Abstract
The main types of models related to the origin of biological asymmetry are reviewed and new models are proposed. It is shown that in polymerization (in contrast to Yamagata's hypothesis) only a temporary amplification of asymmetry occurs. Models have been constructed in which always the same enantiomer survives, independently of any fluctuations or asymmetric initial conditions. Therefore, the question of the "by chance" or the causal origin of biological asymmetry remains still open, although with a slight preference for a causal origin.
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