Author Archives: Dr Colin Holloway

Why the clitoris doesn’t get the attention it deserves – and why this matters

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Why the clitoris doesn’t get the attention it deserves – and why this matters

March 10, 2016 6.00am AEDT

Don’t know much about the clitoris? It’s probably not your fault. Jen/Flickr, CC BY-SA

Did you know the clitoris is a large and complex organ? If not, it’s probably not your fault: in anatomical textbooks, few words and diagrams are devoted to understanding the clitoris. Most label the very small portion of the organ visible on diagrams of the vulva, when in fact it’s almost entirely under the skin.

Studies of historical anatomical textbooks have shown that depictions of the clitoris were significantly limited and often omitted completely from the mid-19th into the 20th century.

During these times there were ideologies and subsequent theories relating to women’s bodies that likely encouraged and sustained censorship of the clitoris. For instance, there was Freud’s now defunct theory that clitoral stimulation was a sign of sexual immaturity and neurosis. Women were also taught not to enjoy sex; women had sex for reproductive purposes, while men had sex for pleasure.

These fallacies led to the neglect of the clitoris in research, literature and the public domain.

Although more recent research and feminist lobbying have improved the quality of information on the clitoris in current textbooks, most texts are still brief. These include minimal information, or information only on the external portion of the clitoris (the glans). This brevity has impacts on health care for women with clitoral and related pain.

This figure, published in 2014, depicts the clitoris as only the external clitoral glans and prepuce (hood).

What is the clitoris?

The clitoris lies at the junction of the labia minora (the inner lips of the vulva), just above the urethra. It is made up of four main parts: the glans, body, two crura and two bulbs. The glans is the only external part of the clitoris and is covered by a hood of skin.

The body, corpora, crura and bulbs of the clitoris are all made up of erectile tissue and converge below the glans. The body of the clitoris is generally 1-2cm wide and 2-4cm long.

Left: the clitoris from an anterior view. All four parts of the clitoris are visible in this view: the glans (external portion), the body, the bulbs and the crura. Right: the clitoris from a side view. Only one crus (plural: crura) and bulb are shown from this view. Note, the clitoris is a tri-planar organ, with each component lying in a different plane to one another. Author provided

The crura extend laterally from the body of the clitoris and are on average around 5-9cm long. The bulbs of the clitoris are generally 3-7cm long and lie between the body, crura and the urethra.

The clitoris is highly innervated, with twice as many nerve endings as the penis, and receives a rich blood supply. This rich blood supply allows the erectile components to swell up, with the body and glans of the clitoris becoming up to three times larger during arousal – and you thought a penile erection was impressive!

The clitoris (left) and penis (right) emerge from the same cells in a zygote. Screenshot/Huffington Post

Foetus genital and reproductive organs are differentiated at six weeks’ gestation. While the clitoris and penis arise from the same group of cells in a zygote, we now know they clearly have different forms and functions.

The penis has an obvious and well-researched role in the reproductive and urinary systems, while the function of the clitoris is usually stated as being purely for pleasure.

However, few studies have actually investigated the function of the clitoris. The close proximity of the clitoris to the urethra and vagina has led to suggestions that it plays a much larger role than sexual pleasure, such as assisting in maintaining immune health.

What we don’t know can hurt us

Censoring the clitoris in textbooks means doctors and other health-care professionals won’t be equipped to treat patients with clitoral concerns. Women are at risk of sexual dysfunction (such as lack of desire or arousal, decreased lubrication, inability to orgasm) from operations on their urinary and reproductive organs. This shows doctors need more in-depth knowledge, and we need further research into understanding the anatomy of the clitoris.

Don’t you forget about me. Towe My/Flickr, CC BY

Because of its delicate yet complex make-up, the clitoris is prone to infections, inflammation and diseases. Some common examples are itching and soreness due to thrush infections, swelling due to bruising or inflammation, and pain of unknown origin (called clitorodynia).

Although it is not often spoken about, clitoral and vulvar pain are very common in women.

Educating patients about their condition can improve pain outcomes. Yet this may be difficult for doctors treating conditions such as clitorodynia, given they may not be receiving adequate information about the clitoris themselves.

On average, one-third of university-aged women are unable to find the clitoris on a diagram. We frequently use synonyms of females’ reproductive organs as derogatory terms (“pussy” to mean weak, “cunt” to mean an unpleasant person) and many women are often not comfortable using anatomically correct terms.

More than 65% of women say they feel uneasy using the terms vagina and vulva. Instead they use code names such as “lady parts”, even when discussing gynaecological issues with their doctors.

Given there is evidence to suggest our sense of body ownership can influence pain, perhaps this lack of body ownership over the clitoris helps to explain why conditions such as clitorodynia are

common

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Starving cancer cells of sugar could be the key to future treatment

Starving cancer cells of sugar could be the key to future treatment

September 24, 2015 2.36am AEST

Is sugar the answer for tackling cancer cells? Flickr/Wellcome Images, CC BY-ND

All the cells in our bodies are programmed to die. As they get older, our cells accumulate toxic molecules that make them sick. In response, they eventually break down and die, clearing the way for new, healthy cells to grow. This “programmed cell death” is a natural and essential part of our wellbeing. Every day, billions of cells die like this in order for the whole organism to continue functioning as it is supposed to.

But as with any programme, errors can occur and injured cells that are supposed to die continue to grow and divide. These damaged cells can eventually become malignant and generate tumours. In order to avoid their programmed cell death in this way, cancer cells reorganise their metabolism so they can cheat death and proliferate indefinitely.

Cancer researchers have known for decades that tumours use a faster metabolism compared to normal cells in our body. One classic example of this is that cancer cells increase their consumption of glucose to fuel their rapid growth and strike against programmed cell death. This means that limiting glucose consumption in cancer cells is becoming an attractive tool for cancer treatments.

A new hope?

You may have seen articles or websites advocating that starving patients of sugar is crucial for getting rid of tumours or that eating less sugar reduces the risk of cancer. The story is not that simple. Cancer cells always find alternatives to fuel their tank of glucose, no matter how little sugar we ingest. There is not a direct connection between eating sugar and getting cancer and it is always advisable to talk to your doctor if you have doubt about your diet.

Chemotherapy – the most common cancer treatment. www.shutterstock.com

Researchers have demonstrated that cancer cells use glucose to generate the building blocks of the cellular compounds needed for rapid tumour growth. They also use it to generate molecules that guard against the toxic accumulation of reactive oxygen species, the cell-damaging molecules that activate programmed cell death. This means that glucose serves as a master protector against cell death.

If the amount of sugar we eat doesn’t affect this process, the question we need to answer is how the cancer cells are instructed to consume more glucose. Who is filling the fuel tank? We have discovered that what allows tumours to evade their natural cause of death in this way is a protein that is overproduced in virtually every human cancer but not in normal cells.

Turbocharged growth

In a recent study published in Nature Communications we showed that cancer cells stimulate the over-production of the protein known as PARP14, enabling them to use glucose to turbocharge their growth and override the natural check of cell death. Using a combination of genetic and molecular biology approaches, we have also demonstrated that inhibiting or reducing levels of PARP14 in cancer cells starves them to death.

The best news is that by comparing cancer tissues (biopsies) from patients that has survived cancer and those that have died, we have found that levels of PARP14 were significantly higher in those patients that have died. This means that levels of PARP14 in cancer tissues could also predict how aggressive the cancer would be and what the chances are of a patient’s survival.

This means that a treatment which could block the protein could represent a significant revolution in the future of cancer treatment. What’s more, unlike traditional chemotherapy and radiotherapy, the use of PARP14 inhibitors would only kill cancer cells and not healthy ones. The next step is to design and generate new drugs that can block this protein and work out how to use them safely in patients.

Benefits of fish oil.

Circulation. 2018 May 17. pii: CIR.0000000000000574. doi: 10.1161/CIR.0000000000000574. [Epub ahead of print]

Seafood Long-Chain n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: A Science Advisory From the American Heart Association.

Abstract

Since the 2002 American Heart Association scientific statement “Fish Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease,” evidence from observational and experimental studies and from randomized controlled trials continues to emerge to further substantiate the beneficial effects of seafood long-chain n-3 polyunsaturated fatty acids and cardiovascular disease. A recent American Heart Association science advisory addressed the specific effect of n-3 polyunsaturated fatty acid supplementation on clinical cardiovascular events. This American Heart Association science advisory extends that review and offers further support to include n-3 polyunsaturated fatty acids from seafood consumption. Several potential mechanisms have been investigated, including antiarrhythmic, anti-inflammatory, hematologic, and endothelial, although for most, longer-term dietary trials of seafood are warranted to substantiate the benefit of seafood as a replacement for other important sources of macronutrients. The present science advisory reviews this evidence and makes a suggestion in the context of the 2015-2020 Dietary Guidelines for Americans and in consideration of other constituents of seafood and the impact on sustainability. We conclude that 1 to 2 seafood meals per week be included to reduce the risk of congestive heart failure, coronary heart disease, ischemic stroke, and sudden cardiac death, especially when seafood replaces the intake of less healthy foods.

Can Cranberry Juice Help Women with UTIs?

Can Cranberry Juice Help Women with UTIs?

Am J Clin Nutr; 2016 Jun; Maki, Kaspar, Curtin, et a

June 14, 2016

The number of clinical urinary tract infection (UTI) episodes in women with a recent history of UTI was lowered with the consumption of a cranberry juice beverage. This according to a double-blind, placebo-controlled clinical trial in which 373 women with a history of recent UTI were assigned to consume a 240 mL serving of cranberry beverage/day (n=185) or a placebo (n=188) beverage for 24 weekends. Primary outcome was a reduction in the total number of clinical UTI events per unit of observation time. Researchers found:

• There were 39 diagnosed episodes of clinical UTI in the cranberry group vs 67 episodes in the placebo group (antibiotic use-adjusted incidence rate ratio, 0.61).

• Clinical UTI with pyuria was also significantly reduced (incidence RR=0.63).

• Time to UTI with culture positively did not differ significantly between groups (HR=0.97).

Citation: Maki KC, Kaspar KL, Khoo C, Derrig LH, Schild AL, Gupta K. Consumption of a cranberry juice beverage lowered the number of clinical urinary tract infection episodes in women with a recent history of urinary tract infection. Am J Clin Nutr. 2016;103:1434-42. doi:10.3945/ajcn.116.130542.

Commentary: Recurrent UTIs are common, with a quarter of young women who have a first UTI experiencing a recurrence within 6 months. Sexual intercourse, spermicide/diaphragm use, and previous UTIs are the strongest risk factors for recurrent UTIs. Various strategies have been used to decrease recurrence, ranging from post-coital voiding, cranberry juice, probiotics, post-coital antibiotics, and daily antibiotic prophylaxis.1 The results of the present study showing that cranberry juice decreases recurrences of UTIs is consistent with the results of a systematic review and meta-analysis that shows an approximate 40% decrease in the incidence of recurrent UTIs with the use of cranberry containing products.2 This study lends further evidence to support using daily cranberry juice for prophylaxis of UTIs in women with multiple UTI recurrences, a simple approach that has the advantage of avoiding issues of antimicrobial resistance associated with antibiotic prophylaxis. —Neil Skolnik, MD

1. Hooton TM, Gupta K. Recurrent UTIs in women. UpToDate. https://www.uptodate.com/contents/recurrent-urinary-tract-infection-in-women?source=search_result&search=uti+prophylaxis&selectedTitle=1%7E150.

2. Wang CH, Fang CC, Chen NC, et al. Cranberry-containing products for prevention of urinary tract infections in susceptible populations: a systemic review and meta-analysis of randomized controlled trials. Arch Intern Med. 2012;172:988–96. doi:10.1001/archinternmed.2012.3004.

When should you take antibiotics?

When should you take antibiotics?

September 8, 2015 1.38pm AEST

The more we take antibiotics, the more likely we are to have superbugs down the line. Brandice Schnabel/Flickr, CC BY-NC-ND

Antibiotic-resistant superbugs are on the rise and we’re being urged to forgo antibiotics wherever possible to limit their spread. But serious bacterial infections can only be dealt with effectively using these drugs.

So when should you take antibiotics? The easy answer, of course, is when your doctor tells you to. But there’s more to it.

We know that rates of bacterial resistance track antibiotic usage rates. So, as a community, the more we take these drugs, the more likely we are to have superbugs down the line. And Australia may face a bleak future in these terms.

Antibiotic myths and facts

The Australian government’s 2015-2019 National Antimicrobial Resistance Strategy highlighted some interesting, if somewhat disturbing, facts:

• a 2014 poll of Australian workers showed 65% believed taking antibiotics would help them recover faster from a cold or flu

• 20% of people expect antibiotics for viral infections, such as a cold or the flu

• nearly 60% of GPs surveyed would prescribe antibiotics to meet patient demands or expectations

• surgical prophylaxis (giving antibiotics before or during surgery to minimise the risk of infection) is used in 41% of cases, which is much higher than the recommended best practice of less than 5%.

Clearly, we still don’t understand that antibiotics won’t kill viruses responsible for the flu and many common colds. And a majority of doctors take a seemingly lackadaisical approach to antibiotic stewardship. It’s no surprise then that the 2013 National Antimicrobial Prescribing Survey showed 30% of antibiotic prescriptions were inappropriate.

Antibiotics are amazing drugs that can prevent serious harm and stop infections becoming fatal. They’re often used for:

• lung infections, which include bacterial pneumonia and pertussis (whooping cough)

• urinary and genital infections, some of which are sexually transmitted

• eye infections (conjunctivitis)

• ear, nose and throat infections (otitis, sinusitis and pharyngitis)

• skin infections (from impetigo in schoolchildren through to more serious diabetic foot ulcers)

• diarrhoea and more serious gut infections, such as those caused by Clostridium difficile.

Antibiotics are often used for serious gut infections, such as those caused by Clostridium difficile. Francisco Bengoa/Flickr, CC BY-NC

In general, a patient will be given antibiotics if her symptoms are severe (a high fever or skin rash, for instance, or inflammation spreading around an infection site); she has a higher risk of complications (such as an elderly patient with suspected pneumonia); or if the infection is persistent.

Getting it right

To prescribe, the doctor makes an educated guess as to what may be causing the infection. This is based on knowledge of what type of bacteria are normally found in these cases and, if available, the patient’s history. But she doesn’t know exactly what type of bug is causing the infection. In the absence of an accurate diagnosis, as well as to minimise potential risk to the patient, a broad-spectrum antibiotic is used to “cover as many bases” as possible.

Until we can develop point-of-care technology that can identify a bug on demand, such broad-spectrum drugs (the grenade approach to bacteria) are a better option for doctors than targeted specific drugs (a sniper against superbugs). But the latter is the better long-term option for the patient and the community, although it may not always work.

One key problem with broad-spectrum “grenade” antibiotics is that they can cause collateral damage by killing a lot of good bacteria. We now know that we have about a kilogram and a half of good bacteria in our guts that help us digest food. They also “crowd out” potential nasty infections caused by bad bacteria.

There are cases where patients on antibiotics end up with diarrhoea, thrush (a vaginal infection caused by Candida that goes wild when protective bacteria are wiped out), or nasty infections, such as Clostridium difficile, that can lead to severe colitis.

And it gets worse: a recent Danish study that followed more than a million patients found an association between frequency of antibiotic use and Type II diabetes, generating considerable media interest. It found people who received more than four courses of the drugs over 15 years were 53% more likely to develop diabetes.

Of course, there’s the cause-effect corollary. People who were already heading towards the disease may simply have been less healthy, more prone to infection, and hence had more visits to the doctor to get antibiotics. The study showed an association between antibiotics and diabetes, not causality.

So where do we stand now? Remember bacterial infections can kill, and antibiotics save lives, so if you’re really feeling crook, go to your doctor and take her advice. But also think twice. If you have a bad cold or think you have the flu, remember this may be due to a viral infection. And using antibiotics could do you more harm than good in the longer term.

The real game changer in all of this will be a “tricorder” diagnostic that can identify a bug on site. With such a technology, a doctor could prescribe the right drug, the first time, in time. So be sensible about using antibiotics and let’s keep our eyes on this prize.

Cooking the books: when that sensational new research finding isn’t all it seems

I get concerned when some patients are very excited about some new treatment/cure/product that sounds like a dream come true for their particular problems. Unfortunately, it is misleading and not true. Some people get quite upset when I point this out to them, as they are so convinced that this will be the answer to their symptoms. I have seen many spurious “cures”come and go over the years, so am naturally sceptical over some of these claims.

 

Cooking the books: when that sensational new research finding isn’t all it seems

November 11, 2015 1.51pm AEDT

Few media reports in the health sphere generate as much attention as those with screaming headlines about a new link between food and cancer.

The level of interest is understandable. It’s estimated that around one in three cancers (approximately 40,000 cases a year in Australia alone) would be avoided if we modified our lifestyle. Along with smoking, obesity, alcohol consumption and sun exposure, diet is one of these modifiable risk factors.

Who could forget the recent scare about cancer risk from processed meats such as bacon? Or an earlier scare about risk from chemical exposure? Imagine the looming panic when the International Agency for Research on Cancer and the World Health Organisation release their upcoming review of evidence linking coffee with cancer.

A common mistake in reporting these findings is to confuse the strength of evidence with the degree of risk.

This week we’ve had an explosion of reports suggesting that “new” research had linked consumption of fried foods to cancer. The primary source of all the fuss appears to be this newspaper report published over the weekend in the United Kingdom, which was subsequently republished worldwide, including by the Herald Sun and Sunday Age in Australia. Numerous derivative reports appeared on TV, radio and online and were shared widely on social media.

But here’s the problem. None of these media reports refer specifically to any new scientific publication.

Evidence in health reporting

I’m deeply sceptical of most medical/health articles in the Sunday papers, with their lifestyle and wellness sections full of barely disguised advertorials. When a quick search of the PubMed or Google Scholar databases didn’t show any new research published on the topic, I decided to dig a little deeper.

The quoted expert, Professor Martin Groonvelt, suggested that media reports were probably referring to this 2014 article he authored for an industry magazine published by the American Oil Chemists’ Society. This is not a peer-reviewed journal – an instant red flag to any scientist.

Peer review is a fundamental, if not imperfect, aspect of science. It acts as a quality-control filter – with experts checking methodology, analysis and interpretation of new research before publication.

Oils and cancer

There is an existing body of peer-reviewed science showing that heating cooking oils (such as frying) can generate compounds with carcinogenic capacity. Among other things, these chemicals can modify DNA, potentially causing mutations that may lead to cancer.

However, there is very little evidence that these compounds can be absorbed into cells in our bodies at levels high enough to have an effect in humans. To a cancer biologist like me, this is a key question that remains unanswered.

There is evidence heating up some oils can cause carcinogenic compounds, but little to show how these can affect human cells in the body. James Jordan/Flickr, CC BY

Hidden agendas

There is another aspect to these reports worth considering. The food industry is huge, with big dollars at stake. We need to be on the lookout for conflicts of interest in the study and reporting of food science.

Many scientists legitimately consult with industry, but these arrangements need to be transparent. On the flipside, a lot of people are making big money from generating fear and panic.

This was highlighted by a recent scare campaign around brain cancer risk from mobile phone use. There is little convincing evidence that mobile phones cause brain cancer, but that didn’t stop a Melbourne doctor generating loads of sensationalist coverage in an attempt to sell magic patches that would apparently reduce radiation.

Existing dietary guidelines already advise that we limit intake of fried food, but ignoring dietary advice seems to be somewhat of an Australian tradition. An occasional reminder is probably justified but to spin this reminder as some kind of new research breakthrough is not necessarily helpful.

There is a real risk that the constant sensationalism will instead generate fatigue. Expert advice and informed choices need to be made on the best available science, and not on sensationalist reports that present as fact something the science doesn’t necessarily support.

Laugh a Little

The history of natural progesterone, the never-ending story.

Most of my patients on Bio-identical hormones would be on the natural progesterone. Many doctors confuse, or mislead, by referring to Progestogens (synthetic) as progesterone. There is a huge difference. The medical profession do not recommend progesterone if you have had a hysterectomy. This makes no sense as progesterone has major benefits to the neurological system of women. See the articles below.
Climacteric. 2018 May 28:1-7. doi: 10.1080/13697137.2018.1462792. [Epub ahead of print]

The history of natural progesterone, the never-ending story.

Author information

1
a Consultant at Besins Healthcare Global , Department of R & D, Scientific & Medical Affairs , Brussels , Belgium.

Abstract

The term progesterone should only be used for the natural hormone produced by the ovaries or included in a registered drug. The modern history of progesterone begins with the first book-length description of the female reproductive system including the corpus luteum and later with the Nobel Prize winner, Adolf Butenandt who took a crucial step when he succeeded in converting pregnanediol into a chemically pure form of progesterone, the corpus luteum hormone. The deficient production of progesterone was shown first to be the cause of the luteal-phase deficiency responsible for infertility and early pregnancy loss due to inadequate secretory transformation of the endometrium. Later, progesterone was confirmed to be the best and safest method of providing luteal-phase support in assisted reproductive technology. Progesterone provides adequate endometrial protection and is suggested to be the optimal progestagen in menopausal hormone therapy in terms of cardiovascular effects, venous thromboembolism, probably stroke and even breast cancer risk. Neuroprotective effects of progesterone have also been demonstrated in several of experimental models including cerebral ischemic stroke and Alzheimer’s disease. Vaginal progesterone was shown to decrease the risk of preterm birth in women with a mid-trimester sonographic short cervix and to improve perinatal outcomes in singleton and twin gestations.

Climacteric. 2018 May 23:1-6. doi: 10.1080/13697137.2018.1463982. [Epub ahead of print]

Non-clinical studies of progesterone.

Author information

1
a Center for Biomedical Research , Population Council , New York , NY , USA.

Abstract

Progesterone is a steroid hormone that is essential for the regulation of reproductive function. Progesterone has been approved for several indications including the treatment of anovulatory menstrual cycles, assisted reproductive technology, contraception during lactation and, when combined with estrogen, for the prevention of endometrial hyperplasia in postmenopausal hormonal therapy. In addition to its role in reproduction, progesterone regulates a number of biologically distinct processes in other tissues, particularly in the nervous system. This physiological hormone is poorly absorbed when administered in a crystalline form and is not active when given orally, unless in micronized form, or from different non-oral delivery systems that allow a more constant delivery rate. A limited number of preclinical studies have been conducted to document the toxicity, carcinogenicity and overall animal safety of progesterone delivered from different formulations, and these rather old studies showed no safety concern. More recently, it has been shown in animal experiments that progesterone, its metabolite allopregnanolone and structurally related progestins have positive effects on neuroregeneration and repair of brain damage, as well as myelin repair. These recent preclinical findings have the potential to accelerate therapeutic translation for multiple unmet neurological needs.

How long does sex normally last?

 

Health Check: how long does sex normally last?

April 4, 2016 1.50pm AEST

Disclosure statement

Brendan Zietsch receives funding from The Australian Research Council.

Partners

University of Queensland provides funding as a member of The Conversation AU.

If you’re a non-scientist, you might have once asked yourself, propped against the bedhead after disappointingly quick intercourse, how long does sex “normally” last?

A scientist, though, would phrase the same question in an almost comically obscure way: What is the mean intravaginal ejaculation latency time?

I know there’s a lot more to sex than putting the penis into the vagina and ejaculating, but the rest is not always easy to define (kissing? Rubbing? Grinding?). To keep things simple and specific, we’ll just focus on the time to ejaculation.

Measuring an average time to ejaculation is not a straightforward matter. What about just asking people how long they take, you say? Well, there are two main problems with this. One is that people are likely to be biased upwards in their time estimates, because it’s socially desirable to say you go long into the night.

The other problem is that people don’t necessarily know how long they go for. Sex isn’t something people normally do while monitoring the bedside clock, and unassisted time estimation may be difficult during a transportative session of love-making.

What does the research say?

The best study we have estimating the average time to ejaculation in the general population involved 500 couples from around the world timing themselves having sex over a four-week period – using a stopwatch.

That is as practically awkward as it sounds: participants pressed “start” at penile penetration and “stop” at ejaculation. You may note this could affect the mood somewhat, and might perhaps not exactly reflect the natural flow of things. But – science is rarely perfect, and this is the best we’ve got.

So what did the researchers find? The most striking result is that there was a huge amount of variation. The average time for each couple (that is, averaged across all the times they had sex) ranged from 33 seconds to 44 minutes. That’s an 80-fold difference.

Yeah, sexy. Matthew/Flickr, CC BY

So it’s clear there’s no one “normal” amount of time to have sex. The average (median, technically) across all couples, though, was 5.4 minutes. This means that if you line up the 500 couples from shortest sex to longest sex, the middle couple goes for an average of 5.4 minutes each time they do it.

There were some interesting secondary results, too. For example, condom use didn’t seem to affect the time, and neither did men’s being circumcised or not, which challenges some conventional wisdom regarding penile sensitivity and its relationship to staying power in the sack.

It didn’t much matter which country the couples came from either – unless they came from Turkey, in which case their sex tended to be significantly shorter (3.7 minutes) than couples from other countries (Netherlands, Spain, the United Kingdom, and the United States). Another surprising finding was that the older the couple, the shorter the sex, contrary to the prevailing wisdom (probably peddled by older men).

Why do we have sex for so long?

As an evolutionary researcher, all this talk of how long sex lasts make me wonder: Why does it last any time at all? All sex really needs to achieve, it seems, is to put sperm into the vagina. Why all the thrusting and bumping? Instead of sliding the penis in and out many hundreds of times per sexual session, why not just put it in once, ejaculate, and then go have a lemonade and get on with the rest of the day?

Despite the ‘in-out’ being fun, does it serve a purpose biologically? from http://www.shutterstock.com

Before you say, Because it’s fun to go in and out!, remember evolution doesn’t care about fun per se – it generally only “designs” things to be enjoyable if they helped our ancestors pass on their genes to future generations. For example, even though we like eating food, we don’t chew each mouthful of it for five minutes just to make the enjoyment last longer. That would be inefficient, and so we’ve evolved to find it gross.

Why we last so long is a pretty complicated question with no clear answer, but a clue may be in the way the penis is shaped. In 2003, researchers showed – using artificial vaginas, artificial penises, and artificial sperm (corn syrup) – that the ridge around the head of the penis actually scoops out pre-existing syrup from the vagina.

What this suggests is that men’s repeated thrusting might function to displace other men’s semen before ejaculating, ensuring their own swimmers have a better chance of reaching the egg first. Incidentally, this could explain why it becomes painful for a man to continue thrusting after ejaculating, since that would risk scooping out his own semen as well.

So what to do with this information? My advice would be to try not to think about it during the throes of passion.

Estrogen protects against MS

Biomed J. 2015 May-Jun;38(3):194-205. doi: 10.4103/2319-4170.158509.

Estrogen-mediated protection of experimental autoimmune encephalomyelitis: Lessons from the dissection of estrogen receptor-signaling in vivo.

Author information

1
INSERM, U1043; CNRS, U5282; Université de Toulouse, Université Paul Sabatier, Centre de Physiopathologie de Toulouse Purpan (CPTP), Toulouse, F-31300, France.

Abstract

A growing body of evidence from basic and clinical studies supports the therapeutic potential of estrogens in multiple sclerosis (MS), originating from the well-established reduction in relapse rates observed among women with MS during pregnancy. The biological effects of estrogens are mediated by estrogen receptors (ERα and ERβ). Estrogens or selective ER-agonists have been shown to exert potent neuroprotective or anti-inflammatory effects in experimental autoimmune encephalomyelitis (EAE), the mouse model of MS. A central question in EAE is to identify the cellular targets that express a functional ER isotype, and the mechanisms underlying the neuroprotective and anti-inflammatory effects of estrogens. Using pharmacological approaches targeting ER-specific functions, and genetic tools such as conditional knockout mice in which ERα or ERβ are selectively deleted in specific cell populations, a clearer picture is now emerging of the various cellular targets and downstream molecules responsible for estrogen-mediated protection against central nervous system autoimmunity.

Endocr Rev. 2016 Aug;37(4):372-402. doi: 10.1210/er.2016-1007. Epub 2016 May 19.

Estrogens, Neuroinflammation, and Neurodegeneration.

Author information

1
Center of Excellence on Neurodegenerative Diseases and Department of Pharmacological and Biomolecular Sciences, University of Milan, 20133 Milan, Italy.

Abstract

Inflammatory activation of microglia is a hallmark of several disorders of the central nervous system. In addition to protecting the brain against inflammatory insults, microglia are neuroprotective and play a significant role in maintaining neuronal connectivity, but the prolongation of an inflammatory status may limit the beneficial functions of these immune cells. The finding that estrogen receptors are present in monocyte-derived cells and that estrogens prevent and control the inflammatory response raise the question of the role that this sex steroid plays in the manifestation and progression of pathologies that have a clear sex difference in prevalence, such as multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease. The present review aims to provide a critical review of the current literature on the actions of estrogen in microglia and on the involvement of estrogen receptors in the manifestation of selected neurological disorders. This current understanding highlights a research area that should be expanded to identify appropriate replacement therapies to slow the progression of such diseases.