Biology subjects

Volzke, H.

Publications and source records attributed to Volzke, H..

3 recordsLinked to original sources

bioRxiv2025

Lifestyle, Early-life, and Genetic Health Risk Factors Underlying the Brain Age Gap: A Mega-Analysis Across 3,934 Individuals from the ENIGMA MDD Consortium

BackgroundLarge-scale studies show that adults with major depressive disorder (MDD) generally have a higher imaging-predicted age relative to their chronological age (i.e., positive brain age gap) compared to controls, though considerable within-group variation exists. This study examines lifestyle, early-life, and genetic health risk factors contributing to the brain age gap. Identifying risk and resilience factors could help protect brain and mental health. MethodsUsing an established model trained on FreeSurfer-derived brain regions (www.photon-ai.com/enigma_brainage), we generated brain age predictions for 1,846 controls and 2,088 individuals with MDD (aged 18-75) from 12 international cohorts. Polygenic risk scores (PRS) were calculated for major depression, C-reactive protein, and body mass index (BMI) using large-scale GWAS results. Linear mixed models were applied to assess lifestyle (BMI, smoking, education), early-life childhood trauma, and genetic (PRS) health risk associations with the brain age gap. Additionally, we evaluated the link between the brain age gap and peripheral biological age indicators (epigenetic clocks). ResultsHigher brain age gaps were significantly associated with BMI ({beta}=0.01, PFDR=0.02) and smoking ({beta}=0.11, PFDR=0.02), while lower brain age gaps were linked to higher education ({beta}=-0.02, PFDR=0.02). Higher childhood trauma scores predicted a higher brain age gap ({beta}=0.04, P=0.01). Higher brain age gaps were positively associated with all PRS ({beta}s=0.04-0.16, PsFDR=0.02-0.03). There were no significant interactions between diagnosis and assessed factors on the brain age gap. In a multivariable model, only modifiable health factors--BMI, smoking, and education--remained uniquely associated with brain age gaps. ConclusionsGenetic liability for depression and related traits is linked to poorer brain health, but health behaviors potentially offer a key opportunity for intervention. This study underscores the importance of targeting modifiable lifestyle factors to mitigate poor brain health in depressed individuals, an approach perhaps under-recognized in clinical practice.

neuroscience↗

bioRxiv2020

Universal salt iodization contributes to health equity: socio-economic status does not affect iodine status in children in Macedonia

Many studies have shown that socio-economic status (SES) contributes to health inequalities, with nutrition as one of the major risk factors. Iodine intake entirely depends on external sources, and deficiencies are known to be more prevalent in lower social groups, especially in countries with limited access to iodized salt. This study aimed to determine the influence of SES on iodine status and iodine availability from household salt in North Macedonia. Using cluster sampling, 1,200 children were recruited, and 1,191 children participated (response rate: 99.2%). Iodine status was assessed through urinary iodine concentration (UIC), and iodine availability through iodine content in household salt requested from participants. SES was assessed using standardized Family Affluence Score (FAS). No statistically significant correlation was found between FAS and iodine in salt. Median regression revealed no significant associations of middle vs. low FAS ({beta}=0.00; 95%-confidence interval (CI)=[-0.61, 0.62]; p=0.999) or high vs. low affluence ({beta}=0.48; 95%CI=[-1.37, 0.41]; p=0.291) with iodine content in household salt. UIC levels were significantly lower in middle FAS children compared to low FAS children ({beta}=-16.4; 95%CI=[-32.3,-0.5]; p=0.043). No statistically significant differences in UIC were found between children with high and low affluence ({beta}=-12.5; 95%CI=[-35.5, 10.5]; p=0.287), possibly due to lowered statistical power for this comparison. Universal salt iodization (USI) proves to be cost-effective measure for appropriate iodine intake in healthy children and adults, irrespective of their social status. It can thus be concluded that USI contributes to reducing health inequalities related to iodine status among population of different social strata.

physiology↗

bioRxiv2020

Contrasting recruitment of skin-associated adipose depots during cold challenge of mouse and human

Mammalian skin impacts metabolic efficiency system-wide, controlling the rate of heat loss and consequent heat production. Here we compare the unique fat depots associated with mouse and human skin, to determine whether they have corresponding function and regulation. For human, we assay a skin-associated fat (SAF) body-wide depot to distinguish it from the subcutaneous fat pads characteristic of abdomen and upper limbs. We show that the thickness of SAF is not related to general adiposity; it is much thicker (1.6-fold) in women than men, and highly subject-specific. We used molecular and cellular assays of {beta}-adrenergic induced lipolysis and found that dermal white adipose tissue (dWAT) in mice is resistant to lipolysis; in contrast, the body-wide human SAF depot becomes lipolytic, generating heat in response to {beta}-adrenergic stimulation. In mice challenged to make more heat to maintain body temperature (either environmentally or genetically), there is a compensatory increase in thickness of dWAT: A corresponding {beta}-adrenergic stimulation of human skin adipose (in vivo or in explant) depletes adipocyte lipid content. We summarize the regulation of skin-associated adipocytes by age, sex, and adiposity, for both species. We conclude that the body-wide dWAT depot of mice shows unique regulation that enables it to be deployed for heat preservation; combined with the actively lipolytic subcutaneous mammary fat pads they enable thermal defense. The adipose tissue that covers human subjects produces heat directly, providing an alternative to the brown adipose tissues. KEY POINTS SUMMARYO_LISeveral distinct strategies produce and conserve heat to maintain body temperature of mammals, each associated with unique physiologies, with consequence for wellness and disease susceptibility C_LIO_LIHighly regulated properties of skin offset the total requirement for heat production C_LIO_LIWe hypothesize that the adipose component of skin is primarily responsible for modulating heat flux; here we evaluate the relative regulation of adipose depots in mouse and human, to test their recruitment to heat production and conservation C_LIO_LIWe found that insulating mouse dermal white adipose tissue accumulates in response to environmentally- and genetically-induced cool stress; this layer is one of two adipose depots closely apposed to mouse skin, where the subcutaneous mammary gland fat pads are actively recruited to heat production C_LIO_LIIn contrast, the body-wide adipose depot associated with human skin produces heat directly, potentially creating an alternative to the centrally regulated brown adipose tissue C_LI

physiology↗