Predicting lying, sitting, walking and running using Apple Watch and Fitbit data.

OBJECTIVES: This study's objective was to examine whether commercial wearable devices could accurately predict lying, sitting and varying intensities of walking and running. METHODS: We recruited a convenience sample of 49 participants (23 men and 26 women) to wear three devices, an Apple Watch Series 2, a Fitbit Charge HR2 and iPhone 6S. Participants completed a 65 min protocol consisting of 40 min of total treadmill time and 25 min of sitting or lying time. The study's outcome variables were six movement types: lying, sitting, walking self-paced and walking/running at 3 metabolic equivalents of task (METs), 5 METs and 7 METs. All analyses were conducted at the minute level with heart rate, steps, distance and calories from Apple Watch and Fitbit. These included three different machine learning models: support vector machines, Random Forest and Rotation forest. RESULTS: Our dataset included 3656 and 2608 min of Apple Watch and Fitbit data, respectively. Rotation Forest models had the highest classification accuracies for Apple Watch at 82.6%, and Random Forest models had the highest accuracy for Fitbit at 90.8%. Classification accuracies for Apple Watch data ranged from 72.6% for sitting to 89.0% for 7 METs. For Fitbit, accuracies varied between 86.2% for sitting to 92.6% for 7 METs. CONCLUSION: This preliminary study demonstrated that data from commercial wearable devices could predict movement types with reasonable accuracy. More research is needed, but these methods are a proof of concept for movement type classification at the population level using commercial wearable device data.

Ensemble learning for detecting gene-gene interactions in colorectal cancer.

Colorectal cancer (CRC) has a high incident rate in both men and women and is affecting millions of people every year. Genome-wide association studies (GWAS) on CRC have successfully revealed common single-nucleotide polymorphisms (SNPs) associated with CRC risk. However, they can only explain a very limited fraction of the disease heritability. One reason may be the common uni-variable analyses in GWAS where genetic variants are examined one at a time. Given the complexity of cancers, the non-additive interaction effects among multiple genetic variants have a potential of explaining the missing heritability. In this study, we employed two powerful ensemble learning algorithms, random forests and gradient boosting machine (GBM), to search for SNPs that contribute to the disease risk through non-additive gene-gene interactions. We were able to find 44 possible susceptibility SNPs that were ranked most significant by both algorithms. Out of those 44 SNPs, 29 are in coding regions. The 29 genes include ARRDC5, DCC, ALK, and ITGA1, which have been found previously associated with CRC, and E2F3 and NID2, which are potentially related to CRC since they have known associations with other types of cancer. We performed pairwise and three-way interaction analysis on the 44 SNPs using information theoretical techniques and found 17 pairwise (p < 0.02) and 16 three-way (p ≤ 0.001) interactions among them. Moreover, functional enrichment analysis suggested 16 functional terms or biological pathways that may help us better understand the etiology of the disease.