Women who smoke have been observed to reach menopause earlier than non-smokers, thereby shortening their reproductive life span. Basal FSH (follicle stimulating hormone) levels are said to be between 60 per cent and 70 per cent higher in active smokers than in non smokers.
Recent data have suggested that oxidative stress plays a crucial role in the patho-physiological process involved in fertility reduction, in relation to the quality of both gametes. There is evidence that polycyclic aromatic hydrocarbons in tobacco could trigger premature cell death, which causes early menopause.
However, no research has been able to demonstrate ‘safe’ levels of smoking correlated with preserved fertility. It implies that even light smoking leads to reduced fecundity.
Many of the effects of tobacco on infertility may be ultimately related to the oxidative impacts. The reactive oxygen species are capable of damaging every molecule present inside the cell: carbohydrate, proteins, lipids, and DNA.
Exposure to tobacco can also 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 depends on the quantity of cigarettes that a woman smokes and the length of time that she spends smoking. 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 proportional to the amount of exposure to smoke in both active and passive smokers.
Nicotine and other hazardous substances in cigarettes interfere with the body’s ability to create estrogen, a hormone that regulates follicular growth and ovulation. Nicotine by-products have been traced in the semen of such men and they have been found to reduce sperm motility and their fertilization potential.
Smoking interferes with the complex processes, from egg formation to the growth of the embryo in the uterus. It 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 quitting 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. At the same time, levels of ascorbic acid and the activity of other components of the antioxidant defense are reduced considerably, thus affecting the scavenging capacity of the antioxidant defense system of the body.
The incidence of impotence is approximately 85 per cent higher in male smokers, compared to non-smokers and it is a primary cause of erectile dysfunction.
Fathers who smoke heavily (greater than 20 sticks per day) at the time of conception increases the child’s risk of childhood Leukaemia (cancer of the blood system) and shortens the reproductive lifespan of their daughters.
Evidence has also suggested that female infertility can be damaged in utero if the woman’s mother was exposed to second-hand smoke during pregnancy. 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, in particular, attempt to quit smoking when they are pregnant than at any other time. Support should come from the baby’s father, family members and friends, as well as the healthcare system, 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 given available literature and studies, critics are of the opinion that the strength of the association is varied. However, this does not mean that the association is not clinically relevant. Studies on sperm production, for instance, make this particularly pertinent.
Stop smoking interventions in primary, secondary and tertiary centers should be introduced 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 legislation against public smoking and smoking at workplaces should be enacted to reduce the effects of passive smoking. Indoor tobacco and smoking in vehicles should also be strictly discouraged. Designated smoking areas, especially in public places, should be created. The government should also mandate tobacco companies to inform the public of the harmful effects of smoking on fertility and general well being.
In conclusion, cigarette smoking has been shown to reduce female fertility natural, as well as in assisted reproductive cycles. Embryos generated from the sperm of smokers have reduced implantation potentials. Clinical evidence is in support of the deleterious effects of nicotine on conception.
Anyone planning for conception should stop smoking. If, however, there has been prior smoking and planned to have a baby, a good detoxification therapy (www.martlifedetoxclinic.com), where all the toxins can be eliminated using various strategies, will be advisable.
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