Higher Body Weight Predicts Moderately Lower Hypomania for Population

Higher Body Weight Predicts Moderately Lower Hypomania for Population

Contents

Variables

A
Body Weight 1140
A
Hypomania 111

Categories

A
Physique 41
A
Symptoms 13336

Tags

Medium Confidence
Moderate Effect Size
Negative Relationship
Population Study
cause image gauge image effect image
Participants reported a 18.5% average decrease in Hypomania following above average Body Weight.

Abstract

Hypomania was generally 16.1% lower than average after 140 pounds of Body Weight per 7 days.

Aggregated data from 1 study participants suggests with a MEDIUM degree of confidence (p=0.0283, 95% CI -0.746 to -0.21) that Body Weight has a moderately negative predictive relationship (R=-0.478) with Hypomania.

The highest quartile of Hypomania measurements were observed following an average 139 pounds Body Weight.

The lowest quartile of Hypomania measurements were observed following an average 140 pounds of Body Weight.

After an onset delay of 0 seconds, Hypomania is typically 8% lower than average over the 7 days following around 140 pounds of Body Weight Body Weight.

Keywords: Body Weight, Hypomania, N-of-1 trials, real-world evidence, causal inference, observational study

Preliminary: Based on 1 participants. Results may change as more data is collected.

Results

Primary Findings

Analysis of 34 paired observations from 1 participants revealed a moderate reduction in Hypomania following above-average Body Weight exposure.

-16.1%
Change from Baseline
Moderate effect on Hypomania
0.05
Predictor Impact Score
Insufficient evidence for causal relationship

Supporting Statistics

Low
Confidence
-0.478
Correlation (r)
p = 0.185
Significance
z = 1.09
Effect Magnitude
φ = 1.00
Temporality

What This Means

When participants had above-average Body Weight:

  • Hypomania decreased by 16.1% on average
  • Temporal analysis supports Body Weight as the predictor (not the outcome)

Interpreting the Predictor Impact Score

The Predictor Impact Score (PIS) integrates multiple Bradford Hill causal criteria into a single metric. Use this guide to interpret the score:

PIS Range Interpretation Recommended Action
≥ 0.5 Strong evidence High priority for RCT validation
0.3 - 0.5 Moderate evidence Consider for experimental investigation
0.1 - 0.3 Weak evidence Monitor for additional data
< 0.1 Insufficient evidence Low priority; may be noise

Note: PIS is a prioritization heuristic, not proof of causation. High scores indicate relationships worth investigating, not confirmed causal effects. With only 1 participants, these scores are preliminary and will become more reliable as additional data is collected.

Optimal Daily Values

No clear dose-response relationship detected. The Body Weight values associated with high and low Hypomania are too similar to provide meaningful dosing guidance. This may indicate a threshold effect (any amount works equally well), no effect, or insufficient data variance. With more participants, a clearer pattern may emerge.

Population Correlation

Body Weight Distribution

Hypomania Distribution

Statistical Summary

Relationship Statistics

Property Value
Cause Variable Name Body Weight
Effect Variable Name Hypomania
Sinn Predictive Coefficient 0.045487712772123
Confidence Level MEDIUM
Confidence Interval 0.26839388694908
Forward Pearson Predictive Coefficient -0.478
Critical T Value 1.684
Average Body Weight Over Previous 7 days Before ABOVE Average Hypomania 139 pounds
Average Body Weight Over Previous 7 days Before BELOW Average Hypomania 140 pounds
Duration of Action 7 days
Effect Size moderately negative
Number of Paired Measurements 34
Optimal Pearson Product 0.23004776793122
P Value 0.028281292515404
Statistical Significance 0.185
Strength of Relationship 0.26839388694908
Study Type population
Analysis Performed At 2026-01-04
Number of Participants 1

Body Weight Info

Property Value
Variable Name Body Weight
Aggregation Method MEAN
Analysis Performed At 2020-09-23
Duration of Action 7 days
Kurtosis 29.271534088526
Maximum Allowed Value 1000 pounds
Mean 168.9619340574 pounds
Median 168.27481272906 pounds
Minimum Allowed Value 0 pounds
Number of Aggregate Predictors 883
Number of Aggregate Outcomes 257
Number of Measurements 108822
Number of Measurements (including those generated by tagged, joined, or child variables) 21092
Public true
Onset Delay 0 seconds
Standard Deviation 8.7190661755282
Unit Pounds
User Variables 417
UPC 875011003902
Variable Category Physique
Variable ID 1486
Variance 594.35417755402

Hypomania Info

Property Value
Variable Name Hypomania
Aggregation Method MEAN
Analysis Performed At 2020-10-09
Duration of Action 24 hours
Kurtosis 2.0157105937037
Maximum Allowed Value 5 out of 5
Mean 1.9950666666667 out of 5
Median 2.0555555555556 out of 5
Minimum Allowed Value 1 out of 5
Number of Aggregate Predictors 90
Number of Aggregate Outcomes 21
Number of Measurements 56
Number of Measurements (including those generated by tagged, joined, or child variables) 56
Public true
Onset Delay 0 seconds
Standard Deviation 0.67580769229388
Unit 1 to 5 Rating
User Variables 20
UPC 0
Variable Category Symptoms
Variable ID 87350
Variance 0.93111672278339

Introduction

Background

Body Weight (Physique) and Hypomania (Symptoms) are both important factors in understanding human health and well-being. This study investigates the relationship between these two variables using real-world observational data.

Traditional randomized controlled trials (RCTs), while the gold standard for causal inference, are often impractical, expensive, or unethical for studying many health relationships. Aggregated N-of-1 observational studies offer a complementary approach that leverages within-subject comparisons across large populations to identify meaningful patterns.

Research Question

Does Body Weight affect Hypomania?

Additionally, we seek to determine:

  1. What is the direction and magnitude of any effect?
  2. How confident can we be in this relationship based on the available data?
  3. What are the optimal levels of Body Weight for maximizing Hypomania?

Study Objective

The objective of this study is to determine the nature of the relationship (if any) between Body Weight and Hypomania. Additionally, we attempt to determine the Body Weight values most likely to produce optimal Hypomania values.

Study Overview

This is a population-level observational study using aggregated N-of-1 methodology. By aggregating individual N-of-1 experiments, we can identify population-level patterns while accounting for the substantial individual variation that exists in most health relationships. Effect sizes are reported as percent change from baseline, enabling intuitive interpretation and comparison across different measures.

Full Methodology: Framework for Real-World Evidence-Based Pharmacovigilance: Aggregated N-of-1 Trials for Quantifying Treatment Effects

Discussion

Interpretation of Findings

Participants experienced a 16.1% reduction in Hypomania following above-average Body Weight exposure. The Predictor Impact Score (PIS) of 0.05 indicates insufficient evidence for a causal relationship.

Statistical Significance

Using a two-tailed t-test with alpha = 0.05, it was determined that the change in Hypomania is statistically significant at a 95% confidence interval. The p-value of 0.1850 indicates there is less than a 18.50% probability that this result occurred by chance.

After treatment, a 18.5% decrease (-0.367 out of 5) from the mean baseline 2.27 out of 5 was observed. The relative standard deviation at baseline was 14.7%. The observed change was 1.0949 times the standard deviation.

A common rule of thumb considers a change greater than twice the baseline standard deviation on two separate pre-post experiments may be considered significant. This occurrence would have only a 5% likelihood of resulting from random fluctuation (a p-value < 0.05).

T-Test Details
Observed t-value: 2.301
Critical t-value: 1.684

Since t = 2.30 > 1.68, we reject the null hypothesis.

Biological Plausibility

A plausible bio-chemical mechanism between predictor and outcome is critical for interpreting observational findings. This is where human judgment excels beyond statistical analysis.

Community feedback on the biological plausibility of this relationship is still being collected. Consider the known mechanisms by which Body Weight might influence Hypomania.

Bradford Hill Criteria Assessment

The Bradford Hill criteria provide a framework for assessing causality in observational studies. Our methodology operationalizes six of the nine criteria through the Predictor Impact Score (PIS):

Criterion How Addressed Metric
Strength Effect size magnitude Percent change from baseline (Δ%), z-score
Consistency Cross-participant replication Number of users (N), number of pairs (n)
Temporality Predictor precedes outcome Temporality factor (φ), onset delay (δ > 0)
Biological Gradient Dose-response relationship Gradient coefficient (φgradient)
Plausibility Biological mechanism assessment Community votes on mechanism plausibility
Specificity Category appropriateness Interest factor (finterest)

Predictor Impact Score (PIS)

The PIS integrates multiple Bradford Hill criteria into a composite metric quantifying how reliably a predictor affects an outcome. Higher scores indicate stronger evidence:

Population-Level PIS:

$$\text{PIS}_{\text{agg}} = |r_{\text{forward}}| \cdot w \cdot \phi_{\text{users}} \cdot \phi_{\text{pairs}} \cdot \phi_{\text{change}} \cdot \phi_{\text{gradient}}$$

Where φ-factors are saturation functions approaching 1 as evidence accumulates:

  • φusers = 1 - e-N/10 (user saturation)
  • φpairs = 1 - e-n/nsig (pair saturation)
  • φchange = 1 - e-Δspread/Δsig (effect spread saturation)
  • w = weighted average of plausibility votes

Temporality Assessment

We assess evidence for correct causal direction using the temporality factor:

$$\phi_{\text{temporal}} = \frac{|r_{\text{forward}}|}{|r_{\text{forward}}| + |r_{\text{reverse}}|}$$

Values approaching 1 indicate the predictor precedes the outcome (supporting causation); values near 0.5 suggest ambiguous directionality; values near 0 suggest reverse causation or confounding by indication.

Limitations

As with any observational study, correlation does not prove causation. Key limitations include:

  • Unmeasured confounders: Variables not tracked may influence results
  • Self-selection bias: Health trackers may differ from the general population
  • Measurement error: Self-reported data may contain recall bias
  • Confounding by indication: Sicker individuals may use more treatments

However, within-subject comparison and temporal precedence analysis partially mitigate these limitations. If the relationship is merely coincidental, as participants independently modify their Body Weight values, the observed strength will decline over time. Spurious correlations naturally dissipate as more data is collected.

Future Directions

Future research should examine:

  • Subgroup analyses to identify individual differences in response
  • Potential confounders and mediators of the observed relationship
  • Optimal dosing and timing for Body Weight
  • Confirmation through prospective or randomized designs
  • Biological mechanisms underlying the observed effects

Conclusion

📊 Preliminary Findings: With 1 participants, these results are based on limited data. Effect sizes and confidence will improve as more participants contribute data. Consider these findings directional rather than definitive.

Above-average Body Weight was associated with a 16.1% reduction in Hypomania—a moderate effect. The Predictor Impact Score of 0.05 indicates this relationship is requiring additional data before conclusions.

Bottom Line: Based on a PIS of 0.05 and a 16.1% effect size, this relationship currently lacks sufficient evidence. Continue monitoring as more data becomes available. Note: These conclusions may strengthen or change direction as more data is collected.

These findings contribute to our understanding of how Body Weight may influence Hypomania in real-world conditions. While preliminary, these results may inform future research directions. As more participants contribute data, the reliability and precision of these findings will improve substantially.

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Methods

Study Design

This study is based on data donated by 1 participants. Thus, the study design is equivalent to the aggregation of 1 separate n=1 observational natural experiments.

This within-subject design is powerful because it controls for all stable individual characteristics (genetics, baseline health status, socioeconomic factors) that might otherwise confound the relationship between variables.

Data Analysis

Temporal Assumptions

The analysis incorporates temporal assumptions about the relationship between variables:

  • Onset Delay: It was assumed that 0 seconds would pass before a change in Body Weight would produce an observable change in Hypomania.
  • Duration of Action: It was assumed that Body Weight could produce an observable change in Hypomania for as much as 7 days after the stimulus event.

Statistical Methods

For each participant, we calculated the Pearson correlation coefficient between Body Weight values and subsequent Hypomania values. Individual correlations were then aggregated using Fisher's z-transformation to produce a population-level estimate:

Individual Correlation:

$$r_i = \frac{\sum(x_{ij} - \bar{x}_i)(y_{ij} - \bar{y}_i)}{\sqrt{\sum(x_{ij} - \bar{x}_i)^2 \sum(y_{ij} - \bar{y}_i)^2}}$$

Fisher's Z-Transformation:

$$z_i = \frac{1}{2} \ln\left(\frac{1 + r_i}{1 - r_i}\right)$$

Aggregated Correlation:

$$\bar{r} = \tanh(\bar{z}) \quad \text{where} \quad \bar{z} = \frac{1}{N}\sum_{i=1}^{N} z_i$$

Effect Size Calculation

Effect sizes are reported as percent change from baseline. For each participant, we compare the outcome following above-average predictor values to the overall baseline outcome:

$$\Delta\%_{\text{baseline}} = \frac{\bar{O}_{\text{follow-up}} - \bar{O}_{\text{baseline}}}{\bar{O}_{\text{baseline}}} \times 100$$

Effect Magnitude (Z-Score)

To assess effect magnitude relative to natural variability, we calculate the z-score:

$$z = \frac{|\Delta\%_{\text{baseline}}|}{\text{RSD}_{\text{baseline}}}$$

where RSDbaseline is the relative standard deviation of outcome during baseline period

A z-score > 2 indicates statistical significance (p < 0.05), meaning the observed change exceeds typical baseline fluctuation and is unlikely due to random variation.

Statistical Significance

Correlation significance is assessed using a two-tailed t-test:

$$t = \frac{r\sqrt{n-2}}{\sqrt{1-r^2}}$$

We reject the null hypothesis (ρ = 0) at α = 0.05 when |t| exceeds the critical value, providing statistical evidence that the observed relationship is not due to chance.

Data Sources

Body Weight data was primarily collected using Fitbit. Fitbit makes activity tracking easy and automatic.

Hypomania data was primarily collected using QuantiModo. QuantiModo allows you to easily track mood, symptoms, or any outcome you want to optimize in a fraction of a second. You can also import your data from over 30 other apps and devices. QuantiModo then analyzes your data to identify which hidden factors are most likely to be influencing your mood or symptoms.

Data Quality

Data quality measures were applied to ensure reliable results:

  • Minimum Data Requirement: Only participants with sufficient paired observations were included in the analysis.
  • Outlier Handling: Extreme values were winsorized to reduce the influence of measurement errors.
  • Missing Data: Days with missing values were handled using appropriate filling strategies based on the variable type.
  • Test User Exclusion: Test accounts and invalid users were excluded from all analyses.

Principal Investigator

Program & Methods

Mike P. Sinn
Sinn, M. P.

Designed and implemented data collection, aggregation, causal inference pipeline, and automated study generation framework. Developed the Predictor Impact Score methodology operationalizing Bradford Hill criteria for ranking causal relationships in observational data. When he tells people this at parties, they usually say they have to go check on their car.

Individual study outputs are automated, reproducible, and open to external audit. (Which I would seriously recommend.)

Contact

Cite This Study

APA Format
Sinn, M. P. (2026). Causal Analysis: Does Body Weight Affect Hypomania?. The Journal of Citizen Science. https://studies.crowdsourcingcures.org/study/cause-1486-effect-87350-population-study
BibTeX 
@misc{sinn_cause_1486_effect_87350_population_study_2026,
  author = {Sinn, Mike P.},
  title = {Causal Analysis: Does Body Weight Affect Hypomania?},
  year = {2026},
  publisher = {The Journal of Citizen Science},
  url = {https://studies.crowdsourcingcures.org/study/cause-1486-effect-87350-population-study},
  note = {Accessed: January 11, 2026}
}
Chicago/Turabian
Sinn, Mike P. "Causal Analysis: Does Body Weight Affect Hypomania?." The Journal of Citizen Science. Accessed January 11, 2026. https://studies.crowdsourcingcures.org/study/cause-1486-effect-87350-population-study.
Harvard
Sinn, M.P., 2026. Causal Analysis: Does Body Weight Affect Hypomania?. [Aggregated N-of-1 Study] The Journal of Citizen Science. Available at: https://studies.crowdsourcingcures.org/study/cause-1486-effect-87350-population-study [Accessed January 11, 2026].

Study Type: Aggregated N-of-1 Observational Mega-Study
Evidence Level: Level II (Real-World Evidence)
Methodology: Bradford Hill Criteria with Predictor Impact Score (PIS)

References

This framework was originally developed in 2013 based on the Bradford Hill criteria. Subsequent literature has independently validated similar approaches to causal inference from observational data:

  1. Hill, A.B. (1965). The environment and disease: association or causation? Proceedings of the Royal Society of Medicine, 58(5), 295-300. [Bradford Hill criteria]
  2. Lillie, E.O., et al. (2011). The n-of-1 clinical trial: the ultimate strategy for individualizing medicine? Personalized Medicine, 8(2), 161-173. [N-of-1 methodology]
  3. Pearl, J. (2009). Causality: Models, Reasoning, and Inference . Cambridge University Press. [Causal inference]
  4. Hernán, M.A., & Robins, J.M. (2020). Causal Inference: What If . Chapman & Hall/CRC. [Free textbook]
  5. FDA (2018). Framework for FDA's Real-World Evidence Program . U.S. Food and Drug Administration. [Regulatory context]
  6. Duan, N., et al. (2013). Single-patient (n-of-1) trials: a pragmatic clinical decision methodology . Journal of Clinical Epidemiology, 66(8), S21-S28.
  7. Platt, R., et al. (2018). The FDA Sentinel Initiative—an evolving national resource . New England Journal of Medicine, 379(22), 2091-2093.

This information is for research and educational purposes only, not medical advice. Consult a healthcare provider before making health decisions. Terms of Service

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