of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibito

Non-Steroidal Anti-Inflammatory Drugs – NSAIDs - are among the world's most widely prescribed drugs, and the most frequently purchased over the counter (OTC) medicines. They treat pain and according to pharmaceutical industry estimates, about one quarter of the entire world’s population suffers from moderate to severe chronic pain.

NSAIDs are drugs containing anti-inflammatory and analgesic ingredients that help relieve inflammation, fever and pain. Since inflammation is one of the chief causes of pain, the search for effective anti-inflammatory agents has been intense. Aspirin was the first commercially significant NSAID, but since it, in common with other NSAIDs, can irritate the stomach lining and causing internal bleeding, the drug companies began the search for a better solution.

NSAID and Pain

When tissue cells are damaged -for example by arthritis - inflammation is created and the enzyme, PLA (phospholipase), is released. The PLA enzyme breaks down the outer membrane, not only of the damaged cell, but of neighbouring cells. These cell walls are made of fatty acids called phospholipids – which then break free.

The broken-down fatty acids are then processed by three further enzymes called COX 1, COX 2 and LIPOX.

The end result of the process is the creation of another fatty acid called a prostaglandin which is recognised by pain receptors on nerve endings and transmitted to the brain as pain.

Prostaglandins also make the original inflammation worse which creates a vicious circle – because more PLA is created and therefore more cell membranes breakdown and therefore more phospholipids are released and therefore more prostaglandin is produced. The circle continues.

NSAIDs work by preventing the broken down phospholipids from reaching COX1 or COX2 – which is why they are called COX Inhibitors. But they can’t block the pathway to LIPOX.

Moreover, they only affect the symptoms – the pain – they do not address the cause. And, they can be a cause for gastric ulceration, estimated to affect as many as 20% of NAISD long-term users.

Indeed the US experiences about 7,600 NSAID-related deaths and 76,000 NSAID-related hospital admissions per year. According to one research group NSAIDS cause as many as 40 deaths per week in the UK.

Given the serious side effect issues, scientists unsurprisingly began to look for better NSAID’s and in the ‘70’s found there were two forms of COX, designated COX-1 and COX-2. It became apparent that inhibiting COX-1 was the cause of the ulceration problem, and drug companies began to search for compounds that blocked COX-2 without affecting COX-1.

This more specific (magic bullet) approach, it was hoped, would produce a safer product. It eventually produced the COX-2 inhibitors Celebrex (sold by Searle and Pfizer), Vioxx (sold by Merck & Co.), and Bextra (sold by Pfizer). But safety was to prove elusive.

COX-2 Inhibitors and Cardiovascular Disease

There was suspicion quite early that COX-2 inhibitors could increase blood pressure. In 2005 this was confirmed by a very large meta-analysis, (an examination of 19 separate studies of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibitor

olution.

NSAID and Pain

When tissue cells are damaged -for example by arthritis - inflammation is created and the enzyme, PLA (phospholipase), is released. The PLA enzyme breaks down the outer membrane, not only of the damaged cell, but of neighbouring cells. These cell walls are made of fatty acids called phospholipids – which then break free.

The broken-down fatty acids are then processed by three further enzymes called COX 1, COX 2 and LIPOX.

The end result of the process is the creation of another fatty acid called a prostaglandin which is recognised by pain receptors on nerve endings and transmitted to the brain as pain.

Prostaglandins also make the original inflammation worse which creates a vicious circle – because more PLA is created and therefore more cell membranes breakdown and therefore more phospholipids are released and therefore more prostaglandin is produced. The circle continues.

NSAIDs work by preventing the broken down phospholipids from reaching COX1 or COX2 – which is why they are called COX Inhibitors. But they can’t block the pathway to LIPOX.

Moreover, they only affect the symptoms – the pain – they do not address the cause. And, they can be a cause for gastric ulceration, estimated to affect as many as 20% of NAISD long-term users.

Indeed the US experiences about 7,600 NSAID-related deaths and 76,000 NSAID-related hospital admissions per year. According to one research group NSAIDS cause as many as 40 deaths per week in the UK.

Given the serious side effect issues, scientists unsurprisingly began to look for better NSAID’s and in the ‘70’s found there were two forms of COX, designated COX-1 and COX-2. It became apparent that inhibiting COX-1 was the cause of the ulceration problem, and drug companies began to search for compounds that blocked COX-2 without affecting COX-1.

This more specific (magic bullet) approach, it was hoped, would produce a safer product. It eventually produced the COX-2 inhibitors Celebrex (sold by Searle and Pfizer), Vioxx (sold by Merck & Co.), and Bextra (sold by Pfizer). But safety was to prove elusive.

COX-2 Inhibitors and Cardiovascular Disease

There was suspicion quite early that COX-2 inhibitors could increase blood pressure. In 2005 this was confirmed by a very large meta-analysis, (an examination of 19 separate studies of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibito

e more cell membranes breakdown and therefore more phospholipids are released and therefore more prostaglandin is produced. The circle continues.

NSAIDs work by preventing the broken down phospholipids from reaching COX1 or COX2 – which is why they are called COX Inhibitors. But they can’t block the pathway to LIPOX.

Moreover, they only affect the symptoms – the pain – they do not address the cause. And, they can be a cause for gastric ulceration, estimated to affect as many as 20% of NAISD long-term users.

Indeed the US experiences about 7,600 NSAID-related deaths and 76,000 NSAID-related hospital admissions per year. According to one research group NSAIDS cause as many as 40 deaths per week in the UK.

Given the serious side effect issues, scientists unsurprisingly began to look for better NSAID’s and in the ‘70’s found there were two forms of COX, designated COX-1 and COX-2. It became apparent that inhibiting COX-1 was the cause of the ulceration problem, and drug companies began to search for compounds that blocked COX-2 without affecting COX-1.

This more specific (magic bullet) approach, it was hoped, would produce a safer product. It eventually produced the COX-2 inhibitors Celebrex (sold by Searle and Pfizer), Vioxx (sold by Merck & Co.), and Bextra (sold by Pfizer). But safety was to prove elusive.

COX-2 Inhibitors and Cardiovascular Disease

There was suspicion quite early that COX-2 inhibitors could increase blood pressure. In 2005 this was confirmed by a very large meta-analysis, (an examination of 19 separate studies of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibito

began to look for better NSAID’s and in the ‘70’s found there were two forms of COX, designated COX-1 and COX-2. It became apparent that inhibiting COX-1 was the cause of the ulceration problem, and drug companies began to search for compounds that blocked COX-2 without affecting COX-1.

This more specific (magic bullet) approach, it was hoped, would produce a safer product. It eventually produced the COX-2 inhibitors Celebrex (sold by Searle and Pfizer), Vioxx (sold by Merck & Co.), and Bextra (sold by Pfizer). But safety was to prove elusive.

COX-2 Inhibitors and Cardiovascular Disease

There was suspicion quite early that COX-2 inhibitors could increase blood pressure. In 2005 this was confirmed by a very large meta-analysis, (an examination of 19 separate studies of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibito

of the effects of COX-2 inhibitors), published in the Archives of Internal Medicine. This paper concluded that they did indeed have a tendency to raise blood pressure – a known risk factor for heart attacks and strokes.

In parallel with this research, a team at the University Of Pennsylvania School Of Medicine (Zhang ’03, Rudic ’05) had more or less established how the COX-2 inhibitors created this problem. COX-2 has more than one role in the body. COX-2 is involved in the synthesis of substances that cause pain and inflammation; but it is also responsible for producing an oily substance called prostacyclin – a fat molecule.

Prostacyclin controls the way in which blood vessels adapt to stresses such as high blood pressure. By reducing levels of prostacyclin, the COX-2 inhibitors increase blood pressure. But they also accelerate the process of atherosclerosis (hardening of the arteries), interfere with key healing mechanisms, and possibly increase the risk of blood clots.

This ‘perfect storm’ combination of effects, the researchers suggested, could all interact to increase the risk of heart attack and stroke even in previously healthy individuals.

Fighting Pain with Nutritional Food Ingredients

Long ignored by the drug companies, many leading scientists have nonetheless studied the therapeutic power of natural food ingredients and their active constituents. The best documented anti-inflammatory is the food spice turmeric, which has a long history of use in Ayurvedic medicine in the treatment of painful conditions from sore throats to arthritis.

The curcuminoids in turmeric reduce pain and inflammation by inhibiting COX-1 and COX-2, plus the other inflammatory enzyme known as lipooxygenase or LIPOX. They are powerful antioxidants that lower LDL (the ‘bad’) cholesterol and protect against oxidation. They reduce blood pressure and make the blood less likely to clot.

Curcuminoids belong to a wider category of phytonutrients called ‘flavonoids’, a family of compounds which occur in many plant foods such as berry fruits and which are associated with better health prospects – including a lower risk of Alzheimer’s.

The role of curcumin and flavonoids in reducing inflammation and controlling pain is explained in detail by the international health expert Dr Paul Clayton in his book Health Defence and at www.drpaulclayton.com.

Dr Paul Clayton has also aided in the design of the Uni-Vite JointShield a safe and natural nutritional product of interest to osteo-arthritis sufferers that combines curcuminoids with glucosamine hydrochloride, pomegranate extract, beta sitosterol, Vitamin D and Vitamin K.