Tea and weight loss and other health effects

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ARBOR CLINICAL NUTRITION UPDATES ©

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Dear subscriber,

This is the final part of a three-part series on tea and health.

In the first two parts (already distributed as Premium issues) we looked at

clinical applications of tea against cancer, cardiovascular disease,

hyperlipidaemia, osteoporosis, as an antimicrobial agent and on the central

nervous

system.

In this issue we focus on the potential benefits of tea in relation to

weight control, diabetes, skin protection, gut and oral health. We also

consider

possible side-effects.

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NUTRITION RESEARCH REVIEW

Study 1: Tea consumption and skin cancer

A recent North American study has looked at the relationship between tea

drinking and skin cancer.

Method: Observational case-control study of 770 patients with basal cell

(BCC) and 696 with squamous cell carcinoma (SCC) compared to 715 controls.

Results: Having ever consumed tea regularly (³.1 cup/day for ³1 month) was

inversely associated with skin cancer incidence, especially SCC and in those

drinking more often (³2 cups/day OR = 0.49; 95% CI 0.29-0.83, p for trend =

0.008) or long term (³ 47 yrs consumption OR = 0.49; 0.29-0.83, p=0.008).

There

was a weak inverse association with BCC (OR = 0.79; 95% CI 0.63-0.98).

Ref.:J Am Acad Dermatol. 2007 May;56(5):781-5.

Study 2: Green tea, fat and glucose tolerance

A new clinical trial investigated the effect of green tea on metabolic

parameters in healthy subjects.

Method: Two separate randomised, placebo-controlled crossover trials, the

first involving cycling exercise (to 60% maximal O2 consumption) and the second

a glucose tolerance test, both before and after taking capsules containing

either green tea extract or placebo. The subjects were healthy adult

volunteers (n=12 and 11 respectively).

Results: Subjects taking green tea when compared to placebo had significant

increases in fat oxidation rates (by 17%, p<0.05, see Graph), contribution of

fat oxidation to total energy expenditure at the expense of lesser

carbohydrate contribution (p<0.05), lower insulin levels in both serum

concentrations

(p<0.01) and area under the GTT curve (p<0.05).

Ref.: Am J Clin Nutr. 2008 Mar;87(3):778-84.

Study 3: Green tea for obesity

A new RCT from Thailand used green tea powder to treat obese patients.

Method: 60 obese adults (BMI ³25) took green tea as part of a standard 2,000

kcal/day diet.

Results: There was a significantly greater weight loss in the green tea

compared to placebo group at 8 and 12 weeks (5.1 and 3.3 kg respectively, both

p<0.05), associated with higher respiratory quotient (by 0.02, p<0.05) and

higher resting energy expenditure (by 183.4 kJ/day p<0.001).

Ref.: Physiol Behav. 2008 Feb 27;93(3):486-91.

COMMENTARY

These three new studies illustrate the range of mechanisms by which tea has

potential clinical benefit.

Weight management

A considerable number of mechanisms that could affect weight balance have

been demonstrated in animal and in vitro research for green tea as a whole,

green tea catechins in general and the specific catechin epigallocatechin

gallate (EGCG) (ref.1, 2).

For example, EGCG increased thermogenesis in obese men in one recent German

trial (ref.3), as it did in new Study 3. Other mechanisms may include:

reducing fat mass, fat absorption, adipocyte differentiation and proliferation

and

lipogenesis (ref.1). A number of clinical trials have been conducted, so far

with modest results. A very recently published Taiwanese RCT, for example,

failed to find any benefit from green tea on weight in obese women (ref.4), as

did an Australian trial using modest EGCG doses (ref.5), whereas a benefit

was seen after 12 weeks in obese Japanese adults (ref.6), and after 24 weeks in

obese Japanese children (but only in the more obese of the subjects)

(ref.7). Positive results were reported from three of another four earlier RCTs

(ref.1).

Diabetes

A weight reducing effect might also follow from the impact of tea on glucose

control. There is epidemiological, animal and human clinical evidence that

green tea and to a lesser extent black tea can improve glucose control and

enhance insulin activity, although some RCTs have failed to show any clinical

benefit (ref.8-11). More work needs to be done in this area before we can say

whether there is a real clinical application here or not.

Skin disease

Tea polyphenols may protect against skin cancer and photo-aging. Tea

protects skin against UV radiation damage, and green tea has already found its

way

into skin care products (ref.12, 13). Whilst most of the data is from

laboratory studies, one RCT on subjects with moderate photo-aged skin found

significant histologic improvement in elastic tissue content after a

combination of

topical and oral green tea (ref.14). The mechanisms involve anti-oxidation

countering free radicals, something which applies both to black and green tea

(ref.15, 16), as well as anti-inflammatory and immune modulatory actions

(ref.17, 18). There is some data suggesting EGCG may stimulate hair growth

(ref.19).

Gastrointestinal tract

The antioxidant and anti-cancer effects of tea give rise to potential

benefits in the GIT (ref.20). Tea can change the balance of bowel flora and it

has

been suggested that it could be useful in irritable bowel syndrome (ref.21,

22). Observational data has found an inverse relationship between tea

consumption and chronic liver disease (ref.23). The tea compound theanine has

been

shown in mice to protect against alcohol caused liver damage (ref.24).

A few studies have investigated tea’s therapeutic potential in oral health,

for example to treat oral leukoplakia, prevent oral cancer, dental caries and

periodontal disease (ref.26-29). Not only does tea have useful

anti-microbial properties, but it is also a source of fluoride 30. However, the

evidence

overall of a clinical benefit is not yet convincing (ref.31).

Side-effects and some practical issues

The fact that tea is the most popular drink in the world after water

(ref.16) must provide some comfort in relation to its safety and side-effects.

However, if it is going to be used as a nutraceutical, perhaps in high doses or

in

extracts such as EGCG, this and other practical questions of dosage and

optimal administration have to be looked into.

For example, the question of how adding milk to tea might change its

properties. The answer appears to be not much, although milk can reduce the

anti-oxidant effect of tea somewhat (ref.31, 32).

Safety issues that have been raised include impaired iron absorption,

aluminium or fluoride toxicity, and adverse effects from caffeine (such as

overstimulation of the central and autonomic nervous system) (ref.32).

The phenols in tea can chelate iron in the gut and thus theoretically

contribute to iron deficiency (ref.33). There is some observational data

linking

tea intake with lower iron status in those with marginal iron intake, but other

studies have failed to find any association (ref.34-36). Some remain

unconvinced that this is a practical problem (ref.31), whilst others suggest

that it

may be advisable for people with marginal intake of bioavailable iron to

consume their tea between, rather than with meals (ref.33).

Both fluoride and aluminium tend to accumulate in leaves of the tea plant

and concentrations are higher in tea bags than tea leaves, and in black more

than green tea (ref.32, 37). This presents a theoretical risk of excessive

doses, for example in children, but we found no evidence that this is so in

reality.

In relation to caffeine, black tea has a higher concentration than either

green or oolong, but this is still less than found in coffee (ref.32).

Overall, these dangers seem more potential than actual, certainly at normal

levels of tea consumption (ref.31, 38). Exactly what doses will be needed to

achieve therapeutic effects is still uncertain, although these may well be

greater than typical tea intakes (ref.38).

In summary, tea - both black and green - appears to offer a range of

exciting potential clinical applications, but in all of which a lot more

clinical

trials are needed.

References:

1. Mol Nutr Food Res. 2006 Feb;50(2):176-87.

2. Mol Nutr Food Res. 2006 Feb;50(2):188-210.

3. J Am Coll Nutr. 2007 Aug;26(4):389S-395S.

4. Clin Nutr. 2008 May 9. [Epub ahead of print]

5. J Am Coll Nutr. 2007 Aug;26(4):396S-402S.

6. Obesity (Silver Spring). 2007 Jun;15(6):1473-83.

7. Obesity (Silver Spring). 2008 Mar 20; [Epub ahead of print]

8. Ann Intern Med. 2006 Apr 18;144(8):554-62.

9. J Am Coll Nutr. 2007 Oct;26(5):471-7.

10. Metabolism. 2007 Oct;56(10):1340-4.

11. J Agric Food Chem. 2002 Nov 20;50(24):7182-6.

12. Photodermatol Photoimmunol Photomed. 2007 Feb;23(1):48-56.

13. Skin Pharmacol Appl Skin Physiol. 2001 Mar-Apr;14(2):69-76.

14. Dermatol Surg. 2005 Jul;31(7 Pt 2):855-60; discussion 860.

15. Prev Med. 2005 Jun;40(6):910-8.

16. J Nutr. 2003 Oct;133(10):3285S-3292S.

17. Curr Drug Targets Immune Endocr Metabol Disord. 2003 Sep;3(3):234-42.

18. Arch Dermatol. 2000 Aug;136(8):989-94.

19. Phytomedicine. 2007 Aug;14(7-8):551-5.

20. Eur J Pharmacol. 2004 Oct 1;500(1-3):177-85.

21. J Nutr. 2004 Feb;134(2):473-8.

22. Med Hypotheses. 2006;67(2):419.

23. Gastroenterology. 2005 Dec;129(6):1928-36.

24. Biol Pharm Bull. 2005 Sep;28(9):1702-6.

25. Nutrition. 2002 May;18(5):443-4.

26. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD001829.

27. Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):132-7.

28. J Med Microbiol. 2001 Apr;50(4):299-302.

29. J Periodontal Res. 2002 Dec;37(6):433-8.

30. J Ir Dent Assoc. 1998;44(4):100-5.

31. Eur J Clin Nutr. 2007 Jan;61(1):3-18.

32. J Am Coll Nutr. 2006 Apr;25(2):79-99.

33. Crit Rev Food Sci Nutr. 2000 Sep;40(5):371-98.

34. Eur J Clin Nutr. 2002 May;56(5):379-86.

35. J Hum Nutr Diet. 2004 Feb;17(1):43-54.

36. Eur J Clin Nutr. 2007 Oct;61(10):1174-9.

37. Food Chem Toxicol. 2006 Jul;44(7):1131-7.

38. Alt Med Rev.1999; 4(5): 360-70.

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