Not everyone affected by these foods is diagnosed with a chronic disease; more than 60 million Americans experience episodes of acid indigestion as often as once each month and some studies suggest that as many as 15 million experience episodes of acid indigestion daily. Many people self-medicate with antacids when they could adjust their diet including reducing coffee and caffeine consumption in order to find relief. These conditions are serious: at least 10 million people are hospitalized each year for gastrointestinal disorders and the annual total of health care costs associated with these exceeds $40 billion. 1

Heartburn Acid Reflux & GERD

Heartburn, or pain behind the breastbone, is a condition in which there is reflux of acid from the stomach into the sensitive esophagus, often caused by a relaxation or weakening of the lower esophageal sphincter, the ring of muscle between the esophagus and the stomach. Foods, including dietary fat, chocolate, mints, coffee, onions, citrus fruit, and tomatoes, have been associated with increased incidence of acid reflux in susceptible persons.2

When symptoms are recurrent or esophageal tissue is damaged, GERD develops. GERD affects 5-7% of the global population.3, 4 When untreated, it can cause complications such as chest pain, bleeding, esophageal stricture (narrowing or obstruction of the esophagus) or Barrett�s esophagus (a pre-malignant condition). Symptoms that indicate damage to the esophagus has occurred include: pain, dysphagia (difficulty swallowing), bleeding and choking. Some risk factors of these more serious conditions are alcohol use, pregnancy, weight gain and coffee consumption.5

Ulcers

Ulcers are another common problem, afflicting approximately 20 million Americans, according to the American College of Gastroenterology. Ulcers can occur in the stomach or duodenum, and are regions where the lining has been destroyed by stomach acids or digestive juices. Even small areas of damage can cause intense pain. The presence of the bacteria Helicobacter pylori is also implicated as a predisposing factor in ulcer development, but not everyone infected with H. pylori develops ulcers. It is unknown why this is the case, although a strong immune system provides protection against the bacters ability to colonize damaged areas of the stomach lining. Increased levels of cortisol and other stress hormones stimulated by caffeine consumption and coffee drinking suppress the activity of the immune system and raise stress levels which are associated with ulcer formation. Other predisposing factors include: being male, family history, prolonged stress, skipping meals, cigarette smoking and coffee ingestion⁶.

Of all the dietary habits that people find difficult to change, coffee drinking is one of the most challenging because it is so entrenched in cultural habits and caffeine addiction.⁷ Withdrawal symptoms can involve painful headaches, nausea, vomiting, and loose stools.⁸ People whose health problems would be ameliorated if they gave up coffee can improve their chance for successfully quitting coffee if they have both a satisfying alternative and a method to slowly decrease their caffeine intake to reduce withdrawal symptoms.

The Following Characteristics of Coffee have an Adverse effect on the upper GI tract:

• Coffee Decreases Pressure in the Lower Esophageal Sphincter
  • Coffee has been shown to decrease pressure in the lower esophageal sphincter, contributing to gastroesophageal reflux. This suggests that coffee can either cause or exacerbate heartburn in susceptible individuals.^{9, 10, 11}
  • The type of coffee bean roasting method used does not reduce the tendency of coffee to produce gastroesophageal reflux. Sensitive individuals, even when consuming coffee produced through different roasting processes, while fasting or after a meal, experienced heartburn, regurgitation and dyspepsia.¹²
  • Coffee consumption has been associated with greater incidence of heartburn than drinking other fluids such as water.¹³
  • Both caffeinated and decaffeinated coffee exacerbate gastroesophaeal reflux, and coffee creates more reflux than caffeine added to water, suggesting that other components of coffee contribute to its aggravating effect.¹⁴

• The Acidity of Coffee Irritates the Stomach
  • Coffee is highly acidic and it can stimulate the hypersecretion of gastric acids. Decaffeinated coffee has been shown to increase acidity to a greater degree than either regular coffee or caffeine alone.¹⁵ Both caffeine and coffee stimulate gastric acid secretion and decaffeinated coffee raises serum gastrin levels.^{16, 17} A study comparing the ability of decaffeinated coffee with that of a high protein meal to increase gastric acid secretion and gastrin levels found that decaffeinated coffee was a more powerful stimulant of acid secretion and gastrin release than the high protein.¹⁸
  • Coffee tends to speed up the process of gastric emptying, which may result in highly acidic stomach contents passing into the small intestine more rapidly than normal. This may lead to injury of the intestinal tissue.¹⁹
  • There is a clear relationship between reduction of stomach acid and heartburn relief.²⁰

• Coffee Is a Risk Factor Associated with Ulcer Susceptibility
  • Coffee is linked to ulcer susceptibility. Both caffeinated and decaffeinated coffees have an acid-stimulating effect, and therefore it is recommended that people with ulcers restrict not only caffeinated but also decaffeinated coffee intake.²¹

• Coffee Elevates Stress Hormones
  • Caffeine in coffee elevates the stress hormones cortisol, epinephrine (also known as adrenaline) and norepinephrine.^{22, 23, 24, 25} These hormones are responsible for increased heart rate, increased blood pressure, and a sense of “emergency alert”. Blood is diverted from the digestive system which can cause indigestion. The circulation of oxygen to the brain and extremities is decreased and the immune system is suppressed.
  • The purpose of the body’s “fight or flight” response initiated by the release of cortisol, epinephrine and norepinephrine is to provide the body with a temporary energy boost for intense physical activity. With today’s sedentary lifestyle, the continual state of increased stress resulting from caffeine consumption may affect symptoms of heartburn and GERD. Although the relationship between stress and symptoms of gastroesophageal reflux is still unclear, evidence suggests that anxiety, along with exhaustion resulting from sustained stress, are both associated with exacerbation of heartburn and esophageal reflux.²⁹

• Coffee Supresses Immune System Function
  • Immune system suppression caused by chronic increased levels of stress hormones induced by caffeine intake can create a situation in which the bacteria Helicobacter pylori can thrive in the stomach. Infection by H. pylori is implicated in ulcers.

• Caffeine Interferes with GABA Metabolism
  • GABA (Gamma-aminobutyric acid) is a neurotransmitter that is naturally produced in the brain and nervous system as well as the GI tract. It plays an important role in mood and stress management and it exerts a calming effect on the GI tract.
  • Caffeine has been found to interfere with binding of GABA to GABA receptors, preventing it from performing its calming function.²⁶ Studies suggest that stimulation of GABA receptors may be beneficial for people with reflux arising from low lower oesophageal sphincter pressure.^{27, 28} In addition to its direct effect on the GI tract, GABA�s role in stress management is also compromised in the presence of caffeine. This is significant as psychological stress has been shown to be an exacerbating factor in heartburn and ulcers.²⁹

Recommendation:

Individuals who suffer from or are susceptible to problems with the upper gastrointestinal tract, would do well to avoid coffee as it has been demonstrated to be a contributing factor associated with increased incidence of gastritis, ulcers, acid reflux and GERD. Dietary changes that include weaning off of coffee and all other sources of caffeine can help relieve symptoms of these disorders.30 Nutrition professionals can support gastrointestinal patients by guiding them through the process of substituting a non-caffeinated, alkaline herbal coffee that brews and tastes just like coffee.

Kicking the Caffeine Habit:

The social prevalence of coffee drinking and the addictive side effects of caffeine can cause problems with patient compliance. Caffeine-free herbal coffee marketed under the brand name of Teeccinoi helps coffee drinkers replace their regular or decaf coffee with a satisfying alternative. Coffee drinkers need a dark, full-bodied, robust brew to help satisfy their coffee craving. Teeccino satisfies the 4 needs coffee drinkers require in a coffee alternative:

1. Teeccino brews just like coffee, allowing coffee drinkers to keep their same brewing ritual.
2. It has a delicious, deep roasted flavor that is very coffee-like.
3. It wafts an enticing aroma.
4. People experience a natural energy boost from nutritious Teeccino.

Teeccino offers the following health benefits to people suffering from upper GI tract disorders:

The Pain-free Way to Wean off of Coffee

Start by mixing normal coffee 3/4 to 1/4 Teeccino Herbal Coffee. Gradually reduce the percentage of coffee over a two to three week period until only 100% Teeccino Herbal Coffee is brewed. Gradual reduction of caffeine is recommended.31 Side effects such as headaches, fatigue, and brain fogginess can be avoided as the body gradually adjusts to less reliance on stimulants.

Example: Use the following proportions if you make a 10-cup pot of coffee daily:

References

1. American College of Gastroenterology. Copyright 2004.
2. Terry P, Lagergren J, Wolk A, Nyren O. 2000. Reflux-inducing dietary factors and risk of adenocarcinoma of the esophagus and gastric cardia. Nutrition and Cancer. 38(2): 186-91.
3. International Foundation for Functional Gastrointestinal Disorders. Copyright 2004.
4. Richter JE, Katz PO, Waring JP. Gastroesophageal Reflux Disease. IFFGD, 2000.
5. Wang, J.H., Luo, J.Y., Dong, L., Gong, J. and Tong, M. 2004. Epidemiology of gastroesophageal reflux disease: a general population-based study in Xi’an of Northwest China. World Journal of Gastroenterology. 10(11):1647-51.
6. Abu Farsakh, N.A. 2002.Risk factors for duodenal ulcer disease. Saudi Medical Journal. 23(2):168-72.
7. Braun, S. Buzz: The Science and Lore of Alcohol and Caffeine. Copyright 1996.
8. Strain, E.C., G.K. Mumford, K. Silverman, and R.R. Griffiths. 1994. Caffeine dependence syndrome. Journal of the American Medical Association, 272:1043-1048.
9. Thomas, F.B., Steinbaugh, J.T., Fromkes, J.J., Mekhjian, H.S., and Caldwell, J.H. 1980. Inhibitory effect of coffee on lower esophageal sphincter pressure. Gastroenterology, Dec; 79(6): 1262-6.
10. Boekema, P.J., Samsom, M., van Berge Henegouwen, G.P. and Smout, A.J. 1999. Coffee and Gastrointestinal function: facts and fiction. A Review. Scandinavian Journal of Gastroenterology Supplement. 230: 35-9.
11. Cohen, S. 1980. Pathogenesis of coffee-induced gastrointestinal symptoms. New England Journal of Medicine. 303(3):122-4.
12. DiBaise, JK. 2003. A randomized, double-blind comparison of two different coffee-roasting processes on development of heartburn and dyspepsia in coffee-sensitive individuals.Digestive Diseases and Sciences. 48(4):652-6.
13. Feldman, M. and Barnett, C. 1995. Relationships between the acidity and osmolality of Popular Beverages and reported Postprandial Heartburn. Gastroenterology. 108(1): 125-31.
14. Wendl, B., Pfeiffer, A., Pehl, C., Schmidt, T. and Kaess, H. 1994. Effect of decaffeination of coffee or tea on gastro-oesophageal reflux. Alimentary pharmacology & therapeutics. 8(3):283-7.
15. Cohen, S. and Booth, G.H. Jr. 1975. Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine. New England Journal of Medicine. 293(18):897-9.
16. Coffey, R.J., Go, V.L., Zinsmeister, A.R. and DiMagno, E.P. 1986. The acute effects of coffee and caffeine on human interdigestive exocrine pancreatic secretion. Pancreas. 1(1):55-61.
17. Borger HW, Schafmayer A, Arnold R, Becker HD, Creutzfeldt W. 1976. The influence of coffee and caffeine on gastrin and acid secretion in man. Deutsche medizinische Wochenschrift. 101(12):455-7.
18. Feldman EJ, Isenberg JI, Grossman MI. 1981. Gastric acid and gastrin response to decaffeinated coffee and a peptone meal. JAMA. 246(3):248-50.
19. H. Glatzel and K. Hackenberg, Effects of Caffeine Containing and Decaffeinated Coffee on the Digestive Functions: X-ray Studies of the Secretion and Peristalsis of Stomach, Intestines and Gallbladder, Medizinische Klinik, April 21, 1967;62(16):625-28.
20. Huang, J.Q., Hunt, R.H. 1999. pH, healing rate, and symptom relief in patients with GERD. Yale Journal of Biology and Medicine. 72(2-3): 181-94.
21. Marotta, R.B. and Floch, M.H. 1991. Diet and nutrition in ulcer disease. The Medical Clinics of North America. 75(4): 967-79.
22. Robertson, D., Frolich, J.C., Carr, R.K., Watson, J.T., Hollifield, J.W., Shand, D.G. and J.A. Oates. 1978. Effects of caffeine on plasma renin activity, catecholamines and blood pressure. New England Journal of Medicine. 298(4):181-6.
23. Lane, J.D., Adcock, R.A., Williams, R.B. and C.M. Kuhn. 1990. Caffeine effects on cardiovascular and neuroendocrine responses to acute psychosocial stress and their relationship to level of habitual caffeine consumption. Psychosomatic Medicine. 52(3):320-36.
24. Lane, J.D. 1994. Neuroendrocine Responses to Caffeine in the Work Environment. Psychosomatic Medicine. 546:267-70.
25. Kerr, D., Sherwin, R.S., Pavalkis, F., Fayad, P.B., Sikorski, L., Rife, F., Tamborlane, W.V. and During, M.J. 1993. Effect of caffeine on the recognition of and responses to hypoglycemia in humans. Annals of Internal Medicine. 119(8):799-804.
26. Roca, D.J., G.D. Schiller, and D.H. Farb. 1988. Chronic Caffeine or Theophylline Exposure Reduces Gamma-aminobutyric Acid/Benzodiazepine Receptor Site Interactions. Molecular Pharmacology, May;33(5):481-85.
27. Cantu, P., Carmagnola, S., Savojardo, D., Allocca, M. and Penagini, R. 2003. Effect of non-selective gamma-aminobutyric acid receptor stimulation on motor function of the lower oesophageal sphincter and gastro-oesophageal reflux in healthy human subjects. Alimentary pharmacology & therapeutics. 18(7):699-704.
28. Koek GH, Sifrim D, Lerut T, Janssens J, Tack J. 2003. Effect of the GABA(B) agonist baclofen in patients with symptoms and duodeno-gastro-oesophageal reflux refractory to proton pump inhibitors. Gut. 52(10): 1397-402.
29. Naliboff BD, Mayer M, Fass R, Fitzgerald LZ, Chang L, Bolus R, Mayer EA. 2004. The effect of life stress on symptoms of heartburn. Psychosomatic Medicine. 66(3):426-34.
30. Roberfroid MB. 1997. Health benefits of non-digestible oligosaccharides. Advances in experimental medicine and biology. 427: 211-9.
31. Silverman, K., Evans, S.M., Strain, E.C. and Griffiths, R.R. 1992 Withdrawl Syndrome after the Double-Blind Cessation of Caffeine Consumption. The New England Journal of Medicine. 16(327): 1109-14.
32. Cherniske, S. Caffeine Blues: Wake Up to the Hidden Dangers of America�s #1 Drug. Copyright 1998.
33. Fetrow, C.W. and J.R. Avila. Professional�s Handbook of Complementary and Alternative Medicines. Second Edition. Copyright 2001.
34. Murray, M., and J. Pizzorno. Encyclopedia of Natural Medicine, Revised Second Edition. Copyright 1998.
35. Physicians Desk Reference for Herbal Medicines. Second Edition. Copyright 2000.
36. Roehl, E. Whole Foods Facts: The Complete Reference Guide. Copyright 1996.
37. Biddle, W. 2003. Gastroesophageal reflux disease: current treatment approaches. The Official Journal of the Society of Gastroenterology Nurses and Associates 26(6): 228-36.

(Reviewed by Meri Rafetto, RD, Theresa Grumet, RD, and Gerri French, RD, MS, CDE)

* the common cold, as shown in a case-control study involving preschool and school-age children. After being given a water-based preparation of propolis (Nivcrisol®) throughout the whole colds season in 1994-1995, the children had fewer cases of acute or chronic symptoms, as well as a decrease in disease-causing microorganisms carried in their upper airways (Rom J Virol, 1995; 46: 115-33).

In a study carried out in Poland, 50 people with colds treated with propolis had symptoms for an average of 2.5 times shorter duration than those who took a placebo (Otolaryngol Pol, 1989; 43: 180-4).

* recurrent genital herpes, as proven in a randomised, single-blind, controlled study of 90 sufferers. Of the 30 patients treated with propolis ointment for 10 days, 24 had healed, compared with 14 of the 30 using an acyclovir ointment and 12 of the 30 using a placebo (Phytomedicine, 2000; 7: 1-6).

* candidiasis due to Candida albicans and other species of this yeast (Mycoses, 2001; 44: 375).

* fungal skin infections (dermatophytoses) caused by Trichophyton rubrum and T. mentagrophytes (Mycoses, 2005; 48: 205), at least in the lab.

* liver diseases, as evidenced by a marked decrease in fatty degeneration of the liver induced by chronic alcohol abuse, at least in rats given 30 mg/kg of propolis ethanol extract (so it may not apply to humans) (Am J Chin Med, 1997; 25: 325-32). There is also laboratory evidence that propolis can promote liver-tumour-cell death (Int J Mol Med, 1999; 4: 29-32).

* rheumatic diseases, as shown in a single-blind, placebo-controlled Hungarian trial of 190 patients, who used purified propolis and propolis saturated with anti-inflammatory trace metals, respectively applied locally and by iontophoresis (where the affected joints are immersed in a conductive solution through which a tiny electrical charge is transmitted). Symptoms such as pain and inflammation were significantly improved, especially with the latter form of propolis treatment (Orv Hetil, 1996; 137: 1365-70).

* stomach ulcers, as shown by a study wherein a propolis ethanol extract prevented damage to the stomach lining (Am J Chin Med, 2002; 30: 245-54). However, this was a study in rats, so the results may not necessarily apply to humans.

Raynaud’s syndrome (or disease) tends to strike women aged 20-40. Left uncontrolled, it can lead to brittle, deformed nails and slow-healing ulcers at the fingertips or around the nails. In severe cases, the blood vessels can collapse and die, leading to gangrene.

What causes it?
The exact cause of Raynaud’s is unknown. One theory suggests that the abnormal blood vessel constriction could be due to infection by Helicobacter pylori (a cause of stomach cancer). Raynaud’s patients with H. pylori had a complete recovery or a reduction of vasospasms once the bacteria were eradicated (Dig Dis Sci, 1998; 43: 1641-5; Int J Angiol, 1998; 7: 307-9).

Raynaud’s can also be secondary to other conditions such as scleroderma, lupus and rheumatoid arthritis. Such cases are considered to be more serious as patients are more likely to develop skin ulcerations and tissue death.

Certain drugs can also induce Raynaud’s, including over-the-counter cold and weight-control medications, and beta-blockers, which decrease blood flow.

People who work with vibrating tools are also at risk of a similar condition known as ’vibrating white finger’.

What doctors tell you
An effective cure for Raynaud’s remains elusive. Calcium-channel blockers, which open up the arteries, are prescribed to control the vasospasms. But effectiveness is limited – and come at the cost of a raft of side-effects such as dizziness, headaches, nausea, oedema, hot flushes, abnormal heartbeats, sleep disturbances, psychosis and jaundice.

Other drugs for Raynaud’s include blood-thinners (like aspirin) and vasodilators (such as reserpine and guanethidine).

Surgery is often the final option, such as a sympathectomy, where the nerves controlling vascular constriction in the fingers are cauterised. However, this is rarely done as it is invasive and unpredictable in outcome.

An experimental treatment is H-O-U therapy (heat, ozone, ultraviolet light). Patients are reinjected with their own blood, pretreated with H-O-U (Int Angiol, 1997; 16: 250-4).

Antibiotic therapy is useless in ‘a significant proportion’ of patients, says Peter Jenks, a microbiologist at University Hospital in Nottingham, for other reasons as well, such as age, smoking and the type of bacteria in the gut.

But, by far, the biggest concern is antibiotic resistance. Up to 70 per cent of H. pylori strains in the West are resistant to the antibiotic metronidazole, and up to 15 per cent are resistant to clarithromycin, another antibiotic. Resistance to amoxycillin is vastly underreported, which leaves just tetracycline among the antibiotics as an effective antidote to the bug (BMJ, 2002; 325: 3).

So, researchers recently tested a COX-2 on patients who were taking an NSAID for arthritis, but who had suffered bleeding ulcers as a result. But the COX-2 was no better, and ulcer bleeding recurred in most cases. (Source: New England Journal of Medicine, 2002; 347: 2104-10).

For more information about NSAIDS and the treatments for arthritis, buy The WDDTY Arthritis Handbook. It’s available from our website: http://www.wddty.co.uk/shop/details.asp?product=5

But now, researchers at Nottingham University have revealed that the COX-2s are just as bad as the NSAIDs they are meant to replace. In a study of more than 9400 patients diagnosed with a stomach ulcer or GI bleeding, the researchers found an increased risk of GI problems that was associated not only with the conventional NSAIDs such as ibuprofen, but with the COX-2s as well (BMJ, 2005; 331: 1310-6).

In other words, years of COX-2 commercial success have been based on claims that turn out not to be true.

This astonishing discovery, which has taken around 15 years to make, was based on patients’ records from 367 general practices in the UK. The data showed that rofecoxib was the most likely to cause a serious GI problem – hardly a surprise, given that this drug was withdrawn in 2004, after a new clinical trial showed an increased risk of serious thrombotic events (including heart attack and stroke) with long-term use.

The safety risk was deemed slightly less for celecoxib, the only COX-2 selective NSAID left on the market after valdecoxib (Bextra), like rofecoxib, was recalled due to concerns over cardiovascular events. However, a recent study found that the patients taking this drug developed even more dyspepsia than those taking the conventional NSAID naproxen (Am J Med, 2005; 118: 1271-8).

In fact, the large number of COX-2 prescriptions – due, no doubt, to the avid promotion of their better tolerability – has been linked to the growing number of cases of GI haemorrhage (Prescrire Int, 2005; 14: 177-8).

Celebrex: the sole survivor
Celebrex was the first COX-2 to be approved, in 1998, by the US Food and Drug Administration (FDA). The results of the CLASS (Celecoxib Long-Term Arthritis Safety Study) claimed that it caused fewer GI side-effects compared with the traditional NSAIDs. However, among patients given aspirin as a just-in-case medicine to prevent heart disease, those patients given celecoxib had similar GI problems (such as ulcers) as those given diclofenac and ibuprofen (JAMA, 2000; 284: 1247-55).

Then heart problems came to light. The Adenoma Prevention with Cele-coxib (APC) study, co-sponsored by the US National Cancer Institute and Pfizer, which makes the drug, revealed that patients taking 200 mg twice daily of the drug were nearly two and a half times more likely to suffer a heart attack or stroke. This risk rose to 3.4 times with 400 mg twice daily. Needless to say, the authors recommended that the cancer study be discontinued before it had run its intended course (N Engl J Med, 2005; 352: 1071-80); also, for more evidence about celecoxib, see http://www.cancer.gov/clinicaltrials/results/cox inhibitor-trials0205).

Even more damning for Pfizer, an unpublished study from 1999 had shown that elderly (Alzheimer) patients had four times the risk of a heart attack or stroke with the drug vs a placebo – a finding which only recently came to light.

A recent study of 2035 patients showed that Celebrex was associated with a dose-related, two- to threefold increase in death from cardiovascular causes, including stroke, heart attack and heart failure (N Engl J Med, 2005; 352: 1071-80). In terms of thromboembolic events (blood clots leading to stroke), Celebrex was no better than its banned sister Vioxx (Drug Saf, 2005; 28: 803-16).

Given these findings, a reconsideration of the cardiovascular safety profile of all NSAIDs – selective and non-selective – would seem warranted. Indeed, the FDA now recommends that all such drugs carry a ‘black-box’ warning for GI and cardiovascular risks (Curr Pain Headache Rep, 2005; 9: 377-89).

Kim Wallace

* Avoid supplementing with copper, which significantly boosts the effects of the drug (J Med Chem, 1976; 19: 135-48), with iron, which can cause further gut irritation, and with potassium, as blood-potassium levels are increased in patients taking NSAIDs.

No area offers the potential for a major moneyspinner than something that will take away the pain of arthritis, a market possibly bigger than any, excluding vaccination. Such is the desperation of medicine to find a breakthrough for arthritis that they are currently experimenting with chemotherapy that was originally developed to combat non-Hodgkin’s lymphoma – a drug so toxic that it can cause acute respiratory failure within an hour of taking it (Hoffmann-LaRoche, Rituxan product monograph, 21 June 2000).

Although non-steroidal anti-inflammatory drugs (NSAIDs) had firmly staked out the arthritis market as their own, there was a long list of problems with this class of drugs. Patients might enjoy relief from the pain of arthritis, but were then beset with gastrointestinal ulcers. A good number of patients with arthritis were in the situation of having to take ‘chaser’ drugs to alleviate the pain and side-effects caused by the original drugs they were taking for their condition.

Enter the COX-2 inhibitors. These are the fair-haired boys in arthritis treatment at the moment – the ‘super-aspirins’, drugs that have been marketed as a pain reliever with no strings attached. Indeed, the first two to be marketed – Celebrex and Vioxx (virtually all of these drugs have an ‘x’ incorporated into their names, making them the weirdest drug names of all time) – were, virtually overnight, the most successful drugs in medical history, snatching the mantle from Viagra.

As is usually the case in modern medicine, much of the fanfare over the COX-2s has been seriously overplayed. For one thing, as the postmarketing evidence begins pouring in, it seems that COX-2 inhibitors cause the same side-effects as their predecessors. Numerous trials show that many of these drugs can cause ulcers (BMJ, 1999; 319: 1518). Indeed, a recent Norwegian study concluded that COX-2s were actually more dangerous than NSAIDs and caused more side-effects (Tidsskr Nor Laegefor, 2002; 122: 476-80). In fact, Bextra (valdecoxib), among the latest of the COX-2s, was approved less than a year ago and has already been linked to many life-threatening skin conditions, such as Stevens-Johnson syndrome, as well as anaphylactic shock. Other drugs, such as Celebrex (celecoxib), were linked to deaths from gastrointestinal ulcers and heart problems. Studies have emerged showing that patients taking Vioxx (rofecoxib) are twice as likely to suffer a cardiovascular problem, such as a heart attack, than those given an NSAID (JAMA, 2001, 286: 954-9). Such are the questions lingering over the heart dangers with COX-2s that the Food and Drug Administration in America is considering the use of a warning.

As is so often the case with a modern ‘miracle’ drug, the hype was premature and the testing was inadequate. The COX-2 inhibitors are not super-aspirins – they are just aspirin in a more dangerous suit of clothes. If I were trying to come up with a clever drug name for this batch of beauties, I’d be inclined toward ‘Nothanx.’
Lynne McTaggart

The drug that caused limb deformities in newborns and which single handedly changed the way pharmaceuticals are controlled, has been tested on AIDS patients.

Of the 29 patients with advanced HIV, 16 responded well to treatment, and their mouth ulcers cleared up. Quite what else it may have done remains to be seen.

Over 1 per cent of the population of Great Britain undergoes some form of endoscopic screening every year, usually to detect ulcers and particularly if they already suffer from dyspepsia. The procedure can be rather upsetting, however, and so is sometimes done under a general anaesthetic.

Researchers at Glasgow’s Western Infirmary compared the outcomes of patients who had been screened with either an endoscopic examination or a simple breath test. In all, they followed 708 patients, aged under 55, who had been randomly assigned to one or the other procedure.

Having found that both techniques similarly did not miss any cases of H. pylori infection, they now recommend that the breath test should be the preferred screening procedure (BMJ, 2002; 324: 999-1002).