood glucose values over several
weeks. Prior to that time, she had not consumed aspartame products. In
a subsequent visit, the patient complained of extreme sleepiness, fatigue,
depression and intense sweats. Her FBS concentrations now ranged up to 160 mg
percent, and the blood pressure had risen to 180/112. When asked about
aspartame use, she stated that she began drinking considerable amounts of diet
sodas on the advice of a dietitian. Five days after stopping all aspartame
products, without any change in insulin dosage, the FBS values averaged 130 mg
percent and the afternoon glucose values ranged from 90-120 mg percent.
Concomitantly, her blood pressure declined to 155/90. Case
XIII-11 This
80-year-old active diabetic had been controlled on diet and tolbutamide
(Orinase) for several years. She then was shifted to insulin because of elevate
blood glucose concentrations that persistently exceeded 200 mg percent. The
dosage of insulin had to be increased over the ensuing eleven months from 12
units to 28 units. Her FBS on 8/14/86 was 230 mg percent. She also experienced
severe headaches. This
patient happened to hear my discussion about aspartame disease, and stopped
using it. The headaches promptly disappeared. Her FBS declined to 101 mg
percent within two weeks, at which point the insulin dosage was reduced. Case
XIII-12 An
elderly diabetic woman had been doing well on 10-12 unit NPH insulin before
breakfast, and 6-8 units NPH before her evening meal. The FBS progressively
rose to 209-214 mg percent over the next five months, notwithstanding several
increases of the insulin dosage. No infection or other contributory factor
could be uncovered. Within five days after discontinuing aspartame, her FBS
declined to 110 mg percent, and the insulin dosage reverted to her prior
requirements. Case
XIII-13 A
48-year-old insulin-dependent diabetic began using aspartame products to avoid
sugar. She reported, "It increased my blood sugar, making it necessary to
take an extra shot of insulin to counteract it." Associated nausea and
extreme irritability interfered with her performance as a teacher. She had a
longstanding allergy to penicillin. Her daughter also experienced severe nausea
and dizziness after ingesting aspartame. Case
XIV-14 An
insulin-dependent diabetic described her problems with aspartame in these
terms: "When
using this sweetener, I have increased blood sugar, and more difficulty controlling the diabetes. It
also caused a more rapid heartbeat. I am fighting to get this sweetener out of everything!
There is not a diabetic 'treat' I can have because they are loaded with this sweetener. That
includes diet pop." Case
XIII-15 A
67-year old insulin-dependent diabetic woman presented with severe headache,
leg pains, and lightheadedness. These complaints disappeared after avoiding
aspartame for three weeks. The previously unexplained rise of her FBS (from
130-165 mg percent to 313-331 mg percent) declined to 131 mg percent. The blood
glucose concentration after breakfast now did not exceed 191 mg percent. Case
XIII-16 A
husband shifted to diet colas when diabetes was diagnosed, and "got used
to the taste" in the transition from regular cola. Symptomatic retinopathy
with retinal bleeding subsequently developed. He also suffered severe joint
pain, and non-healing of a sore. Learning about aspartame disease, he
discontinued such products. "Within a month, the numbness in my hands was
gone, the sore on my right index finger healed (and has not come back), and my
joints don't hurt anymore." Case
XIII-17 The
diabetic wife of Case XIII-16 had been unable to maintain her blood glucose
level below 200 mg percent for several years despite exercise and trying to
lose weight. Observing the beneficial effect of aspartame avoidance in her
husband, she also abstained. Within two weeks, she lost fifteen pounds, coupled
with a decline of her blood glucose to 152 mg percent. C. POOR CONTROL ON ORAL DRUGS FOR
DIABETES More
than a score of non-insulin-dependent diabetics who were being treated with
oral hypoglycemic drugs unexpectedly manifested high morning and afternoon
blood glucose concentrations while consuming aspartame drugs. Representative
Case Reports Case
XIII-18 A
67-year-old diabetic woman had been maintained relatively well on diet and
tolazamide (Tolinase). Her blood glucose concentrations increased during August
1986 - the morning values ranging from 180-247 mg percent, and the afternoon
values up to 248 mg percent. During this period, she was taking two to three
diet colas and other aspartame products daily. Fungal involvement of a thumb
(reflecting loss of diabetic control) also developed. The
patient then stopped aspartame. She felt much improved one week later. The nail
infection already had begun to improve. Her serial FBS values were now 108,
106, and 108 and 82 mg percent. The pre-supper values were 198, 64, 94, and 82
mg percent. Case
XIII-19 A
prominent engineer sent the following letter to Aspartame Victims and Their
Friends. "I
am a Type II (adult onset) diabetic. I am normally able to keep my blood sugar
under reasonable control with the use
of oral medication. "When
an aspartame tabletop sweetener first appeared on the market, I purchased the pre-prepared packets to use in
place of the saccharin sweetener I had been using. I had concern about saccharin due to
its reported carcinogenic effects. "Very
shortly after beginning aspartame, my blood sugar jumped to 268, then to 351, 321, and 333 over a period of 18 days.
Suspecting that this sweetener might be the cause of the rapid rise in blood
sugar, I discontinued its use. My blood sugar dropped back to 200 in six days. I am
still controlling it within an acceptable range three years later. "The
doctor to whom I was going to at the time of this surge ridiculed the idea that
such a small amount of aspartame could trigger
this dramatic effect in my blood sugar. I
changed doctors shortly thereafter. I am personally convinced that the
usage of aspartame was the cause of my
high blood sugars. "I
have definite knowledge of one Type I diabetic on insulin who was using the
same tabletop sweetener and monitoring his blood
sugar. When he visited his doctor, the test (as run by the laboratory)
showed his blood sugar to be out of control. "I
try to avoid aspartame in any form, and am very disturbed by its presence in so
many products." Case
XIII-20 A
51-year old stockbroker began consuming one can of diet cola and two packets of
an ATS daily after diabetes was diagnosed. Even though he conscientiously
followed a diet and took tolbutamide, there was difficulty in controlling his
blood glucose concentrations. He also developed marked ringing in the left ear,
"distorted vision" in the left eye (attributed to "macular
degeneration of unexplained cause"), severe drowsiness, memory loss, and a
marked personality change. Case
XIII-21 A
48-year-old truck driver saw the author in consultation for poorly controlled
diabetes, intense neuropathic discomfort of the feet and left hand, and
progressive blurring of vision. The latter had been attributed to "some
oozing in the right eye." His FBS on tolbutamide was 278 mg percent; a
random blood glucose was 178 mg percent. The total serum cholesterol (normal,
over 35 mg percent), and the triglyceride level 1,468 mg percent (normal, up to
160 mg percent). The
patient was drinking four diet sodas daily. He had not ingested alcohol for
several years. Striking improvement of vision
was noted within less than one week after stopping aspartame, especially
the absence of a blur while driving. His FBS declined to 146-163 mg percent
within one week. Concomitantly, the blood pressure decreased from 150/100 to
134/84. There was subsequent improvement of the neuropathic symptoms, and a
lowering of his cholesterol to 192 mg percent, and triglyceride to 273 mg percent. D. REACTIONS TO INSLUIN AND ORAL DRUGS Many
diabetics noted a greater tendency to insulin reactions/hypoglycemia while
using aspartame products. Insulin Several
diabetic patients unequivocally attributed more frequent and severe insulin
reactions to the use of aspartame. A contributory factor in some may have been
marked confusion and memory loss (Chapter VI-C), causing them to repeat doses
of insulin or to forget their interval feedings. Representative
Case Reports Case
XIII-23 A
41-year old housewife developed insulin-dependent diabetes at the age of 22.
Its control had become a problem the previous five years because of frequent
and severe insulin reactions. Her husband at times had to force-feed her. This
posed a considerable challenge inasmuch as aggression and "complete
obstinance" characterized her attacks. Concomitant problems included
weight gain, bloat, fluid retention, marked personality changes, and a striking
loss of short-term memory. She
consumed considerable amount of aspartame products - including sodas (averaging
two liters daily), hot drinks, chewing gum, mints, and diet hot chocolate. Case
XIII-24 A
36-year-old woman with insulin-dependent diabetes (25 years) initially had
denied any contributory role of aspartame products because she left that the
negative allegations were "reactionary." Moreover, a dietitian told
her they were "perfectly safe." As a result, "I just went wild
eating it in everything." She wrote "My
blood pressure went from difficult to horrible. My appetite was running
rampant. I was waking up with 500 blood
sugars, and also going to lows of 35-40. No one could figure out what
was wrong with me. I didn't want to have sex with y husband. I even began
having hot flashes. I had some minor tingling, which I always passed off as
'just one of those diabetic things.' I was gaining weight, feeling
uncoordinated and spacey, and felt like hell. "I
then remembered the correspondence about aspartame, and decided to give it up
as a trial. The next day, my blood sugars
were perfect, as they have been now for almost two weeks. It is uncanny. I am so beside
myself with glee I can hardly stand it. My insulin dosage has gone from 37 units to 17 units
daily. I have, simply put, been reborn." Case
XIII-25 A
37-year old woman was diagnosed as having diabetes seven years previously. She
then began using aspartame products. There was a strong family history of
diabetes. The
patient experienced many unexplained symptoms. Her family physician and
endocrinologist initially attributed them to her diabetes medication. They
included confusion, loss of memory, anxiety attacks, unexplained chest pains,
headache, dizziness, joint pains, weight loss, and drastic declines of the
blood glucose concentration... at times with loss of consciousness. Her family
had to stay with her constantly, and feed her frequently. She wrote,
"Without warning, I was fine one minute, and the next minute the room
would be spinning and I was looking for a place to lay down. It was like being
in a dream or fog. I even had to leave work." She
stopped all aspartame products when a friend sent her an article about
aspartame disease. Dramatic improvement ensued. "I had to leave work due to blood sugar levels
dropping. My loved ones haven't had to feed me or be with me. I haven't had to
drive in a mental fog. I haven't had nearly as many headaches, joint aches or
dizzy spells." Case
XIII-26 A
businessman expressed appreciation for being informed about the probable role
of aspartame disease relative to his problems with diabetes and memory loss. "I
am a diabetic who consumes large amounts of sugar-free beverages containing aspartame.
For about three months, I have been experiencing a loss of memory the following
ways: a. About
five days per week I will forget if I ate lunch that day. When I get home in
the evening, I will be ravished, but I don't know if or what I ate. This is
dangerous for a diabetic on insulin who should be eating three meals on time to
balance the insulin dosage. b. I
will see people I've known for years, but cannot remember their names." Case
XIII-27 A
21-year-old insulin-dependent teacher suffered more frequent insulin reactions
(both at work and at home) while consuming 15 or more cans of aspartame colas
daily. He stated, "When we cut down on aspartame, I stopped having so many
reactions." Oral
Drugs Type
II diabetic patients who did not receive insulin by injection also experienced
more frequent and sever hypoglycemic attacks while consuming aspartame
products. Representative Case Report Case
XIII-28 A
diabetic woman had been controlled on diet and tolazamide. During the two years
she consumed aspartame, her FBS values decreased. She then suffered grand mal
seizures and transient paralysis on one side. Swelling of the mouth and tongue
also occurred on two occasions after taking aspartame. Her condition stabilized
on the prior regimen after avoiding aspartame, with no recurrence of the
seizures or mouth reactions. E. REAL OR SIMLUATED DIABETES COMPLICATIONS Diabetic
patients who react to aspartame products face an additional major problem: the
aggravation or simulation of diabetes complications - namely, neuropathy,
retinopathy, and nephropathy (kidney involvement). In turn, failure to
recognize aspartame disease invites needless or hazardous treatments, including
eye (laser) surgery. Erroneous
Diagnoses The
role of aspartame disease relative to visual impairment (Chapter IV), headache
(Chapter V), dizziness (Chapter VI-B), limb pain (Chapter VI-H), diarrhea
(Chapter IX-D) became evident when these symptoms abated after aspartame
products were discontinued. ·
Cases IV-25 to IV-29
reported striking and prompt improvement of blurred vision and eye pain after
stopping aspartame. ·
Case I-29 had prompt
improvement of severe difficulty in focusing after abstinence from aspartame,
proving she did not have a suspected symptomatic retinopathy. ·
A diabetic who drank
four liters of aspartame sodas daily complained of severe changes in vision. An
ophthalmologist reassured him that there was no demonstrable retinopathy. After
reading about blindness in an aspartame reactor, he stopped such products...
with marked improvement. ·
75-year-old physician
(reported by Barbara Mullarkey in the Wednesday
Journal of Oak Park & River Forest March 26, 1986, p. 37) had enjoyed
regular sexual activity. Within 10 days of using an ATS for recently diagnosed
diabetes, he noted " a complete and total loss of libido." This might
have been ascribed to diabetic neuropathy except for the fact that his vigorous
sex life returned within six weeks after avoiding aspartame. ·
A diabetic woman
developed agonizing pains "from my knees to y ankles which I was not able
to handle." They began shortly after drinking two cans of an aspartame
beverage. Other symptoms included "large sores over my head, face and
back, plus I was on the verge of fainting and sick all the time." At the
insistence of an physician-daughter, four specialists saw her for a presumed
diabetic neuropathy. The provoking cause could not be determined. The patient
then "took it upon myself to cut out the soft drinks. I was immediately
normal with the exception of my leg pain." ·
Case IV-1, a
66-year-old diabetic man, had been controlled with diet and an oral
hypoglycemia drug. He then experienced temporary "loss of vision" and
pain in both eyes, as well as "dry eyes" requiring the frequent use
of artificial tears. Other complaints included severe drowsiness, decreased
hearing in both ears, itching, and "red blotches." These features
subsided after stopping aspartame, but promptly recurred during one
re-challenge. He abstained from these products thereafter because "I was
afraid I'd go blind." Aggravation
of Diabetic Complications Repeated
reference was made in previous chapters to the aggravation or simulation of
diabetic retinopathy (Chapter IV) and diabetic neuropathy (Chapter VI-E) in
aspartame disease. Mention of this subject on talk shows predictably evoked
calls from diabetic patients about the onset of severe complications when they
began using aspartame products after having been in "good control." The
metabolic stress superimposed upon diabetes by aspartame disease can be
intensified when kidney failure coexists, as in Case XIII-21. (See Introduction
to Section 3). The
aggravation or simulation of neurologic complications by aspartame was
considered in Chapter VI and elsewhere. Suspicion about the diagnosis of
multiple sclerosis in a diabetic consuming considerable aspartame is paramount.
Terms such as "diabetic dementia" and "diabetic encephalopathy"
should raise suspicion about aspartame disease in the case of patients who
consume these products. The variety of other misdiagnoses included
"polyradiculoneuropathy" and the Guillain-Barre syndrome. Hemochromatosis
(iron storage disease; bronze diabetes) might be aggravated in its
pre-cirrhotic state by aspartame through the stimulation of insulin (Chapter
XIV). This association is suggested by Case XIII-I. In addition to
hyperinsulinemia, other evidences of insulin resistance include obesity,
elevated lipids, and abnormal glucose tolerance. The primary action of
transferrin receptors to the cell surface where extracellular iron uptake is
mediated (Ferrannini 2000). Representative
Case Reports Case
XIII-29 A
50-year-old surgeon with diabetes began consuming considerable amounts of diet
sodas. He had to give up surgery and driving when his vision deteriorated to
20/100 in both eyes. Laser therapy was administered to one eye. Once he
discontinued diet drinks, his vision improved to 20/30 and 20/40, and his blood
sugar values were generally normal. Case
XIII-30 During
an interview on Philadelphia Station WWDB, the mother of a 20-year-old diabetic
woman called. She stated that a hemorrhage in one eye of her daughter had
caused virtual blindness notwithstanding careful control of diabetes with
insulin, and severe impairment was beginning in the other eye. This mother had
pleaded with her to reduce or stop the considerable use of diet sodas, but to
no avail. She then wrote "My
suspicions that aspartame might be responsible for losing her sight in the left
eye were raised. I realize that most people, including many physicians I have
spoken to, will blame this on her diabetes. But they have also admitted to me
that her problem as a diabetic who is very well controlled under the care of a
diabetologist, and with regular visits (every six months) to an eye surgeon, is
very unusual. "It all happened so quickly. We are
suffering from shock even though it has been almost a year since she lost all
central vision. One reason for our panic is that now she is experiencing
blurring, etc. in her right eye. I was even afraid to mention any suspicion
about aspartame to the family or friends as I thought they would think me
grasping at straws or just a 'hysterical' mother." Case
XIII-31 This
case, reported to Dr. Richard J. Wurtman of Massachusetts Institute of
Technology, is part of the public record. The
patient had longstanding diabetes with renal failure. A kidney transplant was
unsuccessful, necessitating hemodialysis. She subsequently died at the age of
37. Four
months prior to her death, she began consuming increasingly large amounts of
aspartame-sweetened tea and lemonade. Her mother tried to dissuade her from
doing so after reading about aspartame reactions. The patient, however,
insisted that "it was safe because the F.D.A. had approved it."
Within two months, she experienced severe muscle spasms, slurred speech,
difficulty in swallowing, inability to control the limb muscles, and seizures. The
attending physician stated that he did not know enough "to make a
judgment" about the possible contributory role of aspartame. The parents
thereupon went to the hospital library, and found an article by Dr. Wurtman on
aspartame-induced seizures which they handed to the physician. The mother
subsequently wrote, "I honestly believe that the aspartame may have been
the cause of her seizures. Surely any one with kidney failure would be at high
risk." Increased
Triglyceride and Cholesterol Concentrations Elevated
blood triglyceride and cholesterol concentrations are commonly found in
patients with diabetes. Indeed, they may serve as clues to this underlying
metabolic disturbance. A large literature exists concerning the
impaired ability of diabetics with insulin resistance to metabolize a glucose load
- as reflected by their increased insulin concentrations after meals, and
associated triglyceride elevation. Aspartame
can evoke or aggravate hypertriglyceridemia and hypercholesterolemia, as in
Case XIII-20. The problem may be compounded when high-fiber laxatives containing aspartame are recommended because they
reduced blood cholesterol levels in short-term studies. Case
II-2 evidenced clinical diabetes for the first time after more than two decades
under the author's care. She recently began drinking large amounts of aspartame
beverages. Concomitantly, her triglyceride levels rose to 1,284 mg percent and
1,616 mg percent (normal, up to 160 mg percent) and her serum cholesterol to
354 and 349 mg percent (normal, up to 225 mg percent). These
metabolic aberrations could be viewed as reflections of compensatory, albeit
inefficient, mechanisms whereby the body attempts to provide basic energy needs
for vital organs (Roberts 1964, 1967b, 1964c, 1971b). The superimposed adverse
effects of aspartame are discussed in Section 5. Many
diabetic patients conducted "self-experiments" with aspartame
products, and independently confirmed my observations. A
woman with Type I diabetes decided to "experiment with the use of
aspartame from time to time to satisfy my own curiosity about its effects on my
body." She stated "Invariably, if I use aspartame - just one or two diet sodas per day and a few sticks
of aspartame gum - my former symptoms
of aspartame poisoning return with a vengeance. My blood sugars go haywire.
Only one tiny unit of insulin would drop my blood sugar over 100 points in
under half a hour, sending me into a series of hypoglycemic reactions. Rebound
into high blood sugars followed. The tingling along my spine and under my
breast bone, which had disappeared after I gave up aspartame, returned. And my
menstrual periods, which had been very irregular prior to giving up aspartame
but came every 28 days for three days like clockwork after giving up aspartame,
came on two weeks early, then three weeks early, two days after re-introducing
aspartame into my diet." GENERAL CONSIDERATIONS Public
Health Ramifications The
Center for Disease Control and Prevention reported a striking 33 percent rise
in the incidence of diabetes nationally between 1990 and 1998. While various
factors were incriminated (most notably overweight, stress, fast foods and less
exercise), the possible contributory role of aspartame products was apparently
not considered. Consumption of Aspartame and Sugar by
Diabetics FDA
Commissioner Dr. Frank E. Young testified as to the United States Committee on
Labor and Human Resources on Nov. 3, 1987 that 60 percent of diabetics were
using aspartame products, compared to 35 percent of the total sample
population. Yet, Farkas and Forbes (1965) concluded there was "...no basis
for generalizing on the effect that the use of non-caloric sweeteners has or
will have on adherence to a carbohydrate-restricted diet by patients with
diabetes in the age range of 40 to 70 years." There
has been a paradoxical rise in the consumption of all sugar products over the
past two decades, concomitant with the dramatic increased use of artificial
sweeteners. The Department of Agriculture noted that the per capita consumption
of sugar in 1985 was 130 pounds compared to 118 pounds in 1975. (The
consumption of artificial sweeteners, including aspartame and saccharin, rose
from 6.2 pound in 1975 to 17.0 pounds in 1985). Many diabetics add aspartame to
coffee or tea, which they then proceed to take with cake, pie, or ice cream. The excessive use of aspartame
products helps explain the proneness of women with insulin-dependent diabetes
mellitus (IDDM) to bulimia (Stancin 1989). Such behavior involves self-induced
vomiting, the taking of laxatives, diuretics and enemas, and even the
intentional reduction of insulin in order to lose weight (Chapter IX-B). Legal
Ramifications The
problems considered in this chapter have potential legal ramifications. Special
mention is made of pregnant women, children, older persons, epileptics, and
other high-risk groups. Several examples are cited. ·
An insulin-dependent
diabetic who suffered seizures after using an ATS sued the manufacturer for
alleged breach of an "implied warranty" that these sweeteners were
"fit for ordinary use" (The Grand
Rapids Press March 6, 1986, p. C-6). ·
Aspartame-related
hypoglycemia may have caused or contributed to the "dead-in-bed
syndrome" in diabetics with hypoglycemia unawareness. Diabetes: A Brief Overview Diabetes
mellitus is a chronic disease in which there is insufficient insulin - total or
relative (resistance to insulin action) - for deriving adequate energy from
ingested food. It tends to be familial. There
are more than ten million diabetics in the United States, but less than half
have been formally diagnosed. Most (85 percent) do not require insulin, and are
termed "Type II." Paradoxically, many persons in this category,
especially when overweight, release considerable insulin after taking sugar or
a meal, and then experience reactive hypoglycemia ("low blood sugar
attacks"). I have used the term diabetogenic hyperinsulinism (see
Introduction and Chapter XIV) to describe this transitional phase (Roberts
1964, 196, 1966, 1967, 1968, 1971b, 1973). The remaining 15 percent are
referred t as having "Type I" insulin-dependent or juvenile-type
diabetes. Most
diabetics desire sweets. This may represent an inborn characteristic, an
acquired habit, or both. ·
A survey of 500
diabetic patients conducted in West Germany (cited by Horwitz 1983) revealed
that only 84 could abstain from sweets. ·
A comparable situation
exists among juvenile diabetics. Court (1976) found that 72 percent of mothers
used artificial sweeteners in preparing the meals of their diabetic children to
achieve compliance. The
hazards of aspartame for diabetics require further clarification in light of
statistics concerning premature mortality. The years of potential life lost
(YPLL) increased only for the categories of diabetes mellitus and chronic
obstructive pulmonary disease in the Morbidity
and Mortality Weekly Report (December 1986 Supplement). Mechanisms
of Aspartame's Diabetognic Potential The
adverse metabolic, hormonal, toxic, and other undesirable effects of aspartame
and its components are detailed in Section 5. Many could contribute to the
aggravation of diabetes and its complications. They encompass the wasting of
insulin, impaired insulin-stimulated glucose transport, increased growth
hormone and glucagon release after phenylalanine administration, other effects
of its amino acids (see below), and additional pharmacologic activities.
Another mechanism whereby aspartame-induced stimulation of insulin could
aggravate diabetes involves the generation of insulin receptor antibodies
capable of blocking the access of insulin to liver receptors (Dozio 2001). With
reference to aspartame-induced insomnia (Chapter VI-F), sleep debt has a
detrimental impact on carbohydrate metabolism and endocrine function -
including decreased glucose tolerance, and altered thyrotropin and cortisol
concentrations (Spiegel 1999). Some
of the scientific observations that pertain to the effects of aspartame and its
amino acid components on insulin release, other hormones, and metabolism are
briefly reviewed. ·
Phenylalanine and
aspartic acid might enter the brain of diabetics more readily due to altered
permeability of the blood-brain barrier. They could then aggravate fetal
development during gestational diabetes in conjunction with elevated sorbitol
concentrations because of increased polyol metabolism (Eriksson 1986) -
conducive to eye and neurologic complications ·
Limited insulin
reserves could be further depleted by pancreatitis (Chapter IX) or
phenylalanine-induced pancreatitis stimulation (Chapter XXIV). This and other
amino acids, as well as protein, increase insulin and blood glucose levels.
Years ago, Conn and Newburgh (1936) demonstrated comparable elevations of the
blood sugar in diabetic patients consuming either dextrose or beefsteak. ·
Schusdiziaria et al
(1981) reported that digested gluten elicited a more rapid and significantly
greater rise in postprandial (after a meal) peripheral vein insulin and
glucagon levels than undigested gluten. ·
Wahren et al (1972)
found accelerated splanchnic uptake of amino acids in diabetic patients (24
hours after withdrawal of insulin), compared to healthy controls. This increase
was most notable for phenylalanine, glycine, serine, threonine, methionine, and
tyrosine. ·
Atawa et all (1990)
noted the high frequency of aspartic acid at 57 of the HLA -DQ Beta-chain in
Japanese patients with insulin-dependent diabetes mellitus. ·
Another influence of
phenylalanine and its analogs on glucose and insulin metabolism involves the
binding and activation of glucose-dependent insulinotropic polypeptide (GIP)
receptors by the photoactivable p-benzyl-L-phenylalanine (Yip 1999). GIP, an
important regulator of insulin receptor of the insulin receptor as well as
insulin action on target issues. Sardesai
et al (1987) concluded on the basis of experimental data that aspartame may
adversely influence the control of diabetics. They found that a single dose
of aspartame administered to both normal and streptozotozin-induced diabetic
rats increased liver tryptophan oxygenase by 12 percent. Furthermore, aspartame
decreased blood and brain tryptophan, and increased serum glucose and glucagon
in the diabetic animals. The chronic administration of aspartame to both
groups also resulted in increased tryptophan oxynase activity, hyperglycemia,
and a further rise of glucose in the diabetic animals. Insulin/Hypoglycemia
Reactions The
subject of hypoglycemia reactions in aspartame disease and the mechanisms
involved will be considered in Chapter XIV. Excessive
insulin may be released by aspartame through a reflex mechanism involving the
cephalic phase of insulin release. This is exaggeration of normal
physiology relative to anticipating the arrival of food. It could result in
hypoglycemic symptoms, or aggravation of diabetes mellitus when the binding of
more insulin at cell membranes creates "insulin resistance." Severe caloric restriction and other
forms of metabolic stress in noninsulin-dependent diabetics increases the release
of endorphins and enkephalins. These endogenous peptides with opiate-like
activity have been shown to have important glucose-regulating effects in humans
- notably, significant increases in plasma insulin and glucose concentrations
(Giugliano 1987). Such effects can also lead to clinical hypoglycemia and
insulin resistance. Diabetic
patients who receive increased doses of insulin for "tight control,"
as occurred while using aspartame, are at greater potential risk for the
adverse cerebral consequence of hypoglycemia. This problem is compounded by
reduced release of counter regulatory hormones (epinephrine; growth hormone;
cortisol; glucagon) in response to severe hypoglycemia. These altered counter
regulatory hormonal thresholds in well controlled Type II diabetics, even at
normal blood glucose concentrations (Spyer 2000), can further compound
complications by aspartame-induced hyperinsulinemia. ·
Widom and Simonson
(1990) demonstrated that diabetic patients may develop cognitive impairment before
the onset of symptoms attributable to the release of epinephrine and
norepinephrine. ·
Amiel et al (1991)
reported a threefold increase in the incidence of both severe and asymptomatic
hypoglycemia among diabetic patients treated intensively with insulin.
Furthermore, they are more likely to develop EEG abnormalities during
hypoglycemia. Criticism
of Related Research (see Chapter XXVIII) The
administration of aspartame as capsules to evaluate its effect on diabetic
control, rather than "real world" products, is relevant. This
introduces the deficiency of not invoking the cephalic phase of insulin release
associated with the taste of sweet (see
above). If insulin production is already strained, such suerimposed stimulation
could result in a state termed "high-output failure of
insulinogenesis" (Roberts 1964 ,1965). Professional
Confusion and Disagreement (see Chapter XXVIII) Many
physicians and other health care professionals disagree with the author's
concerns about aspartame use by diabetics. ·
Filer and Stegink
(1989) reviewed aspartame metabolism in diabetic subjects, and concluded
"aspartame may be safely ingested at projected levels of use." (These
investigators received considerable corporate support). ·
John D. Fernstrom,
Ph.D. (1987) opined that the "pros" of aspartame in improving the
quality of life for "millions of diabetics in the population" far
outweigh "any imagined cons" of this and related products. He argued
against wasting effort by "being obsessive about something that isn't
really there." ·
Dr. F. Xavier
Pi-Sunyer, a physician-representative of the American Diabetes Association,
reaffirmed this organization's approval of the safety of aspartame - both for
diabetics and the general population in testimony given in an U.S. Senate
hearing on Nov 3, 1987. He asserted that there had been no significant input
from physicians concerning problems in managing diabetics related to aspartame
use. Moreover, he expressed concern over the unwarranted anxiety created by
this hearing, and objected to spending any more money for research
"already done." Furthermore,
most physicians accept the assertion by diabetologists that aspartame is
harmless for diabetics. ·
Horwitz and
Bauer-Nehrling (1983) concluded that there is "no evidence of alteration
of diabetic control because of aspartame ingestion." ·
Visek (1984) stated
that aspartame does not interfere with the basic treatment of diabetic
patients. ·
Stern et all (1976)
followed 43 non-insulin-dependent diabetics at two centers. They were given
either two capsules of aspartame three times daily with meals, or a comparable
placebo, for 90 days. These investigators stated that "diabetic control
was unaffected by the chronic administration of these substances." The author's interpretation of the
fasting blood sugar (FBS) concentrations in the subgroups of patients treated
and followed at the Jewish Hospital and Medical Center of Brooklyn, based on
the published data, differs from this assessment The FBS values at one, five,
nine, and 14 weeks for the 9-10 patients given aspartame were 115.7, 116.2,
136.5, and 134.9 mg percent, respectively. The FBS values for the placebo group
(ranging in number from 10 to 11) at one, five, nine, and 14 weeks were 88.9,
107.2, 117.7, and 95.5 mg percent, respectively. The P values at one, five,
nine, and 14 weeks were 0.10, >0.50, >0.40, and >0.10, respectively. ·
Nehrling et al (1985)
gave aspartame and an identical-looking placebo containing corn starch to
insulin-dependent and non-insulin-dependent diabetics in a randomized,
double-blind study over an 18-week period. Three capsules were taken with each
meal (total of 9 capsules daily). They concluded that adverse reactions were n
more common with aspartame. These investigators, however, did not compare the
corn starch with an inert non-carbohydrate placebo (e.g. alanine). Moreover,
one subject developed severe diarrhea while receiving aspartame. (It disappeared
when the aspartame was discontinued, and recurred after re-challenge). ·
The inclusion of
monosodium glutamate (MSG) in presumed placebos raises another problem. Resistance The
author asserted in many publications and written testimony to Congress that the
current wholesale ingestion of aspartame products constitute a perceived
"imminent public health hazard," especially for diabetics. Yet the
FDA and the American Diabetes Association (ADA) continue to express the unequivocal
opinion that aspartame is "completely safe" for diabetics. As
a case in point, it has been virtually impossible to present these observations
at national meetings of diabetologists and other physician groups. For example,
the ADA (of which I had been a member for over three decades) refused to print
an abstract of adverse reactions
encountered in 58 diabetics patients that was submitted for its 1987 annual
meeting. Clinical Research
subsequently published (1988; Vol. 3:489A). The
following letter indicates the resistance this subject provokes. The
correspondent, a 60-year-old diabetic woman with many ailments, had a sister
and multiple relatives who suffered severe reactions (including convulsions) to
aspartame products, but defended their use. "How
in the world can someone take a product that is relied upon by diabetics to
live, and make it bad? This was a big hoax. I just wonder how many people are
depriving themselves of a pleasure just because someone scared them into not
using it (an aspartame tabletop sweetener). The
American Diabetes Association approves its use." Patient
Input Diabetic
aspartame reactors have expressed severe disapproval over the continued
recommendation of aspartame products by the American Diabetes Association. Some
averred that this is tantamount to helping diabetics die. Patients
have expressed this attitude in dramatic confrontations with doctors,
even resorting to ridicule (see Case XIII-9). For example, a diabetic patient
with aspartame reactions was dismissed by her physician, "a diabetes
specialist," when she became irate over his lack of knowledge or interest
on the subject - especially after providing him considerable information on
aspartame disease obtained from the Internet. The
virtual unconditional approval of aspartame products by endocrinologists
astonished parents of diabetic children when they learned the adverse
effects of this chemical. For example, the outraged mother of a 9-year-old
diabetic boy stated, "His endocrinologist backs aspartame 1001 percent,
and highly recommends diet sodas. When I questioned any side effects from
drinking so much, he assured me that the boy would have to drink over 100
cans/bottles of diet soda for the rest of his life to have any damaging side
effects." end of chapter More information on aspartame on www.mpwhi.com Also on www.wnho.net,
www.holisticmed.com/aspartame,
and www.dorway.com
files on www.mpwhi.com Dr. Betty Martini, D.Hum, Founder Mission Possible World Health Intl 9270 Riverclub Parkway Duluth, Georgia 30097 770 242-2599
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