The combination matters--distinct impact of lifestyle factors on sperm quality: a study on semen analysis of 1683 patients according to MSOME criteria.
TL;DR: Combinations of adverse lifestyle factors could have a detrimental impact on sperm, not only in terms of motility and sperm count but also in Terms of sperm head vacuolization.
Abstract: Background
Poor sperm quality can negatively affect embryonic development and IVF outcome. This study is aimed at investigating the influence of various lifestyle factors on semen quality according to MSOME (motile sperm organelle morphology examination) criteria.
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TL;DR: It is suggested that greater focus on collection of DNA fragmentation and progressive motility in a clinical setting may lead to better patient outcomes during fertility treatments of aging couples, even though sperm concentration did not decline with increasing male age.
257 citations
TL;DR: Results showed that alcohol intake has a detrimental effect on semen volume and normal morphology, and studies evaluating the effect of changes on semen parameters on the reproductive outcomes are needed in advance of providing recommendations regarding alcohol intake other than the advice to avoid heavy alcohol drinking.
Abstract: Alcohol consumption is widespread in the Western world. Some studies have suggested a negative association between alcohol intake and semen quality although others have not confirmed this. MEDLINE and Embase were searched using ‘alcohol intake' OR ‘alcohol consumption' OR ‘alcohol drinking' OR ‘lifestyle' combined with ‘semen quality' OR ‘sperm quality' OR ‘sperm volume' OR ‘sperm concentration' OR ‘sperm motility' for full-length observational articles, published in English. Reference lists of retrieved articles were searched for other pertinent studies. Main outcome measures were sperm parameters, if provided as means (standard deviation or standard error) or as medians (interquartile range). Fifteen cross-sectional studies were included, with 16,395 men enrolled. Main results showed that alcohol intake has a detrimental effect on semen volume (pooled estimate for no/low alcohol consumption 0.25 ml, 95% CI, 0.07 to 0.42) and normal morphology (1.87%, 95% CI, 0.86 to 2.88%). The difference was more marked when comparing occasional versus daily consumers, rather than never versus occasional, suggesting a moderate consumption did not adversely affect semen parameters. Hence, studies evaluating the effect of changes on semen parameters on the reproductive outcomes are needed in advance of providing recommendations regarding alcohol intake other than the advice to avoid heavy alcohol drinking.
125 citations
TL;DR: Severe male factor impairs early embryonic competence in terms of fertilization rate and developmental potential, however, the euploidy rate and implantation potential of the obtained blastocysts are independent from sperm quality.
96 citations
TL;DR: The literature suggests that caffeine intake, possibly through sperm DNA damage, may negatively affect male reproductive function, and well-designed studies are essential to reach a consistent evidence on the effect of caffeine on semen parameters and male fertility.
Abstract: Semen quality, a predictor of male fertility, has been suggested declining worldwide. Among other life style factors, male coffee/caffeine consumption was hypothesized to influence semen parameters, but also sperm DNA integrity. To summarize available evidence, we performed a systematic review of observational studies on the relation between coffee/caffeine intake and parameters of male fertility including sperm ploidy, sperm DNA integrity, semen quality and time to pregnancy. A systematic literature search was performed up to November 2016 (MEDLINE and EMBASE). We included all observational papers that reported the relation between male coffee/caffeine intake and reproductive outcomes: 1. semen parameters, 2. sperm DNA characteristics, 3. fecundability. All pertinent reports were retrieved and the relative reference lists were systematically searched in order to identify any potential additional studies that could be included. We retrieved 28 papers reporting observational information on coffee/caffeine intake and reproductive outcomes. Overall, they included 19,967 men. 1. Semen parameters did not seem affected by caffeine intake, at least caffeine from coffee, tea and cocoa drinks, in most studies. Conversely, other contributions suggested a negative effect of cola-containing beverages and caffeine-containing soft drinks on semen volume, count and concentration. 2. As regards sperm DNA defects, caffeine intake seemed associated with aneuploidy and DNA breaks, but not with other markers of DNA damage. 3. Finally, male coffee drinking was associated to prolonged time to pregnancy in some, but not all, studies. The literature suggests that caffeine intake, possibly through sperm DNA damage, may negatively affect male reproductive function. Evidence from epidemiological studies on semen parameters and fertility is however inconsistent and inconclusive. Well-designed studies with predefined criteria for semen analysis, subject selection, and life style habits definition, are essential to reach a consistent evidence on the effect of caffeine on semen parameters and male fertility.
90 citations
Cites background from "The combination matters--distinct i..."
...Wogatzky, 2012 [39] Mean (SD) Mean (SD) Mean (SD) Mean (SD)...
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...Wogatzky, 2012 [39] Not estimated Cups of coffee per day 204 men out of 1321 drinking coffee had an intake of more than 3 cups of coffee per day....
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...Wogatzky, 2012 [39] Austria 1683 Cross-sectional Fertility clinic: infertile couples Semen variables 40....
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TL;DR: Smoking, coffee/cola/fried foods consumption, and the effects of environmental/sociopsychobehavioral factors act on semen quality are found to be significantly associated with semen quality from the baseline investigation.
61 citations
Cites result from "The combination matters--distinct i..."
...But in other studies, decreased semen quality or its tendency was also observed.(55,56,63) Similar result was found for cola consumption in this study, but lower semen volume and lower total sperm count were found in cola consumers....
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References
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TL;DR: The results suggest that zones without chromatin in the sperm nucleus reflect underlying chromosomal or DNA defects in severe teratozoospermic men, and should be considered in the evaluation of male fertility.
Abstract: Sperm morphology has consistently been the best indicator of male fertility. Transmission electron microscopy currently provides the most information on the subcellular details of sperm structure. Recently, assessment of sperm DNA damage has been employed to assess fertility potential. The purpose of this work was to link sperm DNA damage, evaluated by an intercalated fluorescent dye, with the structural characteristics of sperm. Conventional semen analysis was performed on samples from men undergoing fertility evaluation. Thirty men were evaluated and assigned to three subgroups based on strict criteria for sperm morphology: normal morphology (>14% normal forms), intermediate morphology (5-14% normal forms), and poor morphology (<5% normal forms). By quantifying acridine orange-positive cells and ultrastructural sperm defects, we found that the poor morphology pattern group showed a positive association between sperm carrying damaged DNA and the percentage of sperm nucleus with vacuoles (P = 0.01). No statistically significant correlations were established in other ultrastructural characteristics of sperm, including immature chromatin, lytic changes, or abnormal sperm tails. These results suggest that zones without chromatin in the sperm nucleus reflect underlying chromosomal or DNA defects in severe teratozoospermic men. This association should be considered in the evaluation of male fertility.
33 citations
"The combination matters--distinct i..." refers background in this paper
...Nevertheless, several recent studies demonstrated that nuclear vacuoles were correlated to DNA damage and/or failures in chromatin packaging [20-23]....
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TL;DR: Responses on a lifestyle questionnaire were correlated with results from traditional semen analysis and a newer functional sperm assay, namely, the ability of sperm to bind to a hyaluronan-coated slide.
32 citations
"The combination matters--distinct i..." refers background in this paper
...Over- and underweight is seen as a risk factor for low sperm quality [2,28-30]....
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TL;DR: The research clearly indicated that an association between paternal age and autism in offspring can be detected in most populations and is not an artifact of confounding by maternal age or of pooling across birth cohorts.
Abstract: King et al.1 addressed 2 questions using data from the California Department of Developmental Services. The first concerned possible bias in estimating the association between parental age and autism as a result of pooling data across birth years. In their analysis, pooling caused a “reversal paradox” for paternal age—that is, the association between paternal age and autism was substantially inflated in pooled data. On this basis, they argued that the relation between paternal age and autism has been overestimated in previous research.
We, however, do not agree with this conclusion. Previous studies have considered birth years and the effects of pooling data. Birth year is often included as a confounder in the statistical models, and data by birth year are often inspected by researchers to check for such possible pooling artifacts.2–6 In fact, a recent study by Grether et al.5 used the same California data source as King et al. and found no evidence for an inflated paternal-age effect when pooling data. For every 10-year increase in paternal age the pooled odds ratio (OR) for autism was 1.22 (95% confidence interval [CI]=1.18, 1.26). The equivalent OR for individual years was lower than was the pooled OR in 7 of the 14 individual years and higher in 6 (Table 2 in Grether et al.5). These results suggested that bias, if it exists, is only minimal. Furthermore, the research clearly indicated that an association between paternal age and autism in offspring can be detected in most populations and is not an artifact of confounding by maternal age or of pooling across birth cohorts.
The Maneki Neko (literally “Beckoning Cat”) is a common Asian sculpture, often made of ceramic, which is believed to bring good luck to the owner. The sculpture depicts a cat (traditionally a Japenese Bobtail) beckoning with an upright paw, and is usually displayed—many times at the entrance—in shops, restaurants, pachinko parlors, and other businesses. In the design of the sculptures, a raised right paw supposedly attracts money, while a raised left paw attracts customers. Image from Punchstock.com. Printed with permission.
The second question that King et al. addressed is the relative importance of paternal or maternal age. The authors used a statistical method of decomposition—about which we have some qualms—to examine this. However, is it really important whether the association with autism is stronger for paternal or for maternal age? Is there a “competition” between the two? At this point, an abundance of large and well-designed studies have demonstrated that advancing maternal and paternal age are associated with autism. One can draw different conclusions about their relative importance depending upon the perspective adopted. For example, men can and often do conceive at much later ages than can women, broadening the paternal age range. So, even if 10 years of maternal age confers greater risk than does 10 years of paternal age, the oldest men carry greater risk than do the oldest women (Table 1 in Grether et al.5).
Regardless of the relative importance of paternal and maternal age, it is noteworthy that so many credible epidemiologic studies (including that conducted by King et al.) have now confirmed that paternal and maternal age at birth are related to autism risk. The evidence is substantial enough to justify a search for the underlying mechanisms. Genomic alterations could be involved in either the case of men or of women,7 as could other factors. All possible mechanisms can and should be studied in both human and animal models.8
32 citations
"The combination matters--distinct i..." refers result in this paper
...In concordance to these findings, it could be further demonstrated by several studies that advanced paternal age results in a higher risk of schizophrenia, autism, bipolar disorders or impaired neurocognitive capability in their offspring [32-35], indicating that sperm quality substantially decreases during the aging process....
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27 citations
"The combination matters--distinct i..." refers background in this paper
...Schnall was the first to describe nuclear vacuoles in human spermatozoa as small, non-membrane bound cavities of irregular outline distributed at random throughout the condensed chromatin in 1952 [45]....
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TL;DR: APA at conception appears to be a risk factor for schizophrenia in offspring of fathers older than 35 years, and two main hypotheses could explain these results.
Abstract: BACKGROUND: Schizophrenia is an aetiologically heterogeneous syndrome, with a strong genetic component. Despite a reduced fertility in this disorder, its prevalence is maintained and could be explained by de novo genetic mutations. Advanced paternal age (APA) is a major source of new mutations in human beings and could thus be associated with an increased risk of developing schizophrenia in offspring. New mutations related to APA have been implicated as a cause of sporadic cases in several autosomal dominant diseases and also in neurodevelopmental diseases, autism, intellectual disabilities, and social functioning. The aim of the present study was to summarize the results of studies investigating the role of APA, and to discuss some interpretations. METHODS: All relevant studies were identified through the National Library of Medicine (PubMed(®) database). Keywords used for research were "age" and "schizophrenia" linked to "paternal or father". We have identified and analysed eight cohort studies, five case-control studies, two meta-analyses, and one review concerning different father's mutations potentially transmitted, two studies comparing paternal age at conception between sporadic versus familial cases of schizophrenia. All studies selected have been published between 2000 and 2009. RESULTS: After controlling for several confounding factors including maternal age, the relative risk of schizophrenia increased from 1.84 to 4.62 in offspring of fathers with an older age of fatherhood. Mother's age showed no significant effects after adjusting for paternal age. There was a significant association between paternal age and risk of developing schizophrenia, there was a weaker association with psychosis. DISCUSSION: The results of these different studies are confirmed by two recent meta-analyses which found an increased risk of schizophrenia in offspring of fathers older than 35 years. Two main hypotheses could explain these results. The first one is based on the presence of new mutations in the spermatogonia, possibly because of accumulating replication errors in spermatogonial cell lines. This hypothesis is confirmed by Malaspina et al. (2002) [19], who found that patients without a family history of schizophrenia had significantly older fathers than probands with a positive family history of schizophrenia. However, this result has not been confirmed by other studies, and paternal age effect could be also explained by a mechanism called imprinting, which is a form of gene regulation. The second hypothesis is based on the fact that fathers with schizophrenia spectrum personality disorder, known to be genetically related to schizophrenia, could have an advanced age at conception. However, regarding this hypothesis, advanced maternal age at conception should be a risk factor for schizophrenia, and this is not the case. Thus, the first hypothesis seems more plausible than the second. APA has been identified as a risk factor for other psychiatric disorders such as autism, bipolar disorder, obsessive-compulsive disorder, and phobia, and thus seems to be a non-specific risk factor. Furthermore, its association with impaired neurocognitive outcomes during infancy and childhood in normal populations raises the question of the phenotype linked to APA. CONCLUSION: APA at conception appears to be a risk factor for schizophrenia. This risk factor probably interacts with genetic factors in a gene-environment interaction. To date, there is no validated cut-off at which the risk is significantly increased in offspring. In the future, studies could benefit from analyzing the phenotype related to APA.
22 citations