Rob Knell considers the relationship of monogamy and STDs @ConversationUK

How sexually transmitted diseases might have driven the evolution of monogamy

Rob Knell, Queen Mary University of London

Exactly why so many humans choose monogamous pair bonds over juggling multiple partners has long been a mystery to scientists. After all, having several partners at the same time should lead to more offspring – an outcome you’d think evolution would favour. Now a new study has linked the phenomenon to sexually transmitted diseases, arguing that monogamy could have evolved because it offered protection against the threat of infection.

Monogamy is, of course, the norm in Western societies. But there are many cultures where a husband can have more than one wife (polygyny) or, less commonly, a wife can have more than one husband (polyandry). This diversity of human mating systems is also hard to explain. What we do know, however, is that many hunter-gatherer societies, living in small groups, were most often polygynous (and many remaining groups still are). But with the rise of agriculture, societies tended to become more complex – and less polygynous. In the most strictly monogamous societies, there was often a social punishment for polygynists, either informally or, as in many modern societies, through a legal system.

Many explanations for this evolution have been put forward, including changes to the way that women chose their partners, such as being faithful to men who invested in provisioning for them. Another possibility is that groups of monogamists may have performed better than groups of polygynists. But the new research adds a further option: could an increased risk of infection from sexually transmitted infections associated with polygyny have contributed to – or even driven – the overall move from polygyny to monogamy?

Sexually transmitted diseases have been infecting humans for a long time. Prior to modern medicine, they also often caused significant harm – especially to the reproductive system. Clearly, these diseases infect polygynists more than monogamists, and it has been argued that when a polygynist and a serial monogamist have the same number of partners overall, the polygynist is more likely to pick up a dose of something nasty than the monogamist. According to computer modelling, this is because contact networks are more connected when you have concurrent partners than when you have serial partner change. Either way, overall, these effects could have had a big enough impact on the well-being of polygynists to allow monogamous individuals to take over a population.

The challenges of modelling

It’s certainly a good argument. But it’s hard to assess how likely it is to be true. This is because we know very little about the risk of sexually transmitted diseases in hunter-gatherer societies or historical societies transitioning to agriculture. This is a common problem in science: we can only make progress when we can test an idea, but plausible ideas are sometimes very hard to evaluate without massive effort.

One option in these cases is to do your experiment in the form of a computer simulation. This is what the researchers behind the new study did, modelling the impact of a bacterial sexually transmitted disease similar to gonorrhoea or chlamydia. Their results strongly back the hypothesis that such diseases could have triggered monogamy.

In their model, sexually transmitted diseases tend to “fade out” from small groups such as polygynist hunter-gatherers. This occurs because of random chance events that are more likely to be important in small groups, such as all the infected people suddenly getting better or dying. In larger, agricultural groups, however, such fade-out is much less likely, so sexually transmitted diseases tend to persist, damaging the health and reducing the birth rates of polygynists while allowing monogamists to take over.

What’s more, the monogamists that are most likely to take over a group for a long period are those that follow a “punishment strategy”, which fits with what we observe in many societies today.

So is the puzzle solved? Not quite yet. Computer simulations are useful and can tell us important things, but they are always limited and necessarily simplify the real world. In this case, for example, the researchers assumed that the disease they were modelling had similar pathological effects on men and women, whereas in reality many sexually transmitted diseases affect women more severely than men, potentially changing the effect of the disease on polygynists.

Further questions are raised by research into sexually transmitted diseases in animals, which hasn’t really found a clear relationship between promiscuity and disease. In fact, computer modelling work focused on animals has found that promiscuous and monogamous individuals can coexist even in the presence of a dangerous disease. What’s more, there are examples of highly promiscuous animals which are heavily infected with sexually transmitted diseases yet carry on regardless (two-spot ladybirds in Continental Europe are one example, believe it or not).

As the researchers themselves point out, there are indeed some challenges associated with this idea. More detailed simulations or better data on sexually transmitted infections in societies where people live in small groups would make the picture clearer. For now, it remains an intriguing and plausible suggestion that we should explore further. Given the continuing threats posed by sexually transmitted diseases today it’s surprising that it’s taken this long for someone to put two and two together and suggest that the advent of monogamy may have served a very practical purpose.

The Conversation

Rob Knell, Senior Lecturer, Queen Mary University of London

This article was originally published on The Conversation. Read the original article.

Measles and Pertussis outbreaks tied to vaccine refusal @NIHDirector #science

Parents have a responsibility not only to their own children, but to their communities—it’s only by achieving a very high level of population immunity that outbreaks can be prevented. Vaccination is particularly crucial for children with cancer and other diseases that cause immunosuppression. They cannot be vaccinated safely, but are at high risk of severe consequences if they are infected—and, thus, they depend on the community’s so-called “herd immunity” for protection against a potentially fatal illness.

While some parents continue to express concern about a possible link between vaccines and autism spectrum disorders, the original report claiming this connection has been debunked and retracted.  A large number of carefully designed follow up studies have been carried out, and the overwhelming weight of scientific evidence shows no evidence for such a link. That’s why it continues to be so important to get the word out to parents: Have your kids vaccinated.

Top 6 #GMO news stories from @GeneticLiteracy #GLPTop6!

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  1. Moms Across America claims GM salmon not kosher, but Jewish law, tradition say otherwise by Stephan Neidenbach

  2. Cellular clock may help improve cancer treatment, forensic science by Nicholas Staropoli

  3. Genetic engineering in Africa: Part 1: Bananas and Cassavas  || Part 2: Cautious embrace of biotechnology by Steven Cerier

  4. Enviro activists reject synbio solution for Indonesian palm oil-orangutan crisis by Nicholas Staropoli

  5. Life without allergies? Detecting genetically-based food allergies at birth by Meredith Knight

  6. Knowledge of genetic risks from personal DNA tests may not help in changing behavior by Arvind Suresh

WHO update on Zika Virus – Focus on neurological disorders

whoCheck out the latest on Zika virus from the World Health Organization – including new information on the potential association of Zika with neurological disorders. WHO has called for intensified research into these associations. See the link for the full report.

The second meeting of the Emergency Committee (EC) convened by the Director-General under the International Health Regulations (2005) (IHR 2005) regarding clusters of microcephaly cases and other neurological disorders in some areas affected by Zika virus was held by teleconference on 8 March 2016, from 13:00 to 16:45 Central European Time.

The WHO Secretariat briefed the Committee on action in implementing the Temporary Recommendations issued by the Director-General on 1 February 2016, and on clusters of microcephaly and Guillain-Barré Syndrome (GBS) that have had a temporal association with Zika virus transmission. The Committee was provided with additional data from observational, comparative and experimental studies on the possible causal association between Zika virus infection, microcephaly and GBS.

Plethora of information on Zika virus from @CDCgov!!

The CDC website has tons of info on Zika virus, both for travelers and others. Definitely check it out for up to date information on cases, and the outbreak itself. Our just for information! Including the infographic below, and about 10 more!!

what-we-know-infographic

How bad is double-dipping?? Paul Dawson explains @US_Conversation

Is double-dipping a food safety problem or just a nasty habit?

Paul Dawson, Clemson University

What do you do when you are left with half a chip in your hand after dipping? Admit it, you’ve wondered whether it’s OK to double dip the chip.

Maybe you’re the sort who dips their chip only once. Maybe you look around the room before loading your half-eaten chip with a bit more dip, hoping that no one will notice.

If you’ve seen that classic episode of Seinfeld, “The Implant,” where George Costanza double-dips a chip at a wake, maybe you’ve wondered if double-dipping is really like “putting your whole mouth right in the dip!

‘You doubled-dipped the chip.’

But is it, really? Can the bacteria in your mouth make it onto the chip then into the dip? Is this habit simply bad manners, or are you actively contaminating communal snacks with your particular germs?

This question intrigued our undergraduate research team at Clemson University, so we designed a series of experiments to find out just what happens when you double-dip. Testing to see if there is bacterial transfer seems straightforward, but there are more subtle questions to be answered. How does the acidity of the dip affect bacteria, and do different dips affect the outcome? Members of the no-double-dipping enforcement squad, prepare to have your worst, most repulsive suspicions confirmed.

Start with a cracker

Presumably some of your mouth’s bacteria transfer to a food when you take a bite. But the question of the day is whether that happens, and if so, how much bacteria makes it from mouth to dip. Students started by comparing bitten versus unbitten crackers, measuring how much bacteria could transfer from the cracker to a cup of water.

We found about 1,000 more bacteria per milliliter of water when crackers were bitten before dipping than solutions where unbitten crackers were dipped.

In a second experiment, students tested bitten and unbitten crackers in water solutions with pH levels typical of food dips (pH levels of 4, 5 and 6, which are all toward the more acidic end of the pH scale). They tested for bacteria right after the bitten and unbitten crackers were dipped, then measured the solutions again two hours later. More acidic solutions tended to lower the bacterial numbers over time.

The time had come to turn our attention to real food.

But what about the dip?

We compared three kinds of dip: salsa, chocolate and cheese dips, which happen to differ in pH and thickness (viscosity). Again, we tested bacterial populations in the dips after already-bitten crackers were dipped, and after dipping with unbitten crackers. We also tested the dips two hours after dipping to see how bacterial populations were growing.

We tested All Natural Tostitos Chunky Hot Salsa (pH 4), Genuine Chocolate Flavor Hershey’s Syrup (pH 5.3) and Fritos Mild Cheddar Flavor Cheese Dip (pH 6.0).

So, how dirty is your dip? We found that in the absence of double-dipping, our foods had no detectable bacteria present. Once subjected to double-dipping, the salsa took on about five times more bacteria (1,000 bacteria/ml of dip) from the bitten chip when compared to chocolate and cheese dips (150-200 bacteria/ml of dip). But two hours after double-dipping, the salsa bacterial numbers dropped to about the same levels as the chocolate and cheese.

After two hours, levels of bacteria in the salsa were similar to levels in the cheese and chocolate dips.
Paul Dawson, Author provided

We can explain these phenomena using some basic food science. Chocolate and cheese dips are both pretty thick. Salsa isn’t as thick. The lower viscosity means that more of the dip touching the bitten cracker falls back into the dipping bowl rather than sticking to the cracker. And as it drops back into the communal container, it brings with it bacteria from the mouth of the double-dipper.

Salsa is also more acidic. After two hours, the acidity of the salsa had killed some of the bacteria (most bacteria don’t like acid). So it’s a combination of viscosity and acidity that will determine how much bacteria gets into the dip from double-dipping. As a side note about party hosting: cheese dip will run out faster than salsa since more of the cheese sticks to the cracker or chip on each dip. That could reduce the chances of people double-dipping. And yes, this is something we discovered during the experiment.

Should I freak out about double-dipping?

Double-dipping can transfer bacteria from mouth to dip, but is this something you need to worry about?

Anywhere from hundreds to thousands of different bacterial types and viruses live in the human oral cavity, most of which are harmless. But some aren’t so good. Pneumonic plague, tuberculosis, influenza virus, Legionnaires’ disease and severe acute respiratory syndrome (SARS) are known to spread through saliva, with coughing and sneezing aerosolizing up to 1,000 and 3,600 bacterial cells per minute. These tiny germ-containing droplets from a cough or a sneeze can settle on surfaces such as desks and doorknobs. Germs can be spread when a person touches a contaminated surface and then touches their eyes, nose or mouth.

That’s why the Centers for Disease Control and Prevention strongly recommends covering the mouth and nose when coughing and sneezing to prevent spreading “serious respiratory illnesses like influenza, respiratory syncytial virus (RSV), whooping cough, and severe acute respiratory syndrome (SARS).” With that in mind, there may be a concern over the spread of oral bacteria from person to person thanks to double-dipping. And a person doesn’t have to be sick to pass on germs.

One of the most infamous examples of spreading disease while being asymptomatic is household cook Mary Mallon (Typhoid Mary), who spread typhoid to numerous families in 19th-century New England during food preparation. Science has left unanswered whether she was tasting the food as she went along and, in effect, double-dipping. Typhoid Mary is obviously an extreme example, but your fellow dippers might very well be carrying cold or flu germs and passing them right into the bowl you’re about to dig into.

If you detect double-dippers in the midst of a festive gathering, you might want to steer clear of their favored snack. And if you yourself are sick, do the rest of us a favor and don’t double-dip.

The Conversation

Paul Dawson, Professor of Food Science, Clemson University

This article was originally published on The Conversation. Read the original article.