The aim of the present piece is to present an evolutionary hypothesis relating to the role of deconditioning in the prevalence of low back pain (LBP) in humans. LBP is a multifactorial issue with many associated symptoms and potential causes. Prevalence is high in westernised populations and also rural and indigenous populations. Other diseases common in western populations, such as obesity, diabetes, heart disease, and cancer are almost absent in populations devoid of western influence who follow a traditional diet and lifestyle. It therefore seems counter-intuitive that LBP should also be high in traditional populations. The hypothesis that an evolutionarily determined factor might predispose LBP across a wide range of Homo sapiens populations seems plausible to examine. Fossil data from the infra-order Anthropoidea suggest adaptations in predominant habitual locomotion styles from 1) arboreal quadruped, to 2) semi-terrestrial quadruped, to 3) biped over the past ~20 million years. These adaptations were accompanied and permitted by anatomical evolutionary changes occurring in the lumbar spine and pelvis including development from 1) a long mobile lumbar vertebral column, laterally facing pelvis and large lumbar extensors to 2) a short lumbar vertebral column, posterior location of the transverse process, lengthening of the ilia, general reduction of the lumbar extensor musculature and increase in passive rigidity through entrapment and invagination and 3) to re-lengthening of the vertebral column, reduction in length and broadening of the ilia and sacrum. Comparative musculature anatomy between old world monkeys and modern humans suggests the presence of relatively smaller, and potentially weaker, lumbar extensor musculature in humans. Further, hip/trunk extensor musculature of short backed primates is well developed. Anatomically modern humans therefore may bear the compromise of relatively strong hip/trunk extensors and relatively weak lumbar extensors in combination with a long flexible lumbar spine. This may contribute to disuse atrophy of the lumbar extensors which may explain the consistent association of their deconditioning in LBP, and also predispose modern humans to the high prevalence of LBP presently observed.