These data suggest with a high degree of confidence (p=0) that Acetyl-L-Carnitine (Treatments) has a weakly positive predictive relationship (R=-0.574) with Inflammatory Pain (Symptoms). The highest quartile of Inflammatory Pain measurements were observed following an average 0mgAcetyl-L-Carnitine. The lowest quartile of Inflammatory Pain measurements were observed following an average 460.53mgAcetyl-L-Carnitine.
In order to reduce suffering through the advancement of human knowledge, I have chosen to share my findings regarding the relationship between Acetyl-L-Carnitine and Inflammatory Pain.
The objective of this study is to determine the nature of the relationship (if any) between the Acetyl-L-Carnitine and the Inflammatory Pain. Additionally, we attempt to determine the Acetyl-L-Carnitine values most likely to produce optimal Inflammatory Pain values.
This study design is consistent with an n=1 observational natural experiment.
Acetyl-L-Carnitine data below 0 mg was assumed erroneous and removed. 0 mg was assumed for days without Acetyl-L-Carnitine data. It was assumed that 0.5 hours would pass before a change in Acetyl-L-Carnitine would produce an observable change in Inflammatory Pain. It was assumed that Acetyl-L-Carnitine could produce an observable change in Inflammatory Pain for as much as 7 days after the stimulus event.
Acetyl-L-Carnitine 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 Acetyl-L-Carnitine 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 Acetyl-L-Carnitine (Treatments) generally predicts LOWER Inflammatory Pain (p = 0). Inflammatory Pain is, on average, 20% HIGHER after around 0 Acetyl-L-Carnitine. After an onset delay of 168 hours, Inflammatory Pain is, on average, -11% LOWER than its average over the 168 hours following around 460.53 Acetyl-L-Carnitine. 51 data points were used in this analysis. The value for Acetyl-L-Carnitine changed 8 times, effectively running 4 separate natural experiments. The top quartile outcome values are preceded by an average 0 mg of Acetyl-L-Carnitine. The bottom quartile outcome values are preceded by an average 460.53 mg of Acetyl-L-Carnitine. Forward Pearson Correlation Coefficient was -0.574 (p=0, 95% CI -0.695 to -0.453 onset delay = 0.5 hours, duration of action = 168 hours) . The Reverse Pearson Correlation Coefficient was -0.371 (P=0, 95% CI -0.492 to -0.25, onset delay = -0.5 hours, duration of action = -168 hours). When the Acetyl-L-Carnitine value is closer to 0 mg than 460.53 mg, the Inflammatory Pain value which follows is, on average, 20% percent higher than its typical value. When the Acetyl-L-Carnitine value is closer to 460.53 mg than 0 mg, the Inflammatory Pain value which follows is 0% lower than its typical value.