Curcuma

Clinical

Clinical Monitor BY KERRY BONE

The Cranberry Letters Two letters have recently been published on the theme of understanding the mechanism of action of cranberry in preventing urinary tract infections. The first letter challenges the hypothesis that proanthocyanidins are responsible for this effect.1 Some scientists have proposed in the past that these compounds inhibit the adherence of organisms such as E. coli to the bladder wall, thereby reducing the likelihood of bladder infection. The authors point out that proanthocyanidins are large polar molecules (found in red wine, grape seed extract and hawthorn) which are unlikely to be absorbed as such and unlikely to be excreted unchanged in the urine. They suggest that this issue highlights the fact that it is unwise to extrapolate from cell culture (in vitro research) to the human body, especially with complex herbal extracts. According to these scientists, identifying and testing metabolites or compounds in the urine of humans consuming cranberry is a more realistic approach to characterise the mechanism(s) involved in its beneficial effects. The second letter, written by a different research team and published around the same time, examined the effect of urine from healthy female volunteers given cranberry juice on the adherence of antibioticresistant strains of E. coli. 2 Urine excreted after cranberry juice cocktail consumption prevented adhesion of 31 (80%) of the 39 E. coli isolates in all bioassays. Normal urine was inactive. Antiadhesion activity was evident in the urine within 2 hours and persisted for up to 10 hours following cranberry intake.

Comment In the light of these two letters we can conclude that cranberry consumption definitely does create urine which is capable of preventing adhesion of pathogenic bacteria. But the compounds responsible for this are yet to be found and are unlikely to be proanthocyanidins (unless one believes in pharmacokinetic miracles). Another possibility is that, rather than containing compounds or precursors which prevent adherence, cranberry induces the body to produce its own factors which prevent adherence. For professional use only. Not for Public Distribution.

Some readers may be questioning the value of such research to their clinical use of cranberry. However, if we find out the mechanism of action, this might lead to a better understanding of the dosage and quality issues involved and a more effective cranberry product could be the outcome. REFERENCES 1

Dearing MD, Appel HM, Schultz JC. Why do cranberries reduce incidence of urinary tract infections? J Ethnopharmacol 2002; 80(2-3): 211

2

Howell AB, Foxman B. Cranberry juice and adhesion of antibioticresistant uropathogens. JAMA 2002; 287(23): 3082-3083

Turmeric and Prevention of Alzheimer’s Disease Studies have noted that elderly people living in Indian villages appear to have the lowest incidence of Alzheimer’s disease (AD) in the world, with just 1% of those aged 65 years and older suffering this terrible condition. Scientists at the University of California, Los Angeles speculated that curcumin, a common element of the Indian diet, could hold the key given that it is known to be a powerful antioxidant and anti-inflammatory agent.1 They examined the effects of dietary curcumin intake (the major antioxidant component of turmeric) on two different animal models of Alzheimer’s disease.2,3 In one model the effect of turmeric on induction of beta-amyloid damage in elderly rats was compared with the non-steroidal anti-inflammatory drug ibuprofen (also thought to protect against AD).2 Curcumin, but not ibuprofen suppressed oxidative brain damage. Both treatments reduced the accumulation of beta-amyloid and associated brain damage compared to controls. Dietary curcumin also resulted in better performance in memory-dependent maze tests. In the second study, transgenic mice which develop a brain pathology like AD were fed two doses of turmeric.3 Only the lower dose (which corresponds to typical supplemental or dietary intake of turmeric) decreased beta-amyloid plaque buildup. Both doses significantly lowered measures of oxidation and inflammation.

Modern Phytotherapist 25

Clinical

Comment It is too early to suggest that regular turmeric intake will help to prevent AD. There could be many other factors which could lead to the low incidence observed in Indian villages. Nonetheless, this is a promising finding for a spice which has also been linked to protective activity against cancer and cardiovascular disease.1 In an article several years ago I referred to turmeric as the “spice of life”. Contemporary research is certainly supporting this assertion.

by minimising reperfusion injury, but other favourable mechanisms could also apply.3 I maintain that there is now sufficient evidence to justify a regular consumption of green tea, grape seed extract and turmeric as part of a health maintenance program. These complex herbal antioxidants which have been part of human diet for thousands of years are very unlikely to be harmful and could provide considerable health benefits. REFERENCES 1

Mukamal KJ, Maclure M, Muller JE et al. Tea consumption and mortality after acute myocardial infarction. Circulation 2002; 105(21): 2476-2481

REFERENCES 1

Mills S, Bone K. Principles and Practice of Phytotherapy: Modern Herbal Medicine. Churchill Livingstone, Edinburgh, 2000, pp 569-580.

2

2

Frautschy SA, Hu W, Kim P et al. Phenolic anti-inflammatory antioxidant reversal of Abeta-induced cognitive deficits and neuropathology. Neurobiol Aging 2001; 22(6): 993-1005

Geleijnse JM, Launer LJ, Van der Kuip DA et al. Inverse association of tea and flavonoid intakes with incident myocardial infarction: the Rotterdam Study. Am J Clin Nutr 2002; 75(5): 880-886

3

Imai K, Nakachi K. Cross sectional study of effects of drinking green tea on cardiovascular and liver diseases. BMJ 1995; 310(6981): 693-696

3

Lim GP, Chu T, Yang F et al. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci 2001; 21(21): 8370-8377

Tea Consumption and Deaths from Heart Attacks Heavy drinkers of tea, be it black or green, are more likely to survive a heart attack according to a recent survey.1 Scientists from Harvard surveyed 1900 patients hospitalised with a confirmed heart attack between 1989 and 1994 and then followed them for an average of around 4 years. In the year prior to their heart attack 1019 people consumed no tea (nondrinkers), 615 consumed less than 14 cups per week (moderate tea drinkers) and 266 consumed 14 or more cups per week (heavy tea drinkers). After adjusting for confounding factors such as age, smoking, blood pressure and so on, moderate tea drinkers experienced a 28% lower death rate than nondrinkers. For heavy tea drinkers the death rate was 44% lower than nondrinkers. The scientists are certain that caffeine was not the protective factor in tea, because caffeine intake from other sources (such as cola drinks) was monitored and found to have no protective association.

Comment There is increasing evidence that herbal antioxidants could play a valuable role in preventing age-related degenerative disorders such as heart disease and Alzheimer’s disease. This study is consistent with the protective effects on cardiovascular disease reported for the Rotterdam study in Holland.2 In this context the antioxidant phenolic compounds in tea could act 26 Modern Phytotherapist

Memory Enhancing Effect of Bacopa Confirmed in Trial An Australian clinical trial examined the long-term effects of an extract of Bacopa monnieri on cognitive function in 46 healthy human volunteers.1 The study was of double-blind, placebo-controlled design in which subjects were randomly allocated to receive Bacopa or placebo. Neuropsychological testing was conducted before treatment and at 5 and 12 weeks after treatment. After 12 weeks the largest cognitive change from Bacopa treatment (which was also statistically significant compared to placebo, p<0.05) was a time reduction for the Inspection Time (IT) test (64.5 ± 16.7 min vs 75.9 ± 25.3 min). IT is regarded as a measure of the integrity of the early stages of information processing and may act as a rate-limiting factor for cognition. This indicates that Bacopa significantly improved the speed of visual information processing. Verbal learning rate and memory consolidation as assessed by the Rey Auditory Verbal Learning Test were also somewhat improved against placebo at 12 weeks (p<0.05). But the most striking finding was the highly significant (p=0.001) reduction in anxiety in volunteers receiving Bacopa. The percentage of adverse effects was similar for both groups, except that there was a higher incidence of nausea, dry mouth and fatigue in the Bacopa group.

Comment In the introduction to their paper the authors review the link between Bacopa and cholinergic modulation For professional use only. Not for Public Distribution.