Continued from the last post here…

Women who smoke have been observed to reach menopause earlier (1 – 4 yrs earlier) than non-smokers, shortening their reproductive life span. Basal FSH (Follicle stimulating hormone) levels are said to be 60 – 70 per cent higher in active smokers than in non-smokers.

Recent data have suggested that oxidative stress plays a crucial role in the pathophysiological process involved in fertility reduction related to the quality of both gametes. Evidence showed that polycyclic aromatic hydrocarbons food in tobacco can trigger premature cell death which causes early menopause.

No research has been able to demonstrate ‘safe’ levels of smoking correlated with preserved fertility. This implies that even light smoking is associated with reduced fecundity. Many of the effects of tobacco on infertility may be ultimately related to oxidative effects. It is known that reactive oxygen species are capable of damaging every molecule present inside the cell: carbohydrate, proteins, lipids and DNA.

Tobacco exposure was also shown to alter the structural component of the eggs in women, leading to inborn errors in the babies. In females, smoking potentially affects the ovaries adversely. The degree of damage is dependent upon the quantity and length of time a woman smokes.

Cotinine (an alkaloid) is a metabolite of nicotine, a tobacco end product which results in oxidative stress to the gametes. Studies by Zenzes et al. showed that cotinine is detectable in follicular fluids. Its presence in the blood is proportionate to the amount of exposure to smoke in both active and passive smokers.

Nicotine and other hazardous substances in cigarette interfere with the body’s ability to create oestrogen, a hormone that regulates follicular growth and ovulation. Nicotine by-products have been traced in the semen of such men and have been found to reduce sperm motility and their fertilisation potential.

Smoking interferes with the complex processes from egg formation to the growth of the embryo in the uterus. Smoking decreases the chances of IVF producing a live birth by 34 per cent and increases the risk of an IVF pregnancy miscarrying by 30 per cent. Some damage is irreversible, but stopping smoking can prevent further damage.

In males, oxidative stress occurs in the seminal fluid of smokers. Increased concentrations of cadmium, lead and ROS are significantly higher; and at the same time, concentrations of ascorbic acid and the activity of other components of the antioxidant defence are significantly reduced, affecting the scavenging capacity of the antioxidant defence system of the body.

Incidence of impotence is approximately 85 per cent higher in male smokers compared to non-smokers and is a major cause of erectile dysfunction.

Fathers who smoke heavily (greater than 20 sticks per day) at the time of conception increase the child’s risk of childhood Leukaemia (cancer of the blood system) and shorten the reproductive life span of their daughters.

Evidence also suggests that female infertility can be damaged in-utero if the woman’s mother was exposed to second-hand smoke while pregnant. It has also been found that women exposed to cigarette smoke while undergoing IVF or other assisted reproduction technologies treatment can have adverse pregnancy outcomes.     .

Many men and women of reproductive age continue to smoke with only a small proportion of them considering quitting. Women, particularly when pregnant, attempt to quit than at any other times. Support should come from the baby’s father, family members and friends as well as the health care system – e.g. pregnancy smoking helpline, smoking cessation groups, etc.

Couples of reproductive age should be strongly advised to quit smoking. Although the causal effect of smoking and decline in fecundity have not been as unanimous as expected in view of available literature and studies, critics are of the opinion that the strength of the association is varied and a larger sample size is required. However, this does not mean that the association is not clinically relevant. Studies on sperm production, for instance, make this particularly relevant.

Stop smoking interventions in primary, secondary and tertiary centres should be advocated for and implemented with appropriate published guidelines.

Health care practitioners are also encouraged to work in unison to reduce smoking during pregnancy and postpartum (after delivery).

Government legislations against public smoking and smoking at workplaces should be enacted to reduce the effects of passive smoking. Indoor smoking and smoking in vehicles should also be strictly discouraged. Designated smoking areas, especially in public places, should be created. Government should also mandate tobacco companies to inform the public duly of the harmful effects of smoking on fertility and general well being.

In conclusion, cigarette smoking has been shown to reduce female fertility naturally, as well as in assisted reproductive cycles. Embryos generated from the sperms of smokers have reduced implantation potentials. Clinical evidences are in support of the negative effects of nicotine on conception.

It is advised that anyone planning for conception should stop smoking. If, however, they have been smoking and plan to have a baby, a good detoxification therapy where all the toxins can be eliminated using various strategies would be advisable.

Concluded.