DCSIMG

Ruby’s ruminations on...the science of depression

Ruby Hryniszak is a regular columnist and guest writer for the Mail.

Ruby Hryniszak is a regular columnist and guest writer for the Mail.

  • by Ruby Hryniszak
 

Depression is a plague that has afflicted a vast proportion of the population for years. In fact, there are medical reports of depression going as far back as 200AD, and back then it was known as ‘melancholia’.

In the 20th century, a German psychiatrist described the different melancholic states as depression, which introduced its modern name. The term ‘depression’ is derived from the Latin verb ‘deprimere’, which means ‘pressing down’.

Emotions are chemically balanced in the body and depression is caused by a chemical imbalance. However, scientists have now discovered the molecule that triggers feelings of depression: protein receptor CRF1.

We’ve all been there before: Laying in bed, you roll over and wrench the duvet up over your eyes. “If I can’t see the time, it isn’t time to leave” you mutter, refusing to move from the fortress of solitude and sulking you’ve built up in the darkness of your room.

It’s just too much effort to get out of bed. I’ve definitely been there before and I know I’m not the only one. Depression is a serious mental illness and doesn’t get nearly as much attention as it deserves.

As with most mental illnesses, it falls under the assumption that if you can’t see it...it doesn’t exist.

Chemicals, though, are all too real and being caused by chemicals in the body that must make depression real. Modern science refuses to ignore depression, though, and have been giving it a lot of attention and the discovery of CRF1’s influence on our response to stress could be a breakthrough in creating an effective cure.

As I mentioned above, our emotions are all responses to different neurotransmitters in the brain. For example, serotonin creates feelings of happiness, dopamine is euphoria or love and acetylcholine aids memory and dreaming.

These three neurotransmitters just happen to be the most critical to creativity. That’s how our feelings work and those three are just a tiny example of the complex chemical structures perpetually influencing our thinking.

Of course, not all chemicals in the body are going to trigger feelings of pleasure of satisfaction, and CRF1 is just one of them. The hormones released by this protein are related to feelings of anxiety and depression over extended periods of time. The key cause for release of these hormones is stress.

Upon the receival of stress molecules from the hypothalamus (brain), CRF1 responds by making us feel worried or melancholic. Along with other protein receptors, it manages our response to stress, and as scientists have found out, controlling its activity could lead to a highly effective cure.

The prescribed drugs used to combat depression work by changing the activity of neurotransmitters, such as serotonin and norepinephrine. Low levels of these two molecules in the synapse are associated with depression, and so it makes sense that these are the things most affected by anti-depressants. For the most part, they’re helpful drugs, although they don’t work for everybody. Anything is better than nothing, but it can certainly be said that these medications leaves room for improvement.

It would seem that the method for tackling depression is to trigger increased production of hormones that cause feelings of happiness.

Whilst it is possible to fight chemicals with more chemicals (the drugs wouldn’t work otherwise, would they? Well, I suppose they could, because of the placebo effect but that’s another story), a more efficient way to fight depression would be to identify the opprobrious molecule that causes it in the first place.

It’s far more effective to prevent something than it is to have to overcome it. The discovery of depression’s creator is the beginning of this process, as now a way of deactivating CRF1 has been found.

Scientists used a particle accelerator called the Diamond Light Source to study the structure of CRF1, which, through the X-ray machine’s powerful beams, illuminated a chink in its molecular armour: a small crevice.

This could, potentially, be targeted for drug therapy and the information gained from the study is going to be used to design small molecule drugs, that will fit into the precipice in the protein receptor’s surface, thus treating depression.

By blocking this crevice, CRF1 becomes inactive and as such the biochemical cascade that leads to stress and depression is ended.

As far as scientific discoveries go, this is most importunate as this new knowledge can be used not just to treat depression, but to aid the development of drugs for other, closely-related diseases, such as Type 2 diabetes and osteoporosis.

These diseases are caused by hormones secreted by receptors of a similar structure and class, so once we have an effective drug to deactivate one protein receptor, we can begin working in the same way to shut off others.

This discovery is a huge leap for medical science as until now there have been methods only to lessen the symptoms of these diseases, but no way of curing them directly.

Having unearthed a weakness in receptors of this class, we’re now able to begin the process of curing health problems which have otherwise been impervious.

Though the development of drugs is a long process, having the basis to begin work and the knowledge to, eventually, succeed in this task is of no lesser importance than any other newly-concocted medicines brewed to alleviate other serious health problems.

It’s no secret that I’ve gone through extremely long periods of depression, spanning over years of what is still a short life.

It’s a serious mental illness that affects so many people and a genuine cure would help so many people. I’ve known friends who’ve suffered with depression and have been prescribed anti-depressants, which they always claimed were useless and did nothing to improve their condition.

As such, it’d be a truly jubilant occasion to see such a drug created that can successfully treat depression.

Story by Mail guest writer Ruby Hryniszak

Follow Ruby on Twitter, @13eautifulLife.

 

Comments

 
 

Back to the top of the page