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Author Topic: Tomato compound improves sperm quality  (Read 44 times)
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14 October 2019 - by Jen Willows
A new study has shown that sperm quality but not quantity may be improved by an antioxidant related to the red pigment in tomatoes.
Lycopene is a powerful antioxidant naturally found in tomatoes. It has been previously linked to male fertility, but previous studies lacked a control group, making findings uncertain. Because lycopene is difficult for the human body to absorb, the researchers used the more bioavailable lactolycopene, which was specifically developed as a supplement.
The study was led by Allan Pacey, professor of andrology reproduction, and Dr Liz Williams, a specialist in human nutrition, both at the University of Sheffield and published in the European Journal of Nutrition.
'When we decoded the results, I nearly fell off my chair. The improvement in morphology - the size and shape of the sperm - was dramatic,' said Professor Pacey.
The study looked at sperm in 60 healthy men over 12 weeks. The volunteers, all aged between 19 and 30 were randomly assigned to receive either lactolycopene or a placebo neither the volunteers nor researchers knew which were which.
The volunteers provided sperm samples at the beginning of the experiment, halfway through and at the end of the 12 weeks.
Analysis of the samples revealed that among the men who took lactolycopene the results did not show an increase in numbers of sperm. However, the proportion of sperm that were able to swim fast increased by 40 percent by and the proportion that were a healthy shape and size also increased significantly.
'The next step is to repeat the exercise in men with fertility problems and see if lactolycopene can increase sperm quality for those men and whether it helps couples conceive and avoid invasive fertility treatments,' said Dr Williams.
It is estimated that one in six UK couples are affected by subfertility, and that around 40 percent of these are due to problems with sperm production.
Professor Richard Sharpe from the University of Edinburgh's MRC Centre for Reproductive Health, welcomed the research, calling it a 'methodical small ray of sunshine' in a field where 'our understanding of the causes of poor semen quality (and consequent poor fertility) in men is lamentably bad' which 'explains why there are few if any treatments to offer affected men.'
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Rare genetic quirk twice as common as thought
14 October 2019 - by Laura Riggall
Inheriting two copies of a chromosome from a single parent is more common than previously thought, according to a new study.
The phenomenon, called uniparental disomy (UPD), occurs due to an error in meiosis, the process that forms eggs and sperm. Because of the error, the affected individual inherits both copies of a chromosome from one parent only. Documented cases of UPD are rare, with only around 3300 recorded in total worldwide.
Using a dataset of 4,400,363 participants from 23andMe and another of 431,094 UK BioBank participants, US researchers identified 675 instances of UPD. To determine how often UPD occurs in the general population, they also looked at the rate of UPD among trios of parents and children, finding 105 cases within 214,915 trios in the 23andMe dataset. This amounts to roughly one in every 2000 births, compared with a previous estimate of one in every 3500.
'So that's about twice as common as was previously thought,' lead author Dr Priyanka Nakka told Gizmodo.
Existing research has linked UPD to developmental disabilities and a greater risk of cancer. However, while the study found some association between the UPD of chromosome 22 and the risk of autism, it identified no significant associations with deleterious traits in the 23andMe database.
'Our work challenges the typical view that errors in recombination are strongly deleterious, showing that even in extreme cases where individuals are homozygous for an entire chromosome, those individuals can be, to the best of our knowledge, phenotypically normal and healthy,' wrote senior study author Dr Fah Sathirapongsasuti at 23andMe, and colleagues, in their paper.
'We found that a little surprising,' said Dr Nakka, who did the study while at Brown University in Providence, Rhode Island, and 23andMe. 'Because in the past, UPD is always been written about as this genetic phenomenon that can cause imprinting disorders or unmask deleterious mutations.'
To identify UPD in such large datasets, the researchers developed a machine-learning classifier that assessed the degree of homozygosity (possessing two identical alleles of at least one gene).
The classifier struggled, however, with data from populations with higher-than-average levels of homozygosity, such as Ashkenazi Jewish, Middle Eastern, and South Asian populations. This was acknowledged by Dr Nakka and her co-authors, who suggested that individuals who have so far signed up for 23andMe aren't completely representative of the general population.
Nevertheless, the study has provided a clearer picture of UPD. 'I was really excited to see this paper,' Dr Wendy Robinson, a medical geneticist at the University of British Columbia in Vancouver, Canada, who was not involved in the study, told The Atlantic. She had suspected that UPD occurs in healthy people more often than reported.
The study was published in the American Journal of Human Genetics.
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