For half the population, it comes three to five days each month, 12 months each year, for 40 years of our lives. Menstruation can be debilitating, relieving, disappointing, or simply an inconvenient fact of life.

But why do humans menstruate, when most animals don’t? When you shake the tree of life, you find that only a handful of mammals aside from us – primates, a small number of bat species, and the elephant shrew – have opted for the monthly bleed.

Each month the uterus prepares a thick and luxurious lining in preparation for the arrival of a fertilised egg – an embryo that will develop into a fetus and after nine months, a full-term baby. If no embryo arrives, there will be no pregnancy and menstruation sheds the thickened lining.

Evolution is often viewed in terms of a cost-benefit ledger: if something is costly, it must have some benefit. Women lose over half a standard glass of wine’s worth in iron-rich blood and tissue – about 90 millilitres – each time they menstruate, so the process does seem quite costly. And in the predator-filled environs of our early ancestors, leaving a trail of blood was presumably not advantageous.

So how did menstruation arise? Over recent decades, evolutionary biologists have come up with three key theories to explain human menstruation.

Cleansing mechanism

One controversial theory, proposed in the 1990s by self-taught biologist Margie Profet, suggested menstruation was a cleansing mechanism. Being the amorous species that we are, human females require a mechanism to regularly flush out the infection-laden sperm that gathers from our sexual conquests.

This argument was soon found to have more than a few flaws. For a start, women are more susceptible, not less, to infections such as chlamydia and gonorrhoea during menstruation, as the cervical mucus thins out.

The iron-rich blood also serves as an attractive food source for Staphylococcus aureus, of tampon-associated toxic shock syndrome notoriety.

And there is no correlation between level of promiscuity in us and our close primate relatives and heaviness of bleeding, as the theory predicts.

Invasive embryos

A more plausible explanation for menstruation is that it evolved to accommodate the peculiar way in which human embryos embed into the lining of the uterus – the endometrium – during pregnancy.

In some mammals with a placenta, a fertilised embryo attaches to the endometrium only superficially. In humans and other menstruating species, implantation is deep and invasive, and requires an especially luxurious lining to develop in preparation for implantation.

While other mammals are able to reabsorb the lining that adorns their fertile womb, the volume of tissue in humans is too great, so if no pregnancy ensues, it is expelled instead.

In the evolutionary cost-benefit analysis, building up the lining only when a pregnancy is on the cards – only when we ovulate once a month – could be less costly than maintaining this expensive lining indefinitely.

Another key difference between menstruators and non-menstruators is in the impetus for uterine thickening. In non-menstruating mammals, the final thickening of the endometrium (a process called decidualisation) only occurs once the lining senses the bleating signals from the embryo saying, “I’m here, now make my bed!”

Somewhere along the human evolutionary path, the dialogue between embryo and uterus shifted, so that the signals causing the endometrium to thicken came not from the embryo, but from the mother herself. Instead of being linked to the presence of the embryo, uterine thickening became linked to ovulation and the choreographed hormonal up-and-down that each woman cycles through on a monthly basis.

Maternal self-defence

But what’s with all this pre-emptive pampering? Not all mammals prepare for pregnancy so hopefully each month. Rabbits, for example, only ovulate and thicken their endometrium when they copulate.

American evolutionary biologists Deena Emera, Roberto Romero and Günter Wagner argue that the spontaneous thickening of the uterine lining is in fact a defence mechanism. Except the defence is against our own parasitic offspring, rather than sperm-borne infection.

Since mother and child do not share identical genes, their purposes are at odds. From the embryo’s perspective, the maximum benefit is gained from squeezing as many resources from its mother as possible. It even dampens its mother’s response to insulin, ensuring that a greater slice of the circulating sugar pie is placenta-bound during its nine-month residence.

Click to enlarge

The mother, meanwhile, prefers to be frugal with her resources, so that she can survive this pregnancy and go on to populate the next generation with additional children endowed with her unique genetic contribution.

There are two reasons that this maternal–fetal tug of war could have resulted in spontaneous thickening of the uterus. First, with implantation already invasive in humans and other menstruating species, the pre-thickened lining could be an evolutionary push-back to prevent the embryo from burrowing even deeper into the uterine wall.

The second reason is to protect the mother from expending valuable resources on faulty fetuses. The thickened lining could be an efficient way to sense – and if necessary, jettison – any tainted, and therefore unwanted, embryos. Around 30% to 60% of all human embryos are unceremoniously discarded in this way, before any signs of pregnancy occur.

While its evolutionary origins are firmly rooted in what takes place during pregnancy, the reality is that for most menstrual cycles, no embryo arrives. The decidual cells that have thickened the uterine lining pack up shop, the extracellular matrix keeping them all together breaks down, and the lining becomes as deciduous as the autumn leaves.

For Western most women who bear few children, this menstrual cycle is repeated 450 to 480 times over.

Choosing Olive Oil

Olive oil, once used in the U.S. primarily by immigrants from Mediterranean countries and adventurous gourmets, is now mainstream. In 2012, Americans consumed over 320 metric tons – more than 10 times the amount consumed in 1972. This is good news, as olive oil has the highest percentage of heart-healthy monounsaturated fat of any edible oil, and quality brands contain abundant antioxidants – substances that have been shown to provide cardiovascular and anti-cancer effects.

When choosing olive oil, Dr. Weil recommends buying small bottles of certified organic, extra virgin olive oil. Check the label for the ICEA (Istituto per la Certificazione Etica e Ambientale, which means Ethical and Environmental Certification Institute) logo, and that of another organic certification body such as the USDA’s green-and-white ORGANIC logo. Quality extra virgin olive oil should have a natural peppery finish and a deep, “green” aroma of grass and artichoke. Such oils are not cheap, because they rely on careful cultivation that preserves olive oil’s legendary taste and health benefits. But the reward is more than worth it.

Healthiest Bread Spread?

When it comes to spreads for your bread, Dr. Weil is a longtime proponent of extra virgin olive oil. Its heart-healthy fats are a much better choice than margarine. Margarine was originally developed as a cheap substitute for butter, and has evolved from some fairly unappealing animal-based ingredients into a vegetable-oil based spread with added chemicals that make it more flavorful and easier to spread. To achieve that solid, spreadable consistency, margarine manufacturers add hydrogenated vegetable oil, creating unhealthy compounds that may contribute to heart disease and stroke. In addition, the heat and chemicals used to harden vegetable oils produce trans-fatty acids (TFAs), which can contribute to heart disease, increase cancer risks, promote inflammation and accelerate tissue degeneration.

Butter is definitely the better choice. In fact, some recent studies suggest that natural saturated fats, such as those found in butter, may not significantly contribute to cardiovascular disease, though further study is warranted. In any case, butter is closer to a whole food than margarine. If you must opt for a spread that is not extra virgin olive oil, try natural, organic butter in limited quantities.

You’ve got a high fever, severe cough and find it hard to breathe – all symptoms of severe pneumonia. Before antibiotics, you’d likely be dead within ten days. In fact, before we had these amazing drugs, infections caused by bacteria were the leading cause of death.

Today, take a course of antibiotics and most of time you’ll be completely fine. But just what is an antibiotic, and how does it work? And what’s all this talk about antibiotic resistance and superbugs?

An antibiotic is a compound that cures infections by killing or slowing the growth of bacteria. The word literally means “anti-life”, from the Greek “bios” meaning life. The original antibiotics were made by bacteria or fungi to prevent growth or kill other bugs in what was effectively “chemical warfare” between the species during the colonisation of our planet by microorganisms billions of years ago.

Antibiotic drugs

Thousands of antibiotics have been discovered over the years, but most have only been shown to kill bacteria in the laboratory. Very few have become drugs because in order to do that, an antibiotic must be selective – it must kill the bacteria while not harming the cells of the human body.

An antibiotic must also have the right properties to last long enough in the body to get to the site of the infection and kill the bacteria quickly. The first antibiotic, a blue-green pigment extract from a bacterium called Pseudomonas aeruginosa, was a compound called pyocyanase. It was used to treat infections in the 1890s, but was quite toxic.

Most antibiotic drugs today are variations of substances that were originally isolated from bacteria or fungi, such as penicillin, which was isolated from a fungal mould in 1928, or vancomycin, which came from a soil-dwelling bacteria collected in Borneo in 1953.

Some commercial antibiotics used today are still isolated from bacteria grown in large fermentation vats, while others are modified chemically by scientists to improve their activity or reduce the extent of side effects. Totally synthetic antibiotics produced by chemists have been developed in the last 40 years.

While antibiotics were “discovered” around 100 years ago, they are actually ancient – microorganisms have been producing them for billions of years. Some antibiotics were produced as defence mechanisms against other bacteria, while others started off as messenger molecules between bacteria and then evolved into killing agents to allow different species of bacteria to out-compete others.

How antibiotics work

Antibiotics work by attacking the parts that a bacterium needs to grow, survive and replicate. A number of antibiotics, such as penicillin and vancomycin, inhibit the growth of the outer casing of the bacteria, which is called a cell wall. Just like the walls of a house, without a strong cell wall, the bacteria collapses.

Bacteria have a very different type of cell wall to what we find in human cells (think a double brick insulated bungalow in cold Canberra for bacteria versus a timber Queenslander in warm Brisbane for humans). This is because in people, cells are protected by being surrounded by other cells inside our bodies, while bacteria are exposed out in the environment and need stronger cell walls.

In this analogy, antibiotics such as penicillin and vancomycin are designed to attack and destroy the bricks, but not touch timber, which means they kill bacteria but don’t harm us. This image shows how vancomycin, chemically modified to glow blue, selectively attaches to the cell wall of bacteria.

Other antibiotics (such as aminoglycosides, erethromycins and tetracyclines) work by inhibiting protein synthesis, which means the bacteria can’t function (there is no kitchen or furniture inside the house). Or they block DNA replication (metronizadole and the quinolones, such as ciprofloxacin), which stops the bacteria from reproducing or replicating (so only one house is built in the suburb).

Some of these effects are bacteriostatic – they stop the bacteria growing. This gives our body’s immune system time to kick in and clear the infection naturally.

Antibiotic resistance and superbugs

Bacteria develop resistance to antibiotics by rapidly evolving to create ways of neutralising them, actively pumping them out of their cells, or preventing them from entering in the first place. Resistance to antibiotics is now a global problem that is increasing all the time.

Paradoxically, antibiotic resistance is also ancient. Excavations of permafrost in Canada have demonstrated that genes coding for a common type of resistance to vancomycin were present over 30,000 years ago. This is because bacteria developed most of the antibiotics we use today millennia ago, and at the same time, other bacteria were evolving ways to defend themselves and resist them.

So antibiotics are a very precious, finite natural resource that we need to take much more care of.

Resistance to antibiotics is a growing problem in treating infections, and is often due to incomplete treatments. Not taking the whole course of antibiotics leads to the survival of a small number of bacteria that can tolerate the drug.

Feeding sub-lethal doses of antibiotics to livestock as growth promoters is another potential source of resistance because it creates resistant populations of bacteria within the livestock. It also results in low levels of antibiotic contamination in the environment.

Research has shown that this leads to superbugs in animals that can then get transferred to humans via our food chain. Bacteria are very promiscuous, and are able to quickly swap genes coding for resistance between different species, in a kind of “bacterial sex”. This has led to the global spread of “superbugs”, bacteria that are resistant to many types of antibiotics, and, in some cases, all antibiotics.

In 2010, bacterial infection killed more people than cancer, based on data from the WHO’s Global Health Observatory Database. Despite this enormous human cost, most pharmaceutical companies have left the field of antibiotic drug discovery, primarily for economic reasons. They make more money with drugs people take for a long time, such as the cholesterol-lowering drug Lipitor, than an antibiotic you may only need for two weeks.

The train is heading down the tunnel, but we are still walking towards it. We may be re-entering an era where simple infections can once again be death sentences.

Osteoporosis experts have urged the public to ensure they get adequate calcium, weight-bearing exercise and vitamin D to prevent bone problems, warning that children who swap milk drinks for soft drink may be at greater risk of fractures later in life.

Around 1.2 million Australians suffer from osteoporosis, where bones become so frail they fracture at low levels of trauma. A further 6.3 million have osteopenia, a precursor condition where bones have lower density than normal.

Both conditions are caused by inadequate consumption of calcium and vitamin D, which is needed to absorb calcium, as well as insufficient weight-bearing activities and sports like running and tennis.

In a white paper published today by the Medical Journal of Australia, osteoporosis experts said more needed to be done to boost public awareness of a problem that added billions to the public health bill every year.

“Osteoporosis was designated a National Health Priority Area in 2002; however, implementation of national plans has not yet matched the rhetoric in terms of urgency,” the authors of the paper said.

It is never too late to take action to reduce your osteoporosis risk, the authors said, adding that calcium and exercise needs will change throughout life.

The paper urged people to:

• Consume three to five serves of calcium-rich foods daily (such as dairy or calcium-fortified foods).
• Get enough vitamin D from sunlight. Fair people should get around 6 minutes a day (during summer) or up to 40 minutes a day (during winter) of sun, avoiding peak UV times. Dark-skinned people should aim for up to 42 minutes during summer and up to four hours during winter. People who cannot get adequate sun exposure should consider vitamin D supplements.
• Partake in regular weight-bearing sports or exercise for at least half an hour three to five days a week and do muscle-strengthening exercises on at least two days per week.

“The main finding is there are three key things that we all need to consider to optimise our bone health: ensuring we get adequate calcium, vitamin D and exercise. Each one alone is not sufficient if we want to prevent fractures in later life,” said one of the authors of the paper, Professor Robin Daly, Chair of Exercise and Ageing at Deakin University’s School of Exercise and Nutrition Sciences.

“We are trying to encourage people to consider various forms of dairy products and avoid drinking sugary soft drinks. Dairy products not only contain calcium, they contain other good nutrients and there are some good options on the market for people who are lactose intolerant.”

Professor Daly said it was understandable Australians should be cautious of getting too much sun but to remember that a little could help reduce their osteoporosis risk.

“We published a study on 11,000 Australians that showed a third of the general population from 25 years up had low vitamin D levels. You don’t need much sunlight to get adequate amounts of vitamin D,” he said.

Associate Professor Mark Kotowicz from Deakin University’s School of Medicine said the white paper was “an important and well-researched document that highlights the burden of osteoporosis in the community.”

“The white paper provides some practical guidelines as to vitamin D and calcium requirements at different ages and critically reviews the evidence relating to exercise and bone health, highlighting regimens that have evidence to support their efficacy,” he said.

However, the white paper’s focus on public health meant it did not address the treatment gap in the management of osteoporosis, said Associate Professor Kotowicz, who was not involved in the white paper.

“Osteoporosis is under-diagnosed and under-treated throughout the world and this treatment gap could be the subject of another white paper on osteoporosis,” he said.

“The evidence that interventions to make the “first fracture the last fracture” are cost-effective in reducing the burden of osteoporosis is mounting, yet health authorities have been reluctant to invest in fracture prevention programs.”

Dr Peter Rich, a senior lecturer in RMIT’s School of Medical Sciences, said the white paper was “an excellent document” because it emphasised weight-bearing exercise and vitamin D as well as calcium consumption.

“People tend to think ‘Oh well, all I have to do is drink enough milk and I won’t get osteoporosis’. But that is not enough,” said Dr Rich, who was not involved in the paper.

“I would like the idea of emphasising the exercise part. It’s a lot easier to go and drink milk but the exercise part is harder to change.”

Dr Rich said it was important to remember that only certain types of exercise helped prevent osteoporosis.

“A lot of people think, ‘Well, I go swimming, so I do a lot of exercise’. Swimming is good and we would not discourage it but it is not weight-bearing exercise,” he said, adding that people who count walking as their primary form of exercise should consider including strength training or gym exercises too.

“And the paper mentions that, depending on your age group, you may want to increase walking to brisk walking or hill walking.

<!– — Updated: 11:25 am –>16 Comments

Ask Well: How Often to Exercise

Phil Mansfield for The New York Times A class at an Equinox gym in Manhattan led members through treadmill exercises.

Does it really matter if I work out three days in a row, rather than spreading my exercise through the week?

It probably does matter. As Dr. Michael Joyner, a physiologist at the Mayo Clinic in Rochester, Minn., points out, exercise has long-lasting, cumulative effects on your health and fitness, but it also produces acute effects that don’t necessarily linger.

A brisk walk can lead to almost immediate improvements in blood-sugar control and blood pressure for many people, he says. But if you then don’t walk or otherwise exercise for several consecutive days, those health benefits can evaporate. “There is good data in animals,” he says, ”showing that when running wheels are locked,” and the animals can’t exercise, “the positive metabolic aspects of training start to dissipate within days.”

Endurance also fades if you skip exercising for too many days in a row. The same is true, sadly, with motivation. In study after study, researchers have found that one of the primary reasons people continue exercising is that they enjoyed yesterday’s exercise or the exertions of the day before; they felt healthier and more physically masterful afterward and wish to relive that sensation. Longer periods between exercise sessions potentially could dull that enthusiasm.

Similarly, there is some evidence that injury rates can rise after a multiday layoff, especially in activities requiring well-honed technique. A 2011 study of circus performers found that two-day breaks between performances lessened injury rates, but the rates rose again if performers rested for three days or more.

“The key is probably to not miss more than two days in a row,” Dr. Joyner says, “and skipping only one day is even better.”

How to Thaw Frozen Fish

Wild-caught Alaskan salmon is one of my favorite foods. It is an excellent source of high-quality protein and essential omega-3 fatty acids, lowering the risk of heart attack, stroke, cancer, inflammatory diseases such as rheumatoid arthritis, and mental and emotional problems. Wild salmon is available fresh, frozen and canned, and according to the National Fisheries Institute, freezing fish and other seafood will cause minimal loss of the health-protective omega-3 fatty acids they contain. To thaw frozen salmon (or any other type of frozen fish), place the original, sealed package under a stream of cold water or put in a basin of cold, clean water. When the fish has just become pliable it is properly thawed and ready to cook. (It’s okay if the fish still seems slightly frozen.) Another method is to put the fish in your refrigerator to thaw – timing depends on the thickness of fish, but check the progress every few hours. Do not thaw frozen fish by setting it out at room temperature, submerging it in hot water or defrosting it in a microwave oven.

Dr Weil.

This is a very important message for all menopausal women, and their gynecologists. I have also just added a new page to my website, Titled” Menopause- recommendations” Read it, as these recommendations  have  just been published by the British Menopause Society.   This is as mainstream as you can get, and yet they now recommend natural progesterone as the safest form of progestogen, and transdermal ( through the skin – like troches) as the best way to introduce hormones. They also now recommend that women can take HRT for as long as they benefit by it. It is gratifying to see the major menopause bodies moving in the direction that I have been advocating for many years. This has been opposed by most specialists and GPs, as many of you will have experienced. I have recently posted the benefits of oestrogen for women (Look back in Archives) and now this adds more spice to what I wrote.

Estrogen deficiency: Education for all!

In July 2011, the Royal College of Obstetricians and Gynaecologists published the Expert Advisory Group Report High Quality Women’s Health Care: A Proposal for Change. ¹ This landmark publication highlighted a new concept – the continuum of important aspects of women’s health through puberty, the reproductive years, menstruation, pregnancy, contraception and fertility, through to the menopause and postreproductive health.

We feel the concept of a life-course approach to healthcare should be widely adopted with an emphasis on the fluid and changing challenges in women’s health. Healthcare providers need to be reminded that many conditions and disease processes evolve during the process of aging. This means that the same condition may have different manifestations depending upon her age and consequently her endocrinological status. For example, a history of polycystic ovarian syndrome increases the risk of endometrial cancer and so would influence the threshold for investigation of increased perimenopausal bleeding or postmenopausal bleeding; pregnancy-related problems such as pre-eclampsia increase the risk of cardiovascular disease in later life; the use of hormonal contraceptives may influence a woman’s views, and those of her doctor, on the use of hormone replacement therapy (HRT); diabetes influences the use of contraception, pregnancy and management of the menopause as clearly outlined in this issue in the review paper by Morling.²

So has this concept been applied to the care of women experiencing the menopause, and to the management of postmenopausal health? There has certainly been a broadening of interest in postmenopausal health and focus has moved away simply from ‘the menopause’ and the pros and cons of HRT, but it appears that the concept of changing health as life progresses after the point of the menopause has not been widely adapted. When women attend gynaecology clinics with postmenopausal bleeding, is full assessment taken of the number of years since the menopause, i.e. since she became estrogen deficient, whether or not she is still experiencing vasomotor symptoms, what has been the effect of estrogen deficiency on her vagina and bladder, how healthy are her bones and what is her cardiovascular risk? The same can be applied to women attending with prolapse, continence problems, and even when asymptomatic and attending for cervical or breast screening after the age of 50. If these assessments of the effects of estrogen deficiency are not being made, then surely opportunities are being lost?

While cognisance has to be made of time limitations and what is realistically achievable, surely at least gynaecologists should take on the broader, life-course view of women’s health and of the continuum of estrogen deficiency in particular and address the possible effects in any woman attending their clinics who is in an estrogen-deficient state. How can this message be adapted? It is time that primary care doctors and nurses, gynaecologists, physiotherapists, physicians, indeed all healthcare professionals caring for estrogen-deficient women had a broad understanding of the consequences of estrogen deficiency not only in the short term but throughout the years after periods stop and understood the life-course of women’s health. How? Education, education, education!

References

↵ RCOG Press. High

Former Olympic swimmer Lisa Curry has announced she will undergo fertility treatment to try to have a baby with her partner of three years. News reports say doctors estimate she has less than a 10% chance of success.

Given her doctors also note Curry’s ovaries are in “much better shape than expected”, why is it that her chances of having a child through IVF are so low? After all, Curry already has three children, which shows she has been fertile. The main factor is her age – 51.

While age also affects male fertility (sperm quality decreases with age), men generate new sperm throughout most of their lives. A woman, on the other hand, is born with a finite number of oocytes (eggs) that start to develop soon after she is conceived.

Declining numbers

At birth, a girl will have approximately one million eggs but, through natural cell attrition, she’ll have around 400,000 left by the time she reaches puberty. These eggs will have remained in a quiescent, dormant stage until the onset of puberty.

In response to hormone surges, one egg (on average) will undergo the final stages of growth and be ovulated approximately every 28 days for between four and five decades.

The ovum is unique for being the largest cell in the body and the fact that can’t be regenerated. By the time it has ovulated and is ready to be fertilised, it’ll be at least a couple of decades old. Indeed, an ovum awaiting fertilisation can be up to 40 years old.

At peak fertility (between the ages of 17 and 25), a sexually active woman has a 20% to 25% chance of becoming pregnant each month. At 32, her fertility starts to decline and by 40, it has halved.

She now also has a higher risk of miscarriage, pregnancy complications, gestational diabetes and birth defects.

So what is happening?

Deteriorating function

We carry 46 chromosomes, with each parent contributing 23 of these. For this inheritance to go smoothly, eggs and sperm need to contain half the number of chromosomes as normal cells.

If sperm and eggs contained a full set of chromosomes (46), at the time of fertilisation, the resulting embryo would contain 92 chromosomes. Your parents contributing equal numbers of chromosomes also aids genetic variability (allowing you to inherit traits from both your mum and dad).

When the final stages of egg growth is triggered just before ovulation, it undergoes a process called meiosis. The main purpose of meiosis is to shed half the number of chromosomes in the egg (from 46 to 23). In order for meiosis to occur correctly, chromosomes are moved around the cell on scaffolding called spindles.

As women get older, the components of meiosis, including the expression of genes that control its rate, the spindles and other repair mechanisms, deteriorate. This results in increasing numbers of eggs with incorrect numbers of chromosomes (this is called aneuploidy).

While most aneuploidies result in implantation failures (the inability for the embryo to embed in the uterine wall) or miscarriage, not all of them are lethal to the embryo. Incorrect numbers of chromosomes also result in Downs Syndrome, where a child has an extra chromosome 21.

Studies in mice have revealed that the rate of chromosome misalignments increases from 15% in young mice (six to eight weeks old, which is their peak fertility) compared to 50% in aged mice (12 months old).

Chromosome quality

The quality of the chromosomes themselves is also compromised by age.

Telomeres are structures that protect chromosomes from damage, similar to the plastic bit at the end of shoelaces. Shortening of telomeres is associated with cell ageing throughout the body, including ageing eggs.

Eggs have shorter telomeres from decades of inactivity. In comparison, telomere length within sperm is not affected as sperm-producing cells contain high levels of telomerase, the enzymes involved in repairing telomeres.

The ability of eggs to produce energy also decreases with age. All cells contain organelles called mitochondria that produce energy. Comparisons between aged and young mice show that ageing results in a 40% decrease in energy levels, 44% lower mitochondrial DNA and significant changes in the mitochondrial structure within the egg.

The combination of these and other factors, as well as the natural decline of the egg pool as women age, contribute to their decreasing fertility.

The introduction of the contraceptive pill, increased education and career opportunities have contributed to the increasing age of mothers.

Lisa Curry may have brought this issue into the spotlight but it is something that affects all of us, one way or another.

Research from The University of Queensland has reconfirmed oily fish or fish supplements are vital for heart health and debunked popular myths about coconut oil.

Associate Professor David Colquhoun, a cardiologist from UQ School of Medicine and Wesley and Greenslopes Private Hospitals, said the value of fish oil and its health benefits have been questioned.

“My research review confirms oily fish or fish supplements are important for heart health and should be a regular part of our weekly diet,” Associate Professor Colquhoun said.

According to the Heart Foundation, healthy adults should consume about 500 milligrams of omega-3 oil from marine sources per day to lower their risk of coronary heart disease.

This can be achieved by eating two to three serves of oily fish a week or by taking fish oil supplements.

Associate Professor Colquhoun also debunked popular myths about krill oil and coconut oil.

“Krill oil is a good source of omega-3s however it is no better for you than fish oil and is usually more expensive,” he said.

“Don’t take too much notice of krill oil labeled ‘organic’, ‘sustainable’ or ‘eco-friendly’ – the current harvesting of krill is less than 1 per cent of what is in the ocean, so it is all wild and sustainable.

“There have also been bizarre claims that coconut oil lowers cholesterol, cures Alzheimer’s disease and even prevents heart disease, however the research does not support this.

“In fact, coconut oil is full of unhealthy saturated fat which raises bad cholesterol levels, clogs the arteries and increases the risk of heart disease.

“With over 90 per cent saturated fat I would definitely be keeping coconut oil off the menu.”

Associate Professor Colquhoun presented his findings at the Heart Foundation Conference (16-18 May) in Adelaide.