Effects of Ethanol on Nutrition RoseAnn L. Shorey Associate Professor of Nutrition University of Texas at Austin Austin. TX 78712 Alcoholism is the most frequent cause of malnutrition in the adult population of the United States. A recent survey found that almost 90% of a randomly selected municipal hospital population hospitalized for illness caused or exacerbated by alcoholism, was frankly deficient in one or more nutrients as determined by standard clinical assays. T h e number of alcoholics is increasing, over nine million by a recent surgeon general's estimate. Alcoholics die eight to twelve wars nrematurelv and morhiditv statistics note that they are , two to three times more likely than the general population to suffer from heart disease, cirrhosis, gastritis, respiratory disease, and trauma. The alcoholic employee costs twice as much in problems related to productivity, interpersonal friction, absenteeism, health, and accidents. The current trend toward increasine consumotion of ethanol by young males and females-&out two:thirds of persons aged 18-29 use alcohol-has resulted in a national focus on teen as well as adult drinking habits. Teens are more susceptible to the nutritional effects of ethanol because of requirements for growth and maturation. In addition, the effects of alcohol intake on pregnant females, particularly teenagers, and on the developing fetus are critical concerns. The following discussion of the nutritional and physiological ramifications of the consumption of ethanol will include examples of four major effects of ethanol ----A
1) Energy from the metabolism of ethanol contributes toobesity, in
itself a known health hazard. 2) Malnutrition and resultant metabolic handicaps are likely since sources of ethanol devoid of must nutrients replace more nutritious foods in the alcoholic's diet. :3) Absorption or activation of some vitamins is inhibited by ethanol
and excretion of some minerals is increased hy ethanol, an additional factor in alcoholic malnutrition. 4) Ethanolper se and its metabolites are toxic to cells of organ systems, particularly the liver.
Obesity T h e resemblance between ethanol and water is visual but not metabolic. Despite folklore to the contrary, ethanol is a concentrated and usable source of energy. Ethanol has more energy per gram, 7 kcallg or 5.5 kcallml, than carbohydrate, 4 kcallg, and only slightly less than fat, 9 kcallg. One jigger, 1.5 fluid ounces, of 86-proof distilled liquor contains 101 kcal. 28 rnl 86 5.5 kcal 1.5 fl oz X -X -X ---- = 101 kcal 1 fl oz 200 ml The net effect of an extra jigger of liquor beyond energy needs each day is a weight gain of approximately 10 lh per year for an already overweight population. Beer and wine are more dilute; 12 oz of 3.6% (wtlwt) beer furnishes 68 kcal, and 4 oz of table wine furnishes 64 kcal of energy from ethanol in addition to energy from carhohydrate for totals of 151 and 99 kcal, respectively. In 1971 the consumption of absolute alcohol from distilled spirits, wine, and beer was 2.6 gallons per drinking age person, up 32% from 1958, and equivalent to 210 kcal, per drinking age person per
article 532 1 Journal of Chemical Education
day. Obviously, consumption is not equally distributed across the population. At times when the body needs energy, ethanol is metaholized to watw and carbon dioxide hy the action of enzymes, which are highly specialized biolog~ralprorein ca1a.yst.i. As illuitmtrd helow, the major mute of the metabolism of ethanol inwlves a two-step uxidation process. The first step involves nn enzyme called ulcohol dehydrogt:nase which includes the lj vitamin niacin in its roenzvme fmm, nicotinnmide adenine dinucleotide ( N A D t ).The renction v~eldsacetaldehydeand thr remwed hydrogen furms reduced NAIIH. Further oxidation of the acrtal(lt.hyde with a second unit of N A D t catd y e d by an rnzyme called a l d e h y d ~drhydrogenase yields acetic arid and a second unit of SADH. The c n o ~ l a s mof liver cells is the primary site of the oxidation oiethanol to acetate. H H H H alcohol aldehyde
I I I
H
I 1
dehydrogenane
dehydrogenase
/ HC-C=O
HC-COH
I
NAD+
I
NADH
H
NAD+
NADH
H
ethanol
acetaldehyde
H
I HC-C I H
acetate
@O O 'H
thiokinase
ATP CoenzymeA
H
0
I 11 HC-C-Coenzyme I H
A
acetic acid acetyl-CoA Acetic acid is then converted with thiokinase enzyme and adenosine triphosphate (ATP) to acetyl-Coenzyme A (CoA), which can be oxidized to COz and H 2 0 with the concomitant formation of utilizable energy in the form of ATP. The metaholic pathway for this last step, the oxidation of acetyl-CoA from ethanol, is the same whether the acetyl-CoA is produced from ethanol or from carhohydrate, protein, or fat. The NADH formed in the cytoplasm by the dehydrogenase enzymes is shuttled to the mitochondriabf cells where it too vields the enerev currencv of ATP. At times when this would produce an energy excess, when ATP is adeouate for bodv needs. the NADH and acetvl-CoA are utilized'in the synthksis of fatty acids, which liver cells package into triglycerides (fat) and ship to the adipose or fat cells for storage. In addition to the well-known beer-belly fat stores of excessive drinkers, increased fat in the liver contributes to the fatty liver that typically precedes alcoholic hepatitis and cirrhosis in alcoholics. The body normally utilizes the full energy potential of ethanol; however, when ethanol is consumed in very large quantities over short periods of time, some is lost via kidney and lung. The Breathalyzer test, which detects small amounts of ethanol in expired air, is based on this fact. In the metabolism of ethanol the initial oxidation step, to acetaldehyde limits the amount of ethanol that the hodv can handle, and its rate is governed by the activity of alcohol dehydrogenase enzvme and the availability of NAD+. The liver metabolizes alcihol a t a rate of 5-7 g & about two-thirds of an ounce of 86-proof alcohol per hour. Intake greater than this amount results in elevated blood ethanol levels and intoxication. Some orientals exhibit an alcohol dehydrogenase with a much lower maximum velocity, hence, lesser activity, and their blood
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ethanol remains elevated longer fnr thesame intake ofethanol. The presence of fat or food mixtures in the stomach delays stomach emntvine . . time and slows the rate of entry of ethanol into the bloodstream. Food mixtures also protect the gastric mucosal cells from the irritating effects of ethanol.
Malnutrition Wine, beer, and liquor contribute energy but do not contain significant quantities of other nutrients; these beverages thus merit the t&m "empty calories." A teenage male would have to drink 9 beers or 200 glasses of wine, representing energy intakes of 50% and 700% of total requirement, respectively, to provide the amount of niacin recommended for his age eroun hv theFood and Nutrition Board of the National Academy of Science. Provisions for other B vitamins such as thiamine from alcoholic beverages are even more ludicrous. The teenage male would have 6 drink 11/2 times his energy requirement to meet his thiamine needs from beer. (This is about 135beers a day!) The level of iron in red wine has been touted as significant, yet the same teenager would have to drink 2125 kcal of wine (21 4-02. glasses) to obtain 10 mg of iron. From these few examples, it is apparent that when any substantial nart of the diet is alcoholic beverages the nutritional adequncy of the diet is jeopardized. It is not surprising I hat manv alcoholics are malnourish~.d.When diets are also high in nutrient-poor fat and sugar, as in the American diet, nutritional status is even more vulnerable. Both males and females are affected by the high energy content of ethanol and its contribution to obesity; however, females particularly must be aware of the danger of maluutrition from any substantial intake of ethanol. The total energy needs of females are lower and therefore a smaller amount of energy requirements can be allocated to items with low nutrient density such as ethanol, fat, and sugar. There is extensive documentation in the literature of dietary deficiencies of B vitamins, notably folic acid, thiamine, niacin, and vitamin B6 in heavy drinkers. Many alcoholics exhibit symptoms related to these deficiencies, including anemia, intestinal malabsorption, and low hlood protein levels.
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Vitamin and Mineral Absorption and Utilization The nutritional status of alcoholics, already a problem due to inadequate diet, is further complicated by the overt effects of ethanol on specific vitamins and minerals. Absorption of folic acid from the gut is diminished in the alcoholic as is the absorption of thiamine and vitamin BIZ.Even in well-nourished subiects given ethanol, thiamine and Biz absorption are decreased. Vitamin BF. occurs in food in the form of pyridoxine, analcohol. The co&ersiou of pyridoxine to pyridoxal, an aldehyde, and its subsequent conversion to the active form is inhibited in alcoholics. The conversion of Vitamin D to the active form that maintains calcium balance in the body has been reported to be impaired in the kidneys of alcoholics. Vitamin A and retinol-binding protein in alcoholics are quite low, perhaps as the result of inhibition of protein synthesis by liver. Some investigators cite low vitamin A levels to exnlain the sterility of male alcoholics. Zinc and . typical .. magnesium deficiencies resulting from increased urinary excretion in alcoholics are well established. The condition of delirium tremens in alcoholics has been treated with intravenously administered magnesium sulfate solution.
0 Toxicity The liver, hlood, central nervous system, and gastrointestinal tract of alcoholics display evidence of overt toxic effects of ethanol and/or its metabolites. Of the organ systems, the liver is the most vulnerable since it is the major site of the detoxification of ethanol by oxidation. The accumulation of
fat in the liver leading to alcoholic hepatitis and ultimately, cirrhosis. correlates with the duration and the degree of alcoholism: Most individuals with cirrhosis have been drinking more than 11of wine or 8 oz of 86-proof per day for 5 years. The Wernicke-Korsakoff syndrome is typified by mental confusion, ataxia (loss of muscle coordination), abnormal ocular motility (uncontn~lledeye movement), and polyneuropathy (generali~eddrterioration of wries). This s y n h m e in- thc nutritionallv debilitated alcoholic a evidence ~ ~ - - chronir of severe effects of ethanol i n the central nervous system. The Wernicke-Korsakoff svndrome is associated with thiamine deficiency and with permanent pathological changes. Many alcoholics have decreased numbers of red and white blood cells. The anemia has been postulated to be the result of folic acid deficiency and interference with vitamin Be,,both required for rapidly proliferating cells. Ethanol increases gastric inflammation and bleeding. This effect, coupled with folic acid deficiency that decreases the number of intestinal epithelial cells available for normal ahsorption of nutrients contributes to the primary and secondary malnutrition of alcoholics. Alcohol also is associated with oancreatitis. inflammation of the pancreas, resulting in low levels of many pancreatic enzymes which are necessary for dirrestion. The nutritional imnliration of the resulting poor digestion of foods is that pan&eatitis in alcoholics decreases the calories available in an already deficient diet. Loss of weight is a typical effect. Some data suenest ethanol per se may he responsible for liver damage; nth& data implicate the aiwtaldehyde formed in the metabolism of ethanol as theu)xic by-product of alcohol ahuse. Kthanol disrupts cellular membranm hy solubili7ing lipid compments. Also the metabolism of ethanol alters the normal~-~~ cellular ratiu of NADt to NADH. with consequences --.----that include a decrease in the body's use i f carbohydrate and an increase in the synthesis of fat and cholesterol. Acetaldehyde, akhougb present only in small amounts, may wreak havoc in biological systems by virtue of its high reactivity. I t may combine with -OH groups to form hemiacetals; with -SH groups. . . such as those on glutathione, Coenzyme A, and cysteine, 'to form mer~a~tohkmiacetals; and with -NHz moups. .. . such as found in proteins, epinephrine and dopamine, to form Schitri hases. 'l'hvse fawri& the aretaldehyde theory of toxiritv note that the administration of the drug antalluse, chemicafiy identified as disulfiram, to an incompletely reformed alcoholic results in an increase in hlood acetaldehyde levels as well as symptoms including nausea, vomiting, headache, weakness, convulsions and even death, to quote the Physician's Desk Reference. From this brief summary of the effects of ethanol, it can be concluded that substantial intakes of ethanol represent a nutritional and physiological hazard. Effects range from obesity to malnutrition of protein, B-complex vitamins, and minerals, to overt toxic manifestations on liver, hlood, and other organ systems. Additional Readlngs ~~~~
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id1 Bndy..I.. and Mills. G.."On Considering Alcuhol apaRisk Factor in SpeificDiseaspa.' Arne,. J. Epidemiology. 107.462 119781.
Glossary of Biochemical Terms Adenosine triphosphate. A major energy donor ATP in energy transfer processes. Heat-stable organic mdecules that must be Coenzymes loosely associated with an enzyme in order for the enzyme to function. The protoplasm in a cell that is outside of the Cytoplasm nucleus of that cell. Volume 56, Number 8. August 1979 / 533
Folie acid
Mitochondria Niacin Thiamine
A member of t h e vitamin-B complex which is necessary for DNA synthesis and, hence, cell division. It can effect, for example, red blood cell formation. Small bodies within the cytoplasm of a cell. They are the sites of energy production. A B-complex vitamin required in energy derivation pathways and for the prevention of pellagra. A B-complex vitamin necessary for carbohydrate metabolism; maintenance of normaineural activity, and the prevention of
Vitamin A Vitamin BE Vitamin BIZ
Vitamin D
heri-heri. A vitamin that is required t o maintain the integrity of epithelial cells. Insufficient Vitamin A can result in blindness. A vitamin active in orotein transformations in human metabolism. A mmplea courd~natimcomp~mndcontainmy cobalt whish I? required in cell replicstwn. Insufficient \'ltnmm BI, ra aiauriatrd with neural degeneration. A vitamin required for normal hone growth.
The Metabolism of Carbohydrates 'The human h d y r e q u i m a varirty ofchemical substances (nutr~rnts)m maintain health. Fwd, ar a result i.f digestiun. yields a pool of earhohgdrates, lipidb, proteins, vitamins, and mincrnls. n porlitrn of which is used for the rynthcsis of new structural molecules; the major part of these nutrients, however, is used for the production of energy to support organism81 activity. The immediate source of energy is a compound called adenmine triphasphate (ATP) which contains high-energy chemical bonds; the pyrophosphate honds in ATP are high-energy bonds in the sense that much free energy is released when they are hvdrolvzed. Hvdrolvsis of ATP nrovides enerev , ... t o sunnort . . orocesses such as muscle contraction and transoort across memlranrs. A numtwr ofmrtahdic reactions areconcrrnrd with the transfer denergy i n m theclnenlirnl bcmdi in the nutrients to ccmpuunds that will ultimately form ATP. One of the principal nutr~cnwrequired in the iurmatian oi ATl' is the six-carbur sugar glucose. Relraw vf the energy stored i l l glucose prcw~edsin a .tq-wi3r fnshwn, each step of which is controlled or catalyzed by specific enzymes.
.
.
CfiH120fi+ 6 0
2
----
6 COz
+ 6 Hz0 + 686 kcal
Overall, the 686 kcal released hy the (aerobic) breakdown of a single mole of glucose yields 38 moles of ATP. Organisms exist in a dynamic steady state. The energy-requiring processes leading to the synthesis of new structural molecules (anabolism) occur simultaneously with processes which release energy (catabolism). Thus,the atoms and molecules that constitute the human hody are in a constant state of flux, and it is useful to consider the existence of nutrient pools within the body that can be tapped to meet the body's needs. There are two major nutrient pools: the amino acid pool and the carbohydrate and fat pwl. Ingested proteins can he broken down into amino acids to form a pool which is used for the synthesis of nitrogen-containing macromolecules required by the hody. Amino acids can also he converted into carbohydrates or fats, the nitrogen being removed as ammonia. The hody does not store excess amino acids or proteins, but converts these substances into carbohydrate or fat. The ammonia produced in this process is transformed into urea and excreted by the kidneys. The second large nutrient pool consists of carhahydrates and fats. These nutrients are usually considered together because they can he interconverted in the body. Carbohydrates and fats are the major energy sources. Indeed, aminoacids must he converted intocarbohydrates if they are to be used as energy sources. The hody is able tostore excess fatsand carbohydrates. The fat and carbohydrate pool and its relationship tosome of the important bodily processes areshown in the figure. Surface Excretions and Sloughed Cells
r--
Specialized Derivatives (Steroids, ete.)
a n d Glycogen)
34
t
journal of Chemical Education
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Carbohydrate a n d F a t Pool (Carbohydrate 2 F a t )
I
I
Excretion
I
1
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Structural Carbohydrates and F a t
Catabolism t o CO,, H,O a n d Energy
