Monthly Archives: February 2020

What is irritable bowel syndrome and what can I do about it?

Explainer: what is irritable bowel syndrome and what can I do about it?

November 29, 2018 6.07am AEDT Women are twice as likely to be diagnosed with irritable bowel syndrome as men. from shutterstock.com

Author

  1. Suzanne Mahady Gastroenterologist & Clinical Epidemiologist, Senior Lecturer, Monash University

Disclosure statement

Suzanne Mahady does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Partners

Monash University

Monash University provides funding as a founding partner of The Conversation AU.

Victoria State Government

Victoria State Government provides funding as a strategic partner of The Conversation AU.

Irritable bowel syndrome (IBS) is a common disorder that affects one in ten Australians, and twice as many women as men. Its symptoms include chronic abdominal pain, constipation or diarrhoea, and bloating. These have a significant impact on a person’s quality of life.

Many people use the term irritable bowel syndrome to describe general symptoms of gut and bowel dysfunction. But diagnosis requires meeting strict, diagnostic criteria. Known as the ROME criteria, these require a person to be experiencing abdominal pain, on average, at least one day per week. The pain must be associated with two or more of the following:

  • defecation
  • a change in the frequency of stool
  • a change in the form (appearance) of stool
  • having occurred over the last three months with symptom onset at least six months before diagnosis.

Tests aren’t always needed for a diagnosis if these symptoms are present. But an accurate diagnosis of IBS is important as some symptoms, such as pelvic pain, may overlap with other diseases such as endometriosis or inflammatory bowel disease. If other symptoms are present, a doctor may need to perform blood tests, pelvic ultrasound, endoscopy or stool tests to rule out similar disorders.


Read more: I have painful periods, could it be endometriosis?


Some symptoms are considered “red flag” symptoms and should prompt further testing and specialist referral. For example, if you have rectal bleeding, weight loss and are aged over 50 when symptoms start, it is not IBS.

What causes it?

A single cause for IBS has not been identified. IBS may run in families, but we still don’t know if this is due to shared genetics or environmental factors. An episode of gastroenteritis, an infection caused by viruses or bacteria, increases the risk of developing IBS. But this is usually temporary and symptoms gradually improve.

People with IBS often also have anxiety and depression. Research suggests early childhood trauma can predispose some people to IBS in later life. This is because the gut and brain talk to each other through nerve signals, the release of gut or stress hormones, and other pathways.

We have long known that emotions can directly alter gut function. But studies now show that gut function also affects emotions. One Australian study indicated that for some people gut symptoms occur first and the psychological symptoms occur as a result. But this is not true for all people with IBS.


Read more: Stomach and mood disorders: how your gut may be playing with your mind


What do I do?

Non-drug treatments should be considered initially, and more than one treatment strategy may be needed to help improve symptoms.

Good-quality evidence shows a low-FODMAP diet reduces IBS symptoms. FODMAPs are carbohydrates that produce excess gas when digested. They can be found in roots such as onions and garlic, and fruits (or seeds) like legumes, apples, pears and mangoes. For the best result, a person should start a low-FODMAP diet under the guidance of an experienced dietitian.

It’s a common misconception that people should keep to a low-FODMAP diet for life. Foods like onions, which are high in FODMAPs, are also good prebiotics and promote the growth of friendly gut bacteria. Restricting these can result in low gut bacterial diversity, which is linked to autoimmune diseases and obesity. That’s another reason a dietician should guide people through the diet over a few weeks and avoid unnecessary dietary restriction.

FODMAP foods include onions, but these also promote the growth of friendly gut bacteria. from shutterstock.com

Simple dietary measures include adding more soluble fibre to the diet. This can include psyllium, which can be bought as a powder from chemists and health food shops. Insoluble fibres like bran are generally unhelpful.

A trial of probiotics might help. These could be trialled for one month and then re-evaluated by the GP, but are unlikely to be useful if used indefinitely. Exercise has been shown in randomised trials to improve gut symptoms in people with IBS.

Managing stress and anxiety are key to improving symptoms for many people. Psychological therapies have been shown in trials to help symptoms more than placebo or other interventions. This is particularly so when the psychologist is interested in IBS.

Clinical trials have also shown that, for some people, hypnotherapy that is directed at the gut is just as effective as a low-FODMAP diet. The benefits are still seen at six months. Hypnotherapy is not for everyone, however, and multiple sessions are needed for symptoms to improve.

Peppermint oil can help reduce stomach cramps related to IBS. from shutterstock.com

What about medications?

IBS affects quality of life but it doesn’t change a person’s risk of early death or cancer. So, treatments should have few side effects to be acceptable. Clinical trials have shown that medications such as peppermint oil (usually given in capsules) can reduce troublesome abdominal cramps with minimal side effects.

Melatonin can improve symptoms through better sleep quality where sleep is disturbed.

The choice of drug should be tailored to each person’s symptoms. For instance, low-dose antidepressants can be helpful for some people, especially where significant depression or anxiety symptoms exist together with IBS. Medications that reduce inflammation are generally unhelpful, as consistent and clinically apparent inflammation is not part of the syndrome.


Read more: So you think you have IBS, coeliac disease or Crohn’s? Here’s what it might mean for you


A few new approaches are being trialled for IBS, including faecal transplants and new medications. But all of these need better long-term data before they appear on the market.

The effect of Hop (Humulus lupulus L.) on early menopausal symptoms and hot flashes

How the diets of early humans explain our eating habits

How the diets of early humans explain our eating habits

August 28, 2015 6.07am SAST

The size of the human brain had a great deal to do with the food choices of our ancestors. Shutterstock
Much attention is being given to what people ate in the distant past as a guide to what we should eat today. Advocates of the claimed palaeodiet recommend that we should avoid carbohydrates and load our plates with red meat and fat. Its critics, on the other hand, argue that these are the same ingredients that would set us up for heart attacks. Moreover, these animal-derived foods require more space to produce on our crowded planet filled with starving humans.

A factual foundation for the debate is provided by a review of the eating patterns of early humans and how we adapted to digest starches softened by cooking. The researchers contend that it was digestible starches that provided extra energy needed to fuel the energy needs of bigger brains, rather than extra protein from meat to grow these brains.

But the most striking thing about human diets is just how variable they have been and the adaptations that have taken place. Furthermore, the American evolutionary biologist Marlene Zuk in her book Paleofantasy contends that these dietary adaptations are not fixed on what our ancestors ate in caves at some time in the past.

So are our energy, or protein, needs much different from other mammals of similar size? Brains demand a lot of energy but so does the liver and the digestive tract. The extra nutrition that we need for brain work may be counterbalanced, at least partially, by a lesser need for:

  • a long gut to process poor quality foods, or
  • a large liver to handle nasty chemicals in these plant parts.

Once built, a large brain does not require extra sources of protein to maintain its activities.

My studies on the dietary requirements of savanna-inhabiting herbivores highlight how these animals must cope with the dry season when most herbage is brown and indigestible even with the aid of microbial symbionts in the gut.

But carnivores do not have this problem because the dry season is when weakened herbivores are most readily killed, especially when they concentrate around scarce waterholes.

The role of carbs among early humans

Meat has long been part of human diets, along with carbohydrates provided by fruits, tubers and grains. We can get by without it, obtaining protein from milk or, with some planning, from legumes.

The early humans that consumed most meat were the Neanderthals, who lived in Europe many thousand years ago, but were not our ancestors. Meat formed the crucial lean-season food for the Neanderthal people during successive winters when plants were seasonally buried under deep snow, but later also for the modern humans who spread through Eurasia and displaced them around 40 000 years ago.

Unlike tropical Africa, meat could be stored during the freezing winters of the far north to provide a reliable food source, especially in the form of large carcasses of elephant-like proboscideans.

This led to a wave of large mammal extinctions as humans spread rapidly into Australia and entered the Americas towards the end of the last Ice Age. By that time hunting technology had been honed and meat routinely supplemented plant food, but the latter remained the dietary staple for African hunter-gatherers like the Bushmen or San people into modern times.

The food journey within evolution

Coping with the intensifying dry season in the expanding African savanna was a critical issue for human ancestors during the evolutionary transition from ape-men to the first humans between three and two million years ago. How did our ape-men ancestors gather sufficient to eat during this time of the year when nutritious fruits and leaves were scarce?

This was when meat, or at least the marrow left within bones, could have become a nutritional fallback, probably acquired by scavenging from animal carcasses not completely consumed by big fierce carnivores, along with underground storage organs of plants.

Obtaining this meat required more walking and hence longer limbs, hands freed to carry, security in numbers and stone weapons to throw at threatening carnivore fangs, but not much expansion in cranial capacity. These were features of the early Australopithicines.

At this early time, another branch of ape-men, placed in the genus Paranthropus, took a different adaptive route. They developed huge jaws to chew on tough plant foods extracted from underground storage organs to get them through the dry season.

The last representative of this genus faded out nearly a million years ago when this strategy eventually became unviable. About that time the lineage leading to early humans discovered cooking, or at least how to use it effectively to make starches stored by plants more readily digestible, according to the article in The Quarterly Review of Biology.

Adding this reliably found source of energy to the proteins acquired more opportunistically by hunting animals or gathering shellfish provided the means to survive through seasonal bottlenecks in food availability and build even bigger brains and the adaptations that followed.

A supporting adaptation was to store more body fat to get through the lean periods, especially among women supporting dependent offspring. This works against us now that foods supplying carbohydrates are plentiful.

The modern day dilemma

The problems we currently face are that we retain a craving for sugar, which was scarce the past, while most of the starchy carbohydrates we eat are highly refined. This means losing out on the other nutrients in plant parts like minerals and vitamins, and most basically fibre.

A meat-based diet could have a role to play for people who have a propensity to store fat by filling the gut for longer and alleviating desires to snack on sweets between meals. More important generally is the need to exercise so that we are hungry enough to consume sufficient food to provide the scarce micronutrients that we also require for healthy bodies.

The best advice is to eat lots of things: meat if you can afford it and justify its planetary costs to produce, but also all kinds of good food, as least refined and processed as you can obtain (apart from wines).

Self-Help Anxiety Management

Self-Help Anxiety Management

31 August, 2015 0 comments Read Later

Self-Help Anxiety Management

This app was developed by University of the West of England psychologists to help patients with anxiety manage their condition.

If the user needs immediate help for their anxiety, they can use the calm breathing tool, where they breathe in time with the moving timer, or they can rub the screen to gradually reveal a calming picture.

The user can also monitor their anxiety using a tracker, which may help to identify anxiety triggers.

The self-help section has a range of activities to practice, including breathing exercises, meditation and muscle relaxation techniques, while users can also anonymously share self-help tips.

The large range of exercises, tips and functions can make the app a little hard to navigate, but it also means that there’s something for everyone.

Specifications:

COST: Free.

COMPATIBLE WITH: iPhone, iPad, iPod touch; and Android.

REQUIRES: iOS 7.0 or later; Android 4.0.3 and up.

Unravelling the mysteries of sleep: how the brain ‘sees’ dreams

Unravelling the mysteries of sleep: how the brain ‘sees’ dreams

August 12, 2015 4.27pm AEST

Dreams and their purpose have been one of the enduring mysteries of sleep. diastème (Sarah Giboni)/Flickr, CC BY

We’ve known for some time that our eyes move around during the dreaming phase of sleep, much like when we’re awake and looking at a visual scene. The phase of sleep is called rapid eye movement sleep, or REM sleep.

New research, published today in the journal Nature Communications, shows brain activity during the dreaming phase of sleep is remarkably similar to brain activity when we’re awake and processing new visual images, suggesting the brain “sees” dreams.

While researchers have suspected this may be the case, it’s the first time investigators have been able to record brain activity from within the brain.

A quick history of dream research

Dreams and their purpose have been one of the enduring mysteries of sleep. Early dream theorists, such as Sigmund Freud, argued that the function of dreaming was to preserve sleep by expressing unfulfilled desires or wishes in the unconscious state.

More recently, researchers have investigated the function and processes of sleep and dreams by measuring the physiological signals that characterise this state of consciousness.

Just over 60 years ago, American sleep researcher Eugene Aserinsky stumbled across rapid eye movements during sleep almost accidentally, during an overnight sleep study recording of his eight-year-old son. His seminal 1953 paper reported “rapid, jerky and binocularly symmetrical” eye movements during periods of sleep.

These eye movements were also associated with increased brain activity, thus discounting the idea that sleep is a completely passive phenomenon. During REM sleep, our brains are active and behave similarly to wakefulness or light sleep. But muscle activity is suppressed so we can’t physically carry out our dreams.

In a pioneering 1957 paper, American researchers William Dement and Nathaniel Kleitman examined the relationship between eye movements and dream content. They woke participants during REM sleep and asked them to describe their dream. The researchers then looked at how their dream description related to the type of eye movements they were experiencing at the time (vertical, horizontal, or a mix of both).

Participants who were woken after a series of vertical movements reported “climbing up a ladder”, and “standing at the bottom of the cliff operating a hoist and looking up at climbers”, whereas one participant who was woken after horizontal eye movements reported dreaming about “two people throwing tomatoes at each other”. In contrast, those who had mixed eye movements tended to be watching people close to them with no description of distance or vertical vision.

When climbing, dreamers’ eyes move vertically. Håkan Dahlström/Flickr, CC BY

Since this study, the evidence for this association between the REMs and dream content is not consistent. Individuals who have been blind from birth, for instance, have REMs but no visual dream content.

But in support of Dement’s finding, a recent study in patients with REM behaviour disorder (where people act out their dreams due to a lack of muscle paralysis), found a strong association between goal-oriented limb and head action and eye gaze direction during REM sleep.

Brain activity during sleep

In everyday life, when we see things, our eyes and brain behave in characteristic ways to gather and process the information in our visual field and give it meaning. But the function of eye movements during sleep and dreaming are relatively unknown. Today’s Nature Communication paper provides some insights.

Usually, brain activity is measured non-invasively from the scalp. But the investigators, from Tel Aviv University, recorded the activity of the brain, from within the brain, in patients with epilepsy.

Patients whose epilepsy cannot be controlled with medication have electrodes surgically placed within the brain as a clinical means to map their epileptic activity, and assess suitability for surgery as a treatment. These electrodes were implanted in the medial temporal lobe – a region that is associated with visual awareness.

Researchers compared brain activity of these patients across three settings: REM sleep brain activity, wakeful eye movements in darkness (no visual processing) and wakeful fixed-gaze visual processing (no eye movements). They wanted to test whether brain behaviour during sleep was more closely related to physical movement, or the processing of visual information.

Results showed that during rapid eye movements in sleep, the brain activity was more closely related to the brain activity during visual processing during wakefulness (without movement) than physical movements of the eyes in darkness where no visual processing was taking place.

Eye movements suggest dreamers’ brains were processing images rather than trying to move . Ali T/Flickr, CC BY

These results suggest that the rapid eye movements that occur in sleep are linked to visual processing rather than just physical activation or movement. So, the participants may have actually been looking at a dream image, rather than these eye movements simply reflecting motor discharge in the brain.

While much remains unknown, this detailed processing of our dream images suggests that rapid eye movements may actually modulate our brain activity during sleep. We know that sleep is needed for rest and rejuvenation, but it’s likely to have other important functions as well.

In line with the earliest of theories about why we dream, are we processing content that has been consciously or unconsciously avoided during wakefulness, but somehow “needs” to be dealt with at least during sleep to maintain our psychological well-being?

Are the eye movements a simple byproduct of the visual processing that occurs of the images we dream?

Is there a psychological basis to why we need to process these images during sleep, and does this lend to better psychological outcomes in a similar way to sleep aiding physical functioning?

These and many questions drive the ongoing research into why we sleep, and what its precise benefits are.

Are we sleep-deprived or just darkness-deprived?

One of the most common complaints I have from my menopausal patients is insomnia. I have posted more blog on this subject than any other. Search this web-site by typing “sleep” in the search section to see  many of the other posts. 

Are we sleep-deprived or just darkness-deprived?

October 26, 2015 9.10pm AEDT

Not dark enough. People in bed via www.shutterstock.com.

The Centers for Disease Control and Prevention (CDC) state that insufficient sleep is a serious public health concern, because it can lead to many immediate dangers such as car crashes as well as long-term health problems like diabetes. The blame for sleep deprivation is often pinned on our fast-paced, 24/7 lifestyle, made possible by electric lighting at all times of day and night.

But are we really getting too little sleep?

A new study challenges that idea from a unique perspective, and it is getting wide media attention.

Researchers, led by Jerome Siegel at UCLA, followed three small preindustrial societies, two in Africa and one in South America, reasoning that the best way to judge whether sleep habits in the industrialized world are unnatural is to compare them to sleep habits in those few remaining societies on Earth that still live without electricity.

They found that the average period of time people spent trying to sleep was 7-8½ hours each night. Of this, only 5½-7 hours was confirmed as time asleep. This is about the same as, or less than, what is reported by most Americans and Europeans, and is considered too little for optimum health.

So maybe 5½-7 hours of sleep is natural and not the problem the CDC and many other health organizations say it is.

However, a crucial aspect of the findings of the new study has not been discussed in either the news stories or the paper itself: people in preindustrial societies spend much more time in darkness than people living in the industrialized world.

What does this study tell us about sleep patterns?

Besides finding that people in preindustrial societies without electricity sleep about the same amount as people in the electrified world, researchers also found that sleep didn’t start until several hours after sunset, although almost everyone woke up close to sunrise.

The researchers looked at temperature fluctuations, finding that it influenced the time of awakening in the morning. But for people sleeping in the modern built environment, temperature fluctuations in our bedrooms are minimal.

The researchers also found sleep in these societies was usually interspersed with periods of awakening that lasted for over an hour. These routine awakenings call into question the conventional wisdom that “ideal” sleep should be compacted into one stretch. Waking for a while at night is not necessarily a sleep disorder. Compacted sleep (“sleeping like a log”) is evidently not the way in which sleep evolved in humans.

But the big difference between sleep in the industrial world and sleep in the preindustrial world is about light and darkness. Electric light can delay or shut down nighttime physiology, whereas light from a wood fire or flame cannot. The researchers did not directly assess the quality of sleep, and this may be the part that matters.

The subjects in the preindustrial societies, living close to the equator, were exposed to darkness (with maybe an occasional wood fire) for 11 or 12 hours each night. In industrialized societies, people are typically exposed to darkness only as long as they are trying to sleep, often about seven hours.

Normal sleep and nighttime physiology

We humans have an endogenous circadian rhythmicity in physiology that is adapted to the solar cycle of day and night (as does almost all life on the planet). This means that in constant darkness we would still cycle about 24 hours in body temperature, hunger, activity and sleep.

When the sun is up, we are in daytime physiology: alert, active and hungry. When the sun sets in the evening, we begin the transition to nighttime physiology: body temperature drops, metabolism slows and sleepiness builds. In the world before electricity, each lasted about 11 hours near the equator, with time also for the transitions from one to the other at dawn and dusk. Of course, farther from the equator, the length of night increases or decreases according to season.

Part of nighttime physiology is sleep, but it is difficult to define what “normal” sleep is. Until the late 20th century, sleep was ignored by most biologists because it’s hard to study, and was thought by many ambitious people to be a vast waste of time. In recent years, this attitude has changed radically. It is now believed that modern life has led to unhealthy sleep habits and widespread sleep deprivation with a multitude of adverse health and productivity consequences.

 

Blue light disrupts melatonin production. Sleeping boy via www.shutterstock.com.

Looking at sleep in the industrialized world

In 1991, Thomas Wehr, a prominent sleep researcher, published the results of a landmark experiment he conducted in Bethesda, Maryland. In a sense, it mimicked sleep in the preindustrial world where there are naturally long, dark nights – the environment studied directly by Siegel and colleagues.

First, seven volunteers spent eight hours in the dark at night in the laboratory for four weeks; they then switched to 14 hours of dark each night without access to clocks and alarms. During the short nights, they slept a little more than seven hours on average. During the long nights they slept only about an hour more, a little over eight hours, and the sleep was broken into two stretches with an hour or two awake in between.

Importantly, the duration of melatonin production increased by about two hours after the long night. The hormone melatonin is a marker of nighttime physiology that helps regulate sleep and wake patterns. It has many important biological functions, and its production requires dark but not sleep.

So whether awake or not, these subjects produced melatonin, and maintained nighttime physiology, for the long duration of dark. But this is not how people actually live in the modern world. People use electric lights and electronic gadgets in the evening, and often late into the night.

The type of light we use at night matters

A useful term in the context of sleep and health is “circadian effective light” because bright, short wavelength light (blue, for instance) is much more effective than dim, longer wavelength light (yellow/red) in suppressing melatonin during the night and causing a premature transition to daytime physiology. There is also evidence from studies in humansthat bright blue light in the evening decreases the quality of sleep compared to an evening of dimmer, longer wavelength light.

In industrial societies, people are bathed in blue light from smartphones, computers and some kinds of light bulbs all day, and for a good chunk of the night. Our preindustrial counterparts may stay up late too, but it’s in the dark or in the light of a flame.

 

Candlelight doesn’t interfere with our circadian rhythm like electric light. The Night School circa 1660-1665. Gerrit Dou, via Wikimedia Commons

In the preindustrial time before electricity, sleep occurred within a much longer period of circadian dark; in the modern world it does not. Dark is restricted only to the sleep period, if even then; many people do not sleep in a truly dark bedroom. Seven hours of sleep embedded within 11 hours of circadian dark may be far more restorative than seven hours with bright, blue-containing light preceding it in the evening. The Siegel study might suggest that preindustrial people don’t sleep any more than people in industrialized societies, but perhaps they just get a better night’s sleep, and much more circadian dark.

For us in the industrialized world, it might be wise to use dimmer, longer wavelength lighting (like low wattage incandescent bulbs, if you can still find them) in the evening before sleep to allow an earlier transition to nighttime physiology. Fortunately, such circadian-friendly lighting is currently being designed with the new lighting technologies now available.

And during those inevitable periods of awakening in the middle of the night, try to enjoy the calm of darkness.

Female sexuality and vaginal health across the menopausal age.

Vaginal dryness is a major problem in the menopause, causing pain and discomfort during sex. Women seem to be reluctant to discuss this with their doctors, and often just accept it as a normal part of menopause. Treatment is readily available, if women would just mention to their doctors. I am just as much to blame as anyone else because I don’t ask women frequently enough about vaginal discomfort. (Note to myself – make an effort to ask more often)

Menopause. 2020 Jan;27(1):14-19. doi: 10.1097/GME.0000000000001427.

Female sexuality and vaginal health across the menopausal age.

Cagnacci A1, Venier M1, Xholli A1, Paglietti C1, Caruso S2; ANGEL Study.

Author information

Abstract

OBJECTIVE:

The primary aim was to evaluate changes in female sexuality across the menopausal period, and the secondary objective was to test the associations of female sexuality domains with vaginal atrophy and its symptoms.

METHODS:

A cross-sectional multicenter study was performed involving 518 women, 40 to 55 years of age, consulting outpatient gynecological services at 30 centers across Italy. Vaginal atrophy was identified by the contemporaneous presence of a pH >5, subjective vaginal dryness, and an objective sign. The relationships between vaginal atrophy and its main symptoms (vaginal dryness and dyspareunia), and Female Sexual Function Index (FSFI) score and its domains (desire, arousal, orgasm, dyspareunia, lubrication, and sexual satisfaction) were analyzed.

RESULTS:

The prevalence of sexual dysfunction, as defined by a FSFI score <26.55, was 70.6%, increasing from 55% in the years 40 to 45, to 82.8% (P < 0.01) in the years 52 to 55 of age. Mean FSFI score decreased from 40 to 45, to 46 to 48 years of age (23.13 ± 9.76 vs 19.49 ± 9.88; P < 0.05), and from 48 to 51, to 52 to 55 years of age (21.3 ± 8.06 to 17.59 ± 9.11; P < 0.01). Independent determinants of FSFI were age, vaginal atrophy, and the presence of vaginal dryness and dyspareunia (R2 0.208; P = 0.011). FSFI score was independently correlated (R2 0.116) with weight (CR -0.067; 95% confidence interval [CI] -0.126, -0.006; P < 0.032), menopausal status (CR -2.406; 95% CI -4.180, -0.63; P < 0.008), and vaginal dryness (CR -5.647; 95% CI -7.677, -3.618; P < 0.0001). Vaginal dryness was the only variable correlated independently with each FSFI domain, including desire (also correlated with menopausal status), arousal (with age and menopausal status), lubrication (with age), orgasm (with age), satisfaction (with vaginal atrophy and being an ex-smoker), and dyspareunia (with age and spontaneously referred dyspareunia).

CONCLUSIONS:

In the perimenopausal years, FSFI score decreases and sexual dysfunction increases by about 30%. Vaginal dryness is the symptom of vaginal atrophy most closely related to all domains of female sexuality.

The real reason women live longer than men – new study

Jekatarinka/Shutterstock

The real reason women live longer than men – new study

January 21, 2020 11.12pm AEDT

Author

  1. Maarten Wensink Assistant Professor, Epidemiology, Biostatistics and Biodemography, University of Southern Denmark

Disclosure statement

Maarten Wensink does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Partners

University of Southern Denmark

University of Southern Denmark provides funding as a member of The Conversation UK.

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CC BY NDWe believe in the free flow of information

Ask your smartphone how to drive from Copenhagen to Berlin and it will give you an estimate of how long the trip will take, based on current traffic. If there is a traffic jam in Hamburg, say, the extra time this traffic jam takes will be included in the estimate. But, of course, you are not at all the points of your journey now. Rather, you’ll be in Copenhagen first, then at Odense, then Kolding, and so forth. By the time you get to Hamburg, there may no longer be a traffic jam. The estimate your smartphone gave you will be off. Life expectancy is calculated in much the same way.

Life expectancy in 2019 is calculated using the chances of survival for all ages in 2019: those who turned 70 in 2019, those who turned 69 in 2019, those who turned 71 … you get the point. But nobody actually has all their birthdays in 2019. People have at most one birthday a year (less than one for some of those who died that year and those born on February 29). Since I turned 35 in 2019, why should the 2019 chances of survival for a 70-year-old matter to me? By the time I turn 70, the world will have changed. The estimate will be off.


Read more: Mortality rates are still rising in the UK – and everyone is ignoring how many more people are dying


But your smartphone also tells you something like “31 minutes extra travel time due to a traffic jam”. With this information, you can guess how long the trip will take assuming that the traffic jam will be resolved by the time you get there: just subtract those 31 minutes. Every part of the journey has a travelling time and you can pick those pieces apart.

Similarly, life expectancy is built up out of many small pieces, one for each age, and demographers can pick those pieces apart. We did that to answer questions such as: “what is the part of life expectancy lived between ages 50 and 85?” (which will be a number between 0 and 35). And “suppose that in 2015 no 70-year-old died of smoking (for example through lung cancer), what would that life expectancy have been?” And “how has the importance of smoking-related deaths been changing, and was that different for men and women?”

Throw all that in the mixer and you get some interesting results, which my colleagues and I – a team from the University of Southern Denmark and University of Groningen – published in BMC Public Health.


Read more: Improving life expectancy used to be the UK’s forte – now it’s falling behind


We studied the part of life expectancy lived between ages 50 and 85 for high-income North America, high-income Europe and high-income Oceania for the period 1950-2015. Around 1950, males lived about two and a half years less than females. Around 1980, this difference had increased to about four and a half years. Then the difference in life expectancy declined to new lows of about two years in 2015.

All of that increase and subsequent decrease was due to smoking. Remove smoking and you get an almost flat line at only two years, which is what the difference in life expectancy between ages 50 and 85 would have been if nobody had smoked.

Long time coming

If smoking is so bad, why are we seeing all of these early deaths? Why aren’t people smarter? Well, if cigarettes killed you right away, nobody would touch them. The problem is that cigarettes do kill you – only decades later.

Because, historically, men started smoking earlier and heavier than women, any effect of smoking on life expectancy shows in males first. While medical doctors were coming to the conclusion that smoking is bad – basing their conclusions on evidence from men – women decided it was time to take up smoking. Now, decades later, the effect of smoking (death) is declining in males but still increasing for older females who smoked in the past. This gives rise to a four-wave pattern dubbed “the smoking epidemic”: first men smoke, then men start dying from smoking at around the same time women start smoking, then women start dying from smoking.

In some countries, such as the UK and the Netherlands, more women than men may soon die of smoking. Photographee.eu/Shutterstock

In the final phase of the smoking epidemic, people get smarter and stop smoking. This last part of the smoking epidemic, however, is the more difficult part. Unfortunately, people keep smoking (big tobacco is doing just fine).

But our study also showed some good news. Recently, there was a big drop in smoking-related deaths for people of around 50 years old. While smoking is certainly not down and out, at least some people seem to get that tobacco is a killer.

How marketers condition us to buy more junk food

How marketers condition us to buy more junk food

September 10, 2015 6.14am AEST

People queue outside the first KFC restaurant in Yangon, Myanmar, which opened last month. Nyein Chan Naing/EPA/AAP

While excess weight and obesity is a growing global concern, there has been more and more advertising and promotional effort encouraging the consumption of unhealthy food.

In many cases this marketing is targeted at children, and takes place online. In our recent study we investigated the impact of online marketing communications on children and their intention to consume unhealthy food. We found fast food ads on social networking sites can manipulate young audiences – their purchasing likelihood, their views of fast food and their eating habits.

The qualitative study included a sample of 40 Australian children who use social networking sites. Half (21) of the children were male and the average age was 14 (the youngest being 12 and the oldest 16). Their parents were also present during the interview, however they agreed not to intervene during the conversation.

A growing problem

The prevalence of excess weight and obesity among Australians has been growing for the past 30 years. Between 2011 and 2012, around 60% of Australian adults were classified as overweight, and more than 25% of these fell into the obese category. In 2013, more than 12 million, or three in five Australian adults, were overweight or obese. On top of that, one in four Australian children were overweight or obese. Excess weight and obesity is only beaten by smoking and high blood pressure as a contributor to a burden of diseases.

Despite this, the food industry is succeeding in using marketing communications to change attitudes, perceptions and perceived norms associated with unhealthy food.

Consumers are lured by surprisingly cheap deals, which are especially attractive to teenagers and young adults with low income. But sales promotions such as discounts and coupons often offer only short-term benefits to consumers and are usually not effective among middle-age adults.

However, if a promotion is offered for a long period of time (i.e. more than three months), it can actually influence customer habits, encouraging repeat purchases – for example, the $1 frozen Coke.

Similarly, sales promotions can make other brands be perceived as less attractive by customers after a period of time. For instance, the $1 frozen Coke campaigns by McDonald’s and Hungry Jack’s affect the perception of frozen Coke in terms of monetary value. Many consumers become less willing to buy a frozen Coke that is more expensive than $1. The same can be said of $2 burgers or $5 pizzas.

The role of social networks

More than half (16 out of 30) of the respondents admitted they tended to change their eating habits after repeatedly being exposed to advertisements on social networking sites.

“Yes, many people say that it is not good to eat fast food. I used to think so but not anymore. Look at their ads, they are colourful, many options and cheap.”

“I just cannot resist it… I had been looking at the ads day after day and I decided that I needed to try these”.

Interestingly, fast food was associated with socialisation and fun among young consumers.

“The ads make me feel like this is where we belong to. This is our lifestyle…where we hang out and can be ourselves.”

“This is about our culture, young, active and free. We are kids but also not kids. We are different.”

Peer pressure

Peer pressure is heavily related to eating habits, especially during puberty when there is usually a shift from home influence to group motivation. Teenagers and young adults in particular tend to choose a particular type of food under peer pressure.

More than 70% of teenagers will choose a food according to the preference of their friends. This means marketing communications promoting fast food consumption can create a snowball effect within this group of customers. For example, Jack, Sara and Park go out together. If Jack and Sara order Big Burgers with extra cheese, the likelihood that Park will order another Big Burger with extra cheese is approximately 75%. In contrast, only 2.7% of people aged over 40 choose fast food because of their peers.

It’s clear marketing efforts by fast food chains can promote unhealthy eating habits. Also, peer influence plays an important part in forming eating habits. This means the intervention of government and health organisations should concentrate on increasing customers’ attention to health issues, self-efficacy and perceived norms, and at the same time, lessening the influence of marketing efforts aimed at motivating unhealthy eating habits.

Is breast cancer risk the same for all progestogens?

I often get the comment from patients, that their doctors said that the Bioidentical hormones are the same as what most GPs prescribe. This is patently false as the natural progesterone is far better and it is what I have been prescribing for over 25 years for my menopausal patients. Recently, a commercial preparation has become available, which is the same as the natural, micronised progesterone.

Is breast cancer risk the same for all progestogens? – PubMed – NCBI

Arch Gynecol Obstet. 2014 Aug;290(2):207-9. doi: 10.1007/s00404-014-3270-0.

Is breast cancer risk the same for all progestogens?

Author information

  • 1Department of Obstetrics and Gynecology, University of Berne, Bern, Switzerland, petra.stute@insel.ch.

Abstract

The population-based case–control study CECILE investigated the impact of various menopausal hormone therapy (MHT) products on breast cancer (BC) risk in 1,555 postmenopausal women [1]. The case group (n = 739) included incident cases of in situ (!) or invasive BC in postmenopausal women. The control group (n = 816) included women from the general population within predefined quotas by age and socio-economic status (SES). While quotas by age were applied to obtain similar distributions by age among controls and among cases, quotas by SES in control women were applied to reflect the distribution by SES of women in the general population in the study area. Data of participants were obtained by a structured questionnaire during in-person interviews, and from pathology reports if applicable, respectively. Women were divided into current and past MHT user. MHTs were classified in estrogen-only therapy (ET), estrogen combined with progestin therapy (EPT) and tibolone. EPT was subdivided in three subtypes according to the progestogen constituent: natural micronized progesterone, progesterone derivatives, and testosterone derivatives. In comparison to never MHT users, any current or past MHT use (ET, EPT, tibolone) was not associated with an increased BC risk. However, in subanalysis BC risk was significantly increased for current use of EPT for 4 or more years (n = 73 cases and n = 56 controls, adjusted OR 1.55; 95 % CI 1.02–2.36). Within the group of current EPT users for 4 or more years, 14 cases had used estrogens combined with micronized progesterone (n = 17 controls), and 55 a combination with a synthetic progestogen (n = 34 controls), respectively. Compared to never MHT use, current use of EPT containing a synthetic progestogen for 4 or more years was associated with a significantly increased BC risk (adjusted OR 2.07; 95 % CI 1.26–3.39), but EPT containing micronized progesterone was not (adjusted OR 0.79; 95 % CI 0.37–1.71). 73 % of current MHT users started treatment within the first year of onset of menopause. Early EPT (n = 52 cases and n = 38 controls, adjusted OR 1.65; 95 % CI 1.02–2.69), but not early ET, starters had a significantly higher BC risk compared to never MHT users. In contrast, MHT initiation beyond 1 year after menopause was not associated with an increased BC risk.

The authors concluded that: (1) ET and EPT containing natural progesterone did not increase BC risk whereas, (2) BC risk was increased in users of tibolone or EPT containing a synthetic progestogen, respectively, and that (3) MHT use early after onset of menopause was associated with an increased BC risk as compared to women who delay MHT beyond 1 or more years.