​Why is that that the same thing can be a trigger and a treatment? Headache sufferers have had a love-hate relationship with caffeine, going from complete avoidance due to its triggering potential, to relying on a cup a day to keep pain at bay!
 
Hidden amongst our morning tea and coffee, soft drinks and chocolate is a potent drug that has very complex interactions that go right to the heart of headache and migraine.

​Caffeine is a chemical compound in the alkaloid family, (chemical name 1,3,7-Trimethylpurine-2,6-dione) that occurs naturally in over 60 plant species including tea, kola nuts, coffee beans, mate leaves, guarana plants, and cocoa nuts. As such caffeine is one of the most widely consumed psychoactive agents (able to change brain function/mental state) in the world. [1]

​When entering the body caffeine looks exactly the same to nerve cells as a substance called adenosine. Adenosine is active in a number of regions in the brain and is a key building block in our energy pathways, but doesn’t instantly boost energy. In fact adenosine binding to nerves in the brain causes drowsiness by slowing down nerve activity and promotes sleep. During this time our blood vessels dilate allowing more blood into the brain to nourish it during sleep.
Caffeine blocks the ‘drowsiness effect’ by binding to adenosine receptors, leading to increased nerve activity and an increase in our ‘alertness’.
In response to this increased activity the pituitary gland releases adrenaline – our fight or flight hormone. The result is what most people will feel when they drink coffee in increased activity of the central nervous system: increased heart and breathing rate, increased blood pressure, increased diuresis, cardiac muscle contraction and gastric, lacrimal (tear), nasal mucous secretions vasoconstriction of blood vessels in the brain. Blood will be moved from your periphery to your core and the liver will release more glycogen into the blood stream for extra energy.

​Caffeine causes vasoconstriction in the brain, and was added to numerous migraine medications on the mistaken assumption that migraine was a vascular headache.
‘Now that migraine is thought to be a neurological and not a vascular disorder, caffeine’s common inclusion in migraine treatments suggests an alternative, non-vascular mechanism of action behind its efficacy in migraine patients.’(Nathan Fried 2017)
While there may be some mild benefits with the vasoactive effects of caffeine, it is caffeine’s action in blocking adenosine receptors in the brainstem that is having the positive impact. In the brainstem (the home of the migraine circuit) adenosine is involved in pain transmission and sensitization. By blocking adenosine receptors here caffeine may help stop the spread of ‘excitability’ and abort a migraine or ease a headache. [2] 
 
Despite the anecdotal evidence or a ‘strong black coffee’ aborting migraines, research into caffeine as a monotherapy (not combined with another drug) shows it is no more effective than placebo in time taken to 50% reduction in symptoms. [3]
 
The most commonly understood mechanism for helping headache and migraine sufferers comes from caffeine’s effect on your stomach. Ingesting Caffeine causes rapid lowering of gastric pH (more acidic), improving the absorption of analgesic medication. When the ergot family of drugs was in use a combination therapy known as cafergot was widely used. This has since been removed in most forms (still available as a suppository under prescription), due to deleterious cardiovascular effects of ergotamines. Today we see panadol extra on the market with caffeine combined with paracetamol. Despite some research to support its use as a combined therapy there isn’t currently a caffeine plus NSAID (like ibuprofen) on the market. This will be because both agents cause lowering of gastric pH, which indeed is the most common and concerning side effect of NSAID’s leading to stomach upset and ulcers.
 
Once again we see the double-edged nature of caffeine. On the one hand, here there seems to be good reason to use it as either an adjuvant to other rescue medication, or for its own effects in dampening brainstem excitability, however there is evidence to the contrary. Not unlike the opioids (with similar dependence and withdrawal profiles) caffeine may seem to ne helping with one hand, but worsening things in the long run.

​A study of 36 children and adolescents (aged 6-18) who were heavy cola drinkers (minimum 1.5L per day or 192gms caffeine) and suffered daily headache examined the effect of ceasing caffeine consumption. Two weeks after stopping their caffeine intake researchers saw a complete cessation of daily headache in 33 of the 36 children in the study. [4]
 
 
Another study examining the factors that lead to chronification of headaches found daily consumption of caffeine to be a significant factor in the development of analgesic overuse headache and chronic migraine. [5]
This study was followed up 2 years later looking more closely at the amount of caffeine used, and found a history of heavy caffeine use (> 300mg daily) was associated with chronic daily headache compared to episodic headache control groups. [6]
 
In 2016 Lee and associates looked at the effect of caffeine cessation on the effectiveness of acute migraine medication. The two groups (abstinence and coffee groups) had a mean caffeine intake of 192mg per day. Given it’s adjuvant effect with analgesics one might assume that cessation of caffeine use would decrease the effectiveness of acute migraine treatment. In fact they found the exact opposite. Discontinuing caffeine use actually significantly improved the efficacy of acute migraine medication. [7]

​There appears to be a complex association of caffeine with headaches. On the one hand many properties seem to make it a useful medication for helping relieve pain, but daily use appears to have some negative effects in increasing the likelihood on transforming from episodic to chronic headaches. 
 
It’s the same story we have been hearing for opioid analgesics like codeine, recently taken off the shelves as an OTC (over the counter) medication. Adenosine homeostasis also plays a crucial role in narcotic drug responses and plays a role in neurobehavioural features associated with opiate addiction and withdrawal. [8]
Caffeine also affects dopamine by increasing its production in the brain. Dopamine is our ‘pleasure drug’ so it makes you feel euphoric. This action is very similar to two banned drugs in heroin and cocaine which both slow down dopamine reabsorption. It’s the action on dopamine that may be even stronger cause of addiction and withdrawal with caffeine.
In other words the effect of caffeine and its interaction with adenosine and dopamine receptors results in the same withdrawal/addiction responses in our central nervous system as narcotic drugs.

​The Food Standards Code (Australian government) restricts the caffeine content of energy drinks. Whilst they have not set an upper limit in Australia, they have commented on the limit that appears to be linked to anxiety as being 3mg of caffeine per kg of body weight. This equates to around 200mg per day for an adult, and that seems to be a similar figure in the headache studies above. [9]
 
At the end of all this you firstly need to figure out whether caffeine has any interaction with your headaches at all, as triggers are a hugely individual aspect of headaches.
 
If you believe caffeine is a sensitive trigger with either not enough or too much (i.e. you have a ‘sweet spot’ in terms of it being helpful), you may want to monitor how much you have on a longer-term basis. 200mg per day, whilst in the short term may seem like its helping, in the longer term may actually be making you worse.
 
An espresso shot may contain anywhere from 30mg to 90mg per shot. This variation is in the bean and roast type with lighter roasts having more caffeine. Caffeine in other foods drinks as per Food Standards Code [9]:
Black tea – 20-80mg/250ml (longer brewed = higher caffeine)
Coca Cola – 48.75 mg per 375ml
Milk Chocolate – 20mg /100g
Dark Chocolate – 81mg/100g
Energy drinks – 80mg/250ml
 
So one double shot of light roasted barista espresso coffee could have you close to the 200mg level. In the USA the recommended daily intake for caffeine is 400mg. The discussion around triggers always comes back to dealing with the common underlying theme which is an overactive brainstem. Lots of people consume caffeine but don’t get headaches, even when they stop or withdraw.
 
So what makes headache and migraine sufferers prone to the positive and negative impacts of caffeine. Indeed why do all these different triggers result in headache? The underlying problem is overactivity in the brainstem – in the area housing the nerves for the head/face and neck.
 
Regardless of the impact of triggers, the neck is the most common source of overactivity in this part of the brainstem and is the easiest to assess and treat.
 
Treat the underlying causes today and get your neck assessed.

 [1] Neurology advisor Caffeine-migraine-headache-trigger-treatment
 
[2] Fried, N.T, Elliot, M. B. and Oshinsky (2017) The Role of Adenosine The Role of Adenosine Signaling in Headache: A Review. Brain Sciences, 7 (3), 30.
 
[3]Diener HC, et al. The fixed combination of acetylsalicylic acid, paracetamol and caffeine is more effective than single substances and dual combination for the treatment of headache: a multicentre, randomized, double-blind, single-dose, placebo-controlled parallel group study. Cephalalgia. 2005;
 
[4] Hering-Hanit R, Gadoth N (2003) Caffeine-induced Caffeine-induced headache in children and adolescents.Cephalalgia, 23, 332-335.
 
[5] Bigal, M.E. Sheftell, F.D, Rapoport, A.M., Tepper, S.J. and Lipton, R.B. (2002) ChronicChronic daily headache: identification of factors associated with induction and transformation.Headache, 42 (7), 575-581.
 
[6] Scher, A.I., Stewart, W.F, and Lipton, R. B. (2004) Caffeine as a risk factor for chronic daily headache: a population based studyNeurology, 14; 63 (11) 20022-7.
 
[7] Lee, M.J., Choi, H.A., Choi, H, and Chung, C.S. (2016) Caffeine discontinuation improves acute migraine treatment: a prospective clinic-based study.Journal of Headache and Pain; 17 (1); 71 
[8] Mohong, Wu et al (2013) Opiate-induced Changes in Brain Adenosine Levels and Narcotic Drug Responses. Neuroscience, 3, 228; 235-242. 
[9] Food Standards Code (2018) Caffeine
 
[10] Heckman et al (2010) Caffeine (1, 3, 7-trimethylxanthine) in Foods: A comprehensive Review on Consumption, Functionality, Safety and Regulatory MattersJournal of Food Science, 75, (3).
 

Up to 53% of migraineurs report weather changes as a consistent trigger making it one of the most commonly reported triggers for migraine behind stress, hormones and skipped meals. [1]
 
A subject of interest as far back as 1974, researchers have spent decades trying to examine the question: Does weather actually trigger migraine attacks, and if so, what are the factors related to weather change that is causing attacks in people?
Theories over the years have included temperature and barometric pressure changes, high and low humidity, high winds, stormy weather, and changes in light conditions (very bright or dull light as well as changes in daylight hours). 
The science however has provided contrasting and often confusing results making it difficult to understand what is happening.
 
In 1979 [2] researchers in London asked 310 migraineurs about the day and time of their attacks (subject to recall bias) and found no correlation with changes in wind, barometric pressure, humidity and temperature. 
 
Jump ahead to 2011 and Karin Zebenholzer and colleagues [3] undertook a 90-day prospective diary study in Vienna. Whilst they found trends when analyzing change in temperature, wind speed, sunshine duration in isolation, analysis of multiple variables to account for attacks yielded no positive findings.
Their conclusion was ‘the influence of weather factors on migraine and headache is small and questionable.

​In 2013 [4] researchers studied the effect of lightening strikes on 90 migraineurs who kept diaries for 3-6 months. When they analysed the data they also accounted for rainfall, and barometric pressure.
 
When there was a lightening strike within 25 miles (40kms) there was a 25-30% increased risk of both new-onset headache or new-onset migraine. They are following up with further research to try and determine what it is that lightening strikes do that can cause a slight increase in migraine incidence.

The odds of having a new headache or migraine start increased on days with lightening that had a more negative charge leading researchers to suggest that something to do with the electromagnetic interaction is causing some irritation of the nervous system and triggering an episode. 
 
Lead researcher Dr Vince Martin [5], explained that other environmental factors change in thunderstorms, in particular related to fungi and mold. Rain increases mold counts, and if lightening strikes the ground it aerosolizes the fungi. In other words we breathe in a lot of fungi and molds in the air during thunderstorms, contributing to our now famous ‘Thunderstorm Asthma’ events.
When this is coupled with the fact that migraineurs tend to have a higher incidence of non-allergic rhinitis (nasal and sinus irritation) it provides another possible mechanism for triggering an attack, but it is still interacting with a sensitized system as Dr Martin explains:
 
“I think that what we don’t realize is all these different things in our lives can influence that (migraine) threshold. So how much sleep you got the night before, how much stress you are under, whether you fasted for a prolonged period of time. All these things have a neurologic effect on migraine patients and can seek to lower that threshold and make people more vulnerable to migraine.”
 
The threshold to which he refers of course is the ‘explosiveness’ or the trigeminal nucleus. Read on for ideas on how to fix this sensitivity.

Barometric pressure is what we see weather forecasters referring to with weather patters. Low pressure allows clouds to form and typically rain and storms. High pressure is typically associated with clear blue skies and warmer weather.
 
The challenge is that pressure changes ahead of the weather that comes with it, so you won’t often ‘see’ the weather that might trigger you. This might result in many migraineurs claiming to be able to ‘predict the weather’ as they might be sensitive to falling barometric pressure. 
 
Dr Martin [5] explains that ‘some (migraineurs are) triggered by falling or rising barometric pressure. Interestingly if falling pressure does it then rising pressure is usually ‘protective’ and vice versa.’
 
Researchers in Japan [6] studies the effects of changing Barometric pressure in 34 migraineurs compared to a control group of tension-type headache sufferers. On face value there appears to be a link between small decreases in barometric pressure (6-10hPa) and increased incidence of migraine compared to tension-type headache controls. Unfortunately the diary-recording period only went for 18 days. The problem is that we don’t know if the migraine group had a higher incidence of attacks and whether either incidence was different to the previous 18-days prior to recording.
 
Cioffi and colleagues [7] investigated the effects of changing weather in patients with temporomandibular disorders (TMD) and migraine. Their results indicate that decrease in atmospheric pressure increased the intensity of TMD pain, however increase in pressure and temperature increased the intensity of migraine symptoms. Again the study is very limited, in part by a ‘lost' or 'not captured'  data rate of 25% and no indication of the baseline activity in both groups – in other words we don’t know whether the pain fluctuations can be attributed to the weather or if these are normal fluctuations.
 
More disturbingly, the authors claim as a starting point in their introduction that:
‘The pain course of subjects suffering from migraine is influenced by weather conditions’
citing two publications to support the statement. On reviewing these two publications the conclusions the authors draw themselves are quite the opposite:
‘The influence of weather factors on migraine and headache is small and questionable” [3]
and
“In a sub-group of migraineurs, a significant weather sensitivity could not be observed”. [8]

So this all seems a bit confusing, and we want a simple answer – do changes in weather cause migraines or not?
 
The answer is a simple as does chocolate, or wine, or perfume cause a migraine. The answer is obviously yes………..and no.
 
That is to say migraineurs as a group are heterogeneous. Some things that may trigger one migraineurs may not trigger another, so pooling together large groups to study effects of anything, be it a trigger (or a treatment for that matter) can dilute the effect that it might have on sub-groups. The difficulty is in discerning the sub-group in a way that allows better predictions of the effects of
The results of Hoffmann’s 12-month study [8], though inconclusive, did show trends leading to the conclusion that “only a sub-group of migraineurs is sensitive to specific weather conditions, explaining why previous studies, which commonly rely on pooled analysis, show inconclusive results”. 
 
One might expect a better result in migraineurs who report weather changes as a trigger, however Zebenholzer and colleagues looked at perceived weather changes compared to weather data and found a poor correlation. [3]
Not unsurprisingly, the ability of a migraine brain to accurately detect weather may be impaired (similar to its response to noise, light, smells in some cases), leading to inaccurate forecasting, and the feeling that ‘the weather is changing and here comes my migraine’ whereas in fact the sense that the weather is changing may be a part of the migraine itself. 
 
Another problem is that changes in weather do not influence migraineurs in isolation. What were the other factors occurring at the time of the study with regards to amount of sleep – over-sleeping, under-sleeping, dietary influences, hydration levels, stress levels etc 
As with many other triggers, often in isolation or at low doses they may be ok, but when a strong dose or in conjunction with others triggers may cause problems.
 
At the end of the day the research has failed to show what we know and see in the clinic, and that is, without question, migraine can be triggered by changes in the weather – but as with many other things migraine, the exact mechanism’s have eluded researchers and remains an area of ongoing focus for some.

What does chocolate, perfume, bright light, red wine, stress, hormones changes and weather changes have in common? Nothing apart from the fact that they can all (amongst a host of other things) be considered triggers for some peoples migraine.
 
Focusing on triggers can be helpful if you only have a small number. If on the other hand you have multiple triggers, then this line of migraine management often proves futile and frustrating as the next doctor pulls out yet another migraine diary for you (scream!).
 
The thing that ties these and every other migraine trigger together is that they all interact with a sensitized trigeminal nucleus to cause the symptoms we associate with primary headache conditions.
 
So aside from moving to somewhere with stable weather patterns that has just the right mix of heat, humidity, wind and small changes in pressure to prevent your weather related migraines, what else can you do.
 
I would urge you to ignore the triggers and focus on the sensitized brainstem.
 
The nerves from the top of the neck feed directly into this area making it the number one suspect in the frontline of fighting the underlying problems in migraine.
 
In recent years the migraine community has shifted away from the vascular theories to focus on a sensitized brainstem model. This brings the neck back into focus, and even Dr Andrew Charles has moved from:
‘this (neck pain) is just a symptom of their migraine’ in 2012 [9] to a 'greater appreciation of the potential role of the cervical nerves' acknowledging the 'frequent occurrence of neck pain could indicate a role for the upper cervical nerves in the transmission of migraine pain' in 2018 [10].
 
Come and get the underlying problem assessed and treated with the only technique developed specifically to lower trigeminal nucleus sensitivity. 
 
For those wanting more tips on how to minimise weather related migraine:

• Stay indoors with windows shut. This may minimise the impact of aerosolized molds and fungi.
• Monitor Weather forecasts for migraineursI’m not sure how they account for individual variation is triggers, but it may be of some help.
• If you know the upcoming changes that are forecast may be a trigger try to minimise your other triggers at that time – in other words be more watchful about skipping meals, careful with sleep patterns, drink plenty of fluids etc

[1] Pavlovic J. M. et al (2014) Trigger Factors and Premonitory Features of Migraine Attacks: Summary of Studies.Headache, Nov/Dec, 1670-1679.
 
[2] Wilkinson M and Woodrow J. (1979)Migraine and Weather. Headache. 19: 375–378.
 
[3] Zebenholzer K, Rudel E, Frantal S, Brannath W, Schmidt K,
Wober-Bingol C et al. (2011) Migraine and weather: a prospective diary-based analysis.Cephalalgia. 31:391-400
 
[4] Martin, G.V. et al (2013) Lightening Lightening and its association with the frequency of headache in migraineurs: an observational cohort study.Cephalalgia, 33 (6), 375-383
 
[5] Martin, G.V. (2018) Surviving weather-related Migraine.  Migraine World Summit. (2018)
 
[6] Okuma, H et al (2015) Examination of fluctuations in atmospheric pressure related to migraine.  SpringerPlus Open Journal.
 
[7] Cioffi, I et al (2017) Effect of weather on temporal pain patterns in patients with temporomandibular disorders and migraine.Journal of Oral Rehabilitation. 44; 333-339.
 
[8] Hoffmann, J et al (2015) The influence of weather on migraine – are migraine attacks predictable?Annals of Clinical and Translational Neurology, 2 (1); 22-28
 
[9] Charles, A (2012) Migraine ResearchMigraine Research.ABC Health Report.
 
[10] Charles, A (2018) The pathophysiology of migraine; implications for clinical management.
Lancet Neurology. 17; 174-182.