Archive for August, 2008


Meditating Away Pain (Part 1)

2008 August 30


Today I want to start a three part Saturday Series to go with the last one on migraines. In this series, I will try to teach you basic meditation. The aim is to finish with my own meditation method to manage migraine pain. You should be able to use this method with other forms of acute pain – pain that goes away. I haven’t tried it on pain that stays – chronic pain. If anyone does find it useful, or not, for chronic pain please let me know.

Before we start one word of caution. Although I draw on Buddhist meditation, it is not my aim to teach Buddhist meditation. To learn this you should find an ordained, qualified teacher. You do not need to be a Buddhist or learn other forms of meditation! Anyone may follow the method I will teach to manage pain. You can also apply the method to coping with other things you may dislike, like noise and other distractions. You may, though, like to know the origin of the “counting the breaths” and “pleasant, neutral, and unpleasant” aspects. I give the references at the end of this post. If you are interested in Buddhist meditation, these books are a great place to start.

Finally, I have heard back from others who I have talked to. They suggest that pretty much any form of meditation can relieve pain. So if my method does not work for you, you may still want to try other ones.

“Counting the Breaths”

Meditation is a method to relax the mind and body while sharpening mental focus. Relaxation itself may help with pain management. The mental focus will help when we come to parts two and three.

The most basic form of meditation is simple. Anyone can learn to do it. But in order to learn to meditate, you will need a quiet, comfortable space free from disturbances. If you have others around you, you will need to make sure they will not disturb you. Later on, as you go along, this will be less essential. You may also need pain-free time in which to start to learn meditation.

Most teachers recommend some form of Eastern sitting posture. But for our purpose this is not necessary. The most important thing is that you are comfortable and undisturbed. You can sit in a full-lotus position if that works for you. But sitting on a chair, or cross-legged or lying down will each do fine. You can close your eyes, or keep them open. But you are more likely to fall asleep if you close them!

All forms of meditation start with the breath. This is because it is a simple process we all do. So to begin with, simply sit (or lie) and be aware of each breath. Let the breaths come naturally as they will. Simply be aware of breathing in, and then of breathing out.

After a while you may notice the slight, natural pause after each breath in and each breath out. This forms the usual cycle of breathing: breathe in, pause, breathe out, and pause, and so on.

Do not worry if thoughts stray into your head. This is normal even for seasoned meditators! Simply think “I acknowledge this thought”, and return to being aware of your breathing. Also, do not worry if sometimes you cannot relax. This too happens even to seasoned meditators! Just acknowledge whatever happens. The important thing with meditation here is to just sit (or lie) and be aware of your breathing.

After a while (in each sitting), or even straight away, you can move on to the “counting of the breaths”. This is the first method to get used to. It is a simple one that helps to focus on breathing and removing stray thoughts. With each in-breath count, and count the same number with the out-breath:

  • Breathing in, thinking “one”,
    Breathing out, thinking “one”,
    Breathing in, thinking “two”,
    Breathing out, thinking “two”…

And so on until ten. When you reach ten, simply begin at one again. If you should find yourself distracted, again simply acknowledge the distraction and begin counting at one.

This is the method of counting the breaths. You should start by practising this simple method for a few days or weeks. Once you get used to just sitting (or lying) and counting breaths, you can move on to part two.

Don’t worry! This series will be here when you’re ready to return!

Counting the breaths, from p. 35 of Zen Master Thich Nhat Hanh’s Breathe! You are alive.
Pleasant, neutral, unpleasant aspects, from the Satipatthana Sutta, from p. 20 of Zen Master Thich Nhat Hanh’s Transformation and Healing.

Nhat Hanh, Thich. (1990). Breathe! You are Alive: On the Full Awareness of Breathing. Rider.
Nhat Hanh, Thich. (2006). Transformation and Healing: Sutra on the Four Establishments of Mindfulness. Parallax Press.


Who Can we Trust to Keep our Data Safe?

2008 August 28

A cursory search of the BBC website shows how much data loss is in the media at the moment. I found seven stories about data that was lost this year alone. The culprits ranged from government departments losing data affecting four million people in the period January to April, to a Royal Bank of Scotland hard disk with bank account details of millions of credit card applications turning up on e-Bay. Yet these are not the only examples of how poorly it seems government and private business is treating our private data. And this treatment potentially puts our identities at risk. We have so far been lucky, as far as we know, that criminals have not stolen identities through such negligence.

It beggars belief how sensitive data like account details, signatures, phone numbers and family details – enough to open fraudulent accounts – can be stored unencrypted. Yet time and again we hear how data like this turns up in places like trains and online auctions.

Now there’s a new low in data security. When I applied for Incapacity Benefit, I had to undergo a medical. The government contracts out this to a private company, ATOS Healthcare. Out of the blue they phoned me one Saturday afternoon. I later discovered that it was to arrange this medical. But they started out, without introduction, asking me to confirm my postcode and date of birth. Assuming it was a phishing call (to try to get personal data in order to steal my identity), I asked for proof of who they were. I even rang the police, who said I’d done the right thing (but couldn’t do anything even if it was a phishing call). Eventually, they sent me a written form.

Thinking this was a one off, I forgot about it. Then I bought an item in America, on the Internet, by credit card. This is something I do rarely, and my credit card company flagged it. Their security team then phoned my mobile, again out of the blue. This time I got an automated system claiming to be the card company. It too began asking for sensitive security data. This time I phoned the number I had for them and sorted it out that way.

It seems to me that cold calling, starting out asking for sensitive data, is dangerous. Imagine I rummage through your bin and find a letter from FictionCard. You’re careful. You shred any sensitive data. This letter had nothing more than your name, address and phone number and saying how proud they were to offer such a great customer a lower rate. I now know you’re a Fictioncard customer. I have your basic details, and a number to call you on.

“Hello, is that Mr. Smith? Hello, it’s Fred here from FictionCard. We’ve had an unusual transaction on your credit card and want to check out that it’s a genuine purchase. Can I start by confirming your postcode and date of birth please…?” Which of course I don’t offer you. After all, I’m genuinely from FictionCard so you know I know this already. Right?

Crazy. Would your granny think before giving out this information?

Here are the items I found in a five minute search (United Kingdom):-

Health board lost patients’ data:
When financial data goes missing (RBS):
Firm ‘broke rules’ over data loss:
Extent of data losses is revealed:
Discs loss ‘entirely avoidable’:
Tougher data laws needed, say MPs:
‘Lax standards’ on data security:


Tuesday Round-up For Friends

2008 August 26

It won’t be until the end of next week till I see my doctor. In the meantime, my migraines have continued to get more frequent. I’ve already missed a friend’s wedding reception. I’d rather have missed, knowing she has other guests, than turned up and fallen ill on her big day.

I’m knocking the Friday Funnies on the head for the moment. I have to find time to do other things than blog! And illness makes that time too short at the moment.

Plus my PC died at the weekend, so I’ve had to rebuild it.

I do plan, this Saturday or next, to start a short series on pain meditation. (Not medication!) This may be helpful to my readers (thank you) who have migraine, or any pain.


Migraines (Part 4) (Last Edited: 2009 Nov 19)

2008 August 23

Go back to Part 3

This is the final part of a four part series about migraine. You can use the links above or at the end of this page to go back. Or you can jump to any part from the Migraine FAQs page link.

There is difference of opinion over the exact mechanism for migraine pain. Both agree that the trigeminal nerves, that registers pain, are central to the mechanism. These relay pain signals to the thalamus. The thalamus processes them and then passes information to the cerebral cortex that registers it as pain. But the mechanism for pain signal generation in the trigeminal nerve differs between the two theories.

One school suggests that the cortical spreading depression directly stimulates the trigeminal nerves through the release of neurotransmitters and ions as the wave spreads. These then stimulate the trigeminal nerves to register pain. There is evidence supporting this mechanism, even in patients who do not necessarily experience aura during the spreading depression. This is also supported by the observation of increased, then decreased, blood flow in migraine without aura. This theory also helps explain vaguer symptoms observed such as fatigue or difficulty concentrating.

The second school places the cause of pain in the brain stem. This is the control centre for pain sensitivity, as well as other functions. Positron-emission tomography (“PET scans”) during migraine attack show that three clusters of cells called “nuclei” are active during and after migraine. This school suggests that abnormal activity here induces two pathways to pain. These nuclei normally inhibit the trigeminal nerves, reducing pain sensitivity. The nuclei’s misbehaviour may activate the trigeminal nerves causing them to fire and register “phantom pain”. It is suggested the nuclei may even trigger cortical spreading depression. These nuclei also control the flow of sensory information like light, noise and smell. Misfiring in the nuclei may explain the sensitivity to these during some migraine attacks.

There is also a minority opinion that migraine begins in neck pain.

The activity of the nuclei are also changed by behavioural and emotional states, which are also accepted as possible migraine triggers. The nuclei receive input from only two parts of the cortex; those that regulate arousal, attention and mood. These links could explain the mood fluctuations sometimes observed during migraine and the statistical association between migraine, depression and anxiety disorders.

The neurotransmitter serotonin seems to play some role in migraine. It also plays a part in mood regulation and in anxiety disorders and depression. Its role in blood vessel dilation may be important. Triggers like stress, bright lights, dehydration and so on are thought to increase serotonin levels in the brain. This disrupts the normal functioning of the hypothalamus and may trigger the blood vessel changes in migraines. Studies have shown how injection of a drug called reserpine, that releases serotonin, induces migraine headaches in sufferers, but not other people.

Both these new approaches may eventually offer relief for migraine sufferers. At present, few drugs can prevent migraine. None of the drugs used today were developed specifically for migraine. Only around one in two sufferers are helped by them and the potential side effects can be serious. Those that tend to be most effective, anti-hypertensives, anti-epileptics and antidepressants, have all been shown to inhibit cortical spreading depression. This supports the theory that this neural phenomenon contributes to migraine both with and without aura. New drugs are now in development that target “gap junctions” – a type of ion channel – effectively halting calcium flow between brain cells.

Go back to Part 3


MacGregor, Dr Anne. 2005. Understanding Migraines and Other Headaches. Family Doctor Publications Limited/British Medical Association


The Midwives of Hell

2008 August 21

This week the BBC aired a documentary on pedigree dog breeding. The documentary, two years in the making, looked at how breeds today were suffering. It claimed that their suffering was a direct result of breeding methods.

The problem, the documentary suggested, was that breeders selected offspring on the basis of appearance at the expense of health. It highlighted the major cause of this as inbreeding.

Before show dog breeding, dogs tended to be bred as working dogs. The artificial selection mimicked natural selection. Fit and healthy dogs make better working dogs. This means that fit and healthy offspring were also selected for breeding from. The prevalence of genetic disease was kept low, as in natural selection. But in show dog breeding it is appearance that is stressed over fitness and health. This removes the natural barrier to genetic disease. The result is that today pedigree dog owners spend over £10m in vet fees weekly.

The programme highlighted Kennel Club breed standards that included inherent health problems. It also suggested exaggerated traits bred into dogs trying to win rosettes as a causative factor. The Kennel Club continues to register dogs bred from mother-to-son and brother-to-sister matings.

Scientists an Imperial College, London, looked at the population of pugs. They found that the population of 10,000 was the same as just 50 distinct individuals. This makes the breed more genetically compromised that the giant panda.

The result of this behaviour of human beings is the suffering of individual dogs. As a result responsible owners also suffer. Here are some examples of problems found in pedigree breeds:

  • Pugs cannot breathe easily. Their faces are so flat that they are prone to eye damage from bumping into things.
  • King Charles spaniels are prone to a painful disease called syringomyelia. This happens if their skulls are too small for their brains.
  • Boxers are prone to epilepsy, heart disease and high cancer rates.

But the final cause of this scandal in dog breeding is human fashion. Dogs are selected on cosmetic grounds. The demand for show dogs that flatter their owners drives breeding. Champion show dogs continue to father puppies despite serious genetic disease. Some breeders cull perfectly healthy puppies because they are cosmetically “wrong”.

The Kennel Club far from being open to change defends its position. It insists that “the vast majority of dog breeds are healthy”. This despite scientific evidence that, for example, up to one third of King Charles spaniels suffer syringomyelia. The programme showed a disturbing video of one dog writhing in agony due to this condition.

If the dogs were human beings, we may have little difficulty describing some of them as being in Hell. The breeders, and the people who buy from them, are directly responsible for this suffering. While some continue to turn a blind eye to the problem they remain the Midwives of Hell. Many owners do not even realise they are buying dogs whose genes are compromised.

One vet said that if a human being beat a dog to cause it the pain some suffer, he would be prosecuted. Yet they can breed dogs into a life of such pain legally.

Continuing in this way is not even in the interest of those involved in the business. Steve Jones, Professor of Genetics, UCL, said, “If the dog breeders insist on going further down that road, I can say with confidence really that there is a universe of suffering waiting for many of these breeds – and many if not most of these breeds will not survive.

“They will get so inbred that they will be unable to reproduce and their genes will come to a dead end.”

Links and sources

Warning! I have not checked all the videos included on these pages. It is possible they may contain scenes you may find distressing.


Tuesday Round-up For Friends

2008 August 19

I saw my optometrist. (Apparently, there’s a difference between optician, optometrist and ophthalmologist in increasing order of qualifications.) She could find no physical problem with my eyes or eyesight. So she said I should go back to my doctor. She said, though admitting she’s no expert, she suspects the visual phenomena relate to migraines.

On that subject, the sweet little things have gone up quickly in frequency since June. Again. Back now to almost one every other day as at their peak. So far I cannot find anything from my exhaustive migraine diary to show a trigger. But then I have two kinds of headache/migraine according to my specialist.

Still, at least between times it gives me some time to study the Buddhist sutras. And to practise mindfulness. I have chosen the lineage of Zen Master Thich Nhat Hanh. Thay (teacher) was the first I read online. Thay’s writings are wonderfully clear. I am fortunate and grateful to have found his books. I hope one day to be able to hear a talk from him. And to be able to learn from a teacher in his lineage.

Perhaps these migraines are a blessing in disguise?


Migraines (Part 3) (Last Edited: 2009 Nov 19)

2008 August 16

Go back to Part 2 | Go on to Part 4

This is part three of a four part series about migraine. You can use the links above or at the end of this page to go back or forward. Or you can jump to any part from the Migraine FAQs page link.

The exact triggers for migraine attack are uncertain, and may vary widely. Sufferers usually keep a diary to try to identify:

  1. Triggers,
  2. Other things affecting migraine frequency,
  3. Things that may prevent attacks,
  4. Things that might predict impending attack.

Commonly suggested triggers include: allergies, things in the environment like lighting, noise or scents, stress, changes in sleep patterns, cigarette smoke, alcohol, certain foods, and weather or seasonal changes.

All auras are the results of “cortical spreading depression”. This is a self-propagating wave of cell depolarisation that travels through the cortex. The cortex is the crinkled outer or “higher” part of the brain. During this phase, the affected neurons go into a kind of hibernation. The exact mechanism of neuronal “firing” depends on a critical flow of sodium, potassium and calcium ions. During the depressed state, neurons rest high in potassium, and low in sodium and calcium. Cell “firing”, releases neurotransmitter chemicals, when the inside of the cell is positively charged relative to the outside. After firing the cells become strongly negatively charged on the inside by allowing potassium ions to flow out. This returns the neurons to their resting states. But neurons can become hyper-polarised, or inhibited, for some time after intense stimulation.

The phase of hyper-excitability followed by inhibition in cortical spreading depression may explain the changes in blood blow recorded before the pain phase of migraine. Active neurons need energy, which is transported by blood. When inhibited, they need less blood.

Further studies link cortical spreading depression with description of visual aura. The wave travels across the cortex at between two and three millimetres per minute. The visual aura match with those expected given that rate of spread. The change of sensations also match observed spreading depressions.

Migraine is a complex disorder that shows a strong genetic component. But studies show that it is a range of genetic mutations that affect migraine rather than a single gene. This is called a poly-genetic disorder. There is also evidence of non-genetic parts. The strongest evidence for both comes from identical twin studies. These show that identical twins are more likely to share migraine that non-identical twins. But even identical twins do not necessarily both share migraine. One may suffer migraine, while the other does not.

Recent evidence also supports the view that at least one type of migraine is caused by faulty genes. These govern the ion channels talked about earlier. This is a newly recognised condition called “channelopathy”, which is also responsible for other conditions like cardiac arrhythmia and seizures. But it is not yet known whether this mechanism is common to all forms of migraine.

There is also another controversial theory about a common heart defect. It is called “patent foramen ovale” or PFO. It is where a small hole in the heart allows oxygen-rich and oxygen-poor blood to mix. It is controversial because the way PFO may cause migraine is unclear. Closing the hole in migraine patients has shown some results, but they are not statistically significant.

Go back to Part 2 | Go on to Part 4


Spot the Difference

2008 August 15

This week, this story caught my eye. It is probably familiar to UK readers:

The City Council of Birmingham, England – note, England – sent out a leaflet which showed the skyline of Birmingham, Alabama – note, Alabama – to promote the city. The English city, not the Alabaman one.

An eagle eyed resident called Jon Cooper spotted the difference and wrote to the council. They replied, the “generic skyline [was] intended to symbolise an urban area”.

  • I found that particularly funny: The generic skyline intended to symbolise an urban area just happened to be Birmingham, Alabama, then?

What followed was even funnier: “Birmingham is immensely proud of its recycling record and this leaflet has helped to get the recycling message across to thousands of our enthusiastic citizens over the last 15 months.”

  • It took them 15 months to deliver all the leaflets…?

The Georgian-Russian Conflict

2008 August 14

One of the big news items in this last week has been the conflict between Russia and Georgia. But what is the background to the conflict?

The fighting erupted over the status of two Georgian regions, South Ossetia and Abkhazia. Both regions have majority populations favourable to independence. In the war of 1992-3, more than 250,000 ethnic Georgians were “ethnically cleansed” from Abkhazia. The Abkhaz separatists were aided by North Caucasian volunteers, including Chechens. More than 25,000 Georgians were expelled from Tskhinvali in South Ossetia. At the same time many Ossetian families were expelled from Borjomi to Russia. In effect, both South Ossetia and Abkhazia are independent of Georgia. Though their independence has no international recognition.

Since the Russian operations against Georgia, hundreds of civilians are reported to have been killed and tens of thousands displaced. It is still unclear who broke the ceasefire between Georgia and South Ossetian separatists on the 8th August that began the crisis. Leaders have criticised Russia for over-reacting in its attack, as well as Georgia of being foolish in their shelling of Tskhinvali, capital of South Ossetia.

I have researched the conflict and the history behind it. I include this below. Just click on the “continue reading” link. I include a list of sources at the end.

Whether Russia’s claimed intentions of protecting South Ossetian and Abkhazi civilians is genuine or not is debatable. Even if true, Russia does appear to have left itself open to accusations. These accusations are that its aims are to bully Georgia and the Ukraine into withdrawing NATO membership applications. Whatever their aims, they have risked relations with the West.

Avaaz has organised a petition for a Georgian ceasefire:

Read the rest of this entry ?


Tuesday Round-up For Friends

2008 August 12

I saw my doctor on Monday about the “visual snow” I’m seeing before my eyes. I figured the best thing to do was just go with that. I thought if I loaded him with a mass of “symptoms” he might just ignore me. He gave me a quick eye exam, and suggested I see my optician. So I’m booked to do so on Friday. I’ll see what she finds.

As I expected, the back spasms I had in my late teens and early twenties weren’t in my medical records. So that’s something I’ll have to make sure my specialist knows about next time I see him. That won’t be until November now. Whether that makes any practical difference now, who can say?