j. lipid res.-1984-crouse-486-96.pdf

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peared to be less active during the period of alcoholingestion than during the control period, but none becameovertly intoxicated. In none of the patients did liver func-tion tests become abnormal during alcohol feeding.

Effects of alcohol on body weight

One aim of this study was to maintain a constancy of

weight throughout all periods. In general, this aim wasachieved: nine patients either gained or lost less than 1.5kg (Table 2). Seven patients (Nos. 1, 2, 7, 8, 10, 1 1, 12)actually lost small amounts of weight when alcohol wasadded to weight maintenance calories; the mean weightloss for these seven was 0.85 kg (range = -0.1 to -1.9kg). On the other hand, four obese patients (Nos. 3, 4,5, 6) gained weight when alcohol was added to weightmaintenance calories. Despite reduction of non-alcoholcalories during the “test” period by 300 cal/day in patient3 and by 380 cal/day in patient 6, these two patientsgained 1.3 and 1.8 kg, respectively, during feeding ofalcohol. One obese patient (No. 4) received alcohol inthe first period, and on discontinuation of alcohol, hisweight began to decline; consequently, his non-alcoholcalories were increased by 200 cal/day and his weightremained constant thereafter.

Patient 9 was the first patient studied. After the controlperiod, and upon substitution of alcohol for non-alcoholcalories, he experienced a weight loss of 2.6 kg throughout

TABLE 2. Weight ch anges durin g alcohol administration

WeightPatient Alcohol

No. Control Alcohol Minus Control

t kg t

1 105.2 1.22 (24)“ 103.8 0.59 (25) -1.42 95.4 f 2.7 (26) 94.3 f .34 (33) -1.1

5b 86.9 f .55 (35) 87.1 f .50 (31) +0.2

Sb 101.7 f 0.38 (31) 103.0 f .60 (27) +1.34b 79.4 f .60 (27) 80.2 f .52 (25) +0.8

6’ 82.7 f .47 (25) 84.5 f .67 (29) +1.87 84.8 f 0.74 (34) 84.3 f .41 (34) -0.58 75.2 f .75 (32) 74.6 f .77 (29) 0.69‘ 77.8 f .61 (20) 75.2 0.55 (34) -2.6

10 73.0 f .49 (37) 73.6 f 0.44 (31) -0.311 62.6 f .78 (34) 60.7 f .42 (26) -1.912 55.6 f .50 (28) 55.5 *0.63 (28) -0.1

Mean f SD (n).Non-alcoho l calories were redu ced during the alcohol test period

or ncreased during the control pe riod (when that followed the alcoholtest period) in four patients to prevent excess weight gain or loss.Reductions were: from 3100 to 2800 calories/day in patient No. 3;from 2800 to 2600 calories/day in patient No. 5; and from 2330 to1950 in patient No. 6. In patient No. 4 calories were increased from2400 calories/day during the alcohol test period t 2600 during the(following) control period.

Alcohol calories were initially substituted for rather than a ddedto formula calories in patient No. 9. Calories in this patient werereduced from 2730 calories/day t 2091 calories/day when alcohol(90 g daily = 6 3 0 calor ies) was started.

the period. His was the greatest weight change experi-enced by any of the patients, and on the basis of hischange, alcohol was added to baseline calories rather thansubstituted for them in the remaining volunteers.

Plasma lipids and lipoproteins

The effects of alcohol on plasma cholesterol and tri-

glycerides and on lipoprotein lipids are summarized inTable 3. For the whole group, the feeding of alcohol wasassociated with small but statistically significant increasesin both plasma lipids. A similar increase occurred inVLDL-CH and VLDL-TG. Five patients had a statisticallysignificant increase in total triglycerides when tested asindividuals; four of these were obese and three of thesetended to gain weight during. alcohol feeding.

Levels of LDL-CH and LDL-TG were unchanged byalcohol feeding, but concentratins of both HDL-CH andHDL-TG rose significantly with alcohol. AH ten patientstested had a numerical increase in HDL-CH, and in seventhe rise was statistically significant for the individuals.

Triglyceride metabolism

Transport of VLDL-TG was estimated in all patients(Table 4). Four patients (Nos. 2, 3, 4, 6) responded toalcohol feeding with at least a 45 increase in productionof VLDL-TG and a resultant rise in VLDL-TG concen-trations. All four of these patients were obese; in theremainder of the patients, alcohol feeding had no effecton production of VLDL-TG.

Clearance rates of chylomicron-TG were determinedin ten patients before and during feeding of alcohol (Table4). In four obese patients (Nos. 2, 3, 5, 6 alcohol pro-longed the residence time in plasma of chylomicron-TG.Thus, delayed clearance of chylomicron-TG appeared tobe related to enhanced production of VLDL-TG. In gen-eral, when alcohol did not stimulate production of VLDL-TG , clearance of chylomicron-TG was not retarded.

Measurements of postheparin lipolytic enzymes [hepatictriglyceride lipase (HTGL) and lipoprotein lipase (LPL)]were determined in the fasting state in six patients (Nos.1, 2, 6, 9, 11, 12). Alcohol feeding had no effect on theactivities of these enzymes (Table 5). For postheparinLPL, activity in the control period was 13.0 5pmol FFA/hr per ml, and was 12.0 3 pmol FFA/hrper ml during alcohol administration. Activity of post-

heparin HTGL was 29.7 16 pmol FFA/hr per ml forthe alcohol-feeding period, vs. 3 1.3 f 14 pmol FFA/hrper ml for the control. None of these differences wasstatistically significant.

Cholesterol and bile acid metabolism

The effects of alcohol on fecal excretion of neutralsteroids and bile acids are presented in Table 6. Excretionof neutral steroids in the control period averaged 495

Crouse and Grundy Alcohol and lipids 489


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TA B L E 3. Total plasma and lipoprotein cholesterol and triglyceride

Patient

Very Low Density High DensityTotal Lipoprotein Low Density Lipoprotein Lipoprotein

NO. Period (n)B CH TG CH TG C H TG Chol TG

1

2

3

4

5

6

7

8

9

10

11

12

Meanf D)

P

C

E T O HA

CE T O H

A

CE T O HA

CE T O H

A

CE T O H

A

CE T O HA

CE T O HA

CE T O HA

CE T O HA

CE T O HA

CE T O H

A

CE T O HA

CE T O HA

204 f 28

235 f 1031

184 19175 17

-9

205 f 5207 f 10

2

183 f 10225 15

42'

2 1 4 f 6233 6

196

285 f 233 0 8 f 6

23

179 f 111 8 3 f 9

4

186 f 18192 13

6

171 10171 f 7

0

2 1 9 f 5220 f 10

1

166 131 8 0 2 9

14

216 f 15229 f 20

11

201 f 32213 f 38

12


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TABLE 4. Metabolismof VLDL-TG and chylomicron-TG

VLDL Lipids VLDL -TGPatient Plasma Residence Chylomicron-TG

NO. Period Volume CH T G CH /TG VLDL T G Transport Tim e Residence Time

1

2

3

4

5

6

7

8

9

10

11

12

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

CE T O H

36043602

35323502

37383748

30063036

33453338

32753292

33893379

30243012

31653145

31693164

28132768

24982462

7790

4557

3140

2751

145152

2127

2632

3739

8285

2815

4381

mgldl

359389

192318

194270

76233

142249

537729

95135

130168

153174

347342

9770

308406

0.2 130.233

0.2360.179

0.1620.149

0.1870.199

0.2700.209

0.2200.203

0.2010.188

0.2420.224

0.2380.248

0.2910.214

0.1400.200

m g l k r

247 12676

12481793

15082408

6261252

8171003

14772256

649826

877688

692914

14741331

483370

11231080

'' C, control; E TO H, alcohol feeding period.

Absorption of cholesterol was estimated in ten patients.Mean absorption was 44.5 f (SD) during the controlperiod and 46.7 f (SD)9 during alcohol feeding (Table7). This difference was not statistically significant.

Lipid composition of gal lbladder bile was determinedin nine patients. Overal l, feeding of alcohol did not alter

TABLE 5. Postheparin lipoprotein lipase (LPL) and hepatictriglyceride lipase (HT GL ) in control and

alcohol treatment periods

L P L H T G L

Patient No. Control ET OH Control ET OH

pmol FA1 kr p r r i n 1

1 16.2 13.6 28.6 35.52 16.7 11.2 35.8 37.06 8.5 8.2 55.9 50.59 19.3 13.3 13.0 13.3

11 10.8 15.3 14.2 15.012 6.5 10.1 31.2 36.8

Mean SD 13 5 12 3 30 f 16 31 14

mgl hr p p r kg

23.725.7

12.919.1

14.823.3

8.015.5

9.411.7

17.026.8

7.69.8

11.79.3

9.112.2

19.918.1

7.76.0

20.219.7

mglhr per kglBW

33.836.6

17.024.5

19.431.0

9.519.1

11.514.2

21.132.2

9.011.4

13.510.6

10.213.3

21.219.2

6.75.1

17.116.4

min

218218

226258

200175

152235

242358

495442

200230

186306

289249

310337

235218

285385

min

1.725.7

6.216.0

5.38.5

17.840.9

12.740.7

3.64.0

8.79.7

5.06.3

2.88.8

9.411.1

the composition of bile (Table 8). Four patients showeda decrease in saturation of bile with cholesterol; two hadan increase; and three were unchanged. Saturation ofgallbladder bile averaged 1 17 27 in the control periodand 114 f 18% during alcohol feeding.

DISCUSSION

Effects of alcohol on body weight

An unexpected finding in the first patient of this studywas that substitution of alcohol calories for non-alcohol

calories caused a progressive loss of weight. This obser-vation substantiated the claim of Pirola and Lieber (17)that alcohol does not contribute to maintenance of bodyweight, and led us to alter the experimental design andadd, rather than substitute, alcohol for baseline calories.In lean patients the consumption of additional alcoholcalories did not produce weight gain. How can this lackof weight gain be explained?

Was the period of alcohol supplementation too short



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TA B L E 6. Fecal excretion of cholesterol and metabolites during control and alcohol test periods

Fecal Steroid Excretion

Patient Days Cholesterol Neutra l Acidic Total CholesterolNo. Period .3 Intake Steroids Steroids Steroids Balance

1

2

3

4

5

6

7

8

9

10

1 1

1 2

C

E T O HA

CE T O H

A

CE T O H

A

CE T O H

A

CE T O HA

CE T O H

A

CE T O H

A

CE T O H

A

CE T O H

ACE T O H

A

CE T O H

A

CE T O HA

mgldl

120

134

120120

133120

103103

111111

103103

111111

103103

10090

107107

9494

8585

466 108

663 135-197'

520 133400 f 29

120

451 f 37498 f 131

-47

643 f 2069 4 0 f 9 1

-297

604 f 70408 f 40

196'

363 f 1084 1 7 f 6 9

-54

5 0 9 f 6 6596 44

-87

570 120468 110

102

585 299341 f 37

244594 f 1195 2 3 f 6 9

71

320 61579 ? 165

-259

326 f 29424 98

-98

mglday f D

267 49

3 9 6 f 6 1- 29'

247 f 129289 f 65

-42

11 2 9 f 5 31413 f 110

-284'

545 f 94751 f 115

-206

297 f 233 4 9 f 5 0

-52

284 65213 f 56

71

4 1 0 f 5 8488 f 44

-78

516 257353 f 85

163

293 129267 f 100

26493 43499 f 52

-6

622 f 132777 f 243

-155

2 7 0 f 2 9293 f 64

-23

733 f 128

1059 186-326'

767 f 246689 83

78

1580f 711911 f 230

-331

1188 2491167 f 1

-479

902 f 69757 75

145'

647 1416 3 0 f 6 4

17

9 1 9 f 8 41084 f 10

- 65'

1086 155821 f 93

265'

878 f 330607 f 125

27 11087 f 1511022 67

65

941 1071356 f 406

-415

596 f 16717 f 35

-121'

mglday f D

613 128

925 186-312'

647 f 246569 f 83

78

1447 f 711791 230

-344

1085 f 2451564 I

-479

791 f 69646 f 75

145'

544 f 1415 1 9 f 6 4

17

808 f 84973 10

-165

983 1557 1 8 f 9 3

265'

778 330517 f 125

26 1980 f 151915 67

65

847 f 1071262 f 406

-415

5 11 f 1 6632 35

-121'

Period: C, control; E T O H , alcohol 90 g/day, added to or substituted for (one patient, #9) baseline formula calories; A, difference, control

(n), Number of determinations. Stools from this period were combined into three to six pools. Th e quotient is the average number of days

Alcohol period significantly different from control ( P < 0.05 or less).

alcohol.

per pool.

to have detected reliably an increase in adipose tissueweight? The ingestion of an extra 630 calories per dayfor 30 days should have produced an increment of 5.25pounds (2.39 kg). A weight gain of this magnitude shouldhave been noted, and our inability to detect a change

probably cannot explain the lack of weight gain. Ther e-fore we might ask whether there could have been a si-multaneous increase in adipose tissue weight and a dec-rement in body water, so that no net change in bodyweight occurred. This is a possibility; alcohol is known

492 Journal of Lipid Research Volume 2 5 , 1984


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TABLE 7. Cholesterol absorption

Control Alcohol DifferencePatient 11) 111 (11 1)

1234678

101112

Mean f SD

8 01)

45 (3)42 (4)41 (3)

40 (4)48 (4)47 (4)36 (3)45 (3)54 (3)47 (4)

44.5 f 5

8-9-2+4+5+1

+13+7+1-6

2.2

, Absorption; n, number of determinations.

to induce a transitory diuresis ( 30 ,3 ) , and a net reductionin body water could have occurred. A longer durationof alcohol feeding might be needed to prove the presence

or absence of adipose tissue gain. Another possible reasonfor lack of weight gain is malabsorption of calories. Inprevious studies of patients with chronic alcoholism, it isdifficult to separate the effects of alcohol from those ofmalnutrition; the latter frequently accompanies alcoholabuse and also is associated with malabsorption (32). Theinfluence of alcohol on absorption of various nutrientsis no exception: early work demonstrated that alcoholinterfered with absorption of thiamine, folic acid, vitaminB12, and d-xylose (33-35). In another study, in whichalcohol provided 46 to 66% of calories, an adequate dietand folic acid supplements prevented malabsorption ofd-xylose and fat (36).

Interference with nutrient absorption thus cannot beimplicated in the calorie wastage apparently induced byalcohol consumption. This has led investigators o evaluatethe possibility that chronic alcohol ingestion leads to ahypermetabolic state not unlike that induced by hyper-thyroidism or thyroxine administration (3'7). In rats,chronic treatment with alcohol increases oxygen con-sumption, and this effect is thought to result from in-creased hepatic mitochondrial sodium-potassium ATPaseactivity. The rise in ATPase activity can account for therise in oxygen consumption in these animals (37). Thus,further studies on effects of alcohol on energy consump-tion in man might prove revealing.

Finally, the apparent lack of weight gain during alcoholsupplementation seemed to be related to the initial weight.Most patients who failed to gain weight with addition ofalcohol were nonobese. Previous investigators have ob-served that enhancement of caloric intake does not nec-essarily cause weight gain in nonobese people. The reasonfor this is unknown. Therefore, we do not know whether

alcohol is unique among nutrients in its failure to causeweight gain in nonobese subjects. Pirola and Leiber (1 7)showed that addition of alcohol calories to a baseline dietwas not as effective in causing weight gain as was theaddition of an equal amount of carbohydrate calories.However, they added a great deal more ethanol (2000Kcal per day) than we did. In this study only 63% Kcalof alcohol was administered and this accounted for anincrease of, on average, only 24 above baseline calories(range 20-30%). In the present study the weight gainnoted in four obese patients given alcohol provides astriking contrast to results in nonobese subjects. Whetherobese patients are more likely than nonobese subjects to

TABLE 8 . Biliary lipid composition~

Control Ethanol

Lipid Composition Lipid CompositionBile

Patient No. CH BA PL Saturation* CH BA PL Bile Saturation*

moirs8 8

1 9.2 67.3 23.6 132 (2)2 5.9 76.6 17.7 96 (3)3 8.9 69.5 22.2 114 (4)4 10.7 70.1 19.2 158 (4)5 10.0 66.7 23.3 133 (3)6 9.3 59.7 30.9 112 (1)7 6.1 7.3 19.6 93 (1)

11 4.6 76.7 18.7 73 (2)9 9.6 68.0 22.4 141 (4)

Mean f SD 117 f 27 (9)

molrs8

8.8 66.3 25.06.7 74.1 19.29.3 72.2 18.59.0 71.5 19.57.6 72.0 20.48.4 67.0 24.66.1 76.0 18.16.5 74.0 19.45.9 77.3 16.8

8

114 (2)101 (3)152 (3)133 (2)110 (3)109 (5)99 (2)

99 (1)106 (5)

114 f 18 (9)

a Abbreviations: CH , cholesterol; BA, bile acids; PL, phospholipids.Percent saturation of gallbladder with cholesterol accordin g t Carey and Small (29) assuming 10

solids for (n) samples.



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to be related to body weight. Overweight individuals re-sponded to alcohol feeding by increasing their bodyweight, by transient increases in VLDL-TG levels, andby an increase in VLDL-TG production. Concomitantly,these individuals had a reduction in clearance of chylo-micron-TG that was most likely the result of competitionfor LPL with VLDL-TG rather than a reduction in LPL.

These metabolic responses of the obese were not notedin lean individuals who did not gain weight when fedalcohol and in whom metabolism of triglyceride-rich li-poproteins was unaffected. In spite of the rise in TGlevels in overweight individuals, alcohol feeding causeda paradoxical increase in levels of HDL-CH in overweightas well as in lean subjects. Alcohol feeding resulted in nochanges in levels of LDL-CH, although we cannot ruleout the possibility of an increased flux of LDL. Further-more, we could not detect changes in the metabolism ofeither cholesterol or bile acids, and alcohol feeding didnot cause a tendency for increased saturation of gall-bladder bile. This study suggests that the most adverse

metabolic effects of alcohol are in obese subjects, whoalready are at increased risk in other ways.l

T h e authors express their appreciation to the Nursing and Die-tetic Services of the Special Diagnostic Unit of the VeteransAdministration M edical Cente r, San D iego, CA. W e acknowledgethe excellent technical supp ort ofJann a Naylor, Elliott Groszek,Susan Butler, Michael Gardner, Lynne Lesh, and MarjorieWhelan. This work was supported by the Veterans Adminis-tration and grants HL-1497 and AM -16667, NIH/H DS/D HH S.Dr. Grundy was a Medical Investigator and Dr. Crouse was aResearch Associate of the Veterans Administration.Manuscript received 3 August 1983

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252: 228-234.

PYOC.4: 2052-2059.

496 Journal of Lipid Research Volume 25, 1984

j. lipid res.-1984-crouse-486-96.pdf

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