Oura Ring Gen 4 sensor data — not clinical measurementsN=1 case study — not validated for clinical decisionsHEV diagnosed Mar 18; interpret findings cautiously in this Day 73 post-ruxolitinib window

Causal Inference: Ruxolitinib

Data period: 2026-01-08 to 2026-05-26 (140 days) | Total runtime: 1.0s
Generated 2026-05-28 07:29 · Post-HSCT Patient
Four complementary causal analysis methods explore whether Oura biometrics shifted after ruxolitinib (10 mg BID, started 2026-03-16) on Oura Ring biometrics. Data period: 2026-01-08 to 2026-05-26 (140 days).
Pre-intervention
Info
67days
Post-intervention
Normal
73days
Raw p<0.05
Info
0/0
FDR-significant
None
0/0
Lowest raw p
Not significant
p=1.000
N/A | q=1.0000
Methods used
Info
4
CI + PCMCI+ + TE + Mediation
Table of contents:
  1. Individual Metric Treatment Response
  2. CausalImpact - Bayesian Structural Time Series
  3. Statistical Power & Interpretation
  4. Placebo tests (falsification)
  5. Granger Causality Network (PCMCI+)
  6. Transfer Entropy
  7. Intervention Response Decomposition
  8. Clinical Interpretation

0. Individual Metric Treatment Response

Method: Non-parametric Mann-Whitney U test compares pre- vs post-ruxolitinib distributions for each core biometric. Effect sizes reported as Cohen's d with bootstrap 95% CI (2000 iterations). These direct statistical tests provide intuitive per-metric significance before the multivariate causal methods below.
HRV (RMSSD)
Significant
p<0.001
d=+1.63 (large)
Lowest HR
Significant
p<0.001
d=-1.56 (large)
Average HR
Significant
p<0.001
d=-1.50 (large)
Sleep Efficiency
Significant
p<0.001
d=+0.81 (large)
Metric Pre-Rux Mean Post-Rux Mean Change Cohen's d Mann-Whitney 95% CI (diff)
HRV (RMSSD)10.00 ms24.06 ms+14.06 ms+1.63 (large)Sig p<0.001[+11.29, +16.85]
Lowest HR76.72 bpm65.41 bpm-11.31 bpm-1.56 (large)Sig p<0.001[-13.77, -8.75]
Average HR85.17 bpm74.32 bpm-10.85 bpm-1.50 (large)Sig p<0.001[-13.33, -8.32]
Sleep Efficiency78.62 %82.02 %+3.39 %+0.81 (large)Sig p<0.001[+1.94, +4.78]
Note: These per-metric tests complement the Bayesian CausalImpact analysis below. For full changepoint detection and multi-patient comparison, see the Comparative Treatment Response report.

1. CausalImpact - Bayesian Structural Time Series Analysis

Method: Bayesian Structural Time Series (BSTS) models pre-intervention dynamics and generates a counterfactual prediction for the post-period. The difference between actual and counterfactual estimates the causal effect, with full posterior uncertainty. MCMC: 5,000 iterations, weekly seasonal component (nseasons=7). Benjamini-Hochberg FDR correction for multiple testing.

FAILED CausalImpact package not installed. Install with: pip install pycausalimpact

1a. Statistical Power & Interpretation

Purpose: All 11 metrics sorted by statistical significance, with Benjamini-Hochberg corrected q-values for multiple testing.

No CausalImpact results available for statistical power analysis.

1b. Placebo tests (intervention date falsification)

Method: CausalImpact is run with 3 random placebo dates in the pre-period on the 3 most significant metrics. Placebo dates should NOT show significant effects.

CausalImpact failed, skipping placebo

2. Granger Causality Network (PCMCI+)

Method: PCMCI+ (tigramite) tests for time-lagged causal relationships between biometric variables using partial correlation. Tau_max = 7 days.

Full period (0 days): No significant causal links found.

Pre-ruxolitinib (0 days): No significant causal links found.

3. Transfer Entropy

Method: Transfer entropy quantifies directional information flow between biometric streams. Comparison of TE matrices for pre- and full period reveals changes in information coupling after ruxolitinib start.

Full period (139 days)

SourceTargetTE (bits)Net TE
REMdurRespRate0.8796+0.2450
DeepDurRespRate0.8796+0.2727
SpO2RespRate0.8796+0.1466
REMpctRMSSDmax0.8679+0.1359
TotalSleepRMSSD0.8679+0.2326
DeepDurRMSSD0.8679+0.2611
DeepDurRMSSDmax0.8679+0.2610
SpO2RMSSDmax0.8679+0.1643

Pre-ruxolitinib (67 days)

SourceTargetTE (bits)Net TE
REMdurRespRate0.5564+0.1891
TotalSleepRespRate0.5564+0.3064
DeepDurRespRate0.5564+0.2439
RMSSDmaxRespRate0.5564+0.3689
LowestHRRespRate0.5564+0.2127
AvgHRRespRate0.5564+0.1071
SpO2RespRate0.5564+0.1132
REMpctRespRate0.5252+0.0835

Change in information flow

Largest increase: REMpct -> RMSSDmax (+0.6804 bits)

Largest decrease: REMdur -> REMdur (+0.0000 bits)

4. Intervention Response Decomposition

Method: Linear mediation analysis (Baron-Kenny) decomposes total ruxolitinib effect into four mediating pathways. Bootstrap (2000 iterations) for confidence intervals.
+8.7
Total effect (readiness score)
64.8 -> 73.5
Pre -> Post average
p<0.001
Raw p-value Significant
PathwayMediator (pre->post)a (T->M) b (M->Y)Indirect effect [95% CI] % mediatedp-value
Direct cardiac
Ruxolitinib -> HR change -> Readiness
92.57 -> 85.02-0.756-0.566+0.4280
[+0.2378, +0.6537]
46.5%0.0000 Sig
Autonomic
Ruxolitinib -> HRV change -> Readiness
10.00 -> 24.55+1.296+0.673+0.8725
[+0.6543, +1.1101]
94.9%0.0000 Sig
Sleep-mediated
Ruxolitinib -> Sleep efficiency -> Readiness
78.62 -> 82.02+0.753+0.249+0.1880
[+0.0403, +0.3844]
19.7%0.0110 Sig
Inflammatory
Ruxolitinib -> Temperature deviation -> Readiness
0.06 -> 0.01-0.193-0.257+0.0497
[-0.0341, +0.1709]
5.4%0.2880 NS

5. Clinical Interpretation

Executive summary

N/A
Strongest signal: p=1.000
0/0
Metrics trending in expected direction
73
Post-intervention days (Day 14 target)
  • N/A: strongest hypothesis-generating raw p-value signal (p=1.0000, q=1.0000). It does not survive FDR correction, so confirmation still depends on more post-treatment follow-up.
  • CausalImpact: 0 of 0 biometric streams show significant causal change (p < 0.05). After Benjamini-Hochberg FDR correction: 0 of 0 remain significant (q < 0.05).
  • Placebo validation: N/A - ?/? placebo tests reached significance. This keeps the result vulnerable to false positives rather than establishing a confirmed intervention effect.
  • PCMCI+: 0 significant time-lagged causal links identified in the biometric network
  • Mediation analysis: 3 of 4 mediating pathways show significant indirect effect

Limitations

  • Short post-period (73 days): All results are preliminary. Minimum 14-21 days of post-intervention data recommended for robust causal inference.
  • Confounders: Linear methods cannot capture non-linear interactions. Seasonal variation, activity level, and other medications are not controlled for.
  • Wearable data: Oura Ring is not a medical device. Measurements have inherent noise that can affect causal estimates.
  • Single patient: N=1 study without control group. Causality cannot be definitively established, but Bayesian posterior probability of effect provides a strength measure.
  • HEV diagnosis: HEV was diagnosed 2026-03-18 (2 days after ruxolitinib start). Hepatitis may confound biometric changes.

Recommendations

  1. Repeat analysis after 2-3 weeks of ruxolitinib treatment for robust causal inference
  2. Add HEV-related biomarkers (ALT, bilirubin) as time-varying covariates
  3. Consider synthetic control method when longer time series are available
  4. Combine with clinical endpoints (GVHD scoring, ferritin) for multimodal analysis