Past research has associated stress with a number of health problems, including heart disease, asthma, obesity and depression. Now, a new study suggests stress can reduce sperm and semen quality, which could have implications for male fertility.
According to the American Society for Reproductive Medicine, in around 40% ofinfertilecouples the male partner is the sole cause or contributing cause of infertility.
The main cause of male infertility is sperm abnormalities, including low sperm production or misshapen or immobile sperm. Medical conditions – such asundescended testiclesor ejaculation problems – can lead to sperm abnormalities, as well as health and lifestyle factors.
In this latest study – published in the journalFertility and Sterilityand led by researchers from Columbia University’s Mailman School of Public Health in New York, NY, and Rutgers School of Public Health in Piscataway, NJ – the team investigated whetherstressmay affect sperm and semen quality.
Life stress ‘led to lower semen quality’
To reach their findings, the researchers assessed 193 men aged 38 to 49 between 2005 and 2008. All men were a part of the Study of the Environment and Reproduction at the Kaiser Foundation Health Plan in Oakland, CA.
Men who experienced two or more stressful life events in the past year had lower sperm quality than men who did not experience any stressful life events, according to researchers.
As part of the study, the men were required to complete a series of tests that measured levels of stress, including that from the workplace, stressful life events and overall perceived stress.
They were also required to provide semen samples. Using standard fertility testing methods, researchers from the University of California, Davis, analyzed semen concentration, and sperm shape (morphology) and movement (motility) in each sample.
The researchers found that men who experienced two or more stressful life events in the past year had a lower percentage of sperm motility and a lower percentage of sperm of normal morphology, compared with men who did not experience any stressful life events. They note this finding remained even after accounting for other factors that may influence semen quality, such as age, other health problems and history of reproductive health problems.
Although workplace stress did not directly affect semen quality in the men, the researchers found that those who experienced job strains had lower levels of the hormonetestosteronein their semen, which could affect reproductive health.
In addition, they found that regardless of the levels of stress experienced, men who were unemployed had lower semen quality than those who were employed.
How can stress affect semen quality?
Although the researchers are unable to pinpoint exactly how stress affects the quality of semen, they do present some theories.
They say stress could activate the release of glucocorticoids – steroid hormones that affect the metabolism ofcarbohydrates, fats and proteins – which could reduce testosterone levels and sperm production.
Furthermore, they say stress could trigger oxidative stress – physiological stress on the body caused by damage from unneutralized free radicals – which has been associated with semen quality and fertility.
Commenting on the findings, first study author Teresa Janevic, PhD, an assistant professor at Rutgers School of Public Health, says:
“Stress has long been identified as having an influence on health. Our research suggests that men’s reproductive health may also be affected by their social environment.”
The researchers note that this is the first study to use subjective and objective measures of stress and, as a result, find links with reduced semen quality.
In what is deemed the “most comprehensive global study to date,” researchers have found that over the past 3 decades, there has been a “startling” increase in rates of obesity worldwide, with no significant decline in any country.
A team of international researchers, led by Prof. Emmanuela Gakidou of the Institute for Health Metrics and Evaluation at the University of Washington, recently published their findings inThe Lancet.
For their study, the team conducted a comprehensive review of surveys, reports and scientific literature looking at overweight and obesity prevalence among adults aged 20 years or older and children ages 2-19 years between 1980 and 2013. Data was drawn from 188 countries over all 21 regions of the world.
Overweight was defined as a body mass index (BMI) of 25 kg/m2or higher and obese was defined as a BMI of 30 kg/m2or higher.
Significantly high adult obesity increases in the US
The researchers found that over the past 33 years, worldwide overweight and obesity rates among adults have increased by 27.5%, while such rates among children and adolescents have increased by 47.1%. Collectively, the number of overweight and obese people worldwide has increased from 857 million in 1980 to 2.1 billion in 2013. Of these, 671 million are obese.
The biggest increases in overweight and obesity rates occurred between 1992 and 2002, primarily among adults ages 20-40.
The researchers found that over the past 33 years, worldwide overweight and obesity rates among adults have increased by 27.5%.
At present, more than half of the obese worldwide population reside in only 10 countries, including the US, China, Russia, Brazil, Mexico, Egypt, Germany, Pakistan and Indonesia.
The team found that 62% of the world’s obese individuals live in developed countries. The US had the highest increases in prevalence of adult obesity – a third of the population are now obese. This is followed by Australia – where 28% of men and 30% of women are obese – and the UK – where around a quarter of the adult population are obese.
Developed countries also saw very high increases in overweight and obesity rates among children. Rates increased from 17% to 24% between 1980 and 2013 among boys, and from 16% to 23% among girls in the same period.
Significantly high rates of overweight and obesity were reached in Tonga, where obesity levels among both men and women are over 50%. More than 50% of women are obese in Kuwait, Libya, Qatar, the Pacific Islands of Kiribati, Federated States of Micronesia and Samoa.
Among men, those living in the US, New Zealand, Bahrain, Kuwait and Saudi Arabia saw the highest increase in obesity levels over the past 3 decades, as did women living in Egypt, Oman, Saudi Arabia, Bahrain and Honduras.
But it is not all bad news. The researchers note that in developed countries, the rate of increase in adult obesity has slowed over the past 8 years. Furthermore, the team says that recent birth cohorts indicate a slower weight gain, compared with previous birth cohorts.
Prof. Gakidou says that unlike other major global health risks, such as smoking, obesity rates are not falling. But he says the statistics do offer some hope:
“Our findings show that increases in the prevalence of obesity have been substantial, widespread, and have arisen over a short time. However, there is some evidence of a plateau in adult obesity rates that provides some hope that the epidemic might have peaked in some developed countries and that populations in other countries might not reach the very high rates of more than 40% reported in some developing countries.”
WHO obesity campaign ‘ambitious and unlikely to be attained’
Last year, members of the World Health Organization (WHO) launched a campaign to stop increases in obesity by 2025. But the research team says that based on these latest findings, this target is “very ambitious and unlikely to be attained.”
The team says that in order to reduce rates of obesity worldwide and reach this target set by WHO, “urgent global leadership” is needed to implement strategies that discourage excessive caloric intake, physical inactivity and promotion of food consumption.
In an editorial linked to the study, Prof. Klim McPherson of Oxford University in the UK agrees. He says:
“An appropriate rebalancing of the primal needs of humans with food availability is essential, which would entail curtailing many aspects of production and marketing for food industries. To prevent unsustainable health consequences, BMI needs to return to what it was 30 years ago.”
The researchers note that there are some limitations to their study. For example, they included surveys that collected self-reported weights and heights. Although they corrected such data as best they could, this may have influenced figures.
They also point out that the statistics are based on BMI, but this measure does account for body variations across different ethnic groups.
WHOEVER first described the UK and US as two nations divided by a common language probably wasn’t thinking about a molecule called N-acetyl-p-aminophenol. But there is possibly no better example of the cultural divide. Brits call it paracetamol; Americans call it acetaminophen. And attitudes towards the painkiller are equally divergent.
People in the UK are aware that a paracetamol overdose can kill. That goes back to 1998, when the government restricted the number of tablets that could be bought in one purchase and ran an information campaign explaining the change. The measures prevent an estimated 1000 deaths a year.
US awareness is much lower. When investigative journalism group Propublicarevealed last yearthat 1500 Americans die from accidental overdoses annually, it was big news.
That would be an overreaction. As the British experience shows, people can understand and act on nuanced messages. Paracetamol doesn’t need to be banned: people simply need to be made aware of its limitations and dangers so that they can make the right call.
On 18 September, the people of Scotland will vote on whether their country should become independent of the UK. This article is part of our “Four futures for an independent Scotland” special report, looking at the choices a newly independent Scotland could make
AS DUSK falls, Grangemouth starts to glow. Cloaked in clouds of steam and lit by flares like giant candles, Scotland’s biggest oil refinery has a strange beauty. Situated roughly halfway between Edinburgh and Glasgow on the Firth of Forth, the 700-hectare petrochemical complex is a vital hub of UK oil production. Should Scotland vote for independence, it will be one of the new government’s key assets.
According to the industry, there are between15 and 24 billion barrelsof recoverable oil and gas left under the North Sea. About 42bn barrels have been extracted since production began there in 1967. Because prices have risen, 24bn barrels could be worth £1.5 trillion – more than the value of all the oil and gas extracted so far. “That gives us one of the best financial safety nets of any country in the world,” theScottish government says. If the UK’s Trident nuclear submarine base moves from the river Clyde after independence – as Scottish nationalists say it must – then prospecting off the west coast could begin too. It is currently banned in case it interferes with naval operations there.
There will be a few other tricky issues to resolve, like where the lines are drawn to demarcate which fields belong to an independent Scotland and which to the UK, and how the £35-£50bn cost of decommissioning old oil rigs would be divided up.
Ultimately the plan is to emulate Norway, and invest at least some of the created wealth for the future. Scotland’s first minister, Alex Salmond, has promised to put aside about £1bn a year, with the aim of generating a £30bn oil fund over a generation.
Norway’s equivalent, theNorwegian Pension Fund Global, has amassed over£500bnfrom oil and gas revenues since it was set up in 1990. It is the world’s largest sovereign wealth fund and owns 1.3 per cent of all the world’s listed companies.
According to Bjørn Vidar Lerøen, an adviser to Norway’s industry body, Norwegian Oil and Gas Association, there was political consensus on the fund from the start. “The oil belongs to the people and revenues from oil production shall be used to build a better society,” he says. The Norwegian fund has a wide-ranging ethical policy that forbids investments in more than 60 companies involved in tobacco, arms, environmental or human rights abuses. Ironically, it is now reviewing whether to disinvest from fossil fuel companies because of the damage they do to the climate.
But there is one way in which Scotland would probably not be able to copy Norway: the Norwegian government’s 67 per cent ownership of the oil company Statoil. “To try to nationalise companies would not be politically possible either in Scotland or the UK,” saysUisdean Vass, an oil specialist at legal firm Bond Dickinson in Aberdeen.
Perhaps the biggest conundrum, though, is the climate. According to WWF Scotland, burning 24bn barrels of oil and gas could put more then 10bn tonnes of carbon dioxide into the atmosphere – more than 120 times Scotland’s current annual emissions. “The science is clear,” says the environmental group’s director,Lang Banks. “The planet certainly can’t afford to allow all the oil left in the North Sea to be burned.”
First the bad news. Humans are driving species to extinction at around 1000 times the natural rate, at the top of the range of an earlier estimate. We also don’t know how many species we can afford to lose.
Now the good news. Armed with your smartphone, you can help conservationists save them.
The new estimate of the global rate of extinction comes fromStuart Pimmof Duke University in Durham, North Carolina, and colleagues. It updates a calculation Pimm’s team released in 1995, that human activities were driving species out of existence at 100 to 1000 times the background rate (Science, doi.org/fq2sfs).
It turns out that Pimm’s earlier calculations both underestimated the rate at which species are now disappearing, and overestimated the background rate over the past 10 to 20 million years.
“Twenty years ago we simply didn’t have the breadth of underlying data with 70,000 species assessments in hand,” says team memberThomas Brooksof the IUCN in Gland, Switzerland.
By studying animals’ DNA, biologists have also created family trees for many groups of animals, allowing them to calculate when new species emerged. On average, it seems each vertebrate species gives rise to a new species once every 10 million years.
It’s hard to measure the natural rate of extinction, but there is a workaround. Before we started destroying habitats, new species seem to have been appearing faster than old ones disappeared. That means the natural extinction rate cannot be higher than the rate at which they were forming, says Pimm.
For the most part, the higher estimate of the modern extinction rate is not caused by any acceleration in extinctions since 1995. One exception is an increase in threats to amphibians, partly due tothe global spread of the killer chytrid fungus.
Still, it seems unlikely that extinctions running at 1000 times the background rate can be sustained for long. “You can be sure that there will be a price to be paid,” says Brooks.
Pimm’s team has also compileddetailed global maps of biodiversity, showing the numbers of threatened species and total species richness in a global grid consisting of squares 10 kilometres across.
Such maps can help conservationists decide what to do.
For instance, Pimm and his colleagueClinton Jenkinsof the Institute for Ecological Research in Nazaré Paulista, Brazil, noticed high numbers of threatened species on Brazil’s Atlantic coast. Local forests were being cleared for cattle ranching. So they are working with a Brazilian group, the Golden Lion Tamarin Association, tobuy land and reconnect isolated forest fragments.
But conservationists need more data, and you can help, through projects likeiNaturalist. Users share photos of the creatures they see viaiPhoneandAndroidapps, and experts identify them. “Right now, someone is posting an observation about every 30 seconds,” says co-directorScott Loarieof the California Academy of Sciences in San Francisco.
Now it seems diclofenac has the same effect on eagles, which also feed on cattle carcasses. Yet the drug has recently been approved for use in Spain and Italy, home to some of Europe’s biggest populations of vultures and eagles.
In February 2012, two dead steppe eagles (Aquila nipalensis) turned up in a dump for cattle carcasses near Bikaner, in Rajasthan, India. Anil Sharma and his colleagues from theIndian Veterinary Research Institutein Izatnagar found telltale signs of kidney failure such as uric acid crystals.
Kidney failure is also typically seen in vultures that have diedafter eating cattle treated with diclofenac. Sharma also found traces of diclofenac in the eagles’ tissues, at the same levels seen in killed vultures.
This does not prove that diclofenac killed the eagles, says Sharma, but this is how the drug kills vultures. If the drug is to blame, it is bad news for steppe eagles, many of which winter in India and rely on cattle carcasses.
Steppe eagles may not be the only birds at risk. At least five of the eight species in theGypsgenus aresusceptible to diclofenac. If the steppe eagle is susceptible, the rest of its genusAquilacould be too.
There are 14Aquilaspecies including several more in south Asia, a few in Africa, and Europe’sgoldenandSpanish imperialeagles. All scavenge cattle carcasses.
And all are now exposed. Diclofenac was registered for use in cattle in Italy and Spain in November 2013. It has been sold in Africa for veterinary use since 2007, and conservation organisation BirdLife International saysthe drug is already affecting vulture populations there.
The Vulture Conservation Foundation (VCF)wants diclofenac banned in Europeand has set up apetition. But they say officials are only offering to change the drug’s label, to recommend it not be given to cattle that are likely to be eaten by vultures.
Europe has spent millions of euros to bring back vultures and eagles, and in 2012 authorised farmers to leave dead animals out for the birds to eat. ” We do not think that a warning will ensure the safety of vultures and eagles,” says Sharma’s colleagueToby Galliganof the Royal Society for the Protection of Birds in Sandy, UK.
Such carcasses may pose a particular threat to eagles. They range widely, particularly golden eagles, whereas EuropeanGypsvultures are restricted to limited feeding places. Toxicologists have calculated thatthe liver of one treated cow can kill 15 vultures, and eagles are smaller so probably need less to die.
In a new study published in the journalCell Metabolism, researchers from the Karolinska Institutet in Sweden have identified a gene that they believe is responsible for the development of unhealthy human body fat. The team says the gene could be a risk factor for insulin resistance and type 2 diabetes.
Adipose tissue, commonly known as body fat, is loose connective tissue mainly consisting of fat cells called adipocytes. These fat cells are important for storing and releasing energy in the body.
Humans have two types of body fat; white fat (white adipose tissue) and brown fat (brown adipose tissue). In recent years, brown fat has been deemed the “good” fat. Its main function is to generate body heat. Scientists have found that people of a healthy weight are more likely to have brown fat and, when stimulated through exercise, it can burn calories.
White fat, on the other hand, is believed to be “bad” fat. Those who are overweight or obese tend to accumulate excessive amounts of white fat.
According to the research team, an increase in the size or number of fat cells can lead to an overproduction of white adipose tissue. They note that past research has associated a low number of large fat cells – known as hypertrophy – with development of type 2diabetes.
In this latest study, the researchers found that a gene called EBF1 may be closely linked to hypertrophy.
Low EBF1 expression ‘promotes hypertrophy and insulin resistance’
To reach their findings, the team collected adipose tissue samples from participants who had either small or large fat cells.
Researchers say the EBF1 gene may be responsible for the development of white adipose tissue – or “bad fat – in humans.
They found that subjects with large fat cells had much lower EBF1 expression in their adipose tissue, compared with those who had small fat cells. They also had altered lipid movement in their blood and insulin resistance.
Insulin resistance is the inability of the body’s cells to effectively respond to the hormone insulin when blood glucose levels increase, usually after a meal. The team explains that insulin resistance is an important risk factor for diabetes in people who have hypertrophy. Those with insulin resistance tend to have higher circulating glucose and lipid levels in the blood.
To investigate their findings further, the researchers analyzed mice that had been genetically modified to produce lower levels of the EBF1 gene.
The mice developed hypertrophy in their adipose tissue and showed higher lipid movement from fat cells. When the mice were fed a high-fat diet, they also developed insulin resistance.
The researchers found that the EBF1 gene acts a “transcription factor.” It binds to a protein that controls other genes and regulates fat cell formation and metabolic function.
Study co-leader Prof. Peter Arner says the team’s findings may open the doors to new treatments for type 2 diabetes:
“Our findings represent an important step forward in the understanding of how adipose tissue links to the development of metabolic disease.
This is the first time someone has identified a gene that may cause malfunctioning adipose tissue in man. In the future, it might be possible to develop drugs that improve EBF1 function in adipose tissue, which could be used to treat type 2 diabetes.”