ライフサイエンスコーパス: alcohol intake

1 activity of this neuronal population reduces alcohol intake.

2 a causal relationship between D2R levels and alcohol intake.

3 in the transition from moderate to excessive alcohol intake.

4 nd adjusted for sex, education, smoking, and alcohol intake.

5 e important mediators of this stress-induced alcohol intake.

6 d prevented withdrawal-induced escalation of alcohol intake.

7 ns with diet have been convincing other than alcohol intake.

8 ce observed in sP rats and to their elevated alcohol intake.

9 wo inbred strains of mice known to differ in alcohol intake.

10 sensitivity in patients with sustained heavy alcohol intake.

11 ids, education, race/ethnicity, smoking, and alcohol intake.

12 ignificant for a model using the most recent alcohol intake.

13 sure and withdrawal known to drive excessive alcohol intake.

14 -to-NAcore inputs sustain aversion-resistant alcohol intake.

15 usting for age, body mass index, calcium and alcohol intake.

16 its in the NAcore reduced aversion-resistant alcohol intake.

17 ctivity, vegetable consumption, and moderate alcohol intake.

18 by JC-1 fluorescence) and ATP production in alcohol intake.

19 by mandated folic acid (FA) fortification or alcohol intake.

20 amygdala, a region involved in regulation of alcohol intake.

21 fied by time exposed to FA fortification and alcohol intake.

22 matched on age, gender, IQ, BMI, and weekly alcohol intake.

23 ss of developing a common summary measure of alcohol intake.

24 cancer risk after controlling for cumulative alcohol intake.

25 ats with and without a history of adolescent alcohol intake.

26 ral or lateral shell or in the core, reduced alcohol intake.

27 etween each biomarker and cumulative average alcohol intake.

28 x, current smoking status, total energy, and alcohol intake.

29 ns with a high body mass index and excessive alcohol intake.

30 t within a 4-year period following increased alcohol intake.

31 subtypes were inconsistently associated with alcohol intake.

32 own of CRMP-2 in the NAc decreases excessive alcohol intake.

33 re to measure lifetime use or the pattern of alcohol intake.

34 ved stress, depression, dietary factors, and alcohol intake.

35 d portal hypertension in patients with heavy alcohol intake.

36 g properties, which could promote subsequent alcohol intake.

37 l relevance of kinase activity for excessive alcohol intake.

38 l appear to be a crucial factor in promoting alcohol intake.

39 diabetes, smoking, sedentary behaviors, and alcohol intake.

40 restored BDNF levels and decreased excessive alcohol intake.

41 , family history of diabetes, and energy and alcohol intakes.

42 , riboflavin, vitamin B-6, vitamin B-12, and alcohol intakes.

43 risk was attenuated in subjects with higher alcohol intakes.

44 g years-of-life-lost were 0.5 years for high alcohol intake, 0.7 years for obesity, 3.9 years for dia

45 under the curve=0.90-0.99) for current heavy alcohol intake (42 g per day in men and 28 g per day in

46 re most effective at achieving reductions in alcohol intake across the 3 trauma centers.

47 alcohol deprivation effect (the increase in alcohol intake after a period of abstinence) while havin

48 f the neurokinin 1 receptor (NK1R) decreases alcohol intake, alcohol reward, and stress-induced alcoh

49 Furthermore, we demonstrate that alcohol intake also blocks glycogen synthase kinase-3bet

50 jective of this study was to examine whether alcohol intake alters the associations between carbohydr

51 30a-5p in the mPFC produced an escalation of alcohol intake and a preference over water.

52 MICs, higher income, being divorced/widowed, alcohol intake and abdominal obesity had higher odds of

53 The authors observed no association between alcohol intake and advanced prostate cancer and an inver

54 serotonin receptor agonist) robustly reduced alcohol intake and BALs in HDID-1 mice, providing the fi

55 ctive was to examine the association between alcohol intake and BMD in women around menopause in the

56 the established association between lifetime alcohol intake and breast cancer and provide evidence fo

57 idence for an association with postdiagnosis alcohol intake and breast cancer survival.

58 al studies assessing the association between alcohol intake and cardiovascular events in the followin

59 hol intake or dose-response relationships of alcohol intake and cardiovascular events.

60 istone (RU38486) prevented the escalation of alcohol intake and compulsive responding induced by chro

61 e response to the metabolic stress caused by alcohol intake and could potentially play a role in many

62 tios for the association between smoking and alcohol intake and development of colorectal adenoma.

63 ion which was not explained by adjusting for alcohol intake and drinking patterns (mean adjusted dysf

64 significant interactions between smoking and alcohol intake and each index on HNC risk.

65 administration, increased aversion-resistant alcohol intake and enhanced stress-induced relapse to al

66 studies of ALD have focused on pathological alcohol intake and few mechanistic studies of moderate a

67 serology, age, nutritional status, smoking, alcohol intake and gastric pH were also analysed.

68 and Signature E4 is unique in ESCC linked to alcohol intake and genetic variants in alcohol-metaboliz

69 estimate associations between previous day's alcohol intake and hormone concentrations, whereas Poiss

70 re was a U-shaped relationship between total alcohol intake and incident HF (P=0.0004).

71 aimed to investigate the association between alcohol intake and incident HF.

72 ssion was used to assess RR of cycle-average alcohol intake and menstrual cycle function.

73 ssociations were shown between cycle-average alcohol intake and menstrual cycle function.

74 idence intervals for the association between alcohol intake and myocardial infarction, ischemic strok

75 ude starches and red meats, whereas moderate alcohol intake and polyunsaturated fat and vegetable con

76 ventral tegmental area (VTA) rapidly reduces alcohol intake and relapse, and increases dopamine (DA)

77 est that relaxin-3/RXFP3 signaling regulates alcohol intake and relapse-like behavior, adding to curr

78 tive synaptic changes that lead to excessive alcohol intake and relapse.

79 ntake might modulate the association between alcohol intake and risk of hormone-dependent cancer.

80 n and place preference, as well as excessive alcohol intake and seeking in preclinical rodent models

81 e also found an inverse relationship between alcohol intake and sTNFRII levels, but no associations w

82 dorsolateral striatum PDE10A in facilitating alcohol intake and support further investigation of PDE1

83 bjectives were to study the relation between alcohol intake and the risk of hormone-dependent cancers

84 rsive effects negatively modulates voluntary alcohol intake and thus may be important in vulnerabilit

85 ts suggest that repeated cycles of excessive alcohol intake and withdrawal potentiate glutamatergic s

86 pioid receptor antagonist, on both voluntary alcohol-intake and alcohol-seeking behaviors.

87 e, other chronic diseases linked to moderate alcohol intake, and a framework in which Mr Q can discus

88 use, adjusted for body mass index, smoking, alcohol intake, and concomitant use of medications.

89 ly attenuated by the adjustment for smoking, alcohol intake, and intelligence measured at conscriptio

90 ass index, diabetes, chronic kidney disease, alcohol intake, and lipid-lowering therapy.

91 cation, total energy intake, smoking status, alcohol intake, and menopausal status as potential covar

92 ass index change, lipid medication, smoking, alcohol intake, and physical activity conveyed similar r

93 Smoking, diet quality, alcohol intake, and physical activity did not further ac

94 such as hedonic responses to palatable food, alcohol intake, and reinstatement of cocaine seeking.

95 baseline body mass index, physical activity, alcohol intake, and several aspects of diet.

96 ur results suggest that television watching, alcohol intake, and sleep deprivation are not merely cor

97 inent lifestyle factors-television watching, alcohol intake, and sleep deprivation-had significant sh

98 y and behaviors such as television watching, alcohol intake, and sleep deprivation.

99 nt of age, sex, Townsend deprivation scores, alcohol intake, and smoking history.

100 position, physical activity, diet, smoking, alcohol intake, and use of oral contraceptives (per 1-un

101 ed risks include physical activity, moderate alcohol intake, and vegetable consumption.

102 ge, adiposity, physical activity, energy and alcohol intakes, and perceived stress.

103 Moderate alcohol intake appears to be positively associated with

104 e mineral density, urticaria pigmentosa, and alcohol intake are easy to collect in clinical practice.

105 Alcohol intake associates with overeating in humans.

106 04) when compared with those who reported no alcohol intake at baseline, having adjusted for sex, age

107 ensity, absence of urticaria pigmentosa, and alcohol intake at the time of ISM diagnosis were indepen

108 of association between maternal or paternal alcohol intake before or during pregnancy and offspring

109 Prior alcohol intake blocked the pro-aggressive effects of ket

110 baseline categories of age, body mass index, alcohol intake, blood pressure, metabolic syndrome, high

111 Alcohol intake both earlier and later in adult life was

112 related to mortality in this cohort-smoking, alcohol intake, caffeine consumption, exercise, body mas

113 Combining such measures of alcohol intake can cause heterogeneity and exposure misc

114 Damaging levels of alcohol intake can occur in the absence of dependence.

115 sted HRs over increasing cumulative averaged alcohol intake categories were 1.00 (reference) for nond

116 light drinkers who modestly increased their alcohol intake, compared with men who either drank less

117 the point of dependence displayed increased alcohol intake, compulsive drinking measured by progress

118 ol consumption, but, by 24 hours, only heavy alcohol intake conferred continued risk.

119 There was a nadir at light-to-moderate alcohol intake: consuming 7 to <14 standard drinks per w

120 ex, physical activity level, smoking status, alcohol intake, depression, self-reported general health

121 Blink reflex recovery cycle before and after alcohol intake did not differ between groups.

122 idal antiinflammatory medications, and daily alcohol intake did not modify these effects; baseline-re

123 nal assessments of body mass index, smoking, alcohol intake, diet quality, physical activity, and ant

124 utions of health-related behaviors (smoking, alcohol intake, diet, physical activity, and sedentary t

125 body mass index, smoking, physical activity, alcohol intake, dietary glycemic index, family history o

126 Although recent moderate alcohol intake does not appear to have adverse short-ter

127 ear, based on self-reported information: any alcohol intake (drinker/non-drinker status) and the regu

128 between education, beverage and non-beverage alcohol intake, drinking patterns, and acute alcohol-rel

129 enetic and behavioral rhythms and influences alcohol intake during chronodisruption.

130 d behavioral circadian timing and influences alcohol intake during chronodisruption.

131 expectation, D2R upregulation did not reduce alcohol intake during continuous or intermittent access

132 Parental age, body mass index, and alcohol intake during pregnancy, child's birth weight, a

133 ificant reductions of relapse-like excessive alcohol intake during the post-abstinence drinking days,

134 In the home cage, increased alcohol intake emerged in 118GG mice with increasing alc

135 ping behaviors in real life, including binge alcohol intake, emotional eating, and frequency of argum

136 , body mass index, cigarette smoking status, alcohol intake, energy intake, physical activity, educat

137 , smoking, physical activity, coffee intake, alcohol intake, family history of T2D, total energy inta

138 mes (ie, body mass index [kg/m(2)], diet and alcohol intake [Food Frequency Questionnaire], and smoki

139 oes provide support for a benefit of limited alcohol intake for cardiovascular and overall survival i

140 cancer risk was observed for higher lifetime alcohol intake (for >/=230 drinks/year vs. <60 drinks/ye

141 ceived a motivational intervention to reduce alcohol intake from either the hygienist or dentist.

142 , we observed a positive association between alcohol intake (from wine but not from beer or spirits)

143 actors (in particular, tobacco and excessive alcohol intake), genetic susceptibility, environmental e

144 I: 0.60, 1.65; P-trend = 0.82) in women with alcohol intakes >/=15 g/d (P-interaction = 0.02).

145 obesity (body mass index > or = 30 kg/m(2)), alcohol intake (> or = 7 ounces of pure alcohol/week), h

146 Our findings suggest that a higher alcohol intake (>/=15 g/d) attenuates the positive assoc

147 tribution of acute withdrawal relief to high alcohol intake has been difficult to model in animals.

148 Although habitual low-to-moderate alcohol intake has been linked with reduced all-cause mo

149 l consumption, the immediate risks following alcohol intake have not been well characterized.

150 le factors (e.g. diet, physical activity and alcohol intake) have been suggested as risk factors for

151 and cardiovascular mortality independent of alcohol intake, have been reported in several prospectiv

152 , lifestyle (smoking, physical activity, and alcohol intake), health history and medication use, and

153 s later (year 20): not overweight/obese, low alcohol intake, healthy diet, physically active, nonsmok

154 e, field center, physical activity, smoking, alcohol intake, high-density lipoprotein-cholesterol, to

155 body mass index <25 kg/m(2), no or moderate alcohol intake, higher healthy diet score, higher physic

156 ng (HR = 1.00, 95% CI: 0.84, 1.21), or heavy alcohol intake (HR = 1.00, 95% CI: 0.74, 1.35).

157 [CI], 1.16; 3.25; P = 0.012); past excessive alcohol intake (HR, 1.55; 95% CI, 1.02; 2.36; P = 0.041)

158 Clinically, low and moderate alcohol intake improves human health with protection aga

159 entration, naltrexone selectively suppressed alcohol intake in 118GG animals to a level virtually ide

160 nine dinucleotide (CpG) sites in relation to alcohol intake in 13 population-based cohorts (ntotal=13

161 We assessed pre- and postdiagnostic alcohol intake in a cohort of 22,890 women with incident

162 receptors, was shown to significantly reduce alcohol intake in a rat model.

163 cess during acute withdrawal increased later alcohol intake in a time-dependent manner, an effect tha

164 eceptor (GR) antagonist mifepristone reduces alcohol intake in alcohol-dependent rats but not in nond

165 GSK1521498) reduced both alcohol seeking and alcohol intake in compulsive and non-compulsive rats, in

166 nnel inhibitor apamin into the NAc increased alcohol intake in control C57BL/6J mice, while spontaneo

167 e conditioning response rate decreased under alcohol intake in controls, it increased in patients (an

168 naptome found cross-species genetic links to alcohol intake in discrete proteins (e.g., C2CD2L, DIRAS

169 dian dysfunction may contribute to increased alcohol intake in ENT1 KO mice.

170 es of chronic liver disease, including daily alcohol intake in excess of 20 g.

171 er and how ghrelin administration may impact alcohol intake in humans is not clear.

172 We also observed that voluntary alcohol intake in K-ras heterozygous null mice (K-ras(+/

173 contraceptive pills in females, smoking and alcohol intake in males did not differ significantly amo

174 14 days dose-dependently decreased voluntary alcohol intake in Marchigian Sardinian rats.

175 ing in the dorsolateral striatum (DLS) keeps alcohol intake in moderation.

176 Cs) and that intra-CeA LTCC blockade reduces alcohol intake in nondependent rats.

177 g LTCCs, and intra-CeA LTCC blockade reduces alcohol intake in nondependent rats.

178 containing rs26907, the SNP associated with alcohol intake in our previous metaanalysis.

179 tory factor and was recently found to reduce alcohol intake in rats by approximately 50%.

180 High alcohol intake in rats during adolescence has been shown

181 ole of the mPFC and CeA in the escalation of alcohol intake in rats with a history of binge drinking

182 inputs to DA cells and CB1 receptors affect alcohol intake in rodents, we hypothesized that the endo

183 ntake in the instrumental context as well as alcohol intake in the choice procedure.

184 uced both cue-controlled alcohol seeking and alcohol intake in the instrumental context as well as al

185 iable lifestyle factors, such as smoking and alcohol intake, increase this risk.

186 Mechanistically, alcohol intake increased RA levels in serum and adipose

187 We have reported that alcohol intake increases Pol III gene transcription to p

188 There was a trend of alcohol intake increasing the risk of colorectal adenoma

189 rget for the prevention/treatment of chronic alcohol intake induced intestinal barrier dysfunction an

190 Moderate alcohol intake induces thermogenic brown/beige adipocyte

191 In conclusion, moderate alcohol intake induces thermogenic brown/beige adipocyte

192 f a highly prevalent form of drinking, binge alcohol intake, influences enzyme priming or the functio

193 tially attenuated by adjustment for smoking, alcohol intake, intelligence, educational level, and lat

194 The lack of reliable measures of alcohol intake is a major obstacle to the diagnosis and

195 Compared with no alcohol consumption, heavy alcohol intake is associated with a higher rate of heart

196 Withdrawal from excessive alcohol intake is associated with a reduction in NAc DA

197 Alcohol intake is associated with increased circulating

198 Alcohol intake is associated with increased risk of brea

199 derly community-based population, increasing alcohol intake is associated with subtle alterations in

200 o measure population-level association where alcohol intake is stratified by sex.

201 ctor for stroke, but the effect of stroke on alcohol intake is unknown.

202 , a behavior characterized by rapid repeated alcohol intake, is most prevalent in young adults and is

203 triatal, and limbic structures that regulate alcohol intake, it has been difficult to disentangle how

204 Repeated alcohol intake leads to mesostriatal neuroadaptations, r

205 Kcnn3 in the NAc negatively correlated with alcohol intake levels in BXD strains, and alcohol depend

206 However, reported alcohol intake may be unreliable, and associations are l

207 ol drinking.SIGNIFICANCE STATEMENT Long-term alcohol intake may lead to neuroadaptations in the mesos

208 ied into 4 categories based on self-reported alcohol intake: nondrinkers, drinkers of </=7, >/=7 to 1

209 ing by age, sex, smoking (in the analyses of alcohol intake), number of colonoscopies during the foll

210 the transition from moderate to uncontrolled alcohol intake occurs, in part, upon a breakdown of this

211 mass index (weight (kg)/height (m)(2)), and alcohol intake (odds ratio = 0.82, 95% confidence interv

212 ects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats.

213 ects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats.

214 : 1.11, 1.49; P-trend < 0.001) in women with alcohol intakes of 0 to <5 g/d, 1.34 (95% CI: 0.93, 1.92

215 I: 0.93, 1.92; P-trend = 0.05) in women with alcohol intakes of 5 to <15 g/d, and 0.99 (95% CI: 0.60,

216 However, more modest levels of alcohol intake on a regular basis may also increase the

217 as used to examine the effect of categorized alcohol intake on BMD adjusted for cluster of lifestyle

218 e regarding the largely adverse influence of alcohol intake on cardiovascular health in an Asian popu

219 ortality and morbidity, the effect of recent alcohol intake on female reproductive function has not b

220 States, the established effects of moderate alcohol intake on key pathophysiological biomarkers and

221 In order to assess the potential impact of alcohol intake on sensory information processing, metric

222 were to investigate the effects of moderate alcohol intake on thermogenic brown/beige adipocyte form

223 and Laird random-effects models to model any alcohol intake or dose-response relationships of alcohol

224 adult socioeconomic status, current smoking, alcohol intake or physical activity.

225 icity, sex, body mass index, smoking status, alcohol intake, or diabetes status.

226 oL, cancer-related fatigue, fruit, fiber, or alcohol intake, or smoking.

227 e of lower mortality risk with low levels of alcohol intake over time but higher mortality risk for t

228 association remained consistent when we used alcohol intakes over different latency periods (0-4, 4-8

229 ors, such severe overweight and a history of alcohol intake (P = 0.005).

230 Myoclonus improved significantly after alcohol intake (p = 0.016).

231 re not attributable to differences in weekly alcohol intake, pharmacokinetic effects (eg, absorption

232 otential confounders such as sleep duration, alcohol intake, physical activity, and current smoking.

233 variables, body mass index, smoking status, alcohol intake, physical activity, and major comorbiditi

234 of cigarettes smoked, cups of coffee taken, alcohol intake, physical activity, parental premature hy

235 ational position, 25 x 25 risk factors (high alcohol intake, physical inactivity, current smoking, hy

236 social class, education, physical activity, alcohol intake, plasma vitamin C, history of cardiovascu

237 x, body mass index, blood pressure, smoking, alcohol intake, plasma vitamin C, social class, educatio

238 Alcohol intake prevented body weight gain, induced the f

239 Here, we show that a history of excessive alcohol intake produces neuroadaptations in the DLS that

240 Together, these data suggest that alcohol intake produces profound functional and structur

241 hat exposure to environments associated with alcohol intake reinstates alcohol seeking after extincti

242 a premorbid risk factor or a consequence of alcohol intake remains unclear.

243 blink reflex recovery cycle before and after alcohol intake resulting in a breath alcohol concentrati

244 bacco smoking (RR, 2.47; 95% CI, 2.12-2.87), alcohol intake (RR, 1.33; 95% CI, 1.17-1.52), body mass

245 odel, adjusted for age; sex; smoking status; alcohol intake; SBP; DBP; cholesterol:high-density lipop

246 , when associated with severe overweight and alcohol intake, severe steatosis.

247 We observed that alcohol intake severely reduced the levels of complex I

248 access to alcohol leads to the escalation of alcohol intake, similar to binge drinking in humans.

249 Survival models were adjusted for age, sex, alcohol intake, smoking history, and educational attainm

250 onal hazards regression, after adjusting for alcohol intake, smoking, body mass index, diabetes, and

251 vation, urban or rural residence, education, alcohol intake, smoking, leisure physical activity, recr

252 eg, hypertension, hyperlipidaemia, excessive alcohol intake, smoking, obesity, and sedentary lifestyl

253 ge, sex, race, clinic site, body mass index, alcohol intake, smoking, physical activity, LDL choleste

254 l adjusting for age, sex, race, clinic site, alcohol intake, smoking, prevalent coronary heart diseas

255 ohol in rats with a history of escalation of alcohol intake specifically recruited GABA and corticotr

256 r, LM11A-31, significantly reduces excessive alcohol intake suggesting that the drug may be developed

257 in patients who improved significantly with alcohol intake suggests a crucial role of cerebellar net

258 and D-cycloserine on this aversion-resistant alcohol intake (that persists despite adulteration with

259 In the presence of obesity and chronic alcohol intake, the variant is associated with even more

260 the most consistent measure being cumulative alcohol intake throughout adult life.

261 el, a higher triglyceride level, and a lower alcohol intake to be independently associated with great

262 cally or intra-PLmPFC, interacted with prior alcohol intake to escalate aggression in ANAs.

263 on adjusted for age, education, smoking, and alcohol intake to estimate the associations between lead

264 imitations of observational evidence linking alcohol intake to lower risk of coronary heart disease,

265 We related alcohol intake to measures of cardiac structure and func

266 mentation and modifying risk factors such as alcohol intake, tobacco use, and lack of exercise.

267 g, body-mass index (BMI), physical activity, alcohol intake, type 2 diabetes and parity, use of hormo

268 ined associations between AMD prevalence and alcohol intake using 20,963 participants from the Melbou

269 factors (dietary pattern, physical activity, alcohol intake, usual sleep, smoking status, and body ma

270 Median alcohol intake was 1013 (range 366-5880) g/week over the

271 Alcohol intake was ascertained every 6 months and use ca

272 In this prospective study, current heavy alcohol intake was associated with a reduced risk of NHL

273 In men, increasing alcohol intake was associated with greater left ventricu

274 Increased alcohol intake was associated with increased BCC risk in

275 In both genders, increasing alcohol intake was associated with larger left ventricul

276 In women, increasing alcohol intake was associated with lower left ventricula

277 ex-specific median of dietary fiber intake), alcohol intake was directly associated with hormone-depe

278 Overall, alcohol intake was directly associated with the risk of

279 Alcohol intake was measured using a detailed food freque

280 Alcohol intake was more strongly associated with B-cell

281 Alcohol intake was repeatedly assessed every 2-4 y over

282 Importantly, compulsive alcohol intake was reversed by overexpression of the wil

283 characteristics of patients were comparable; alcohol intake was the most common etiology of cirrhosis

284 In nondependent rats, the decrease in alcohol intake was transient and returned to normal the

285 cent genome-wide association metaanalysis of alcohol intake, we identified a suggestive association o

286 k factors, overall HRs per 10-g increment in alcohol intake were 0.94 (95% CI: 0.89, 0.98) for CAD an

287 Pretreatment drinking patterns and total alcohol intake were both unrelated to SVR rates.

288 averages of GI, GL, total carbohydrates, and alcohol intake were calculated every 2-4 y from validate

289 HRs and 95% CIs for BCC in association with alcohol intake were computed with the use of Cox proport

290 Body mass index, smoking, and alcohol intake were determined by questionnaire at basel

291 Effects of naltrexone or nalmefene on alcohol intake were examined in continuous access home c

292 , smoking, physical activity, and energy and alcohol intakes were pooled by using a random-effects mo

293 A as a neuroadaptation maintaining excessive alcohol intake, which may contribute to the propensity t

294 Postdependent rats showed escalated alcohol intake, which was associated with increased DNA

295 s in the association of obesity, smoking, or alcohol intake with prostate cancer risk and mortality b

296 The authors examined associations of alcohol intake with risk of NHL and NHL subtypes in the

297 ted inverse associations of coffee, tea, and alcohol intake with risk of type 2 diabetes, but none ha

298 glycemic index (GI), glycemic load (GL), and alcohol intake with type 2 diabetes (T2D).

299 , vitamin B-6, vitamin B-12, methionine, and alcohol intakes with postmenopausal breast cancer among

300 ensin receptor antagonists), smoking status, alcohol intake, years of education, temperature, and sea