Table 2.
Correlates of Hair Cortisol Concentrations
| Study | Sample size for analysis | Summary of Findings |
|---|---|---|
| Hair-Related Factors | ||
| Natural Hair Color | ||
| Raul et al (2004) | 8 black, 3 blond, 24 brown, 7 grey | No differences in HCC of different hair colors (p=0.9773) AB Mean±SD: (black: 16.63±7.99; blond: 16.97±6.84; brown: 15.52±7.85; grey: 15.86±5.21) pg/mg |
| Sauvé et al (2007) | 4 blond, 4 brown, 4 black | No difference in HCC of different hair colorsCD |
| Kirschbaum et al (2009) | 142 womenE | No difference in HCC of different hair colors (p>0.20)CD |
| Manenschijn et al (2011) | 10 black, 75 brown, 94 blond, 6 red, 9 grey | No difference in HCC of different hair colors (p=0.413)D |
| Dettenborn et al (2012) | 33 light blond, 36 dark brown | No difference in HCC of different hair colors (p=0.524) Mean±SD: (light blond: 20.22±11.2; dark brown: 21.88±10.4) pg/mg |
| Dettenborn et al (2012) | 79 light-middle blond, 71 dark blond-light brown, 84 middle-dark brown |
No significant difference in HCC of different hair colors F(2,232)=2.538, p=0.081D |
| Groeneveld et al (2013) | 42 children (mean age, 50.1 months, SD=0.42 months, 45% boys)E |
HCC was not significantly related to hair colorCD |
| Hair Wash Frequency and Temperature | ||
| Kirschbaum et al (2009) | 142 womenE | No significant association between frequency of hair washes per week and HCC (p>0.20)CD |
| Manenschijn et al (2011) | 50 hair samples (≤2 times per week) 143 hair samples (≥3 times per week) |
No significant association between frequency of hair washes per week and HCC (p=0.673)D |
| Dettenborn et al (2012) | Frequency of hair washing: (0–1, 1.5–2, 2.5– 3, 3.5–4, 4.5–5, 5.5–6, 6.5–9 times per week) | No significant association between frequency of hair wash and HCC in first two segments: (first 3-cm segment: r=−0.061, p=0.335, n=249), (second 3-cm segment: r=−0.102, p=0.168, n=184). However, in third segment, HCC was inversely correlated with frequency of hair wash (r=−0.248, p=0.008, n=113) |
| Li et al (2012) | 3 participants | After immersion in shampoo solution for four hours, HCC decreased from 30.5±9.6 to 6.5±5.9 pg/mgC Mean±SD cortisol loss ratio was 75.5±27.4%, range: 45.1–98.4% |
| 8 participants | After 20 hour immersion, mean HCC decreased from (at 40°C: 13.8±5.8 to 4.4±2.9 pg/mg, p<0.001), (at 65°C: 8.8±4.1 to 1.4±0.4 pg/mg, p<0.01) and (at 80°C: 8.8±4.1 to 0.6±0.2 pg/mg, p<0.01) |
|
| Stalder et al (2012) | 155 individuals in study I (mean±SD of number of hair washes in the entire sample: 3.1±2.3)E 58 individuals in study II (mean±SD of number of hair washes in the entire sample: 3.7±1.6)E |
No significant association between frequency of hair washes per week and HCC (p>0.10 in study I, p>0.30 in study II)CD |
| Groeneveld et al (2013) | 42 children (mean age, 50.1 months, SD=0.42 months, 45% boys)E |
HCC was not significantly related to hair washing frequencyCD |
| Stalder et al (2013) | 1258 men and womenE | HCC was not correlated with number of hair washes per week (r =−0.046, p>0.05)C |
| Hair Dyeing and other Hair Treatments | ||
| Sauvé et al (2007) | 25 untreated hair, 14 dyed hair | Dyed hair had lower HCC (p=0.036)D |
| Dowlati et al (2010) | 5 dyed hair, 78 non-dyed hair | No difference in mean HCC of dyed and non-dyed hair (4.77±0.70 vs. 4.95±0.57, p=0.49) |
| Karlén et al (2011) | 95 students (40 students had colored/permed hair) |
There seemed to be a difference between mean HCC of colored/permed hair vs. non colored/permed hair (mean±SD 13.0±16.0pg/mg vs. 24.8±40.9 pg/mg, p=0.09), but it was not statistically significant |
| Manenschijn et al (2011) | 152 untreated hair, 43 treated hair (women) 90 used hair products, 104 did not use hair products |
Treated hair (dyed, bleached, permanent waved/straightened) had lower mean HCC than untreated hair (24.27 vs. 29.38 pg/mg, p=0.051) Use of hair product (hair spray, mousse, gel, wax) on the day of hair collection was not significantly associated with HCC: 24.83 pg/mg (product use) vs. 28.44 pg/mg (no product use), p=0.109 |
| Manenschijn et al (2012) | 96 healthy, non-obese controls, 14 patients with Cushing’s Syndrome, 6 patients suspected of cyclic Cushing’s syndromeE |
HCC was slightly lower in healthy women with treated hair, i.e. hair dyeing or bleaching (p=0.06)D No difference between HCC of treated and untreated hair in Cushing’s patientsCD |
| Stalder et al (2012) | Study I: 59 treated hair, 96 untreated hair Study II: 21 treated hair, 37 untreated hair |
Study I: No difference between treated semi-permanent color, coloration or permanent wave) and untreated hair (p>0.10)CD Study II: No difference between treated (as described above) and untreated hair (p>0.30)CD |
| Stalder et al (2013) | 1258 men and womenE (15.5% reported use of hair treatment) |
HCC was negatively associated with hair treatment after adjustment for sex (F1, 1195=4.22, p=0.04, ŋp2=0.0004) |
| Hair Segment | ||
| Xie et al (2011) | 8 female participants | Average linear HCC decline rate of 2.9±0.6 pg/mg (r=−0.948, p<0.05) per centimeter in the first five 1- cm hair segments |
| Manenschijn et al (2011) | 28 healthy women | HCC was not significantly different in six consecutive 3-cm segments (p=0.249)D |
| Steudte et al (2011) | 30 participants | HCC decreased 17.4% from the proximal 3-cm segment to the second 3-cm segment, then decreased 18.3% from the second 3-cm segment to the third |
| Dettenborn et al (2012) | 155 individuals | HCC decreased by 16.32% from first 3-cm hair segment to the second hair segment (p<0.001). HCC also decreased 12.29% from second 3-cm hair segment to third (p<0.001) |
| Skoluda et al (2012) | 273 individuals | HCC decreased from proximal to distal hair segments (F(1.55, 273.05)=131.9, p<0.001)D |
| Luo et al (2012) | 20 non-traumatized controlsE | HCC linearly declined from proximal to distal in the nontraumatized control group (F=41.07, p <0.0001) |
| Krumbholz et al (2013) | 1 woman (hair examined across pregnancy) | HCC decreased by >50% after 4 months of hair growth |
| Hair Texture and UV-Irradiation | ||
| Kirschbaum et al (2012) | 142 womenE | Hair curvature was not significantly related to HCC (p>0.20)D |
| Dettenborn et al (2012) | 360 individuals (70% of whom were aged 18–49 years old)E |
There was no influence of curls (p=0.468)D or waves (p=0.633)D on HCC when compared with straight hair in individuals aged 18–49 years old |
| Li et al (2012) | 12 hair samples exposed to 9-hour UV irradiation |
HCC decreased from 26.1±8.8pg/mg to 18.9±8.0pg/mg (p=0.047) The average loss ratio in HCC was 26.5±20.9% (r=0.616, p<0.05) |
| Stress-Related Factors | ||
| Demographic, Social and Occupational Factors | ||
| Dettenborn et al (2010) | 31 unemployed, 28 employed | Unemployed individuals had higher HCC for first 3-cm segment (p<0.05)D and second 3-cm segment (n=52, p<0.05)D |
| Manenschijn et al (2011) | 33 shift workers, 89 day workers | Workers who had a fast-forward rotating shift schedule had higher mean HCC compared with those who only worked during the day (mean(95% CI): 47.32(38.37–58.21) vs. 29.72(26.18–33.73) pg/mg, p<0.001). However, in individuals <40 years of age, shift workers had higher HCC (mean(95%CI): 48.53(36.56–64.29) vs. 26.42(22.91–30.55) pg/mg, p<0.001) while for those >40 years, there was no effect of shiftwork. There were no individuals who were exactly 40 years old |
| Chen et al (2013) | Cohort A (13 had elementary school education, 34 had high school education or below, 6 had college education or above) Cohort B (4 had elementary school education, 27 had high school education and below, 19 had college education or above) |
No significant difference in HCC among all three educational groups in cohort A (F=0.31, p=0.74) and in cohort B (F=1.98, p=0.15) |
| Groeneveld et al (2013) | 42 children (mean age, 50.1, SD=0.42 months); mean parental educational was 14.8 years (SD=1.9)E |
HCC was not significantly related to parents’ educational levelCD |
| Saleem et al (2013) | 56 cardiac rehabilitation patients with CAD (26 with normal HCC (median 111 ng/g) and 30 with elevated HCC (median 263 ng/g) |
Normal vs. high HCC group: total years of education (mean±SD: 16.5±3 vs 17±3.5 years, p=0.45), married (88.5% vs. 73.3% married, p=0.20) |
| Vaghri et al (2012) |
333 preschoolers |
Parental income was inversely correlated with HCC from 1–2cm hair segment (r=-0.18, p=0.001); in a subsample of 275 preschoolers, annual family income was not correlated with HCC (r=-0.07, p=0.235) |
| Age | ||
| Raul et al (2004) | 44 individuals | Linear regression predicting HCC from age (β=0.0296, standard error=0.0541, p=0.139)AB There was no relationship between HCC and age category (mean±SD: 0–15 years: 15.2±7.1; 16–30 years: 14.4±8.4; 31–50 years: 16.2±7.6; 51–90 years: 17.3±6.3 pg/mg, p=0.878) |
| Manenschijn et al (2011) | 195 individuals (18–63 years); Mean age: 36 years |
HCC was not correlated with participant age (p=0.388)D |
| Dettenborn et al (2012) | 360 individuals (1–91 years) | HCC was positively related with age (R2=0.010, p=0.030) For children 0–5 years, age in months was negatively correlated with HCC (r=−0.428, p=0.023). Children (1–9 years old, n=28) had significantly higher HCC compared with adults (n=34, 18–38 years old) (p<0.001)D |
| Kirschbaum et al (2012) | 103 mothers of newborns 2–4 days of age (mean±SD age: 29.7 ±5.5years), 19 mothers of toddlers 3–9 months (mean±SD age: 30.4± 2.8years) and 20 nonpregnant nulliparas (mean±SD age: 25.8±6.4years) |
HCC was not significantly associated with age across the entire group (p>0.20) CD |
| Manenschijn et al (2012) | 14 Cushing’s syndrome patients, 6 individuals with suspected cyclic Cushing’s Syndrome, 96 healthy controlsE |
HCC was not significantly related with age in either the patient or control groupCD |
| O’Brien et al (2012) | 135 adults (18–66 years old) | No correlation of age and HCC (r=0.07, p>0.05) HCC was not significantly correlated with tertiles of age (age ranges: young=18–21 years, n=44; middle=22–29 years, n=45; older=30–66 years, n=43) |
| Stalder et al (2012) | 155 individuals (18–46 years) Mean±SD age: 24.1±14.2 years |
HCC was not correlated with participant age (r=−0.02, p>0.05) CD |
| Stalder et al (2012) | 58 individuals (20–70 years) Mean±SD age: 30.5±12.1 years |
HCC was not correlated with participant age (r=−0.06, p>0.05) CD |
| Vaghri et al (2012) | 339 preschoolers (mean±SD age: 4.6±0.5 years) |
No statistically significant correlation between age and log-transformed, winsorized HCC variable (r=− 0.09, p=0.098) |
| Chen et al (2013) | Cohort A (23 participants 21–40 years; 29 participants >40 years); Cohort B (21 participants aged 21–40 years; 23 participants >40 years) |
No significant difference in HCC of those aged 21–40 years and those >40 years in cohort A (z=−0.179, p=0.86), and in cohort B (z=−0.51, p=0.61) |
| Gerber et al (2013) | 42 university male and female students | Age was not significantly associated with HCCCD |
| Manenschijn et al (2013) | 283 elderly adults (65–85 years) | HCC was not correlated with age (r=−0.02; p=0.76) |
| Saleem et al (2013) | 56 cardiac rehabilitation patients with CAD (26 in normal HCC (median 111 ng/g) and 30 in the elevated HCC (median 263ng/g) |
Age was not significantly associated with HCC |
| Stalder et al (2013) | 1258 men and womenE(age: 16–64 years) | HCC was positively correlated with age (r=0.11, p<0.0001)C |
| Sex | ||
| Raul et al (2004) | 16 males, 26 females | No differences in HCC of males and females (mean±SD: 15.6± 8.8 vs. 16.1±6.3 pg/mg, p=0.859) |
| Karlén et al (2011) | 95 students (24 males, 71 females) | No difference in HCC of males and females (mean±SD: 17.8±13.4 pg/mg vs 20.6±37.7 (p=0.73) |
| Manenschijn et al (2011) | 90 men, 105 women | No significant effect of gender (p=0.353)D |
| Manenschijn et al (2012) | Bipolar patients: 34 men, 62 women Healthy controls: 90 men, 105 women |
No sex differences in HCC of bipolar patients (p=0.12)D and healthy controls (p=0.87)D |
| Steudte et al (2011) | PTSD patients: 4 men, 6 women Controls: 11 men, 6 women |
No significant effects of gender on HCC (F(1,23)=1.01, p=0.33, ŋp2=0.04)D |
| Dettenborn et al (2012) | 252 adults (18–49 years) 52 children (1–9 years) 25 adolescents (10–17 years) 31 elderly (50– 91 years) |
Males had higher HCC in first 3-cm segment compared with females for adults 18–49 years (F(1,251)=9.573, p=0.002, ŋp2=0.037).D Males had higher in first 3-cm segment HCC compared with females for children 1–9 years (F(1,51)=5.304, p=0.025, ŋp2=0.078).D No sex differences were seen in HCC of adolescents (F(1,24)=0.837, p=0.370)D or elderly (F(1,30)=0.064, p=0.803)D |
| Manenschijn et al (2012) | 14 Cushing’s syndrome patients, 6 individuals with suspected Cushing’s Syndrome, 96 healthy controls E |
HCC was not significantly related with sex in either the patient or control groupCD |
| O’Brien et al (2012) | 135 adults (60% female) | Men had slightly higher HCC compared with women t(129) = 2.91, p<0.01 |
| Skoluda et al (2012) | Athletes: 304 individuals (58.9% female), Controls: 70 individuals (82.9% female) |
No significant differences in HCC between the sexes in athletes (p=0.06)D nor in controls (p=0.62)D Across the entire sample, males had higher HCC (F(1,372)=8.13, p<0.01)D |
| Stalder et al (2012) | Study I: N=155 (73.5% females) Study II: N=58 (67.2% females) |
Study I: No significant difference in HCC of males and females (F(1.154)=0.006, p>0.05)CD Study II: Non significant linear trend for higher HCC in males compared with females (F(1,57)=3.58, p=0.06, ŋp2=0.06)D |
| Vaghri et al (2012) | 167 preschool boys, 172 preschool girls | No statistically significant correlation between age and log-transformed, winsorized HCC variable (biserial correlation=−0.01, p=0.790) |
| Chen et al (2013) | Cohort B (41 men, 9 women) | No significant gender difference in HCC (z=−1.25, p=0.22) |
| Gerber et al (2013) | 42 university students (22 women, 20 men) |
Sex was not significantly associated with participants’ HCCCD |
| Groeneveld et al (2013) | 42 children (mean age, 50.1 months, SD=0.42 months, 45% boys) |
HCC was not significantly related to genderCD |
| Hinkelmann et al (2013) | 43 major depressive disorder patients, 41 age- and sex-matched controlsE |
HCC was not significantly associated with sex (p>0.10)CD |
| Manenschijn et al (2013) | 283 elderly adults (66.1% female) | HCC were significantly higher in men than in women (median, 26.3 pg/mg hair [interquartile range (IQR), 20.6 – 35.5 pg/mg hair] vs 21.0 pg/mg hair [IQR, 16.0 – 27.0 pg/mg hair]; p<0.001) |
| Saleem et al (2013) | 56 cardiac rehabilitation patients with coronary artery disease (26 in normal HCC group (median 111.4 ng/g) and 30 in the elevated HCC group (median 262.8 ng/g) |
Gender was not significantly different between normal HCC group (92.3% male) and high HCC group (80% male) (p=0.19) |
| Stalder et al (2013) | 1258 men and womenE (about 84.8% were men) |
HCC was not significantly with sex (F1, 1216=1.83, p>0.05)CD |
| Race and Ethnicity | ||
| O’Brien et al (2012) | 135 adults categorized into two groups: minorities (African-Cuban, Afro-Cuban, Asian, Brazilian, Indian, Latino-Hispanic and Pacific Islander (n=67)); and non-minorities (European or White American (n=68)) |
HCC was not correlated with race (r=−0.09, p>0.05). However, there was significant interaction of race and SES on HCC (F(2, 122)=3.26, p<0.05, ŋp2=0.16) |
| Psychiatric Symptoms and Disorders | ||
| Dowlati et al (2010) | 34 depressed patients, 87 non-depressed patients (all attending a cardiac rehabilitation center) |
Mean HCC was not different between depressed and non-depressed patients (log mean±SD: 4.96±0.58 vs. 5.04±0.59, p=0.53) |
| Karlén et al (2011) | 95 students (20 with serious life events) | Mean HCC were higher students who had experienced serious life events within the last 3 months vs. those who had not (mean±SD: 33.0±57.0 vs 16.3±22.5 pg/mg, p=0.045) |
| Steudte et al (2011) | 10 traumatized individuals with PTSD, 16 traumatized controls without PTSD | Traumatized PTSD patients had significantly higher HCC compared with traumatized non-PTSD controls (F(1,25)=5.35, p=0.03, ŋp2=0.18)D |
| Steudte et al (2011) | 15 generalized anxiety disorder patients (GAD), 15 controls |
HCC were significantly lower in GAD patients compared with controls for first 3-cm segment (F(1,27)=11.80, p=0.002, ηp2=0.304)D and second 3-cm segment (F(1,24)=8.894, p=0.006, ηp2=0.270)D. A non-significant trend for lower HCC in GAD patients was observed for the third segment (F(1,17)=4.138, p=0.058, ηp2=0.196)D |
| Dettenborn et al (2012) | 23 depressed patients, 64 healthy controls | Depressed patients had elevated HCC in the first 3-cm (mean±SD: 26.7±20.8 vs. 18.7±11.5 pg/mg, p<0.05) and second 3-cm hair segments (mean±SD: 21.9±23.7 vs. 13.4±9.6 pg/mg, p<0.05) compared with controls |
| Luo et al (2012) | 32 individuals with PTSD, 32 traumatized non-PTSD controls, 20 non-traumatized non-PTSD controls |
For the hair segment corresponding to 2 months before and 1 month after the earthquake, HCC were elevated in traumatized individuals (PTSD and non-PTSD) compared with the non-traumatized non- PTSD controls (F=3.88, p=0.0499 and F=6.27, p=0.013, respectively)D. For the hair segment corresponding to 2 to 4 months after the earthquake, traumatized non-PTSD controls had significantly higher HCC compared with traumatized PTSD individuals (F=6.17, p=0.0137)D and non-traumatized non- PTSD controls (F=11.74, p=0.0007)D. For the period corresponding to 5 to 7 months after the earthquake, traumatized non-PTSD controls had higher HCC compared with traumatized individuals with PTSD (F=4.11, p=0.0438)D |
| Manenschijn et al (2012) | 100 bipolar disorder (BD) patients, 195 healthy controls |
No difference between mean HCC of BD patients and that of controls (mean(95%CI): 31.84(28.38– 35.81) vs. 28.18(25.94–30.62) pg/mg, p=0.233). However, in a subsample, individuals with older age of onset (≥30 years) had higher HCC compared with those with early onset (<30 years old) (β=0.335, p=0.004) |
| Gerber et al (2013) | 42 undergraduate students (22 women, 20 men) |
HCC were negatively associated with depressive symptoms (as assessed using the Beck Depression Inventory (BDI)), β=−0.24, p=0.009. |
| Grassi-Oliveira et al (2012) | 23 treatment seeking crack cocaine- dependent women |
HCC was significantly related with negative life events exposure 90 days before hospital admission (r =0.56; p=0.007) and 30 days (r =0.42; p=0.048) prior to admission at the hospital, but not with 60 days prior to admission (r=0 .23; p =0.293) |
| Groeneveld et al (2013) | 42 children (mean age, 50.1 months, SD=0.42 months, 45% boys); 21 children scored high on a fearfulness questionnaire |
HCC significantly increased after the start of school, but only in children who scored high for fearfulness F(1, 19)=4.67, p=0.04, ŋp2=0.20. |
| Hinkelmann et al (2013) | 43 major depressive disorder patients, 41 age- and sex-matched controlsE |
HCC was not associated with current depression, nor with atypical depressionCD |
| Saleem et al (2013) | 56 patients who completed a one-year cardiac rehabilitation program(26 of whom had normal HCC at baseline, 30 had normal HCC a baseline)E |
The prevalence of depression did not differ between the normal HCC group (26.9%) and the high HCC group (30%) (p=0.80) |
| Steudte et al (2013) | 25 PTSD patients, 25 traumatized controls, 28 non-traumatized controls |
HCC was 59% lower in PTSD patients and 51% lower in traumatized controls (TC), compared to non- traumatized controls (NTC) (mean±SD HCC: PTSD 6.44±6.05 pg/mg; TC 7.78±7.01 pg/mg; NTC 15.75±14.77 pg/mg; p<0.05). No differences in HCC between PTSD and TC groups (p=0.535). HCC was not correlated with Beck Depression Index (BDI-II) scores (r=−0.127, p=0.256). HCC was inversely correlated with number of different lifetime traumatic events, frequency of traumatic experiences, time since traumatization, and severity of intrusion symptoms. |
| Other Medical Conditions | ||
| Cardiovascular Disease, Cardio-Metabolic Syndrome, and Chronic Pain | ||
| Van Uum et al (2008) | 15 chronic pain patients receiving opioid treatments, 39 non-obese controls |
Chronic pain patients had higher HCC compared with controls (mean(range): 83.1(33.0–205) pg/mg vs. 46.1(27.2–200) pg/mg, p<0.01) |
| Pereg et al (2010) | 56 acute myocardial infarction patients (AMI), 56 non-AMI hospital controls |
AMI patients had significantly elevated median HCC compared with non-AMI hospital controls (median (range): 295.3(105.4–809.3) vs. 224.9(76.58–949.9) ng/g, p<0.01) |
| Karlén et al (2011) | 95 students (28 reported taking pharmaceuticals) |
No difference in HCC according to use of pharmaceuticals (mean±SD: 22.9±44.9 pg/mg vs 18.6±27.2 pg/mg, p=0.57) |
| Manenschijn et al (2011) | 46 healthy participants | No correlation between HCC and systolic (p=0.109)D or diastolic blood pressure (p=0.365)D |
| O’Brien et al (2012) | 135 adults (18–66 years, 65% female, 48% minority) |
HCC was positively correlated with systolic blood pressure (r=0.25, p<0.01); however no significant correlation was observed between HCC and diastolic blood pressure (r=0.08, p>0.05) |
| Manenschijn et al (2013) | 283 elderly adults (age range: 65–85 years) | HCC was significantly associated with CVD. The odds ratio (OR) was 1.9 (p=0.09) for the second, 2.0 (p=0.08) for the third and 2.7 (p=0.01) for the fourth quartile. Highest levels of HCC quartile assocated with type 2 diabetes mellitus (OR 3.2, p=0.04). |
| Saleem et al (2013) | 56 patients who completed a one-year cardiac rehabilitation program(26 of whom had normal HCC at baseline, 30 had normal HCC a baseline)E |
High baseline HCC (i.e. HCC ≥153.2 ng/g) predicted less improvement in verbal memory performance after one year (F(1, 50)=5.50, p=0.02,.Number of weeks since acute coronary event, percutaneous coronary intervention, and myocardial infarction did not differ between normal and high HCC groups, however history of coronary artery bypass surgery differed. Between the normal and high HCC groups: prevalence of hypertension (53.8% vs 63.3%, p=0.47), diabetes (7.7% vs 16.7%, p=0.31), maximum heart rate (118±18 vs 121±22 bpm, p=0.55), SBP (176±24 vs 177±27 mmHg, p=0.90), DBP (76±9 vs 80±11 mm Hg, p=0.18), and maximal oxygen intake (20±5 vs 20±5, p=0.98) seemed to differ, though the p-values were not significant. |
| Stalder et al (2013) | 1258 men and womenE (about 24% had metabolic syndrome (MetS)) |
HCC was positively associated with metabolic syndrome (MetS): [mean(±SD), no MetS: 7.70 (±8.12) pg/mg; MetS: 10.78 (±11.37) pg/mg, p<0.0001]. Furthermore, in the adjusted partial correlations, HCC was not significantly associated with mean arterial pressure (r=0.047, p>0.05), high-density lipoprotein cholesterol (r=−0.037, p>0.05), triglycerides (r=−0.015, p>0.05), and glucose (r=0.005, p>0.05). However, HCC was associated with low-density lipoprotein cholesterol (r=−0.080, p<0.01), and glycated hemoglobin (r=0.116, p<0.001) |
| Adrenocorticoidal Conditions | ||
| Thomson et al (2010) | 6 female Cushing’s syndrome patients, 32 healthy controls (21 females, 11 males) |
Cushing’s patients had significantly higher HCC compared with controls: (median(range): 679(279–2500) vs. 116(26–204) ng/g, p<0.001) |
| Gow et al (2011) | 93 adrenal insufficiency (AI) patients on hydrocortisone replacement therapy, 62 household partners |
AI patients had higher median HCC than controls (median(range): 230.7(22.7–1377) vs. 184.7(57.7– 1479) ng/g, p=0.08), although the result was not significance. Hydrocortisone dose was also correlated with HCC (r=0.03, p=0.004) |
| Manenschijn et al (2011) | 195 healthy controls, 9 hypercortisolemics | Hypercortisolemics had significantly elevated HCC compared with healthy controls (p<0.0001)CD |
| Manenschijn et al (2012) | 14 patients with Cushing’s syndrome (CS), 6 patients with cyclic Cushing’s syndrome, 96 non-obese healthy controls |
Patients with CS (excluding cyclic CS patients) had significantly elevated mean HCC compared with healthy individuals (mean(95%CI): 399.7(171.8–930.0) vs. 27.3(24.6–30.4) pg/mg, p<0.0001) |
| Adiposity | ||
| Manenschijn et al (2011) | 39 shift workers, 89 day workers | HCC positively correlated with participant BMI (b=0.262, p<0.05). HCC increased across BMI groups as follows: (mean(95%CI): (BMI<25kg/m2: 31.26(26.79–36.48)); (BMI 25–30kg/m2: 36.06(30.48–42.76)); (BMI >30 kg/m2: 60.95(43.95–84.72) pg/mg, p=0.002) |
| Manenschijn et al (2011) | 195 healthy people, 9 hypercortisolemic, 1 hypocortisolemic |
HCC was positively correlated with waist circumference (r=0.392, p<0.05) and WHR (r=0.425, p<0.05). HCC was not significantly correlated with BMI (p=0.646)D or hip circumference (p=0.096)D |
| Manenschijn et al (2012) | Bipolar patients: 100 individuals; BMI median (IQR): 25.3(23.5–28.0 kg/m2) Healthy controls: 195 people: BMI median (IQR): 23.7(21.7–26.5 kg/m2) |
No significant relationship between HCC and BMI in bipolar (r=0.163, p=0.11) and control individuals (r=0.042, p=0.59) |
| O’Brien et al (2012) | 135 adults | HCC was not significantly correlated with waist-to-hip ratio (r=−0.03, p>0.05) |
| Stalder et al (2012) | 155 adults; BMI: (mean±SD: 22.2±3.4; range:16.5–35.8) kg/m2 |
HCC positively correlated with participant weight (r=0.29, p≤0.001) and BMI (r=0.33, p≤0.0001) |
| Stalder et al (2012) | 58 university students; BMI: (mean±SD:24.0±4.9; range:16.9–42.1) kg/m2 |
HCC positively correlated with participant weight (r=0.36, p<0.05) and BMI (r=0.42, p≤0.001) |
| Manenschijn et al (2013) | 283 elderly adults (65–85 years old, 66.1% female) |
No significant correlation between HCC and BMI (r=0.06, p=0.36), waist circumference (r=0.11, p=0.08) |
| Saleem et al (2013) | 56 patients who completed a one-year cardiac rehabilitation program(26 of whom had normal HCC at baseline, 30 had normal HCC at baseline)E |
Between the normal and high HCC groups, mean±SD of BMI did not differ (27.1±5.0 kg/m2 vs 27.4±3.5 kg/m2, p=0.75), neither did waist circumference (96.2±10.1 cm vs. 98.8±8.8, p=0.29) |
| Pregnancy | ||
| D’Anna-Hernandez et al (2011) | 21 non-smoking pregnant women (<17 weeks gestational age) |
HCC increased across successive trimesters and then decreased during the first 2 to 3 months postpartum. HCC in third trimester was higher than in the first (t=4.1, p=0.001)D as well as post-partum (t=2.9, p=0.004)D |
| Kirschbaum et al (2012) | 103 mothers with newborn 2–4 days of age, 19 mothers of toddlers 3 to 9 months, 20 non-pregnant nulliparous women (n=20). |
HCC of mothers of newborns 2–4 days of age (their hair corresponded with the third trimester) was significantly elevated in the first 3-cm segment compared with that of control women (t(1,120)=4.77, p<0.0001) D; however there was no significant difference in HCC of the two groups of women for segments 2 and 3 |
| Krumbholz et al (2013) | 1 woman (HCC over a pregnancy) | The highest HCC (13.4 pg/mg) was observed for the hair segment that reflected the last month of pregnancy and first month postpartum |
| Early Life Adversity | ||
| Yamada et al (2007) | 60 NICU infants > 25 weeks gestational age, NICU term infants, healthy term infants |
HCC for NICU infants was elevated compared with HCC for healthy term infants (mean±SD: 2.06±2.05 vs. 0.11±0.42 nmol/g, p=0.004). Total number of days on the ventilator was associated with HCC (increased 0.2 nmol/g, p=0.03, on average, for each additional day). There was no difference between HCC of term infants in NICU and HCC of preterm infants in NICU |
| Grassi-Oliveira et al (2012) | 23 treatment seeking crack cocaine- dependent women |
No correlation between HCC and severity of early life stress CD |
| Hinkelmann et al (2013) | 43 major depressive disorder patients, 41 age- and sex-matched controlsE |
HCC was lower in subjects who experienced childhood maltreatment compared to controls (F1,71=4.11, p=0.05)C |
| Steudte et al (2013) | 25 PTSD patients, 25 traumatized controls, 28 non-traumatized controlsE |
No significant correlation was observed between HCC and childhood trauma scores (r=-0.144, p=0.197) |
| Lifestyle and Behavioral Factors | ||
| Alcohol Use | ||
| Stalder et al (2010) | 23 alcoholics in acute withdrawal, 25 abstinent alcoholics, 20 controls |
HCC (mean±SD) was highest in acute withdrawal alcoholics (51.99±43.30 pg/mg), compared with abstinent alcoholics (13.98±10.63 pg/mg, p<0.001) and controls (16.35±12.59 pg/mg, p<0.001). No |
| difference between HCC of abstinent alcoholics and controls (p=0.91) | ||
| Manenschijn et al (2013) | 283 elderly adults (17.4% who had never drank, 52.8% light drinkers, 26.2% moderate drinkers, 3.6% (very) excessive drinkers) |
HCC was positively associated with alcohol consumption. HCC were 21.2 pg/mg hair (IQR, 15.2–29.4) in non-drinkers, 21.7 pg/mg hair (IQR, 16.9–28.9) in light drinkers, 24.5 pg/mg hair (IQR, 17.1–36.3) in moderate drinkers, and 30.4 pg/mg hair (IQR, 25.0–45.0) in excessive drinkers (p=0.05) |
| Stalder et al (2013) | 1258 men and womenE (43% reported regular consumption of ≥3 alcoholic drinks/week) |
No association between HCC and self-reported alcohol consumption (F1, 1208 = 0.11, p>0.05)D; HCC was positively associated with serum γ-glutamyltransferase (γGT), (r=0.11, p<0.0001) |
| Cigarette Smoking | ||
| Dettenborn et al (2012) | 18–49 year oldsE | No influence of smoking status on HCC (p=0.836)D |
| Stalder et al (2012) | Study I: 155 adults (17.6% smokers), Study II: 58 students at the Technical University of Dresden (27.6% smokers) |
Study I: No association between smoking status and HCC (p>0.10)D Study II: No association between smoking status and HCC (p>0.30)D |
| Skoluda et al (2012) | 304 amateur endurance athletes (7.1% habitual smokers); 70 controls (20% habitual smokers) |
Smoking was not associated with HCC (F(1, 364)=0.02, p=0.88)D |
| Hinkelmann et al (2013) | 43 major depressive disorder patients; 41 age- and sex-matched controlsE |
HCC was not significantly associated with smoking status (p>0.10)CD |
| Manenschijn et al (2013) | 283 elderly adults (38.2% never smoked; 52.7% former smokers, 8.8% current smokers) |
No difference in HCC based on smoking status. HCC were 21.2 pg/mg hair (IQR, 16.6–26.9) in those who never smoked, 22.1 pg/mg hair (IQR, 17.4–33.6) in former smokers, and 26.3 pg/mg hair (IQR, 18.7- 32.3) in current smokers (p=0.22) |
| Stalder et al (2013) | 1258 men and womenE (33.5% smokers) | HCC was not associated with smoking status (p>0.05)CD |
| Oral Contraceptives and Medication Intake | ||
| Dettenborn et al (2012) | (16.7% of 360 individuals in the sample used oral contraceptives)E 252 individuals aged 18–49 years oldE 29 elderly individuals (medication intake analysis)E |
No influence of oral contraceptive use on HCC in 18–49 year old women (p=0.110)D No influence of overall medication intake on HCC in 18–49 year olds (p=0.610)D No influence of medication intake in elderly group (F(1,29)=0.245, p=0.625)D |
| Stalder et al (2012) | Study I: 72 oral contraceptive users, 42 not taking oral contraceptives Study II: 16 oral contraceptive users, 23 not taking oral contraceptives |
Study I: No association between oral contraceptive use and HCC (p>0.10)D Study II: No association between oral contraceptive use and HCC (p>0.30)D |
| Groeneveld et al (2013) | 42 children (mean age, 50.1 months, SD=0.42 months, 45% boys)E |
HCC of children was not related to use of corticosteroids or other medicationsCD |
| Hinkelmann et al (2013) | 43 major depressive disorder patients, 41 age- and sex-matched controlsE |
HCC was not associated with antidepressant treatment (p>0.1)D |
| Saleem et al (2013) | 56 patients who completed a one-year cardiac rehabilitation program(26 of whom had normal HCC at baseline, 30 had normal |
Use of concomitant medications seemed to differ with specific drugs between normal and high HCC groups, however no statistically significant difference was observed; beta-blocker (80.8% vs 70%, p=0.35); calcium channel blocker (26.9% vs 10%, p=0.10); diuretics (23.1% vs 20%, p=0.78); |
| HCC at baseline)E | antihypertensives (50% vs 63.3%, p=0.32); antidiabetics (3.8% vs 16.7%, p=0.12); antidepressants (3.8% vs 10%, p=0.37) ; anxiolytics (11.5% vs 3.3%, p=0.23) |
|
| Steudte et al (2013) | 25 PTSD patients (36% used regular medication (RM)), 25 traumatized controls (20% used RM), 28 non-traumatized controls (29% used RM)E |
No relationship between HCC and medication intake (p>0.31)D |
| Steudte et al (2013) | 25 PTSD patients (96% female, 7 women used oral contraceptives (OC)), 25 traumatized controls (92% female, 4 used OC), 28 non-traumatized controls (89 female, 9 used OC)E |
No relationship between HCC and oral contraceptive use (p>0.31)D |
| Physical Activity | ||
| Skoluda et al (2012) | 304 amateur endurance athletes, 70 controls |
On average, athletes had higher HCC compared with controls (mean±SD: 18.18±9.6 vs. 12.43±6.2 pg/mg; and gender did not alter the effect of endurance sports on HCC, p=0.048). Additionally, they observed a significant correlation between HCC and training kilometers run per week (r=0.32, p<0.001), training hours per week (r=0.22, p<0.001) and number of competitions per year (r=0.29, p<0.001), but not with number of training years (r=0.008, p=0.89). |
| Stalder et al (2013) | 1258 men and womenE (physical activity score range: 3–15) |
No association of HCC with light or moderate physical activity; positive association with vigorous physical activity (p>0.05)CD |
| Gerber et al (2013) | 42 university students (vigorous physical activity: 0–213 weekly minutes; moderate physical activity: 164– 775 weekly minutes) |
HCC positively correlated with vigorous physical activity (β=0.33, p=0.05, ?R2=0.106). HCC was not significantly correlated with moderate physical activity (r=−0.08, p>0.05) |
| Diet | ||
| Stalder et al (2013) | 1258 men and womenE (self-reported daily fruit and vegetable consumption) |
No association between HCC and fruit and vegetable consumption (p>0.05)CD |
A
We used SAS 9.2 to calculate these values
B
We excluded two outlier values
C
Authors did not report exact p-values
D
Authors did not report mean HCC, median HCC, correlation or odds ratio
E
Sample size used in analysis might be different from total sample size (and/or) authors did not specify the proportion of subjects in comparison groups