The Dangers of Painkillers

  • 4 Jan 2010
  • Reading time 16 mins
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There’s a good and a bad side to inflammation and to the drugs used to treat it. When it first appears, it’s a sign that your body is responding to a problem and trying to deal with it.

Before we look at what happens in your body when pain occurs, and the mechanism behind painkilling drugs and natural painkilling nutrients and herbs, let’s gauge your pain level. Unlike diabetes, which is principally measured by your blood sugar level, the main indicator of pain and inflammation is simply how you feel. The effectiveness of treatments is rated by how much patients say their pain has gone down. Different types of questionnaires are used for different kinds of pain. (For example, the WOMAC check is used for hip and knee pain, while the Oswestry test is used for back pain.) Check yourself out on the questionnaire below.

How's Your Pain?
Do you have aching or painful joints?
Do you suffer from arthritis?
Do you have painful or aching muscles?
Do you suffer from muscle stiffness which limits your movement?
Do you wake up with physical pain?
Do you suffer from headaches?
If so, how often? 
On average once a week (score 1), twice a week (score 2) or more (score 3)? 
Does your level of pain make you feel tired?
Does it make you feel weak?
Does it limit your ability to move around?
Does it limit your ability to sit for more than 30 minutes?
How intense is your pain, without medication? No pain (score 0); mild (score 1); discomforting (score 2); distressing (score 3); horrible (score 4); excruciating (score 5)

Score 1 point for each ‘yes’ answer.

Less than 5: Your level of pain may be reduced by following the advice here. If not, we recommend you seek advice from a nutritional therapist or nutritionally oriented doctor.

5 to 10: You have a moderate level of pain and should definitely explore each of the options here as well as seeking advice from a nutritional therapist or nutritionally oriented doctor.

More than 10: You have a high level of pain and we advise you to consult a nutritional therapist or nutritionally oriented doctor.

The problem with anti-inflammatories

By now it will probably come as no surprise that the drug approach to dealing with pain is to block one or more of the inflammatory chemicals. NSAIDS, for instance, work by stopping the formation of prostaglandins, which in turn are made from one of the omega-6 fats, arachidonic acid, which is abundant in meat and milk. The human body needs some of this fat, but too much can be harmful. Here’s why.

Arachidonic acid makes two inflammatory chemicals known as type 2 prostaglandins and leukotrienes. The NSAIDs go to work on an enzyme involved in a crucial step in these chain reactions, which turns arachidonic acid into a type of prostaglandin called PGE2, which in turn causes pain. The enzyme’s name is ‘cyclo-oxygenase’ or cox. Blocking this cox enzyme is where all the action is, as far as NSAID drugs are concerned.

Why some NSAIDS cause heart problems

As we have seen, blocking some element – such as an enzyme – that is part of a network as complex as the body almost never has just one effect, which is why drugs nearly always have damaging side effects. To see exactly why NSAIDS can be so harmful we need to delve a bit further into their biochemical pathways. As Figure 16 shows, there are two kinds of cox enzyme – cox-1 and cox-2. Figure 16 – How COX 1 and COX 2 Painkillers induce side effects

You could think of cox-1 as the ‘good’ cox, because it helps to protect the gut and the kidneys and promotes normal blood clotting, while cox-2 is the ‘bad’ one because it leads to the painful prostaglandins. One of the first NSAIDs was aspirin, which targets both of these enzymes. Thus it’s good for stopping pain and inflammation, but also likely to put patients at risk by causing gastro-intestinal bleeding when used over the long term, and also taxes the liver. Ibuprofen also targets both enzymes. Because of the gastrointestinal problems, the thinking was that the ideal NSAID would be one that blocked only cox-2 and left cox-1 alone. And the launch of drugs such as Vioxx and Celebrex caused huge excitement because that’s exactly what they did. But problems with these drugs also began emerging a few years after they appeared on the scene. As you can see in Figure 16, the cox-1 pathway, besides making mucus to protect the guts, also makes a fat-like substance called thromboxane A2.

This promotes the narrowing of blood vessels and makes blood cells called platelets more ‘sticky’. The cox-2 pathway, on the other hand, makes what might be thought of as the antidote – a substance called prostacyclin which helps prevent platelets from clumping together and helps dilate the blood vessels. In a healthy system, the action of these two would be balanced. But by powerfully inhibiting the cox-2 pathway (and so blocking prostacyclin in the blood), the new generation of so-called ‘coxib’ drugs created a fresh problem, doubling or in some cases quadrupling a person’s risk of a heart attack.[1] This effect of coxibs also caused another problem, increasing the level of damage to brain cells in the event of a stroke.[2]

There may be as many as 100,000 people killed by these drugs. These ‘new-generation’, ‘safer’ painkillers were principally designed for patients who were at increased risk of gastrointestinal damage from NSAIDS. However, according to a study by researchers at the University of Chicago, ‘63% of the growth in COX-2 use occurred in patients with minimal risk of suffering gastrointestinal bleeding with NSAIDS.’ [3]

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