These data suggest with a high degree of confidence (p=0) that Omega 3 Fatty Acids (Treatments) has a weakly positive predictive relationship (R=-0.504) with Inflammatory Pain (Symptoms). The highest quartile of Inflammatory Pain measurements was observed following an average 7 mg Omega 3 Fatty Acids. The lowest quartile Inflammatory Pain measurements were observed following an average 360 mg Omega 3 Fatty Acids.
In order to reduce suffering through the advancement of human knowledge, I chose to share my findings regarding the relationship of Omega 3 Fatty Acids on Inflammatory Pain.
The objective of this study is to determine the nature of the relationship (if any) between the Omega 3 Fatty Acids and the Inflammatory Pain. Additionally, we attempt to determine the Omega 3 Fatty Acids values most likely to produce optimal Inflammatory Pain values.
This study design is consistent with a n=1 observational natural experiment.
Omega 3 Fatty Acids data below 0 mg was assumed erroneous and removed. 0 mg was assumed for days without Omega 3 Fatty Acids data. It was assumed that 0.5 hours would pass before a change in Omega 3 Fatty Acids would produce an observable change in Inflammatory Pain. It was assumed that Omega 3 Fatty Acids could produce an observable change in Inflammatory Pain for as much as 7 days after the stimulus event.
The QuantiModo platform was used to aggregate data from the data sources.
Omega 3 Fatty Acids data was collect using: Med Helper.
Inflammatory Pain data was collected using: Cardiograph.
Using a two-tailed t-test with alpha = 0.05, it was determined that the change in Inflammatory Pain is statistically significant at 95% confidence interval.
As with any human experiment, it was impossible to control for all potentially confounding variables. The confidence in a causal relationship is bolstered by the fact that time-precedence was taken into account in all calculations. Furthermore, in accordance with the law of large numbers (LLN), the predictive power and accuracy of these results will continually grow over time. 51 paired data points were used in this analysis. Assuming that the relationship is merely coincidental, as the participant independently modifies their Omega 3 Fatty Acids values, the observed strength of the relationship will decline until it is below the threshold of significance. Furthermore, it will be very enlightening to aggregate this data with the data from other participants with similar genetic, diseasomic, environmentomic, and demographic profiles.
This analysis suggests that HIGHER Omega 3 Fatty Acids (Treatments) generally predicts LOWER Inflammatory Pain (p = 0). Inflammatory Pain is, on average, 5% HIGHER after around 7.95 Omega 3 Fatty Acids. After an onset delay of 168 hours, Inflammatory Pain is, on average, -27% LOWER than its average over the 168 hours following around 359.74 Omega 3 Fatty Acids. 51 data points were used in this analysis. The value for Omega 3 Fatty Acids changed 29 times, effectively running 15 separate natural experiments. The top quartile outcome values are preceded by an average 7.95 mg of Omega 3 Fatty Acids. The bottom quartile outcome values are preceded by an average 359.74 mg of Omega 3 Fatty Acids. Forward Pearson Correlation Coefficient was -0.504 (p=0, 95% CI -0.592 to -0.417 onset delay = 0.5 hours, duration of action = 168 hours) . The Reverse Pearson Correlation Coefficient was -0.389 (P=0, 95% CI -0.477 to -0.301, onset delay = -0.5 hours, duration of action = -168 hours). When the Omega 3 Fatty Acids value is closer to 7.95 mg than 359.74 mg, the Inflammatory Pain value which follows is, on average, 5% percent higher than its typical value. When the Omega 3 Fatty Acids value is closer to 359.74 mg than 7.95 mg, the Inflammatory Pain value which follows is 0% lower than its typical value.