The number of eggs in a woman’s ovaries could tell a lot more than just how fertile she is. It may provide a window onto how fast her cells are ageing and, in particular, reflect her risk of developing heart disease.

Women are born with all of their eggs and, throughout their life, the number they have declines. The onset of menopause is triggered by this decline.

. Women who experience it early – before the age of 46 – are .

Several factors that coincide with menopause compound this risk, including a shift in the type of cholesterol the body produces, the redistribution of body fat and increased blood pressure. The drop in oestrogen levels is also thought to play a role as the hormone helps keeps blood vessels elastic. But at the University of California, San Francisco, wondered if the increased risk to women who experience early menopause might have a more fundamental cause. “Perhaps women who go through menopause early are intrinsically aging at a different rate,” says Cedars.

Telling telomeres

To find out, Cedars’ team took blood samples from 1100 non-menopausal women aged 25 to 45 and measured their amount of anti-Müllerian hormone (AMH), an indicator of how many eggs are in the ovaries. They confirmed the number of eggs by counting the pockets of fluid, called follicles, around each egg using an ultrasound.

To measure the women’s biological age, the researchers looked at the length of telomeres in their white blood cells. Telomeres are the dangly bits at the end of chromosomes that shorten every time a cell divides. Their length is considered a measure of cellular age.

Between three and five years later, 250 of the women came back so researchers could calculate their risk of developing heart disease in the next decade – known as their . This takes account of risk factors such as cholesterol levels, blood pressure and body weight.

As expected, the team found that women with lower egg counts had higher Framingham scores, but they also had shorter telomeres. Previous studies have suggested that shorter telomeres are linked with heart disease, dementia and cancer, and also with a shorter lifespan. So women with fewer eggs may also be at higher risk of other age-related diseases, although epidemiological studies will be needed to bolster this link.

Early warning

“We think the ovary may be more sensitive to the processes of aging,” says Cedars, making it like a canary in a coal mine for a general state of accelerated aging.

“It is a very promising hypothesis that reproductive ageing could serve as a window into cardiovascular health and the cellular aging process,” says , an epidemiologist at Harvard School of Public Health in Boston, Massachusetts.

Confirming that number of eggs, as well as age at menopause, is associated with risk of cardiovascular disease is important because heart disease is the . Women are often diagnosed later than men and also tend to have a worse prognosis after being diagnosed, so finding ways to identify those at higher risk is crucial, says Cedars. Many women undergo AMH testing for fertility purposes and those with low egg counts could be monitored for cardiovascular health and advised to make lifestyle changes at a relatively young age, she says.

The researchers presented their findings this week at the in Honolulu, Hawaii.

Whence the female orgasm? After 40 years of debate evolutionary biologists are no closer to deciding whether it evolved to give women a reproductive boost, or whether it is simply a by-product of male orgasm evolution. The latest attempt to settle the dispute involves quizzing some 10,000 twins and pairs of siblings on their sexual habits.

Some evolutionary biologists reckon the female orgasm is adaptive and possibly influences mate choice, strengthens pair bonds or indirectly helps to suck sperm into the uterus. Others argue that women have orgasms for the same reason that men have nipples – being highly adaptive in one sex, the traits tag along for the ride in the other.

at the University of Queensland, Australia, and Pekka Santtila at Abo Akademi University in Turku, Finland, think they can help to settle the question. If female orgasm is a simple by-product of male orgasm, the duo argue, then similar genes would underlie orgasmic function in both men and women. As a consequence, opposite-sex twins and siblings will share more similarities in their susceptibility to orgasm – “orgasmability” as Zietsch calls it – than pairs of unrelated people.

Timing’s everything

To measure this orgasmability, the researchers used survey data from just under 5000 sets of identical and non-identical twins and pairs of regular siblings. The questionnaire asked about the time to orgasm in men and the frequency and ease of orgasm in women.

In keeping with previous findings, Zietsch and Santtila found that same-sex identical twins had more orgasmic similarity than same-sex non-identical twins and siblings, showing that genes do play a role in orgasmic function and apparently providing some evidence that the by-product scenario might be correct.

However, contrary to the expectations of the by-product scenario, the two researchers found that opposite-sex twins and siblings had virtually no correlation in orgasmability.

Premature extrapolation

“This indicates that the genes that influence orgasmic function in men are not the same as those in women,” says Zietsch. In other words, male and female orgasm evolved through different genetic routes, and the by-product hypothesis is incorrect.

Those who favour the by-product hypothesis think such a firm conclusion is premature. at Emory University in Atlanta, Georgia, points out that the study measured different things in men and women – timing to orgasm versus likelihood of orgasm – and so a correlation would be unlikely. Zietsch counters that different measures were necessary because of the different nature of male and female orgasm.

“Of course, it’s possible that different questions would reveal different results,” says , a behavioural anthropologist at Pennsylvania State University in University Park, who places himself in the adaptive camp. “But this study certainly isn’t helping the by-product theory.”

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AS HUMANS migrated out of Africa around 50,000 years ago and moved across the planet, evolution may have latched onto a gene linked to risk-taking and adventurousness.

The idea, first put forward by , was originally met with scepticism. Now of Harvard University and Paul Butler of Boston University have shown that a link between two versions of a specific gene and ancient migration patterns stands up to rigorous analysis.

The DRD4 gene codes for a dopamine receptor in the brain. It exists in several versions, or alleles, and studies have shown that people tend to have slightly different personality traits depending on which they have. The 4R allele, for instance, is associated with being even-tempered, reflective and prudent. The less common 7R and 2R versions have been linked to impulsive and exploratory behaviour, risk-taking and the ability to shrug off new situations. Matthews and Butler think that migrants with these versions were better able to deal with dangerous, fluctuating situations and more likely to survive and reproduce under those conditions.

They looked at the frequency of 7R and 2R in 18 indigenous populations spread along the routes humans took from Africa to Europe, Asia and the Americas. The further away from Africa they were, the more likely they were to have either of these two versions (American Journal of Physical Anthropology, ).

The problem with Chen’s 1999 study was that populations can share alleles simply by chance, which might create the illusion of a link between, say, distance travelled and certain alleles. To overcome this, Matthews and Butler modelled how alleles randomly show up in populations. They discovered that the distribution of 7R and 2R is not random, and were able to demonstrate a statistically significant link between the alleles and migration.

The study suggests that some small portion of the behaviours that characterise populations may be down to genetics, and that cultural actions like mass migration can modify our genes, says Matthews.

Marcus Munafò, at the University of Bristol, UK, cautions that variations in the DRD4 gene are numerous and complex, making its exact behavioural effects hard to pin down. But he agrees that it is likely that some differences in behaviour have been generated by genetic selection.

Researchers are beginning to play with the idea that our culture could be influencing evolution, says of the University of California, Irvine. He has shown that 7R arose as a rare mutation 40,000 to 50,000 years ago, after we left Africa, then spread rapidly in human populations. The 2R allele is a modified version that arose in Asia less than 10,000 years ago.

He has also shown that people diagnosed with attention deficit hyperactivity disorder are twice as likely to have the 7R allele. He thinks some of what we consider ADHD symptoms, like rapidly shifting focus and quick movements, are actually survival traits that were selected for during our migration out of Africa.

Newly hatched sea turtles can sense their longitudinal position – something that took sailors hundreds of years and many lost ships to figure out. Surprisingly, they do so using the Earth’s magnetic field.

Recently, it was discovered that a handful of species – including older sea turtles and migratory birds – seem able to perceive longitude. But it was unclear what cues they could be using.

The Earth’s magnetic field, which animals can use to gauge latitude, was considered an unlikely candidate because of how little it varies in the east-west direction around the globe.

However, in certain parts of the world at the same latitude there are subtle differences in the intensity and angle of the magnetic field. Could these be used by animals to figure out longitude?

One such area is in the Atlantic Ocean, where Puerto Rico in the western Atlantic and the Cape Verde Islands in the eastern Atlantic have the same latitude but different longitudes. In between these locations is the .

Loggerhead sea turtles (Caretta caretta) in Florida navigate the North Atlantic Gyre during their five to 10 year migration around the Atlantic Ocean. During this trip the turtles manage to avoid areas where they would get swept up by other currents and ejected out of the gyre.

Staying put

, and colleagues at the University of North Carolina in Chapel Hill wanted to find out if a knowledge of their longitude helped the turtles stay in the gyre.

To do this, the team placed newly hatched turtles in a circular tank equipped with a magnetic field generator. They tethered each turtle to a rotating arm to measure its swimming direction, and exposed it to a magnetic field simulating that at Puerto Rico or the Cape Verde Islands.

In both cases the turtles tended to swim in a direction that would put them back into the gyre. “They were aiming for ocean currents that would carry them home,” says Putman. Since these were hatchlings that had never been in the ocean, the response must be inherited, he says.

“Their nervous system may be hardwired for this,” says , a behavioural physiologist at Virginia Tech in Blacksburg. Turtles that swim the right way in a given magnetic field are more likely to make it home and reproduce.

How the turtles sense the magnetic field is still unknown, but of the Russian Academy of Sciences in Rybachy thinks they probably have organs similar to the magnetoreceptors found in the upper beaks of migratory birds. His team has preliminary data showing these receptors allow the birds to sense their position based on a magnetic map, much like the turtles seem able to do.

Journal locations

LEARNING and memory problems have been reversed in mice with a syndrome that mimics Down’s.

Catherine Spong and colleagues at the National Institutes of Health in Bethesda, Maryland, found they could prevent developmental problems in mice engineered to have Down’s syndrome by injecting their mothers with two proteins, called NAP and SAL, while they were still in the womb. This treatment would carry many risks for humans, so the team wondered whether the proteins might also help adult mice.

Spong’s team engineered mice to have an extra chromosome 16, which causes similar problems to those caused by an extra chromosome 21 in humans, the trigger for Down’s (see picture). The mice then had to find a submerged platform in a water maze using visual cues. Down’s mice usually take twice as long to find the platform as healthy mice. However, after four days of oral treatment with NAP and SAL, the Down’s mice learned to navigate the maze just as easily as normal mice.

NAP and SAL are fragments of proteins normally produced by glial cells – brain cells that provide nourishment to neurons. We know that glial cells malfunction in people with Down’s. Mice treated with the proteins had markers of healthy glial function that were missing in the untreated Down’s mice.

In a second experiment, the team investigated whether the treatment caused changes in chemicals known to be involved in “long-term potentiation” (LTP) – a type of brain activity key to memory formation. People and mice with Down’s have decreased levels of many chemicals involved in this process. However, treated mice appeared to have increased levels of a receptor called NR2B that is responsible for initiating LTP (). , co-director of Stanford University’s Down Syndrome Research Center in California, says this study makes one thing clear: “Learning disabilities and mental retardations that were considered permanent are treatable.”

If you have the face of a fighter but can’t handle yourself, you’ll be made to suffer. And the same will happen if you really are tough but don’t look the part. Yes – wasps don’t like it when they meet a faker.

When female fight it out for nest dominance, they can judge each other’s fighting ability through facial patterns: those with more fragmented patterns are tougher.

It is a situation that seems ripe for cheating. Any mutation giving a weaker wasp a tougher-looking face should spread through the population like wildfire – and yet they don’t.

To figure out what keeps wasps honest, of the University of Michigan in Ann Arbor and colleagues used paint to make weaker wasps look more fearsome, then pitted them against a rival they had never met before.

The rivals submitted at first, but then seemed to change their minds and became aggressive. In fact they gave the cheaters more of a pounding than they gave undisguised wasps, with more incidents of intense aggression, such as biting and mounting, perhaps in an attempt to confirm the cheaters’ true abilities.

Power potion

In a contrasting experiment, the team used hormones to artificially enhance the fighting prowess of weak wasps, making them stronger than their faces indicated. These wasps also had a hard time. Despite their boosted powers, their rivals refused to submit to them.

The results show that wasps with any kind of mismatch between facial pattern and behaviour get punished by their peers, says Tibbetts, which explains why they haven’t evolved a strategy of lying and cheating to get to the top.

Journal reference: , DOI: 10.1016/j.cub.2010.07.042

Junk food may seem like an addictive drug because it is. In rats, at least, too much fatty food raises the threshold for feelings of satisfaction, sparking a cycle of compulsive overeating.

In people, addictive drugs such as heroin and cocaine desensitise the brain by raising the threshold of “reward” activity that is needed to feel satisfied: more drug is needed to achieve the same effect.

and colleagues at the Scripps Research Institute in Jupiter, Florida, wondered if a diet rich in high-calorie, fatty food might also cause desensitisation and lead to obesity.

They used electrodes to measure the sensitivity of rats’ brains to reward activity. Some ate normal rat food while others had limited or unlimited access to junk foods, tasty to both rats and humans. After 40 days, the brains of those that ate junk freely were less sensitive to reward activity than those in the other groups. They were also obese.

Compulsive eaters

To see if these rats would display compulsive eating in the face of negative consequences – a telltale sign of addiction – all the rats were taught that a flash of light led to a painful electric shock.

Rather than try to avoid the shock when the light came on, as the rats with limited or no access to junk food did, “addicted” rats just kept on eating. “We see the same thing in animals with extended access to cocaine,” says Kenny. Like drug-addicted humans, the obese rats also had fewer receptors for the reward chemical dopamine.

The term “food addiction” is slowly becoming accepted in the field of psychiatry, says , an addiction biologist at the University of Cincinnati in Ohio.

“Once we start to consider obesity and pathological overeating as a psychiatric illness we’re going to move a lot closer towards understanding how to come up with therapies or treatments,” he says.

, a neuroscientist at Boston University, is not surprised that an excess of tasty food might “short-circuit” the brain’s reward sensing system. “In western societies, we are observing a sudden increase in food availability. We didn’t evolve to survive under these conditions,” he says.

Journal reference: , DOI: 10.1523/jneurosci.6107-09.2010

It is still unknown if the protein plays a similar role in people. But the finding is intriguing because the natural process of memory decay remains shrouded in mystery. “We know very, very little about what causes normal forgetting,” says , a neurobiologist at the University of California, Irvine, who was not involved in the new work.

If the protein does play a similar role in humans, it could lead to new techniques for either enhancing or erasing memory. Until now approaches to erasing unwanted memories have largely focussed on interfering with the laying-down of memories, rather than our natural ability to forget.

Flies, forget

After learning that some humans with cognitive disabilities have mutations in genes that control the activity of a protein called Rac, and his colleagues at Cold Spring Harbor Laboratory in New York reasoned that the protein might be involved in memory.

They tested this idea in fruit flies by using genetic engineering to enhance or repress the activity of Rac in the parts of the flies’ brains associated with short-term memory. Then they measured how quickly the flies’ memories seemed to disappear.

The flies were taught to associate a certain smell with an electric shock. Those with enhanced Rac activity forgot the association faster than normal flies, and those with suppressed activity retained the memory longer. “A memory that was supposed to disappear after a few hours lasted for more than 24 hours,” says Zhong.

The researchers also investigated what happens to processes that would normally speed up forgetfulness, including new odour associations designed to either distract or conflict with the original odour associations. They found that lowered Rac activity also caused rats to hold on to their original memories longer when faced with these new associations.

Head eraser

If this mechanism holds true in mammals, it could shed light on the molecular basis of forgetting in humans.

To that end, Zhong is looking at Rac activity in people with schizophrenia, who also have unusually good memories. If their Rac activity is lower than in people with normal memory capability, this might suggest the protein’s ability to melt memories away carries over into people.

His team is also testing to see if Rac might influence the retention of long-term memories in flies. “We believe this forgetting mechanism might be universal, that it could erase any kind of memory,” he says.

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Instead, generosity – or the desire for fairness – seems automatic and arises from activation in a brain area that controls intuition and emotion.

Neuropsychologists define “prosocial” people as those who prefer to share and share alike, and “individualists” as those who are primarily concerned with maximising their own gain.

Inequality aversion

According to one theory, the difference between these two groups is that prosocial people actively suppress their selfish tendencies with the help of their prefrontal cortex. But of Tamagawa University in Tokyo, Japan wondered if some people might instead have an automatic aversion to inequality.

Haruno, along with of University College London used functional MRI to scan the brains of 25 prosocial people and 14 individualists (presorted using a standard behavioral test) while they rated their preference for a series of money distributions between themselves and a hypothetical other person. As expected, the prosocial group preferred even splits while the individualists favoured distributions where they got the most money.

Active amygdala

A less predictable finding was that the only brain region that differed in activity between the two groups was the amygdala. When presented with unfair money distributions the activity in the amygdala increased significantly in prosocial people but not in the individualists. “And the more they disliked the split, the more activity you saw in this region,” says Frith.

“The amygdala tends to respond automatically, without thought, or even without awareness,” says Frith. Combined with the fact that there was no difference in activity in the prefrontal cortex – responsible for suppressing urges – this suggested that the suppression theory might not be borne out.

To further test if the prosocial aversion to unfairness was automatic, the researchers repeated the test, this time giving the participants a memory task to complete at the same time as they rated the splits.

They found that the prosocials’ brains still reacted to the unfair distributions, even when the parts of their brain responsible for deliberative processes were taken up by other tasks, suggesting they were not suppressing selfish desires.

Knee-jerk morality

, a neuroeconomist at the University of Antwerp, Belgium, says the results fit with her own, as yet unpublished, data showing that prosocials seem to be driven by an automatic sense of morality. “So far, all our behavioural and fMRI experiments confirm that prosocials are intrinsically motivated to cooperate,” she says.

Haruno will next try to figure out how this difference in the activity of the amygdala arises. It’s partly genetic, but also likely influenced by a person’s environment, he says, particularly the social interactions during childhood. He says it is interesting to think there might be ways to promote this activity to “realise a more prosocial society.”

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