MD · MBA
Physician specializing in genetic analysis and personalized preventive medicine, and author of Outsmart Your Genes.
Brandon Colby is a physician-expert in the fields of genetic analysis and Personalized Preventive Medicine. He holds an MD from the Mount Sinai School of Medicine, an MBA from Stanford University's Graduate School of Business, and a degree in Genetics from the University of Michigan.
Dr. Colby is the author of the book Outsmart Your Genes and has developed numerous technologies that improve the analysis, interpretation, and actionability of genome sequencing data. He is an Affiliate Specialist of the American College of Medical Genetics and Genomics (ACMG), an Associate of the American College of Preventive Medicine (ACPM), and a member of the National Society of Genetic Counselors (NSGC).
Articles by Brandon Colby, MD are reviewed for accuracy by Sequencing's medical and scientific team. This page is for informational purposes and does not constitute medical advice.
Dystonic movements combine with brief muscle twitches, and sometimes epilepsy or cognitive symptoms, from childhood; MRI and DNA analysis narrow the diagnosis.
Changes in a gene that guides nervous system development can bring intellectual disability, speech and motor delays, autism spectrum disorder and seizures.
How the body absorbs, metabolizes and clears this HIV medication varies with CYP2B6 activity; the page covers pharmacokinetics and the limits of testing results.
Discover the EMM-null phenotype, a rare genetic disorder, and learn about its diagnosis, complications, and the crucial role of genetic testing in managing the condition.
Seizures, intellectual disability and dysmorphic features trace back to CDKL5 changes on the X chromosome; sequence and deletion tests can confirm them.
Episodes of lost coordination with continuous muscle twitching define this disorder; EMG, MRI and KCNA1 or CACNA1A testing separate EA1 from EA2.
Tumor tissue can be checked for EGFR mutations that predict benefit, KRAS mutations that signal resistance and ALK rearrangements before erlotinib is chosen.
Patients with rheumatoid arthritis, psoriasis or ankylosing spondylitis respond differently to etanercept; TNF and HLA gene variants may explain part of that.