was provided by a clinic affected society. Scientific interests Pearl's main focus of interest was in biostatistics. As one of the first biostatisticians to use mathematics as a way to interpret population genetics, Pearl published a book called Modes of Research in Genetics in 1915 and another book called Introduction to Medical Biometry and Statistics in 1923. They were both widely read and were influential in showing the importance of statistics in the genetic and medical fields. Even though many of his books were well-received, some of his beliefs still caused controversy. One such belief was that when a brother and sister reproduce, there would not be an increase in homozygosity. Pearl believed that with brother-sister breeding and no selection past the F3 generation, heterozygosity would not fall below 50%. Even though his main interest was biostatistics, Pearl had a wide range of interests in biology and was known for his broad knowledge of the subject. He published works on animal behavior, population growth, food and prices, Jewish and Christian marriages, and vegetarianism. In the 1920s and 1930s, Pearl focused on the effect that the environment, which included disease, alcohol, and tobacco, has on longevity. He published a book called Alcohol and Longevity in 1926, where he claimed that moderate consumption of alcohol could be beneficial for cardiovascular health, which was met with much debate due to prohibition. Controversy continued when Pearl conducted a study on tobacco in which he demonstrated that smoking decreases longevity while drinking does not. Pearl is regarded as one of founders of biogerontology. In 1908 Max Rubner observed that mammals of different size and longevity had equal mass specific metabolic output. Partly based on the observation that the longevity of fruit flies varies inversely with ambient temperature, Pearl (like Rubner) also asserted that maximum life span is inversely proportional to basal metabolic rate. Pearl accepted Alexis Carrel's erroneous ideas that normal somatic cells don't age, and that aging must therefore be due to dysfunction at the body level. Pearl speculated that lifespan was limited by vital cell components that were depleted or damaged more rapidly in animals with faster metabolisms. Denham Harman's free-radical theory of aging later provided a plausible causal mechanism for Pearl's hypothesis. The Rate of Living Hypothesis enjoyed prominence as one of the foremost theories of aging for nearly 50 years. The Rate of Living Hypothesis is undermined by the observation that