We all know the scene. It’s a scene that’s played out in households around the world every morning. Half-asleep, mindlessly stirring your coffee… stumbling over to put the teaspoon in the fridge… return the milk to the sink… sitting down, eagerly awaiting that first sip… only to discover that you’ve forgotten to boil the kettle/insert the coffee pod/add the filter coffee… delete as appropriate. Cue the world-weary sigh! One would be hard-pressed to dispute the miraculous transformation from near-zombie state to sentient being, capable of stringing together whole sentences! All as a result of this real-life magic bean.
We’ve all seen the myriad memes about coffee enabling us to do the together putting of words and even put on pants.
Short-term pick-me-ups and funny memes aside, however, there is growing evidence that coffee can have numerous health benefits, including (but by no means limited to) combatting type II diabetes and obesity through to reducing the risks of Alzheimer’s or Parkinson’s disease.
Historically coffee has had a bad press, owing to its association with unhealthy habits such as smoking or sedentary lifestyles. Despite this, moderate consumption (3-4 cups per day) has been shown to be good for human health.
First discovered in Keffa, Ethiopia in the 6th century (hence the name, coffee), over the ensuing seven hundred years it became known throughout the Islamic world for its restorative properties and was subsequently sold in Europe, eventually becoming one of the most widely consumed beverages globally.
Coffee, Obesity and Type II Diabetes Mellitus (T2DM)
Regular coffee consumption has been linked to the metabolism of glucose and insulin. Ding et al. (2014) observed similar benefits in decaffeinated coffee suggesting that other components in the coffee, besides caffeine, could also be involved. These include cafestol and chlorogenic acid (CGA). Regardless of the mechanisms, numerous reviews indicate a link between regular coffee consumption and reduced risk of obesity and T2DM.
The link between type II diabetes and obesity is well-known with co-existence of the two associated with 90% of the world’s 382 million people with T2DM. Oversized intra-abdominal fat cells (adipocytes) display increased fat breakdown. This appears resistant to the insulin which tries to inhibit it. The end result is increased fatty acids in the circulation going to the liver and muscle and leading to altered insulin actions.
Caffeine appears to aid weight loss in T2DM by “thermogenesis”, increased energy production which boosts exercise without the associated increased effort sensation. (Note to self: even though you consume coffee by the bucket, you still need to get up off the sofa to do said exercise in order to boost it!)
In vitro studies into cafestol indicated an increase in insulin secretion in addition to increased glucose uptake by skeletal muscle cells. These actions could potentially make meaningful contributions to the prevention of T2DM.
Chlorogenic acids (CGAs) impact glucose metabolism in three different tissues. In the gastrointestinal tract, they affect glucose absorption; within skeletal muscle, the liver and adipose tissue, they affect glucose storage and, in the pancreas, they alter the hormonal regulation of glucose metabolism. Combined, these effects reduce glucose within the blood. Additionally, CGAs are thought to enhance energy metabolism by altering lipid metabolism, suppressing the accumulation of fat within the body. This could reduce the likelihood of obesity and its associated T2DM risk, provided the coffee is taken alongside a healthy diet and lifestyle.
Coffee and Neurodegenerative Disease – Alzheimer’s Disease (AD)
Alzheimer’s Disease (AD) is typically associated with the accumulation of β amyloid (Aβ) in the brain.
Epidemiological studies indicate that coffee consumption is associated with reduced risk of several neurological disorders including AD.
In a culture medium, coffee was noted to reduce Aβ accumulation to 80% of the control level after a twenty-four-hour period.
Though there are several possible mechanisms involved, one receiving the most attention and showing some promise is via the adenosine receptors of which there are four subtypes (A1, A2A, A2B and A3). Caffeine appears to act as an A2A receptor antagonist, preventing lipid peroxidation and increasing the activity of antioxidant enzymes in brain regions of different neurodegenerative disease models. As antioxidants are known to neutralise harmful free radicals, this could potentially explain some of the apparent neuroprotective properties of caffeine.
Coffee ingestion of 1.5 mg per day in young adult and aged transgenic mice (human equivalent, five cups per day) prevented memory loss and cognitive impairment and reduced A2A in the central nervous system.
Coffee and Neurodegenerative Disease – Parkinson’s Disease (PD)
Parkinson’s Disease (PD) is characterised by the progressive loss of dopaminergic neurones in the brain (the substantia nigra pars compacta if we’re being pedantic!) and this deficit has a profound impact on motor control.
Caffeine and its metabolites, theophylline and paraxanthine, have been shown to have neuroprotective properties in rodent models of PD.
The A2A receptors have been implicated in PD as well, proving vital in the regulation of dopaminergic neurotransmission in the basal ganglia (the main centre for motor control) so natural antagonists may enhance dopamine replacement therapies. In fact, A2A receptor blockade reduced dopamine depletion and degeneration of dopaminergic neurones in the brains of animal models, even when caffeine was given after the degenerative process was initiated.
Coffee to the rescue…
It would appear then that coffee is more than just the drink that enables us to stand up and do the talking and dressing thing. It has potential in preventing and treating many of the major public health issues we face today. Additionally, coffee and its various components have been shown to be antibacterial; antiviral; antifungal; chemo-preventative; hepatoprotective; pro-oxidant; anti-genotoxic; anti-inflammatory… one could write a whole book on the wonders of this magical brew (one won’t at this point – one needs coffee)!
For those of us who already enjoy a good cup of java then, be it straight up Americano, flat white, cappuccino, mocha, drink up and reap the benefits of a healthy mind and body (and remember to put on pants)!
References:
AGUIAR, L.M. et al., 2006. Neuroprotective effects of caffeine in the model of 6-hydroxydopamine lesion in rats. Pharmacology, Biochemistry and Behaviour, 84, pp. 415-419.
CAO, C. et al., 2009. Caffeine suppresses amyloid-beta levels in plasma and brain of Alzheimer’s Disease transgenic mice. Journal of Alzheimer’s Disease, 17, pp. 681-697.
CHEN, J.F., 2014. Adenosine receptor control of cognition in normal and disease. International Review of Neurobiology, 119, pp. 257-307.
DING, M. et al., 2014. Caffeinated and decaffeinated coffee consumption and risk of type 2 diabetes: a systematic review and dose-response meta-analysis. Diabetes Care, 37, pp. 569-586.
GOKCEN, B.B. and SANLIER, N., 2019. Coffee consumption and disease correlations. Critical Reviews in Food Science and Nutrition, 59(2), pp. 336-348.
GOLDSTEIN, E. et al., 2010. Caffeine enhances upper body strength in resistance-trained women. Journal of the International Society of Sports Nutrition, 7, p. 18.
GUERREIRO, S. et al., 2008. Paraxanthine, the primary metabolite of caffeine, provides protection against dopaminergic cell death via stimulation of ryanodine receptor channels. Molecular Pharmacology, 74, pp. 980-989.
MELLBYE, F.B. et al., 2015. Cafestol, a bioactive substance in coffee, stimulates insulin secretion and increases glucose uptake in muscle cells: studies in vitro. Journal of Natural Products (Washington, D.C.), 78(10), pp. 2447-2451.
MIRMIRAN, P. et al., 2018. Long-term effects of coffee and caffeine intake on the risk of pre-diabetes and type 2 diabetes: findings from a population with low coffee consumption. Nutrition, Metabolism and Cardiovascular Diseases, 28(12), pp. 1261-1266.
NOBRE, H.V. Jr. et al., 2010. Caffeine and CSC adenosine A2A antagonists offer neuroprotection against 6-OHDA-induced neurotoxicity in rat mesencephalic cells. Neurochemistry International, 56, pp. 51-58.
ONATIBIA-ASTIBIA, A., FRANCO, R. and MARTINEZ-PINILLA, E., 2017. Health benefits of methylxanthines in neurodegenerative diseases. Molecular Nutrition and Food Research, 61(6), pp.1600670-n/a.
RANHEIM, T. and HALVORSEN, Bente., 2005. Coffee consumption and human health – beneficial or detrimental? – Mechanisms for effects of coffee consumption on different risk factors for cardiovascular disease and type 2 diabetes mellitus. Molecular nutrition and food research, 49(3), pp. 274-284.
SANTOS, C. et al., 2010. Caffeine intake and dementia: systematic review and meta-analysis. Journal of Alzheimer’s Disease, 20(1), pp. S187-S204.
SANTOS, R.M.M. and LIMA, D.R.A., 2016. Coffee consumption, obesity and type 2 diabetes: a mini-review. European Journal of Nutrition, 55(4), pp.1345-1358.
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SONSALLA, P.K. et al., 2012. Delayed caffeine treatment prevents nigral dopamine neuron loss in a progressive rat model of Parkinson’s disease. Experimental Neurology, 234, pp. 482-487.
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About the author – meet Carly Bezensek:
I started out studying for a degree in Neuroscience at Glasgow University, being utterly amazed at the sheer complexity of the human brain controlling everything from the movements in our little toes to whether or not we like coffee (yes please)! As I delved deeper, I discovered the wonders of the research process, from planning through to implementation and eventually turning a mass of data into something that made sense and hopefully gave a better understanding of disease processes or led to better treatments. This led to a Masters in Research in Biomedical Sciences where I was let loose in a lab and told: this is what you’re investigating. Go! Off the back of this I ended up working as a research scientist in a biomedical firm in Glasgow.
When my partner was offered a job up in Aberdeen, I tagged along and ended up taking a detour into nursing where I got to see the direct impact of disease processes on the people we’re aiming to help. I ended up working with patients with a number of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s, Huntington’s and multiple sclerosis.
Fast forward eight years and I’m under new management in the form of a tiny three-year-old tyrant and I realised the pull of the scientific world was just too strong so I’m back! Currently studying part time for an MSc in Analytical Sciences (Drug Analysis and Toxicology) and part time as a referencing monster working towards making the medical and scientific world accessible and understandable for all. On the odd occasion I’ve a minute spare, you’ll find me torturing myself in Cross fit classes or on a run in rural Aberdeenshire.
