Fwd: Report: Aspartame- Methanol and the Public Health

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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 new 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 toxin8.

 

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 level55. 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 model42. There are no human

or

mammalian studies to evaluate the possible mutagenic, teratogenic, or

carcinogenic effects of chronic administration of methyl alcohol55.

 

The average intake of methanol from natural sources varies but limited

data suggests an average intake of considerably less than 10 mg/day8.

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 beverages15.

 

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 (Table 1). Ethanol inhibits metabolism of methanol and

allows

the body time for clearance of the toxin through the lungs and

kidneys40,46.

 

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.

of the Food Science and Nutrition Laboratory Arizona State

University Tempe, Arizona 85287

 

ASPARTAME

 

Aspartame (L-aspartyl-L-phenylalanine methyl ester) has recently 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, 198148.

 

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)47. When

digested, these components are released into the bloodstream48.

 

Phenylalanine and aspartic acid are both amino acids which are found

in

natural proteins14, 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 bloodstream40. The

quaternary structure of protein also slows the digestion of these

amino

acids: the 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 form

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 absorptioin47.

This happens very quickly with the potential to raise component blood

levels rapidly52. The methyl ester bond of phenylalanine is the first

to cleave due to its susceptibility to pancreatic enzymes40. This is

highly unusual; the methyl esters associated with pectin for instance

are completely impervious to all human digestive enzymes6.

 

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

of

Technology, 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 system61 (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 sleep61.

 

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

rat52 and release of pituitary gonadotropins and prolactin in the

rhesus

monkey58. The amount of luteinizing hormone in the blood is a major

determinant of menstrual cycling in the human female39.

 

METHANOL

 

Methanol (methyl alcohol, wood alcohol), a poisonous substance60, is

added as a component during the manufacture of aspartame47. This

methanol is subsequently released within hours of consumption51 after

hydrolysis of the methyl group of the dipeptide by chymotrypsin in the

small intestine40 as it occurs in soft drinks after decomposition of

aspartame during storage or in other foods after being heated48.

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 consumption51.

 

Methanol has no therapeutic properties and is considered only as a

toxicant20. The ingestion of two teaspoons is considered lethal in

humans19.

 

Methyl alcohol produces the Methyl alcohol syndrome, consistently,

only

in humans and no other test animal, including monkeys42,54. There is

a

clear difference between " toxicity " , which can be produced in every

living thing, and the " toxic syndrome " 54.

 

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 enzymes18 during evolution sets man apart from

all

laboratory animals including the monkey42. There is no generally

accepted animal model for methanol toxicity42,59. Humans

suffer " toxic

syndrome " 54 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, respectively43; ethyl

alcohol is more toxic than methanol to these test animals43. No human

or experimental mammalian studies have been found to evaluate the

possible mutagenic, teratogenic or carcinogenic effects of methyl

alcohol55, though a 3.5% chromosomal aberration rate in testicular

tissues of grasshoppers was induced by an injection of methanol51.

 

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

party

per million, with a recommended limit of consumption below 7.8

mg/day8.

This report clearly indicates that methanol:

 

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

once

it is absorbed. In the body, methanol is oxidized to formaldehyde and

formic acid; both of these metabolites are toxic. " 8

 

Role of Formaldehyde

 

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

been

questioned34. No skeptic can overlook the fact that, metabolically,

formaldehyde must be formed as an intermediate to formic acid

production54. Formaldehyde has a high reactivity which may be why it

has not been found in humans or other primates during methanol

poisioning59. The localized retinal production of formaldehyde from

methanol is still thought to be principally responsible fro the optic

papillitis and retinal edema always associated with the toxic syndrome

in humans20. This is an intriguing issue since formaldehyde poisoning

alone does not produce retinal damage20.

 

If formaldehyde is produced form 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 know

carcinogen57 producing squamous-cell carcinomas by inhalation exposure

in experimental animals22. The available epidemiological studies do

not

provide adequate data for assessing the carcinogenicity of

formaldehyde

in man22,24,57. However, reaction of formaldehyde with

deoxyribonucleic

acid (DNA) has resulted in irreversible denaturation that could

interfere with DNA replication and result in mutation37. 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 animals52. 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

the

production of formic acid19. Insufficient formic acid is generated to

account for the severity of metabolic acidosis produced and,

therefore,

other organic acids may be involved32.

 

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

compounds20.

 

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

poisoning20. Other striking clinical features associated only with

the

oral administration of methanol are elevated serum amylase are the

finding of pancreatitis or pancreatic necrosis on autopsy20,55.

 

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

are

interested in observing the effect of increased methanol consumption

on

a population.

 

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

The

individuals 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 conditions20.

 

Many of the signs and symptoms of intoxication due to methanol

ingestion

are not specific to methyl alcohol. For example, headaches, ear

buzzing, 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 neuritis55. The most characteristic

signs

and symptoms of methyl alcohol poisoning in humans are the various

visual disturbances which can occur without acidosis55 although they

unfortunately do not always appear20. 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 vision20,55.

 

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 (Table 1). 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 deficiency21

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 alone56. The fascinating

similarities linking unusual clinical features of methanol toxicity

and

alcoholism are worth noting.

 

 

Neuritis:

 

Chronic occupational exposure to methanol often produces human

complaints of neuritis with paresthesia, numbing, prickling and

shooting

pains in the extremities4,55.

 

Alcoholic polyneuropathy36 or multiple peripheral neuritis21 differs

symptomatically from the methanol induced syndrome only in its first

and

often exclusive affinity for legs. The unpleasant sensations of

intolerable pain associated with slight tactile stimulation36 is not

an

uncommon 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 polyneuropathy36. 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

repetition

of 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 inflammation16,20. Microscopic findings of pancreatic

necrosis on autopsy have been reported after acute oral methanol

poisoning55. In fact, pancreatic injury probably accounts for almost

universal violent epigastric pain17 and occasional elevated serum

amylase levels55 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 attack16. The fact

that

40% of all cases of acute pancreatitis complaints are attributable to

alcoholics21, however, must be taken into consideration to avoid

artifactual association. Pancreatitis has been a complaint associated

with 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

the

organ 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 period56.

 

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

50

percent of the cases of congestive cardiomyopathy56. 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

nondrinker56

seems 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.

The

chronic 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

humans

is very well established in the literature46,55. The timely

administration of ethanol is still considered a vital part of methanol

poisoning management11,12,19,20,50. 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 ethyl alcohol was only 1/16th

that

of methanol62. 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 ethanol2,46.

 

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

the blood concentration, but a rate only one seventh20 to one fifth12

that of ethanol.

 

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

catalyzing toe elimination of formic acid41. If this process proves

to

be a protective for humans as has been shown in other organisms50,38

it

may account, in part for the tremendous variability of human responses

to acute methanol toxicity. Folacin in a nutrient often found lacking

in 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

methanol

equivalent 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 daily

consumption level of aspartame48. The child would also absorb over 70

mg 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 methanol55,59. 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

one

tenth 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,

not

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

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

methyl alcohol appears in other natural food products increases

greatly

the danger of chronic toxicity developing by adding another unnatural

source 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 pectin6,25,

particularly

the pectin esterase required for its hydrolysis to methanol26.

Fermentation in the gut may cause disappearance of pectin6 but the

production of free methanol is not guaranteed by fermentation3. In

fact, bacteria in the colon probably reduce methanol directly to

formic

acid or carbon dioxide6 (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 atmosphere49. Entrapment of these

volatiles

probably accounts for the elevation in methanol levels of certain

fruit

and vegetable products during canning31,33.

 

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

for a public hearing on this issue13, the claim is made by them that

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

(a

range of between 15-640 parts per million). This often used average

originates from a informative table in a conference paper presented by

Francot and Geoffroy15. The authors explain that the data presented

in

the table " may not " represent their work but " other authors " 15. There

is 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 substances15. 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

(265

ppm) 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 per

million (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 of

484 mg/liter. This is a ratio of almost eight times ethanol/methanol

l28. Testing done recently in Spain showed orange juice with 33

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

for grapefruit juices are similar, ranging form 0.2 mg methanol/liter

27

to 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

ethyl

alcohol was only 1/16th that of methanol62. 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

competition46.

 

Another factor reducing the potential danger associated with methanol

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

500

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

their consumption level and rate.

 

[begin webmaster note]

*following numeric colums*

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(28) 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(28) 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(48)

2 and 5 liters

Uncarbonated Drinks(48)

55 8 6875 0 110 mg 275 mg

Cola (Carbonated)(48)

56 8 7000 0 112 mg 280 mg

Orange (Carbonated)(48)

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 day1

*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 of

173.9 gm of grapefruit juice while only 1.8% drink approximately 201

gm

of tomato juice daily. Table 1 shows that under normal conditions

these

individuals would only be expected to consume between 1 and 7 mg of

methanol a day from the sources. 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 mammal55,59. Yet, if predictions

are

correct5 it won't be long before an additional 2,000,000 pounds of it

will be added to the food supply yearly53.

 

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).

 

2.Bartlett, G.R., Inhibition of Methanol Oxidation by Ethanol in the

Rat.Am. J. Physiol., 163:619-621 (1950).

 

3.Braverman, J.B.S. and Lifshitz, A., Pectin Hydrolysis in Certain

Fruits During Alcoholic Fermentation. Food Tech., 356-358, July,

(1957).

 

4.Browning, E., Toxicity and Metabolism of Industrial Solvents, New

York: Elsevier Publishing Company, (1965).

 

5.Bylinsky, G., The Battle for America's Sweet Tooth. Fortune, 28-32,

July (1982).

 

6.Campbell, L.A., Palmer G.H., Pectin in Topics in Dietary Fiber

Research. Edited spiller, G.A. and Amen, R.J. Plenum Press, NY (1978).

 

7.Casey,J.C., Self, R. and Swain, T., Origin of Methanol and Dimethyl

Sulphide from Cooked Foods. Nature, 200:885 (1963).

 

8.Cleland, J.G. and Kingsbury, G.L., Multimedia Environmental Goals

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

 

( " 'Richard T. Murray' " <rmforall@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

woody.monte@a...

 

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

 

[Notes by Rich Murray rmforall@e... 3.17.99: PubMed lists

14

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 .]

--- End forwarded message ---