Today is my last day at work until the 6th Jan. I wish you all a safe, healthy, and hormonally happy Christmas and New year. My posts will be sporadic until then, so I close with a light-hearted but important look at kissing.

Love Well

October 28, 2013, 4:48 pm

<!– — Updated: 12:16 pm –>        149 Comments

Now, a Kiss Isn’t Just a Kiss

Menopause education: needs assessment of American obstetrics and gynecology residents.

Abstract:

Antioxidants are a commonly promoted feature of health foods and supplements. They’re portrayed as the good forces that fight free radicals – nasty molecules causing damage thought to hasten ageing and cause chronic diseases.

The simple logic that antioxidants are “good” and free radicals are “bad”, has led to the idea that simply getting more antioxidants into our bodies, from foods or supplements, can outweigh the impacts of free radicals.

Sadly, biology is never this simple, and antioxidants are not a free radical free pass.

We are exposed to free radicals every day; they’re produced in our bodies as part of normal functioning. Such normal levels are easily tolerated.

But habits such as smoking, drinking, and eating processed foods all increase exposure. These additional free radicals may increase the risk of lifestyle and age-related diseases, such as cancer and cardiovascular disease.

Free radicals explained

Free radicals are very reactive molecules. In the body, a chemical reaction occurs between free radicals and the molecules that make up our cells.

This inactivates the free radical, but turns the other molecule into a new free radical. The process continues in a chain reaction, damaging each molecule as it goes on.

These reactions can alter the structure and function of molecules; when enough molecules are damaged, cells can stop functioning correctly, or die.

Damage to DNA by free radicals can result in mutations and promote cancer. Free radicals can also oxidise low-density lipoprotein or LDL (“bad” cholesterol), making it more likely to get trapped on the artery walls, clogging blood vessels and leading to cardiovascular disease.

Sometimes, free radicals are very helpful, for example, in an oxidative burst. This happens when special immune cells, known as phagocytes, deliberately release free radicals as part of a cocktail of chemicals to kill and digest bacteria and viruses.

Our antioxidant heroes

Antioxidants can stop the free radical chain reaction. They can react with free radicals without getting damaged or becoming a free radical themselves.

There are hundreds of substances that can act as antioxidants. Well-known antioxidants include vitamin C and vitamin E, both of which are found in fruits and vegetables.

Vitamin C is mainly found in citrus fruits and berries, while vitamin E is abundant in nuts and green leafy vegetables.

The ability of antioxidants to scavenge free radicals has led to the suggestion that consuming large amounts of antioxidants might lessen the free radical damage that leads to chronic diseases and ageing.

And there’s little doubt that a diet including sources of antioxidants is necessary for good health. Indeed, studies have shown that cancer rates are lower in people with diets rich in fruits and vegetables.

Not all roses

But the benefits of supplementing diets with additional antioxidants are yet to be shown. In fact, some studies have shown that taking antioxidant supplements can sometimes increase the risk of cancer.

This might be because antioxidants may be actually harmful under certain conditions. At high concentrations, substances that normally act as antioxidants can have the opposite effect and act as a pro-oxidant. This may be because antioxidants compounds, such as vitamin C, react with other molecules in the body, not just free radicals.

Some of these reactions, such as the Fenton Reaction, actually produce additional free radicals. When antioxidant concentrations get too high, the free radical-producing effect can outweigh the free radical-fighting effect.

Also, not all antioxidants are the same; each has unique chemical behaviours and biological properties. This means that no single substance can replace the multiple functions of a variety of antioxidants.

A growth industry

Despite these uncertainties about their efficacy, supplemental antioxidants are a boom industry, sold as a health panacea and added to a range of processed foods, including juices, cereals, chocolate bars, and alcoholic beverages.

But the benefits of antioxidant-rich food is likely due to the entire nutritional package that comes from a diet rich in natural and whole foods. Adding antioxidants to processed foods means many healthy components of whole foods are missing.

So it’s unlikely that antioxidant supplements will be as successful in preventing disease as a healthy, varied and balanced diet. And while antioxidants may help protect the body from free-radical damage, as is often the case in nutrition, more is not always better.

The myriad other components of foods that are natural sources of antioxidants may also be responsible for their beneficial effects.

The best thing you can do for good health is to keep eating between five and eight servings of fruit or vegetables every day and to steer clear of unnecessary, and potentially harmful supplementation.

Research claiming that men are to blame for menopause has gone viral in the popular media in the past week. But does the theoretical model’s fundamental assumption – that men prefer young women – stack up?

It may surprise some to discover that, in many respects, humans are remarkably unremarkable. Our physiology and morphology is similar to other higher primates. In fact, it follows a broadly similar blueprint for primates and mammals more generally.

Nevertheless, we clearly lack the impressive size dimorphism of gorillas, the extraordinarily large testes of chimpanzees, and only a tiny fraction of our species share the fabulous hair colour of orangutans.

Humans also align unremarkably with conventional life-history theory, which attempts to understand how natural selection has shaped the principal events in an organism’s lifetime. Recent comparisons of mortality schedules in natural populations of primates, including humans, for instance, reveal similar patterns.

But we are unusual in at least one respect. In the vast majority of species, males and females die shortly after they cease producing and caring for dependent offspring. Several species of small marsupials of the genus Antechinus spectacularly illustrate this effect. Male and female Antechinus typically survive only one reproductive cycle.

In contrast, human females typically remain alive for many years after they cease to reproduce. This change in reproductive activity, menopause, is unusual and seems to be confined to only a handful of species of mammals, such as killer whales and humans.

Menopause represents something of an evolutionary puzzle. Natural selection will favour reproductive or life-history strategies that maximise the number of surviving offspring. As our bodies deteriorate with age, we expect the end of female reproductive activity to coincide with the time when our bodies can no longer function.

More bluntly, males and females are expected to be able to produce offspring until they die.

Explanations for menopause treat it as either an adaptive reproductive strategy, or a non-adaptive consequence of extended lifespans. Chief among the former is the “grandmother” effect. Here, females can improve their fitness through the survival of grandchildren, without bearing the risks of giving birth at an older age.

Empirical tests of this idea have had mixed success. But importantly, these studies recognise the challenge of controlling for cultural, socioeconomic effects when examining human life-history features.

The recent, novel explanation of menopause takes a more cavalier approach. Using a computer simulation model, Rama Singh and his team claim that menopause is the consequence of male mating preferences for young females, which leads to the accumulation of mutations that are deleterious to female fertility.

The novelty of this model is that it doesn’t assume that diminished fertility in older females predates menopause, or that offspring survival is enhanced by the presence of grandmothers.

Ultimately, the success of theoretical models that make novel claims must stand on their underlying assumptions. The crucial assumption of this model is that males prefer to mate with young females. Apparently, Singh and colleagues believe this is self-evident, because they detail no supporting evidence.

Perhaps this isn’t surprising, since the required evidence may not be available. Popular wisdom comes from David Buss’ classic 1986 survey of human mate preferences across 33 countries. This study suggested that females prefer relatively older and males prefer relatively younger partners. This is not quite the same kind of mating preference that appears to characterise the Singh model.

In any case, it’s impossible to discern, from these kinds of data, whether male mate preferences have a genetic basis or are influenced by the local culture. Indeed, we don’t really know whether these preferences reflect real life.

This is a crucial issue. If the Singh model has any evolutionary significance, mate preferences must have a genetic basis.

A recent study of human mate preferences suggests not. The degree of preference for many mate preference attributes, including age, vary predictably between countries according to an index of gender parity (the Global Gender Gap Index).

This means that either mate preferences are strongly influenced by society, or the preference can experience truly impressive rates of evolution.

More generally, explanations that rely on male mate choice in mammals are skating on thin ice. Sexual selection theory is unlikely to predict male mate choice in mammals, because the typically lower reproductive rate of females predisposes them to be the more choosy sex.

And the relative rarity of menopause among mammals begs the question of why a male preference for young female mates is confined to humans and a handful of other species. In this context, it is telling that male chimpanzees in their natural environment prefer to mate with older females.

The point is that humans are remarkable in one crucial aspect. In all other animals, behaviour is shaped by a combination of genes and environment, but in humans the sociocultural influence is particularly potent.

Distinguishing between these effects is crucial for unravelling the evolutionary significance of those aspects of human biology that involve behaviour.

Studies of human life-history strategies that carefully negotiate through this challenge reveal intriguing patterns that offer broad insights. Those that don’t, can’t.

In the past few days since the passing of Nelson Mandela, the father of the South African nation, it has become apparent just how much Madiba meant not only to us, but to the rest of the world.

He is a part of all our lives, and his humanity has touched us all. For those of us working in the field of HIV, this was embodied by his stance on the inaction of our government as HIV exploded in South Africa.

Although Mandela had acknowledged the looming threat of AIDS in 1992, during his years as the first president of the new South Africa after 1994, he admitted that he had not paid attention to the new epidemic that was unfolding in the country – something he later lamented.

Opposing the denialists

Under the leadership of the next president, Thabo Mbeki, our work in HIV became increasingly difficult. We were leading local research on the prevention of mother-to-child transmission of HIV in Soweto, but research findings weren’t being implemented.

Where once we had had a warm relationship with the Department of Health, we became increasingly maligned. The special committee set up to advise the department on HIV and AIDS was disbanded, and the department refused to embrace affordable interventions to prevent mother-to-child transmission of HIV.

All of this was happening against a background of a growing presence of AIDS denialism in the corridors of power, which culminated in the “Presidential International Panel of scientists on HIV/AIDS in South Africa”, where Mbeki invited a number of dissident scientists to debate the the so-called “orthodoxy” about the etiology of AIDS.

In Mbeki’s opening address at the International AIDS Conference in 2000 in Durban, he again reiterated his doubts about the gravity of the epidemic. In contrast, Mandela was becoming increasingly vocal about the AIDS matter in South Africa.

It was Mandela who gave the closing speech at the very same conference, in which he said that the dispute over the cause of AIDS was “distracting from the real life-and-death issues we are confronted with”.

Later he became even more direct in public, and accused Mbeki of dereliction of duty for not leading the fight against HIV. He began lambasting the government for not providing anti-retrovirals and told a newspaper: “This is a war. It has killed more people than has been the case in all previous wars and in all previous natural disasters … We must not continue to be debating, to be arguing, when people are dying”.

Mandela began to increasingly use his presence and influence to counter the Mbeki administration’s denialism. In 2001, he celebrated his birthday on a freezing winter day at Baragwanath hospital with children from our clinic. A few months later, in February 2002, we were awarded the Nelson Mandela Health and Human Rights Award for pioneering work done in the field of mother-to-child transmission.

This “coup de grâce” award ceremony was intended to make maximum impact and was scheduled for the day before Mbeki was due to give his annual state of the nation address to parliament. The award traditionally happened with the full support of the government, but that year the audience was thin on Mbeki’s government politicians.

Core concern

Mandela drew attention to the plight of mothers and babies with HIV and he spoke of the benefits of medical science, saying that debate over “some fundamental issues” about AIDS “unfortunately continues to rage in manners that detract attention from what needs to be our core concern”.

In stark contrast to the public views of Mbeki and his Health Minister, Manto Tshabalala- Msimang, Mandela used the award speech to say that our work emphasised “the centrality of fighting mother-to-child transmission in HIV prevention strategies … (which) we accept to be beyond argument and doubt.”

The response by the Mbeki administration to Mandela’s perceived treachery was swift and vindictive, and Mandela was chastised by members of the ANC’s National Executive Committee. But his actions and words created the space for others to speak up, and helped support the fight against AIDS denialism.

A visit from Madiba

In March of 2002, Mandela came to visit one of our programmes in Soweto, together with former US president, Jimmy Carter, and Bill Gates who used the opportunity to further reprimand the government for their slow adoption of mother-to-child transmission prevention strategies. Mandela said: “If the government says you don’t take any move even in regard to public hospitals until we have completed our researches, babies, young people, are going to die in scores every day.”

But, as so often with Mandela, his actions spoke even louder than his words. On arrival at the clinic, accompanied by a swarm of press photographers, he immediately asked to hold one of the children of an HIV-positive mother, and every photographer’s lens focused on him, with Carter and Gates following his example. The picture of three elderly men, each dangling a baby on their knee, with no sense of stigma or fear of HIV, flashed around the world.

‘HIV positive’

More determined, Mandela’s campaign continued, and in mid-2002 at the International AIDS Conference in Barcelona, Mandela urged world leaders to do more to reduce the stigma of HIV/AIDS. Visiting the AIDS activist Zackie Achmat later that year, he begged Achmat to start taking antiretrovirals, and famously donned a T-shirt, with the slogan “HIV POSITIVE” and was photographed in it.

According to Judge Edwin Cameron, this may have been the intervening moral voice that made the change in the government’s resistance to antiretroviral drugs inevitable. Within a year, the Mbeki government had relented and committed, albeit reluctantly, to an antiretroviral treatment programme.

We have no doubt that Mandela’s public support for our work on mothers and babies, and for the HIV treatment struggle in those years, changed the course of AIDS in South Africa. Without his moral authority, his unerring truthfulness and his public courage, it is unlikely that the government would have changed course and antiretrovirals would not have been available in the country for many years.

But the slow change in attitude would come too late for Mandela’s son, Makgatho, who died from AIDS in 2005. But even in the face of this immense personal sadness, Mandela spoke publicly of his son’s cause of death, facing down the stigma that he knew was still evident.

We were privileged to be supported by this great man, and to see his humanity and integrity in action. He changed our lives and the way in which we work, and he changed, yet again, the face of South Africa.

• Joanna Blythman and Rosie Sykes
• The Guardian, Saturday 29 June 2013

Cherries are good for you. Photograph: Jill Mead for the Guardian

There’s only one bad thing about cherries: they’re expensive, so you never get to eat enough of them. But at this time of year, when the English crop is ripe and the European harvest is going full tilt, put austerity on hold for a week or two and binge on cherries.

Throughout the year, global sourcing offers us shipped southern hemisphere cherries that can have spent three or four weeks in cold storage. A freshly picked cherry, only recently cooled to remove its orchard heat, is quite a different proposition. Assuage your financial guilt by thinking of them as a health food. Who needs sweets when you can pop cherries into your mouth?

Why are cherries good for me?
Anthocyanins in cherries appear to have a marked anti-inflammatory action. Specifically, these compounds seem to be highly effective in treating gout, a condition that causes painful swelling in joints. Last year, a Boston Medical Center study reported that eating cherries reduces gout attacks by 35%. Cherries are also one of the few food sources of the hormone melatonin, which regulates sleep patterns. A study published in 2011 in the European Journal of Nutrition, reported that eating tart montmorency (or morello) cherries significantly raised levels of melatonin and improved sleep. Compared to most other fruits, cherries are low in sugar, which makes them an ideal choice for people who want to lose weight.

Where to buy and what to pay
In Kent, Sussex and Herefordshire, our main cherry-growing counties, look out for pick-your-own farms and pop-up cherry stalls on roads through the orchard areas. In shops, expect to pay around £1 per 100g. Two-kilo boxes from greengrocers and markets are much better value, working out at around half that price.

Joanna Blythman is the author of What To Eat (Fourth Estate, £9.99). To order a copy for £7.99 with free UK p&p, go to guardianbookshop.co.uk

The Gift of Siblings
By FRANK BRUNI
Published: May 25, 2013 195 Comments

GIVEN what a mouthy thing I grew up to be, it’s shocking to me that I began talking later than most children do. But I didn’t need words. I had my older brother, Mark.

The way my mother always recounted it, I’d squirm, pout, mewl, bawl or indicate my displeasure in some comparably articulate way, and before she could press me on what I wanted and perhaps coax actual language from me, Mark would rush in to solve the riddle.

“His blanket,” he’d say, and he’d be right.

“Another cookie,” he’d say, and he’d be even righter.

From the tenor of my sob or the twitch of one of my fat little fingers, Mark knew which chair I had designs on, which toy I was ogling. He decoded the signs and procured the goods. Only 17 months older, he was my psychic and my spokesman, my shaman and my Sherpa. With Mark around, I was safe.

This weekend he’s turning 50 — it’s horrifying, trust me — and we’ll all be together, as we were at his 40th and my 40th and seemingly every big milestone: he and I and our younger brother, Harry, and our sister, Adelle, the last one to come along. We marched (or, rather, crawled and toddled) into this crazy world together, and though we had no say in that, it’s by our own volition and determination that we march together still. Among my many blessings, this is the one I’d put at the top.

Two weeks ago, the calendar decreed that we Americans pause to celebrate mothers, as it does every year. Three weeks hence, fathers get their due. But as I await the arrival of my brothers, my sister and their spouses in Manhattan, which is where we’ll sing an off-key “Happy Birthday” to Mark and drink too much, my thoughts turn to siblings, who don’t have a special day but arguably have an even more special meaning to, and influence on, those of us privileged to have them.

“Siblings are the only relatives, and perhaps the only people you’ll ever know, who are with you through the entire arc of your life,” the writer Jeffrey Kluger observed to Salon in 2011, the year his book “The Sibling Effect” was published. “Your parents leave you too soon and your kids and spouse come along late, but your siblings know you when you are in your most inchoate form.”

Of course the “entire arc” part of Kluger’s comments assumes that untimely death doesn’t enter the picture, and that acrimony, geography or mundane laziness doesn’t pull brothers and sisters apart, to a point where they’re no longer primary witnesses to one another’s lives, no longer fellow passengers, just onetime housemates with common heritages.

That happens all too easily, and whenever I ponder why it didn’t happen with Mark, Harry, Adelle and me — each of us so different from the others — I’m convinced that family closeness isn’t a happy accident, a fortuitously smooth blend of personalities.

IT’S a resolve, a priority made and obeyed. Mark and his wife, Lisa, could have stayed this weekend in the Boston area, where they live, and celebrated his 50th with his many nearby college buddies. Harry and his wife, Sylvia, could have taken a pass on a trip to New York: they’re traveling all the way from the Los Angeles area, their home. But we made a decision to be together, and it’s the accretion of such decisions across time that has given us so many overlapping memories, which are in turn our glue.

I’m also convinced that having numerous siblings helps. If you’re let down by one, you can let off steam with another. “There’s always someone else to turn to,” said George Howe Colt, the author of “Brothers,” a 2012 book about brothers through history and about his own three siblings, all male.

“It’s like a treasure chest: you have access to a lot of different personalities,” Colt told me. “With my brothers, I turn to them all. But I turn to them for different things.” That’s how it is in our brood, too.

Perhaps because the four of us belong to the same generation — just over eight years separate Mark and Adelle — each understands the others better than our mother, now gone, could ever understand us, or than our father ever will. And while our parents gave us values, we inadvertently assigned ourselves the roles we play. Popularity came more easily to Mark, so I resolved to be the more diligent student, needing to find my own way to stand out. Because Mark and I made relatively conventional choices, Harry, for a while, made less conventional ones: his claim to a distinct identity.

That’s how it goes in a pack of siblings, and I sometimes wonder, when it comes to the decline in fertility rates in our country and others, whether the economic impact will be any more significant than the intimate one. For better or worse, fewer people will know the challenges and comforts of a sprawling clan.

Those comforts are manifold, at least in my lucky experience. With siblings to help shoulder the burden of your parents’ dreams and expectations, you can flail on a particular front with lower stakes and maybe even less notice. Siblings not only pick up the slack but also act as decoys, providing crucial distraction.

They’re less tailored fits than friends are. But in a family that’s succeeded at closeness, they’re more natural, better harbors. As Colt observed of his siblings, and it’s true of mine as well, they aren’t people he would have likely made an effort to know or spend time with if he’d met them at school, say, or at work. And yet a reunion with them thrills him more than a reunion with friends, who don’t make him feel that he’s “a part of a larger quilt,” he said. His brothers do.

My friend Campbell, who’s as fond of her two sisters as I am of my siblings, put it this way: “With a friend, I have to be more articulate. With my sisters, I can be my most primal self: inarticulate, childishly emotional. I’ll have a fight with my sister and say, ‘O.K., I know we’re in a fight, but I need your advice on something,’ and we can just put the fight on hold. They’re the only people in the world you can be your worst self with and they’ll still accept you.”

My siblings have certainly seen me at my worst, and I’ve seen them at theirs. No one has bolted. It’s as if we signed some contract long ago, before we were even aware of what we were getting into, and over time gained the wisdom to see that we hadn’t been duped. We’d been graced: with a center of gravity; with an audience that never averts its gaze and doesn’t stint on applause. For each of us, a new home, a new relationship or a newborn was never quite real until the rest of us had been ushered in to the front row.

This weekend we clap for Mark, and as I plot his dinner menu and hit the liquor store, I have to decode what he wants. It won’t be difficult. I have decades of history to draw from, along with an instinct I can’t even explain.

A new test could help doctors better understand which prostate cancers are likely to remain slow growing and could be managed with surveillance only, potentially sparing thousands of men from unnecessary prostate removal surgery or invasive procedures.

Diagnosing the likely rate of a prostate cancer growth is notoriously tricky, leading many clinicians to err on the side of caution and recommend treatment where it may not be needed.

In a new paper titled “A Molecular Signature Predictive of Indolent Prostate Cancer” and published in the journal Science Translational Medicine, researchers from the Columbia University Medical Centre said they had discovered that the expression of certain genes associated with ageing could be used to predict whether a prostate cancer was going to become aggressive or stay indolent (slow growing).

The researchers looked at prostate cancers that had a low Gleason score, a grading system that aims to give patients and clinicians an idea of how aggressive a prostate cancer is.

A low Gleason score means the cancer is currently slow-growing, but until now, there was no way of accurately predicting how long it would stay indolent.

“Distinguishing the many indolent tumours from the minority of lethal ones remains a major clinical challenge,” the researchers wrote in their paper.

“The current lack of reliable and reproducible assays to identify tumours destined to remain indolent has resulted in substantial over-treatment of patients who would not have died from prostate cancer if the disease had been left untreated.”

The researchers discovered that the expression of three genes — called FGFR1, PMP22, and CDKN1A — allowed them to accurately predict the outcome of low Gleason score tumours. Tumours in which this biomarker was not expressed or expressed at low levels were deemed aggressive.

“The three-gene biomarker could take much of the guesswork out of the diagnostic process and ensure that patients are neither over-treated nor under-treated,” said lead author Dr Cory Abate-Shen, lead author of the study and head of the lab that made the discovery.

The researchers put their theory to the test on 43 patients who had been monitored for at least 10 years for a slow growing prostate cancer.

Of the 43 patients, 14 ultimately developed advanced prostate cancer. All 14 were correctly identified by the test, the researchers said.

Holy grail

Ian Haines, Adjunct Associate Professor of Medicine at Monash University said that the new finding was “a useful first step towards the holy grail of prostate cancer diagnosis.”

“This study pursues the noble and so far elusive goal of identifying in advance which low or intermediate risk prostate cancers may become aggressive in their behaviour and eventually threaten the patient’s survival,” said Dr Haines, who was not involved in the study.

“If these preliminary results are replicated in the proposed larger study, this three-gene biomarker will represent a significant advance that will help to define more accurately which patients can be offered watchful waiting as their treatment of early stage prostate cancer.”

Dr Haines said it was important to remember that most prostates have multiple independent sites of cancerous growths.

“Hence, you really have to do the analysis on multiple independent sites,” he said.

Dr Haines said the tests do not help in reducing the over-diagnosis of early stage prostate cancer caused by the use of PSA (prostate-speficic antigen) screening, “but they may prove very effective in helping to reduce the current over-treatment of early stage prostate cancer.”

Ian Olver, Clinical Professor of Oncology at Cancer Council Australia said that to be able to predict which of the low grade prostate cancers is aggressive by a simple three-gene test is “an important finding, if it stands up to further trials.”

“We have not been able to do that from microscopic examination of the cancer. This will mean that we will be able to select which patients with low grade prostate cancers need to be treated immediately, and which can be safely kept under surveillance,” said Professor Olver, who was not involved in the study.

“This will reduce the problem of over-treatment where currently prostatectomies are performed, but the prostate cancer would never have caused a problem. It will also provide more reassurance to men who select a watch policy, that their disease is slow growing.”

NEVER talk about where you’re staying while on the plane, and make sure to leave your TV on while you’re gone.

They are the hotel security tips you need to know, according to flight attendant Sara Keagle in an article on the Huffington Post.

Well, who would know more about hotels than someone who is constantly on the move?

Here are her top words of accommodation wisdom:

1. Zip it

Never talk about where your staying on the plane or in the airport – especially if you’re travelling solo. You don’t know who could be listening. This is just as important when you arrive at the hotel – don’t let others see your room number. If you’re travelling with others, write it on a piece of paper and give it to them.

2. Excess baggage

When you arrive in your room, use your bags to prop open the door and look inside before it closes. It hasn’t happened to me but I know flight attendants who’ve encountered strangers in their rooms.

3. Be wary

If someone knocks at your door, don’t open it unless you’re expecting someone, for example if you’ve ordered room service. If in doubt call the front desk.

4. Noisy

When you’re out and about leave your television on in your room – this will deter thieves.

5. Write it down

Place a note on the table detailing yourself and your plans, this could assist police if something does happen to you.

6. Use the deadbolt

Keagle says: “I have walked in on people sleeping because the hotel inadvertently gave me a key to a room already occupied. This will also stop housekeeping from coming in while you’re in the shower should you forget the do not disturb sign.”

7. Know the nearest exit

Leave a torch and a room key on the floor near the door, so if there’s a fire you can grab them on the way out. That way, if you encounter thick smoke down the hall you can go back to your room and call for help.