A post to remember?


When I was young, I used to ask my mum what it was like when she was a child. Her response of ‘I don’t remember it was so long ago’ always astounded me. I was convinced that I would remember everything! Flash forward, and while I have some strong, distinct memories from my childhood, much of it is gone, just like my mum’s. So what are memories? How are they formed and stored and, how do we lose them?

I remember

Memory is the retention of knowledge. Both neuroscientists and physiologists agree that this is a broad term covering different aspects of knowledge accumulation. In a general sense, this covers whether the knowledge is purely emotional, linked to a time and place, or if it is related to environmental stimuli.

Much of what has been gleaned about memory comes from medical conditions in which people cannot retain memory or demonstrate memory loss. For example, in individuals with Alzheimer’s, it has been demonstrated that the hippocampus region of the brain is necessary to memory formation. It has been found that there are certain proteins in the hippocampus that are targeted by beta-amyloid peptides (small proteins that are found in the brain tissue of individuals with Alzheimer’s) that result in memory loss. Restoring the levels of these proteins in mouse models of Alzheimer’s restores the ability to learn and remember.

The hippocampus has been shown to be integral in the formation of episodic memories. An episodic memory is one which recall is via the stimuli of a place and/or time. New episodic memories can use the ‘parameters’ of a previous episodic memory and retrieval can involve thoughts and emotions of other memories. This can be why one place or emotion can trigger a multitude of memories! This has been shown experimentally from imaging of the brain. The area of the brain involved in performing an activity associated with a particular place was the same area used to conduct recall of an episodic memory associated with the same location. It has also been demonstrated that stimulation of the hippocampus produces a similar neural response to novel stimuli.

I will remember for ever and ever

So how is it that we fail to remember a conversation we had yesterday but can recall the phone number of the first house we ever lived in?

This comes down to short-term memory versus long-term memory.

Short-term memory is often also referred to as working memory (WM), and is retained for approximately 15-30 seconds. These memories are in a readily available state and usually apply to a task being performed. Repetition of the task or repeated exposure to the stimuli shunts the memory to long-term recall.

A process termed long term potentiation (LTP), is the persistent strengthening of neural cell structures called synapses in response to recent repeated activity. These synapses also exhibit plasticity, a term for the ability of synapses to weaken or strengthen in response to increases or decreases in activity. Memories that ‘fade’ are a phenomenon that neuroscientists call memory extinctionwhere a conditioned response is forgotten as older memories are replaced with new experiences.

Physiologists have demonstrated that dopamine plays a role in memory formation, in particular short-term memory. Neurons in the hippocampus that are receptive to dopamine will respond rapidly to novel stimuli, but as the stimuli become more familiar, the cells no longer respond. And, interfering with dopamine can block LTP, while making cells more receptive to dopamine enhances LTP.

As it is known that there are also learned responses based on both reward and behaviour, how are memory systems (i.e. WM vs LTP vs reward-based memory formation) recruited?

It is the general consensus that in the case of dopamine and LTP, it is only for stimuli that will be behaviourally advantageous. For other memory systems, recruitment of a system is based on the anticipated demands of a memory and can involve a feedback mechanism that predicts the outcome from interaction with stimuli.

This is where it can become a little confusing! The different parts of the brain control different memory systems. As discussed, the hippocampus is involved in LTP while the prefrontal cortex, for example, is involved in the maintenance and manipulation of WM.

One study demonstrated that if an individual was distracted or had increased delay between memory recall during a task that required WM, LTP increased with a decline in WM accuracy. The authors concluded that the anticipation of increased difficulty in completing or performing WM tasks led to a shift away from WM in order to preserve high-level performance.

It’s in the genes?

Very little is known about the biology of memory. Studies into Alzheimer’s have yielded much of the information about proteins that are crucial to retaining memories.

Neuroscientists combine the memory tests with investigating what is going on at the genomic level, and have found that different genes are activated along with differences in protein production. This can depend on the memory system. However, it is increasingly obvious that epigenetics plays a very important role. Modifications to DNA and proteins that change their activity without changing the genetic or protein code are rapid and occur in response to environmental stimuli. Furthermore, these changes are plastic, which as discussed, is important to memory formation and retention. This is an exciting area of research, with much more to come!

It has been demonstrated that diet can affect memory. In particular, a high fat diet (HFD) can result in poor memory retention, and in animal studies, disrupts learning and performance. It is known that a HFD results in insulin resistance of cells in the hippocampus that impairs insulin signalling.

One study observed that mice on a HFD exhibited reduced exploration time of a novel object, and when re-introduced to the object, spent more time investigating the new object compared to control diet mice. These results indicated that both WM and LTP were affected by the HFD. When the diets were changed, the effects on memory were reversed. Food for thought?!

 Liar, liar pants on fire!

The demonstrated plasticity of memory formation and recall can also result in false memories. A false memory is the recall of experiencing something that wasn’t actually experienced.

There are two types of false memories, misinformation-formed and spontaneous false memory formation.

Studies have demonstrated that children seem particularly susceptible to spontaneous false memory formation, while in adults sleep deprivation can be a cause. If a person is sleep-deprived at the time of being presented with the stimuli and later provided with misinformation, their recall of the events can be different to what occurred.

This has also been demonstrated in individuals who exhibit ‘total recall’. These people have an ability to recall memories in rich detail unaided by mnemonics or memory aids. Memory recall from these individuals can also be corrupted by misinformation or misleading suggestions.

I forget

With all that we have learned about memory formation and retention, what about age-related memory loss?

Age-related memory loss is associated with a reduction in the activity of genes involved in plasticity, degradation or loss of neurons, and decreased plasticity. The hippocampus in particular appears to exhibit age-related decay that can lead to a loss of autobiographical recall.

However, not all memory systems are affected by age. One study showed that there were not age-related differences in the ability to learn configural tasks, but that there were delayed response times i.e. older adults repeated the tasks more slowly. The older adults did show a deficit in recalling tasks associated with newly learned episodic memories, with higher false memory recall. This was further confounded if several cues could initiate the retrieval of a memory.

However, all is not lost. A recent study demonstrated that the injection of blood from young mice could counteract ageing at the molecular, structural, functional and cognitive levels in the hippocampus of aged mice!

While the authors observed these changes, they had no data to explain why and how the changes occurred. They cited that it was possibly ‘pro-youthful’ factors that promote regeneration of decaying tissue or affect the activity of ‘pro-ageing’ factors. Current literature suggests that stem cells in the young mouse blood may play a role.

Stress is also linked to poor memory retention and recall, as is a lack of sleep.

Final thought

While it appears much is known about memory, it is acknowledged that there is still a long way to go to understand the brain and memories. Unfortunately, progress is generally made by understanding how something has gone wrong.














You are what you eat?


We all know that our environment affects our health and well being. Breathing polluted air results in respiratory problems, being out in the sun too long results in sunburn, not having enough sunlight can result in seasonal-affective disorder, exercising improves cardiovascular health….the list goes on.

Researchers like to know why and how the environment can control our bodies and cellular functions. What we know now, is that some people are genetically programmed or predisposed to react to environmental cues.

This is most commonly observed in the case of cancer risk, and a well known example is the influence of diet on colorectal cancer (CRC) risk. World wide, CRC is the 3rd most common cancer in men and the 2nd most common cancer in women. In Australia, CRC was the cause of death for 1.1% of the males and 1.12% of the females who died in 2015.

CRC has a high hereditary factor, where a family history of CRC is a greater predictor of a person’s risk for developing the disease. CRC most often arises due to mutations that disrupt normal cellular processes. Commonly, these mutations can be found in genes that encode for molecules that repair DNA following exposure to damaging agents.

The good, the bad, the ugly.

So, how does diet influence risk if we know that there are hereditary risk factors? In order to discuss this, I want to share a quote that appeared in my social media news-feed the other day:

‘Eat bad food and bad genes are activated. If the same person, with bad genes activated from bad food, eats good food……those bad genes turn off and good genes turn on. Genes don’t control anything, they react to our environment…..mostly our food choices…… The “genetic causation of disease myth” is intended to make sure the public never understands that their food choices control the way their genes express themselves’.

There are so many problems with this statement. First, let’s start with ‘bad genes’. Is there such a thing? No. Genes exist because they produce molecules (proteins) that cells need.

Sometimes, a mutation can occur that can alter the function of the gene or of the proteins it produces. In a sense, it could now be a ‘bad gene’ but, eating ‘good food’ cannot turn off a ‘bad gene’. It is possible that the author of this post is confusing epigenetics with genetics. Epigenetics, as I have discussed previously, is the alteration of gene expression without changing the DNA sequence, and can be influenced by external factors such as diet. It is also possible that the author is confusing physiological effects with the genetic effects. An example of this could be the development of Type II diabetes due to obesity, where the body stops reading cues in regards to glucose production and consumption. But it is important to remember that this is also controlled by genes!

There is control, and then there is controlling.

Second, ‘Genes don’t control anything, they react to our environment. This simply is not  true. Genes control everything. However, in turn, genes can be influenced by other factors, which changes how they affect or ‘control’ cellular processes. If we come back to the epigenetics thread, the change in expression of gene can be altered by diet, but the alteration induced by the diet influences the expression of another gene producing the epigenetic change. Therefore, genes are still controlling expression!

CRC risk is influenced by both genetics and environment.

Finally, the last statement ‘The “genetic causation of disease myth” is intended to make sure the public never understands that their food choices control the way their genes express themselves’. This brings us back to the CRC diet-associated risks, where genetic predisposition can be enhanced by diet. In this sense, diet increases the risk of developing CRC in predisposed individuals, but is not the cause. Someone following the guidelines for ensuring good bowel health, who doesn’t smoke, exercises daily and eats plenty of  ‘good foods’ as the author of the post suggests, could still develop CRC due to the familial risk.


Final Thought

Massive genome sequencing studies have demonstrated that there are untold gene-environment connections that can influence cancer risk and other physiological alterations. However, as not everyone has cancer (as an example), it is obvious that it needs to be the right ‘mix of ingredients’ to initiate the disease. For example, studies are now showing that gut microflora can influence predisposition to disease!

Humans have evolved, and this means alterations to genes, in response to the environment, but the genes have also influenced how we respond to these environmental cues!




Statistics obtained from the Australian Bureau of Statistics and the World Health Organisation





Dose matters


Do you ever think about how much radiation you receive when you fly long-distance, have a dental X-ray or undergo a CT scan?

Much of what we know about the risks arising from radiation exposure come from studies on the Hiroshima and Nagasaki bombings during WWII. Despite only having data for high doses, it was concluded that all doses, no matter how small, were harmful and that the risk of cancer increases exponentially with dose. This is termed the linear no-threshold model (LNT). LNT is in contrast with what radiation biologists have demonstrated experimentally for more than two decades, that below a certain dose, where the LNT is extrapolated, risk is reduced and often the low dose appears to have a ‘protective effect’. This has been termed the radioadaptive response.


Radiation can be ionising (e.g. X-rays) or non-ionising (e.g.. microwaves). Non-ionising radiation does not have enough energy to displace electrons and therefore cannot cause damage to cells and other molecules such as DNA.

Why is this important? Understanding safe low dose exposure is an increasing concern where legislation and safe work practices are concerned. Increasing availability to the masses of medical imaging devices such as CT scans or dental X-rays, airport whole body scanners, increased air travel as well exposure to background radiation in mines means that greater understanding of safe radiation exposures is required.

So many factors can confound the determination of safe levels. At the simplest level it can be whether the exposure is single or repeated, whether it is whole body or targeted at an individual organ (important as different organs display different radiation sensitivities). And then, there is the agreement on what a low dose of radiation is. Even in research laboratories this can differ. Further adding to this is the consideration of natural background radiation arising from naturally emitting materials such as granite, or radon carried in the air. Even bananas are radioactive! Did you know there are some countries in the world where the natural background radiation is as high as receiving a CT scan or a dental X-ray, without increased rates of cancer or other radiation-induced problems?!

My own PhD lab has demonstrated that a low dose of X-rays can protect against DNA damage induced by a high dose, when given before or after the high dose exposure, while others have demonstrated that the incidence of tumours in radiation-sensitive mice can be reduced if the mice are given a low dose first.

Recently, a study into the deaths of nuclear industry-workers in France dating back 60 years reported that there was an increased, proportional risk in leukaemia. But only for extremely low doses. These individuals were exposed to doses just a little higher than background radiation doses, but accumulative. The only problem with studies like this, and it was pointed out by the authors, is that the risk was calculated based on mathematical model and the accumulated radiation doses cannot be directly linked to the deaths.

Based on increasing evidence that the LNT model cannot be used to justify exposures, there are many who say that a new model for radiation exposure and risk needs to be proposed. Public understanding of radiation, and what constitutes damaging radiation, also need to be addressed by scientists and legislators.

The take home message should be that radiation is harmful, but the question is still “at what dose does risk become neglible, if at all?”







Hooker et al. Radiation research 162.4 (2004): 447-452.
Dayet al. Radiation research 167.6 (2007): 682-692.
Mitchel et al. Radiation research 159.3 (2003): 320-327.

The rise of the lifestyle guru and information cherry picking


So I have only posted several times refuting facts that people share on the social medias’. This is mainly because I am not interested in the deluge of responses located in the comments section of said links. My biggest gripe is people using the internet to push unverified data and anecdotal evidence, usually with the tag line “what scientists aren’t telling you about [insert item here]”.

This is why I was surprised when a link  appeared in my news feed (that I initially dismissed as tripe) had sound science with links to high-quality peer reviewed journals. *Gasp*.

‘And you won’t believe what this common foodstuff does!!…”

The article describes how the active ingredient in turmeric, curcumin, appears to be able to improve endothelial cell functioning. What this means is that it can alter the way that the endothelial cells that line blood vessels contract, restricting or promoting blood flow through the vessels. There is also evidence that curcumin may be an interesting adjuvant (additional to other therapies) chemotherapeutic agent, although further investigation is required. My literature search showed that there are a lot of articles supporting these facts, BUT, it should be noted that doses tested in the laboratory do not necessarily translate to the amount that you obtain from consuming turmeric. And, there are other considerations such as, was it tested in cells, using animal models, or in human clinical trials?

Money, money, money

Now back to the link that was posted. While it was scientifically sound, a quick search of the author of the article showed that he has a vast financial investment in what he discusses in his blog. Books, seminars, videos and so on all selling the ‘lifestyle’ that he promotes. Interestingly, a science blog from McGill University in Canada also discussed the lifestyle blog and that despite the use of peer reviewed research, there is an agenda and therefore the information presented is cherry picked.

The deluge will continue

As long as the internet will exist, there will be sites that support or refute opinions (most likely refuting concrete scientific data). Evidence shows that when searching for information, people themselves will cherry pick what data they choose to believe. Using the anti-vaccination movement as an example, providing anti-vaccinators with evidence contrary to their beliefs, including images of sick children, fails to change their views against the plethora of sites that will support their ideas.

Adding to this are the personalised search results and advertising, which further cement beliefs and opinions.

Final thought

To me the internet is like a store that sells ‘dust collectors’. Pretty to look at, you consider for a second to buy the bauble, but ultimately realise it is a cheap trinket that will collect dust. But, at the same time, one person’s trash is another’s treasure. The jury is still out amongst scholars on how to prevent the spread of misinformation, false news and potentially health damaging opinions and ideaologies, without completely censoring information and internet use. However, while there is a dollar value linked to the promotion of these opinions, these sites will persist. I implore you that if a link appears purporting the health benefits of [insert name of ‘natural product’] and how scientists/ doctors are lying to you, take it with a grain of salt.

Rant over (!)



So the other week I was fortunate to witness Guy Fawkes’ Day/Bonfire Night. As I was watching the different coloured fireworks and effects, I began to wonder how fireworks work.

The art of chemistry

The art of pyrotechnics comes down to basic chemistry, oxidation (if anyone remembers previous posts on oxidation, it is the process of losing or gaining electrons) and the addition of chemicals which create heat (exothermic reactions). In the case of fireworks, a fuel source (usually a metal) is oxidised by an oxygen source other than atmospheric oxygen. Traditionally, nitrates, perchlorates and chlorates are used as oxidisers.

So what about the colours? The range of colours that we see during a fireworks display are due to the addition of metal salts. Sodium is used for yellow, strontium for red, barium salts for green, and copper for blue. The white/incandescent effects are due to white hot burning metals such as magnesium (does anyone remember during Chemistry class watching Mg burn when it came into contact with air??!!).

A little bit of timing, a little bit of engineering

The chemistry is actually the easiest part of creating fireworks. The next step is to send the fireworks into the sky. This is where the engineering comes into it. Fireworks are traditionally shaped like a missile, with a long stick, a fuse, a charge, and a head that contains the pyrotechnic chemicals (sometimes with several housing units making up the head).

The fireworks also normally contain several fuses attached to different housing heads. The fuses are timed, so as to create the differently timed explosions that we see. Gunpowder is most often used as a charge, which propels the missile into the air and creates the first explosion that promotes the secondary reactions containing the coloured salts. Et voilà!

Simple chemistry, a little bit dangerous

Although the principle behind fireworks is simple and it seems relatively straightforward to make them, they are explosives and are therefore dangerous. The ratio of chemicals, the amount of gunpowder used, and fuse and tail length all need to be precise. If not, premature explosions can occur which can result in injuries.

So my take home message? Enjoy the show, appreciate the chemistry and the feats of engineering, but don’t try it at home!!




Toothbrushes and their little friends



So today’s post might have some people cringing and others reaching for a new toothbrush.

I, like many other big city dwellers, live in a small apartment where my toilet is located in the bathroom. It is in very close proximity to the sink where I keep my toothbrush. Hence I always keep the lid closed on the toilet, particularly when flushing. It seems to me, however, that I may be in the minority of people who do this.

So why am I writing about this? Why should it matter, you ask? Simple. Aerosols. Aerosols from the toilet landing on my toothbrush.

I’ll let you savor that image.

It’s all about the microbiota

A study in 2012 demonstrated that bathrooms were covered in microbes found in toilet aerosols generated by flushing a toilet with the seat up. These microbiota were also found on toothbrushes. While this study highlighted how far the toilet aerosols can travel, it also revealed that toothbrushes are inherently contaminated.

A review of the literature into studies investigating toothbrush contamination revealed that toothbrushes are coated in oral microbiota as well as microbiota from the surrounding environment. Interestingly, contamination was found to be influenced by the size of the handle and bristles.

While this sounds horrifying to think that our toothbrushes are contaminating us, we should remember that toothbrushes actually remove the bacteria from our mouths that can cause periodontal disease. Furthermore, bacteria that make it to the gut can be outcompeted by the gut microbiota. Only people who are immune compromised or who are suffering from severe periodontal disease should be worried.

A final word

Despite these unsettling discoveries, it is recommended that you change your toothbrush frequently and, to add my own two cents, perhaps put the lid down when you flush the toilet if your toothbrush is nearby??


Montero, Elly A., et al. “The Effects of Proximity on Aerosol Distribution of Bacteria on Toothbrushes.” Journal of the California Dental Hygienists’ Association 27.2 (2012).

Frazelle, Michelle R., and Cindy L. Munro. “Toothbrush contamination: a review of the literature.” Nursing research and practice 2012 (2012).



All the leaves are brown



So the falling, gold, red and brown leaves tell me that Autumn (fall, l’Automne) is here. The colours are amazing, but why do the leaves change from green to these colours?

Green is the colour of fuel

Leaves are green because of chlorophyll, a pigment molecule found within the leaves (and in bacteria and some algae). This green pigment absorbs sunlight and utilises its energy to transform water obtained from the roots, and carbon dioxide in the air, into glucose (which the plants use as a fuel source) and oxygen.

These reactions take place in cells called chloroplasts in two stages. In stage one, chlorophyll is energised by sunlight to make ATP (a chemical energy transporter). At the same time, water molecules are ‘split’ to make electrons available to another molecule which along with ATP, in stage two of photosynthesis, turns carbon dioxide from the air into the components required to make glucose.

So why the transition to brown?

A sign of the times

The colour change signals a decrease in moisture (water) and sunlight, meaning that chlorophyll becomes degraded and leaves become less green. This is of course associated with seasonal transitions.

Interestingly, longer ‘green seasons’ has been found to be a marker of increased carbon dioxide availability, warmer temperatures and altered precipitation. It has also been discussed that these changes in Autumn length can affect competiveness between plant species, promoting greater growth of parasitic or destructive plant species.

Plants in space?

Because plants absorb carbon dioxide from the air and produce water, using plants as a life support in space exploration is an attractive idea. However, much needs to be known about the effect of zero gravity, altered atmospheric gas concentrations and cosmic radiations on plant growth and function.

It is already known that there are subtle micro -structural differences between terrestrial and space grown plants. For instance, some proteins were found to be less abundant in space grown plants meaning basic plant functions could be reduced. Conversely, there were also groups of proteins that were more abundant resulting in increased activity for certain plant functions. For example, proteins involved in flavour, were found to be over abundant in space grown plants!

Another consideration is light cycling. Terrestrial plants have evolved in a 12-hour light/dark cycle, and during dark cycles, plants release carbon dioxide that can affect the breathable gases concentrations in enclosed spaces such as spacecraft.

Finally, the effect of gravity needs to be considered. Water is drawn up from the roots into the main stem of the plants to the leaves. The effect of zero gravity on this function needs to be understood and researched further, as well as the affect on the cell membranes.

Final thought

Before you stop to smell the roses, maybe you should consider the browning of the leaves as well, and how one chemical is in part responsible for the air that we breathe, and possibly allowing humans to survive space exploration!








Fats, what are they good for?


So I have been away from the blog for a week due to manuscript preparation, revisions and submissions, and, a  good ol’ Autumn cold. But I’m back and with a topic that is the result of a conversation over dinner.

It went something like this, “what exactly am I losing now that I have increased my training?” Me, “well you are losing fat, but it is actually quite hard to lose fat because you don’t lose fat cells. This means that it is easy to gain weight again” Friend, with very confused expression, “but, where is it going then?” Me “umm…..I think I should blog about this”.

I went to the trusty search engines and stupidly typed in “Where does fat go when you exercise?” Oh the deluge of weight loss tips, super food advice and ‘buy these fat burning tablets’. Hmm, that wasn’t what I was hoping to find. So I tried a different tactic.

What is fat?

What exactly is fat? Fat (which can consist of tri-, di- and monoglycerides) is a type of macromolecule known as a lipid, and is distinguished by a chemical structure that renders is hydrophobic. This means that it does not dissolve in water. And, because of the specific structure of fats, they store large amounts of energy.

So, fats are an energy source and are therefore important fuel for the body.

Fats are stored in specific cells known as adipocytes. Fats are made up of 3 (tri-) fatty acids. Fatty acids can be obtained from the diet, or produced by our own cells. Importantly, fatty acids can be reassembled into triglycerides, aka fat.

Ahhh, so this is where the penny drops. Fatty acids that are not used will form triglycerides and stored in fat cells.

Calorie in, calorie out.

The food we eat is digested into its macronutrients that can be used by cells as building blocks for proteins, or, for energy. Calories are the energy obtained from food. So, if you are exercising and your muscles require large amounts of quick energy, consumed calories obtained from carbohydrates in the form of glucose will be utilised first before fat cell stores. Energy will be obtained from triglycerides in between meals.

So, calories in, calories out. If you consume more calories than required, these will be converted to triglycerides and stored within fat cells. If your body never needs to use the triglycerides stored in the fat cells, the fat will remain.

So…when do we use energy from fat?

It has been demonstrated that fat cell triglyceride energy production occurs during low intensity exercise or after in the recovery phase, whereas carbohydrate triglyceride comsumption is favoured during high intensity exercise. Consumption of fat triglycerides decreases with incresing exercise intensity.

So….where does the fat go?

This is the question, isn’t it? Well as you can guess, it is removed from fat cells (which then shrink) and used for energy. The energy production also produces carbon dioxide and oxygen as a by-product, which is excreted from the lungs. So, in essence, you are breathing out the fat.

Final thought

The metabolism of alcohol results in triglyceride storage in fat cells. It is also preferentially metabolised as an energy source. Therefore, a big night out will not only leave you with a hangover, but also with extra fat stores……



Arner, Peter. “Human fat cell lipolysis: biochemistry, regulation and clinical role.” Best practice & research Clinical endocrinology & metabolism 19.4 (2005): 471-482.