Report: Aspartame, Methanol & Public Health - Dr. Woodrow Monte

[Guest guest]

Report: Aspartame, Methanol and Public Health -Dr. Woodrow Monte

 

 

 

JOURNAL OF APPLIED NUTRITION, VOLUME 36, NUMBER 1, 1984

REPORT ASPARTAME: METHANOL AND THE PUBLIC HEALTH

 

DR. WOODROW C. MONTE

 

ABSTRACT

 

Aspartame (L-aspartyl-L-phenylalanine methyl ester), a sweetener

marketed under the trade name NutraSweet*, releases into the human

bloodstream one molecule of *methanol* for each molecule of aspartame

consumed.

 

This new methanol source is being added to foods that have considerably

reduced caloric content and, thus, may be consumed in large amounts.

 

Generally, none of these foods could be considered dietary methanol

sources prior to addition of aspartame.

 

When diet sodas and soft drinks, sweetened with aspartame, are used

to replace fluid loss during exercise and physical exertion in hot

climates,

the intake of *methanol* can exceed 250 mg/day or 32 times

the Environmental Protection Agency's recommended limit of consumption

for this cumulative *toxin*.

 

There is extreme variation in the human response to acute methanol

*poisoning*,

the lowest recorded lethal oral dose being 100 mg/kg with one individual

surviving a dose over ninety times this level.

 

Humans, due perhaps to the loss of two enzymes during evolution, are

more sensitive to methanol than any laboratory animal;

even the monkey is not generally accepted as a suitable animal mode.

 

There are no human or mammalian studies to evaluate the possible

mutagenic, teratogenic, or carcinogenic effects of chronic

administration of methyl alcohol.

 

The average intake of methanol from natural sources varies but limited

data suggests an average intake of considerably less than 10 mg/day.

 

Alcoholics may average much more,with a potential range of between 0 and

600 mg/day,

depending on the source and in some cases the quality of their

beverages.

 

Ethanol, the classic antidote for methanol toxicity, is found in natural

food sources of methanol at concentrations 5 to 500,000 times that of

the toxin.

 

Ethanol inhibits metabolism of methanol and allows the body time for

clearance of the toxin through the lungs and kidneys.

 

The question asked is whether uncontrolled consumption of this new

sweetener might increase the methanol intake of certain individuals to a

point beyond which

our limited knowledge of acute and chronic human

methanol toxicity can be extrapolated to predict safety.

 

*NutraSweet is a trademark of G.D. Searle & Co.

 

ASPARTAME-

 

Aspartame (L-aspartyl-L-phenylalanine methyl ester) has been

approved as a sweetener for liquid carbonated beverages.

 

It has had wide acceptance as an additive in many dry food

applications after Food and drug Administration approval on July 24,

1981.

 

The Food and Drug Administration, Dr. Richard Wurtman and myself have

received well over a thousand written complaints relative to aspartame

consumption.

 

By far, the most numerous of these include dizziness, visual impairment,

disorientation, ear buzzing, high SGOT, tunnel vision, loss of

equilibrium, severe muscle aches,

numbing of extremities, pancreatitis, episodes of high blood pressure,

retinal hemorrhaging, menstrual flow changes, and depression.

 

The validity of these complaints has yet to be scientifically

evaluated.

However, a thorough knowledge of just what makes this new sweetener

stand apart from other nutritional substances might aid physicians in

making dietary recommendations for their patients.

 

Aspartame (NutraSweet)* is a small molecule made up of three

components:

 

Phenylalanine, aspartic acid, and methanol (wood alcohol).

When digested, these components are released into the bloodstream.

 

Phenylalanine and aspartic acid are both amino acids which are found

in natural proteins, and under normal circumstances are beneficial,

if not essential, for health.

 

Proteins are complex molecules which contain many chemically bonded

amino acids.

 

it takes several enzymes to break these bonds and liberate the amino

acids.

This is a slow process and the amino acids area released gradually into

the bloodstream.

 

The quaternary structure of protein also slows the digestion of these

amino acids:

 

amino acids in the center of the protein molecule aren't released until

the outer layers of amino acids on the surface have been swept away.

 

This natural time release process saves the body from large numbers of

any one of the 21 amino acids being released into the bloodstream at any

one time.

 

Aspartame requires the breaking of only two bonds for absorption.

 

This happens very quickly with the potential to raise component blood

levels rapidly.

The methyl ester bond of phenylalanine is the first to cleave due to its

susceptibility to pancreatic enzymes.

 

This is.highly unusual;

the methyl esters associated with pectin for

instance are completely impervious to all human digestive enzymes.

 

AMINO ACID COMPONENTS-

Phenylalanine

 

Phenylalanine is an essential amino acid, the daily consumption of

which is required to maintain life.

However, Dr. Richard J. Wurtman, Professor of Neuroendocrine Regulation

at the Massachusetts Institute ofTechnology, presented data to the FDA

demonstration that in humans the feeding of a carbohydrate with

aspartame significantly enhances

aspartame's positive effect on plasma and brain phenylalanine and

tyrosine levels (48 Federal Register at 31379).

 

There are sound scientific reasons to believe that increasing the brain

levels of these large neutral amino acids could affect the

synthesis of

neurotransmitters and in turn affect bodily functions controlled by

the autonomic nervous system (e.g., blood pressure).

 

The proven ability of aspartame to inhibit the glucose-induced

release of serotonin within the brain may also affect behaviors,

such as satiety and sleep.

 

Aspartic acid-

 

Aspartic acid, is not an essential amino acid but is normally easily

utilized for human metabolism.

 

However, under conditions of excess absorption it has caused

endocrine disorders

in mammals with markedly elevated plasma levels of luteinizing hormone

and testosterone in the rat and release of pituitary gonadotropins and

prolactin in the rhesus monkey.

The amount of luteinizing hormone in the blood is a

major determinant of menstrual cycling in the human female.

 

METHANOL-

Methanol (methyl alcohol, wood alcohol), a poisonous substance,

is added as a component during the manufacture of aspartame.

 

This methanol is subsequently released within hours of consumption

after hydrolysis of the methyl group of the dipeptide by chymotrypsin

in the small intestine as it occurs in soft drinks after decomposition

of aspartame

during storage or in other foods after being heated.

 

Regardless of whether the aspartame-derived methanol exists in food in

its free form or still esterified to phenylalanine,

10% of the weight of aspartame intake of an individual will be absorbed

by the bloodstream

as *methanol* within hours after consumption.

 

Methanol has no therapeutic properties and is considered only as a

*toxicant*.

The ingestion of two teaspoons is considered *lethal* in humans.

 

Methyl alcohol produces the Methyl alcohol syndrome, consistently,

only in humans and no other test animal, including monkeys.

 

There is a clear difference between " toxicity " , which can be produced in

 

every living thing, and the " toxic syndrome " .

 

The greater toxicity of *methanol* to man is deeply rooted in the

limited biochemical pathways available to humans for detoxification.

 

The loss of uricase (EC 1.7.3.3.), formyl-tetrahydrofolate synthetase

(EC 6.3.4.3.)42 and other enzymes during evolution sets man apart from

all laboratory animals including the monkey.

 

There is no generally accepted animal model for *methanol* toxicity.

 

Humans suffer " toxic syndrome " at a minimum lethal dose of 1 gm/kg,

much less than that of monkeys, 3-6 g/kg42,59.

 

The minimum lethal dose of methanol in the rat, rabbit, and dog is 9.5,

7, and 8 g/kg, respectively;

ethylalcohol is more toxic than methanol to these test animals.

 

No human or experimental mammalian studies have been found to

evaluate the possible mutagenic, teratogenic or carcinogenic effects

of methylalcohol,

though a 3.5% chromosomal aberration rate in testicular tissues of

grasshoppers was induced by an injection of methanol.

 

The United States Environmental Protection Agency in their Multimedia

environmental Goads for Environmental Assessment recommends

a minimum acute toxicity concentration of methanol in drinking water

at 3.9 part per million, with a recommended limit of consumption below

7.8 mg/day.

 

This report clearly indicates that methanol:

" is considered a cumulative poison due to the low rate of excretion

onceit is absorbed. In the body, methanol is oxidized to formaldehyde

and formic acid;

both of these metabolites are toxic. "

 

Role of Formaldehyde-

 

Recently the toxic role of formaldehyde (in methanol toxicity) has

been questioned.

No skeptic can overlook the fact that, metabolically,

formaldehyde must be formed as an intermediate to formic acid

production.

 

Formaldehyde has a high reactivity which may be why it has not been

found in humans or other primates during methanol

poisioning

 

The localized retinal production of formaldehyde from

methanol is still thought to be principally responsible for the optic

papillitis and retinal edema always associated with the toxic syndrome

in humans.

 

This is an intriguing issue since formaldehyde poisoning alone does not

produce retinal damage.

 

If formaldehyde is produced from methanol and does have a reasonable

half life within certain cells in the poisoned organism the chronic

toxilogical ramifications could be grave.

 

Formaldehyde is a known arcinogen producing squamous-cell carcinomas by

inhalation exposure n experimental animals.

 

The available epidemiological studies do not provide adequate data for

assessing the carcinogenicity of formaldehyde inman.

 

However, reaction of formaldehyde with deoxyribonucleicacid (DNA) has

resulted in irreversible denaturation

that could interfere with DNA replication and result in mutation.

 

Glycerol formal, a condensation product of glycerol and formaldehyde

(which may

be formed in vivo), is a potent teratogen causing an extremely high

incidence of birth defects in laboratory animals. even the

staunchest critic of formaldehyde involvement in methanol toxicity

admits:

 

" It is not possible to completely eliminate formaldehyde as a toxic

intermediate because formaldehyde could be formed slowly within cells

and interfere with normal cellular function without ever obtaining

levels that are detectable in body fluid or tissues. " 34

 

Acute Toxicity in man " Toxic Syndrome "

 

A striking feature of methyl alcohol syndrome the asymptomatic

interval(latent period) which usually lasts 12 to 18 hours after

consumption.

This is followed by a rapid and severe acidosis caused partially by

theproduction of formic acid. Insufficient formic acid is generated to

account for the severity of metabolic acidosis produced and,

therefore,other organic acids may be involved.

 

Patients may complain of lethargy, confusion, and impairment of

articulation, all frequently encountered signs in moderate central

nervous system (CNS) intoxications resulting from other toxic

compounds.

 

Patients may also suffer leg cramps,

back pain, severe headache,

abdominal pain, labored breathing,

vertigo and visual loss, the latter

being a very important clue to making a diagnosis

of methanol poisning.

 

Other striking clinical features associated only with

theoral administration of methanol are elevated serum amylase are the

finding of pancreatitis or pancreatic necrosis on autopsy.

 

In fatal cases liver, kidneys and heart may show parenchymatous

degeneration. the lungs show desquamation of epithelium, emphysema,

edema, congestion and bronchial pneumonia12.

 

Chronic Human Exposure

 

This is the most important aspect of methanol toxicity to those who

areinterested in observing the effect of increased methanol

consumption on a population.

 

The data presented here were compiled by the Public Health Service.

Theindividuals studied were working in methanol contaminated

environments.

 

It is interesting to note that the visual signs always associated with

acute toxicity often do not surface under chronic conditions.

 

Many of the signs and symptoms of intoxication due to methanol

ingestionare not specific to methyl alcohol.

 

For example, headaches, earbuzzing, dizziness, nausea and unsteady

gait (inebriation),

gastrointestinal disturbances, weakness, vertigo, chills, memory

lapses,numbness and shooting pains in the lower extremities hands and

forearms,behavioral disturbances, and neuritis.

 

The most characteristic signs

and symptoms of methyl alcohol poisoning in humans are the various

visual disturbances which can occur without acidosis

although they unfortunately do not always appear.

 

Some of these symptoms are the

following: misty vision, progressive contraction of visual fields

(vision tunneling), mist before the eyes, blurring of vision, and

obscuration of vision.

 

ALCOHOLICS: CHRONIC METHANOL CONSUMPTION

 

Alcoholics in general, but particularly those who consume large

quantities of wine or fruit liqueur, would seem, from the available

evidence, to be the only population thus far exposed to consistently

high levels of methanol ingestion.

 

The high ethanol/methanol

ratio of alcoholic beverages must have a very significant protective

effect, though enzyme kinetics mandate some constant but low level of

methanol metabolism.

 

One could speculate that the delicate balance

which maintains this defense might be jeopardized by the general

nutritional neglect and specifically the folic acid deficiency

associated with the meager food intake of some alcoholics.

Alcoholics have a much higher incidence of cancer and other

degenerative diseases,

none of which can be attributed to ethanol alone. The fascinating

similarities linking unusual clinical features of methanol toxicity

andalcoholism are worth noting.

 

 

Neuritis:

 

Chronic occupational exposure to methanol often produces human

complaints of neuritis with paresthesia, numbing, prickling and

shootingpains in the extremities.

 

 

Alcoholic polyneuropathy36 or multiple peripheral neuritis differs

symptomatically from the methanol induced syndrome only in its first

andoften exclusive affinity for legs.

 

The unpleasant sensations of

*intolerable pain* associated with slight tactile stimulation is not

anuncommon anecdotal consumer complaint following long term

consumption of aspartame.

 

In one such case reported to me, my interpretation of an

electromyogram indicated the signs of denervation indicative of

alcoholic polyneuropathy. The individual's ischemic lactate

pyruvate curve, before and after fasting, was flat.

 

Less that six weeks after

aspartame consumption ceased the major symptoms subsided and

repetitionof these tests produced normal responses, although the

individual still experienced intermittent pain.

 

Pancreatitis:

 

Methanol is one of the few etiologic factors associated with acute

pancreatic inflammation. Microscopic findings of pancreatic

necrosis on autopsy have been reported after acute oral methanol

poisoning.

In fact, pancreatic injury probably accounts for almost

universal violent epigastric pain and occasional elevated serum

amylase levels which marks the end of the latent period.

 

There is a generally accepted association between alcoholism and

pancreatitis. Most patients, however, give a history of 5 to 10 years

of heavy drinking before the onset of the first attack. The fact

that40% of all cases of acute pancreatitis complaints are

attributable

to alcoholics, however, must be taken into consideration to

avoidartifactual association. Pancreatitis has been a complaint

associatedwith aspartame consumption.

 

Methanol and the Heart:

 

A 21-year-old non-drinking male who had been exposed daily to the fine

dust of aspartame at the packaging plant he had worked for over a

year,

was complaining of blurred vision, headaches, dizziness, and severe

depression before his sudden death. An autopsy revealed (aside from

theorgan involvement one might expect from methanol toxicity)

myocardial hypertrophy and dilatation with the myocardiopathy and

left ventricle

involvement reminiscent of alcoholic cardiomyopathy.

 

Alcoholic

cardiomyopathy however typically occurs in 30-55 year old men who

have a history of alcohol intake in quantities comprising 30 to 50

percent of their daily caloric requirement over a 10 to 15 year

period.

 

It has been suggested that alcohol is the etiologic factor in a least

50percent of the cases of congestive cardiomyopathy. The

significantly lower hospitalization incidence for coronary disease

among moderate drinkers than among nondrinkers and protection to

coronary risk afforded

the moderate drinker (less than two drinks a day) over the

nondrinkerseems contradictory. However, if we implicate methanol as

the etiologic

factor, then clearly the nondrinker is at a disadvantage with a much

lower ethanol to methanol ration (Table 1) when consuming naturally

occurring methanol in a diet otherwise equivalent to the drinkers.

 

Thechronic alcoholic for reasons already proposed might sacrifice this

protection.

 

As mentioned below, high temperature canning as developed late in the

19th century should increase significantly the methanol content of

fruits and vegetables. The increased availability and consumption of

these food products in various countries over the years may parallel

better than most other dietary factors the increase in incidence of

coronary disease in their populations.

 

Cigarette smoke, a known

coronary risk factor, contains four times as much *methanol* as

formaldehyde and only traces of ethanol.

 

ETHANOL AND FOLIC ACID

 

The importance of ethanol as an antidote to methanol toxicity in

humansis very well established in the literature. The timely

administration of ethanol is still considered a vital part of methanol

poisoning management.

Ethanol slows the rate of

methanol's conversion to formaldehyde and formate, allowing the body

time to excrete methanol in the breath and urine.

Inhibition is seen

invitro even when the concentration of ethyl alcohol was only 1/16th

thatof methanol. The inhibitory effect is a linear function of the

log

ofthe ethyl alcohol concentration, with a 72% inhibition rate at only

a0.01 molar concentration of ethanol.

 

Oxidation of methanol, like that of ethanol, proceeds independently of

the blood concentration, but a rate only one seventh to one fifth

that of ethanol.

 

Folacin may play an important role in the metabolism of methanol by

catalyzing toe elimination of formic acid. If this process proves

tobe a protective for humans as has been shown in other organisms

itmay account, in part for the tremendous variability of human

responsesto acute methanol toxicity. Folacin in a nutrient often

found

lackingin the normal human diet, particularly during pregnancy and

lactation.

 

METHANOL CONTENT OF ASPARTAME SWEETENED BEVERAGES

 

An average aspartame-sweetened beverage would have a conservative

aspartame content of a bout 555 mg/liter48,51, and therefore, a

methanolequivalent of 56 mg/liter (56 ppm).

 

For example, if a 25 kg child consumed on a warm day, after

exercising,

two-thirds of a two-liter

bottle of soft drink sweetened with aspartame, that child would be

consuming over 732 mg of aspartame (29 mg/kg).

 

This alone exceeds

what the Food and drug Administration considers the 99 - percentile

dailyconsumption level of aspartame. The child would also absorb over

70mg of methanol from that soft drink. This is almost ten times the

Environmental Protection Agency's recommended daily limit of

consumption for methanol.

 

 

To look at the issue from another perspective, the literature reveals

death from consumption of the equivalent of 6 gm of methanol. It

would take 200 12 oz. cans of soda to yield the lethal equivalent of 6

gm of methanol According to FDA regulations, compounds added to foods

that are found to cause some adverse health effect at a particular

usage

level are actually permitted in foods only at much lower levels. The

FDA has established these requirements so that an adequate margin of

safety exists to protect particularly sensitive people and heavy

consumers of the chemical. Section 170.22 of Title 21 of the Code of

Federal Regulations mandates that this margin of safety be 100-fold

below the " highest no-effect " level has tragically not been determined

for methanol8,11, but assuming very conservatively that the level is

onetenth of the lethal dose, the FDA regulations should have limited

consumption to approximately 2.4 ounces of aspartame sweetened soft

drink per day,

 

The FDA allows a lower safety margin only when " evidence is submitted

which justifies use of a different safety factor. " (21.C.F.R. 170.22)

No such evidence has been submitted to the FDA for methanol. Thus,

notonly have the FDA's requirements for acute toxicity not been met,

butalso, no demonstration of chronic safety has been made. The fact

thatmethyl alcohol appears in other natural food products increases

greatlythe danger of chronic toxicity developing by adding another

unnaturalsource of this dangerous cumulative toxin to the food system.

 

NATURAL SOURCES OF METHANOL-

Methanol does appear in nature.

 

To determine what impact the addition of a toxin will have on an

environment it is very helpful to accurately determine the background

levels of consumption.

 

Fruit and vegetables contain pectin with variable methyl ester

content.

 

However, the human has no digestive enzymes for pectin,

particularly

the pectin esterase required for its hydrolysis to methanol.

 

Fermentation in the gut may cause disappearance of pectin but the

production of free methanol is not guaranteed by fermentation.

 

In fact, bacteria in the colon probably reduce methanol directly to

formic acid or carbon dioxide (aspartame is completely absorbed before

reaching the colon).

 

Heating of pectins has been shown to cause virtually no demethoxylation:

even temperatures of 120 C produced

only traces of methanol3.

 

Methanol evolved during cooking of high

pectin foods7 has been accounted for in the volatile fraction during

boiling and is quickly lost to the atmosphere.

Entrapment of these

volatiles probably accounts for the elevation in methanol levels of

certain fruitand vegetable products during canning.

 

In the recent denial by the food and drug Administration of my request

for a public hearing on this issue, the claim is made by them that

methanol occurs in fruit juice at an average of 140 parts per million

(arange of between 15-640 parts per million).

 

This often used average

originates from a informative table in a conference paper presented by

Francot and Geoffroy. The authors explain that the data presented

inthe table " may not " represent their work but " other authors " .

 

Thereis no methodology given nor is the original source cited and

only the identity of the lowest methanol source, grape juice (12 ppm),

and the highest, black currant (680 ppm), are revealed. The other 22

samples used to generate this disarmingly high average are left

completely to the imagination.

 

The authors conclude their paper by insisting that

" the content of methanol in fermented or non-fermented beverages

should not be of concern to the fields of human physiology and public

health. "

 

They imply that wines " do not present any toxicity " due to the

presence of certain natural protective substances.

 

When they present their original data relating to the methanol content

of French wines (range

14-265 ppm) or when the methanol content of any alcoholic beverage is

given, the ratio of methanol to ethanol is also presented.

 

Of the wines they tested, the ratio associated with the highest methanol

 

content (265ppm) indicates over 262 times as much ethanol present as

methanol.

 

the scientific literature indicates that a fair estimate of methanol

content of commonly consumed fruit juices is on the order of 40 parts

permillion (Table 1).

 

Stegink, et al. points out that some neutral

spirits contain as much as 1.5 grams/liter of methanol51, what is not

mentioned is the fact if these spirits are at least 60 proof (30%

ethanol) this still represents the presence of over 200 molecules of

ethanol for

every molecule of methanol that is digested.

 

An exhaustive search of the present literature indicates that no testing

of natural substances

has ever shown methanol appearing alone; in every case ethanol is also

present, usually, in much higher concentrations 15, 27, 28, 30, 31,

35,44, 45.

 

Fresh orange juices can have very little methanol (0.8

mg/liter), and have a concomitant ethyl alcohol content of 380

mg/liter28.

 

Long term storage in cans has a tendency to cause an increase in these

levels, but even after three years of storage,

testing has revealed only 62 mg/liter of methanol, with an ethanol

content of484 mg/liter.

This is a ratio of almost eight times ethanol/methanoll28.

 

Testing done recently in Spain showed orange juice with 33mg/liter

methanol and 651 mg/liter ethanol (20/1 ratio)45.

 

The rangefor grapefruit juices are similar, ranging form 0.2 mg

methanol/liter 27to 43 mg methanol/liter 27. The lowest ratio or any

food item was found in canned grapefruit sections with 50-70 mg/liter

methanol and 200-400 mg/liter ethanol 27, thus averaging six molecules

ethanol for every molecule of methanol.

 

This high ethanol to methanol ratio, even a these low ethanol

concentrations, may have some protective effect.

 

As stated previously,ethanol slows the rate of methanol's conversion to

formaldehyde and formate allowing the body time to excrete methanol in

the breath and urine.

 

Inhibition is seen in vitro even when the concentration of ethylalcohol

was only 1/16th that of methanol.

 

The inhibitory effect is a linear function of the log of the ethyl

alcohol concentration, with a 72% inhibition rate at only a 0.01 molar

concentration of ethanol.

 

Therefore if a liter of a high methanol content orange juice is

consumed, with 33 mg/liter of methanol and a 20/1 ratio of

ethanol/methanol, only one molecule of methanol in 180 will be

metabolized into dangerous metabolites until the majority of the

ethanol has been cleared from the bloodstream.

 

If a similar amount of methanol equivalent from aspartame were consumed,

there would be no competition.

 

Another factor reducing the potential danger associated with methanol

from natural juices is that they have an average caloric density of

500Kcal/liter and high osmolarity which places very definite limits to

their consumption level and rate.

 

 

*following numeric columns*

First and last columns below have complete names.

CAL/LIT = Methanol (MG) Caloric Densidty (calorie/liter)

RATIO/1000c = Ration consumed per 1000 calories

* = Methano (MG)

Ethanol (wt.)

Methanol (wt.)

[end note]

 

TABLE 1

 

AVAILABLE METHANOL IN VARIOUS BEVERAGES

 

Juices METHANOL CAL/ RATIO * Consumption

mg/liter LIT /1000c per day

*Orange, fresh(2 1 470 2 475 1

*Orange, fresh(45) 33 470 70 20 6 mg

*Orange, fresh(31) 34 470 72 16 6 mg

*Orange, canned(2 31 470 66 15 6 mg

*Grapefruit, fresh(27) 1 400 1 2000 1 mg

*Grapefruit(31) 43 400 108 5 7 mg

Grapefruit, Canned(31) 27 400 68 9 5 mg

Grape(15) 12 660 18 -- --

 

Alcoholic Beverages

Beer (4.5%) 0 400 -- -- --

Grain Alcoho(l55) 1 2950 1 500000 --

Bourbon, 100 proof 55 2950 19 9090 --

Rum, 80 proof(15) 73 2300 32 5000 --

 

Wines (French)(15)

White 32 800 44 2500 --

Rose 78 800 98 1000 --

Red 128 800 160 667 --

Pear 188 1370 137 250 --

Cherry 276 1370 201 294 --

 

Wines (American)(30)

Low 50 800 62 2500 --

High 325 800 406 385 --

 

Aspartame Sweetened Beverages(4

2 and 5 liters

Uncarbonated Drinks(4

55 8 6875 0 110 mg 275 mg

Cola (Carbonated)(4

56 8 7000 0 112 mg 280 mg

Orange (Carbonated)(4

91 8 11375 0 182 mg 455 mg

Aspartame, pure 25000

 

*17.6% of U.S. Population consume an average of 185.5 gm of Orange

juice a day

 

*1.1% of the U.S. Population consumes an average of 173.9 gm of

Grapefruit Juice a day1

 

Data obtained in a Department of Agriculture survey of the food

intake of a statistically sampled group of over 17,000 consumers

nationwide1, indicate that the 17.6% of the population that consume

orange juice daily take in an average of 185.5 gm of that juice.

 

these statistics indicated that 1.1% of the population consume an

average of173.9 gm of grapefruit juice while only 1.8% drink

approximately 201 gm of tomato juice daily.

 

 

Even if an individual consumed two juices in the same day or a more

exotic juice such as black currant, there would still be some protection

afforded by the ethanol present

in these natural juices.

 

Consumption of aspartame sweetened drinks at levels commonly used to

replace lost fluid during exercise yields

methanol intake between 15 and 100 times these normal intakes (Table

1).

 

This is comparable to that of " winos " but without the metabolic

reprieve afforded by ethanol.

 

An alcoholic consuming 1500 calories a day from alcoholic sources alone

my consume between 0 and 600 mg of

methanol each day depending on his choice of beverages (Table 1).

 

The consumption of aspartame sweetened soft drinks or other

beverages is not limited by either calories or osmolarity, and can

equal the daily water loss of an individual (which for active people in

a

state like Arizona can exceed 5 liters).

 

The resultant daily methanol intake might then rise to unprecedented

levels.

 

Methanol is a cumulative toxin8 and for some clinical manifestations it

may be a human-specific toxin.

 

CONCLUSION

 

Simply because methanol is found " naturally " in foods, we can not

dismiss the need for carefully documented safety testing in

appropriate

animal models before allowing a dramatic increase in its consumption.

 

We know nothing of the mutagenic, teratogenic or carcinogenic

effect of methyl alcohol on man or mammal. Yet, if predictions

arecorrect it won't be long before an additional 2,000,000 pounds of

it will be added to the food supply yearly.

 

Must this, then, constitute our test of its safety?

 

References

 

1.Agricultural Research Service, U.S. Department of Agriculture,

Portion sizes and days intakes of selected foods, ARS-NE-67 (1975).

 

*************************************************************

 

( " 'Richard T. Murray' " <rm-@e...>;;; 3-15-99)

 

Rich Murray

Room For All

1943 Otowi Drive

Santa Fe, NM 87505

505-986-9103 505-920-6130 cellular VoiceStream

 

Keep up the good work. Send me your address and I will mail you a

copy of my original article. You have my permission to post it

anywhere

you wish.

 

(signed)

 

Woodrow C. Monte Ph.D.

Professor of Food Science

6411 South River Drive #61

Tempe, Arizona 85283-3337

United States of America

Phone/Fax 001 602-965-6938

woo-@a...

*************************************************************[Notes by

Rich Murray rm-@e... 3.17.99: PubMed lists

papers and letters by " Monte WC " and various partners, from 1977 to

1994, but not this one. Go figure!

http://www.ncbi.nlm.nih.gov/PubMed/

 

Two L of diet soda contains 1110 mg aspartame, putting 112 mg methanol

into the body.

 

This is 5.6 12-oz cans at 197 mg aspartame per can,

giving 20 mg methanol each can.

 

The Environmental Protection Agency limit in water for methanol, a

cumulative poison, is 7.8 mg/day .]

 

===============================================

 

Posted: Fri Nov 07, 2003 3:05 pm

Post subject: Case Study on Aspartame in Norway

 

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Case Study on Aspartame in Norway

CASE STUDY – December 2001

[A major newspaper in Norway]

Translation:ABSTRACT

 

http://www.dagbladet.no/print/?/dinside/2001/12/17/301529.html

 

 

Introduction: Aspartame (ASM) is a product that was originally made for

diabetics, but today ASM is widely used by healthy people as an

artificial sweetener in many food products.

 

Purpose: The main goal with this research was to see whether ASM was

harmful to brain cells (cerebellar granule cells). We wanted to check if

 

the damage to the neurons is connected to the N-methyl-D-aspartate

(NMDA)-receptors on these cells.

 

 

Procedure: Brain cells from 7 day old mice were used. They were

cultured in 24 Petri well dishes, and different quantities of ASM were

added.

 

After 7 days, the cultures were analysed by two different tests:

Lactate dehydrogenases (LDH) test, which gives a picture of cell death

 

(LDH leakage to the medium in which the cells were cultured).

3-[4,5-dimethylthiazol-2yl]-2,5-diphenyltetrazolium bromid (MTT) test,

which can be used to analyse mitochondrial activity in living cells.

 

To test whether the NMDA-receptor was involved in the damage done by

ASM, the receptor was blocked by (±)-2-amino-5 phosphonopentanocid

(AP5).

 

 

 

Results: Our results showed damage/cell death from an added quantity of

0.06 mg/ml ASM each day for 4 days.

 

As a comparison there is 0.24 mg/ml ASM in Cola Light. MTT- and

LDH-tests showed damage to the neurons at an added quantity of 1.5 and

3.00 mg/ml ASM after 22 hours of incubation.

 

The results also show that ASM is in part acting through the

NMDA-receptor because AP5 reduced or blocked the damage to the granule

cells.

 

Conclusion:

 

In light of these results, our conclusion is that in order to be on the

safe side, it should be warned against use of ASM as a food additive,

maybe especially in products consumed by children, because

NMDA-receptors and the synapses involved also are connected to learning.

 

 

 

 

 

AIM Barleygreen

" Wisdom of the Past, Food of the Future "

 

http://www.geocities.com/mrsjoguest/Diets.html

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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