Colour change in a teacup

As the revision period looms (I mean, when is there a time when we don’t have to revise?), tea becomes my constant companion. Whether this may be in the form of offering a shoulder to cry on as maths questions refuse to make sense or, by living up to its expectations, that tea can, in fact, solve all your problems by creating the polite deception of wanting to boil the kettle for everyone when you just wish to escape the confining shackles of textbooks.

It was as I was pouring over my chemistry notes on hydrogen and hydroxide ions that tea made another unlikely addition to its already enviable personal statement; it is a real-life example of a colour change.

I am sure this has limitations. For example, I drink my tea with lemon and no milk.

However, I was still intrigued about this magic in my tea cup and here is what I found in my educational revision break.

50 shades of tea

By adding a lemon slice or juice, black tea lightens significantly (shown by figures 1 and 2), and although I have never tried this, by adding lemon to green tea, the tea loses its signature colour and becomes colourless [1].


Fig 1. Tea before lemon has been added.


Fig 2. Tea after lemon has been added.

Lemon juice is an example of citric acid, which has the chemical formula of C6H8O7. It is a weak tricarboxylic acid that is found mainly in citrus fruit, but also a variety of different fruit and vegetables. Lemons and limes have a particularly high citric acid content as it can make up to 8% of the dry mass of the fruit and the concentration can reach 0.30 mol/L whereas this is significantly lower in fruit such as oranges and grapefruit where the concentration amounts to 0.005 mol/L.  Citric acid itself was isolated by the chemist Carl Wilhelm Scheele in 1784 by crystallising it from lemon juice. The acid can exist in both an anhydrous form, which is formed when it is crystallised from hot water, and a monohydrate form which is created when the acid is crystallised from cold water instead.

Anyway, back to tea.

Tea leaves are rich in polyphenols-a group of chemicals that accounts for almost one third of the mass of a dried leaf and much of the tea’s colour and flavour is due to these compounds. One group of polyphenols is called thearubigins and they are the red-brown pigments which are found in black tea. This group of polyphenols can make up between 7% and 20% of the total mass of dried black tea, and more interestingly, these thearubigins are weak ionising acids, and the anions (otherwise known as negatively charged ions) they produce are highly coloured. For example, if the water used to brew the tea is alkaline, then the colour of the tea will be deeper because of the greater ionisation of the thearubigins, and because the colour of black tea is influenced by the concentration of hydrogen ions in the water [3].

This means that if lemon juice, i.e. citric acid, is added to the tea, then the hydrogen ions will suppress the ionisation of the thearubigins and this will make the tea a lighter colour [3]. Sorry – no real magic this time.

On a side note, however, you may be interested to know that theaflavins-the yellow-coloured polyphenols present in black tea-are not actually involved in the colour change that is associated with a change in acidity [3].


The colour change that you see in your tea cup as you sip slowly in order to extend the tea-drinking break is in fact just evidence of a change in acidity-much like a change in litmus paper that you may have seen in a Chemistry lab.





Why does Christmas dinner make us sleepy?

I hope you all had a lovely Christmas, and are looking forward to the New Year. At about 5pm on Christmas day I looked round our living room to see my sister, dad and grandparents all fast asleep – the annual post Christmas lunch nap. Something which caused me to ponder why, so I thought I’d do a bit of research and share it with you in a quick blog post.

Initially, the only answer I found was that large meals obviously take a long time to digest, thus blood is diverted away from other body areas to help digest the food at a faster rate. However, after a bit of digging I found some interesting websites and articles which gave more in-depth alternatives. The conclusion I came to is as follows…

Eating triggers the PNS  (parasympathetic nervous system) responsible for preparing the body for rest and increasing the activity of the digestive system. The PNS is part of the autonomic nervous system (thank you 3rd Form biology!) which is responsible for involuntary actions. Fundamentally, the actions of the PNS trigger hormones and neurotransmitters which are what make us feel sleepy.

An old New Scientists article says that ‘high blood glucose levels, similar to those after eating a big meal, can switch off the brain cells that normally keep us awake and alert.’ Additionally to this, high blood glucose levels cause the PNS to stimulate the pancreas to produce insulin – converting these sugars to be stored.  This increased level of insulin consequently stimulates the action of tryptophan, an essential amino acid within the brain. In turn, when the tryptophan is in the brain, it leads to an increased level of serotonin – the universally known ‘happy hormone’. Serotonin is an neurotransmitter which passes electrical signals between connecting neurones, and has many functions, including controlling mood and lethargy. Around 90% of serotonin within the body is found in the abdomen, and is responsible for regulating intestinal movements. However, the remaining 10% is found in the brain.

In short, high blood glucose levels trigger the production of insulin. This stimulates the action of tryptophan in the brain, consequently triggering an increase in the levels of serotonin within the body.

Therefore, it is the increased level of serotonin, responsible for mood and ‘sleepiness’ which makes you feel like all you can do is nap after Christmas dinner!



Nerves, aka the not-so-good wires

Author’s note:

So, just before we explore the workings of message transfer in the human body, I would like to clarify the origins of this blog post. On Saturday 5th November 2016, Cambridge University held a Medicine Taster Day at the Lady Mitchell Hall. This consisted of sample lectures and a run through of the teaching system, among other tips for entry. One of the lectures was titled something along the lines of “How do nerves work?”. As fabulous and interesting as the other lectures were, this one really gave me the most “food for thought”, as they say, and it is on the notes that I made during the lecture that is blog post is based.

Thus, I implore you to understand that writing notes on a topic which a lecturer is comfortably pacing through and later trying to make out the beginning and end of your scrawls is no easy feat (as I’m sure we’ll all find out about in a few years’ time and become masters of note taking). I admit that I wanted to write this solely on my notes to a) review the lecture and b) to see if I understood anything that was being said.

But before any of you future Biology stars start panic (or panic further as may be the case), I did ask for my Biology teacher to look over this post. The message is this: this is a very simplified version of what is happening in real life, especially in the case of amplification. We shall, of course, come to study the topic of nerves in more detail and finesse further in the A Level course.

Oh, and another thing. If any of you dear readers come to learn that any of the figures are incorrect, I sincerely apologise and please do not hesitate to let me know. In the meantime, feel free to blame my poor eyesight (I did find out a while later that my right eye has deteriorated 🙂 ) or my incomprehensible handwriting for any mistakes made.


Nerves work in a similar fashion to wires, but when you look at their basic structure, to be honest, they’re a bit of a disappointment to the wire family.

So, if nerves are the “ok” version of copper wires, how do we manage to stay alive?

Firstly, we’ll look at how nerves work, then the problems they encounter and finally how they try to overcome the issues of transferring current.

Trying hard to be a wire

When a pain fibre is stimulated, pain channels are opened and sodium ions (which have a positive charge) enter at one end of the nerve while the rest remains negatively charged. The next stages are similar to those of a battery, as, the differently charged ions create a current which spreads positive charge through the nerve and this results in the potential of activating something else, such as a synapse.

In comparison to a copper wire in which the speed of this is 28,000,000 m/s, the nerve’s speed is between 0.6 to 100 m/s. However, although this is significantly lower, this is not a limiting factor in the body’s reactions, as the message still travels in milliseconds.

The difficulties begin

As usual, there are problems with all wires, however this is particularly true of nerves, and the problem nerves face is that current leaks out.


Fig 1. Diagram showing longitudinal and membrane resistance in a nerve.

In the diagram above (Fig 1.), RL (red line) is the longitudinal resistance and it is a measure of the resistance the current encounters as it travels along the nerve. The lower this resistance, the easier it is for the current to travel.

Rm (blue line) is the membrane resistance and this is a measure of the resistance given to the current by the cell membrane. The higher this resistance, the less current will escape.

How far can a nerve conduct?

Voltage decreases exponentially, meaning it leaks less.

The distance at which the voltage has decreased by half is called lambda (λ), and it is a ratio of the two resistances aforementioned. In effect, it is a ratio of how much voltage continues travelling along the nerve to how much has leaked out.


This means that high membrane resistance and low longitudinal resistance results in a good signal.

We must also remember that resistance is calculated by:

R = p x l/A


  • R is resistance
  • p is resistivity
  • l is length
  • A is cross-sectional area


Nerves are very narrow as they normally have a diameter between 0.2 to 2.0 micrometres, meaning that RL is large.

The cell membranes are also very thin, typically between 7.0 to 9.0 nanometres, so Rm is small. This is due to the fact that the membrane is made of two molecules – specifically two phospholipids, as cell membranes are bilayers.

In addition, the axon, which is mainly cytoplasm, has a resistivity of 50 To put this into perspective, copper wires have a resistivity of 1.7×108 The poor axon resistivity is because, since nerves are part of the body, they have to be able to change shape, which is the advantage of a conducting liquid.

As a result, a 1 metre long, 1 micrometre diameter nerve has the same resistance as a 22-gauge copper wire, which in other words is a 0.65 nanometre diameter piece of copper stretching to Saturn and back. Five times.

A much-needed rescue

To put it nicely, nerves are probably not the material you would be reaching for if you wanted to transfer some current. As a result of their physical properties of being narrow, thin-walled and not very conductive, their resistance is high, and even non-physics students know that this is not ideal for conducting electricity.

After reading all of this, I’m sure your question is: how are we still alive? This was my question too.

Thankfully, nerves have some tricks up their sleeves, something similar to pulling a rabbit out of a hat.


One of these features is myelination of the nerve fibre. The myelin sheath increases the membrane resistance and it means that the signal can travel 3 millimetres more. However taking into consideration that the length of a nerve fibre running from your foot to the central nervous system can be around 1 metre, in the grand scheme of things, 3 millimetres are not that helpful, although certainly much appreciated.


The real show stopper trick and literal life saver is the nerve’s power of amplification. This process keeps allowing ions to enter the nerve cell by sodium gated voltage channels in order to sustain the voltage. This makes the signal bigger, as when the channel opens, more positive sodium ions enter and this increases the concentration gradient, as there is more positive charge. Furthermore, the channel is also charged, meaning it moves if voltage changes. This means the channel itself detects a change in the voltage and is able to react to make it greater. Figure 2 demonstrates this process.


Fig 2. Graph showing the effect of amplification [1].

Problems persist

Because the amplification process requires sodium channels, and channels are required to stimulate pain, the myelin sheath cannot be too thick, as otherwise the sodium channels could not be present, meaning the effect of myelination is not at its highest potential, as it needs to compromise with the other processes.

Moreover, the transmission takes time because the passive movement of the signal (i.e. when the signal is not aided by amplification) is still faster than the active movement (the points where amplification takes place) since the amplification process, as we now know, involves sodium channels opening, moving and opening again, which overall is time consuming. 

In addition, there is also the factor of positive feedback. The main idea is that it is triggered by something that it causes and so it is an all or nothing response. What this means is that as one sodium channel opens, then more will open. If the stimulus is not powerful enough, then nothing happens, so the stimulus must be greater than the threshold.


Overall, the structure of the nerve results in it being a poor conductor, however it is because of features such as myelination and amplification that we are still here today, reading this biology blog post.


As I have mentioned before: this post has been written from my notes which I took during the lecture: “How do nerves work?” as part of the Medicine Taster Day at Cambridge University. The information is from the lecturer given on the day: 5Th November 2016.



With thanks to:

·Cambridge University for organising the taster day and to the lecturer for providing the fascinating information.

·Miss Lasouska who kindly read this post.

A Trip Which Sparked Curiosity (Part 3)

A Burst Of Colour

imageThe Christmas festivities are well under way, and we all know how colourful this season can be. Red, green, yellow, you name it, chances are there is a decoration in your house of that colour. Thinking about the sheer variety of colour I am surrounded by at the moment led me to dedicate my next post to a smaller, and often forgotten realm – the world of the invertebrates.

Christmas to insects isn’t the same, for many insects can only see the higher part of the visible light spectrum and part of the ultraviolet light spectrum. An exhibit in the Natural History museum showed what some flowers could look like through an insect’s eyes, and I was curious about what difference in anatomy caused this interspecies variation in vision.

It’s all about the receptors

Many insects that can detect ultraviolet light have eyes which contain ultraviolet light receptors which aren’t present in human eyes. Human eyes contain three types of photoreceptors, we are trichromatic; red, blue, and green [1]. When light enters the eye, its wavelength determines whether it is absorbed by these receptors, and the combination of signals produced by the photoreceptors due to the light absorbed is what determines which colour the brain perceives (as a quick side note; discussing colour perception is very theoretical, as, the sensors stimulated and colour of light absorbed can be scientifically proven, however, how the brain of the organism interprets those signals is impossible to state with 100% accuracy. Predictions can be made, but perception of colour is in the eye of the ‘bee-holder’ only after all [2].).

imageInsects are trichromatic also, however they do not possess the receptor which absorbs red light. Instead, insects possess the ultraviolet light receptor, leading to many invertebrates being unable to sense red light but instead being able to sense light towards and in the ultraviolet spectrum. Each of the insect’s prismatic lens containing units (or ommatidia [3]) contains eight light detecting cells; four respond to yellow-green light, two respond to blue light, and the other two respond to ultraviolet light [2]. This fact has forced flowers to develop petals which are attractive to insects not only in the visible light spectrum, but also in the ultraviolet light spectrum.

One hundred and eighty

imageWhen looking at many petals in the visible light spectrum, they may seem drab and a bit boring to you and me, however, when placed under an ultraviolet lamp, or photographed with an ultraviolet camera, these petals reveal a hidden world. Patterns, like dart boards, suddenly appear and offer a small glimpse into the world of the invertebrate. Vibrant colours illuminating the pollen rich areas of the flower act as a target for the insects flying overhead [4]. They have adapted so their petals are not only attractive to the human eye in the visible spectrum, but they exploit the ultraviolet sensing ability of the insects to become highly practical in their marketing strategy. No beating around the bush, if the insect wants nectar, it knows exactly where to find it. With a precise flutter of the wings, the insect hits the bullseye, receiving a sugary reward.


The photoreceptors present in the eye is what makes all the difference when perception of colour is involved. Without the relevant receptor, an entire spectrum of colours is inaccessible and a world is hidden to us. Think about how different Christmas could be with just a simple receptor missing.


[1] HORSE ARMOR. (2016) Insect vision. [Online] Available from: [Accessed: 23rd December 2016]

[2] RIDDLE, S. (2016) How Bees See And Why It Matters. [Online] Available from: [Accessed: 23rd December 2016]

[3] [Online] Available from: [Accessed: 23rd December 2016]

[4] STARR, B. (2013) Hidden Patterns: How A Bee Sees The World Of Flowers. [Online] Available from: [Accessed: 23rd December 2016]