Evidence map›Paper›PMID 26453329›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Sympathetic activation is associated with increased IL-6, but not CRP in the absence of obesity: lessons from postural tachycardia syndrome and obesity.

Luis E Okamoto, Satish R Raj, Alfredo Gamboa, Cyndya A Shibao, Amy C Arnold, Emily M Garland, Bonnie K Black, Ginnie Farley, André Diedrich, Italo Biaggioni

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
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  3. A Randomized Trial of Vitamin D Supplementation on Vascular Function in CKD.Journal of the American Society of Nephrology : JASN · 2017
    Trial
  4. Article
  5. Review
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  7. Postural orthostatic tachycardia syndrome in a Thai male patient.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024
    Article
  8. Article
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  11. Transcutaneous vagus nerve stimulation attenuates autoantibody-mediated cardiovagal dysfunction and inflammation in a rabbit model of postural tachycardia syndrome.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Luis E OkamotoVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Satish R RajVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Pharmacology, Vanderbilt University School of Medicine; and.
Alfredo GamboaVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Cyndya A ShibaoVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Amy C ArnoldVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Emily M GarlandVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Bonnie K BlackVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
Ginnie FarleyVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee;
André DiedrichVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Biomedical Engineering, Vanderbilt University School of Medicine, Nashville, Tennessee.
Italo BiaggioniVanderbilt Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Pharmacology, Vanderbilt University School of Medicine; and Italo.biaggioni@vanderbilt.edu.
Vanderbilt University · US

Funding

The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
Structural genomics of norepinephrine transportersP01HL056693 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BIAGGIONI, ITALO · 1997 to 2016
$30.8M
CLINICAL PHARMACOLOGY TRAINING PROGRAMT32GM007569 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Bjorn C Knollmann · 1985 to 2026
$12.4M
Training CoreU54NS065736 · NINDS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BIAGGIONI, ITALO · 2009 to 2018
$11.6M
Autonomic Nervous System in Chronic Fatigue SyndromeR01NS055670 · NINDS · VANDERBILT UNIVERSITY · PI BIAGGIONI, ITALO · 2006 to 2009
$1.5M
NCATS NIH HHS UL1 TR000445NCATS NIH HHS UL1-TR-000445NHLBI NIH HHS P01 HL056693NHLBI NIH HHS P01-HL-56693NIGMS NIH HHS T32 GM007569NINDS NIH HHS R01 NS055670NINDS NIH HHS R01-NS-055670NINDS NIH HHS U54 NS065736PHS HHS 14CRP20380211
6 · The paper itself

Abstract

Sympathetic activation is thought to contribute to the inflammatory process associated with obesity, which is characterized by elevated circulating C-reactive protein (hsCRP) and interleukin-6 (IL-6). To evaluate whether sympathetic activation is associated with inflammation in the absence of obesity, we studied patients with postural tachycardia syndrome (POTS), a condition characterized by increased sympathetic tone in otherwise healthy individuals. Compared with 23 lean controls, 43 lean female POTS had greater vascular sympathetic modulation (low-frequency blood pressure variability, LFSBP, 3.2 ± 0.4 vs. 5.5 ± 0.6 mmHg(2), respectively, P = 0.006), lower cardiac parasympathetic modulation (high-frequency heart rate variability, 1,414 ± 398 vs. 369 ± 66 ms(2), P = 0.001), and increased serum IL-6 (2.33 ± 0.49 vs. 4.15 ± 0.54 pg/ml, P = 0.011), but this was not associated with increases in hsCRP, which was low in both groups (0.69 ± 0.15 vs. 0.82 ± 0.16 mg/l, P = 0.736). To explore the contribution of adiposity to inflammation, we then compared 13 obese female POTS patients and 17 obese female controls to matched lean counterparts (13 POTS and 11 controls). Compared with lean controls, obese controls had increased LFSBP (3.3 ± 0.5 vs. 7.0 ± 1.1 mmHg(2); P = 0.016), IL-6 (2.15 ± 0.58 vs. 3.92 ± 0.43 pg/ml; P = 0.030) and hsCRP (0.69 ± 0.20 vs. 3.47 ± 0.72 mg/l; P = 0.001). Obese and lean POTS had similarly high IL-6 but only obese POTS had increased hsCRP (5.76 ± 1.99 mg/l vs. 0.65 ± 0.26; P < 0.001). In conclusion, sympathetic activation in POTS is associated with increased IL-6 even in the absence of obesity. The coupling between IL-6 and CRP, however, requires increased adiposity, likely through release of IL-6 by visceral fat.

Indexed as

AdiposityAdultBlood PressureBody CompositionC-Reactive ProteinCytokinesFemaleHumansInflammationInterleukin-6MaleNeurotransmitter AgentsObesityPostural Orthostatic Tachycardia SyndromeSympathetic Nervous SystemC-Reactive ProteinCytokinesIL6 protein, humanInterleukin-6Neurotransmitter Agentsautonomic nervous systemchronic fatigue syndromeinflammationobesitypostural tachycardia syndrome

Identifiers

PMID26453329
PMCPMC4698423
OpenAlexW2291341206

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.