Aspartame industry propaganda generated in response to the criticismsof activists like ourselves claims that since methanol is a “naturallyoccurring substance” and that there is no danger in its consumption asit exists in the form in which it is contained in aspartame products. This1984 University of Arizona clearly indicates that this premise is completelyspurious and misleading, and that NutraSweet knew that this was so whenthey first put their poison on the market.
Woodrow C. Monte, Ph.D., R.D.
Director of the Food Science and Nutrition Laboratory
Arizona State University
Tempe, Arizona 85287
Published in Journal of Applied Nutrition, Volume 36, Number1, 1984
Abstract
Aspartame (L-asparty-L-phenylalanine methyl ester), a new sweetenermarketed under the trade name NutraSweet*, releases into the human bloodstreamone molecule of methanol for each molecule of aspartame consumed.
This new methanol source is being added to foods that have considerablyreduce caloric content and, thus, may be consumed in large amounts. Generally,none of these foods could be considered dietary methanol sources priorto addition of aspartame. When diet sodas and soft drinks, sweetened withaspartame, are used to replace fluid loss during exercise and physicalexertion in hot climates, the intake of methanol can exceed 250 mg/dayor 32 times the Environmental Protection Agency’s recommended limit ofconsumption for this cumulative toxin(8).
There is extreme variation in the human response to acute methanolpoisoning, the lowest recorded lethal oral dose being 100 mg/kg with oneindividual surviving a dose over ninety times this level (55). Humans,due perhaps to the loss of two enzymes during evolution, are more sensitiveto methanol than any laboratory animal; even the monkey is not generallyaccepted as a suitable animal model (42). There are no human or mammalianstudies to evaluate the possible mutagenic, teratogenic, or carcinogeniceffects of chronic administration of methyl alcohol (55).
The average intake of methanol from natural sources varies butlimited data suggests an average intake of considerably less than 10 mg/day(8). Alcoholics may average much more, with a potential range of between0 and 600 mg/day, depending on the source and in some cases the qualityof their beverages (15).
Ethanol, the classic antidote for methanol toxicity, is foundin natural food sources of methanol at concentrations 5 to 500,000 timesthat of the toxin (Table 1). Ethanol inhibits metabolism of methanol andallows the body time for clearance of the toxin through the lungs and kidneys(40,46).
The question asked whether uncontrolled consumption of this newsweetener might increase the methanol intake of certain individuals toa point beyond which our limited knowledge of acute and chronic human methanoltoxicity can be extrapolated to predict safety.
*NutraSweet is a trademark of G.D. Searl & Co.
Aspartame
Aspartame (L-aspartyl-L-phenylalanine methyl ester) has recentlybeen approved as a sweetener for liquid carbonated beverages. It has hadwide acceptance as an additive in many dry food applications after Foodand Drug Administration approval on July 24, 1981 (48).
The Food and Drug Administration, Dr. Richard Wurtman and myselfhave received well over a thousand written complaints relative to aspartameconsumption. By far, the most numerous of these include dizziness, visualimpairment, disorientation, ear buzzing, high SGOT, tunnel vision, lossof 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 scientificallyevaluated. However, a thorough knowledge of just what makes this new sweetenerstand apart from other nutritional substances might aid physicians in makingdietary recommendations for their patients.
Aspartame (NutraSweet)* is a small molecule made up of threecomponents: Phenylalanine, aspartic acid, and methanol (wood alcohol) (47).When digested, these components are released into the bloodstream (48).Phenylalanine and aspartic acid are both amino acids which are found innatural proteins (14), and under normal circumstances are beneficial, ifnot essential, for health. Proteins are complex molecules which containmany chemically bonded amino acids. It takes several enzymes to break thesebonds and liberate the amino acids. This is as slow process and the aminoacids are released gradually into the blood stream (40). The quaternarystructure of protein also slows the digestion of these amino acids; theamino acids in the center of the protein molecule aren’t released untilthe outer layers of amino acids on the surface have been swept away. Thisnatural time release process saves the body from large numbers of any oneof these 21 amino acids being released into the bloodstream at any onetime.
Aspartame requires the breaking of only two bonds for absorption(47). This happens very quickly with the potential to raise component bloodlevels rapidly (52). The methyl ester bond of phenyalanine is the firstto cleave due to its susceptibility to pancreatic enzymes (40). This ishighly unusual; the methyl esters associated with pectin for instance arecompletely impervious to all human digestive enzymes (6).
Amino Acid Components
Phenylalanine
Phenylalanine is an essential amino acid, the daily consumptionof 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 demonstrating that in humans thefeeding of a carbohydrate with aspartame significantly enhances aspartame’spositive effect on plasma and brain phenylalanine and tyrosine levels (48Federal Register at 31379). There are sound scientific reasons to believethat increasing the brain levels of these large neutral amino acids couldaffect the synthesis of neurotransmitters and in turn affect bodily functionscontrolled by the autonomic nervous system (61) (e.g., blood pressure).The proven ability of aspartame to inhibit the glucose-induced releaseof serotonin within the brain may also affect behaviors, such as satietyand sleep (61).
Aspartic Acid
Aspartic acid, is not an essential amino acid but is normallyeasily utilized for human metabolism. However, under conditions of excessabsorption it has caused endocrine disorders in mammals with markedly elevatedplasma levels of luteinizing hormone and testosterone in the rat (52) andrelease of pituitary gonadotropins and prolactin in the rhesus monkey (58).The amount of luteinizing hormone in the blood is a major determinant ofmenstrual cycling in the human female (39).
Methanol
Methanol (methyl alcohol, wood alcohol), a poisonous substance(60), is added as a component during the manufacture of aspartame (47).The methanol is subsequently released within hours of consumption (51)after hydrolysis of the methyl group of the dipeptide by chymotrypsin inthe small intestine (40). Absorption in primates is hastened considerablyif the methanol is ingested as free methanol (40) as it occurs in softdrinks after decomposition of aspartame during storage or in other foodsafter being heated (48). Regardless of whether the aspartame-derived methanolexists in food in its free form or still esterified to phenylalanine, 10%of the weight of aspartame intake of an individual will be absorbed bythe blood stream as methanol within hours after consumption (51).
Methanol has no therapeutic properties and is considered onlyas a toxicant (20). The ingestion of two teaspoons is considered lethalin humans (19).
Methyl alcohol produces the Methyl alcohol syndrome, consistently,only in humans and no other test animal, including monkeys (42,54). Thereis a clear difference between “toxicity”, which can be produced in everyliving thing, and the “toxic syndrome” (54).
The greater toxicity of methanol to man is deeply rooted in thelimited biochemical pathways available to humans for detoxification. Theloss of uricase (EC 1.7.3.3.), formyl-tetrahydrofolate synthetase (EC 6.3.4.3.)(42) and other enzymes (18) during evolution sets man apart from all laboratoryanimals including the monkey (42). There is no generally accepted animalmodel for methanol toxicity (42,59). Humans suffer “toxic syndrome” (54)at a minimum lethal dose of < 1gm/kg, much less than that of monkeys,3-6 g/kg (42,59). The minimum lethal dose of methanol in the rat, rabbit,and dog is 9, 5, 7, and 8 g/kg, respectively (43); ethyl alcohol is moretoxic than methanol to these test animals (43). No human or experimentalmammalian studies have been found to evaluate the possible mutagenic, teratogenicor carcinogenic effects of methyl alcohol (55), through a 3.5% chromosomalaberration rate in testicular tissues of grasshoppers was induced by aninjection of methanol (51).
The United States Environmental Protection Agency in their MultimediaEnvironmental Goals for Environmental Assessment recommends a minimum acutetoxicity concentration of methanol in drinking water at 3.9 parts per million,with a recommended limit of consumption below 7.8 mg/day (8). This reportclearly indicates that methanol:
“is considered a cumulative poison due to the low rate of excretiononce it is absorbed. In the body, methanol is oxidized to formaldehydeand formic acid; both of these metabolites are toxic.” (8)
Role of Formaldehyde
Recently the toxic role of formaldehyde (in methanol toxicity)has been questioned (34). No skeptic can overlook the fact that, metabolically,formaldehyde must be formed as an intermediate to formic acid production(54). Formaldehyde has a high reactivity which may be why it has not beenfound in humans or other primates during methanol poisioning (59). Thelocalized retinal production of formaldehyde from methanol is still thoughtto be principally responsible for the optic papillitis and retinal edemaalways associated with the toxic syndrome in humans (20). This is an intriguingissue since formaldehyde poisoning alone does not produce retinal damage(20).
If formaldehyde is produced from methanol and does have a reasonablehalf life within certain cells in the poisoned organism the chronic toxicologicalramifications could be grave. Formaldehyde is a know carcinogen (57) producingsquamous-cell carcinomas by inhalation exposure in experimental animals(22). The available epidemiological studies do not provide adequate datafor assessing the carcinogenicity of formaldehyde in man (22,24,57). However,reaction of formaldehyde with deoxyribonucleic acid (DNA) has resultedin irreversible denaturation that could interfere with DNA replicationand result in mutation (37). Glycerol formal, a condensation product ofglycerol and formaldehyde (which may be formed in vivo), is a potent teratogencausing an extremely high incidence of birth defects in laboratory animals(52). Even the staunchest critic of formaldehyde involvement in methanoltoxicity admits:
“It is not possible to completely eliminate formaldehyde as atoxic intermediate because formaldehyde could be formed slowly within cellsand interfere with normal cellular function without ever obtaining levelsthat are detectable in body fluids or tissues.” (34)
Acute Toxicity in Man: “Toxic Syndrome”
A striking feature of methyl alcohol syndrome is the asymptomaticinterval (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 (19). Insufficient formic acid is generated toaccount for the severity of metabolic acidosis produced and, therefore,other organic acids may also be involved (32). Patients may complain oflethargy, confusion, and impairment of articulation, all frequently encounteredsigns in moderate central nervous system (CNS) intoxication’s resultingfrom other toxic compounds (20).
Patients may also suffer leg cramps, back pain, severe headache,abdominal pain, labored breathing, vertigo and visual loss, the latterbeing a very important clue to making a diagnosis of methanol poisoning(20). Other striking clinical features associated only with the oral administrationof methanol are elevated serum amylase and the finding of pancreatitisorpancreatic necrosis on autopsy (20,55).
In fatal cases liver, kidneys and heart may show parenchymatousdegeneration. The lungs show desquamation of epithelium, emphysema, edema,congestion and bronchial pneumonia(12).
Chronic Human Exposure
This is the most important aspect of methanol toxicity to thosewho are interested in observing the effect of increased methanol consumptionon 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 withacute toxicity often do not surface under chronic conditions (20).
Many of the signs and symptoms of intoxication due to methanolingestion are not specific to methyl alcohol. For example, headaches, earbuzzing, dizziness, nausea and unsteady gait (inebriation), gastrointestinaldisturbances, weakness, vertigo, chills, memory lapses, numbness and shootingpains in the lower extremities hands and forearms, behavioral disturbances,and neuritis (55). The most characteristic signs and symptoms of methylalcohol poisoning in humans are the various visual disturbances which canoccur without acidosis (55) although they unfortunately do not always appear(20). Some of these symptoms are the following: misty vision, progressivecontraction of visual fields (vision tunneling), mist before eyes, blurringof vision, and obscuration of vision (20,55).
Alcoholics: Chronic Methanol Consumption
Alcoholics in general, but particularly those who consume largequantities of wine or fruit liqueur, would seem, from the available evidence,to be the only population thus far exposed to consistently high levelsof methanol ingestion (Table 1). The high ethanol/methanol ration of alcoholicbeverages must have a very significant protective effect, though enzymekinetics mandate some constant but low level of methanol metabolism. Onecould speculate that the delicate balance which maintains this defensemight be jeopardized by the general nutrition neglect and specificallythe folic acid deficiency (21) associated with the meager food intake ofsome alcoholics. Alcoholics have a much higher incidence of cancer andother degenerative diseases, none of which can be attributed to ethanolalone (56). The fascinating similarities linking unusual clinical featuresof methanol toxicity and alcoholism are worth noting.
Neuritis:
Chronic occupational exposure to methanol often produces humancomplaints of neuritis with paresthesia, numbing, pricking and shootingpains in the extremities (4,55).
Alcoholic polyneuropathy (36) or multiple peripheral neuritis(21) differs symptomatically from the methanol induced syndrome only inits first and often exclusive affinity for legs. The unpleasant sensationsof intolerable pain associated with slight tactile stimulation (36) isnot an uncommon anecdotal consumer complaint following long term consumptionof aspartame. In one such case reported to me, my interpretation of anelectromyogram indicated the signs of denervation indicative of alcoholicpolyneuropathy (36). The individual’s ischemic lactate pyruvate curve,before and after fasting, was flat. Less than six weeks after aspartameconsumption ceased the major symptoms subsided and repetition of thesetests produced normal responses, although the individual still experiencedintermittent pain.
Pancreatitis:
Methanol is one of the few etiologic factors associated withacute pancreatic inflammation (16,20). Microscopic findings of pancreaticnecrosis on autopsy have been reported after acute oral methanol poisoning(55) which marks the end of the latent period.
There is a generally accepted association between alcoholismand pancreatitis. Most patients, however, give a history of 5 to 10 yearsof heavy drinking before the onset of the first attack (16). The fact that40% of all cases of acute pancreatitis complaints are attributable to alcoholics(21), 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 tothe fine dust of aspartame at the packaging plant he had worked for overa year, was complaining of blurred vision, headaches, dizziness, and severedepression before his sudden death. An autopsy revealed (aside from theorgan involvement one might expect from methanol toxicity) myocardial hypertrophyand dilatation with the myocardiopathy and left ventricle involvement reminiscentof alcoholic cardiomyopathy. Alcoholic cardiomyopathy, however, typicallyoccurs in 30-55 year old men who have a history of alcohol intake in quantitiescomprising 30-50 percent of their daily caloric requirement over a 10 to15 year period (56).
It has been suggested that alcohol is the etiologic factor inat least 50 percent of the cases of congestive cardiomyopathy (56). Thesignificantly lower hospitalization incidence for coronary disease amongmoderate drinkers than among nondrinkers and the protection to coronaryrisk afforded the moderate drinker (less than two drinks a day) over thenondrinker (56) seems contradictory. However, if we implicate methanolas the etiologic factor, then clearly the nondrinker is at a disadvantagewith a much lower ethanol to methanol ratio (Table 1) when consuming naturallyoccurring 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 latein the 19th century should increase significantly the methanol contentof fruits and vegetables. The increased availability and consumption ofthese food products in various countries over the years may parallel betterthan most other dietary factors the increase in incidence of coronary diseasein their populations. Cigarette smoke, a known coronary risk factor, containsfour times as much methanol as formaldehyde and only traces of ethanol.
Ethanol and Folic Acid
The importance of ethanol as an antidote to methanol toxicityin humans is very well established in the literature (46,55). The timelyadministration of ethanol is still considered a vital part of methanolpoisoning management (11,12,19,20,50). Ethanol slows the rate of methanol’sconversion to formaldehyde and formate, allowing the body time to excretemethanol in the breath and urine. Inhibition is seen in vitro even whenthe concentration of ethyl alcohol was only 1/16th that of methanol (62).The inhibitory effect is a linear function of the log of the ethyl alcoholconcentration, with a 72% inhibition rate at only a 0.01 molar concentrationof ethanol (2,46).
Oxidation of methanol, like that of ethanol, proceeds independentlyof the blood concentration, but at a rate only one seventh (20) to onefifth (12) that of ethanol.
Folacin may play an important role in the metabolism of methanolby catalyzing the elimination of formic acid (41). If this process provesto be as protective for humans as has been shown in other organisms (50,38)it may account, in part, for the tremendous variability of human responsesto acute methanol toxicity. Folacin is a nutrient often found lacking inthe normal human diet, particularly during pregnancy and lactation (14).
Methanol Content of Aspartame Sweetened Beverages
An average aspartame-sweetened beverage would have a conservativeaspartame content of about 555 mg/liter48, (51) and therefore, a methanolequivalent of 56 mg/liter (56 ppm). For example, if a 25 kg child consumedon a warm day, after exercising, two-thirds of a two-liter bottle of softdrink sweetened with aspartame, that child would be consuming over 732mg of aspartame (29 mg/kg). This alone exceeds what the Food and Drug Administrationconsiders the 99+ percentile daily consumption level of aspartame (48).The child would also absorb over 70 mg of methanol from that soft drink.This is almost ten times the Environmental Protection Agency’s recommendeddaily limit of consumption for methanol.
To look at the issue from another perspective, the literaturereveals death from consumption of the equivalent of 6 gm of methanol (55,59).It would take 200 12 oz. cans of soda to yield the lethal equivalent of6 gm of methanol. According to FDA regulations, compounds added to foodsthat are found to cause some adverse health effect at a particular usagelevel are actually permitted in foods only at much lower levels. The FDAhas established these requirements so that an adequate margin of safetyexists to protect particularly sensitive people and heavy consumers ofthe chemical. Section 170.22 of Title 21 of the Code of Federal Regulationsmandates that this margin of safety by 100-fold below the “highest no-effect”level. If death has been caused by the methanol equivalent of 200 12 oz.cans of aspartame sweetened soda, one hundredth of that level would betwo cans of soda. The relationship of the lethal dose to the “highest noeffect” level has tragically not been determined for methanol (9,11) butassuming very conservatively that the level is one tenth of the lethaldose, the FDA regulations should have limited consumption to approximately2.4 ounces of aspartame sweetened soft drink per day.
The FDA allows a lower safety margin only when “evidence is submittedwhich justifies use of a different safety factor.” (21.C.F.R.170.22) Nosuch evidence has been submitted to the FDA for methanol. Thus, not onlyhave the FDA’s requirements for acute toxicity not been met, but also,no demonstration of chronic safety has been made. The fact that methylalcohol appears in other natural food products increases greatly the dangerof chronic toxicity developing by adding another unnatural source of thisdangerous 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 onan environment it is very helpful to accurately determine the backgroundlevels of consumption.
Fruit and vegetables contain pectin with variable methyl estercontent. However, the human has no digestive enzymes for pectin (6,25)particularly the pectin esterase required for its hydrolysis to methanol(26). Fermentation in the gut may cause disappearance of pectin (6) butthe production of free methanol is not guaranteed by fermentation (3).In fact, bacteria in the colon probably reduce methanol directly to formicacid or carbon dioxide (6) (aspartame is completely absorbed before reachingthe colon). Heating of pectins has been shown to cause virtually no demethoxylation;even temperatures of 120*C produced only traces of methanol (3). Methanolevolved during cooking of high pectin foods (7) has been accounted forin the volatile fraction during boiling and is quickly lost to the atmosphere(49). Entrapment of these volatiles probably accounts for the elevationin methanol levels of certain fruit and vegetable products during canning(31,33).
In the recent denial by the Food and Drug Administration of myrequest for a public hearing on this issue (13), the claim is made by themthat methanol occurs in fruit juices at an average of 140 parts per million(a range of between 15-640 parts per million). This often used averageoriginates from an informative table in a conference paper presented byFrancot and Geoffroy (15). The authors explain that the data presentedin the table “may not” represent their work but “other authors” (15). Thereis no methodology given nor is the original source cited and only the identityof the lowest methanol source, grape juice (12 ppm), and the highest, blackcurrant (680 ppm), are revealed. The other 22 samples used to generatethis disarmingly high average are left completely to the imagination. Theauthors conclude their paper by insisting that “the content of methanolin fermented or non-fermented beverages should not be of concern to thefields of human physiology and public health.” They imply that wines “donot present any toxicity” due to the presence of certain natural protectivesubstances (15). When they present their original data relating to themethanol content of French wines (range 14-265 ppm) or when the methanolcontent of any alcoholic beverage is given, the ration of methanol to ethanolis also presented. Of the wines they tested, the ratio associated withthe highest methanol content (265 ppm) indicates over 262 times as muchethanol present as methanol. The scientific literature indicates that afair estimate of methanol content of commonly consumed fruit juices ison the order of 40 parts per million (Table 1). Stegink, et al. Pointsout that some neutral spirits contain as much as 1.5 grams/liter of methanol(51); what is not mentioned is the fact that if these spirits are at least60 proof (30% ethanol) this still represents the presence of over 200 moleculesof ethanol for every molecule of methanol that is digested. An exhaustivesearch of the present literature indicates that no testing of natural substanceshas ever shown methanol appearing alone; in every case ethanol is alsopresent, 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 havea concomitant ethyl alcohol content of 380 mg/liter 28. Long term storagein cans has a tendency to cause an increase in these levels, but even afterthree 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 eighttimes ethanol/methanol (28). Testing done recently in Spain showed orangejuice with 33 mg/liter methanol and 651 mg/liter ethanol (20/1 ratio) (45).The range for grapefruit juices are similar, ranging from 0.2 mg methanol/liter27to 43 mg methanol/liter (27). The lowest ratio of any food item was foundin canned grapefruit sections with 50-70 mg/liter methanol and 200-400mg/liter ethanol27, thus averaging six molecules ethanol for every moleculeof methanol.
This high ethanol to methanol ratio, even at these low ethanolconcentrations, may have some protective effect. As stated previously,ethanol slows the rate of methanol’s conversion to formaldehyde and formateallowing the body time to excrete methanol in the breath and urine. Inhibitionis seen in vitro even when the concentration of ethyl alcohol was only1/16th that of methanol62. The inhibitory effect is a linear function ofthe log of the ethyl alcohol concentration, with a 72% inhibition rateat only a 0.01 molar concentration of ethanol (2). Therefore if a literof a high methanol content orange juice is consumed, with 33 mg/liter ofmethanol and a 20/1 ration of ethanol/methanol, only one molecule of methanolin 180 will be metabolized into dangerous metabolites until the majorityof the ethanol has been cleared from the bloodstream. If a similar amountof methanol equivalent from aspartame were consumed, there would be nocompetition (46).
Another factor reducing the potential danger associated withmethanol from natural juices is that they have an average caloric densityof 500 Kcal/liter and high Osmolality which places very definite limitsto their consumption level and rate.
Data obtained in a Department of Agriculture survey of the foodintake of a statistically sampled group of over 17,000 consumers nationwide(1), indicate that the 17.6% of the population that consume orange juicedaily take in an average of 185.5 gm of that juice. These statistics indicatethat 1.1% of the population consume an average of 173.9 gm of grapefruitjuice while only 1.8% drink approximately 201 gm of tomato juice daily.Table 1 shows that under normal conditions these individuals would onlybe expected to consume between 1 and 7 mg of methanol a day from thesesources. Even if an individual consumed two juices in the same day or amore exotic juice such as black currant, there would still be some protectionafforded by the ethanol present in these natural juices. Consumption ofaspartame sweetened drinks at levels commonly used to replace lost fluidduring exercise yields methanol intake between 15 and 100 times these normalintakes (Table 1). This is comparable to that of “winos” but without themetabolic reprieve afforded by ethanol. An alcoholic consuming 1500 caloriesa day from alcoholic sources alone may consume between 0 and 600 mg ofmethanol each day depending on his choice of beverages (Table 1).
The consumption of aspartame sweetened soft drinks or other beveragesin not limited by either calories or Osmolality, and can equal the dailywater loss of an individual (which for active people in a state like Arizonacan exceed 5 liters). The resultant daily methanol intake might then riseto unprecedented levels. Methanol is a cumulative toxin (8) and for someclinical manifestations it may be a human-specific toxin.
Conclusion
Simply because methanol is found “naturally” in foods, we cannot dismiss the need for carefully documented safety testing in appropriateanimal models before allowing a dramatic increase in its consumption.
We know nothing of the mutagenic, teratogenic or carcinogeniceffect of methyl alcohol on man or mammal (55,59). Yet, if predictionsare correct (5) it won’t be long before an additional 2,000,000 pound ofit will be added to the food supply yearly (53).
Must this, then, constitute our test of its safety?
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Table 1: Available Methanol In Various Beverages
density calories/liter |
*methanol (mg) |
||||
| *Orange, fresh (28) | |||||
| *Orange, fresh (45) | |||||
| *Orange, fresh (31) | |||||
| *Orange, canned (28) | |||||
| *Grapefruit, fresh (27) | |||||
| *Grapefruit (31) | |||||
| *Grapefruit, canned (31) | |||||
| Grape (15) |
| alcoholic beverages |
density calories/liter |
||||
| Beer (4.5%) | |||||
| Grain Alcohol (55) | |||||
| Bourbon, 100 proof (15) | |||||
| Rum, 80 proof (15) | |||||
| Wines (French) (15) | |||||
| White | |||||
| White | |||||
| Red | |||||
| Pear | |||||
| Cherry | |||||
| Wines, (American) (30) | |||||
| Low | |||||
| High |
aspartame sweetened beverages |
density calories/liter |
||||
| Uncarbonated Drinks (48) | |||||
| Cola (Carbonated)(48) | |||||
| Orange (Carbonated)(48) | |||||
| Aspartame, pure |
*1.1% of the U.S. Population consume an average of 173.9 gm.of Grapefruit Juice a day (1)