The Vices Of Men

By Vincent van Gogh - Scanned from Smoke: a global history of smoking (2004) ISBN 1-86189-200-4, Public Domain, https://commons.wikimedia.org/w/index.php?curid=3857076

The paper linked here is a fascinating review that looks at three major vices of men – drinking alcohol, being overweight/obese, and smoking tobacco – and how these activities can damage male fertility and also negatively affect the health of their offspring. Mechanisms by which these vices can affect fertility and the health of children include epigenetic changes to sperm DNA and non-coding RNA (changes to the modification to DNA and RNA, not including actual sequence mutation, that can affect gene expression), sperm DNA damage (which can cause actual sequence mutation affecting gene expression), changes in sperm chromatin structure (for example, changes in the chromosome structure that can affect which genes are expressed and which are silenced), and changes in seminal plasma (that can affect the function of the sperm cells themselves).  Abstract:

There is growing evidence from animal and human studies that demonstrate that acquired paternal traits can impair both a male's fertility and the health of his offspring, including advanced age, smoking, stress, trauma, under-nutrition, infection, toxin exposure, and obesity. Curiously, many of these factors manifest as impaired neurological, behavioural, and/or metabolic functioning in offspring. The underlying molecular mechanisms that respond to the paternal environment and act as vectors of intergenerational transmission are beginning to emerge. This review focuses on three vices of men (alcohol consumption, overweight/obesity, and tobacco smoking) that damage fertility and pose risks to offspring health. These vices are not only the three most prevalent but are also leading risk factors for death and disability adjusted life years (DALYs) worldwide. Clearly, any epigenetic/genetic alterations induced by the paternal exposures responsible for transmission need to escape/bypass the substantial post-fertilisation reprogramming that occurs during embryo development. For example paternal obesity alters the molecular composition of sperm, alters the developmental trajectory of resultant embryos, and increase the incidence of obesity and metabolic disorders in offspring. Mechanistic candidates of paternal programming include changes to the sperm epigenome (eg DNA methylation, histone/protamine modifications, and sperm borne small non-coding RNAs), increased sperm DNA damage, aberrant sperm DNA chromatin structure, and components of seminal plasma. Understanding the molecular mechanisms underpinning paternal programming may lead to the development of interventions designed to reduce the disease burden in future generations, who were born to fathers exposed to these initiating factors. Given that these vices are predominantly self-inflicted, interventions aimed at mitigating their consequences are readily identified.

Add this information to all the other reasons to avoid these vices.