Caffeine intake is not associated with serum testosterone levels in adult men: cross-sectional findings from the NHANES 1999–2004 and 2011–2012

<p><b>Objective:</b> The association of caffeine intake with testosterone remains unclear. We evaluated the association of caffeine intake with serum testosterone among American men and determined whether this association varied by race/ethnicity and measurements of adiposity.</p> <p><b>Methods:</b> Data were analyzed for 2581 men (≥20 years old) who participated in the cycles of the NHANES 1999–2004 and 2011–2012, a cross-sectional study. Testosterone (ng/mL) was measured by immunoassay among men who participated in the morning examination session. We analyzed 24-h dietary recall data to estimate caffeine intake (mg/day). Multivariable weighted linear regression models were conducted.</p> <p><b>Results:</b> We identified no linear relationship between caffeine intake and testosterone levels in the total population, but there was a non-linear association (<i>p</i>_nonlinearity < .01). Similarly, stratified analysis showed nonlinear associations among Mexican-American and Non-Hispanic White men (<i>p</i>_nonlinearity ≤ .03 both) and only among men with waist circumference <102 cm and body mass index <25 kg/m² (<i>p</i>_nonlinearity < .01, both).</p> <p><b>Conclusion:</b> No linear association was identified between levels of caffeine intake and testosterone in US men, but we observed a non-linear association, including among racial/ethnic groups and measurements of adiposity in this cross-sectional study. These associations are warranted to be investigated in larger prospective studies.</p

Demographic and tumor characteristics of CRC patients according to SMAD4 mutation status.

<p>Demographic and tumor characteristics of CRC patients according to SMAD4 mutation status.</p

Comparison of survival curves in patients with metastatic CRC according to SMAD4 mutation status.

<p>Median OS durations of 29 months (95% CI, 20–48 months) and 56 months (95% CI, 51–63 months) were observed in patients with mutated and wild-type SMAD4, respectively.</p

OncoPrint of genomic alterations in TCGA CRC cases (n = 220) showing mutations of SMAD4, KRAS, NRAS, and BRAF.

<p>OncoPrint of genomic alterations in TCGA CRC cases (n = 220) showing mutations of SMAD4, KRAS, NRAS, and BRAF.</p

Univariate and multivariate Cox regression analyses of OS in metastatic CRC patients (n = 600).

<p>Univariate and multivariate Cox regression analyses of OS in metastatic CRC patients (n = 600).</p

Comparison of the incidences of SMAD4 mutations across different molecular subtypes.

<p>Comparison of the incidences of SMAD4 mutations across different molecular subtypes.</p

The prevalence and spectrum of SMAD4 mutations in the MD Anderson study patients and TCGA data.

<p>(A) The prevalence and spectrum of SMAD4 mutations in the study patients who underwent full-length sequencing (n = 49). (B) The prevalence and spectrum of SMAD4 mutations in TCGA data (n = 220 patients).</p

Progression-free survival curves for CRC patients who received anti-EGFR treatment according to SMAD4 mutation status.

<p>All patients were wild-type for KRAS, NRAS, and BRAF genes.</p

Comparison of the incidences of TGF-β pathway mutations across different molecular subtypes.

<p>Comparison of the incidences of TGF-β pathway mutations across different molecular subtypes.</p

OncoPrint showing the distribution of TGF-β mutations across different molecular subtypes in TCGA CRC samples.

<p>OncoPrint showing the distribution of TGF-β mutations across different molecular subtypes in TCGA CRC samples.</p