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. 2019 Apr 17;75(3):481–494. doi: 10.1093/gerona/glz099

Table 1.

Studies Investigating the Association Between Smoking, Alcohol Consumption, Diet or Body Mass Index and DNAm Age

Ref Study (Country) n: Mean Age (SD) or Range, Sex, Other Information Exposure Sample; Platform Epigenetic Clock ↑ DNAm Age [r With Chronological Age] Adjustments
(31) Publically available data, 3 studies (United States) Total 274. Further details not provided BMI Blood; 27K or 450K AA-Horvath BMI (r = .26, p = .012) in 1 study. NS other 2 studies (r = −.07 to −.18, p ≥ .10). [r = .88] Age
(30) EAS & FACHS studies (United States) EAS 656: age 63 (15), % ♀ not stated, white. FACHS 180, age 49 (9), 62% ♀, black DNAm proxies of smoking, alcohol Blood; not stated AA-Hannum Smoking (β: 8.73, p < .001).
Alcohol, low and high levels of alcohol (nonlinear, p < .05). [r = .71]
None
(53) Esther cohort study (Germany) 1477, 62 (6.5), 49.4% ♀ Cotinine levels in serum, smoking Blood; 450K AA-Horvath, Hannum NS Cotine (β: 0.0011 & β: −0.0013, p > .79, Horvath & Hannum, respectively)
NS Smoking (Horavth current β: −0.13, p = .88; former β: 0.10, p = .79; Hannum current β: −0.34, p = .43; former β: −0.51, p = .16). [r = .75, .78]
Age, sex, BMI, alcohol, health
(27) WHI cohort (United States) from a 9 cohort study 1462 WHI: aged 50–80, 100% ♀. Different racial/ethnic groups. Smoking (3 grps), alcohol (4 grps), BMI Blood; 450K IEAA EEAA NS Alcohol (eg, heavy IEAA β: −0.40, p = .69; EEAA β: −0.83, p = .45).
NS Smoking (eg, current IEAA β: 0.38, p = .72; EEAA, β: 0.12, p = .93).
NS BMI (IEAA β: 0.035, p = .10; EEAA β: 0.045, p = .09) [r = .65 to .93]
Age, sex, cell % education, ethnicity
(51) FACHS (United States) 100: age 48.5 (9.2), 100 ♀, 94% African-American, 17.8% <12th grade education Smoking, alcohol, diet, BMI Blood; 450K AA-Hannum NS Smoking (β: 0.04), NS Alcohol (β: −0.12),
NS BMI (β: −0.08), NS Diet (β: 0.03)
Exact p values not stated. [r = .82]
Education, exercise, trauma, married
(35) WHI (United States) 43: age 61.5 (6.9), 16 year FU. Replication sample of 157, aged 50–79. 100% postmenopausal ♀. BMI Blood; 450K AA-Horvath BMI (β: 0.29, p = .001) & Waist circumference (β: 0.48, p = .03). NS in replication (β: 0.04, p = .56). [r = .89] Age, cell %, ethnicity, smoking
(36) WHI Study (United States) & InCHIANTI study (Italy). 4,173: age 64 (7.1), 100% ♀;
402: age 71 (16), 56% ♀, all
Smoking, alcohol, diet, BMI Blood, serum; 450K. IEAA, EEAA Fish Intake EEAA (β: −2.92, p = .003), NS IEAA β: −0.38, p = .71). ↓ Poultry Intake IEAA (β: −3.30, p = .001), NS EEAA (β: −0.73, p = .46). ↓ Alcohol EEAA (β: −3.23, p = .001), NS IEAA β: −0.36, p = .72).
BMI both (βs: 4.14 to 4.86, p < .001)
NS Smoking (βs: 0.07 to 0.12, p > .90)
Various
(66) YFS, 25 year FU & V90+, 4 year FU (Finland) YFS 183: age 19.2 (3.2), 60.7% ♀; 183: age 44.2 (3.2), 60.7% ♀. V90 + 119: aged 90 (0), %♀ not stated. BMI and 25 year change in BMI Blood; 450K IEAA BMI (β: −0.236, p = .002) & change in BMI in middle-aged adults (r = −.19, p = .009). NS young adults (r = −.11, p = .14) & nonagenarians (r = .12, p = .21). [r = −.14] None
(41) MRC-NSHD cohort; ALSPAC (replication) (United Kingdom) 790: age 53, 100% ♀. Followed until age 60–64.
988: age 46.9 (4.5), 100% ♀.
Smoking, Change in BMI Buccal & Blood; 450K AA-Horvath BMI Buccal (β: 0.085, p = .02), NS Blood (β: 0.04, p = .42), ↑ Blood ALSPAC (β: 0.13, p = .001). ↓ Smoking Buccal (current β: −1.8, p = .001), NS Blood (β: −0.16, p = .30), NS ALSPAC (β: 0.17, p = .43). [r = .02]. Cell %
(62) GOCS (Chile) 94: age 8.1–12, 100% ♀, low-middle income Smoking, BMI, weight Blood; 850K AA-Horvath NS Smoking (r = .01), NS BMI (r = .06), NS Weight (maternal r = .12 & birth r = .14), exact p not stated). [r = .34] Cell %, birth maternal BMI, education
(63) MCC study (Australia) 2,818: age 27–76, 39% ♀, healthy controls matched to cancer cases Smoking, alcohol, healthy eating index, BMI (3 categories) Blood; 450K AA-Horvath,
AA-Hannum, IEAA, EEAA
Smoking (EEAA β: 2.12, p < .001; IEAA β: 1.33, p = .02)
Overweight & Obese (EEAA β: 0.69, p = .01; β: 1.24, p < .001). NS IEAA β: 0.52, p = .09; β: 0.29, p = .47)
NS Alcohol (βs −0.01 to 0.47, p > .10)
NS Healthy Eating (βs −0.01 to −0.02 p ≥ .10) [r = .73 to .76]
Various
(65) Family study, GOLDN (United States) 830: age 48 (16), ~52% ♀, Caucasian. High-fat meal challenge after fasting. Smoking, alcohol Whole blood; 450K IEAA, EEAA Alcohol drinkers >median IEAA (∆+9.0%, p = .01). NS EEAA (∆+4.1%, p = .23).
NS Smokers (IEAA ∆0.2%, p = .89, EEAA ∆1.2%, p = .52). [r = .94, 0.91]
Age, cell % smoking, drinking, lipid
(59) GS-SFHS (Scotland) 5100: age 48.5 (14.0), 61.6% ♀ Smoking, BMI Blood; 850K IEAA, EEAA Smoking (IEAA β: 0.03, p = .03; EEAA β:0.06, p < .001).
BMI (IEAA β: 0.09, p < .001; EEAA β: 0.06, p < .001).
Age, sex

Note: AA = epigenetic age acceleration; BMI = body mass index; EAS = Effects of ageing study; EEAA = extrinsic epigenetic age acceleration; FU = follow-up; GS-SFHS = Generation Scotland- Scottish Family Health Study; GOLDN = Genetics of Lipid Lowering Drugs and diet Network; GOCS = Longitudinal Growth & Obesity Cohort Study; IEAA = intrinsic epigenetic age acceleration; MCC = Melbourne Collaborative Cohort Study; MRC-NSHD = Medical Research Council National Survey of Health & Development; NS = not significant; SD = standard deviation; V90+ = Vitality 90+ (V90+); YFS = The Young Finns Study; WHI = Women’s Health Initiative study.