Smoking cigarettes reduces sperm production and increases oxidative stress, DNA damage and lipid peroxidation levels (Linschooten et al., 2011; Fariello et al., 2012). Spermatozoa from smokers have reduced fertilizing capacity, and embryos display lower implantation rates (Soares and Melo, 2008). Even in utero exposure to tobacco constituents leads to reduced sperm count in adult life (Jensen et al., 2004). Recent male smoking is associated with significantly decreased live birth rates even after adjusting for confounders (Fuentes et al., 2010). In vitro studies using cigarette smoke extract revealed suppression of sperm motility in a concentration- and time-dependent manner as well as an increased number of spermatozoa with low mitochondrial membrane potential (Calogero et al., 2009). In addition, cigarette smoke extract has detrimental effects on sperm chromatin condensation and apoptosis, inducing concentration- and time-dependent increases in the number of spermatozoa with phosphatidylserine externalization (an early apoptotic sign) and fragmented DNA (a late apoptotic sign) (Calogero et al., 2009). Given the adverse effects of cigarette smoking by the male partner on assisted reproductive techniques and the transmission of smoking-induced sperm DNA alterations to preimplantation embryos, which may predispose offspring to a greater risk of malformations, cancer and genetic diseases, men seeking to become fathers should give up smoking.
Nicotine also has established adverse effects on fertility. It can cause sexual dysfunction due to arteriosclerotic changes in the vessels of the penis, and the consequent development of erectile failure. Nicotine can also worsen infertility due to other causes (the so-called ‘co-factor effect’) where smoking may exacerbate the action of a varicocele (Peng et al., 1990).
What should it take to describe a substance or product as ‘sperm-safe’http://humupd.oxfordjournals.org/conten ... _1/i1.full
In a world of deceit open your eyes.