While some medications are safe to use before and during pregnancy, others can affect your chances of getting pregnant, cause problems during pregnancy, or harm your baby. All drugs and medications pass into the bloodstream. Some directly affect sperm or eggs and reduce fertility. For both men and women, taking cocaine, heroin, ecstasy and marijuana can reduce the chance of having a baby. Taken over a long period of time, recreational drugs can cause permanent problems with the reproductive system and infertility.
We excluded these findings because they are not directly related to sperm ecfect or maturation. The entire family can benefit when a family member stops smoking. Impact of cancer and cancer treatment on male fertility. These men will typically take longer to conceive and are more likely to require the assistance of artificial reproduction techniques to do so. These changes were not seen in men taking carbamazepine.
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Scientists at the seminar listed problems including pregnancy loss, low birth weight, increased birth defects and childhood cancers in children fathered by men who were exposed to toxins, from pesticides and prescription drugs to wartime Trans am and catalytic converter. Useful links: Asthma Council guidelines. Life is full of hard truths. Men who use these drugs to treat prostate enlargement will have a decrease in the volume druga the semen and the total number of sperm in the semen, which may make it harder to cause a pregnancy. The impact of these medications is mild and will reverse once the medication is stopped. THC also has a direct Do prescription drugs effect sperm effect on the movement of sperm. Some directly affect sperm or eggs and reduce fertility. Yazigi said. Epigenetic changes are not usually passed to children unless they happen in germ cells such as sperm. The extent of the impact depends on the opiates being used, the dose, and how long the man is using the opiates. Photo via Flickr User Imagens Evangelicas. Some supplements, vitamins, minerals, and herbal medicines are safe to take while trying to get pregnant and during pregnancy, and others Do prescription drugs effect sperm not. Alcohol : Light to moderate alcohol drinking does not appear to affect male fertility. Many studies have been done to look for DNA changes in both non-sperm and sperm cells but have been inconclusive. For that reason, we recommend men stop these medications if dtugs are having trouble creating a pregnancy.
There are potentially many different causes of male infertility, including hormonal, anatomical, and secondary to exposure to exogenous substances.
- Men who wish to father a child should talk to their doctor before starting a new medication or having any treatments.
- Photo via Flickr User Imagens Evangelicas.
- Men should not smoke, drink or take unnecessary drugs if they are planning to become fathers to avoid causing health problems for their children, a health expert has warned.
We herein provide an overview of the single-ingredient U. Food and Drug Administration FDA -approved drugs that affect human spermatogenesis, potentially resulting in a negative impact on male fertility.
To provide this information, we performed an in-depth search of DailyMed, the official website for FDA-approved drug labels.
Not surprisingly, hormone-based agents were found to be the drugs most likely to affect human spermatogenesis. The next category of drugs most likely to have effects on spermatogenesis was the antineoplastic agents. Interestingly, the DailyMed labels indicated that several anti-inflammatory drugs affect spermatogenesis, which is not supported by the peer-reviewed literature.
Overall, there were a total of 65 labels for drugs of various classes that showed that they have the potential to affect human sperm production and maturation. We identified several drugs indicated to be spermatotoxic in the drug labels that were not reported in the peer-reviewed literature.
However, the details about the effects of these drugs on human spermatogenesis are largely lacking, the mechanisms are often unknown, and the clinical impact of many of the findings is currently unclear. Therefore, additional work is needed at both the basic research level and during clinical trials and post-marketing surveillance to fill the gaps in the current knowledge.
The present findings will be of interest to physicians and pharmacists, researchers, and those involved in drug development and health care policy. Reduced, suppressed, or completely lacking spermatogenesis is a common factor associated with male infertility [ 1 ]. There are various causes of suppressed spermatogenesis or spermatogenic failure, including genetic defects [ 2 , 3 ], but acquired factors also play an important role.
For example, men who have been exposed to adverse environmental conditions, such as pesticides or radiation, may become infertile. Lifestyle-related factors such as smoking, heavy drinking, and the use of high-temperature saunas, can also contribute to disorders of sperm production [ 4 , 5 ]. Many therapeutic drugs have also been reported to impair spermatogenesis, leading to temporary or persistent difficulty conceiving.
Any drug that does harm to the spermatogonia, Sertoli cells or Leydig cells can influence the processes of spermatogenesis and sperm maturation. Drugs that induce deleterious changes to the microenvironment of the testes or epididymis may also affect spermatogenesis and sperm maturation, leading to adverse effects on fertility. There have been several reviews published about therapeutic drugs that impair spermatogenesis for example, see [ 1 , 6 — 9 ].
However, all of these previous reviews were based on searches of the peer-reviewed scientific literature. These labels are required to be updated whenever new findings are made, so they provide the latest data known for the drugs [ 10 ]. Importantly, these labels often include information that has not been published.
To the best of our knowledge, this is the first comprehensive review of the FDA-approved prescription drugs that affect human spermatogenesis based on the drug labels.
The objective of the present review was to summarize the relevant information about FDA-approved drugs that can impair spermatogenesis based on the data presented in the drug labels in the DailyMed database. We also briefly discuss the limitations of the current FDA drug labels and reproductive toxicity testing and make recommendations for future studies. The search of the DailyMed database was performed as described in a previous study, with some modifications [ 11 ]. We included only FDA-approved human single-ingredient prescription drugs.
Over-the-counter OTC drugs were excluded because the relevant information was generally not available in the label due to limited testing. The drugs with multiple active ingredients were also excluded to simplify the analysis. When the same agent had more than one route of administration or was produced by different companies, or when the information had been updated at different times, the most recently updated record was used for the review.
The labels for the remaining drugs were downloaded directly from DailyMed in the PDF format on April 22, and were manually examined to collect all information related to spermatogenesis.
We performed a verification of the drug labels on February 16, to identify any new or missed entries that had been added since the previous search. These keywords were used to search for a variety of terms related to spermatogenesis, with many of the stemmed keywords associated with numerous terms, i. When there were differences in the descriptions found between the two authors, they discussed the findings with another author, and the group's consensus regarding the findings was used for the manuscript.
The criteria for drug inclusion and exclusion were discussed among the authors, and a consensus was reached by all of the researchers in the group. All information related to spermatogenesis, including sperm production in the testicles and sperm maturation in the epididymis, was included.
Some symptoms involving pathological changes of the male productive organs, such as Leydig cell tumors, testitis, epididymitis, and orchitis, which are likely to affect sperm production and maturation, were also included in this study. Some descriptions were excluded from further analysis for the following reasons: 1 Many labels had information relevant to sperm ejection, such as ejaculation disorders, delayed ejaculation, retrograde ejaculation, erectile dysfunction, prospermia, etc.
We excluded these findings because they are not directly related to sperm production or maturation. Miltefosine, omeprazole and iloperidone are in this category. These were also excluded from this study. In addition, while the fact that hormones can have a negative impact on fertility is generally well-recognized, and some drugs such as those used to treat prostate cancer are intended to be anti-androgenic, it is still worthwhile to warn patients of the effects on fertility, because they may not know or understand the risk unless they are given explicit information.
We have therefore included some hormone-based drugs where it might seem blatantly obvious that they would have a negative impact simply to insure that they were included in the list, which might eventually be used by non-experts.
As of April 22, , 65, drug labels had been deposited in DailyMed. After excluding the labels for over-the-counter OTC drugs; drugs used only in animals; drugs that were not yet FDA-approved; and the labels for medicinal foods, medical devices, dietary supplements, cosmetics, bulk ingredients, vaccines, plasma derivatives, diagnostic kits, and similar devices or reagents, a total of 22, human prescription drug labels were retained for the subsequent data extraction.
There were multiple labels from different manufacturers for some drugs, as well as drugs intended for different routes of administration, duration of effect, and in different dosage forms.
All of the duplicate labels for the same drugs were deleted manually, and only the most recent label was kept for the study. The final list of human single-ingredient prescription drugs included 1, drug labels, and these were all examined for information about their impact on sperm production and maturation.
As shown in the table, human spermatogenesis was reported to be affected by 65 of the 1, drugs examined. Hormones, antineoplastic agents and anti-inflammatory drugs were the drugs most often reported to affect sperm production and maturation based on the drug information and warning labels.
However, various classes of drugs, such as antibacterial, antiviral and analgesic agents, were also found to affect human spermatogenesis. Hormones, hormone substitutes and hormone antagonists are well-known for their negative impact on male fertility. In addition to changes in libido, these agents also represent a special class of spermatotoxic agents.
Spermatogenesis, which is associated with continuous cell proliferation and differentiation, is regulated by reproductive hormones. Follicle-stimulating hormone FSH and testosterone T secretion are essential for the successful completion of spermatogenesis.
Exposure to exogenous testosterone is considered to inhibit spermatogenesis by suppressing signaling via the hypothalamic-pituitary-gonadal hormonal axis [ 1 ]. Hormones can also affect germ cells by modulating the Sertoli cell function, because these cells express receptors for both FSH and T [ 74 , 75 ].
There is extensive evidence for the negative clinical impact of hormones on the fertility of healthy men see [ 49 , 51 , 52 , 54 , 57 , 62 , 64 , 67 — 69 ] for examples , supporting the warnings included in the drug labels.
Therefore, patients being prescribed any type of male hormone or derivative should be counseled that these agents may decrease their fertility. Antineoplastic agents are also well-known for their negative impact on fertility [ 6 , 76 , 77 ]. Antineoplastic agents have the potential to damage both germ cells and the supporting Sertoli cells in men, leading to severe oligozoospermia or azoospermia immediately following most courses of chemotherapy.
The rapidly dividing differentiating spermatogonia are generally more sensitive to killing by these drugs than are the later-stage, more slowly proliferating cells comprising most of the human body. Most alkylating antineoplastic agents are toxic to stem cells and produce prolonged azoospermia due to their ability to cross-link DNA [ 6 ].
Busulfan is considered to be one of the most highly sterilizing antineoplastic agents, because it kills spermatogonial stem cells [ 78 ]. Anti-inflammatory drugs are used to treat conditions ranging from acute contact dermatitis to chronic lupus erythematosus disorders involving the immune system.
These agents have a broad variety of targets, ranging from immune cells to cell surface receptors, signaling molecules and receptors. However, not much has been published in the scientific literature regarding the spermatotoxicity of anti-inflammatory agents.
In fact, the studies that have been published seem to indicate that the impact of anti-inflammatory agents on fertility may be minimal [ 79 ], non-existent [ 27 ], or even positive under certain conditions [ 80 ]. Of interest, several clinical trials have used anti-inflammatory drugs in an effort to improve the fertility of men with anti-sperm antibodies [ 81 — 83 ]. While these agents especially methylprednisolone and prednisolone consistently reduced the production of anti-sperm antibodies, they did not always lead to improvements in the sperm counts or motility, or in the conception rates.
Most of the drug labels in DailyMed indicated that the anti-inflammatory drugs led to changes in the motility and number of sperm. While these parameters are commonly used to assess the impact of exposure on fertility, decreases in the motility and number of sperm may be due to the type and timing of the studies performed rather than to spermatotoxicity, as there are relatively high variations in these parameters [ 84 ].
Therefore, the true clinical impact of anti-inflammatory agents is currently unclear and should be examined in greater detail.
A variety of other agents were identified to affect spermatogenesis. In fact, almost half of the FDA-approved drugs reported to affect spermatogenesis do not fit into these three main categories, instead ranging across a variety of intended indications. The most common effect of these drugs was epididymitis, although there were various other causes of spermatogenic failure induced by these drugs, many of which have been substantiated in peer-reviewed publications.
For example, tricyclic antidepressants and selective serotonin reuptake inhibitors SSRIs , such as clomipramine and paroxetine, can lead to significant but reversible suppression of spermatogenesis [ 20 — 22 ]. Some drugs have the potential to induce substantial elevation of the serum prolactin level, which suppresses the gonadotropin-releasing hormone GnRH and luteinizing hormone LH secretion.
Most antipsychotic agents block dopamine in the CNS, leading to suppression of the hypothalamic-pituitary-gonadal axis, thereby affecting hormone signaling and subsequent spermatogenesis [ 85 ]. Although detailed mechanistic data is still lacking for most drugs, there does not appear to be any relationship structural, mechanism of action, target s , other side effects, etc.
As noted above, the information reported in the DailyMed drug labels is not always consistent with the published literature. These differences may be due to a lack of publication in peer-reviewed journals, publication bias, differences in the populations studied, differences in the endpoints used for the studies, differences in the dose or frequency of drug administration, or various other factors.
Of the 65 drugs identified to have effects on human spermatogenesis based on the DailyMed labels, there were 13 without any peer-reviewed information available about their effects on spermatogenesis in either animals or humans.
Another seven drugs only reported data for animal studies, with no published information available about the effects of the drugs on human spermatogenesis.
Therefore, nearly one-third of the drugs indicated to have spermatotoxic effects in humans in the DailyMed drug labels would not be found by a search of the peer-reviewed literature. With regard to differences in the conclusions of the studies, the peer-reviewed reports for seven drugs were found to contradict the information present in the DailyMed labels.
Four of the drugs had contradictory findings in human studies pregabalin, colchicine, cortisone, and dexamethasone [ 14 , 24 , 25 , 27 , 28 ] , and one drug had contradictory findings in a study performed in rats gabapentin [ 15 ].
The pro-drug for another agent AZA, which is metabolized to 6-mercaptopurine was reported to have no effects in humans or animals [ 36 , 37 ], and there was conflicting data in the literature regarding the effects of methotrexate in humans [ 40 , 41 ].
The details of the studies that provided the data for the DailyMed labels are not available, so it is unclear whether there were differences in the study design and methods that might have been responsible for the different findings. The U. FDA requires reproductive toxicity testing of almost all new drugs during development. In the guidelines for industry issued by the FDA for new drug development, it is suggested that reproductive or developmental toxicity be evaluated in a variety of relevant studies to estimate the likelihood of risk to humans.
The suggested endpoints include any damage to the reproductive organs; alterations in the endocrine regulation of gamete maturation and release; changes in the sperm count, motility or morphology; alterations in endocrine function; or an overall reduction in fertility [ 86 ].
Findings suggestive of these conditions should therefore appear in the drug labels to guide the selection of treatment for patients. The FDA thus requires the testing and reporting of the impact of drugs on fertility. Most agents are tested at the pre-clinical, clinical, and post-marketing levels, and significant results are subsequently reported in the drug labels.
Despite these guidelines, many of the drug labels currently lack specific information regarding the impact of the drug on spermatogenesis. In some cases, this is because there are no adequate models to test the effects of that drug. In other cases, the drug has been used historically and is generally recognized as safe, permitting its use without stringent testing.
Marijuana may also be laced with heavy metals such as lead to increase its weight or more addictive illicit drugs, such as cocaine. Testosterone supplements, for example, can have a lingering effect, taking many months or even years before sperm production resumes. Doctors usually recommend men bank or freeze sperm beforehand, if possible. It's not anymore, and you are not Jesse Pinkman. Life is full of hard truths. In general, men who are trying to cause a pregnancy should not use any form of testosterone.
Do prescription drugs effect sperm. Sticky Menu
All drugs and medications pass into the bloodstream. Some directly affect sperm or eggs and reduce fertility. For both men and women, taking cocaine, heroin, ecstasy and marijuana can reduce the chance of having a baby. Taken over a long period of time, recreational drugs can cause permanent problems with the reproductive system and infertility.
Some supplements, vitamins, minerals, and herbal medicines are safe to take while trying to get pregnant and during pregnancy, and others are not. Professor Sarah Robertson, from Robinson Research Institute, University of Adelaide, explains why your health before pregnancy is important for your baby's future health.
Share Back to Top. Related links Your Sperm: and how to look after them Better Health Channel What can improve your chance of having a baby? MYTH It's best to stop taking prescription medications while trying to get pregnant. The facts about medications and drugs Many substances can be classified as drugs or medications, including: prescription drugs to treat chronic conditions, such as depression, asthma, thyroid conditions, diabetes high blood pressure, epilepsy, acne, or depression over-the-counter medications to treat headaches, pain, infections and colds complementary medicines, vitamins and mineral supplements and herbal remedies medications for cancer treatment recreational drugs like marijuana, heroin, ecstasy, cocaine or inhalants glues or aerosols.
When does pre-conception health begin? Lassi, Z. Men should not smoke, drink or take unnecessary drugs if they are planning to become fathers to avoid causing health problems for their children, a health expert has warned. Scientists found that toxic chemicals can damage sperm, which then pass altered genes onto babies.
In experiments on rats Matthew Anway of the University of Idaho found that some garden chemicals caused problems such as damaged and overgrown prostates, infertility and kidney problems, all of which were present up to four generations later.
Cynthia Daniels, of Rutgers University in New Jersey, an expert in the relation between a father and child's health, said: "If I was a young man I would not drink beer, I would not be smoking when I'm trying to conceive a child. It is well known that a mother's health is critically important in the resulting health of her baby, but there is now a growing body of evidence from both animal and human studies that paternal exposure to toxins can also adversely effect the development of a foetus, and that this can be passed down the generations.
Daniels, who led a seminar at the American Association for the Advancement of Science annual meeting in Boston, said: "Historically it has been assumed that exposures to the male will not affect his ability to pass defects on to children. Scientists at the seminar listed problems including pregnancy loss, low birth weight, increased birth defects and childhood cancers in children fathered by men who were exposed to toxins, from pesticides and prescription drugs to wartime chemicals.
Vietnam veterans exposed to agent orange, for example, have been shown to have children with increased rates of spina bifida.
Your Fertility medications and drugs | Your Fertility
There are potentially many different causes of male infertility, including hormonal, anatomical, and secondary to exposure to exogenous substances. In many cases of MFI, a definitive cause for abnormalities is never identified. Recently, the research community has given greater attention to identifying causes of MFI ranging from genetic Y chromosome microdeletions to mechanisms of environmental damage on sperm production.
Still evolving, is a clear understanding of how many pharmaceutical medications may cause MFI, which is often treatable and reversible. In this review we will outline the data regarding various pharmaceutical medications that have been investigated as possible causes of MFI. MFI may is generally diagnosed through an abnormal semen analysis SA. While the SA has multiple measured parameters, the most important are abnormalities in sperm count, ranging from fewer than normal sperm oligospermia to undetectable sperm azoospermia , sperm motility, a condition known as asthenospermia, and sperm morphology 5 , 6.
The relative importance of each of these parameters, among other measures of semen quality, are constantly a subject of debate within the fertility community 5 , 7. A further complicating matter is the poor reproducibility of SA as an assessment tool for sperm quality and quantity.
The causes of oligospermia or azoospermia can be divided into three distinct stages: Pre-Testicular, Testicular, and Post-Testicular, depending on the stage of spermatogenesis which is altered or impaired 9. Pre-testicular stage azoospermia results from the pituitary gland, part of the hypothalamic-pituitary-gonadal HPG axis, not producing proper hormones to stimulate the testes to produce sperm and is often due to an underlying endocrinologic abnormality 9.
Testicular stage azoospermia is a failure of testicular function and Post-Testicular azoospermia is due to physical causes such as obstruction 9. In the majority of MFI cases, a definitive cause for abnormalities is never identified 4.
Pharmaceutical medications as well as recreational drugs have been documented to impact semen producticular stages 2 , 10 , In addition, some medications impair ejaculation and erectile function, as well as the ability to decrease libido This review article will focus on the effects of certain pharmaceutical medications that may be associated with male infertility.
Rising levels of depressive disorders have in turn led to an increase in the use of prescription antidepressants, with more than million prescriptions on record for , the second most among all medications in the United States The underlying cause of depression is still being investigated but is thought to include an over-activity of the emotion processing regions of ventral limbic and underactivity of the dorsal prefrontal cortex Antidepressent medications, specifically selective serotonin reuptake inhibitors SSRIs , are currently the treatment of choice for individuals suffering from depression Further complicating the picture is the fact that some studies have linked depression alone, without the use of medications, to altered testosterone levels, which could conceivably contribute to MFI 17 , However, several other studies have failed to demonstrate such a correlation 17 , 19 , In , the same group performed a retrospective study on thirty-five healthy male volunteers The men were asked to provide semen samples at baseline and were then administered the drug paroxetine, an SSRI, for a period of five weeks.
Results indicated that the key sperm parameters of volume, concentration, motility or morphology were not adversely affected during the trial period.
Limitations of the study included a small sample size of healthy volunteers without baseline depression, a lack of placebo pill use in the control group, and the fact that fertility was not evaluated. Another retrospective trial has demonstrated an association between SSRI use and decreased sperm motility Evidence also shows that SSRIs have a spermicidal effect in vitro One group has actually described SSRIs as an acutely helpful therapy to improve increased ejaculate volume in men taking Sildenafil While there have been several small trials that link SSRIs to semen abnormalities, the authors could not identify a large trial that definitively link SSRIs to MFI as defined by in ability to achieve pregnancy.
A summary of the current evidence is offered in Table 1. This table outlines the evidence from the studies discussed in this review. Listed are medication categories and specific medications evaluated. The type of evidence is determined as either including a case report, in vitro, or clinical structure.
The evidence is also determined to have evaluated the impact on fertility and change in sperm count or function. Blank spaces indicate no study evaluated this category among the reviewed articles. They block the movement of free calcium ions, which serve as important secondary messengers, between ion channels and ionophores.
CCBs can have an effect on cardiac muscle, smooth muscle of blood vessels, and neurons 26 , CCBs are indicated as a therapy for various medical conditions including hypertension and heart failure 26 , Since , calcium antagonists have been shown to produce a dose-dependent reduction in sperm motility and viability in vitro In one particular in vitro assay, the dose-dependent effect of Nifedipine, a CCB, was examined with regards to sperm morphology, motility, and phospholipid composition.
The addition of the CCB resulted in significant inhibition of calcium ion uptake. The researchers also elucidated a clear dose-dependent and time-dependent effect of the calcium antagonist on sperm motility for different durations. Additionally, this study showed that exposure to the CCB resulted in structural changes in both the head and tail regions of sperm when evaluated by scanning electron microscope Others have shown that CCB may inhibit the ability of sperm to bind to an egg by altering the lipid bilayer of the sperm plasma membrane Interestingly, researchers have also shown that calcium ions exert a paradoxical effect on human sperm motility, depending on the developmental stage of the sperm Earlier in vitro experiments in non-human mammalian species had shown an increase in sperm motility with the addition of calcium ions, likely through the binding of calcium to a calmodulin-like protein.
One possible hypothesis for this effect was the triggering of a premature acrosome reaction in sperms before they underwent full capacitation and maturation In addition to the in vitro studies outlined above, there are also clinical trials that point to a link between CCBs and MFI. One small trial evaluating sperm from men taking CCB did not show decreased rates of oocyte fertilization when undergoing in vitro fertilization IVF without intracytoplasmic sperm injection However, the pregnancy rate per transfer in embryos derived from men taking CCBs was only While significant data exists to suggest that CCBs may contribute to MFI, the authors could not identify a large prospective trial evaluating fertility outcomes among men taking CCBs.
These drugs have a high affinity for alpha-adrenergic receptors in the smooth muscle cells of the lower urinary tract and blood vessels AABs also have a high binding affinity for various other receptors including dopamine and serotonin The use of AABs has been shown to be associated with significant rates of antegrade ejaculation or even anejaculation 33 , As the process of male ejaculation encompasses a complex coordination of actions, this affect of AABs is thought to be secondary to the effect on dopamine and serotonin, among other mechanisms The degree to which AABs may compromise the ejaculatory efficiency is substantial.
Additionally, AABs have been shown to also negatively impact semen parameters such as sperm concentration and motility However, other trials using AABs other than tamsulosin, such as alfuzosin, have not demonstrated deleterious effects on ejaculatory efficiency or altered semen parameters While significant data exists to suggest that AABs, specifically tamsulosin, may contribute to MFI, the authors could not identify a large prospective trial evaluating fertility outcomes among men taking AABs.
Epilepsy is known to be associated with MFI. Epileptic males have been shown, in large studies, to have significantly lower fertility rates and greater risks of hyposexuality than the general population Studies on anti-epileptic medications including carbamazepine, phenytoin and valproate have suggested specific drug-dependent side effects, including abnormal sperm morphology, reduced motility, lower sperm count, and reduced testicular volume.
The most likely mechanism for these side effects is thought by some to be the interaction between anti-epileptic medications and sex hormones, interfering with normal HPG pathway functioning However, many studies have been inconclusive whether these effects are symptoms of epilepsy itself or side effects of long-term administration of anti-epileptic medications 38 , One month after discontinuing his carbamazepine and starting phenytoin monotherapy, his semen parameters were found to be normal and his wife became pregnant within 6 months 40 , In a selective cohort study, researchers from Norway investigated the effect of carbamazepine and valproate on semen quality in a treatment arm for each medication and a control group receiving no medication.
The study did show an increased rate of abnormalities in the tails of sperm in men taking valproate. These changes were not seen in men taking carbamazepine. Of note, there was no difference in fertility in any of the men, as defined by pregnancy, compared with the controls While significant data exists to suggest that various anti-epileptic medications may contribute to MFI, current data is inconsistent and precludes specific recommendations regarding individual medications.
Furthermore, the welldescribed association between epilepsy and infertility presents a significant confounding variable that the majority of studies have failed to eliminate. The treatment of human immunodeficiency virus HIV has transformed a once quickly lethal disease into a condition that, with proper treatment, may be compatible with a long lifespan 43 , As such, many individuals with well controlled HIV are increasingly interested in the possibility of pursuing parenthood.
The ability of HIV positive men to father children even with HIV seronegative women is now a reasonable proposition through IVF risk reduction programs that involve sperm washing to significantly reduce the risk of HIV transmission Early HIV infection is not thought to significantly impair semen parameters 46 — Highly active antiretroviral therapy HAART is provided to patients with HIV and, despite its tremendous reduction in HIV mortality, has been associated with a number of serious adverse side effects including neuropathy and lipodystrophy One study showed that saquinavir, commonly used in HAART regimens, results in decreased sperm motility in vitro and negatively affects mechanisms that are essential to fertilization of an oocyte such as the acrosome reaction Other studies have shown similar results with reductions in ejaculate volume, increased rates of abnormal sperm morphology, and decreased sperm motility Regardless of the possible adverse effects of HAART on sperm quality, the health benefits of the treatment far outweigh any possible fertility benefit that could be associated with medication discontinuation.
However, these studies may be helpful in counseling HIV positive men who wish to pursue parenthood. Data evaluating the effects of most medications on semen is lacking.
However, the body of data available addressing this topic is ever expanding. The effects of antibiotics on semen quality are largely untested. Many studies have documented the favorable impact of antibiotics on semen quality in the setting of testicular infection, particularly epididymitis 52 — However, some emerging animal data have suggested that some antibiotics, such as tetracycline, may have an independent deleterious effect on semen quality when not given in the context of testicular infection A substantial body of data shows a substantial deleterious effect, even in mild doses, of chemotherapeutic agents and radiation for the treatment of cancer on semen parameters 56 — Specifically, alkylating agents, such as cyclophosphamide, have a particularly long lasting effect on spertamatogensis and may cause permanent oligo or azospermia Therefore, current standard of care is to obtain a semen sample that is cryopreserved before initiation of chemotherapy for fertility preservation Additionally, exogenous medications that alter the hypothalamic pituitary gonadal axis may impact semen quality.
Semen quality is known to be deleteriously affected, for example, with decreased levels of thyroid hormone or changes in prolactin concentration, which can be a side effect of multiple medications Anabolic steroids, generally taken by individuals to increase muscle mass, have been well documented to lead to oligo or azospermia 61 — Recent research has also evaluated the impact of phosphodiesterase inhibitors used to treat male penile impotence, such as sildenafil, on semen quality.
Many studies have found, in animal and human trials, increased motility and other semen parameter improvement with sildenafil 64 — There is conflicting data regarding the effect of sildenafil on oocyte fertilization, however, with some studies documenting a negative effect and others finding no difference from placebo 67 — Male factor infertility is a common cause of infertility.
Only recently has more attention been given to the underlying causes of MFI including the association between semen parameters and certain medications. Establishing clear association between medications and MFI, however, is challenging on several levels. Intra-sample variability is commonly reported among all men who provide multiple sequential semen analyses 8.
Furthermore, the number of days a man abstains from ejaculating prior to semen analysis may affect the results of the evaluation in terms of sperm concentration and sperm quality 71 ,