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Alcohol: Effects on Nutritional Status, Lipid Profile and Blood Pressure

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Abstract

Alcohol consumption can be the cause of several diseases. Depending on the frequency and quantity, the consumption of alcohol may increase the risk of malnutrition, weight-gain, obesity and cardio-vascular diseases. The aim of this study was to review the influence of alcohol intake on nutritional status, lipid profile and blood pressure. The review shows that the additional consumption of ethanol calories will favor weight gain and metabolic changes and may engrave the risk of cardiovascular diseases, altering the lipid profile and promoting hypertension. Recommending a moderate use of alcohol with the purpose of taking advantage of its health benefits must not be done.
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Alcohol: Effects on Nutritional Status, Lipid
Prole and Blood Pressure
Mayla Cardoso Fernandes Toffoloa, Aline Silva de Aguiar-Nemera, c,
Vilma Aparecida da Silva-Fonsecab
Abstract
Alcohol consumption can be the cause of several diseases. Depend-
ing on the frequency and quantity, the consumption of alcohol may
increase the risk of malnutrition, weight-gain, obesity and cardio-
vascular diseases. The aim of this study was to review the inuence
of alcohol intake on nutritional status, lipid prole and blood pres-
sure. The review shows that the additional consumption of ethanol
calories will favor weight gain and metabolic changes and may
engrave the risk of cardiovascular diseases, altering the lipid pro-
le and promoting hypertension. Recommending a moderate use of
alcohol with the purpose of taking advantage of its health benets
must not be done.
Keywords: Nutritional status; Obesity; Ethanol; Cardiovascular
disease
Introduction
Alcohol consumption can be the cause of several diseases,
and it is, well known, the high burden of its consumption
over mortality around the world [1]. Alcohol is the only psy-
choactive drug that provides energy (7.1 kcal/g). However,
alcohol intake can increase the risk of weight-gain and the
development of obesity or malnutrition. Additionally, the
frequency and quantity in which alcoholic beverages are
consumed are important factors that should be included in
the evaluation of the risk for cardiovascular diseases.
Nutritional effects of alcohol are entangled with cardio-
vascular toxicity and there are many aspects to review on the
subject. Depending on the age of the subject, its previous
nutritional state, and dose of alcohol ingestion, the consump-
tion of alcohol can lead to different and opposite effects. For
these reason, the aim of this study was to review the inu-
ence of alcohol intake on nutritional status and the conse-
quent effects on the lipid prole and hypertension.
Alcohol and Malnutrition
Alcohol is the only psychoactive drug that provides energy
(7.1 kcal/g). This drug is an intermediate source of energy
when compared to proteins and carbohydrates, which pro-
vide 4.0 kcal/g, and to the lipids, which provide 9.0 kcal/g
[2]. However, its calories are considered “empty,” because
alcohol ingestion does not provide vitamins and minerals [3]
and its use may cause alterations to the nutritional state [4].
Due to the high energy value of alcohol, it is common
to assume that, when consumed in excess, alcohol increases
the risk of weight-gain and the development of obesity [5].
However, despite its high calorie density, alcohol consumers
do not appear to gain weight when compared to non-con-
sumers [6].
When the alcohol caloric ingestion represents 50% or
more of the total calorie ingestion, the body system may in-
efciently utilize the energy provided by the ethanol inges-
tion due to the activation of the Microsomal Ethanol Oxidiz-
ing System (MEOS) [7]. At the cost of energy waste, the
MEOS is the main liver pathway for ethanol oxidation [8].
Its induction is reversible after alcohol abstinence [9]. Dur-
ing the observational study of 181 hospitalized males that
consumed more than 80 g/day of ethanol, Santolaria et al
[10] observed that 63.1% suffered from anorexia, 58.7% pre-
sented weight loss, and 17.8% had a BMI below 20 kg/m2.
After a period of three months of alcohol abstinence, the use
of caloric energy in alcoholics was normalized, just as the
increase of the Body Mass Index (BMI) and the Waist Hip
Manuscript accepted for publication October 12, 2012
aDepartamento de Nutrição, Instituto de Ciências Biológicas,
Universidade Federal de Juiz de Fora, Juiz de Fora, Minas Gerais,
Brasil
bNucleo de Ciencias Comportamentais e do Desenvolvimento,
Departamento de Fisiologia e Farmacologia, Instituto Biomedico,
Universidade Federal Fluminense, Rio de Janeiro, Brasil
cCorresponding author: Aline Silva de Aguiar Nemer, Universidade
Federal de Juiz de Fora, Instituto de Ciencias Biologicas,
Departamento de Nutricao, Cidade Universitaria/Juiz de Fora, Minas
Gerais, Brasil. Email: aline.nemer@ufjf.edu.br
doi: http://dx.doi.org/10.4021/jem128e
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Toffolo et al
Articles © The authors | Journal compilation © J Endocrinol Metab and Elmer Press™ | www.jofem.org
Ratio (WHP) [11]. The authors suggested the improvement
in the nutritional state during abstinence may have occurred
due to a less active MEOS, decreasing the waste of caloric
energy.
Alcoholic patients presented metabolic and nutritional
disorders due to alcohol consumption, and showed a high
use of energy at a resting state [12], preferential use of lipids
as energy source [13], and a 19% reduction of the adipose
tissue when compared to a healthy control group [14]. Co-
hort studies have shown that women who consume alcohol at
a small or moderate rate (up to 30 g/day) have a lower risk to
gain weight and become obese than those who abstain from
it [15, 16], while other studies have reached the same conclu-
sion regardless of the subjects’ gender [17, 18].
Martin-Gonzalez et al [19] evaluated the prognostic val-
ue of the long-term alterations to the adipose and muscular
tissues of alcoholics and the effects of abstinence on these
changes. The results demonstrate that a loss of lean body
mass during the rst six months after the rst evaluation is
associated to a worse prognosis, whether or not patients were
abstinent during this same period. However, non-abstinence
was greater associated to the loss of lean body mass.
The energy derived from the intake of alcoholic bev-
erages may be added to the diet of those with a moderate
consumption of alcohol or may become a substitute to other
foods to chronic consumers [18] possibly decreasing the
gain of body mass, while increasing alcohol’s toxicity [2].
Therefore, the body’s use of ethanol calories may be associ-
ated with the dosage of alcohol. The consumption of alcohol
dosages below 25-35% of the daily calories may be utilized
as an energy source; however, at higher consumption, the
utilization may not be complete [20].
In humans, caloric malnutrition is a close reality to mil-
lions of people dying of hunger around the world and, due to
low prices and high availability, ethanol is ingested in place
of food. Animal models were created in order to clarify what
happens when a malnourished organism is exposed to etha-
nol. However, results were not what one would have expect-
ed. In fact, in low doses, alcohol consumption represents an
important source of calories, mitigating the effects of malnu-
trition. Animal studies show that the consumption of low to
moderate doses of alcohol (up to 20% of total caloric intake)
causes weight gain in malnourished rats, which suggests an
effective utilization of alcohol energetic content. Eutrophic
rats, however, lose weight when the energetic content of al-
cohol represents 10% or more of the total calorie intake [21,
22].
Could Alcohol be a Risk Factor for Obesity?
The nutritional state of an individual may inuence the uti-
lization of the energy derived from alcoholic beverages. It is
possible that, in humans, lean individuals have a more inef-
cient utilization of ethanol calories, and that in obese indi-
viduals the calories contribute to an increase of body mass
[23].
Although prospective studies have defended a positive
[24, 25] or negative [26, 27] correlations between alcohol
consumption and obesity, a 10-year long prospective study
showed that alcohol consumers had a more stable weight
than non-consumers, indicating that alcohol consumption is
not a risk factor for obesity [28]. Romeo et al [29] veried
that a chronic and moderate monthly consumption of beer
did not modify the weight or the body composition of adult
individuals.
The impact of alcohol drinks over body weight con-
tinues to be a controversial topic, as results vary, showing
sometimes an inverse (or negative) correlation between al-
cohol quantity and the BMI or the weight gain in women
[15, 28, 30-38] and, other times, a positive correlation [39,
40]. Moreover, studies found a positive association among
men, [30, 39-48] as well as an inverse association [34, 36].
Actually, some studies, in both men [49] and women [35,
47], found no associations. Different patterns of consump-
tion may be related to different outcomes [50].
Population studies demonstrate that the increase of body
and abdominal fat is related to a moderate [49, 51] and fre-
quent [52] alcohol consumption. There is also evidence that
the alcohol can result in weight gain in different patterns to
drink. The consumption of ≥ 30 g of alcohol/day may alter
the balance of the energetic homeostasis, prompting an ap-
petite increase and, consequently, body weight gain [53] and
obesity, regardless of type of beverage consumed [43].
On a short-term, alcohol consumption is considered an
appetite stimulant, inuencing neurochemical and peripheral
systems utilized to control appetite, such as, leptin inhibition,
glucagon-like-peptide-1 and serotonin, and enhancing the ef-
fect of gamma-aminobutyric acid, endogenous opioids and
neuropeptide Y. [54, 55] Hence, greater alcohol consump-
tion with an absence of dependency, as well as binge drink-
ing, may increase the risk for obesity. These effects may not
be related to preferences for habitual drinks [56]. Toniolo et
al [57] reported the increase of non-alcoholic energy con-
sumption when an increase in the alcohol consumption was
observed. However, Veenstra et al [58] showed that alcohol
consumers and non-consumers had a similar intake of non-
alcoholic caloric energy.
The association of alcohol consumption with a change in
body weight and its development into obesity appears to be
different depending on gender. Men add alcohol to the daily
ingestion of calories, while women have a tendency to use
alcohol as a substitute to other energy sources [30, 59], such
as reducing the consumption of carbohydrates [16, 18] with-
out an increase of the total calorie ingestion. These differenc-
es must be included when considering the energetic balance,
as they may generate different results regarding bodyweight.
A variety of obesity risk factors are related to alcohol
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Articles © The authors | Journal compilation © J Endocrinol Metab and Elmer Press™ | www.jofem.org
consumption, such increased abdominal fat [60] decreased
capability to oxidize lipids, consumption of high density
calories diets [61, 62] and increase in cortisol secretion [63].
One may say that calories from alcohol are more utilized
in individuals who are overweight or obese, and non-daily
moderate consumers, than in those that are alcoholics and in
a diet rich in fat [64].
Higher values of body, abdominal, and peripheral fat
were also found in female, alcohol consumers, college stu-
dents, showing a positive correlation between higher points
in the AUDIT questionnaire and the BMI, the percentage of
body fat, the waist circumference, the triceps skinfolds, and
the arm circumference [65].
A study based on the data of the National Health Inter-
view Surveys 1997 - 2001 demonstrated strong opposite ef-
fect between the quantity and frequency of alcohol consump-
tion as related to the BMI. Individuals who drank more often
but in small quantities (i.e. a drink a day, every day) had a
lower BMI. On the other hand, individuals that drank less
often, but did so in greater quantities (binge drinking), pre-
sented a higher BMI [39].
Jin et al [66] found an increase of the abdominal obe-
sity risk factor in those individuals consuming ≥ 50 g/day. In
agreement to this nding, in a study conducted with British
individuals, it was noted that a consumption of 30 g or more
of ethanol increased the risk of a high BMI and weight gain
[43].
Similarly, the results provided after a study of the data
of the Third National Health and Nutrition Examination Sur-
vey showed a lower chance of obesity among current alco-
hol consumers in relation to those abstinent, and a greater
chance of obesity among binge drinking individuals or those
who consume four or more doses a day. Obesity risk-factors
were signicantly lower among those reported drinking fre-
quently but consuming less than ve doses per week [40].
Alcohol and Lipid Prole
Alcohol consumption three to four days a week is associ-
ated with a lower risk of myocardial infarct among men and
women. It is estimated that the cardio protector effect of al-
cohol may be attributed to 50% of the HDL-c increase [67,
68]. Moderate consumption of alcohol results (30 g ethanol/
day) increases the concentration of HDL-c in approximately
4 mg/dL, and apoA-I in 8.82 mg/dL, with a reduction to the
risk of cardiac disease estimated at 24.7% [69, 70]. This al-
teration may occur despite the quantity or type of drink con-
sumed (wine, spirits or beer) [71, 72]. Furthermore, alcohol
promotes less degradation of HDL-c and a greater liver me-
tabolism of LDL-c [72].
Although alcohol consumption induces alterations to the
lipid prole and reduces cardiovascular events, the incidence
of strokes, such as brain hemorrhages and subarachnoid
hemorrhage, has shown to be more elevated in heavy drink-
ers than in those who do not consume alcohol [73]. Addition-
ally, there is a progressive increase of diseases attributed to
greater alcohol consumption [74], such as diabetes mellitus,
hypertensive cardiac disease, ischemic heart disease, isch-
emic and hemorrhagic stroke, among others [75].
The variation between alcohol’s risks and benets are
unique to each individual and its utilization as a tool to car-
diovascular protection should not be encouraged as a public
health measure [76]. Filmore et al [77] described the reduc-
tion of the alcohol benets to the prevention of coronary dis-
ease in a meta-analysis study where abstemious and light and
moderate alcohol consumers show the same risk of any death
caused by coronary disease.
Recently, Chen et al [78] found high levels of triglyc-
erides in individuals consuming 10 g/day of alcohol. Con-
sumption greater than 50 g/day signicantly reduced the risk
of developing low levels of HDL-c, but elevated the risks of
developing high levels of cholesterol.
In the post-prandial period, the alcohol is responsible for
an increase in the triglycerides, with the inhibition of the oxi-
dation of free fat acids (FFA) [79]. It is important to highlight
that individuals with coronary disease, the post-prandial hy-
pertriglyceridemia is greater and longer [80]. The hypertri-
glyceridemia or the increase of FFA are associated to a re-
duction of the endothelial vasodilation in normal individuals
[81] and those who are insulin-resistant [82].
Alcohol and Hypertension
The alcohol intake elevates the arterial pressure in a dose-de-
pendent response. Consumption higher than two daily doses
is one of the most common reversible causes of hypertension
[83]. The renin-angiotensin system might be involved in the
mechanisms that alcohol to induce hypertension [84].
A study showed that the acute alcohol intoxication
changed the renin-aldosterone system to humans with nor-
mal hydric and sodium balances. The increase plasma renin
was, probably, caused by dehydration due to ethanol diuresis
or to the inhibiting action of the ethanol in the aldosterone
secretion [85]. No signicative change was found in the os-
molarity, arterial pressure, and cardiac frequency. Later, an
acute increase of renin activity when there is a moderate in-
gestion of alcohol was conrmed, inducing changes to the
uid and electrolyte balance and arterial blood pressure [86].
However, the answer to a low and moderate consump-
tion of alcohol seems to be different, depending on the in-
dividual’s gender. Again, the literature is not in agreement
about the question. In a prospective study developed by the
Women’s Health Study with 28,848 women and in another
one developed by the Physicians’ Health Study with 13,455,
the low and moderate consumption of alcohol decreased the
risk of hypertension in women and increased it in men. The
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threshold value above which alcohol became a risk factor for
hypertension was equal to or larger than four doses a day in
women versus a moderate level equal to or larger than one
a day for men [87]. Nevertheless, some studies have been
controversial when considering whether or not the arterial
blood pressure sensitivity to alcohol is different in men and
women [87-93].
Wakabayashi [94] suggests that an increase of the ar-
terial blood pressure, as a consequence to habitual alcohol
consumption, is more prominent in individuals with low
body weight than in those with an elevated bodyweight.
Therefore, the recommended alcohol consumption limit for
the prevention of hypertension must be lower in women with
low bodyweight than in those with a high bodyweight.
Stranges et al [95] investigated the association of alco-
hol consumption and the current drinking standards to the
hypertension risk in healthy men and women without other
cardiovascular diseases. When compared to abstemious,
those who report alcohol drinks consumption had a higher
risk of developing hypertension, despite the quantity of al-
cohol consumed.
A reduction in the ingestion of alcohol between heavy
consumers signicantly reduces the systolic and diastolic
arterial pressures. Therefore, the reduction of alcohol con-
sumption must be recommended as a life-style modication
measure for the prevention and treatment of hypertension in
heavy drinkers [96].
Conclusion
Alcohol is a drug of complex physiological effects that vary
according to gender, age, race, body weight and consump-
tion patterns. Recommending a moderate use of alcohol with
the purpose of taking advantage of its health benets must
not be done. It must be reminded that there are groups of
increased susceptibility to alcohol exposure. The present
review shows that the additional consumption of ethanol
calories will promote metabolic changes and weight gain in-
creasing the risk of cardiovascular diseases, altering the lipid
prole and promoting hypertension.
References
1. World Health Organization.(WHO). Global status report
on alcohol and health. 2011; Available at: http://www.
who.int/substance_abuse/publications/global_alcohol_
report/msbgsruproles.pdf. Acessed May 2012.
2. Aguiar AV. The medical marketing audit: technique for
today’s competitive extended care environment. Health
Mark Q. 1984;1(4):45-50.
3. Molina PE, Hoek JB, Nelson S, Guidot DM, Lang
CH, Wands JR, Crawford JM. Mechanisms of al-
cohol-induced tissue injury. Alcohol Clin Exp Res.
2003;27(3):563-575.
4. Lieber CS. Medical disorders of alcoholism. N Engl J
Med. 1995;333(16):1058-1065.
5. Wakabayashi I. Impact of body weight on the relation-
ship between alcohol intake and blood pressure. Alcohol
Alcohol. 2009;44(2):204-210.
6. Jequier E. Alcohol intake and body weight: a paradox.
Am J Clin Nutr. 1999;69(2):173-174.
7. Lands WE, Zakhari S. The case of the missing calories.
Am J Clin Nutr. 1991;54(1):47-48.
8. Lieber CS. The inuence of alcohol on nutritional status.
Nutr Rev. 1988;46(7):241-254.
9. Hetu C, Joly JG. Differences in the duration of the en-
hancement of liver mixed-function oxidase activities in
ethanol-fed rats after withdrawal. Biochem Pharmacol.
1985;34(8):1211-1216.
10. Santolaria F, Perez-Manzano JL, Milena A, Gonzalez-
Reimers E, Gomez-Rodriguez MA, Martinez-Riera A,
Aleman-Valls MR, et al. Nutritional assessment in al-
coholic patients. Its relationship with alcoholic intake,
feeding habits, organic complications and social prob-
lems. Drug Alcohol Depend. 2000;59(3):295-304.
11. Addolorato G, Capristo E, Greco AV, Caputo F, Stefa-
nini GF, Gasbarrini G. Three months of abstinence from
alcohol normalizes energy expenditure and substrate
oxidation in alcoholics: a longitudinal study. Am J Gas-
troenterol. 1998;93(12):2476-2481.
12. Addolorato G, Capristo E, Greco AV, Stefanini GF, Gas-
barrini G. Energy expenditure, substrate oxidation, and
body composition in subjects with chronic alcoholism:
new ndings from metabolic assessment. Alcohol Clin
Exp Res. 1997;21(6):962-967.
13. Addolorato G, Capristo E, Greco AV, Stefanini GF, Gas-
barrini G. Inuence of chronic alcohol abuse on body
weight and energy metabolism: is excess ethanol con-
sumption a risk factor for obesity or malnutrition? J In-
tern Med. 1998;244(5):387-395.
14. Addolorato G, Capristo E, Marini M, Santini P, Scog-
namiglio U, Attilia ML, Messineo D, et al. Body com-
position changes induced by chronic ethanol abuse:
evaluation by dual energy X-ray absorptiometry. Am J
Gastroenterol. 2000;95(9):2323-2327.
15. Wannamethee SG, Field AE, Colditz GA, Rimm EB.
Alcohol intake and 8-year weight gain in women: a pro-
spective study. Obes Res. 2004;12(9):1386-1396.
16. Wang L, Lee IM, Manson JE, Buring JE, Sesso HD. Al-
cohol consumption, weight gain, and risk of becoming
overweight in middle-aged and older women. Arch In-
tern Med. 2010;170(5):453-461.
17. Jones BR, Barrett-Connor E, Criqui MH, Holdbrook
MJ. A community study of calorie and nutrient intake
in drinkers and nondrinkers of alcohol. Am J Clin Nutr.
1982;35(1):135-139.
207 208
J Endocrinol Metab • 2012;2(6):205-211
Alcohol on Nutritional Status
Articles © The authors | Journal compilation © J Endocrinol Metab and Elmer Press™ | www.jofem.org
18. Gruchow HW, Sobocinski KA, Barboriak JJ, Scheller
JG. Alcohol consumption, nutrient intake and rela-
tive body weight among US adults. Am J Clin Nutr.
1985;42(2):289-295.
19. Martin-Gonzalez C, Gonzalez-Reimers E, Santolaria-
Fernandez F, Fernandez-Rodriguez C, Garcia-Valdeca-
sas-Campelo E, Gonzalez Diaz A, Alvisa-Negrin J, et
al. Prognostic value of changes in lean and fat mass in
alcoholics. Clin Nutr. 2011;30(6):822-830.
20. Mitchell MC, Herlong HF. Alcohol and nutrition: caloric
value, bioenergetics, and relationship to liver damage.
Annu Rev Nutr. 1986;6:457-474.
21. Aguiar AS, Da-Silva VA, Boaventura GT. Can calo-
ries from ethanol contribute to body weight preser-
vation by malnourished rats? Braz J Med Biol Res.
2004;37(6):841-846.
22. Aguiar AS, Abrahao RF, Freitas TL, da Silva VA. Ear-
ly malnutrition favours heavy ethanol intake in wean-
ing rats without long-lasting effects. Nutr Neurosci.
2009;12(2):65-72.
23. Clevidence BA, Taylor PR, Campbell WS, Judd JT. Lean
and heavy women may not use energy from alcohol with
equal efciency. J Nutr. 1995;125(10):2536-2540.
24. Gordon T, Kannel WB. Drinking and its relation to
smoking, BP, blood lipids, and uric acid. The Framing-
ham study. Arch Intern Med. 1983;143(7):1366-1374.
25. Gordon T, Doyle JT. Alcohol consumption and its re-
lationship to smoking, weight, blood pressure, and
blood lipids. The Albany Study. Arch Intern Med.
1986;146(2):262-265.
26. Camargo CA, Jr., Vranizan KM, Dreon DM, Frey-Hewitt
B, Wood PD. Alcohol, calorie intake, and adiposity in
overweight men. J Am Coll Nutr. 1987;6(3):271-278.
27. Cooke KM, Frost GW, Thornell IR, Stokes GS. Al-
cohol consumption and blood pressure: survey of the
relationship at a health-screening clinic. Med J Aust.
1982;1(2):65-69.
28. Liu S, Serdula MK, Williamson DF, Mokdad AH, Byers
T. A prospective study of alcohol intake and change
in body weight among US adults. Am J Epidemiol.
1994;140(10):912-920.
29. Romeo J, Gonzalez-Gross M, Warnberg J, Diaz LE,
Marcos A. [Does beer have an impact on weight gain?
Effects of moderate beer consumption on body composi-
tion]. Nutr Hosp. 2007;22(2):223-228.
30. Colditz GA, Giovannucci E, Rimm EB, Stampfer MJ,
Rosner B, Speizer FE, Gordis E, et al. Alcohol intake
in relation to diet and obesity in women and men. Am J
Clin Nutr. 1991;54(1):49-55.
31. Hellerstedt WL, Jeffery RW, Murray DM. The associa-
tion between alcohol intake and adiposity in the general
population. Am J Epidemiol. 1990;132(4):594-611.
32. Dallongeville J, Marecaux N, Ducimetiere P, Ferrieres
J, Arveiler D, Bingham A, Ruidavets JB, et al. Inu-
ence of alcohol consumption and various beverages on
waist girth and waist-to-hip ratio in a sample of French
men and women. Int J Obes Relat Metab Disord.
1998;22(12):1178-1183.
33. Ruf T, Nagel G, Altenburg HP, Miller AB, Thorand B.
Food and nutrient intake, anthropometric measurements
and smoking according to alcohol consumption in the
EPIC Heidelberg study. Ann Nutr Metab. 2005;49(1):16-
25.
34. Rohrer JE, Rohland BM, Denison A, Way A. Frequency
of alcohol use and obesity in community medicine pa-
tients. BMC Fam Pract. 2005;6(1):17.
35. French MT, Norton EC, Fang H, Maclean JC. Al-
cohol consumption and body weight. Health Econ.
2010;19(7):814-832.
36. Gearhardt AN, Corbin WR. Body mass index and alco-
hol consumption: family history of alcoholism as a mod-
erator. Psychol Addict Behav. 2009;23(2):216-225.
37. Sherwood NE, Jeffery RW, French SA, Hannan PJ,
Murray DM. Predictors of weight gain in the Pound
of Prevention study. Int J Obes Relat Metab Disord.
2000;24(4):395-403.
38. Skrzypczak M, Szwed A, Pawlinska-Chmara R, Skrzy-
pulec V. Body mass index, waist to hip ratio and waist/
height in adult Polish women in relation to their educa-
tion, place of residence, smoking and alcohol consump-
tion. Homo. 2008;59(4):329-342.
39. Breslow RA, Smothers BA. Drinking patterns and body
mass index in never smokers: National Health Interview
Survey, 1997-2001. Am J Epidemiol. 2005;161(4):368-
376.
40. Arif AA, Rohrer JE. Patterns of alcohol drinking and its
association with obesity: data from the Third National
Health and Nutrition Examination Survey, 1988-1994.
BMC Public Health. 2005;5:126.
41. Prentice AM. Alcohol and obesity. Int J Obes Relat
Metab Disord. 1995;19 Suppl 5:S44-50.
42. Schroder H, Morales-Molina JA, Bermejo S, Barral D,
Mandoli ES, Grau M, Guxens M, et al. Relationship of
abdominal obesity with alcohol consumption at popula-
tion scale. Eur J Nutr. 2007;46(7):369-376.
43. Wannamethee SG, Shaper AG. Alcohol, body weight,
and weight gain in middle-aged men. Am J Clin Nutr.
2003;77(5):1312-1317.
44. Lahti-Koski M, Pietinen P, Heliovaara M, Vartiainen E.
Associations of body mass index and obesity with physi-
cal activity, food choices, alcohol intake, and smoking
in the 1982-1997 FINRISK Studies. Am J Clin Nutr.
2002;75(5):809-817.
45. Wannamethee SG, Shaper AG, Whincup PH. Al-
cohol and adiposity: effects of quantity and type of
drink and time relation with meals. Int J Obes (Lond).
2005;29(12):1436-1444.
46. Sung KC, Kim SH, Reaven GM. Relationship among
209 210
J Endocrinol Metab • 2012;2(6):205-211
Toffolo et al
Articles © The authors | Journal compilation © J Endocrinol Metab and Elmer Press™ | www.jofem.org
alcohol, body weight, and cardiovascular risk factors in
27,030 Korean men. Diabetes Care. 2007;30(10):2690-
2694.
47. Alcacera MA, Marques-Lopes I, Fajo-Pascual M, Puzo
J, Blas Perez J, Bes-Rastrollo M, Martinez-Gonzalez
MA. Lifestyle factors associated with BMI in a Span-
ish graduate population: the SUN Study. Obes Facts.
2008;1(2):80-87.
48. Lukasiewicz E, Mennen LI, Bertrais S, Arnault N, Prezi-
osi P, Galan P, Hercberg S. Alcohol intake in relation
to body mass index and waist-to-hip ratio: the impor-
tance of type of alcoholic beverage. Public Health Nutr.
2005;8(3):315-320.
49. Tolstrup JS, Heitmann BL, Tjonneland AM, Overvad
OK, Sorensen TI, Gronbaek MN. The relation between
drinking pattern and body mass index and waist and hip
circumference. Int J Obes (Lond). 2005;29(5):490-497.
50. Sayon-Orea C, Martinez-Gonzalez MA, Bes-Rastrollo
M. Alcohol consumption and body weight: a systematic
review. Nutr Rev. 2011;69(8):419-431.
51. Dorn JM, Hovey K, Muti P, Freudenheim JL, Russell
M, Nochajski TH, Trevisan M. Alcohol drinking pat-
terns differentially affect central adiposity as mea-
sured by abdominal height in women and men. J Nutr.
2003;133(8):2655-2662.
52. Tolstrup JS, Halkjaer J, Heitmann BL, Tjonneland AM,
Overvad K, Sorensen TI, Gronbaek MN. Alcohol drink-
ing frequency in relation to subsequent changes in waist
circumference. Am J Clin Nutr. 2008;87(4):957-963.
53. Navarro FB, Costa FD, Mulinari LA, Pimentel GK,
Roderjan JG, Vieira ED, Noronha L, et al. Evaluation
of the biological behavior of decellularized pulmonary
homografts: an experimental sheep model. Rev Bras Cir
Cardiovasc. 2010;25(3):377-387.
54. Yeomans MR, Caton S, Hetherington MM. Alcohol
and food intake. Curr Opin Clin Nutr Metab Care.
2003;6(6):639-644.
55. Yeomans MR. Effects of alcohol on food and energy in-
take in human subjects: evidence for passive and active
over-consumption of energy. Br J Nutr. 2004;92 Suppl
1:S31-34.
56. Yeomans MR. Alcohol, appetite and energy balance: is
alcohol intake a risk factor for obesity? Physiol Behav.
2010;100(1):82-89.
57. Toniolo P, Riboli E, Cappa AP. A community study of
alcohol consumption and dietary habits in middle-aged
Italian women. Int J Epidemiol. 1991;20(3):663-670.
58. Veenstra J, Schenkel JA, van Erp-Baart AM, Brants HA,
Hulshof KF, Kistemaker C, Schaafsma G, et al. Alcohol
consumption in relation to food intake and smoking hab-
its in the Dutch National Food Consumption Survey. Eur
J Clin Nutr. 1993;47(7):482-489.
59. Yung L, Gordis E, Holt J. Dietary choices and likelihood
of abstinence among alcoholic patients in an outpatient
clinic. Drug Alcohol Depend. 1983;12(4):355-362.
60. Rissanen AM, Heliovaara M, Knekt P, Reunanen A,
Aromaa A. Determinants of weight gain and overweight
in adult Finns. Eur J Clin Nutr. 1991;45(9):419-430.
61. Kachani AT, Brasiliano S, Hochgraf PB. O impacto do
consumo alcoolico no ganho de peso. Rev Psiquiatr
Clin. 2008;35(1): 21-24.
62. Suter PM, Schutz Y, Jequier E. The effect of etha-
nol on fat storage in healthy subjects. N Engl J Med.
1992;326(15):983-987.
63. Suter PM, Hasler E, Vetter W. Effects of alcohol on en-
ergy metabolism and body weight regulation: is alcohol
a risk factor for obesity? Nutr Rev. 1997;55(5):157-171.
64. Suter PM. Is alcohol consumption a risk factor for weight
gain and obesity? Crit Rev Clin Lab Sci. 2005;42(3):197-
227.
65. Silva ABJ, Oliveira AKV, Silva JD, Quintaes KD, Silva-
Fonseca VA, Aguiar-Nemer A S. Relacao entre consumo
de bebidas alcoolicas por universitarias e adiposidade
corporal. J Bras Psiquiatr. 2011;60:210-215.
66. Jin L, Huang Y, Bi Y, Zhao L, Xu M, Xu Y, Chen Y, et al.
Association between alcohol consumption and metabol-
ic syndrome in 19,215 middle-aged and elderly Chinese.
Diabetes Res Clin Pract. 2011;92(3):386-392.
67. Mukamal KJ, Jensen MK, Gronbaek M, Stampfer MJ,
Manson JE, Pischon T, Rimm EB. Drinking frequency,
mediating biomarkers, and risk of myocardial infarction
in women and men. Circulation. 2005;112(10):1406-
1413.
68. Langer RD, Criqui MH, Reed DM. Lipoproteins and
blood pressure as biological pathways for effect of mod-
erate alcohol consumption on coronary heart disease.
Circulation. 1992;85(3):910-915.
69. Hendriks HF, Veenstra J, Velthuis-te Wierik EJ,
Schaafsma G, Kluft C. Effect of moderate dose of al-
cohol with evening meal on brinolytic factors. BMJ.
1994;308(6935):1003-1006.
70. De Oliveira ESER, Foster D, McGee Harper M, Seid-
man CE, Smith JD, Breslow JL, Brinton EA. Alcohol
consumption raises HDL cholesterol levels by increas-
ing the transport rate of apolipoproteins A-I and A-II.
Circulation. 2000;102(19):2347-2352.
71. Volcik KA, Ballantyne CM, Fuchs FD, Sharrett AR,
Boerwinkle E. Relationship of alcohol consumption and
type of alcoholic beverage consumed with plasma lipid
levels: differences between Whites and African Ameri-
cans of the ARIC study. Ann Epidemiol. 2008;18(2):101-
107.
72. van der Gaag MS, van Tol A, Vermunt SH, Scheek LM,
Schaafsma G, Hendriks HF. Alcohol consumption stim-
ulates early steps in reverse cholesterol transport. J Lipid
Res. 2001;42(12):2077-2083.
73. Reynolds K, Lewis B, Nolen JD, Kinney GL, Sathya B,
He J. Alcohol consumption and risk of stroke: a meta-
209 210
J Endocrinol Metab • 2012;2(6):205-211
Alcohol on Nutritional Status
Articles © The authors | Journal compilation © J Endocrinol Metab and Elmer Press™ | www.jofem.org
analysis. JAMA. 2003;289(5):579-588.
74. Foppa M, Fuchs FD, Duncan BB. Alcohol and athero-
sclerosis. Arq Bras Cardiol. 2001;76(2):165-176.
75. Rehm J, Baliunas D, Borges GL, Graham K, Irving H,
Kehoe T, Parry CD, et al. The relation between differ-
ent dimensions of alcohol consumption and burden of
disease: an overview. Addiction. 2010;105(5):817-843.
76. Criqui MH, Ringel BL. Does diet or alcohol explain the
French paradox? Lancet. 1994;344(8939-8940):1719-
1723.
77. Fillmore KM, Stockwell T, Chikritzhs T, Bostrom A,
Kerr W. Moderate alcohol use and reduced mortality
risk: systematic error in prospective studies and new hy-
potheses. Ann Epidemiol. 2007;17(5 Suppl):S16-23.
78. Chen CC, Lin WY, Li CI, Liu CS, Li TC, Chen YT,
Yang CW, et al. The association of alcohol consump-
tion with metabolic syndrome and its individual compo-
nents: the Taichung community health study. Nutr Res.
2012;32(1):24-29.
79. Brewster AC, Lankford HG, Schwartz MG, Sullivan
JF. Ethanol and alimentary lipemia. Am J Clin Nutr.
1966;19(4):255-259.
80. Patsch JR, Miesenbock G, Hopferwieser T, Muhlberger
V, Knapp E, Dunn JK, Gotto AM, Jr., et al. Relation of
triglyceride metabolism and coronary artery disease.
Studies in the postprandial state. Arterioscler Thromb.
1992;12(11):1336-1345.
81. Vogel RA, Corretti MC, Plotnick GD. Effect of a single
high-fat meal on endothelial function in healthy sub-
jects. Am J Cardiol. 1997;79(3):350-354.
82. Steinberg HO, Tarshoby M, Monestel R, Hook G, Cro-
nin J, Johnson A, Bayazeed B, et al. Elevated circulat-
ing free fatty acid levels impair endothelium-dependent
vasodilation. J Clin Invest. 1997;100(5):1230-1239.
83. Beilin LJ, Puddey IB. Alcohol and hypertension: an up-
date. Hypertension. 2006;47(6):1035-1038.
84. Klatsky AL. Alcohol and hypertension. Clin Chim Acta.
1996;246(1-2):91-105.
85. Linkola J, Fyhrquist F, Nieminen MM, Weber TH, Tontti
K. Renin-aldosterone axis in ethanol intoxication and
hangover. Eur J Clin Invest. 1976;6(2):191-194.
86. Puddey IB, Vandongen R, Beilin LJ, Rouse IL. Alcohol
stimulation of renin release in man: its relation to the he-
modynamic, electrolyte, and sympatho-adrenal respons-
es to drinking. J Clin Endocrinol Metab. 1985;61(1):37-
42.
87. Sesso HD, Cook NR, Buring JE, Manson JE, Gaziano
JM. Alcohol consumption and the risk of hypertension
in women and men. Hypertension. 2008;51(4):1080-
1087.
88. Klatsky AL, Friedman GD, Siegelaub AB, Gerard MJ.
Alcohol consumption and blood pressure Kaiser-Perma-
nente Multiphasic Health Examination data. N Engl J
Med. 1977;296(21):1194-1200.
89. Weissfeld JL, Johnson EH, Brock BM, Hawthorne
VM. Sex and age interactions in the association be-
tween alcohol and blood pressure. Am J Epidemiol.
1988;128(3):559-569.
90. Marmot MG, Elliott P, Shipley MJ, Dyer AR,
Ueshima H, Beevers DG, Stamler R, et al. Alcohol
and blood pressure: the INTERSALT study. BMJ.
1994;308(6939):1263-1267.
91. van Leer EM, Seidell JC, Kromhout D. Differences in
the association between alcohol consumption and blood
pressure by age, gender, and smoking. Epidemiology.
1994;5(6):576-582.
92. Fuchs FD, Chambless LE, Whelton PK, Nieto FJ, Heiss
G. Alcohol consumption and the incidence of hyperten-
sion: The Atherosclerosis Risk in Communities Study.
Hypertension. 2001;37(5):1242-1250.
93. Wakabayashi I. Inuence of gender on the association of
alcohol drinking with blood pressure. Am J Hypertens.
2008;21(12):1310-1317.
94. Wakabayashi I. Inuence of body weight on the relation-
ships of alcohol drinking with blood pressure and serum
lipids in women. Prev Med. 2009;49(5):374-379.
95. Stranges S, Wu T, Dorn JM, Freudenheim JL, Muti P,
Farinaro E, Russell M, et al. Relationship of alcohol
drinking pattern to risk of hypertension: a population-
based study. Hypertension. 2004;44(6):813-819.
96. Xin X, He J, Frontini MG, Ogden LG, Motsamai OI,
Whelton PK. Effects of alcohol reduction on blood pres-
sure: a meta-analysis of randomized controlled trials.
Hypertension. 2001;38(5):1112-1117.
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... Moreover, patients on lipid lowering therapy also have chances of myocardial infarction despite lower levels of LDL-c (Gerszten and Wang, 2008;Stegemann et al., 2014). Risk factors like high fat diet (HFD), obesity, diabetes, smoking and alcohol consumption affect lipid metabolism processes, altering plasma lipid profile and lead to CVD (Jia et al., 2013;Miao et al., 2016;Ozder, 2014;Toffoloa et al., 2012;Yan-Ling et al., 2012). Thus, risk factors for HL are also the contributing factors for development of CVD. ...
... Alcohol Consumption: Alcohol intake significantly affects the lipid profile, blood pressure and nutritional condition (Toffoloa et al., 2012).Numerous studies have shown that alcohol consumption leads to elevation in HDL-c level (De Oliveira et al., 2000;Hendriks et al., 1994;Langer et al., 1992;Mukamal et al., 2005). Moderate consumption of alcohol (30 g ethanol /day) increases HDL-c by 4 mg/dl and Apo-A1 by 8.82 mg/dl (De Oliveira et al., 2000;Hendriks et al., 1994;Toffoloa et al., 2012). ...
... Alcohol Consumption: Alcohol intake significantly affects the lipid profile, blood pressure and nutritional condition (Toffoloa et al., 2012).Numerous studies have shown that alcohol consumption leads to elevation in HDL-c level (De Oliveira et al., 2000;Hendriks et al., 1994;Langer et al., 1992;Mukamal et al., 2005). Moderate consumption of alcohol (30 g ethanol /day) increases HDL-c by 4 mg/dl and Apo-A1 by 8.82 mg/dl (De Oliveira et al., 2000;Hendriks et al., 1994;Toffoloa et al., 2012). It enhances metabolism of LDL-c and reduces degradation of HDLc (van der Gaag et al., 2001). ...
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... It is well established that excess alcohol intake is associated with increased morbidity and mortality since it is accountable for a proportion of cancers, neurophysical diseases, cirrhosis, road accidents, etc. [1][2][3] From a metabolic point of view, obesity, hyperlipidemia and coronary heart diseases have been associated with excess alcohol consumption. [4] However, the effects of moderate consumption of alcohol and especially beer on metabolic health remain controversial. Results from previous studies are heterogeneous with different conclusions drawn. ...
... Nevertheless, a consumption of 30 g alcohol/ day has been viewed as a threshold between alcohol abuse and moderate consumption in some studies. [4,18] However, such studies are rarely including African countries and it is difficult to know whether this 30 g alcohol/day threshold is applicable to the sub-Saharan African context without threatening the health of drinkers. ...
... [37] Population studies show that the increase of body and abdominal fat is related to a moderate [38,39] and frequent [40] alcohol consumption. The consumption of 30 g of alcohol/day or more may alter the balance of the energetic homeostasis, prompting an appetite increase and, consequently, body weight gain [4] and obesity, regardless of type of beverage consumed. [18] However, in our study, significant body composition changes occurred while mean daily alcohol consumption was ranging between 20 and 27 grams for male participants and from 13 to 17 grams for females. ...
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... Depending on the frequency and quantity, the consumption of ethanol may increase the risk of malnutrition, weight gain, obesity, and cardiovascular diseases. 16 On the contrary, alcohol consumption was associated with a lower risk of myocardial infarct among men and women. It is estimated that the cardio protector effect of alcohol may be attributed to 50% of the high-density lipoprotein cholesterol (HDL-C) increase. ...
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... As alcohol and its metabolism prevent the body from properly absorbing, digesting, and using those nutrients, this can lead to deficiencies in proteins and vitamins, especially vitamin A, which might contribute to liver disease and other serious alcohol-related disorders (Lieber, 2003). Furthermore, it can also contribute to weight gain through the additional consumption of ethanol calories (De Aguiar, 2013). ...
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... The aqueous extract of A. muricata, for example, has antidiabetic activity with antioxidant and protective action on pancreatic β cells, which improve glucose metabolism (Florence et al., 2014) and also with the species P. emarginatus (Macedo and Ferreira, 2004) (Latour et al., 1999). These findings were consistent with previous studies indicating that alcohol affected lipid metabolism (Toffolo et al., 2012) with increased cholesterol levels in rats treated with alcohol (Silva et al., 2015). ...
... 180 In short-term, alcohol consumption is considered an appetite stimulant, influencing neurochemical and peripheral systems to control appetite, such as, leptin inhibition, glucagon-like-peptide-1, and serotonin, and enhancing the ef fect of gammaaminobutyric acid, endogenous opioids, and neuropeptide Y. Hence, greater alcohol consumption, may also increase the risk for obesity. 181 Alcohol usage is a more frequent contributor to hypertension than is generally appreciated. It appears to be transitory in most patients, but is not benign. ...
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... The lipid profiles were affected differently in rats exposed to [EP] alcohol [22,23] and pterocarpans [24] [24,29], alcohol toxicity may override these. Regular exposure to alcohol is associated with a variety of secondary effects, some of which relate to hepatocyte homeostasis and lipid metabolism. ...
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... On the other hand, protein synthesis can also be caused by several factors, such as response to a period of stress, an adaptation of the organ, the presence of alcohol or a regenerative process (Baubet et al., 1996;Ogura et al., 2001;Zhu et al., 2013). It is recognized that alcohol, one the components of the tincture, is active on the biological system, especially on the liver metabolic system leading to several alterations in different organs (Epstein, 1997;Das et al., 2009;Toffolo et al., 2012). The interference of alcohol is a reasonable explanation considering that the control group had the same diet and experimental conditions, with no significant change in protein synthesis. ...
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A transição da Educação Pré-Escolar (EPE) para o 1.o Ciclo do Ensino Básico (1.o CEB) pode ser bem-sucedida se a criança vivenciar esta experiência com sentimentos de segurança, satisfação e conforto, permitindo-lhe um ajustamento à nova situação educativa. Para tal, é necessário minimizar possíveis efeitos adversos através de estratégias facilitadoras da transição e da continuidade educativa. Com o presente estudo pretende-se compreender dimensões do processo de transição de um grupo de 119 crianças (EPE N=74 e 1.oCEB N=45), através da caraterização do desenvolvimento socioemocional das crianças, identificação dos sentimentos, competências e dificuldades das mesmas, aquando da transição, e quais as estratégias facilitadoras da transição promovidas num Agrupamento de Escolas (AE) do distrito de Aveiro, Portugal. O estudo envolveu, para além das crianças, 73 pais/Encarregados de Educação (EE) e 14 docentes dos dois níveis educativos (EPE e 1.o CEB). A recolha de dados englobou métodos qualitativos -entrevistas semiestruturadas às crianças- e quantitativos -Questionário de Capacidades e Dificuldades (SDQ) a pais/EE e docentes. A análise dos dados consistiu em análise de conteúdo e análise descritiva e inferencial não paramétrica com recurso aos softwares WebQDA e SPSS-versão 25, respetivamente. Os resultados indicam que as crianças sentem felicidade e satisfação no processo de transição, mas também ansiedade. Quanto ao desenvolvimento socioemocional, na perceção dos pais/EE e docentes, as crianças do 1.o CEB apresentam mais dificuldades do que as crianças da EPE, que apresentam mais competências. O AE promove algumas estratégias facilitadoras da transição, mas pouco consistentes, na promoção do desenvolvimento socioemocional das crianças.
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Background: Smoking and drinking are two predisposing factors for dyslipidemia. Exercise has been proposed as a strategy to improve the blood lipids. However, it remains unclear how smoking and drinking jointly affect blood lipids and whether exercise influences their effects. Objectives: To evaluate the effects of smoking and drinking, either alone or in combination, on lipid-related indices in both exercise and non-exercise groups among Chinese men. Methods: This study was conducted in a health examination center between 2015 and 2016. A sample of 6,179 male subjects was divided into exercise and non-exercise groups. Logistic and linear regression analyses were used to calculate the odds ratios for abnormal lipid-related indices and correlation coefficients between smoking/drinking and lipid-related indices. Results: In the study population, the percentage of stable smokers and stable drinkers was 46.3% (2,860/6,179) and 77.6% (4,795/6,179), respectively. An increased smoking amount was significantly associated with an elevated triglyceride (TG) level and a decreased high-density lipoprotein cholesterol (HDL-C) level. Heavier smokers had higher odds ratios for high TG and low HDL-C. Heavier drinkers had higher levels of total cholesterol (TC), TG, and HDL-C and higher odds ratios for high TC and high TG but lower odds ratio for low HDL-C. The exercise group had lower TG levels and higher HDL-C levels than did the non-exercise group. Conclusions: Both heavier smoking and heavier drinking were associated with poorer TG levels, and the results suggest that drinking may be helpful for HDL-C. Exercise may relieve the negative effects of smoking and drinking.
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CONTEXTO: Considerando-se que o álcool possui um valor energético, ele tem a habilidade de suprimir as necessidades calóricas diárias de um indivíduo, e/ou levá-lo ao sobrepeso, dependendo da quantidade, freqüência e modo de consumo. OBJETIVOS: Revisar o efeito do álcool no metabolismo energético e suas conseqüências no peso corporal. MÉTODOS: Revisão bibliográfica realizada no sistema MEDLINE (Index Medicus) cruzando os descritores "alcohol" e "weight gain". RESULTADOS: O álcool tem prioridade no metabolismo alterando outras vias metabólicas, incluindo a oxidação lipídica, o que favorece o estoque de gorduras no organismo. Dependendo da forma que ele é metabolizado, sua participação como fonte calórica é diferente. CONCLUSÕES: O valor energético dos alimentos adicionados ao consumo alcoólico e o patamar de consumo devem ser observados na relação de ganho de peso. Respostas ao consumo de álcool são diferentes de um indivíduo para o outro e são determinadas por fatores individuais e por possíveis fatores genéticos desconhecidos.
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It was found that following the ingestion of alcohol in an amount comparable to that commonly used by many people as an appetizer triglyceride levels were significantly higher during the postprandial period than when the same meal was ingested without alcohol. Evaluation of gastric emptying and of postheparin lipolytic activity indicated that the alcohol-augmented alimentary lipemia did not result from alteration in either of these functions. Alcohol alone is known to elevate triglyceride levels. The increase in postprandial lipemia produced by alcohol, therefore, must represent increased hepatic triglyceride synthesis and release. This may result from increased peripheral fatty acid mobilization or by a more direct influence of alcohol on fat synthesis.
Article
To determine whether alcohol-associated hypertension (HTN) carries risks similar to those of HTN in abstainers or light drinkers, we prospectively studied cardiovascular sequelae separately in heavy drinkers, light drinkers, and abstainers. The risk of all outcomes was progressively higher for increasing blood pressure categories, with similar associations in each alcohol category. These data indicate that the risks of HTN are independent of the amount of alcohol intake.
Article
Some studies have suggested that drinking in moderation may be beneficial for health, but many of these studies do not address body weight. Evidence suggests that consuming moderate amounts of alcohol is a risk factor for obesity, which is a risk factor for several adverse health outcomes. Recommendations regarding alcohol intake thus should take into account a variety of factors, including baseline body weight, location of body fat, and overall diet.
Article
Objective: To determine whether body weight influences the associations of habitual alcohol drinking with blood pressure and serum lipids in women. Methods: The subjects were 16,805 healthy women at ages of 35-54 years, and data were collected at work places of the subjects in Yamagata Prefecture in Japan from April 1999 to March 2000. The subjects were divided into three tertile groups of body weight and were further divided into three subgroups by average ethanol intake [non-, light (<15 g per day), and heavy (> or =15 g per day) drinkers]. Results: In the first and second tertile groups of body weight, mean systolic and diastolic blood pressure and prevalence of high systolic or diastolic blood pressure were significantly higher in heavy drinkers than in non-drinkers, while these differences were not observed in the third tertile group of body weight. On the other hand, in all tertile groups of body weight, mean serum HDL and LDL cholesterol levels were higher and lower, respectively, in light and heavy drinkers than in non-drinkers, and prevalence of low HDL cholesterol or high LDL cholesterol was significantly lower in heavy drinkers than in non-drinkers. Conclusions: The results suggest that body weight influences the association of alcohol drinking with blood pressure but not the associations of alcohol drinking with serum HDL and LDL cholesterol.
Article
Alcohol has both adverse and protective effects on the individual components of metabolic syndrome (MS). We hypothesize that alcohol consumption increases the risk of developing MS and that the consumption of different types of alcoholic beverages has different effects on the development of MS and its individual components. We enrolled 2358 men for this cross-sectional study. The data were collected from self-reported nutrition and lifestyle questionnaires. Individuals who drank at least once per week for 6 consecutive months were classified as current drinkers. Current drinkers were at a higher risk of developing MS, abdominal obesity, and high triglyceride levels, but they were at a lower risk of developing low levels of high-density lipoprotein cholesterol (HDL-C). The increased risk of developing MS, high triglyceride, and high fasting glucose levels was dose dependent, whereas low HDL-C levels demonstrated a reverse relationship. The dose needed to reduce the risk of having low HDL-C levels was ≧50 g/d. This dose, however, resulted in an increased risk of developing high fasting glucose and high triglyceride levels. Consuming mixed types of alcohol increased the risk of developing MS and abdominal obesity. Meanwhile, those who drank liquor or wine had a greater risk of developing high triglyceride or high fasting glucose levels, respectively. In conclusion, alcohol consumption dose-dependently increased the risk of developing MS and some of its individual components while dose-dependently decreasing the risk of developing low HDL-C levels. The type of alcoholic beverage had different effects on the development of the individual components of MS.
Article
Based on the fact that energy content in 1 gram of alcohol is 29 kJ or 7.1 kcal, alcohol consumption can lead to weight gain. The present review was conducted to analyze the effects of alcohol consumption on body weight. A search of the Medline database for the period 1984 to March 2010 was conducted to identify cross-sectional, prospective cohort studies and intervention trials investigating the relationship between alcohol consumption and the risk of weight gain. Thirty-one publications were selected on the basis of relevance and quality of design and methods. The findings from large cross-sectional studies as well as from well-powered, prospective, cohort studies with long periods of follow-up were contradictory. Findings from short-term experimental trials also did not show a clear trend. The overall results do not conclusively confirm a positive association between alcohol consumption and weight gain; however, positive findings between alcohol intake and weight gain have been reported, mainly from studies with data on higher levels of drinking. It is, therefore, possible that heavy drinkers may experience such an effect more commonly than light drinkers. Moreover, light-to-moderate alcohol intake, especially wine intake, may be more likely to protect against weight gain, whereas consumption of spirits has been positively associated with weight gain. Further research should be directed towards assessing the specific roles of different types of alcoholic beverages. Studies should also take the effect of consumption patterns into account. In addition, a potential effect modifier that has not been evaluated before but might be important to consider is the subjects' previous tendency to gain weight.
Article
The prognostic value of nutritional status and/or lean and fat mass assessed by dual-energy X-ray absorptiometry (DEXA) has been widely analyzed, in both alcoholics and non-alcoholics. However, the prognostic value of changes in fat and lean mass over time in alcoholics has scarcely been studied, nor has the effect of alcohol abstinence on these changes. From an initial cohort of 113 alcoholic patients, 70 prospectively underwent two DEXA assessments six months apart. One hundred and five patients (including 66 of those who underwent two DEXA assessments) were followed up for 34.9 ± 36.4 months (median = 18 months, interquartile range = 7.25-53.75 months). During this follow-up period, 33 died (including 20 of those who had undergone a second DEXA assessment). Forty-two of the 70 patients undergoing a second DEXA assessment had abstained from alcohol. Of these, 69.04% (29) gained left arm lean mass, compared with only 35.71% (10 of 28) of those who had continued drinking (χ² = 7.46; p = 0.006). Similar results were observed regarding right arm lean mass (χ² = 4.68; p = 0.03) and right leg lean mass (χ² = 7.88; p = 0.005). However, no associations were found between alcohol abstinence and changes in fat parameters. Analysis by means of Kaplan-Meier curves showed that loss of total lean mass, right leg lean mass, left leg lean mass and total fat mass were all significantly associated with reduced survival. However, within 30 months of the second evaluation, significant associations were observed between changes of all parameters related to lean mass, and mortality, but no association between changes in fat parameters and mortality. Loss of lean mass over a period of six months after a first assessment is associated with worse prognosis in alcoholics, irrespective of whether they stop drinking during this period or not. Continued drinking is associated with greater loss of lean mass, but not with changes in fat mass.