Monthly Archives: February 2018

Hearing in women at menopause.

Interesting study showing the HRT, mainly oestrogen, protects against hearing loss in menopausal women.
Acta Otolaryngol. 2007 Feb;127(2):149-55.

Hearing in women at menopause. Prevalence of hearing loss, audiometric configuration and relation to hormone replacement therapy.

Author information

Department of Audiology, Karolinska University Hospital, Stockholm, Sweden.



Hormone replacement therapy (HRT) may have a protective effect on hearing impairment in postmenopausal women. New guidelines for classification of audiometric configuration in age-related hearing loss are suggested.


To describe prevalence of hearing loss and audiometric configuration in a group of middle-aged women with respect to menopausal stage and HRT.


A total of 143 women around menopause were sampled through the Swedish population register. The mean hearing threshold levels were compared according to menopausal status. The audiograms in the 57 women with hearing loss were classified according to audiometric configuration.


In all, 57 women (40%) had any kind of hearing loss; 42 had very minute hearing loss; 15 had a 4FA (average of thresholds at 0.5, 1, 2, and 4 kHz) of at least 20-39 dB HL in at least one ear. Two of these had a 4FA of 40-69 dB HL in at least one ear. The most common configurations were: gently sloping (47%), steeply sloping (14%), and high-frequency U-shaped (14%). The postmenopausal women who were not on HRT had poorer hearing mainly at 2 and 3 kHz, compared with pre- and perimenopausal women, and postmenopausal women on HRT.

You’ve been diagnosed with depression, now what

You’ve been diagnosed with depression, now what? October 15, 2015 4.08pm AEDT

Therapy, drugs or exercise? The depression treatment journey can be difficult to navigate. Eduardo Millo/Flickr, CC BY-NC-ND

First stop: talking therapies

Psychotherapy remains the cornerstone of treatment. Cognitive behavioural therapy (CBT) is the most studied of the therapies, but other forms are effective too. CBT works by addressing the thoughts and behaviours that act to entrench depression.

When people are depressed they tend to withdraw from their social networks. They no longer enjoy social interactions and think they’re unappealing company. By spending more time alone, and less time around people whose company they would usually enjoy, the depression gets worse, leading to even more time spent alone, and so on.

CBT and most other therapies act to break this feedback loop by challenging the thoughts and behaviours that reinforce social isolation, and getting people engaged again.

How do you find a therapist?

Your GP should be able to recommend one, or you can find names in the directories at the Australian Psychological Society and Royal Australian and New Zealand College of Psychiatrists. If you’re between 12 and 25, headspace is a good option.

Most therapists are psychologists or psychiatrists, but some have backgrounds in occupational therapy and social work. There is actually no need for a formal qualification to work as a therapist; my five-year-old daughter could put up her shingle. But it becomes important for claiming rebates, as well as feeling confident you’re seeing someone with a degree of competence.

The Medicare Better Access scheme provides rebates for up to ten sessions of therapy a year to see a psychologist, social worker, or occupational therapist.

To access it you need a GP referral, and the amount of the rebate you get will depend on the qualification of the therapist. It might cover all of the therapist’s fee, or there might be a gap.

You can get a higher rebate still if you see a psychiatrist, who can offer up to 50 sessions of therapy a year. Their fees are likely to be higher, though, meaning a bigger gap between what you pay and the rebate you get.

CBT aims to break unhelpful thinking patterns.

The funding for ten sessions per calendar year for non-medical therapists introduces an oddity to the process. If you start seeing a therapist towards the end of the year you can get 20 continuous sessions (ten in one year and ten in the next). But if your depression hits at the beginning of a calendar year you will be cut off after ten.

There are other options, though: you might be eligible for rebates from your health insurance fund and of course, if you can afford to, you can pay for the sessions yourself.

Then there is online therapy, which research suggests is very effective. There are a number of options available in Australia, including MoodGYM, e-couch and This Way Up. They are worth investigating.


Medications for depression have got a lot of bad press in the past few years, with suggestions that pharmaceutical companies have exaggerated their effectiveness by burying equivocal or negative results.

A fair assessment of the evidence suggests that overall they are effective: only modestly so, but taking an antidepressant medication is, on average, more effective than taking a sugar tablet.

Antidepressant medications might be considered when therapy hasn’t been effective, when it isn’t wanted (not everyone wants to see a therapist), or when the depression is severe.

One of the problems with antidepressant medications is they’re often not well-managed. Too often doctors write a script and the person stays on a low and ineffective dose of the medication without review for many months, even years.

Antidepressant use should be closely managed.

Antidepressant medications take four to six weeks before they start working. If there hasn’t been any effect by then, something needs to happen. In the first instance that is usually a dose increase.

But if the medication still hasn’t had any positive effect after another six to eight weeks, another medication should be considered. You need to get to this point before you can determine that a medication hasn’t been effective, but beyond this point there seems little sense in staying on a medication that hasn’t helped.

Any decisions about stopping medication, or changing dose, should be made in consultation with a doctor. Not only can they discuss the options, but they can also monitor your mood while changes are made.

Diet and exercise

People with depression are increasingly told that doing more exercise and eating better – the contemporary version of pulling their socks up – will alleviate their symptoms.

The science shows people who eat well and exercise regularly have lower levels of depression. Good physical health is associated with good mental health. Whether or not interventions that aim to improve diet or increase physical fitness are effective treatments for depression is, however, less certain.

The main problem with these prescriptions, as anyone who has been on a diet or joined a gym will know, is that filling them is hard.

It is always good to be fit and eat well, and doctors should more often recommend that these can help depression. But at this stage, while we work out how best exercise and diet can work as interventions, they should be seen as adjuncts to the more established treatments: pursue them, but in addition to psychotherapy, not instead of it.

Do I need a skin cancer check?

Health Check: do I need a skin cancer check?

November 9, 2015 4.14pm AEDT

Talk to your GP if you notice any moles or lesions that have grown, or changed shape or colour. charnsitr/Shutterstock

Australia has one of the highest rates of skin cancer in the world. Two-thirds of Australians will be diagnosed with skin cancer by the age 70.

The vast majority are non-melanoma skin cancers such as squamous cell carcinomas (SCC) and basal cell carcinomas (BCC). These are relatively easy to treat and rarely spread to other parts of the body.

Thirty years of SunSmart campaigns have raised community awareness – and anxiety – about skin cancer. But while most people know early detection is best, there’s a lot of confusion about whether you need to undergo regular skin checks.

Breast, bowel and cervical cancer prevention programs recommend population-wide screening with mammograms, pap tests and stool tests. But this isn’t the case for skin cancer checks.

Opportunistic screening

Current clinical guidelines recommend examining your own skin and asking your GP for a skin check if you notice anything suspicious.

This means familiarising yourself with your skin and looking for new moles, sores, lumps or lesions – or those that have changed size, shape or colour.

Australian guidelines favour self-detection and opportunistic screening over a population-wide program of regular skin checks because such a program would be incredibly costly and there is insufficient evidence that checking everybody would save lives. This is because:

  • very few people die from non-melanoma skin cancer
  • while advanced melanoma is deadly, the frequency of melanoma in the community does not justify a mass population screening program on economic grounds
  • the instrument that would be used for mass screening (assessment by a general practitioner) is not sufficiently accurate – in other words, GPs may remove too many benign lesions and also fail to diagnose and remove the skin cancers.

What should you do if you find a suspicious spot?

If you find a suspicious spot on your skin, ask your GP for a skin check. Your family doctor knows you, your medical history, your family history and is your first point of call.

There are only three possible diagnoses your doctor can make for you skin lesion: clearly malignant, clearly benign and too close to call.

If your doctor is 100% sure the lesion is a skin cancer, they will arrange for it to be removed. Each GP knows the limits of their surgical skill and will refer you on to a dermatologist as necessary. If you’re particularly concerned about scarring, you can request a referral to a dermatologist or plastic surgeon.

If your doctor is 100% certain the lesion is benign, no treatment is required and you will be reassured. Your doctor will examine any other skin lesions and provide you with advice about sun protection and early diagnosis of skin cancer.

If after examining your skin lesion, your doctor is only 99% sure that the lesion is benign, then a definitive diagnosis is required. Options include diagnostic biopsy, excision biopsy or referral to a dermatologist.

Access to specialists varies and patients may have to wait weeks or months for a definitive diagnosis for a “suspicious lesion”. So GPs often excise lesions they feel are low (but not zero) risk.

Consequently, the number of benign lesions needed to be excised for every skin cancer removed is approximately 20 for melanoma and three for non-melanoma skin cancers.

Some dermatology centres provide rapid assessment clinics for GP-referred patients with suspicious lesions.

High-risk groups

People at higher risk of skin cancer may benefit from asking their doctor for a skin check.

Apart from facilitating early diagnosis, the skin check is an opportunity to discuss your individual risk, what to look for when examining your skin, and ways to protect yourself in the sun.

Medical photography is increasingly popular and there is some evidence to support its use in high-risk patients to help detect melanomas early.

But photographs are not the best way to detect non-melanoma skin cancers. Nor are they a substitute for an examination by an experienced clinician.

People who have had previous skin cancer should see their dermatologist once a year for a skin check.

Those who have had more than 20 solar keratosis (lesions caused by UV rays) treated should see a dermatologist for an initial assessment and then once every two to three years.

People with a first-degree relative who has had a melanoma should ask their GP for a skin check and to assess their risk.

Those with red hair, fair skin, blue eyes and those with lots of moles (more than 50) should consider a skin assessment once they hit 30.

People with blond hair, fair skin and blue eyes could wait until they are 40.

And the rest of us might consider having a check when we turn 50.

Further reading: Spot the difference: harmless mole or potential skin cancer

How our brain controls movement and makes new connections when parts are damaged


How our brain controls movement and makes new connections when parts are damaged

September 29, 2016 6.09am AEST

Disclosure statement

Ross Cunnington receives funding from the Australian Research Council and the National Health and Medical Research Council


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


The brain is key to our existence, but there’s a long way to go before neuroscience can truly capture its staggering capacity. For now though, our Brain Control series explores what we do know about the brain’s command of six central functions: language, mood, memory, vision, personality and motor skills – and what happens when things go wrong.

Having voluntary control over body movements is the only way we can interact with people, objects and our environment. Body movement is not just about controlling arms and legs; it’s also for our head and eyes to visually explore the world, for our facial expressions to show emotion, and for articulation of our lips, tongue and mouth to communicate.

Further reading: What brain regions control our language? And how do we know this?

The devastating effects of the brain losing its ability to control body movements are seen in motor neuron disease – where progressive degeneration and muscle wasting leads to some patients becoming “locked-in”, meaning they can’t move or communicate in any way.

The motor system and primary motor cortex

The brain’s motor system is contained mostly in the frontal lobes. It starts with premotor areas, for planning and coordinating complex movements, and ends with the primary motor cortex, where the final output is sent down the spinal cord to cause contraction and movement of specific muscles.

The primary motor cortex on the left side of the brain controls movement of the right side of the body, and vice-versa, the right motor cortex controls movement of the left side of the body.

Different areas of the primary motor cortex connect to and control movement of different body parts. Wikimedia Commons

Different areas of the primary motor cortex connect to, and control, movement of different parts of the body, forming a kind of body map known as the homunculus.

The size of the area on the homunculus determines the level of fine movement control we have with that part of the body. So, for instance, a large proportion of the motor cortex is devoted to our thumb, fingers, mouth and lips, as they are vital for manipulating objects and speech articulation.

The connection from the primary motor cortex to muscles of the body is so important that any damage leads to an impaired ability to move. If someone suffers a stroke, for instance, that causes damage to the primary motor cortex on one side of their brain, they will develop an impaired ability to move on the opposite side of their body.

Further reading: Some people can’t see, but still think they can: here’s how the brain controls our vision.

If the area of damage is specific to only part of the primary motor cortex, such as the hand area of the homunculus, it will affect movements only of the corresponding part of their body, for example, the hand.

The Conversation, CC BY-SA

Neuroplasticity and movement rehabilitation

As with other parts of the brain, when neurons of the primary motor cortex are damaged they will never regrow or repair. However, the brain can heal itself and regain some lost function through neuroplasticity. This means undamaged parts can change their connections and remap to other areas of the body to take over function, compensating for damaged parts of the motor cortex.

Neuroplasticity is the fundamental principle in physical rehabilitation, such as physiotherapy for patients following stroke, that allows patients to regain motor function and recover. Through neuroplasticity, the more a particular movement is performed, the stronger the brain pathways for that movement become and the easier it gets to perform that movement in the future.

Neuroplasticity is the fundamental principle in physical rehabilitation, such as physiotherapy, for patients following stroke. from

Let’s look at an example of a stroke patient, Harry, who has problems with movement in his left leg. Harry might have altered patterns of walking due to damage in the leg area of the motor cortex of the right side of his brain. To help Harry regain efficient walking ability, the physiotherapist helps him perform sequences or patterns of walking by practising activation and control of specific muscle groups in his left leg.

Further reading: We’re capable of infinite memory, but where in the brain is it stored, and what parts help retrieve it?

At first, Harry will need lots of concentration to use the correct muscles as his brain is laying down new neural pathways to compensate for the damaged areas. But as this practice is repeated and the new pathways are established and strengthened, correct movement becomes easier without much concentration.

This same principle of neuroplasticity also applies for learning in the healthy brain. Anytime we acquire a new skill such as learning to ride a bike, writing our signature or dancing the tango, it’s our brain’s ability to strengthen or make new connections to adapt and change that allows us to learn.

So if you are a ballet dancer or a gymnast, a swimmer or a soccer player, a watch-maker or micro-surgeon, your brain connections in your motor system will be different depending on the practice and skill you have with fine movement of different parts of your body.

This article was co-written with Zita Arends, who is a physiotherapist in stroke rehabilitation and aged care.

More on estrogen and brain function.

Here is more information of the brain benefits of estrogen for those who still remain unconvinced.
Brain Res. 2016 Aug 15;1645:79-82. doi: 10.1016/j.brainres.2016.06.016. Epub 2016 Jun 16.

Reprint of: From the 90׳s to now: A brief historical perspective on more than two decades of estrogen neuroprotection.

Author information

Center for Basic and Translational Stroke Research, West Virginia University, Morgantown, WV 26506, USA; Department of Physiology and Pharmacology, West Virginia University, Morgantown, WV 26506, USA. Electronic address:
Department of Pharmacology and Neuroscience, University of North Texas, Fort Worth, TX 76107, USA. Electronic address:
Center for Basic and Translational Stroke Research, West Virginia University, Morgantown, WV 26506, USA; Department of Physiology and Pharmacology, West Virginia University, Morgantown, WV 26506, USA. Electronic address:


Historical perspective abstract:From the 90׳s to now: a historical perspective on more than two decades of estrogen neuroprotection: In the early 90׳s, estrogens were known to exert organizational and activational effects on reproductive tissues and sexual behavior. As well, the role of sex and gonadal hormones in altering the risk for developing Alzheimer׳s Disease (AD) was only beginning to be elucidated. Preliminary investigations suggested that estrogen-containing therapies typically given for the management of disruptive menopausal symptoms could reduce AD risk, attenuate disease-associated cognitive deficits, and modulate brain substrates known to be dysregulated by the condition, such as the cholingeric system. The findings from our seminal paper demonstrating cognitive benefits and cholinergic impacts with exogenous estrogen treatment in a rodent model of surgical hormone depletion provided initial support for use of estrogen-containing therapies as a treatment for age-related brain disorders. We then went on to demonstrate neuroprotective actions of estrogen in several other in vivo and in vitro models of neurological challenge, including stroke and AD. Further, our findings of the chemical structure requirements for estrogen׳s neuroprotective effects identified a novel approach for optimizing future estrogen-containing hormone therapy options. These early efforts laid the groundwork for later, large-scale clinical investigations into the potential of estrogen-based menopausal hormone therapies for the prevention of a variety of age-related disorders. Although findings of these studies were equivocal, the neuroprotective actions of estrogen, and specifically 17β-estradiol, identified by early investigations, remain well-documented. Future development of interventions that optimize cognitive aging are crucial and, with proper understanding of the factors that influence the realization of beneficial impacts, estrogen-containing treatments may still be among these.


Ovarian steroid deprivation results in a reversible learning impairment and compromised cholinergic function in female Sprague-Dawley rats: We hypothesized that estradiol (E2) serves as a neurotrophomodulatory substance for basal forebrain cholinergic neurons thought to be involved in learning and memory. Learning/memory was assessed using the two-way active avoidance paradigm and the Morris water task. Female Sprague-Dawley rats were either ovariectomized (OVX) or OVX for 3 weeks, followed by s.c. implantation of a Silastic pellet containing 17-βE2 (E2 pellet), resulting in a replacement of E2 to physiological levels. Ovary-intact (INTACT) animals served as our positive control. Active avoidance behavior and choline acetyltransferase (ChAT) activity in the frontal cortex and hippocampus were assessed at 5 and 28 weeks postovariectomy while performance on the Morris water task and high-affinity choline uptake (HACU) were measured only at the 5-week time point. At the 5-week time point, E2 replacement caused a significant elevation in the level of active avoidance performance relative to OVX animals. At the 28-week time point, OVX animals demonstrated a significantly lower number of avoidances relative to controls (61%) whereas E2-pellet animals not only demonstrated superior performance relative to OVX animals but also showed an accelerated rate of learning. Morris water task performance, on the other hand, was not significantly affected by estrogenic milieu despite a trend towards better performance in the E2-pellet group. Neurochemical analyses revealed that 5 weeks of ovariectomy was sufficient to reduce HACU in both the frontal cortex and hippocampus by 24 and 34%, respectively, while E2 replacement was successful in elevating HACU relative to OVX animals in both regions. ChAT activity was decreased in the hippocampus but not the frontal cortex of 5-week OVX animals. E2 replacement resulted in a reversal of this effect. At the 28-week time period, an unexpected decrease in ChAT activity was observed across all treatment groups. Interestingly, E2-pellet animals demonstrated the least severe decline in ChAT. This phenomenon was most evident in the frontal cortex where ChAT decreased by 61 and 56% in INTACT and OVX animals, respectively, whereas the decline in E2-pellet animals was only 16% over the same time period, suggesting a previously unreported cytoprotective effect of E2. Taken together, these findings demonstrate important effects of estrogens on cholinergic neurons and support the potential use of estrogen therapy in treatment of dementias in postmenopausal women. © 1994. This article is part of a Special Issue entitled SI:50th Anniversary Issue.

Role of Estrogen and Other Sex Hormones in Brain Aging.

I have been beating the drum for years now about the benefits of estrogen for women, yet I still get women who say that have been advised to stop their HRT or not to start taking them, by their doctors or friends. I get a bit hot under the collar when I hear this as I know the damage this poor advice will do to these women. Here is more positive reasons for staying on hormones long-term – note the date of this study – a few months ago.
Front Aging Neurosci. 2017 Dec 22;9:430. doi: 10.3389/fnagi.2017.00430. eCollection 2017.

Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair.

Author information

Instituto de Investigaciones Biomédicas (INBIOMED, UBA-CONICET), Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Departamento de Histología, Embriología, Biología Celular y Genética, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Danish Center for Molecular Gerontology and Danish Aging Research Center, Department of Molecular Biology and Genetics, University of Aarhus, Aarhus, Denmark.
Department of Physiology, Faculty of Medicine, Complutense University, Madrid, Spain.


Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed in all tissues, the brain being the most important one due to its main role in the homeostasis of the organism. As our knowledge about the underlying mechanisms of brain aging increases, potential approaches to preserve brain function rise significantly. Accumulating evidence suggests that loss of genomic maintenance may contribute to aging, especially in the central nervous system (CNS) owing to its low DNA repair capacity.

Sex hormones, particularly estrogens, possess potent antioxidant properties and play important roles in maintaining normal reproductive and non-reproductive functions. They exert neuroprotective actions and their loss during aging and natural or surgical menopause is associated with mitochondrial dysfunction, neuroinflammation, synaptic decline, cognitive impairment and increased risk of age-related disorders. Moreover, loss of sex hormones has been suggested to promote an accelerated aging phenotype eventually leading to the development of brain hypometabolism, a feature often observed in menopausal women and prodromal Alzheimer’s disease (AD).

Although data on the relation between sex hormones and DNA repair mechanisms in the brain is still limited, various investigations have linked sex hormone levels with different DNA repair enzymes. Here, we review estrogen anti-aging and neuroprotective mechanisms, which are currently an area of intense study, together with the effect they may have on the DNA repair capacity in the brain.

Can’t teach old dogs new tricks? Nonsense. Tips for learning later in life

Can’t teach old dogs new tricks? Nonsense. Tips for learning later in life

As 90-year-old Thumekile Mthiyane proves, you’re never too old to learn or try new things. Reuters/Rogan Ward

Change, often rapid and disorienting, is today’s norm. Even things our grandparents took for granted – manual typewriters, telegrams, smelling salts, corsets – have disappeared into antique shops and museums. We change jobs and even careers many times in one lifetime. We travel more. It seems like we adapt to new technologies almost weekly.

What hasn’t changed is that human beings need to learn so they can adapt and thrive in new circumstances. Is this possible for older people? It’s common knowledge that children are voracious learners but the famous cliche suggests that you can’t teach an old dog new tricks. This simply isn’t true.

As research conducted by my colleagues and I has shown, learning is a lifelong process. It’s also life-wide: we learn in all kinds of situations besides schools and colleges – in our families, workplaces, communities and through leisure activities. And it’s life-deep: it’s about emotions, morality, cultural and spiritual development, not just the intellect.

Here’s what you need to know to continue on your own lifelong learning process, and to encourage others around you to keep learning.

What older people have going for them

Ageing brings a slight deterioration in functions like short-term memory. But it has the advantage of accumulated experience. This means you know what you want to learn and how you want to apply it, and can link it to experience and concepts you’ve already acquired. Children at school typically learn a prescribed curriculum for future application. Adults tend to choose their learning and want it to count here and now.

Learning as an adult is not easy. You have to admit what you don’t know. Sometimes past learning experiences have been negative and associated with feelings of fear and failure. And adults have multiple responsibilities: work, family, social involvements and ageing parents, to name a few. Learning means negotiating these commitments and your own feelings. When you decide to embark on new studies, it’s important to let those around you know; explain how it will change things and enlist their support.

It’s also good to learn with others so that you can share the challenges and triumphs. Isolation can drive people away from learning at any stage of their lives. Study groups and learning partners, whether online, face-to-face or both, can be a great way of deepening and sustaining learning.

What and where

But what, and where, should you study? Firstly, it’s important to realise that not all, or even most, learning is formal. There’s an enormous modern emphasis on educational institutions, which for the masses is generally only a few hundred years old. And so the ways that humans have always learnt are often taken for granted.

We often learn the most important things informally from others and from experience: how to parent, how to get on with our neighbours, how to surf the Internet, where to find a job; and, perhaps most importantly, how to direct our own learning. Developing social capital – networks of friends, mentors, advisers, instructors – is as important for learning as it’s ever been.

These networks also allow us to connect with people whose voices we don’t usually hear; that helps us to avoid ghettoising our own minds and opens up new opportunities for thought and action.

Local organisations such as churches, mosques and temples often offer learning opportunities. NGOs as diverse as the World Wildlife Fund and Alcoholics Anonymous provide both face-to-face and eLearning opportunities.

In South Africa, community-based organisations such as stokvels – financial cooperatives – can be a great way to learn about money and saving. Keeping the country’s own radical tradition alive, Popular Education South Africa is a catalytic project that “seeks to inspire alternative forms of education provision that benefit working class and poor people”.

The government system of Community Learning Centres, linked to a Community College in each province, offers adult basic education and an alternative route to writing the National Senior Certificate. This is the final school-leaving exam (“matric”) that can equip you to enter tertiary institutions. Although these centres are of uneven quality, many do an outstanding job under difficult circumstances.

Navigating the Internet

The Internet offers a flood of learning opportunities. But how do you negotiate the deluge of options and pathways? It is important to check out the credentials of the websites you use because search engines don’t discriminate. Look out for websites that are linked to universities and research institutes. These and other credible online sources abound.

Though Wikipedia often gets a bad rap, it’s a vast public resource of information on almost every conceivable topic and a fascinating human invention. It’s a good spot to supplement your learning or answer quick queries.

TED Talks are devoted to “ideas worth spreading”, usually in the form of short powerful talks. You can learn anything from how to spot a liar to how to land on a comet. Each talk also offers access to a transcript, a reading list for more sources and an option for posting your own comments and joining the debate.

Learning as never before

It doesn’t matter whether your learning preferences are formal or informal; institutional or self-directed; online, face-to-face or blended.

We live in a learning world as never before, and the quality of our learning as a species is likely to determine our future. So don’t let cliches about old dogs hold you back: keep learning.

Seven essential tips to breaking up with sugar


Seven essential tips to breaking up with sugar

December 8, 2016 6.53am AEDT
As 2017 fast approaches, maybe it’s time for a bitter breakup with some things sweet. Pixabay, CC BY-NC-ND

Global recognition is building for the very real health concerns posed by large and increasing quantities of hidden sugar in our diets. This near-ubiquitous additive found in products from pasta sauces to mayonnaise has been in the headlines and in our discussions. The seemingly innocuous sweet treat raising eyebrows from community groups to policy makers – and resulting change is in the air.

Let’s review some of the sugar-coated headers from the past 12 months:

  • The global obesity epidemic continued to build while more than two-in-three Australian adults faced overweight or obesity – and almost one in four of our children.
  • Science around sugary drinks further solidified, with consumption now linked to obesity, childhood obesity, heart disease, diabetes (type-2), dental caries and even lower fertility.
  • Australians were estimated to consume a staggering 76 litres sugary drinks each since January alone and new reports highlighted that as much as 15% of the crippling health costs associated with obesity could already be resulting from sugary drinks consumption.
  • Meanwhile around the planet, more countries took sound policy measures to reduce sugar consumption in their citizens, with France, Belgium, Hungary, Finland, Chile, the UK, Ireland, South Africa and many parts of the United States implementing, continuing or planning the implementation of pricing policies for sugary drinks.

In short, the overconsumption of sugar is now well recognised as a public health challenge everywhere. With all this in mind and a New Year ahead, it’s time to put big words into local action. With resolutions brewing, here are seven helpful tips to breaking up with sugar in 2017.

1. Understand sugar

When it comes to sugar, things can get pretty confusing. Below, I shed some light on the common misunderstandings, but let’s recheck sugar itself – in simplest terms.

Sugar is type of refined carbohydrate and a source of calories in our diet. Our body uses sugar and other sources of calories as energy, and any sugar that is not used is eventually stored as fat in our liver or on our bellies.

‘Free sugars’ are those sugars added to products or concentrated in the products – either by us or by the manufacturer. They don’t include sugars in whole fruits and vegetables, but more on that later. For a range of health reasons, the World Health Organization recommends we get just 5% of our daily calories from free sugars. For a fully-grown man or woman, this equates to a recommended limit to sugar consumption of roughly 25 grams – or 6 teaspoons. For women, it’s a little less again.

Consume more than this, and our risk of health problems rises.

2. Quit soft drinks

With 16 teaspoons of sugar in a single bottle serving – that’s more than 64 grams – there’s nothing ‘soft’ about soft drinks. Including all carbonated drinks, flavoured milks and energy drinks with any added sugars, as well as fruit drinks and juices, sugary drinks are a great place to focus your efforts for a healthier 2017. Sugary drinks provide no nutritional value to our diets and yet are a major source of calories.

What’s more concerning, evidence suggests that when we drink calories in the form of sugary drinks, our brains don’t recognise these calories in the same way as with foods. They don’t make us feel ‘full’ and could even make us hungrier – so we end up eating (and drinking) more. In this way, liquid calories can be seen as even more troubling than other forms of junkfoods. Combine this with studies that suggest the pleasure (and sugar spike) provided by sugary drinks may make them hard to give up – and it’s not difficult to see why many of us are drinking more, more often and in larger servings. This also makes cutting down harder.

The outcome is that anything up to one-seventh of the entire public cost of obesity in Australia could now result from sugary drinks. In other words, cut out the sugary drinks and you’d be doing your own health a favour – and the health of our federal and state budgets.

3. Eat fruit, not juice

When it’s wrapped in a peel or a skin, fruit sugars are not a challenge to our health. In fact, the sugars in fruit are nature’s way of encouraging us to eat the fruit to begin with. Fruits like oranges, apples and pears contain important fibres. The ‘roughage’ in our foods, this fibre is healthy in many ways but in particular: three. First, it slows our eating down; it is easy to drink a glass of juice squeezed from 7 apples, but much harder to eat those seven pieces whole. Second, it makes us feel full or satiated. And third, it slows the release of the sugars contained in fruit into our blood streams, thus allowing our bodies to react and use the energy appropriately, reducing our chances of weight gain and possibly even diabetes.

Juice, on the other hand, involves the removal of most of those fibres and even the loss of some of the important vitamins. What we don’t lose though, is the 21 grams or more than five teaspoons of sugar in each glass.

In short, eat fruit as a snack with confidence. But enjoy whole fruit, not juice.

4. Sugar by any other name

High-fructose corn syrup, invert sugar, malt sugar and molasses – they all mean one thing… sugar.

As the public awakens to the health challenges posed by sugar, the industry turns to new ways to confuse consumers and make ‘breaking up’ more difficult. One such way is to use the many alternative names for sugar – instead of the ‘s’ word itself. Be on the lookout for:

Evaporated cane juice, golden syrup, malt syrup, sucrose, fruit juice concentrate, dextrose and more…

5. Eat whole foods where possible

Tomato sauce, mayonnaise, salad dressings, gravies, taco sauces, savoury biscuits and breakfast cereals – these are just some of the many foods now often packed with hidden, added sugars.

A study found that 74% of packaged foods in an average American supermarket contain added sugars – and there is little evidence to suggest Australia would be dramatically different. Added to food to make it more enjoyable, and moreish, the next tip when avoiding such a ubiquitous additive is to eat whole foods.

It’s hard to hide sugar in plain flour, or a tomato, or frozen peas. Buying and cooking with mostly whole foods – not products – is a great way to ensure you and your family are not consuming added sugars unaware.

6. See beyond (un)healthy claims

Words like “wholesome”, “natural” and “healthy” are clad on many of our favourite ingredients. Sadly, they don’t mean much.

Even products that are full of sugar like breakfast cereals and energy bars often carry claims that aim to confuse and seduce us into purchase. Be wary – and be sure to turn the package over and read the ingredients and nutrition labelling where possible (and time permits).

7. Be okay with sometimes

The final but crucial message in all of this is that eating or drinking sugar is not a sin. Sugar is still a part of our lives and something to enjoy in moderation. The occasional piece of cake, or late night chocolate; despite the popular narrative painted by industry to undermine efforts for true pricing on sugar, these occasional sweet treats are not the driving challenge for obesity. The problem is that sugary drinks, and sugar in our foods, have become every day occurrences.

With this in mind, let’s not demonise sugar but instead let’s see it for what it is. Enjoy some juice or bubbles from time to time but make water the default on an everyday basis. With the average can of cola containing 39 grams or 9 teaspoons of sugar – be ok with sometimes.

Bitter truth

Let’s be honest, most countries now face serious health challenges from obesity. Even more concerning, so do our kids. While no single mission will be the panacea to a complex problem, using 2017 to set a new healthy goal of giving sugar the kick would see a great start.

Understand sugar, be aware of it, minimise it and see it for what it is – a special treat for a rare occasion.

This New Year’s, make breaking up with sugar your planned resolution.

“Hey sugar – it’s not me, it’s you…”

New study finding fat isn’t as bad as carbs misses the point

New study finding fat isn’t as bad as carbs misses the point

August 30, 2017 2.50pm AEST

What’s more important to examine is whether the fat and carbs come from fruits and vegetables or doughnuts and candy. from

A new study has added weight to the debate as to whether fat is better or worse for you than carbohydrates, in terms of risk of heart disease and early death. Unfortunately based on this study the jury’s still out, but it does highlight that we should focus on what foods people are eating, rather than just looking at components such as fat and carbohydrates.

Researchers looked at intakes of fat, carbohydrates and protein in more than 135,000 people from 18 low income countries (Bangladesh, India, Pakistan, and Zimbabwe), middle income countries (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, Turkey) and high income countries (Canada, Sweden, United Arab Emirates).

They assessed dietary intakes based on questionnaires, and compared the results with death rates from heart disease and from all other causes.

Over 7.4 years of follow-up, 5,796 people died and 4,784 had major cardiovascular disease events, such as a heart attack or stroke. Interestingly, they found those with the highest intakes of total fat and sub-types of fat (saturated, unsaturated) compared to those with the lowest intakes, had a lower risk of dying from all causes.

There was a 21% lower risk of stroke among those with the highest saturated fat intakes compared to the lowest. However, when it came to the risk of having a heart attack or dying from heart disease, fats had no relationship with risk.

Interestingly, those consuming the highest percentage of total energy from carbohydrates had a 28% higher risk of early death, but no higher risk of having heart disease or dying from heart disease.

Although it hasn’t received as much attention, they also found a higher percentage energy intake from protein was associated with a 23% lower risk of early death and 15% lower risk of dying from causes other than heart disease. Animal protein intake was also associated with a lower risk of dying, but there was no significant association between plant protein and risk of early death.

So what does this all mean?

This study highlights that both carbohydrates and fat are important, but which foods you eat that contain fat or carbohydrate is even more important when it comes to how long you live.

The researchers found some differences between results for those living in Asian countries compared to other regions. For example there was no statistically significant difference in early death from all causes between those with the highest, compared to the lowest percentage of energy from carbohydrate for those living in Asian regions. But there was among those from non-Asian countries.

The analysis adds more weight to the global call to go beyond macro-nutrients (protein, fat and carbohydrate which are the major constituents of food) and to look carefully at actual food and drinks consumed. It matters whether your carbohydrates come from an apple, lentils or carrots compared to soft drink, doughnuts or pancakes.

The types of foods actually consumed could inform how changes in the food supply within lower and middle income countries relate to changes in death rates. They could also inform nutrition policies for countries experiencing a nutrition transition as they become more wealthy.

Overall, this study is very important, and a timely reminder of the need to continually update the evidence on diet disease relationships and to factor in what part of the world the individuals under study are from. But it’s not time to throw out the pasta, rice and bread and start guzzling tubs of fat.

It is time to pay more attention to nutrition and to focus on optimal eating patterns within each country. We need to stem the tide of ultra-processed foods that disrupt healthier eating patterns. Studies from around the world show that getting the ratio of ultra-processed to minimally processed foods back in balance is key to improving the nutritional quality of our overall diets.

Dietary patterns and heart disease

We recently reviewed the evidence on dietary patterns and heart disease, where most research has been done in high income countries.

Our report highlighted that a number of dietary patterns that vary in fat and carbohydrate type and quality are associated with lower heart disease risk. What they have in common is that they are all high in vegetables, fruit, wholegrains and most includes legumes.

This new study provides support for a focus on improving the nutritional quality of macronutrients. In other words, it matters what foods you eat that contain high amounts of carbohydrates and fats. For example is the major source of carbohydrate coming from fruit and vegetables or is it added sugars and highly processed foods?

Close examination of the barriers and facilitators of consuming a healthy diet is warranted. In an earlier analysis of data from this new study, the team reported very low intakes of vegetables and fruit with a mean combined intake of 3·8 servings a day. This varied from 2.1 servings of vegetables and fruit per day in low income countries up to 5.4 servings per day in high income countries. They found that the cost of fruits and vegetables relative to household income was high.

This highlights that to improve dietary patterns globally, we need people to eat more vegetables and fruit. To achieve that we must develop nutrition polices that support affordability of healthy food for all and stop arguing about whether fat is better than carbs. That just adds to the current confusion.

Moderate drinking doesn’t cause liver disease

Ignore this junk science – moderate drinking doesn’t cause liver disease

25th January 2018

Sometimes the junk science that comes out of the ‘public health’ lobby is so bad you just have to laugh. Take this study, for example, published yesterday in the apparently reputable Journal of Hepatology. As reported by the Irish Times, it found that ‘alcohol consumption even at very low levels early in life may significantly increase the risk of alcoholic liver disease in men’. It was even suggested that drinking guidelines should be lowered to accommodate this emerging evidence.

Alcoholic liver disease is a relatively rare condition that overwhelmingly affects very heavy drinkers. It would be surprising, to say the least, if ‘very low levels’ of drinking caused it.

And yet the media’s coverage of this study accurately reflected the claims made by its authors. They claim to have shown that ‘consumption of alcohol early in life is associated with an increased risk of developing severe liver disease in men’. They say that ‘men consuming as little as one to five grams [less than one unit] of alcohol per day had an increased risk of severe liver disease compared to abstainers, indicating that the increased risk of severe liver disease might be present even at very low doses of alcohol.’ Moreover, they declare – in the abstract of the study – that: ‘Current guidelines for safe alcohol intake in men might have to be revised.’

How did they arrive at these remarkable conclusions? First, they dug up some old documents from the Swedish army dating back to 1969-70 when conscription was still in force. These documents contain survey data from conscripts aged between 18 and 20, including estimates of how much they drank.

This gave the researchers the baseline figures for alcohol consumption. The men were then ‘followed for a mean period of 37.8 years’ to see what happened to them. This is a rather grand way of saying that the researchers looked at Sweden’s National Patient Register to see how many had developed alcoholic liver disease by 2009.

Of the 43,296 individuals who had provided drinking estimates in 1969/70, 383 had developed severe liver disease (0.9 per cent). When the researchers looked at their alcohol consumption, they found that those who drank the most were the most at risk and those who did not drink at all were the least at risk. Fair enough but, more surprisingly, they also found that those who only drank one or two units a day were at increased risk.

The authors describe these findings as ‘borderline statistical [sic] significant’. In fact, they are nowhere near being statistically significant, but we’ll leave that to one side. The more interesting question is this. In the 39 years between the men being recruited to the army and their medical records being examined, how often do you think the researchers asked them how much they drank?

Every six months? Once a year? Once every five years?

How about never? Because that’s how often they kept abreast of what these men were drinking. Not once. They have no idea how much their subjects’ drinking behaviour changed in the intervening years. All they know is that the people who were teetotal in 1970 were less likely to develop liver disease than the people who were drinkers in 1970. Hold the front page!

In no way does this study show, or even imply, that drinking at low levels causes liver cirrhosis. The authors’ suggestion that their study shows that ‘recommendations for safe alcohol consumption regarding the risk for development of severe liver disease in men might be set too high’ is an absurd non-sequitur.

Quite obviously, the men in this study did not continue drinking at the same level as their 19 year old selves for the rest of their lives. Some of the teetotallers became heavy drinkers (we know this because eleven of them developed alcoholic liver disease), some of the heavy drinkers became teetotallers, and some of the light drinkers became heavy drinkers. It is not drinking at ‘very low levels early in life’ that causes the damage. It is drinking at very high levels later in life. Without knowing anything about what these men were drinking after 1970, the study tells us precisely zero about the relationship between alcohol and liver disease, nor does it inform the discussion about what a ‘safe level’ of drinking is.

Why are journals publishing this pointless rubbish? Judging by the lead author’s comments to the press, the aim is not to tell us anything useful, but to put pressure on the Swedish government to follow the UK in lowering the drinking guidelines.

“If these results lead to lowering the cut-off levels for a ‘safe’ consumption of alcohol in men, and if men adhere to recommendations, we may see a reduced incidence of alcoholic liver disease in the future,” Dr Hagström said.

It would be strangely fitting if the Swedes lower their drinking guidelines based on junk science which claims that alcoholic liver disease is a threat to light drinkers. As the e-mails released under the Freedom of Information Act show, it was only by making this scientifically illiterate assumption that the UK’s Chief Medical Officer was able to lower the guidelines in 2016.

We can expect more studies of this kind in the next few years. The anti-drink lobby will not be happy until the official drinking guidelines are zero and they will go to any lengths to achieve it.