Dr Chris Robinson Brisbane

28/12/2022

Melanoma Part 1- Melanoma and Moles

In the skin there are lots of different types of cells - all with different jobs to do. We have basal cells, squamous cells, merkel cells, fibroblasts, and melanocytes to name but a few. Basal Cell Carcinoma (BCC) skin cancers come from Basal Cells, Squamous Cell Carcinoma (SCC) comes from squamous cells and Melanomas are derived from melanocytes. A BCC or an SCC is not a melanoma and nor can it ever turn into a melanoma - no more than a cat can turn into a dog. They are completely different entities.

So what are melanocytes? Melan is Greek for black, cyte is Greek for cell - so ‘black cell’. And that’s what they are - cells that produce a black/brown pigment protein called melanin. The job of melanin is to help protect the skin from ultraviolet (UV) radiation - sunlight. The accumulation of melanin in the skin gives out skin it’s colour - the more melanin we have the darker we are. When we tan, the melanocytes are stimulated by the damaging UV and produce more melanin to protect our skin.

Melanocytes are spread out pretty evenly throughout the skin as individual cells. However, they can also aggregate together in the skin as ‘nests’. Clusters of nests are referred to as ‘moles’ (aka ‘Neavus’). Most moles are quite safe and will follow a normal pattern of development through life. Some moles were ‘programmed’ to be there from birth, these are ‘congenital moles’. The fleshy ones with hairs in them are an example of a congenital mole. Some moles we ‘acquire’ - and these are usually flat. If we have darker skin types we will usually produce darker moles, if we have fair skin, lighter brown moles.

So what is a Melanoma? A Melanoma is a form of cancer that develops from corrupted melanocytes. In melanomas the melanocytes have begun to grow and divide in an uncontrolled way. Some expanding outwards, sometimes downwards and sometimes both. These proliferations of corrupted melanocytes are called Melanomas. Melanomas are obligate growers. They are an uncontrolled expanding cell population. This is the nature of any cancer. Growth is literally written into its DNA.

Contrary to what people have come to understand, most Melanomas do not come from existing moles. Approximately 70% of melanomas start off life as a melanoma - not as a mole. When this occurs the melanoma was always a melanoma and never a mole (‘de novo melanoma’). The remaining 30% of melanomas that arise are associated with existing moles whose melanocytes have undergone malignant change.

Why is all of this important to know? Because most melanomas start off as melanomas, most melanomas will present as ‘new’ ‘moles’. Any changing ‘mole’ is important to note especially if it changing its size shape, colour and behaviour in any age group. And a new ‘mole’ in the over 50 demographic definitely needs to be assessed.

As always, hope this helps.

Dr Chris Robinson
MBCHB, BSc (1st Class, Hons), MRCGP, FRACGP, Dip Derm (Aus), M Med (Skin Cancer), FSCCA, Senior Lecturer UQ Skin Cancer.

03/10/2021

Basal Cell Carcinoma, Fruit Flies and Sonic The Hedgehog… an Unlikely Connection.

Basal Cell Carcinoma is a type is skin cancer. In fact it’s the most common type of all skin cancer. It comes in different ‘subtypes’ - flavours if you will. Some are ‘superficial’, spreading out under the top layer of the skin (epidermis). Some ‘infiltrate’, sending deep cords of infiltrating carcinoma deep into the surrounding tissue. Some form ‘nodules’ that bud deeper into the dermis (layer of the skin under the epidermis).

It’s important to note that a BCC is not a melanoma and nor can it turn into a melanoma - no more than a cat can’t turn into a dog. ‘Basal cells’ are a distinct type of cell in the skin and so as such they are seperate entities from the cells (melanocytes) that give rise to melanoma.

Each type of BCC can have different ways to manage it. Surgery is often necessary for ‘infiltrating’ and ‘nodular’ BCC subtypes. Management decisions are heavily influenced by where the cancer is. A different management decision may be taken for the same BCC subtype albeit in a different anatomical location - say on the back vs on the nose.

So what does this have to do with Sonic The Hedgehog’ and fruit flies? Surprisingly, everything. Back in the 80’s early gene research was conducted using fruit flies. Drosophila flies , more accurately called vinegar flies and have only 4 chromosomes. Research into these yeast munching blighters has yielded 4 noble prizes no less. Anyhow, whilst unpicking these 4 chromosomes researchers came across a signalling gene that was found to have profound control over embryo development in these flies. These genes are conserved and are found in all different types of animals. This gene has been shown to influence the development of the embryonic central nervous system, legs, arms and ensures that tissues reach their correct location, size, and cellular content.

When this gene was corrupted in the embryonic fruit fly, the tiny fruit fly embryos got covered in spikey growths. The researchers thought these embryos looked like the video game icon Sonic The Hedgehog. The name stuck and the gene was so named the Sonic Hedgehog (SHH) gene. This was after all the 80’s.

The SHH gene provides instructions for making a protein called… you’ve guessed it: Sonic Hedgehog. This protein functions as a chemical signal that is essential for embryonic development. For humans, the SHH pathway normally remains inactive in adult tissues. Reactivation of this pathway results in malignant transformation of the affect tissue - in other words the reactivation of SHH in the skin plays a significant role in triggering BCC development.

With respect to how exactly this happens things at this point get complicated- very complicated. So to summarise a very complex process: essentially a mutation in SHH triggers an intra signalling cellular cascade that can result in the formation of a BCC.

There are genetic conditions in which individuals are born with a defect in the SHH pathway and develop 100’s of BCC’s, the first BCC often presenting when the affected individual are 10-11 years of age. They often have developmental issues, dental issues and skeletal abnormalities. Gorlin’s syndrome is an example of this.

Thankfully for most of us, such genetic abnormalities are rare. Unfortunately, what is not rare are isolated mutations in the SHH gene that can be found in chronically sun damaged skin. Usually the body is pretty good at moping up these defective genes up as part of routine DNA house keeping. However, when the cumulative burden of UV damage is such that the body’s in built repair processes can’t stay on top of the number of defects then BCC formation is more likely to occur.

The ability to repair damaged DNA is also linked to genetics. Some people have better in built DNA repair processes. So, whilst an individual might not have a definite genetic condition - such as the aforementioned Gorlins - they can have a tendency towards BCC formation as their skin’s DNA housekeeping is not able to stay on top of the sun damage. In Australia these individuals will often have multiple BCC’s in their lifetime which can, and do, present in early/ mid adulthood. Sadly, this is not uncommon.

Disclaimer:
All constructive discussion is welcome - even if it is contrary. However, it would be great if any negative/ personal comments are left out. Skin cancer is a large topic and a blog post cannot cover it in any depth.

The above is intended to be general and informative and should not be taken as specific individual advice. Any specific questions related to your own person circumstances need to be discussed with a Dr who is well trained in skin cancer medicine. Please do not send photos or specific patient based questions as I will be unable to respond.

Dr Chris Robinson
MBCHB, BSc (1st Class Hons), MRCGP, FRACGP, Dip Dermatology ( Aus), SCCA Accreditation.

14/06/2019

The physiology of sleep

Going to sleep is simple. Get in bed turn the lights off and away we go - off to dreamworld. But, behind the scenes it’s complicated - very complicated. It’s an orchestra of competing feedback systems all taking inputs from mood, temperature, light, seasons, neurotransmitter availability, intra cellular synchronisation, extra cellular synchronisation, CLOCK genes and the snappily named and grammatically incorrect: Brain and muscle Arnt-like protein-1 (BMAL1) ( no typo - that’s what a a very uninspired scientist named this protein) all playing a delicate complex dance.

The ‘Sleep - Wake cycle’ is driven by two separate but related processes. One is the ‘homeostatic’ drive for sleep. As we expend energy during the day our body accumulates chemical by-products that in turn stimulate the drive for sleep. During the night as we recoup, the homeostatic drive for sleep declines, dwindling between 2-4am. We will come back to that shortly.

The other sleep regulatory system is the Circadian rhythm. The Circadian rhythm is an independent, intercellular, 24-hour oscillating rhythm that regulates the timing of sleepiness and wakefulness throughout the day. All cells in our body have this intracellular clock that controls multiple metabolic processes. The ‘pace maker’ for the clock is situated in the Suprachiasmatic Nuclei (SCN) of the hypothalamus - a tiny bulb like process at the base of the brain.

The SCN is a collection of 10-20k cells - in terms of the brain - this is a very small amount of cells. Very (very) crudely - it works by genes generating proteins that accumulate in the cells of the SCN. These proteins accumulate at a given rate, and it is this rate provides a measurement for time. When these proteins reach a critical threshold (negative feedback) production stops - a bit like a toilet cistern filling and the ball valve engaging. What follows is a chain reaction of chemical messages that drives wakefulness. Over time these proteins then degrade - again at a given rate - and when they reach a low enough volume production fires up and the cycle starts again. This process is so robust that you can literally cut the SCN out of a mouse, set in a culture dish with the right nutrients and it will continue to tick indefinitely with precision. This has been done.

The impulse for sleep generated by the Circadian rhythm dips and rises at different times of the day. For mature adults the strongest sleep drive generally occurs between 2:00-4:00 am. This neatly takes over from when the aforementioned homeostatic drive for sleep starts to ebb .... if it remains synchronised. The Circadian drive for sleep also peaks in the afternoon between 1:00-3:00 pm - the siesta is now making a lot of sense!!!

There is also individual variation - hence morning and evening people. Various disease states, dementia, depression for example, severely alter the circadian clock. Age also dramatically impacts its timings. Neonates are born without this cellular clock ticking - it starts to kick in around 4 months. Old age also affects the circadian timings with early morning waking being a real issue creating a high risk for falls.

Teens literally tick on a different clock. Most teens experience what’s called ‘a sleep phase delay’. This shift in a teenagers circadian rhythm causes them to naturally feel alert later at night, making it difficult for them to fall asleep before 11:00 pm. For teens the strongest sleep drive (called a Circadian dip) is between 3-7am and, depending on how out of sync they are, can still be inducing sleep up to 10am. (I almost feel guilty for dragging my teen out of bed - but then I see the state of their room and feel an odd sense of justice creep over).

The sleepiness we experience during these Circadian dips will be less intense if we have had sufficient sleep, more intense when we are sleep deprived. An individual’s environmental cues, also known as zeitgebers (great word, had to throw it in), modify the Circadian rhythm. Light is the most potent environmental cue - especially blue light - as generates by the sun and iPad/iPhone/ tv’s.

In the mornings, with exposure to light, the SCN sends signals to raise body temperature and produce hormones like cortisol. With light stimulation the SCN stops the release of melatonin. Melatonin is the hormone responsible for us feeling sleepy. When light stimulation to the SCN fades, the signals from the SCN stopping melatonin release ‘dip’ and melatonin released freely inducing sleep. Our body are able to detect not only day to night light signals but also the change in day length that occurs across seasons and our circadian clock tracks accordingly.

Physiological and behavioral cues - the timing of sleep, meals, work/social interactions etc all impact the timing of the ‘sleep-wake cycle’ and the Circadian clock. These cues can be detrimental and have a whole body effect, not just affecting sleep. There are a number of chronic health conditions linked to disturbances in the circadian rhythm: insomnia, diabetes, obesity, depression, bipolar disorder, seasonal affective disorder, and other sleep disorders. I will come to some of these next time.

As always, I hope this helps.

Dr Chris Robinson , MBCHB, BSC, MRCGP, FRACGP, Doctors at Eatons Hill

11/05/2019

The Gut-Brain-Axis and Depression

The term microbiome refers to all microorganisms and their genetic material living in the body. The term microbiota refers to populations of microorganisms present in the body’s various ecosystems - here we are talking about the microbiota of the gut. Altered gut bacterial composition (dysbiosis) has been associated with the pathogenesis (cause) of many inflammatory diseases, infections and mental health issues.

Our gastrointestinal tract represents one of the largest interfaces (250–400 m2) our body has between us, our antigens and environmental factors. At play in this large expanse are approximately 1014 different types of microorganisms. Many of which play a critical role in our health. Lactic acid bacteria, for instance, are key organisms in the production of vitamin B12 - a vital amine (vitamin) which cannot be synthesised by animals, plants or fungi. Bifidobacteria are producers of folate, a vital amine involved in DNA synthesis and repair. The gut microbiota have also been shown to play a role in the synthesis of vitamin K, riboflavin, biotin, nicotinic acid, panthotenic acid, pyridoxine and thiamine. Collectively they contain 150 times more genes than the human genome. Expressed a another way... it’s complicated down there.

To add to that complexity, it’s not a static environment. It’s like the coral reef. Different strains of microorganisms constantly competing with each other to achieve a delicate balance. That balance constantly shaped and reshaped by our age, our geographic location, our genetics, antibiotics and of course our diet.

Research over the past decade has explored the complex relationship between our gut microbiome and our mental health - the ‘Gut-Brain-Axis’. Research has shown that gut bacteria are able to produce active neurotransmitters - brain chemicals involved in loads of things - including influencing mood. For example; Lactobacillus and Bifidobacterium synthesize gamma-aminobutyric acid (GABA), a neurotransmitter. Escherichia coli, Bacillus and Saccharomyces produce norepinephrine another neurotransmitter. Candida, Streptococcus, Escherichia and Enterococcus produce serotonin - a neurotransmitter believed to be involved in the pathology of depression.

Studies in this area have looked at the manipulation of laboratory germ-free animals (usually mice) by targeting specific microorganisms with antibiotics or putting new strains of microorganisms into the mix with probiotics. Other studies have looked altering the composition of the microbiome through dietary restrictions and more radically through wholesale changes to the microbiota with f***l microbial transplantation. In these experiments animals have then been observed on task performance, response to stress, response to pain, feeding behaviour etc. Conclusions have then been extrapolated to potential implications for the human experience.

Unlike our rodent friends, In terms of human studies, there are no high-quality, controlled studies that have studied the effects of interventions of knock-out studies, f***l Microbiol transplants etc - that’s because it extremely tough to conduct these studies with the scale and rigour to derive solid scientific conclusions. Most of the better quality studies in this field that have been conducted involved probiotics. This is because it is hypothesised that probiotics in the GI tract improve symptoms of depression by increasing serotonin availability - a shortage of which is associated with depression.

Studies that have been done do show some benefits of using probiotics in people suffering with depression and anxiety. For unknown reasons this was mainly in the under 65’s. Research demonstrated that non depressed people also reported reduced symptoms of dress and anxiety and probiotics ‘may’ play a protective role in this regard. However, the strain of probiotic, the dosing, and duration of treatment in these studies varied widely. Unfortunately ‘depression’ itself was poorly defined some of these studies. That said, some benefit was realised and importantly there were very few adverse affects reported.

To summarise - that a relationship exists between gut health and mental health is definite. That any definite claims of ‘cause an effect’ are (currently) definitely overreaching. And, in terms of research, it’s definitely an exciting area. Definitely.

Anyone interested in registering for a trial at QUT on this very same topic can register here:

https://www.qut.edu.au/news?id=140448&gclid=CjwKCAjw-4_mBRBuEiwA5xnFIKqNzr_G6TSyc1DKg5IfUV-nKaepMgxRK-tyqS-daBHF3B8vf3kvcRoCEosQAvD_BwE

(Note - Some probiotics may be contraindicated in patients who are immunocompromised or have severe underlying illness, as they have been reported to cause fungaemia and bacteraemia. Please discuss if probiotics are right for you with your doctor.)

As always, hope this helps.

Dr Chris Robinson , MBCHB, BSC, MRCGP, FRACGP, Doctors at Eatons Hill

Do probiotics have a role to play in managing depression? That’s the question QUT-led research is exploring through a clinical trial currently underway.

24/04/2019

The Lyon Diet - the most important diet you’ve never heard of.

No calorie counting, you can eat carbs, you’ll lose weight (slowly) and it could help you live longer.... Too good to be true?

The Lyon Diet heart study took place in 1997. It remains one of the very few randomised controlled dietary interventions trials. Why is this important, most diets out there really don’t have much solid evidence. By that I mean, most diet books/trends arnt based on long term, well organised, well monitored, randomised trials - they are usually based on a good premise - I.e the 5/2 diet, the Keto diet - but the actual claims regarding health benefits haven’t been thoroughly studied and therefore proven per se. The Lyon Heart Study Diet (LHSD) has.

The LHSD was an experimental study. In 1997 evidence of the day was very much in favour of a low fat diet as being key to the prevention of heart disease. Epidemiological evidence emerged that people living around the Mediterranean area didn’t eat a low fat diet but did enjoy a much lower incidence of heart disease. So the ‘experiment’ was to compare a ‘prudent’ low fat diet against a typical diet as consumed in the Mediterranean geographical area. The hypothesis was this: could the natural cardioprotection observed in the Mediterranean diet also be protective when transferred to another group? They picked Lyon, France to conduct this experiment.

So, 605 French patients were recruited from hospital following a heart attack. These patients with established Coronary Artery Disease (CAD) were randomly assigned to two different diets. One group to a prudent low fat diet. The other group was assigned to a diet rich in whole grain products and instructed to have fresh fruit, vegetables and nuts every day. Foods were to be prepared exclusively with either olive oil or rapeseed oil and a margarine rich in a-linolenic acid (ALA) was supplied to them. They were told to limit dairy products. Fish and poultry were to be consumed in low to moderate amounts and red meat sparingly.

As mentioned the patients in the study had established Coronary Artery Disease (CAD) and so many were on necessary heart medications associated with this - this was the same in both groups. The point? These were ‘high risk patients’ - patients who had already had a heart attack.

The results were massive. They really were. The Mediterranean style diet participants had up-to 70% lower ‘recurrence of cardiac events’ - what does this mean? Fewer fatal heart attacks, fewer non fatal hearts, fewer admissions for angina etc. The results were so massive that the study which was originally designed to go for 5 years had to be stopped after 27 months - it wasn’t deemed ethically correct to carry on as too many people following the low fat diet were suffering cardiac events relative to the LHSD group.

A really surprising and unexpected feature of the study was that in terms of classically associated cardiac risk factors: cholesterol, blood pressure, weight - there were no differences between the groups. In both groups the average weight was around 74kg, the average LDL cholesterol (classically taught as ‘bad’) was 4.5 - 5.4 (as they had heart disease they were all basically on statins already), the HDL cholesterol ( ‘good’... [ish]) was around 1.2, blood pressure was well controlled at an average of 120/74.

The LHSD has become more commonly known as the Mediterranean diet. Why it was so powerful at reducing follow on heart attacks and cardiac events is still being debated and has been the grounds for further study. In our rush to reduce everything to its simplest form further studies looked at just adding omega -3, fish oils or ALA to our diet assuming that these were the components that were responsible for the observed health benefits - none of them have been proven to affect hard outcomes - I.e cardiac events.

I understand the temptation, but In my view trying to reduce the cause to a single variable I.e omega 3 , ALA ... cholesterol... detracts from the more important point - it was the holistic Mediterranean diet that conferred the impressive cardioprotective benefits. Just focusing on one variable often means people take false reassurance - my cholesterol is good so I’ll just carry on as is. Reducing the Mediterranean diet to ‘good’ and ‘bad’ components in my view misses the point and ‘we’ need to resist the temptation to take only parts out of a diet that has been proven to be healthy and assume we’re getting the benefits of all of it.

As always, I hope this helps.

Dr Chris Robinson , MBCHB, BSC, MRCGP, FRACGP, Doctors at Eatons Hill

20/03/2019

Anxiety - a brief history

The day starts at around 3-4am. Sleep interrupted by unwanted intrusive thoughts, the rest of the sleep fretful and unrestful. Then the chest tightness starts, it sits there with an on edge feeling that doesn’t leave. Distraction helps but in the quiet moments it comes back. It’s daily, it’s constant, it’s exhausting. It’s anxiety.

Given it’s prevalence today I think that many would see anxiety as a modern condition, however Greek philosophers and Latin physicians recognised anxiety as separate from other types of mood conditions and identified it as a medical disorder. Cicero characterised it as a “constricting” disorder and the word ‘anxiety’ itself derives from the Latin angor - to constrict. Considering the chest tightness that is often felt by those suffering from anxiety I think it was pretty well described.

In the 18th century, medical authors published clinical descriptions of anxiety and panic attacks and it was seen as part of the condition they called ‘melancholia’. French physicians around the same time labelled it as a condition of the vapours - ‘affection vaporeuse et mélancolique’. Vapours being some form of ‘stuff’ coming from the womb - how this got applied to men I’m not sure, but it did.

panophobia phrontis (from the Greek to care, to worry, preoccupation) was a condition in which individuals were described constantly worried and ruminating about potential outcomes which was observed to lead to pain and bodily tension. Again, this aptly observes the physical effects of anxiety. Perhaps they were also observing how other medical conditions, such as a pain syndrome which can, in turn, cause anxiety.

Epicurius (270 BC) a Greek philosopher (Epicureanism) taught that a happy life included reaching a state where the mind was free of worry - ‘ataraxia’. To achieve this, an individual was to get rid of negative cognitions about the past and of fears about the future, with ones focus being in the present - since the only reality is, the present moment. This teaching is essentially not too far from the current tenets of Cognitive Behavioural Therapy (CBT).

In the technical manuals that try to provide a definition for mood disorders (DSM), anxiety is defined as the anticipation of ‘future threat’ and ‘apprehensive expectation’. In this regard, anxiety is a normal emotion. From an evolutionary viewpoint we can see it as an adaptive advantage since it promotes survival by prompting us to avoid perilous places and to cognitively anticipate danger. In this sense, anxiety is ‘normal’ - it’s a strength. Where it becomes pathological, a disease, is where through life events +\- genetic predisposition this process doesn’t get switched off. This heightened state of anticipation is left switched on.

In more clinical language: overactivity in our subcortical and paleocortical fear circuits (these are subconscious) is coupled with under activity in the (conscious) frontal cortex - the processing center that should normally serve to moderate these areas. The result, our hypothalamus-pituitary adrenal system (HPA system) is activated, the adrenal glands fire up, cortisol and adrenaline flow and the body lives in a neuro-biochemical state of ‘fight or flight’ - at its most extreme exhibiting the symptoms of PTSD.

What’s interesting (to me a at least) is that humans through the ages have described, in a language familiar to their time, a set of symptoms that we today can relate to. That’s because today, or a thousand years ago, when the symptoms of anxiety take hold, the battle of managing the complex interplay between our environment and our physical response to it is as ancient as the people who wrote about it.

As always, I hope this helps.

Dr Chris Robinson , MBCHB, BSC, MRCGP, FRACGP, Doctors at Eatons Hill

11/01/2019

Acute Cough - Don’t Worry Honey.

Acute cough caused by viral respiratory tract infections is probably the most common illness to afflict mankind. To unpick some terminology. The Common Cold is an infection of the Upper Respiratory Tract. An Upper Respiratory Tract Infection (URTI). The symptoms of sore throat, sneezing, chilliness, nasal discharge, nasal obstruction, cough and malaise are common. The cough aspect is sometimes called Acute Bronchitis. This sounds better - but its the same thing as the common cold. Its a clinical term that describes anatomically the principle location of where the virus is affecting the respiratory tract - the Bronchi. It’s not a comment on severity of the infection per se.

I say virus, because In at least 90% of cases this is caused by a virus (normally RSV). Antibiotics do nothing for a viral illness. Bacteria are cells and cells have a cell wall. Antibiotics kill bacteria by interacting with cell, often its wall, in some way. Viruses don’t have a cell. They are literally strands of DNA(ish) and they get inside our cells. So antibiotics simply can’t work, as there is no cell to work on. Despite that 85% of people who present to their GP for a viral URTI get…antibiotics. This isn’t to say antibiotics arn’t necessary for chest infections, of course they are, but its about treating the right illness with the right treatment(s) for the right amount of time.

It starts with the aches, the runny nose, the fullness in the face, headaches, then we all know what happens next. Around day 4 the virus that has crept inside and infected the delicate cells of our respiratory tract (the epithelium) has caught the attention of our immune system - chemical warfare ensues. Our immune system takes no prisoners and destroys any infected epithelial cells. The ‘guts’ of these cells spills out and in doing so this sensitises cough receptors nearby and the neuronal pathway of the cough reflex is fired up. More simply put … ‘its gone to my chest…’.

The copious over production of mucus that follows is an effort to protect the damaged delicate tissue of our upper airways. Sometimes this mucus production is excessive - your wet cough, sometimes it not - your dry cough. But, contrary to what we would think, its not the mucus that drives our cough, It is the overstimulation of cough receptors due to the chemical warfare of inflammatory ‘mediators’. It’s brutal. Why does it last so long? Researching this battle ground in mice with the same viral strains that affect us, researchers have found that hyper-reactivity and excessive mucus production of the epithelial cells lasted for at least a year after complete clearance of virus. Ounch. So, In time, the unwell phase of the illness resolves, the mucus production reduces, but in the wasteland of our delicate injured epithelium, the cough receptors are still hypersensitive and the cough persists.

Incidentally, mucus - more specifically the colour of mucus - tells us nothing about what has caused the infection. The notion that yellow/green mucus (sputum) equals a bacterial infection was put to bed in a study in Dusseldorf, Germany, where the mucus was collected for patients at 42 GP practices over a month for people with an URTI. The colour and consistency was noted and then sent to a lab to see if bacteria would grow. It was found, so long as you have no underlying lung condition (asthma, CF, COPD etc) the colour of sputum can’t be used to differentiate between viral and bacterial infections.

Given how common this is and how irritating a persistent cough is you’d think we would have come up with some reasonable options to treat it. O***m is great for a cough. Its the gold standard against which all cough medicines are measured. It has been used for centuries for cough relief….amongst other things. O***m though, has a few issues. He**in followed. He**in was initially marketed as the ‘safer alternative to O***m’. The name came from the German word heroisch, meaning heroic. There are some beautiful victorian adverts of Mum dishing out some he**in to her kids to treat their cough - they threw in Cannabis and Chloroform for good measure to help get their littles ones to sleep - they did. Some forever.

So what works. Codeine probably has the best evidence. The problem with codeine is that it is a pro-drug. It is converted to neat morphine in the liver. But how much morphine is generated depends on the individuals genetics - some make more morphine than others from the same dose of codeine. Why is this a problem? Morphine also reduces the drive to breathe. In young children, people with breathing issues, the elderly, you are, in effect, giving an unknown quantity of morphine. This is a bad idea. Dextromorphan, the main ingredient of robotussin, has some okay evidence behind and is the only FDA approved cough medicine with objective studies behind it that compares to placebo. ‘Compared to placebo’. Thing is, when compared to honey - honey basically works out either the same or better than dextromorphan in controlled studies. In fact, pretty much all OTC cough remedies aside from Dextromorphan, don’t compare to honey. The mighty Cochrane database (a very good source for scientifically based information) note that Honey actually stacks up pretty well against salbutamol ‘ventolin’ in young children with a URTI related cough. It should also be noted that placebo has been compared against antibiotics in an acute URTI cough. Result - no difference. A viral infection…who knew.

So when it comes to the common cold, a viral driven Upper Respiratory Tract Infection, ‘Dont Worry Honey’ - Thats unless its man flu, in which case, call an ambulance.

Some caveats to the above: The above is a summary and not intended as individual medical advice. If your child has been prescribed ventolin/salbutamol, do not stop it without discussion with your treating Dr. Using honey for infants aged up to 12 months is not advised because of poor immunity against bacteria that may be present, which can cause paralysis. Any concerns, again, chat with your Dr.

As always, hope this helps and a happy new year.

Dr Chris Robinson , MBCHB, BSC, MRCGP, FRACGP, Doctors at Eatons Hill