Modifiable and non-modifiable risk factors for poor sperm morphology.

Are common lifestyle factors associated with poor sperm morphology? Common lifestyle choices make little contribution to the risk of poor sperm morphology. Although many studies have claimed that men's lifestyle can affect sperm morphology, the evidence is weak with studies often underpowered and poorly controlled. Unmatched case-referent study with 318 cases and 1652 referents. Cases had poor sperm morphology (<4% normal forms based on 200 sperm assessed). Exposures included self-reported exposures to alcohol, tobacco, recreational drugs as well as occupational and other factors. Eligible men, aged 18 years or above, were part of a couple who had been attempting conception without success following at least 12 months of unprotected intercourse and also had no knowledge of any semen analysis before being enrolled. They were recruited from 14 fertility clinics across the UK during a 37-month period from 1 January 1999. Risk factors for poor sperm morphology, after adjustment for centre and other risk factors, included: (i) sample production in summer [odds ratio (OR) = 1.99, 95% confidence interval (CI) 1.43-2.72]; and (ii) use of cannabis in the 3 months prior to sample collection in men aged ≤30 years (OR = 1.94, 95% CI 1.05-3.60). Men who produced a sample after 6 days abstinence were less likely to be a case (OR = 0.64, 95% CI 0.43-0.95). No significant association was found with body mass index, type of underwear, smoking or alcohol consumption or having a history of mumps. This suggests that an individual's lifestyle has very little impact on sperm morphology and that delaying assisted conception to make changes to lifestyle is unlikely to enhance conception. Data were collected blind to outcome and so exposure information should not have been subject to reporting bias. Less than half the men attending the various clinics met the study eligibility criteria and among those who did, two out of five did not participate. It is not known whether any of those who refused to take part did so because they had a lifestyle which they did not want subjected to investigation. Although the power of the study was sufficient to draw conclusions about common lifestyle choices, this is not the case for exposures that were rare or poorly reported. All participating clinics saw patients at no cost (under the UK National Health Service) and the study population may differ from those in countries without such provision. Even within the UK, low-income couples may choose not to undertake any investigation believing that they would subsequently be unable to afford treatment. Since a computer performed the measurements of sperm morphology, these results may not be comparable with studies where sperm morphology was assessed by other methods. The study was funded by the UK Health and Safety Executive, the UK Department of Environment, Transport and the Regions, the UK Department of Health (Grant Code DoH 1216760) and the European Chemical Industry Council (grant code EMSG19). No competing interests declared.

Pacey AA ，Povey AC ，Clyma JA ，McNamee R ，Moore HD ，Baillie H ，Cherry NM ，Participating Centres of Chaps-UK ... -  《-》

Modifiable and non-modifiable risk factors for poor semen quality: a case-referent study.

Povey AC ，Clyma JA ，McNamee R ，Moore HD ，Baillie H ，Pacey AA ，Cherry NM ，Participating Centres of Chaps-uk ... -  《-》

Body mass index in relation to semen quality and reproductive hormones in New Zealand men: a cross-sectional study in fertility clinics.

Macdonald AA ，Stewart AW ，Farquhar CM 《-》

Risk of childhood mortality in family members of men with poor semen quality.

What is the familial childhood mortality in first-degree (FDR) and second-degree relatives (SDR) of patients undergoing semen analysis (SA)? The relationship between infertility and congenital malformations (CM) in offspring is complex, with an increased risk of death due to CM in FDR, but not SDR, of men with lower semen parameters. Semen quality is an established predictor of men's somatic health. We can gain a better understanding of possible genetic or environmental determinants of the infertility phenotype by exploring familial aggregation of childhood mortality in relatives of men with poor semen quality. Retrospective cohort study from the Subfertility, Health and Assisted Reproduction study (cohort compiled 1996-2011) linked with patient/familial information from the Utah Population Database (UPDB). Index cases included a clinic-referred sample of 12 889 men who underwent SA and had adequate familial and follow-up data in the UPDB. Parameters of semen quality included: semen concentration, sperm count, motility, total motile count, sperm head morphology, sperm tail morphology and vitality. SA data were collected from two tertiary medical center andrology laboratories that have captured ~90% of all SA performed in Utah since 2004. Age- and sex-matched fertile controls were selected to create the comparison group for determining risk of childhood death (to age 20 years) in family members. A total of 79 750 siblings and 160 016 aunts/uncles were used to investigate the familial aggregation of childhood mortality. The main outcome was childhood mortality in FDR and SDR of men with SA and their matched controls. All-cause and cause-specific Cox proportional hazard models were used to test the association between semen quality and childhood mortality in family members. Cause-specific models were considered for cancer and CM. In the cohort of men with SA, there were 406 (1.0%) deaths in FDR and 772 (1.1%) deaths in SDR due to any cause. There was no significant difference in the risk of all-cause childhood mortality between the relatives of men with SA and the fertile control group [hazard ratio (HR)Female = 1.08, 95% CI = 0.88, 1.32; HRMale = 0.88, 95% CI = 0.75, 1.04]. We found no association between semen quality and risk for childhood cancer mortality in FDR or SDR (HRFDR = 0.98, 95% CI = 0.62, 1.54; HRSDR = 1.12, 95% CI = 0.83, 1.50). The FDR of men with SA and fertile controls were followed on average for 19.71 and 19.73 years, respectively. During this period of follow-up, FDR of men with SA had an unadjusted 40% relative risk of increased CM-related death. After stratifying by semen parameters and adjusting for birth year, we found FDR of men with worse semen quality, and notably azoospermic men (HR = 2.69, 95% CI = 1.24,5.84), were at higher risk of CM-related death. A large proportion of men with SA in the study had normal semen parameters. It is important to note that these men themselves may not be subfertile, but they were subfertile at the couple level (i.e. the female partner may be infertile). In addition, care is needed when interpreting our results, as we do not have semen measures on our sample of fertile men. Second, we were unable to include potential confounders such as medical comorbidities, smoking status, or environmental exposures. Third, men with SA were seen at the University of Utah or Intermountain Health Care clinics for a fertility evaluation thereby suggesting a more select population. Fourth, we chose to categorize morphology into equally distributed quartiles as a response to the fact that the World Health Organization threshold for normal motility changed multiple times during our study period. Lastly, we do not know the proportion of female partners with diagnosed infertility. We chose not to subcategorize each infertile male by infertile diagnosis because our goal was to understand how semen parameters influenced familial childhood mortality. We are not the first study to show a relationship between fertility and CMs. Children conceived through ART may be at higher risk of birth defects, however it is not known if the relationship is causal or if there is some underlying factor linking infertility and birth outcomes. This study provides further evidence that the increased risk of congenital birth defects may not be due to the ART, but rather genetic or environmental factors that link the two outcomes. We encourage further research in order to confirm a relationship between semen quality and increased risk for CM. This work was supported by the National Institutes of Health - National Institute of Aging [Grant numbers 1R21AG036938-01, 2R01 AG022095 and 1K12HD085852-01]. Authors have no competing interests to disclose. Not applicable.

Hanson HA ，Mayer EN ，Anderson RE ，Aston KI ，Carrell DT ，Berger J ，Lowrance WT ，Smith KR ，Hotaling JM ... -  《-》

Many women undergoing fertility treatment make poor lifestyle choices that may affect treatment outcome.

What are the lifestyle choices and dietary aspects of women about to undergo fertility treatment in New Zealand? A considerable proportion of women about to undergo fertility treatment make poor lifestyle choices, including the consumption of alcohol and caffeine. Women undergoing fertility treatment are highly motivated to achieve pregnancy, but there are relatively few published data on their lifestyle, lifestyle changes or dietary aspects. This was a cross-sectional study of 250 women aged 20-43 years, taking place between March 2010 and August 2011. Women about to undergo IVF or ICSI treatment in two large fertility clinics in Auckland and Hamilton, New Zealand. Lifestyle and dietary intake questionnaires were individually administered once to each participant 35 days (SD = 22) prior to fertility treatment initiation. Outcome measures included incidence of smoking, consumption of alcohol and caffeinated beverages, BMI, detailed intake of dietary supplements and fertility treatment success. Consumption of certain nutrient supplements was compared with the general female New Zealand population. There were high rates of alcohol (50.8%) and caffeine (86.8%) consumption. Most women (82.8%) reported at least one lifestyle change in preparation for fertility treatment, but less than half of women who consumed alcohol regularly reduced their intake and 60% did not change consumption of caffeinated beverages. Similarly, the majority of women did not change their exercise levels (64.4%) or BMI (83.6%) ahead of fertility treatment. Coffee intake appeared unrelated to treatment outcome, but women who consumed caffeinated herbal tea (36.4% of the study population consumed green tea) had lower odds of becoming pregnant (odds ratio, OR 0.52; P = 0.041 versus those not consuming caffeinated herbal tea). Women who abstained from drinking or reduced alcohol intake had twice the odds of becoming pregnant than those who maintained their drinking habits prior to fertility treatment (OR 2.27; P = 0.049). While 93.2% of women took a folic acid supplement, 16.8% had an inadequate intake compared with the current New Zealand prenatal recommendation of 800 mcg/day. Women who held a university degree or higher qualification had twice the odds of becoming pregnant as women with lower levels of education (OR 2.08; P = 0.017), though this finding appeared to be unrelated to lifestyle or dietary habits. The study involved self-reported behaviours that might have been misrepresented by respondents. In addition, our questionnaires covered the period following the first clinical assessment but ∼5 weeks prior to fertility treatment initiation, so that we cannot ascertain whether dietary intakes and lifestyle choices persisted over the course of treatment itself. Many women about to undergo fertility treatment make poor lifestyle choices that may negatively affect their chances of becoming pregnant. These findings may be more widely applicable to other women attempting to become pregnant. Specific advice for women regarding healthy lifestyle choices while undergoing fertility treatment is warranted. A.A.G. received financial support from Abbott Nutrition Research & Development Asia-Pacific Center; J.C.P. is a shareholder of Fertility Associates; the other authors have no financial or non-financial conflicts of interest to disclose.

Gormack AA ，Peek JC ，Derraik JG ，Gluckman PD ，Young NL ，Cutfield WS ... -  《-》