Chillies Inspire Medicinal Revolution

Chillies Inspire Medicinal Revolution

     The mechanism within our body that explains the burning sensation we feel when eating chillies could prove fundamental in treating chronic pain conditions and even cancerous tumours.The same mechanisms that explain piquant flavours and soothing cooling flavours such as menthol are also vital in the maintenance of internal body temperature. The key component within chillies that is the source of their fire is called capsaicin. Our sensory perception depends on specific channels, known as TRP (transient receptor potential) channels,

on the surface of certain cells, usually neurones, each responding to different stimuli. When the channel is activated, its pores open up, allowing electrical charge in the form of ions to flow in, in turn triggering an electrical impulse. The channel essential for detecting capsaicin is called TRPV1. This channel also responds to extreme temperatures (43^oC or above) which would be enough to damage tissue - this explains why chillies feel as though they are burning the mouth.

      The functions of aforementioned channels are wide-ranging, hence possibly implicating them in a range of disorders. Particular interest in them is a result of their location on nerves that respond to painful stimuli, and consequently their potential for heightening of dampening the nerve’s sensitivity. The radical concept is that these channels present promising avenues for research for new kinds of painkillers that could use the pathway as an entry point. For example, a protein has recently been discovered that controls TRPV1 function during inflammation. AKAP79 shifts the cell’s molecules into certain formations so that when in excess, the TRPV1 channel has a lower threshold for generating nerve impulses. This results in regular temperatures feeling painful – a prevalent issue in chronic pain conditions including migraine and certain injuries. In order to reverse this unwanted effect, a chemical can be used to prevent AKAP79 from binding to the TRPV1 channel, reducing the pain associated with inflammation.

      These channels could also be crucial in delivering drugs to a far more precise region in the body, for better local anaesthetics. Currently, a local anaesthetic at the dentist dampens all your nerve cells, leaving your face temporarily paralysed. One solution is to use capsaicin or similar molecules to unlock pain nerves : by momentarily opening the heat channel a pathway would arise through which an analgesic could progress into the cell. Since the nerves involved in moving  muscles don’t have the same receptor, they would be unaffected.  As a result of  thermal channels on nerve cells, it is highly likely there are other targets – for example cooling has analgesic effects in painful conditions such as osteoarthritis, and has a soothing effect in inflammation. However presently, there is yet to be a drug that ‘achieves a comfortable medium’, without inducing an aching hypersensitivity to cold which emanates from too much activity in several of the pathways (such as TRPM8 and potentially TRPA1) associated with lower temperatures.

    Perhaps a more commercially viable option would be to use the TRP channels to alter the body’s thermostat to control energy expenditure. This could possibly result in loss of excess fat – a welcome prospect for our increasingly obese society. Unfortunately there are currently some issues. It would be seemingly obvious to suggest that removing our heat sensing mechanism would have the same response as a cold temperature, inducing a response such that more energy is used to generate heat. Nevertheless, conflicting studies have illustrated mice lacking the TRPV1 receptor in reality put on weight. On account of this, it is  proposed that the solution should be to gently stimulate these receptors instead. The activation of the TRPV1 channel appears to suppress the production of adipocytes (specialised cells that store energy as fat), whilst other studies have suggested that the body burns fat already stored. Another proposal is that as TRPV1 is involved in taste, we may be fuller after a smaller portion of food. There is so far modest proof that these theories have solid grounding – subjects who took a regular dose of capsaicin every fay showed a noticeable increase in the calories they burned; ‘enough for a steady weight loss over the course of months’.

    What, is in my opinion, most intriguing is the theory that these channels may be involved in tumour growth. For instance TRPM8, which allows us to taste mint, is present at abnormally high levels in prostate cancer – the more the severe the cancer, the higher the levels of said protein in the cancerous cells. The channel may have become integrated in the cellular signalling pathway that triggers cell division, and since they are also found in the cells that line blood vessels, they might contribute to the spread of cancer by promoting the formation of blood vessels which supply tumours with nutrients. Targeting the TRPM8 thus offers the tantalising thought of controlling the growth of cancers, and so far this revelation seems to be entirely true – a recent experiment that used chemicals to inhibit TRPM8 activity reduced the proliferation of cultured prostate cancer cells. Such success has led to the first clinical trial that aims to discover drugs that prevent the spread of the disease. These prospects are compelling and present the possibility of several treatments. For the time being though, at least one thing is evident: these channels are imperative for the future of therapeutics. 

Source: 

http://en.wikipedia.org/wiki/Transient_receptor_potential_channel

http://gbiomed.kuleuven.be/english/research/50000618/50753342/TRPchannels

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