Population-based biobanking is an essential element of medical research that has grown substantially over the last two decades, and many countries are currently pursuing large national biobanking initiatives. The rise of individual biobanks is paralleled by various networking activities in the field at both the national and international level, such as BBMRI-ERIC in the EU. A significant contribution to population-based biobanking comes from large cohort studies and national repositories, including the United Kingdom Biobank (UKBB), the CONSTANCES project in France, the German National Cohort (NAKO), LifeLines in the Netherlands, FinnGen in Finland, and the All of Us project in the U.S. At the same time, hospital-based biobanking has also gained importance in medical research. We describe some of the scientific questions that can be addressed particularly well by the use of population-based biobanks, including the discovery and calibration of biomarkers and the identification of molecular correlates of health parameters and disease states. Despite the tremendous progress made so far, some major challenges to population-based biobanking still remain, including the need to develop strategies for the long-term sustainability of biobanks, the handling of incidental findings, and the linkage of sample-related and sample-derived data to other relevant resources.

We aimed to relate circulating plasma zinc and copper to a broad spectrum of adiposity-related traits in a cross-sectional Northern German study (n = 841, 42% female, age: 61 ± 12 years). Zinc and copper were measured by inductively coupled plasma–mass spectrometry. Subcutaneous (SAT) and visceral (VAT) adipose tissue and liver fat were derived from 534 and 538 participants, respectively, via magnet resonance imaging. Associations were assessed using multivariable-adjusted linear regression analysis. An increase per one standard deviation (SD) in zinc was associated with direct linear increases in body mass index (BMI) (1.17%; 95% confidence interval (95%CI) 0.15–2.20%), waist circumference (0.85%; 95%CI 0.04–1.67%) and waist-to-hip ratio (0.64%; 95%CI 0.18–1.09%). A 1-SD increment in copper was directly associated with BMI (1.64%; 0.41–2.88%) and waist circumference (1.22%; 95%CI 0.25–2.20%) but not waist-to-hip ratio. Independent of fat intake, zinc displayed associations with VAT (5.73%; 95%CI 2.04–9.56%) and with liver fat (3.84%; 95%CI 1.49–6.25%), the latter association being also independent of BMI. Copper was directly associated with SAT (4.64%; 95%CI 0.31–9.15%) before accounting for BMI, but showed no association with VAT or liver fat. Observed associations suggest a possible relevance of zinc and copper to adiposity. Particularly zinc displayed associations with traits of abdominal adiposity and liver fat.

Context: Neck circumference (NC) was proposed as promising marker to assess body fat distribution and cardiometabolic risk. Objective: We aimed to assess associations of NC with anthropometric traits, cardiometabolic risk markers, and self-reported cardiometabolic diseases. Methods: NC was measured in a subsample (5865 participants) of the German National Cohort (NAKO Gesundheitsstudie, NAKO), study region Kiel. Linear and logistic regression models were applied to assess associations of NC with anthropometric and cardiometabolic risk markers and self-reported cardiometabolic diseases, including diabetes, heart failure, gout, and a composite end point “clinical CVD” (cardiovascular disease; combining history of angina pectoris, stroke, myocardial infarction, and peripheral artery disease). Models were adjusted for sex and age, CV risk factors (systolic blood pressure, diabetes, low-density lipoprotein [LDL] cholesterol, use of lipid-lowering and antihypertensive medication, smoking status), and body mass index (BMI). Results: Mean NC values (±SD) were 39.5 ± 3.0 in men and 33.6 ± 2.7 cm in women. NC was positively associated with anthropometric traits, visceral adipose tissue (cm) (β = 1.45 [95% CI, 0.88-2.02]), systolic (β = .37 [0.19-0.56]) and diastolic (β = .17 [0.05-0.29]) blood pressure, glycated hemoglobin A1c (β = .02 [0.01-0.02]), nonfasting glucose (β = .57 [0.31-0.83]), and inversely associated with high-density lipoprotein cholesterol (β = −.73 [−0.91; −0.54]). Furthermore, NC showed associations with diabetes (odds ratio [OR] = 1.08 [1.02-1.15]), heart failure (OR = 1.12 [1.02-1.23]), and gout (OR = 1.09 [1.01-1.17]). Association with “clinical CVD” did not remain statistically significant after BMI adjustment. Conclusion: NC was associated with several cardiometabolic risk factors, including glycemic and lipid traits and self-reported cardiometabolic diseases. These observations suggest that NC may be a useful surrogate marker for cardiometabolic risk.

Coenzyme Q10 (CoQ10) plays an important role in human health; for example, through the antioxidant function of its reduced form (ubiquinol). As the long-term health effects of circulating CoQ10 remain largely unknown, we examined the association of total CoQ10, ubiquinol, ubiquinone (oxidized CoQ10), and CoQ10 redox state (percentage of ubiquinone in total CoQ10) with all-cause mortality in a sample from the northern German general population. In n = 1333 individuals (60.1% females, median baseline age: 48.0 years [37.7; 58.0]), serum total CoQ10, ubiquinol, ubiquinone, and CoQ10 redox state were measured at baseline and found to be related to all-cause mortality using Cox regression models (adjusted for sex, age, body mass index, smoking, systolic blood pressure, total cholesterol, diabetes, and C-reactive protein). After 12.9 years [12.4; 17.1], n = 123 deaths had occurred. A higher CoQ10 redox state was independently associated with a higher risk of all-cause mortality after multivariable adjustment (HR: 1.18 [95% CI 1.02–1.36] per 1-SD increment, HR: 1.92 [95% CI 1.16–3.17] for tertile 3 vs. tertile 1), while higher ubiquinone levels were associated with greater all-cause mortality risk only in the unadjusted model. A higher CoQ10 redox state was associated with a higher risk of all-cause mortality in a population-based sample, possibly indicating detrimental long-term health effects of the lower antioxidant capacity of CoQ10.