Thursday, 10 December 2015

Coffee and Health Part 1 – What is in coffee and how does it work?



It’s one of the most sought after commodities in the world right up there with crude oil and natural gas.  Whilst the former products are used to power cars, planes and industrial factories the humble coffee bean powers us human beings through the latest deadline, early morning, hangover or workout.  In the UK it’s estimated that we consume 70 million cups of coffee each day.  In recent years there has been a substantial growth in businesses specialising in coffee.  The turnover for these outlets was 6.2 billion pounds in 2013, a 6.4% growth from 2012, and 800,000 Britons report visiting a coffee shop at least four times per week.  This upward trend in the consumption of espresso style coffee substantiates the requirement to better understand the health implications of coffee, and the bioactive compounds in coffee.

I believe I come at this topic from a relatively unique perspective.  Not only have I got a fairly deep understanding of the hard science behind coffee and caffeine, I have also worked in a coffee shop on and off throughout my school and university years for eight years.  If I had to count the number of cups of coffee I have made it would most certainly be in the thousands, and similarly I have read hundreds of peer reviewed research articles on coffee.

So a little bit of background on coffee before going into the mechanics of how it does what it does.  Despite it now being grown in a number of countries, coffee originated in Ethiopia.  The coffee blend used to make your morning cuppa will always consist of Arabica beans which may also have added to them Robusta beans.  Arabica beans are very flavourful with less caffeine and tend to grow at higher altitude in comparison to Robusta beans.  Robusta beans are much more bitter and acidic than Arabica and contain much more caffeine, usually 50% or more, and typically grow at lower altitude.  The role of caffeine in plants is actually as a pesticide, hence robusta beans in lower areas have greater concentrations to protect the plant against a greater number or insects.

Coffee and caffeine typically go hand in hand how often have we heard the phrases “I need my caffeine fix”.  There is good reason for this caffeine has the predominant effect out of all the compounds in coffee.  Anyone who has had a strong cup of coffee will have felt that stimulant effect, that buzz that comes from consuming caffeine.  So I will now seek to explain what caffeine actually does in the body. 
The Formula of Caffeine 
When we look at the effects of any substance on the human body it’s important to consider the precise mechanisms of what is actually going on, to full understand the effect it is having.  This means getting quite deep into the science however I will try to make to make it as easy to read as possible.  The primary mechanism of caffeine is to act as an antagonist for adenosine receptors, more specifically the A1 and A2a receptors.  What this means is that caffeine binds to the adenosine receptor sites, therefore preventing adenosine from doing so.  Imagine coming into work to see a life size cardboard cut-out of yourself siting in your office, yes it may look like you and occupy the same space, but that doesn’t mean it can actually do the same job (having said this some days I feel a cardboard cut-out may be just as productive as me!).  This is essentially what happens with caffeine, on a molecular level it is structured very similarly to adenosine, so it binds to the same receptor sites but it can’t actually cause the same action that adenosine would.  
Caffeine Binding to Adenosine Receptor Sites  
The regular function of adenosine is to dilate coronary heart vessels, promote sleep, supress arousal and decrease renal blood flow.  Antagonism of adenosine receptors plays an important role in affect caffeine has on cognitive performance, alongside the inhibition of benzodiazepine receptor ligand (another neurotransmitter that slows down brain activity). Caffeine intake causes increases in neurotransmitters, including noradrenaline, dopamine, acetylcholine, glutamate and gamma-aminobutyric acid.  The increase in these neurotransmitters is what causes the “caffeine high” or “caffeine buzz”.  The net effect is a temporary increase in blood pressure and arterial stiffness, a feeling of alertness or stimulation and a mild diuretic effect.  Chronic consumption of caffeine leads to an up regulation in number and activity of adenosine receptors, also referred to as caffeine adaption.  This is the principle reason why habitual and non-habitual consumers tend to react differently to caffeine in studies.  It is also the reason why regular caffeine consumers often see themselves slowly increasing their intake.  As their body adapts they require more caffeine to get the same “buzz”.

The Structure of Caffeine Versus Adenosine
Another important consideration is the metabolism of caffeine, or the way the body processes caffeine.  Caffeine is absorbed rapidly from the small intestine, and is highly bioavailable.  It reaches peak plasma concentrations 30-45 minutes after consumption, and is delayed with food ingestion. Caffeine is metabolized into more than 25 metabolites in humans, mainly paraxanthine, theobromine, and theophylline.  Seventy two to eighty per cent of the metabolites from caffeine metabolism are paraxanthine.  Cytochrome P-450 1A2, located in the liver, is responsible for ≈ 95% metabolism in humans.  There are variances in the genes encoding for the enzymes that metabolise caffeine, this means that individuals will metabolise caffeine at different rates.  The normal half-life of caffeine is around 2.5-5 hours.  This means that if you consume 200mg of caffeine 2.5-5 hours later there will only be 100mg left in your system.  Carriers of the *1F allele variant metabolise caffeine slower than average, whereas carriers of the A2*1A gene metabolise caffeine at a higher rate.  Studies in regular caffeine consumers have often found increased activity of CYP1A2a, so they metabolise caffeine much quicker compared to non-caffeine consumers.  In fact the half-life of caffeine in these individuals have been reported to be as low as 1 hour.  Again in regular caffeine consumers, variances in the loci near BDNF and SLC6A4 have been detected which could impact consumption patterns by modifying the acute behavioural and reinforcing properties of caffeine.  So these consumers have genetic variances that actually make caffeine consumption seem more pleasurable.
A final factor (for now) when looking into this topic when it comes to coffee is, although caffeine is the main bioactive compound in coffee, there are a ton of other substances in there too!  Other important compounds in coffee include quinic acid, chlorogenic acid, citric acid, phosphoric acid, acetic acid, cafestol and kahweol.  Furthermore not every cup of coffee is created equally variances in blends, roasting process and preparation methods all impact the amounts of caffeine and other compounds in a cup of coffee.  This makes it difficult to thoroughly pool the research together, and draw definitive conclusions.  I have found that preparation method is something that is only staring to be considered in the research.

So there we have it a bit of back ground on coffee and caffeine, how it’s metabolised and what it’s actually doing in the body.  Coffee and caffeine remains a poignant focus of research for good reason.  It’s consumed in vast quantities and there are a number of questions that remain on its effect on short and long term health and performance.  What I’m hoping to do with these series of blog articles is bring evidenced based information on this debated, topic and hopefully provide some answers.  Stay tuned for the parts 2-4 which will be cardiovascular health and heart disease, sports performance and cognitive function.