Sexual reproduction implies high costs, but it is difficult to give evidence for evolutionary advantages that would explain the predominance of meiotic sex in eukaryotes. A combinational theory discussing evolution, maintenance and loss of sex may resolve the problem. The main function of sex is the restoration of DNA and consequently a higher quality of offspring. Recombination at meiosis evolved, perhaps, as a repair mechanism of DNA strand damages. This mechanism is most efficient for DNA restoration in multicellular eukaryotes, because the initial cell starts with a re-optimized genome, which is passed to all the daughter cells. Meiosis acts also as creator of variation in haploid stages, in which selection can purge most efficiently deleterious mutations. A prolonged diploid phase buffers the effects of deleterious recessive alleles as well as epigenetic defects and is thus optimal for prolonged growth periods. For complex multicellular organisms, the main advantage of sexuality is thus the alternation of diploid and haploid stages, combining advantages of both. A loss of sex is constrained by several, partly group-specific, developmental features. Hybridization may trigger shifts from sexual to asexual reproduction, but crossing barriers of the parental sexual species limit this process. For the concerted break-up of meiosis-outcrossing cycles plus silencing of secondary features, various group-specific changes in the regulatory system may be required. An establishment of asexuals requires special functional modifications and environmental opportunities. Costs for maintenance of meiotic sex are consequently lower than a shift to asexual reproduction A complex multicellular organism develops from mitotic divisions of a single initial cell, which passes its genome to all daughter cells. If the initial cell has a thoroughly 'repaired' nuclear genome, all daughter cells will benefit from that because they are a monophyletic group, which has arisen from a single initial cell. In contrast, any later DNA restoration on differentiated cells is less efficient because it has to be done multiple times in specialized tissues. Cell differentiation is connected to an increase of genome size and number of genes (Rokas, 2008), which infers that targeted repair mechanisms become more complex. Mutations and, perhaps, even epigenetic damage accumulate during the life span of the organism in the nuclear DNA. Cellular selection within the organism can erase inviable cells, but cannot act efficiently on mildly disadvantageous mutations or epimutations as long as the whole organism is alive; cellular selection may act in differentiated tissues not efficiently because only a part of the genome is actually expressed. Any restoration of the nuclear genome is most efficient in the initial cell.