Pre-Conceptual Guidelines for Male Infertility: History
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Contributor:
Justine Bold
,
David Swinburne

Male fertility is declining and affects approximately one in seven couples. Reasons for this are multi-factorial and the subject of on-going research, though environmental contaminants (such xenoestrogens) are believed to be contributory factors. Semen parameters can be improved through a healthy diet and nutritional supplementation has also been shown to improve semen parameters, clinical pregnancy and live birth rates significantly.

  • infertility
  • spermatogenesis
  • semen-parameters
  • semen-quality
  • preconception
  • personalised-nutrition

1. Introduction

Clinical infertility is defined as a couple’s failure to conceive following 12 months of unprotected intercourse without pregnancy [1]. It has been reported that male fertility is declining across the world [2], the World Health Organisation (WHO) estimates that there are between 45–80 million infertile couples globally [3][4]. It is estimated that one in seven couples in the UK experience problems conceiving [5], with male factor infertility accounting for 40–50% of all infertility cases [6]. Low sperm count is the most common cause of infertility, responsible for approximately 15% of all cases of male infertility [5]. Many factors may contribute to reduced fecundity such as poor sperm morphology, reduced motility, reduced DNA stability [7], genetics, environmental toxins, reduced testosterone levels and medical conditions.
To determine if a man is infertile, semen analysis and a physical examination are undertaken [8]. Semen analysis typically looks at: volume of ejaculate, sperm count, sperm motility and sperm morphology [9]. DNA fragmentation is not routinely assessed as part of fertility examinations and not considered as a part of typical semen analysis, but it has been shown to significantly increase the incidence of miscarriage [10].
WHO parameters for semen analysis were published in the laboratory guidance for measurement of human sperm [11]. A measure of infertility was not available for men until 1980 when the WHO published its first laboratory manual for the examination of human sperm [12]. In 2010, there were significant reductions to the parameters used to determine infertility. Sperm count was the most significant reduction, reducing from 20 million/mL to 15 million/mL [11]. To generate the WHO semen parameters Cooper et al. [13] pooled data from 5 studies to form centiles and determine upper and lower limits of fertility. Only one study was from the Southern Hemisphere, with the remaining studies from predominantly European cities, which may not accurately reflect fertility in other geographical or rural areas. Fisch & Goluboff [14] concluded there are significant variations in sperm counts by location, which presents an issue when developing global parameters that have not used a world-wide cohort. As a result, the reference values may not be relative or representative of male fertility in many areas of the world, or representative of ethnic minority populations living in western countries. It is estimated that at least 15% of infertile couples will now be classed as being in normal ranges, significantly reducing the number of couples referred for fertility treatment [15]. In the 6th edition of the WHO laboratory manual for the examination of human sperm the researchers did address the concerns regarding the data used for determining the upper and lower limits of sperm parameters [12]. The researchers highlighted that the 5th edition was the first publication that contained a comprehensive data set to determine centiles of sperm count, concentration, motility and morphology [12]. However the narrow range of data selection highlights the need to conduct high quality semen analysis studies in developing countries which can hopefully contribute the global picture of male fertility in time for the next updated manual.

2. Male Emotional Experience of Infertility

Relatively little is known or understood about the mental, emotional and psychological impact of male infertility. Arya and Dibb [16] conducted one of only two UK specific research projects investigating the male experience of infertility and concluded that research is limited globally. A large proportion of the research investigating the psychosocial impact of infertility was investigating the female experience or that of couples [17][18]. The scarcity of research makes drawing conclusions on the true impact of male infertility on men challenging, which may be attributed to the societal notion that men are reluctant to talk about their feelings or emotions [19]. This may explain why it has been suggested that women experience a greater level of distress and sense of loss when undergoing fertility treatment, due to a disproportionate lack of research from the male perspective [20][21]. In contrast, Patel et al. [22] found that stress was pervasive in infertile men, experienced by 72% of men attending a fertility clinic in India and that the level of stress could be predicted by the severity of their diagnosis. However, it is possible that cultural differences and expectations to father a child may contribute to higher levels of perceived stress in Indian men [23]. Indeed, infertility is still a taboo subject among black and minority ethnic (BAME) populations [24].
Stress during male fertility treatment can negatively affect testicular function and fertility [25]. It has been demonstrated that increased levels of stress suppress testosterone production [26]. Research has also linked chronic lifestyle stress as a potential mechanism contributing to reduced sperm quality. The researchers suggested that this is due to glucocorticoid receptor activation which impairs testicular function and germ cell maturation possibly due to a single nucleotide polymorphism (SNP) on the NRC31 gene [25]. Hanna and Gough [27] found that many men in the UK ‘suffer in silence’ for fear of being singled out by their peers. A study by Hanna and Gough [28] qualitatively analysed posts from male fertility support groups which have international reach or included supporting male partners, findings mirror the results of Thorsby & Gill [29]. In both studies men reported having their virility undermined and being subjected to hurtful male culture. Research also suggests that men do not want to discuss their fertility in person [30] but that they are open to seeking help online from men undergoing the same experience [31]. The reluctance to talk about infertility contributes to the scarcity of research on the subject [32]. However, a recent thematic analysis of online male infertility chat forum posts found that men are committed and support each other with lifestyle changes to improve their chances of conception [33]. When men are infertile there is a great burden placed on the female partner as they are the subject for the majority of fertility interventions [34]. Unfortunately, this also leads to men feeling over overlooked and unacknowledged during fertility treatment [16][28].

3. Dietary and Lifestyle Factors Affecting Fertility

3.1. Obesity

Obesity is known to reduce fecundity in both men and women [35]. A systematic review by Sermondade et al. [36] investigating the association of obesity and semen health concluded that obesity is associated with reduced semen concentration. Håkonsen et al. [37] demonstrated that reducing BMI can improve semen parameters during a 14-week intensive weight loss programme with a small cohort of 43 men. Although it is difficult to determine whether the benefits are the result of weight loss or the change in lifestyle, there is no doubt that reducing BMI is beneficial for health overall [38]. High energy diets have been shown to reduce male fertility via alterations in testicular metabolism and increased sperm DNA damage [39][40].

3.2. Dietary Fats

Dietary fats are essential for human health and play a central role in cell membrane formation and normal maintenance of hormone levels in the human body. A recent systematic review and meta-analysis found that low fat diets reduce testosterone levels in men, with the greatest impact being on Caucasian men [41].

3.3. Trans Fatty Acids

Approximately 20% of trans fatty acids (TFA) occur naturally in meat and dairy products, industrially produced hydrogenated fats used in food manufacturing now account for 80% of TFA intake [42]. Most studies suggest a negative association between TFA intake and male fertility through disruptions in testosterone levels, testicular function and sperm cell membrane quality [43]. No studies were found demonstrating a positive association between TFA and sperm health, Chavarro et al. [44] found that there was a linear dose related decrease in sperm count with every increased quartile of TFA intake. A comprehensive review by Cekici & Akdevelioglu [45] reported a significant negative association between TFA intake, sperm health and fertilization rates, however this study had some distinct methodological issues. There were a total of 8 studies included in the review totaling 1355 men. The largest study in the review [46], had a cohort of 701 young Danish men. This one study made up over 50% of the total cohort, however it did not distinguish between saturated fat and TFA, which is a limitation. It is known that TFA intake is associated with several negative health consequences [47] and it is likely that decreased sperm quality is included in that list, however more research and better designed studies are needed to truly assess the risk.

3.4. Saturated Fat

Research relating to saturated fat intake is conflicting. Several studies have correlated increased saturated fat intake to declining sperm concentrations by as much as 38% [44][46][48]. In contrast, a study by Dadkhah et al. [49] only found a correlation between decreased total semen volume and saturated fat, reporting that no differences were observed in any other measure of male fertility. The relationship with saturated fat and sperm health needs further investigation as high saturated fat intake is often related to other unhealthier dietary patterns in general that may adversely affect sperm health.

3.5. Polyunsaturated Fatty Acids

Polyunsaturated fat (PUFA) intake is correlated to a variety of positive health outcomes from improved blood lipid profiles to alleviation of joint pain and depression [50]. Increasing PUFA intake is a common intervention for improving markers of male fertility. Unfortunately, strong evidence is lacking, in the most part due to the nature of dietary analysis using food frequency questionnaires (FFQ), meaning that any relationship outlined cannot prove causation [48][51]. However, supplementation with eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) omega 3 fatty acids have been studied in controlled trails (RCTs). Three RCT’s and one Meta-analysis were found which all showed beneficial effect of omega 3 supplementation on semen parameters at dosages ranging from 500 mg to 2000 mg/day [51][52][53][54].
A double-blind placebo controlled RCT by Gonzalez-Ravina et al. [54] found that DHA supplementation showed a dose dependent improvement in progressive motility and slight improvements in markers of oxidative stress in men with asthenozoospermia at dosages of 0.5 g, 1 g and 2 g per day. The systematic review and meta-analysis by Hosseini et al. [52] found that omega 3 supplementation significantly increased sperm motility and seminal DHA concentrations but no other markers of fertility significantly.

3.6. Mediterranean Diet

Healthy diets are correlated with better semen parameters [55], with higher intakes of foods rich in folates such as fruits and vegetables associated with reduced DNA fragmentation and increased motility [56]. Diet has been shown to effect sperm replication via alterations in ribonucleic acid (RNA) concentrations, both positively and negatively in as little as one week, depending on whether the participant is eating a healthy or unhealthy diet [57]. The Mediterranean diet is considered one of the healthiest diets in the world, typically minimally processed and rich in fruits, vegetables, beans, pulses, fish, nuts and seeds [58] and so naturally a rich source of vitamins and antioxidants including vitamins C, D, E, Beta Carotene, zinc, selenium and omega 3 [59]. This rich source of nutrients and antioxidants is what correlates the Mediterranean diet to increased sperm count, concentration [60] and increased rates of conception among those undergoing assistive reproductive technology (ART) [61]. Unfortunately, there were no randomised interventional studies that could be found investigating sperm health and the Mediterranean diet.

3.7. Caffeine

Evidence regarding caffeine’s impact on sperm health is far from unanimous, with much of the data coming from observational studies. Jensen et al. [62] found that there was a relationship between high intake of caffeine and decreased semen quality although, only a significant relationship for cola consumption. It has been suggested that individuals who consume sweetened beverages regularly, including cola, are more likely to engage in other unhealthy lifestyle behaviors [63], which may also negatively affect semen parameters. Ricci et al. [64] found that men who drank 3 or more cups of coffee per day had higher levels of sperm DNA damage. Conversely the largest meta-analysis investigating the effect of lifestyle factors on fertility, with a cohort of 29,914 found no significant relationship between caffeine and semen health [65]. Therefore, low to moderate caffeine intake does not appear to have any significant impact on sperm health [66]. A recent meta-analysis and systematic review by Ricci et al. [64] found that caffeine was possibly associated with an increase in sperm DNA damage and increased time to pregnancy, although this was associated with high caffeine consumption above 400 mg/day. A large meta-analysis of 201 studies on caffeine and health outcomes by Poole et al. [67] deemed caffeine to have positive health outcomes for the majority of studies except pregnancy, where it was linked to miscarriage and low birth weight in newborns. This highlights the need for individualised lifestyle recommendations for both men and women, as caffeine avoidance can be described as a significant challenge for many men. Low to moderate consumption of tea and coffee should not negatively impact sperm health.

3.8. Alcohol Consumption

It has been suggested that alcohol consumption has a negative impact on semen quality [68]. A lack of heterogenicity of participant selection and classification was a limiting factor for many studies such as the study by Martini et al. [69] in which non-drinkers were classed as those who consumed less than 500 mL wine or equivalent per day. This makes any uniform conclusions between studies difficult. A study by Jensen et al. [62] found that moderate to heavy alcohol consumption was associated with a 33% reduction in sperm concentration. The authors concluded that this was due to disruptions in testosterone and Sex hormone binding globulin (SHBG). The same study also concluded that independent episodes of binging were not associated with decreased semen quality. A recent meta-analysis of 15 cross sectional studies totaling 16,000 participants by Ricci et al. [70] found that there were significant reductions in semen volume and morphology in those who drink daily compared to occasional or never drinkers. The authors concluded that moderate consumption did not adversely affect semen parameters. In chronic heavy drinkers a steady decline in semen quality can be seen, which rapidly returns to normal within 3 months of abstinence [71]. Based on the available evidence it seems clear that moderate to high levels of alcohol have a significant detrimental effect on semen health. Low and occasional alcohol intake does not appear to have any significant effect on semen health.

3.9. Smoke (Tobacco and Surrogates)

Early research on the subject of tobacco smoking from 2004 was confounding, partly due to poor study design where smokers were compared to drinkers and there was no statistical difference in sperm quality in smokers regardless of the level of consumption [69]. However more recent research that analyzed smokers sperm health independently of drinkers found that tobacco smoking was associated with decreased concentration, motility, morphology, increased oxidative damage and increased levels of DNA damage in sperm cells [68].

3.10. Recreational Drugs (Marijuana and Analogues)

No searches here were returned specifically on recreation drugs such as marijuana, so even though these can be significant in terms of male fertility consideration of these is outside of the scope of this research.

4. Micronutrient Supplementation

The most comprehensive review of antioxidants, pregnancy and semen parameters comes from a Cochrane review [72]. Cochrane reviews are a stringent method of conducting systematic reviews and meta-analysis using only data from RCT’s [73]. The study was originally conducted in 2011 with a total of 34 studies reviewed. The updated review in 2019 had 61 studies included dating from 1978 to 2018. Following appraisal with the Critical Appraisal Skills Programme (CASP) checklist for systematic reviews [74] it is unclear if appropriate studies were included in the review as only 18 studies reported on the authors primary outcome, which was live birth or clinical pregnancy. The 43 remaining studies did not report on this outcome, instead focusing on semen parameters. Therefore, it may not be justified for the researchers to conclude that the level of evidence is low due to not reporting on clinical pregnancy, when this was not the objective of the majority of studies in the review. Despite this potential limitation, the authors concluded that supplementation with vitamins and antioxidants may be beneficial in improving male fertility, with an increased in pregnancy rate of 26% compared to 11% for placebo or no treatment. This concurs with the findings of the systematic review and meta-analysis by Majzoub and Agarwal [75], reporting that there is a significant positive effect of antioxidant therapy on semen parameters, assisted reproduction outcomes and live birth rate.

5. Environmental Impacts on Male Fertility

5.1. Testicular Heat Exposure

Keeping the testes cool and avoiding overheating of the testes is advisable, which may happen as a result of being seated for long periods. Heat exposure to the testes may be a contributory factor in the incidence of male infertility [76]. Normal scrotal temperatures are approximately 34 °C, whereas sitting with the legs together raises the average scrotal temperature to 36 °C [77]. In a small study of 9 men, their scrotal temperatures increased by between 1.7–2.2 °C when they were seated compared to when they were walking. This study was limited by the cohort size and also did not seek to determine causation of infertility through increased scrotal temperature [78]. Evidence for this is limited and mostly draws on data from animal studies or associations from observational studies rather than higher quality evidence. It is likely that there are not more RCT’s investigating this subject because it would not be ethical to knowingly cause damage to the participants sperm, therefore correlations can be drawn between heat exposure and sperm quality, but causation could not be determined. One RCT was found, which found that heat exposure to the testes caused severe but reversible reductions in sperm quality and motility [79].

5.2. Mobile Phones and Device Radiation

Over recent years there have been a growing number of studies investigating the link between declining sperm health and exposure to environmental toxins including chemicals, plastics and radiation. Several studies have found a link between mobile phone radiation and increased levels of DNA fragmentation [80] and a reduction in semen parameters. However, the methodology for this study tested the mobile phone in talk mode as opposed to standby mode, at a distance of 5 cm from the semen sample which is not representative of real-world use when talking on the phone. A systematic review and meta-analysis by Adams et al. [81] analyzed data from ten studies with a combined 1492 samples investigating the effect of mobile phone radiation on semen parameters. The authors concluded that exposure to mobile phone radiation significantly reduces semen motility and viability but does not impact sperm concentration. Data on the use of laptops on sperm health is a little sparser, with the first study that could be found being published in 2012. The authors found that exposure to a WIFI connected laptop for 4 h demonstrated a significant reduction in progressive motility and a significant increase in seminal DNA fragmentation [82]. Unfortunately, this study had several methodological flaws that were described by Mortazavi et al. [83]. In a comprehensive review of the literature by Kesari, Agarwal & Henkel, [84] the authors concluded that radiation emitting devices or devices connected to WIFI networks produce deleterious effects on the testes, which may affect sperm count, morphology, motility, and increased DNA damage to sperm and an increase in ROS. The authors noted that the exact mechanism of action is yet to be determined and further studies are needed to determine the link.

5.3. Environmental Contaminants and Endocrine Disrupting Chemicals

Bisphenol A (BPA) is used in the process of plastics manufacturing to make particularly strong and durable plastics and has been linked to reproductive dysfunction in both men and women due to its ability to bind and interact with estrogenic, androgenic and thyroid hormone receptors [85]. Cariati et al. [86] reported that BPA is able to disrupt a host of hormones associated with male reproduction and sperm cell maturation including testosterone, luteinizing hormone (LH), pregnenolone, 5-dehydroepiandrosterone (DHEA) and DHT 5a-dihydrotestosterone (DHT) which resulted in a decrease in sperm count, concentration, motility, and normal forms. In animal models, foetal exposure to BPA has been shown to disrupt testicular development, testosterone production and subsequently spermatogenesis in later life [87]. The toxic effects of BPA are reported to be higher in males than females possibly due to differences in androgen related enzyme activity [88]. BPA is commonly found in food packaging and several studies have reported that BPA is able to leach from plastic containers, bottles and liners of cans into food and beverages, although the European food safety authority (EFSA) concluded that the amount leached was below safe limits [89]. Many products are now marketed and sold as BPA free after concerns were raised regarding its safety [90]. Unfortunately, in plastics manufacturing BPA is often substituted with other types of Bisphenols such as Bisphenol F (BPF) or Bisphenol S (BPS, which have been shown to have the same hormone disrupting abilities as BPA [91].

5.4. Phthalates

Phthalates are fat-soluble synthetic chemicals known for their ability to soften plastic [90]. Phthalates are used in flexible vinyl plastics which are used across many different industry sectors including food processing, pharmaceuticals, cosmetics, personal care products, flooring and wall coverings [92]. The impact of phthalates on male reproductive function is well studied, with in excess of 900 results returned evaluating Phthalates and semen, with the majority of data coming from animal studies. Because of the limited number of human studies, the mechanism of action remains unclear as to how Phthalates impact on fertility in humans [93], with much of the data coming from epidemiological and observational studies. However, there is an undeniable link between urinary Phthalate metabolites and impaired reproductive function in males [94]. The effect of Phthalates on males is an emerging area of research, Phthalate’s exposure on the foetus of boys when in utero is associated with a shortened anogenital distance (AGD), and the prevalence genital birth defects such as hypospadias and cryptorchidism [95]. In animal studies, a shortened AGD from in utero phthalates exposure is associated with testicular dysgenesis syndrome (TDS) which includes undescended testes, reduced testes weight and impaired semen production [96]. Historical evidence for the association of phthalate exposure and male reproductive impairment is limited, however a comprehensive systematic review by Radke et al. [97] concluded that there was sufficient robust evidence to link general, non-occupational exposure to phthalates with decreased AGD, decreased testosterone and increased time to pregnancy for phthalates, di(2-ethylhexyl) phthalate (DEHP) and dibutyl phthalate (DBP).

5.5. Pesticides

The term pesticides covers a broad range of agricultural chemicals including pesticides, herbicides, insecticides and fungicides in which its production dates back to 1952 [98]. Pesticides may interfere with several systems directly related to reproduction [99]. Data from 1061 couples was collected where the male partners were directly exposed to pesticides and found that there was a significant increase in male infertility and spontaneous abortion. There was also a significant increase in still births, neonatal deaths and congenital defects [100]. In a 2016 review of environmental contaminants and spermatogenesis the authors highlighted that exposure to pesticides through dietary, occupational or environmental toxins have been shown to disrupts hormones and spermatogenesis [101]. The mechanisms by which pesticides interfere with male reproductive function remain unclear. It is known that pesticide exposure can lead hormone disruption, germ cell apoptosis, testicular shrinkage and decreased spermatogenesis [102].

This entry is adapted from the peer-reviewed paper 10.3390/dietetics1030016

References

  1. Evers, J.L. Female subfertility. Lancet 2002, 360, 151–159.
  2. Sengupta, P.; Dutta, S.; Krajewska-Kulak, E. The Disappearing Sperms: Analysis of Reports Published Between 1980 and 2015. Am. J. Men’s Health 2017, 11, 1279–1304.
  3. Agarwal, A.; Mulgund, A.; Hamada, A.; Chyatte, M.R. A unique view on male infertility around the globe. Reprod. Biol. Endocrinol. 2015, 13, 37.
  4. Rutstein, S.O.; Shah, I.H. Infecundity, Infertility, and Childlessness in Developing Countries (No. 9); Measure Dhs.; ORC Macro: Calverton, MD, USA; World Health Organisation: Geneva, Switzerland, 2004.
  5. NICE. Fertility Problems: Assessment and Treatment. 2013. Available online: https://www.nice.org.uk/guidance/cg156/ifp/chapter/Treatments-for-men (accessed on 21 April 2022).
  6. Kumar, N.; Singh, A.K. Trends of male factor infertility, an important cause of infertility: A review of literature. J. Hum. Reprod. Sci. 2015, 8, 191–196.
  7. NHS. Diagnosis: Infertility. 2020. Available online: https://www.nhs.uk/conditions/infertility/diagnosis/ (accessed on 4 February 2021).
  8. Khatun, A.; Rahman, M.S.; Pang, M.G. Clinical assessment of the male fertility. Obstet. Gynecol. Sci. 2018, 61, 179–191.
  9. Vasan, S.S. Semen analysis and sperm function tests: How much to test? Indian J. Urol. 2011, 27, 41–48.
  10. McQueen, D.B.; Zhang, J.; Jared, C.; Robins, J.C. Sperm DNA fragmentation and recurrent pregnancy loss: A systematic review and meta-analysis. Fertil. Steril. 2019, 112, 54–60.e3.
  11. World Health Organization. WHO Laboratory Manual for the Examination and Processing of Human Semen, 5th ed.; WHO: Geneva, Switzerland, 2010.
  12. World Health Organization. WHO Laboratory Manual for the Examination and Processing of Human Semen, 6th ed.; WHO: Geneva, Switzerland, 2021.
  13. Cooper, T.G.; Noonan, E.; von Eckardstein, S.; Auger, J.; Baker, H.W.; Behre, H.M.; Haugen, T.B.; Kruger, T.; Wang, C.; Mbizvo, M.T.; et al. World Health Organization Reference Values for Human Semen Characteristics. Hum. Reprod. Update 2010, 16, 231–245.
  14. Fisch, H.; Goluboff, E.T. Geographic variations in sperm counts: A potential cause of bias in studies of semen quality. Fertil. Steril. 1996, 65, 1044–1046.
  15. Murray, K.S.; James, A.; McGeady, J.B.; Reed, M.L.; Kuang, W.W.; Nangia, A.K. The effect of the new 2010 World Health Organization criteria for semen analyses on male infertility. Fertil. Steril. 2012, 98, 1428–1431.
  16. Arya, S.T.; Dibb, B. The experience of infertility treatment: The male perspective. Hum. Fertil. 2016, 19, 242–248.
  17. Greil, A.L.; Slauson-Blevins, K.; McQuillan, J. The experience of infertility: A review of recent literature. Sociol. Health Illn. 2010, 32, 140–162.
  18. Hinton, L.; Miller, T. Mapping men’s anticipation and experiences in the reproductive realm: (in)fertility journeys. Reprod. BioMed. Online 2013, 27, 244–252.
  19. Hanna, E.; Gough, B. A qualitative analysis of men’s forum posts. Health 2016, 20, 363–382.
  20. Devika, D.; Kumar, P.; Sharkel, S. A psychological study of male, female related and unexplained infertility in Indian urban couples. J. Reprod. Infant. Psychol. 2017, 35, 353–364.
  21. Malik, S.H.; Coulson, N. The male experience of infertility: A thematic analysis of an online infertility support group bulletin board. J. Reprod. Infant. Psychol. 2008, 26, 18–30.
  22. Patel, A.; Sharma, P.S.; Narayan, P.; Binu, V.S.; Dinesh, N.; Pai, P.J. Prevalence and predictors of infertility-specific stress in women diagnosed with primary infertility: A clinic-based study. J. Hum. Reprod. Sci. 2016, 9, 28–34.
  23. Van Balen, F.; Bos, H.M. The social and cultural consequences of being childless in poor-resource areas. Facts Views Vis. ObGyn. 2009, 1, 106–121.
  24. Van Balen, F.; Inhorn, M. Interpreting infertility: A view from the Social Sciences. In Infertility around the Globe. New Thinking on Childlessness, Gender and Reproductive Technologies; Inhorn, M., van Balen, F., Eds.; University of California Press: California, CA, USA, 2002; pp. 3–32.
  25. Ilacqua, A.; Izzo, G.; Emerenziani, G.P.; Baldari, C.; Aversa, A. Lifestyle and fertility: The influence of stress and quality of life on male fertility. Reprod. Biol. Endocrinol. 2018, 16, 15.
  26. Nargund, V. Effects of psychological stress on male fertility. Nat. Rev. Urol. 2015, 12, 373–382.
  27. Hanna, E.; Gough, B. The social construction of male infertility: A qualitative questionnaire study of men with a male factor infertility diagnosis. Sociol. Health Illn. 2020, 42, 465–480.
  28. Hanna, E.; Gough, B. Experiencing Male Infertility: A Review of the Qualitative Research Literature. SAGE Open 2015, 5, 2158244015610319.
  29. Throsby, K.; Gill, R. It’s Different for Men. Men Masc. 2004, 6, 330–348.
  30. Miner, S.A.; Daumler, D.; Chan, P.; Gupta, A.; Lo, K.; Zelkowitz, P. Masculinity, Mental Health, and Desire for Social Support Among Male Cancer and Infertility Patients. Am. J. Men’s Health 2019, 13, 1557988318820396.
  31. Richard, J.; Badillo-Amberg, I.; Zelkowitz, P. So Much of This Story Could Be Me": Men’s Use of Support in Online Infertility Discussion Boards. Am. J. Men’s Health 2017, 11, 663–673.
  32. Dooley, M.; Nolan, A.; Sarma, K.M. The psychological impact of male factor infertility and fertility treatment on men: A qualitative study. Ir. J. Psychol. 2011, 32, 14–24.
  33. Hanna, E.; Gough, B.; Hudson, N. Fit to father? Online accounts of lifestyle changes and help-seeking on a male infertility board. Sociol. Health Illn. 2018, 40, 937–953.
  34. Turner, K.A.; Rambhatla, A.; Schon, S.; Agarwal, A.; Krawetz, S.A.; Dupree, J.M.; Avidor-Reiss, T. Male Infertility is a Women’s Health Issue-Research and Clinical Evaluation of Male Infertility Is Needed. Cells 2020, 9, 990.
  35. Ramlau-Hansen, C.H.; Thulstrup, A.M.; Nohr, E.A.; Bonde, J.P.; Sørensen, T.I.A.; Olsen, J. Subfecundity in overweight and obese couples. Hum. Reprod. 2007, 22, 1634–1637.
  36. Sermondade, N.; Faure, C.; Fezeu, L.; Shayeb, A.G.; Bonde, J.P.; Jensen, T.K.; Van Wely, M.; Cao, J.; Martini, A.C.; Eskandar, M.; et al. BMI in relation to sperm count: An updated systematic review and collaborative meta-analysis. Hum. Reprod. Update 2013, 19, 221–231.
  37. Håkonsen, L.B.; Thulstrup, A.M.; Aggerholm, A.S.; Olsen, J.; Bonde, J.P.; Andersen, C.Y.; Bungum, M.; Ernst, E.H.; Hansen, M.L.; Ernst, E.H.; et al. Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men. Reprod. Health 2011, 8, 24.
  38. Washburn, R.A.; Szabo, A.N.; Lambourne, K.; Willis, E.A.; Ptomey, L.T.; Honas, J.J.; Herrmann, S.D.; Donnelly, J.E. Does the Method of Weight Loss Effect Long-Term Changes in Weight, Body Composition or Chronic Disease Risk Factors in Overweight or Obese Adults? A Systematic Review. PLoS ONE 2014, 9, e109849.
  39. Fariello, R.M.; Pariz, J.R.; Spaine, D.M.; Cedenho, A.P.; Bertolla, R.P.; Fraietta, R. Association between obesity and alteration of sperm DNA integrity and mitochondrial activity. BJU Int. 2012, 110, 863–867.
  40. Rato, L.; Alves, M.G.; Cavaco, J.E.; Oliveira, P.F. High-energy diets: A threat for male fertility? Obes. Rev. 2014, 15, 996–1007.
  41. Whittaker, J.; Kexin Wu, K. Low-fat diets and testosterone in men: Systematic review and meta-analysis of intervention studies. J. Ster. Biochem. Mol. Biol. 2021, 210, 105878.
  42. Dhaka, V.; Gulia, N.; Ahlawat, K.S.; Khatkar, B.S. Trans fats-sources, health risks and alternative approach-A review. J. Food Sci. Technol. 2011, 48, 534–541.
  43. Skoracka, K.; Eder, P.; Łykowska-Szuber, L.; Dobrowolska, A.; Krela-Kaźmierczak, I. Diet and Nutritional Factors in Male (In)fertility-Underestimated Factors. J. Clin. Med. 2020, 9, 1400.
  44. Chavarro, J.E.; Minguez-Alarcon, L.; Mendiola, J.; Cutillas-Tolın, A.; Lopez-Espın, J.J.; Torres-Cantero, A.M. Trans fatty acid intake is inversely related to total sperm count in young healthy men. Hum. Reprod. 2014, 29, 429–440.
  45. Cekici, H.; Akdevelioglu, Y. The association between trans fatty acids, infertility and fetal life: A review. Hum. Fert. 2019, 22, 154–163.
  46. Jensen, T.K.; Heitmann, B.L.; Jensen, M.B.; Halldorsson, T.I.; Andersson, A.M.; Skakkebaek, N.E.; Jørgensen, N. High dietary intake of saturated fat is associated with reduced semen quality among 701 young Danish men from the general population. Am. J. Clin. Nutr. 2013, 97, 411–418.
  47. Bhardwaj, S.; Passi, S.J.; Misra, A. Overview of trans fatty acids: Biochemistry and health effects. Diabetes Metab. Syndr. 2011, 5, 161–164.
  48. Attaman, J.A.; Toth, T.L.; Furtado, J.; Campos, H.; Hauser, R.; Chavarro, J.E. Dietary fat and semen quality among men attending a fertility clinic. Hum. Reprod. 2012, 27, 1466–1474.
  49. Dadkhah, H.; Kazemi, A.; Nasr-Isfahani, M.H.; Ehsanpour, S. The Relationship between the Amount of Saturated Fat Intake and Semen Quality in Men. Ir. J. Nur. Midw. Res. 2017, 22, 46–50.
  50. Siriwardhana, N.; Kalupahana, N.S.; Moustaid-Moussa, N. Health benefits of n-3 polyunsaturated fatty acids: Eicosapentaenoic acid and docosahexaenoic acid. Adv. Food Nutr. Res. 2012, 65, 211–222.
  51. Olsen, J.; Ramlau-Hansen, C.H. Dietary fats may impact semen quantity and quality. As. J. Androl. 2012, 14, 511–512.
  52. Hosseini, B.; Nourmohamadi, M.; Hajipour, S.; Taghizadeh, M.; Asemi, Z.; Keshavarz, S.A.; Jafarnejad, S. The Effect of Omega-3 Fatty Acids, EPA, and/or DHA on Male Infertility: A Systematic Review and Meta-analysis. J. Diet. Suppl. 2019, 16, 245–256.
  53. González-Ravina, C.; Aguirre-Lipperheide, M.; Pinto, F.; Martín-Lozano, D.; Fernández-Sánchez, M.; Blasco, V.; Santamaría-López, E.; Candenas, L. Effect of dietary supplementation with a highly pure and concentrated docosahexaenoic acid (DHA) supplement on human sperm function. Reprod. Biol. 2018, 18, 282–288.
  54. Safarinejad, M.R. Effect of omega-3 polyunsaturated fatty acid supplementation on semen profile and enzymatic anti-oxidant capacity of seminal plasma in infertile men with idiopathic oligoasthenoteratospermia: A double-blind, placebo-controlled, randomised study. Andrologia 2011, 43, 38–47.
  55. Gaskins, A.J.; Colaci, D.S.; Mendiola, J.; Swan, S.H.; Chavarro, J.E. Dietary patterns and semen quality in young men. Hum. Reprod. 2012, 27, 899–907.
  56. Oostingh, E.C.; Steegers-Theunissen, R.P.M.; de Vries, J.H.M.; Laven, J.S.E.; Koster, M.P.H. Strong adherence to a healthy dietary pattern is associated with better semen quality, especially in men with poor semen quality. Fertil. Steril. 2017, 107, 916–923.e2.
  57. Nätt, D.; Kugelberg, U.; Casas, E.; Elizabeth Nedstrand, E.; Stefan Zalavary, S.; Henriksson, P.; Nijm, C.; Jäderquist, J.; Sandborg, J.; Flinke, E.; et al. Human sperm displays rapid responses to diet. PLoS Biol. 2019, 17, e3000559.
  58. Davis, C.; Bryan, J.; Hodgson, J.; Murphy, K. Definition of the Mediterranean Diet; a Literature Review. Nutrients 2015, 7, 9139–9153.
  59. Salas-Huetos, A.; Bulló, M.; Salas-Salvadó, J. Dietary patterns, foods and nutrients in male fertility parameters and fecundability: A systematic review of observational studies. Hum. Reprod. Update 2017, 23, 371–389.
  60. Ricci, E.; Bravi, F.; Noli, S.; Ferrari, S.; De Cosmi, V.; La Vecchia, I.; Parazzini, F. Mediterranean diet and the risk of poor semen quality: Cross-sectional analysis of men referring to an Italian Fertility Clinic. Andrology 2019, 7, 156–162.
  61. Karayiannis, D.; Kontogianni, M.D.; Mendorou, C.; Douka, L.; Mastrominas, M.; Yiannakouris, N. Association between adherence to the Mediterranean diet and semen quality parameters in male partners of couples attempting fertility. Hum. Reprod. 2017, 32, 215–222.
  62. Jensen, T.K.; Gottschau, M.; Madsen, J.O.B.; Andersson, A.M.; Lassen, T.H.; Sakkebaek, N.E.; Swan, S.H.; Priskorn, L.; Juul, A.; Jorgenson, N. Habitual alcohol consumption associated with reduced semen quality and changes in reproductive hormones; a cross-sectional study among 1221 young Danish men. BMJ Open 2014, 4, e005462.
  63. Barrett, P.; Imamura, F.; Brage, S.; Griffin, S.; Wareham, N.; Forouhi, N. Sociodemographic, lifestyle and behavioural factors associated with consumption of sweetened beverages among adults in Cambridgeshire, UK: The Fenland Study. Public Health Nutr. 2017, 20, 2766–2777.
  64. Ricci, E.; Vigano, P.; Cipriani, S.; Somigliana, E.; Chiaffarino, F.; Bulfoni, A. Coffee and caffeine intake and male infertility: A systematic review. Nutr. J. 2017, 16, 37.
  65. Li, Y.; Lin, H.; Li, Y.; Cao, J. Association between socio-psycho-behavioral factors and male semen quality: Systematic review and meta-analyses. Fertil. Steril. 2011, 95, 116–123.
  66. Jensen, T.K.; Swan, S.H.; Skakkebaek, N.E.; Rasmussen, S.; Jørgensen, N. Caffeine intake and semen quality in a population of 2,554 young Danish men. Am. J. Epidemiol. 2010, 171, 883–891.
  67. Poole, R.; Kennedy, O.J.; Roderick, P.; Fallowfield, J.A.; Hayes, P.C.; Parkes, J. Coffee consumption and health: Umbrella review of meta-analyses of multiple health outcomes. BMJ 2018, 22, 359.
  68. Joo, K.; Kwon, Y.; Myung, S.; Kim, T. The Effects of Smoking and Alcohol Intake on Sperm Quality: Light and Transmission Electron Microscopy Findings. J. Int. Med. Res. 2012, 40, 2327–2335.
  69. Martini, A.C.; Molina, R.I.; Estofán, D.; Senestrari, D.; de Cuneo, M.F.; Ruiz, R.D. Effects of alcohol and cigarette consumption on human seminal quality. Fertil. Steril. 2014, 82, 374–377.
  70. Ricci, E.; Al Beitawi, S.; Cipriani, S.; Candiani, M.; Chiaffarino, F.; Viganò, P.; Noli, S.; Parazzini, F. Semen quality and alcohol intake: A systematic review and meta-analysis. Reprod. Bio. Med. Online 2017, 34, 38–47.
  71. Sermondade, N.; Elloumi, H.; Berthaut, I.; Mathieu, E.; Delarouzière, V.; Ravel, C.; Mandelbaum, J. Progressive alcohol-induced sperm alterations leading to spermatogenic arrest, which was reversed after alcohol withdrawal. Reprod. Bio. Med. Online 2010, 20, 324–327.
  72. Smits, R.M.; Mackenzie-Proctor, R.; Yazdani, A.; Stankiewicz, M.T.; Jordan, V.; Showell, M.G. Antioxidants for male subfertility. Cochrane Database Syst. Rev. 2019, 3.
  73. Cochrane Library. About Cochrane Library. 2021. Available online: https://www.cochranelibrary.com/about/about-cochrane-library (accessed on 14 November 2020).
  74. Critical Appraisal Skills Programme (CASP). Systematic Review Checklist. 2018. Available online: https://casp-uk.b-cdn.net/wp-content/uploads/2018/01/CASP-Systematic-Review-Checklist_2018.pdf (accessed on 21 February 2021).
  75. Majzoub, A.; Agarwal, A. Systematic review of antioxidant types and doses in male infertility: Benefits on semen parameters, advanced sperm function, assisted reproduction and live-birth rate. Ar. J. Urol. 2018, 16, 113–124.
  76. Levitas, E.; Lunenfeld, E.; Weisz, N.; Friger, M.; Har-Vardi, I. Seasonal variations of human sperm cells among 6455 semen samples: A plausible explanation of a seasonal birth pattern. Am. J. Obstet. Gynecol. 2013, 208, 406.e1–406.e6.
  77. Hjollund, N.H.; Storgaard, L.; Ernst, E.; Bonde, J.P.; Olsen, J. The relation between daily activities and scrotal temperature. Reprod. Toxicol. 2002, 16, 209–214.
  78. Bujan, L.; Daudin, M.; Charlet, J.P.; Thonneau, P.; Mieusset, R. Increase in scrotal temperature in car drivers. Hum. Reprod. 2000, 15, 1355–1357.
  79. Rao, M.; Xia, W.; Yang, J.; Hu, L.-X.; Hu, S.-F.; Lei, H.; Wu, Y.-Q.; Zhu, C.-H. Transient scrotal hyperthermia affects human sperm DNA integrity, sperm apoptosis, and sperm protein expression. Andrology 2016, 4, 1054–1063.
  80. Gorpinchenko, I.; Nikitin, O.; Banyra, O.; Shulyak, A. The influence of direct mobile phone radiation on sperm quality. Cent. Eur. J. Urol. 2014, 67, 65–71.
  81. Adams, J.A.; Galloway, T.S.; Mondal, D.; Esteves, S.C.; Mathews, F. Effect of mobile telephones on sperm quality: A systematic review and meta-analysis. Environ. Int. 2014, 70, 106–112.
  82. Avendano, C.; Mata, A.; Sanchez Sarmiento, C.A.; Doncel, G.F. Use of laptop computers connected to internet through Wi-Fi decreases human sperm motility and increases sperm DNA fragmentation. Fertil. Steril. 2012, 97, 39–45.e2.
  83. Mortazavi, S.A.; Taeb, S.; Mortazavi, S.M.; Zarei, S.; Haghani, M.; Habibzadeh, P.; Shojaei-Fard, M.B. The Fundamental Reasons Why Laptop Computers should not be Used on Your Lap. J. Biomed. Phys. Eng. 2016, 6, 279–284.
  84. Kesari, K.K.; Agarwal, A.; Henkel, R. Radiations and male fertility. Reprod. Biol. Endocrinol. 2018, 16, 118.
  85. Matuszczak, E.; Komarowska, M.D.; Debek, W.; Hermanowicz, A. The Impact of Bisphenol A on Fertility, Reproductive System, and Development: A Review of the Literature. Int. J. Endocrinol. 2019, 2019, 4068717.
  86. Cariati, F.; D’Uonno, N.; Borrillo, F.; Iervolino, S.; Galdiero, G.; Tomaiuolo, R. Bisphenol a: An emerging threat to male fertility. Reprod. Bio. Endocrinol. 2019, 17, 6.
  87. Hong, J.; Chen, F.; Wang, X.; Bai, Y.; Zhou, R.; Li, Y.; Chen, L. Exposure of preimplantation embryos to low-dose bisphenol a impairs testes development and suppresses histone acetylation of StAR promoter to reduce production of testosterone in mice. Mol. Cell Endocrinol. 2016, 427, 101–111.
  88. Caporossi, L.; Papaleo, B. Exposure to Bisphenol a and Gender Differences: From Rodents to Humans Evidences and Hypothesis about the Health Effects. J. Xenobio. 2015, 5, 5264.
  89. Almeida, S.; Raposo, A.; Almeida-González, M.; Carrascosa, C. Bisphenol A: Food Exposure and Impact on Human Health. Comp. Rev. Food Sci. Food Saf. 2018, 17, 1503–1517.
  90. Ohore, O.E.; Zhang, S. Endocrine disrupting effects of bisphenol A exposure and recent advances on its removal by water treatment systems. A review. Sci. Afr. 2019, 5, e00135.
  91. Rochester, J.R.; Bolden, A.L. Bisphenol S and F: A Systematic Review and Comparison of the Hormonal Activity of Bisphenol A Substitutes. Environ. Health Perspect. 2015, 123, 643–650.
  92. Meeker, J.D.; Sathyanarayana, S.; Swan, S.H. Phthalates and other additives in plastics: Human exposure and associated health outcomes. Philos. Trans. R. Soc. Ser. B Biol. Sci. 2009, 364, 2097–2113.
  93. Al-Saleh, I.; Coskun, S.; Al-Doush, I.; Al-Rajudi, T.; Abduljabbar, M.; Al-Rouqi, R.; Palawan, H.; Al-Hassan, S. The relationships between urinary phthalate metabolites, reproductive hormones and semen parameters in men attending in vitro fertilization clinic. Sci. Total Environ. 2019, 658, 982–995.
  94. Pant, N.; Shukla, M.; Patel, D.K.; Shukla, Y.; Mathur, N.; Gupta, Y.K.; Saxena, D.K. Correlation of phthalate exposures with semen quality. Toxicol. Appl. Pharm. 2008, 231, 112–116.
  95. Juul, A.; Almstrup, K.; Andersson, A.M.; Jensen, T.K.; Jørgensen, N.; Main, K.M.; Rajpert-De Meyts, E.; Toppari, J.; Skakkebæk, N.E. Possible fetal determinants of male infertility. Nat. Rev. Endocrinol. 2014, 10, 553–562.
  96. Van den Driesche, S.; Kolovos, P.; Platts, S.; Drake, A.J.; Sharpe, R.M. Inter-relationship between testicular dysgenesis and Leydig cell function in the masculinization programming window in the rat. PLoS ONE 2012, 7, e30111.
  97. Radke, E.G.; Braun, J.M.; Meeker, J.D.; Cooper, G.C. Phthalate exposure and male reproductive outcomes: A systematic review of the human epidemiological evidence. Environ. Int. 2018, 121, 764–793.
  98. Aktar, M.W.; Sengupta, D.; Chowdhury, A. Impact of pesticides use in agriculture: Their benefits and hazards. Interdiscip. Toxicol. 2009, 2, 1–12.
  99. Bretveld, R.; Brouwers, M.; Ebisch, I.; Roeleveld, N. Influence of pesticides on male fertility. Scand. J. Work Environ. Health 2007, 33, 13–28.
  100. Lwin, T.Z.; Than, A.A.; Min, A.Z.; Robson, M.G.; Siriwong, W. Effects of pesticide exposure on reproductivity of male groundnut farmers in Kyauk Kan village, Nyaung-U, Mandalay region, Myanmar. Risk Man Healthc. Pol. 2018, 11, 235–241.
  101. Jenardhanan, P.; Panneerselvam, M.; Mathur, P.P. Effects of environmental contaminants on spermatogenesis. Sem. Cell Dev. Biol. 2016, 59, 126–140.
  102. Mehrpour, O.; Karrari, P.; Zamani, N.; Tsatsakis, A.M.; Abdollahi, M. Occupational exposure to pesticides and consequences on male semen and fertility: A review. Toxicol. Lett. 2014, 230, 146–156.
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