Hospital Form For Vital
ASPARTAME, NEOTAME, NUTRASWEET, AMINOSWEET, E-951,
SPOONFUL,ADVANTAME, SUCRALOSE, CANDEREL, BENEVIA,ACESULFAME
OTHER ALLERGIES AND REACTIONS____________________________________________________________________________________________________________
REASON FOR THIS INFORMATION TO BE ADDED TO MY CHART IS THAT ASPARTAME
IN ITS MANY FORMS IS IN DRUGS AS WELL AS FOODS. IT CAUSES
CHEMICAL HYPERSENSITIZATION USUALLY IN ANYONE WHO HAS USED IT, THE
REASON FOR SO MANY CASES OF DRUG INTERACTION AND SUDDEN CARDIAC DEATH
In the documentary, "Sweet Misery: A Poisoned
Cheryl Kemptner told her hospital not to give her aspartame. A
dietitian gave her some lemonade, Crystal Lite , with it and you see
she became a Code Blue and had to be resuscitated to save her life.
In the movie you will hear from world experts that will answer many
physician's questions. For a lot of info on aspartame and
this particular post you will find a chapter from Dr. H. J.
Roberts, "Aspartame Disease: An Ignored Epidemic" on
drug interaction with aspartame and the mechanism by which is
These pages are being printed out or will be added at the bottom for
the hospital to attach to my file. If any drugs are prescribed
by doctors in this hospital they must check the generics because this
is what is filled because of the insurance industry. Aspartame
is in many generics, especially gastrointestinal and aspartame
triggers gastrointestinal disease.,
front page of Time, August 7, 2017 :" Depression afflicts 16
million Americans, One-Third Don't Respond To Treatment".
Aspartame is a psycho drug and interacts with all antidepressants.
Article by psychiatrist Ralph Walton, M.D., who has done two studies
on aspartame (depression and autism) writes about aspartame and
Medical texts from these experts should be part of every
"Aspartame Disease: An Ignored
Epidemic", 1000 pages, by the late H. J. Roberts, M.D.
Dr. Roberts was a diabetic specialist and explains that aspartame can
not only precipitate diabetes but it simulates and aggravates
diabetic retinopathy and neuropathy, destroys the optic nerve from
the free methyl alcohol, causes diabetics to go into convulsions and
interacts with insulin. The methanol makes them lose limbs.
reviewed studies document the problems:
"Excitotoxins: The Taste That Kills" by
neurosurgeon Russell Blaylock, M.D., www.russellblaylockmd.com
Includes MSG as well as aspartame.
Sleeps: A Sweetener Kills", www.whilesciencesleeps.com
by Dr. Woodrow Monte. Exposes the fact that the original
teratology studies on aspartame were sealed which showed neural tube
defects, spina bifida and cleft palate for starters. Dr. Monte
explains the seriousness of free methyl alcohol. He took
the issue of aspartame triggered seizures and blindness to the
Doctors Roberts and Blaylock have other
texts. There are many books like "Aspartame: King of
Toxins" and can be found on www.amazon.com
hospitals purchase foods that may contain sucralose/Splenda:
Lethal Science of Splenda:
have shown that sucralose can:
*Cause the thymus to shrink by
as much as 40% (the thymus is your immune powerhouse - it produces T
*Cause enlargement of the liver and kidneys
growth rate as much as 20%
*Cause enlargement of the large bowel
*Reduce the amount of good bacteria in the intestines by
*Increase the pH level in the intestines (a risk factor for
*Contribute to weight gain
pregnancy low fetal body weight
*Reduce red blood cell
Particular warning for diabetics: Researchers
found that diabetic patients using sucralose showed a statistically
significant increase in glycosylated hemoglobin, a marker that is
used to assess glycemic control in diabetic patients. According to
the FDA, "increases in glycosolation in hemoglobin imply
lessening of control of diabetes."
Here is how Splenda is
Dr. Morando Soffritti announced a study on Sucralose which
showed it causes cancer.
A safe alternative sweetener made
from organic food is "Just Like Sugar". It's made
from organic orange peel and chicory. Chicory has been used for
70 years to improve the health of diabetics. It can be gotten from
potassium caused cancer and leukemia in original studies.
goes by many names, NutraSweet, Equal, Spoonful, AminoSweet,
Canderel, E951, Benevia and Neotame, for starters. The FDA has
approved Advantame which is half aspartame. Neotame is not
usually labeled. According to the FDA Advantame will only not
be added to meat and poultry. So there is no sign it will be
labeled. There is no PKU warning and Dr. James Bowen says it
importantly there is no pregnancy warning and aspartame in original
studies caused neural tube defects, spina bifida and cleft palate for
starters. The studies were sealed from the public through a
deal by G. D. Searle and the FDA. Autism is rampant. The
last chapter discussing this issue in "While Science Sleeps: A
Sweetener Kills" is free on www.whilesciencesleeps.com
When Jerome Bressler involved in the aspartame investigation
retired from FDA he asked help in finding the FDA information and
studies about this situation sealed from his report. It has now
been added back and you will see from FDA records they confess
aspartame causes birth defects:
Situation: Aspartame can react violently with opioids,.
All hospital patients should be asked if they are using aspartame
before being given opioids. Obviously aspartame has a lot
to do with these deaths. It may not be an overdose. They may simply
be using aspartame and death is the result of the interaction.
Jackson a former Diet Pepsi spokesman is a classic example. He
also had lupus, which is big time precipitated by aspartame.
James Bowen, M.D. wrote: "The
ability of methyl alcohol/formaldehyde to create antigenicity,
especially as combined in aspartame molecules is so great as to cause
severe autoimmune reactions to the tissues deformed by formaldehyde
polymerization, adduct formation. The immune system turns against the
victim's tissues: Lupus." Michael Jackson used Diet Pepsi and it
was a no-brainer that in the end death could happen from interaction.
Example of drug interaction. Headache is #1 on the FDA
the victim goes to a physician he may be prescribed Maxalt. The
pharmaceutical company has been alerted that aspartame causes
headache and they have added it as an ingredient. They refuse
to remove it so a study was done and it showed Maxalt made headaches
worse. They refused. A study was done showing using
Maxalt makes the patient worse and they still refuse to remove it.
form has been prepared by Mission Possible World Health Intl,
Mission Possible is non-profit and a global volunteer force in over
40 countries educating the public that aspartame is a chemical
poison and working to have it removed from the public. It has
no place in a hospital to make the patient worse, and may have
brought him to the ER because of it.
Chapter on Aspartame and Drug Interaction from the This can
be copied with the chapter on drug interaction from "Aspartame
Disease: An Ignored Epidemic" by H. J. Roberts, M.D.
INTERFERENCE WITH DRUG ACTION
The author's clinical observations indicate that aspartame products
can alter the action of important drugs. They include coumarin (Coumadin),
phenytoin (Dilantin), antidepressants, other psychotropic agents, propranolol
(Inderal), methyldopa (Aldomet), thyroxine (Synthroid), and insulin
(Chapter XIII). This phenomenon is illustrated in many case reports
presented in other sections.
It is also likely that some herbs interact with aspartame. Noting
that numerous herb-drug interactions, Fugh-Berman (2000) stated,
"Health care practitioners should caution patients against
mixing herbs and pharmaceutical drugs."
Aspartame may either reduce or
potentiate drug action by various mechanisms. A few of the
possibilities are listed
Alteration of the blood proteins
to which drugs attach.
Alteration of drug receptors on
Changes in the sites at which impulses are
transmitted along nerves and to muscle.
abnormalities in the elderly that are known to enhance their
vulnerability to drug reactions (Weber 1986).This problem increases
in the case of persons taking multiple drugs ("polypharmacy")
prescribed by several physicians.
Interference with drug action by amino acids and protein. An example
is the erratic therapeutic effects when patients with parkinsonism
who were controlled on levodopa began to use aspartame products
(Chapter VI-J). The antagonism if levodopa by dietary protein
presumably reflects impaired transport from serum across the
blood-brain barrier by neutral amino acids (Pincus 1986).
The methanol component of aspartame (Chapter XXI)
might interact with compounds containing ethanol. Examples include
the hypoglycemic sulfonylureas, metronidazole (an antibacterial
drug), and allopurinol (commonly used in the treatment of gout). In
his review of this subject, Posner (1975) emphasized that such
interactions pose "an important area for careful clarification."
Drug Reactions After the Cessation of Aspartame
The phenomenon of increased sensitivity to a drug
after the removal of some interfering factor is known to clinicians.
Examples include severe insulin reactions in diabetics after cure of
an infection, and bleeding from coumarin after terminating a drug
that influenced its binding to carrier proteins. This type of
encounter probably reflects an increase in the "Free" forms
of such drugs, It occurred, for example, when patients on maintenance
coumarin or phenytoin avoided aspartame.
Coumarin is commonly
prescribed as a anticoagulant ("blood thinner") for the
treatment or prevention of serious problems caused by thrombosis
(clot formation) and embolism (the migration of a thrombus). The
vascular beds frequently affected include the coronary arteries, the
carotid arteries, the inner lining of the heart (endocardium) in
patients with heart attacks or irregular heart action (atrial
fibrillation) from which embolism to the 7brain or lower extremities
may originate, and veins in the lower extremities and pelvis that are
frequent sites for pulmonary emboli.
form of therapy constitutes a major commitment for physicians,
particularly the need for continually monitoring the prothrombin
time. Patients may bleed if the anticoagulant effect becomes
excessive. Conversely, the loss of desired anticoagulation invites
recurrence of thrombosis of embolism.
likelihood of interference by aspartame was raised in patients who
had been maintained on coumarin for extended periods with
difficultly. Unexpectedly, their prothrombin times approximated the
control values (meaning a loss of anticoagulant effect), coupled with
recurrent thrombophlebitis or angina pectoris.
Representative Case Reports
An 82-year-old woman had received coumarin for two
reasons: recurrent transient cerebral ischemic attacks ("small
strokes") due to embolism from the carotid arteries, the heart,
or both; and severe thrombophlebitis in the lower extremities with
multiple attacks of pulmonary embolism. A registered nurse
administered her medication daily.
patient's prothrombin time, monitored every 3-4 weeks, had remained
stable a long time. It was found to only 14 seconds (control, 13
seconds) on August 19, 1986. Several days thereafter, she developed
severe pain in the lower extremities and exquisite tenderness over
the deep veins, consistent with recurrent thrombophlebitis. The
dosage of coumarin was increased.
direct injury, it was determined that she recently began to use
aspartame products. These were discontinued. Three days later, blood
was noticed in the urine. At that time, her prothrombin time had
returned to the therapeutic range - namely, 21 seconds. Coumarin was
withheld several days. The failure of urinary bleeding to recur when
coumarin was then resumed probably reflected a return of full
anticoagulation after the loss of aspartame interference.
A 72-year-old woman
had been treated with coumarin for longstanding angina pectoris and
thrombophlebitis. Her prothrombin times generally ranged between
19.5-22 seconds. The patient then developed unstable angina pectoris
and rapid heart action (tachycardia) for which she was hospitalized.
No precipitating cause could be determined. At the time, little
significance was paid to the slight decrease of her most recent
prothrombin time (17 seconds). Even though the dosage if coumarin was
increased, the prothrombin time then declined to 15 seconds.
The occurrence of other complaints suggesting aspartame disease
raised the question as to whether aspartame also had influenced the
They included severe "burning and
swelling" of the lips and tongue, headache, increased visual
difficulty (despite recent cataract surgery and prescription
glasses), marked "nervousness," and unexplained nausea.
Although she initially denied using aspartame, the "diet"
ginger ale she drank did contain it. The prothrombin time rose to 22
seconds (control, 12 seconds) one week after shopping aspartame.
During this time, her intense fatigue and lip-tongue reactions
B. Phenytoin (Dilantin) and Other
Phenytoin is a key in
managing epilepsy. When convulsions are associated with or aggravated
by aspartame products (Chapter III), the patient confronts several
dilemmas. First, the dose of phenytoin is likely to be increased,
possibly to the point of toxicity (see Case III-35). Second, other
anti-epilepsy drugs may be added, thereby increasing the potential
for side effects. Third, the continuation of these drugs in high
doses could result in "rebound" toxicity after stopping
The apparent potentiation of
valproic acid (Depakene; Depacote), another antiepileptic drugs, was
personally reported to the author by a 51-year-old man who drank
considerable diet cola daily. When his physician increased the dose,
he became comatose and required hospitalization.
Representative Case Report
A 28-year-old man suffered seizures after a head
injury while serving in the Marines. As a civilian, his convulsions
unexpectedly increased despite multiple anti-epileptic medications,
causing him to lose his job.
patient's mother noted that he "acted like he was intoxicated."
She expressed concern over his large consumption of aspartame sodas.
Shortly after discontinuing them, he had to be taken to an emergency
room for phenytoin intoxication - presumably representing the rebound
C. Antidepressant Drugs
Aspartame may interfere with the action of important drugs used to
treat depression, particularly imipramine (a tricyclic
antidepressant). Others have made similar observations.
Walton (1986) described a 54-year-old woman with
recurrent major depression who had been well controlled on a
maintenance dose of 150 mg imipramine at bedtime. She subsequently
experienced marked behavioral changes, manic behavior characterized
by inappropriate euphoria and flighty ideas, and a grand mal seizure.
It was then learned that she had been drinking considerable
aspartame-sweetened iced tea for several weeks prior to the seizure.
All evidence of manic activity subsided within four days after
stopping aspartame and the addition of lithium. Her depression
recurred, however, two months later. Imipramine was resumed at the
previous dosage with no recurrence of severe depression or mania over
the ensuing 13 months.
monoamine oxidase inhibitors (MAOIs), another group of antidepressant
drugs, can have additional adverse effects when aspartame is
consumed. These include phenelzine (Nardil), isocarboxazide
(Marplan), and tranylcypromine (Parnate).
It is pertinent that hypertensive crisis have occurred in patients so
treated after they consumed foods and beverages containing tyramine
and tryptophan. This response probably represents vasospasm caused by
amino acid-derived sympathomimetic substances such as norepinephrine
and tyramine (Chapters IX-C and XXIII).
The serotonin-elevating action of fluoxetine (Prozac) for treating
depression could be counteracted by aspartame. It can block
tryptophan entry to the brain, thereby inhibiting synthesis of
serotonin (Chapter VII).
physician called to inquire about a possible interaction between
Prozac and aspartame. He had suffered depression for which Prozac was
prescribed, but without much benefit until he avoided aspartame. At
what point, the drug proved helpful.
The occurrence or aggravation of benign
("essential") tremor by aspartame was described in Chapter
VI-J. This condition usually can be controlled with small or modest
doses of propranolol. Several patients and correspondents stressed
that their tremor intensified after consuming aspartame - even with
increased dosage of propranolol - and improved when they avoided when
they avoided such products.
susceptibility of hypothyroid to aspartame (Chapter IX-E) has been
repeatedly emphasized. Conversely, there may be interference with the
activity of thyroid replacement therapy.
An aspartame reactor had been taking
thyroid hormone several years. After avoiding aspartame products, he
noted "My replacement thyroid dose, which had been steadily
increasing for the last few years, dropped by 30 percent. My doctor
was quite surprised, and had no other explanation for it".
F. Female Hormone Replacement Therapy
Patients with aspartame disease expressed firm convictions about
interactions involving female hormone replacement therapy.
Representative Case Report
A 40-year-old saleswoman consumed considerable
diet sodas and other aspartame products, especially during the
summer. She supplemented her description of reactions in the survey
questionnaire with a two-page analysis of major changes when taken in
conjunction with Premarin/Provera. They included cloudy vision,
dizziness, tenderness and tingling of the feet, joint pains, numbness
of the lower limbs, headache, "foggy thinking," confusion,
slurred speech and extreme fatigue. She took as many as 18 ibuprofen
tablets daily to obtain relief of her constant pain. Extensive
neurologic studies - including electromyography, nerve conduction
studies, x-rays and MRI scanning - failed to revel a cause.
Considering a possible connection to the hormonal
therapy, she reduced Premarin by half and quit Provera. There was
considerable relief from the joint pain and muscle aches within two
days, along with cessation of her neuropathic symptoms. After then
avoiding all aspartame products, she wrote, "I felt IMMEDIATE
relief within two days of what remained of the lumbar ache, muscle
aches, foggy thinking, dizziness, and cloudy vision. All these
improvements continue in the week since. Walking seems less of an
effort; hip pain improved."
There have been references to
enhancement of seizures and other disorders in patients receiving
methyldopa hypertension who also consumed aspartame. Seven of the
initial 397 reactors completing the questionnaire were taking this
drug when they experienced aspartame disease. Maher and Kiritsy
(1987) demonstrated that aspartame administration decreases the entry
of methyldopa into rat brain.
67-year-old retired hypertensive woman had been treated with
methyldopa. She experienced three unexplained seizures while drinking
one can of diet cola and eating various aspartame puddings daily. The
convulsions stopped when she avoided aspartame products, as did her
sensitivity to noise and attacks of rapid heart action.
is an important drug used for local anesthesia and the treatment of
ventricular arrhythmias in intensive care units. Alterations of its
pharmacology by aspartame require study.
Kim et al (1987) reported that the intraperitoneal administration of
aspartame significantly reduced the 50 percent convulsion dose of
lidocaine. They indicated that PKU patients and asymptomatic PKU
heterozygotes may be more sensitive to the toxic effects of this and
relate3d local anesthetics.
Nikfar et al
(1997) noted that aspartame increased morphine analgesia in the early
phase (wherein saccharin had no effect), and further enhanced
morphine analgesia during the late phase. The sister of heavy diet
cola consumer related the apparent potentiation of morphine by
aspartame while he continued drinking it in an intensive care unit
after a heart attack. This interaction became evident when the
aspartame was stopped, coupled with halving the insulin required for
managing his diabetes.
AND LYMPH NODE DISORDERS
Bone marrow and lymph nodes, the organs chiefly responsible for blood
cells, are highly vulnerable to toxic substances. For example,
aplastic anemia and leukemia may occur after treatment with potent
drugs, or exposure to pesticides and other chemicals in the
environment (Roberts 1984, 1990b). Aspartame products could be
another cause of disorders therein.
A. Bone Marrow and
Aspartame disease may be
evidenced by changes involving red blood cells, white blood cells and
platelets. The aspartame reactors reported below and elsewhere
evidenced either anemia, a striking elevation of the white blood cell
count suggestive of leukemia, or markedly decreased platelet counts
patient with recurrent "histiocytic leukemia" following
aspartame ingestion (Case IX-J-1) offers an intriguing clue to the
so-called histiocytosis syndromes in children (The Lancet 1987;
208-209). The Langerhans cell in histiocytosis is a dendritic cell
derived from the bone marrow.
Many drugs and other substances have been implicated in "immune
Case IX-F-6 mentioned the finding of "enlarged red blood cells."
Deficiency of folic acid or its altered metabolism (see below) causes
macrocytic (large red blood cell) anemia, while deficient absorption
of vitamin B12 can result in a similar anemia.
Patients with pernicious anemia may be more vulnerable to aspartame.
For example, a 51-year-old woman with severe aspartame disease gave a
history of treatment for documented pernicious anemia as her only
significant past medical history.
10-year-old girl began consuming various aspartame products at the
age of eight, initially during summer weekends. She developed marked
swelling of one shoulder which then involved the neck. Her arm almost
tripled in size. There was no history of allergies or aspirin use
existed. The patient also evidenced a high fever, pleural effusion
(fluid in the lung cavity), striking enlargement of both the liver
and spleen, and a precipitous decline of the platelet count to 1,000
per cubic mm (normal 150,000 or higher). A striking increase of
histiocytes was found in her bone marrow. Several "liver
enzymes" were markedly elevated - i.e., SGOT 3,080 units/L
(normal, up to 50); CPK 30,000 units/L (normal, up to 50).
Numerous physicians and consultants saw this child.
Most diagnosed histiocytic leukemia. The patient received large doses
improvement and virtual normalization of the foregoing blood changes
occurred when the mother closely monitored her diet and eliminated
additives. The prednisone was then stopped.
The patient subsequently ate several bowls of an aspartame cereal.
Marked swelling of the cheeks developed, coupled with recurrence of
the aforementioned features. When aspartame was discontinued, the
swelling receded without prednisone.
Several months later, the girl was given aspartame chewing gum
without the mother's knowledge. Swelling of her entire body,
recurrent enlargement of the liver and spleen, a dramatic increase of
bone marrow histiocytes, and severe pain in many joints ensued. Total
abstinence from aspartame again effected the disappearance of her
symptoms and the blood abnormalities within six months. At the time
of my last discussion with her mother, the child had minimal
enlargement of the liver, and was receiving prednisone in low doses
This patient had two
sets of head x-rays, three CT scans of the brain, two spinal
punctures, four bone marrow studies, two electroencephalograms, two
heart monitoring studies, two barium enemas, and a host of other
studies. Her mother estimated the medical costs at $750,000!
A 62-year-old man
developed severe gastrointestinal problems while ingesting aspartame
products. He developed "an erratic blood count, with red and
white cell imbalance, and platelets off some." He received
"cortisone" for six months when his condition was diagnosed
as "an immune deficiency problem."
His daughter suffered intense abdominal pain, a bleeding peptic
ulcer, severe headache, and repeated grand mal convulsions when she
used aspartame products. A granddaughter had phenylketonuria (Chapter
XVII) at birth, and subsequently manifested severe learning
A 61-year-old personnel director began drinking diet colas at the age
of 59, and consumed up to one liter daily. His platelet count
declined to 54,000/cu mm thereafter. He also became concerned over
"forgetting to perform things for which I was responsible."
Other complaints included "double vision," severe
sensitivity to light, headache, dizziness, two convulsions, "fits
without convulsions," marked sleepiness during the day,
insomnia, slurred speech, and a nonspecific rash. Extensive studies
failed to uncover a major medical problem.
His symptoms improved within 10 weeks after avoiding aspartame,
although some problems with vision, memory, sleep and "concentration"
persisted. There was an immediate exacerbation during one retest
trial. After avoiding all aspartame products, the platelet count had
increased to 75,000/cu mm at the time of his subsequent
A registered nurse developed hypertension and a platelet count
under 30,000 during her third pregnancy. Neither of these features
had been noted in previous pregnancies. She began using diet colas
after the birth of her second child. Other symptoms included severe
headache, depression, loss of hair, and symptomatic reactive
41-year-old woman consumed diet cola for 14 years. She experienced
many symptoms of aspartame disease for three years, including
headache, visual problems, severe aching of the joints, numbness of
the left hand, and easy agitation. Her white blood cell count was
only 460 (normal 4000-10,000), for which no other cause could be
B. Lymph Node Enlargement
Enlargement of the lymph nodes (lymphadenopathy) occurred in several
aspartame reactors without the finding of another convincing cause.
This featured differed from the striking salivary gland enlargement
in other with aspartame reactors (Chapter IX-D).
Representative Case Reports
A mortgage broker began drinking diet cola in
January 1995. She developed markedly enlarged glands in the neck
("the size of golf balls") one year later, along with a
constant sore throat. These features persisted despite considerable
doctoring. Subsequent symptoms included blurred vision, migraine
headaches, severe joint and muscle pains, constant diarrhea with
bloody stools, ringing in the ears, palpitations, night sweats, "a
tongue as black as leather," a 30-pound weight gain, and
"incapacitating" chronic fatigue. Various suggested
diagnoses - including carbon monoxide poisoning, fibromyalgia, lupus
erythematosus, and Epstein-Barr infection - could not be confirmed.
The patient was "absolutely in
shock" on learning about aspartame disease. Improvement proved
gratifying after discontinuing aspartame products. The tongue
returned to a normal healthy pink state. The enlarged glands in her
neck decreased within several months.
A 44-year-old loan officer experienced headache,
drowsiness, hyperactivity, severe tingling, irritability, personality
changes, palpitations, a recent elevation of blood pressure,
abdominal pain, itching, hives, other rashes, marked frequency of
urine, and joint pains. These symptoms were provoked "immediately"
on three retesting trials with aspartame products.
His son had aspartame disease. It was primarily evidenced as
"noncancerous lumps under the arms" and a rash.
C. Altered Folic Acid Metabolism
Aspartame may deplete important nutrients related to folic acid.
Folic acid assists in eliminating the formic acid derived from methyl
alcohol degradation (Reitbrock 1971). It tends to decrease with
higher methanol concentrations (Chapter XXI). In view of the rarity
of low blood foliate levels in contemporary clinical practice, this
finding could prove a clue to aspartame disease.
Aspartame-induced decrease of folic acid could have clinical
significance, especially anemia and birth defects.
A physician in the State of Washington noted anemia in a patient who
ingested large amounts of aspartame sodas, and suspected folic acid
deficiency. He found the blood methanol level to be elevated.
Unfortunately, the tube sent for a foliate level broke in transit
after he started replacement therapy.
There has been a recent impressive decline in neural-tube following
the fortification of grain products an vitamin formulations with
folic acid, coupled with an associated increase of median serum
foliate concentrations. This decline might be less evident, however,
among pregnant women who consume aspartame products that can deplete
foliate levels as methyl alcohol is metabolized.
The vulnerability of patients with pre-existing liver disease to
aspartame was noted in the introduction of this section. These
disorders include hepatitis, cirrhosis (Case IX-K-5), hemochromatosis
(iron storage disease), and the liver dysfunction complicating many
infections and drug reactions.
aspartame reactors without known liver disease evidenced marked
elevation of blood aminotransferases ("liver enzymes").
They are variously referred to as alanine aminotransferases (ALT;
SGPT), aspartate aminotransferase (AST; SGOT) and glutamyl
transpeptidase (GGT). (Serum levels of ALT and AST in normal persons
are less than 35units/L. In Case IX-J01, a 10-year-old girl, the SGOT
was 3,080 units/L. One such aspartame reactor had been told, "Your
liver is pickled."
Monte (1984) made
a reference to such an association. Taylor (1996) also raised the
issue of liver toxicity caused by aspartame in a 51-year-old man who
evidenced repeated jaundice.
In a recent National Health and Nutrition
Examination Survey, 2.6 percent of the United States population
surveyed had elevated serum ALT for which no cause of chronic liver
disease could be found (James 1999). Even though 70 percent of the
adult population consumes aspartame products, aspartame disease was
not suspected as a likely causative or contributory cause. It is of
historic interest that Dr. Misael Uribe (1982) expressed concern that
the FDA had not adequately considered the potential toxicity of
aspartame patients with liver disease shortly after its forthcoming
release was announced.
cirrhosis of the liver are at increased risk because they may be
unable to metabolize aspartame and its breakdown products adequately
(Jagenberg 1977; Herberer 1980; Dhont 1982).
The possibility of aspartame toxicity should be entertained in
patients diagnosed as having nonalcoholic steatohepatitis. This liver
disorder has become a common liver disorder in North America, and can
progress to cirrihosis (James 1999). Its frequent features of
persistent fatigue, upper abdominal discomfort, diabetes and
hyperlipidemia are also encountered in aspartame disease.
Obese persons and diabetic patients who consume
considerable aspartame appear to be at higher risk for the
development of chronic nonalcoholic steatohepatitis, especially when
addicted to such products (Chapter VII-G). The term "nonalcoholic"
is misleading in this instance because aspartame contains ten percent
Admittedly, it may be
difficult to single out precise symptoms attributable to aspartame
products in patients with liver disease. Yet, few physicians
considered the contributory role of aspartame to hepatic changes
among patients in this series. Some even were hostile to the idea
(see Case IX-K-3).
By contrast, astute
persons and various consumer groups submitted related observations to
the FDA. The husband of one patient, an attorney, became irate over
the absence of any wearing labels on aspartame products for persons
with liver disease.
Representative Case Reports
A 68-year-old housewife
described how she became "incapacitated" form aspartame
products in these terms: "My eyes would not focus. I had
confusion, dizziness, depression, insomnia and memory loss. I could
not drive or leave the house alone." Other complaints included
severe nausea, diarrhea, marked thirst, considerable frequency of
urination, and attacks of hypoglycemia. Her "liver reading"
(presumably the ALT) rose from 44 to 264. It declined to 78 after she
avoided aspartame. Although her physician assumed it was due to
"drinking," the patient empathically stated that she never
drank alcoholic beverages.
A prospective blood donor was surprised, and angered, when a blood
bank would not accept her blood (SGOT and SGPT) were markedly
elevated. She consulted a gastroenterologist. He confirmed the
finding, and by exclusion diagnosed hepatitis C infection. Abdominal
ultrasound studies and other tests were normal. Aside from advice to
stop her modest drinking, the only other treatment option offered was
interferon. She declined the latter because of its inherent severe
Her teats remained
unchanged over the next two years despite total abstention from
alcohol. She would not kiss persons for fear of transmitting the
A friend commented
that aspartame products could harm the liver. As personal proof, she
pointed to the normalization of her own blood studies after
discontinuing diet sodas. The patient thereupon discontinued such
products - including the seven packs per day (!) of aspartame chewing
gum. A dramatic decline of her liver enzymes ensued.
Overwhelmed by this experience, she reported her case to the FDA and
criticized its approval of aspartame as "total disregard for
human health and safety."
A man had consumed 24-60 ounces of diet sodas
daily for a year while on "a very low calorie diet." He
experienced numbness of his left hand, left foot, face, and then the
right hand. Two MRI studies and other neurologic tests were normal.
His liver enzymes, however, were elevated (GGT 350; SGOT 150); repeat
testing confirmed these abnormalities. A CT scan of the liver and an
ultrasound study of the abdomen were not revealing.
This patient was scheduled for consultation with a
gastroenterologist. Learning about aspartame disease in the interim,
he stopped aspartame products, and consumed considerable filtered
water "in an attempt to flush my liver." Repeat liver tests
evidenced progressive declines of the GGT to 15, and of the SGOT to
50. The gastroenterologist disregarded these observations, and
criticized the patient's inference about aspartame being a possible
28-year-old manager of an architectural firm, and mother of a
six-month child, had markedly elevated liver enzymes for four years,
the cause of which eluded multiple physicians. Her AST, ALT and
alkaline phosphates levels average 200, 200 and 1100, respectively.
The bilirubin levels remained normal.
never used drugs of abuse or smoked, and had not ingested alcohol for
three years. No birth control pill was used since the age of 21.
Numerous studies for hepatitis and HIV viruses, and for various
auto-immune diseases were negative. In addition to multiple CT scans
and an MR study, two liver biopsies proved normal.
The patient had "practically lived on" diet cola for ten
years... "drinking more than water or any other beverage."
This soda was avoided during pregnancy.
After reading about aspartame disease, she stopped all diet products.
There was a prompt and striking decrease of all the enzymes, which
progressively normalized with no other interventions.
Case IX-K-5 (FDA Project #3898; Courtesy, Dr. Linda Tollefson)
A 76-year-old woman with longstanding
cirrhosis died in progressive "liver coma." In his
correspondence to a consumer advocate, her husband indicated that she
had been "in pretty good health" until October 1983 when an
elevated blood glucose concentration was found. Tolbutamide and diet
were prescribed. In an attempt to avoid sugar, she used four packets
of an ATS daily in coffee, cereal and desserts.
The patient evidenced dramatic deterioration within two weeks. It was
manifest by indifference to her surroundings, forgetfulness, slurred
speech, dizziness, impaired vision, loss of interest concerning food
and her favorite television programs, and a change in gait. She made
irrelevant statements as if hallucinating. Her condition deteriorated
to the point of becoming incontinent and bedridden. A diagnosis of
"hepatic encephalopathy" was made.
brain function in patients with severe liver disease has been
attributed to the retention of phenylalanine and other amino acids
(Fischer 1971). Striking changes in amino acid metabolism are known
to occur in liver disease - particularly the hydroxylation rates of
phenylalanine, tyrosine and tryptophan. The elevated phenylalanine
concentrations in patients with cirrhosis rise significantly after
protein consumption (Fernstrom 1979). Methanol poisoning (Chapter
XXI) creates another serious problem in patients with liver disease.
The enzymes alcohol dehydrogenase and aldehyde dehydrogenase are
involved in methanol metabolism. The considerable alcohol
dehydrogenase activity of the liver decreases when it is diseased.
One mechanism may be the production of tumor
necrosis factor (TNF)-a. It is an early event in many types of liver
injury that triggers the release of other cytokines, and then the
destruction of liver cells.
cycle involving aggravated hypoglycemia also can occur. Contributory
causes include the tendency to "hepatic hypoglycemia" among
persons with severe liver disease (owing difficulty in storing and
metabolizing glycogen), aspartame-induced hypoglycemia (Chapter XIV),
the use of glucose-lowering drugs for control of diabetes, and the
failure of diabetics receiving such drugs or insulin to take interval
feedings. For example, the physician who prescribed tolbutamide for
Case IX-K-4 "said nothing about diet."
Hemochromatosis (iron storage disease; hepatic iron overload; bronze
diabetes) might be aggravated in its pre-cirrhotic stage by aspartame
consumption (see Case XIII-1), especially through insulin stimulation
(Chapter XIV). Related features of insulin resistance - in addition
to hyperinsulinemia - are increased body mass, elevated lipids, and
abnormal glucose tolerance.
entity of primary hepatic iron overloads differs from genetic
hemochromatosis because transferring saturation is normal, as is the
frequency of the HLA A3 genotype (Ferrannini 2000). It has been
suggested that insulin's primary action in stimulating glucose
transport is coupled with a redistribution of transferring receptors
to the cell surface where they mediate extracellular iron uptake.
Martini: This is the end of the chapter. Please
also see the Aspartame Resource Guide: