Search bioRxiv⌕ Search

bioRxiv · 10.1101/684035

Exploring the Relationship between Geomagnetic Activity and Human Heart Rate Variability

Abstract

Both geomagnetic and solar activity fluctuate over time and have been proposed to affect human physiology. One physiological measurement that has been previously investigated in this context, heart rate variability (HRV), has substantial health implications regarding the ability to adapt to stressors and has been shown to be altered in many cardiovascular and neurological disorders. Intriguingly, previous work found significant, strong correlations between HRV and geomagnetic/solar activity. In an attempt to replicate these findings, we simultaneously measured HRV from 20 healthy participants during a thirty-day period. In agreement with previous work, we found several significant correlations between HRV and geophysical time-series. However, after correction for autocorrelation, which is inherent in time-series, the only significant results were an increase in very low frequency during higher local geomagnetic activity and a geomagnetic anticipatory decrease in heart rate a day before higher global geomagnetic activity. Both correlations were very low. The loss of most significant effects after this correction suggests that previous findings may be a result of autocorrelation. A further note of caution is required since our and the previous studies in the field do not correct for multiple comparisons given the exploratory analysis strategy. We thus conclude that the effects of geomagnetic and solar activity are (if present) most likely of very small effect size and question the validity of the previous studies given the methodological concerns we have uncovered in our work.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Mattoni, M., Ahn, S., Frohlich, C., Frohlich, F.. 2019-06-26. Exploring the Relationship between Geomagnetic Activity and Human Heart Rate Variability. https://doi.org/10.1101/684035

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Selective activation of estrogen receptors modulates electrical activity and insulin secretion in human EndoC-βH1 cells

Estrogen receptors (ERs), ER and ER{beta} have important roles in the physiology of the endocrine pancreas in animal models, but the effects of ER activation on insulin-secreting human cells are still poorly understood. Here, we investigated the role of ER and ER{beta} as modulators of electrical activity and insulin secretion in the insulin-secreting human cell line EndoC-{beta}H1. Immunocytochemical analysis revealed a widespread cellular distribution of ER, while ER{beta} was predominantly localized outside the nucleus. We observed that both estradiol (E2) and the ER{beta} agonist diarylpropionitrile (DPN) led to a decrease in insulin secretion in the absence of stimulatory glucose concentrations, without affecting insulin content. Patch-clamp experiments revealed that a 48-hour treatment with either the ER agonist PPT or DPN resulted in depolarization of the resting membrane potential, increased action potential firing frequency, and altered the action potential waveform in EndoC-{beta}H1 cells. PPT increased voltage-dependent Ca2+ channel currents, while DPN reduced K+ and Na+ currents. These results suggest that activation of ER and ER{beta} modulates beta-cell electrical activity through distinct pathways involving ion channels. The effects of E2, PPT, and DPN were not caused by altered expression levels of ion channel genes after 48 hours of treatment. This suggests that these receptors act extranuclearly without affecting gene expression. Together, our findings demonstrate that selective activation of ER and ER{beta} modulates beta-cell excitability through distinct electrophysiological mechanisms and that E2 and DPN reduce basal insulin secretion in human EndoC-{beta}H1 cells. These results support ER and ER{beta} as potential targets for modulating human pancreatic beta-cell function.

physiology↗

Body weight modifies the efficacy of lifespan-extending interventions in ad libitum-fed mice

Geroprotective interventions are often assessed by extension of lifespan in ad libitum-fed mice. Increased lifespan could therefore reflect rescue of adverse phenotypes of unhealthy controls. We analysed body weight and survival for 33,780 mice in the Interventions Testing Program (ITP) to test whether treatment effects varied with body weight. In males, each added standard deviation of attained adult weight made treatment 6% more favourable (HR 0.94), more apparent for interventions that lowered body weight (HR 0.90). Median lifespan increase rose from 6.2% in mice in the lightest quartile to 20.2% in the heaviest pre-dosing weight quartile among those experiments, mainly because control survival declined more steeply with weight than that of the intervention group. The effect of body weight was consistent across 13 of 14 compounds and reflected weight attained during adulthood rather than in early life. Weight-dependence of intervention effects was weak in ITP females, possibly because median survival of controls exceeded that of every sampled non-ITP female control group. Amelioration of weight-associated risk is therefore implicated as a major contributor to lifespan increases relative to heavy, short-lived controls. The geroprotective effects of these interventions may thus be less apparent in metabolically healthier mice or humans.

physiology↗

Single-nucleus analysis reveals renal STAT1/CEBPB signaling as a modifiable relay of proinflammatory FGF23 effects in diabetic kidney disease

Background Circulating fibroblast growth factor 23 (FGF23) rises dramatically in chronic kidney disease, particularly in diabetic kidney disease (DKD). At high concentrations, and with declining Klotho, FGF23 has been linked to renal inflammation. The cell types and transcriptional programs mediating these off-target actions remain undefined. We asked whether the diseased kidney responds to FGF23 differently from the healthy kidney, and whether any disease-specific response could be targeted. Methods Male and female DBA/2J mice received streptozotocin or vehicle to induce DKD. On day 56, mice received a single dose intravenous injection of FGF23 (0.3 g) or vehicle, with tissue collected 1 h later for single-nucleus RNA sequencing, differential expression and regulon (inferred transcription factor activity) analysis. Candidate pathways were tested in precision-cut kidney slices using the CEBPB inhibitor ST-101. Results Streptozotocin-treated male mice developed early DKD with a 6-fold increase in urinary albumin/creatinine ratio and 50% higher blood urea nitrogen with preserved glomerular filtration rate. All major renal cell types were annotated. Canonical FGF23 signaling was intact in disease, with segment-specific target induction conserved in both conditions (e.g. Cyp24a1 in PT-S1 and DCT1). Superimposed on this were disease-restricted responses, including Wsb1 in DCT1 and Pdk4 in PT-S2, PST, DCT1 and DCT2. Regulon analysis revealed DKD-specific induction of CEBPB regulon activity by FGF23 across all analyzed tubular segments, and of STAT1 in several segments. Pre-treatment with a CEBPB inhibitor suppressed CEBPB activity, downstream NF-KB and pro-inflammatory gene sets, and immune-like cell abundance in diseased slices. Conclusion In the diabetic kidney, FGF23 engages a STAT1-CEBPB-NF-{kappa}B axis absent from healthy kidney and extending beyond its canonical Klotho-dependent target segments, identifying CEBPB as a potential treatment target for FGF23's pathological inflammatory actions.

physiology↗