Lancet Antioxidant Cancer Trial Shows BENEFIT, Not Harm

[Guest guest]

from http://www.patrickholford.com

 

 

Lancet Antioxidant Cancer Trial Shows BENEFIT, Not Harm

 

http://us.f529.mail./ym/ShowLetter?MsgId=2327_721923_14118_998_9626_0_5\

4340_21247_806280222 & Idx=4 & YY=56337 & inc=25 & order=down & sort=date & pos=0 & view= & head\

= & box=Inbox

 

 

 

A study, published in the Lancet currently, on antioxidants and

gastrointestinal cancer, is being

claimed to indicate that antioxidants don't reduce risk, and may even

increase cancer risk.

 

However, experts in nutrition and cancer say the study shows nothing

of the sort.

 

In my opinion this is one of the most biased and unsubstantiated

reports on antioxidants I've ever

read. If you look at the actual results of this supposed comprehensive

analysis of research you

will see that the only really significant finding in a considerable

reduction in gastrointestinal

cancer risk with selenium supplementation. Overall, it shows that

antioxidant supplements reduce the

risk of oesophageal cancer, have little effect on pancreatic or

oesophageal cancer, and slightly

increase the risk of gastric cancer. Overall, the clear trend is

towards protection, not harm. I

believe this is an underestimation of the prevention power of

antioxidants because this claimed

comprehensive analysis of research excludes some very well designed

positive studies, such as a trial

of 864 people with a history of colorectal adenomas, by the National

Cancer Institute (1). The

participants were given either 25mg of betacarotene and/or both 100mg

of vitamin C and 400mg of

vitamin E, versus placebo. While there was approximately a halving of

recurrence of colorectal adenomas

in those who took either the betacarotene or vitamin C and E or both,

there was a modest increase

in cancer recurrence among those who only took betacarotene

supplements and both smoked and drank

alcohol every day. Why was this trial excluded? Perhaps it didn't

give the results the

researchers wanted.

 

The final table in the Lancet study, which is the only one showing a

small negative overall effect

on mortality (the difference between 1 in 14 cancer patients on

antioxidants, versus 1 in 15

cancer patients), was arrived at by removing any positive studies on

the grounds of 'low methodological

quality', leaving only 7 studies out of the original 167 studies! Of

these studies, one is quoted

as showing a massive increased risk. Without this study there is no

such effect. However, this

study actual showed the exact opposite. The study in question, Correa

et al (2), published in the

Journal of the National Cancer Institute, gave people with gastric

cancer either beta-carotene,

vitamin C or anti-Helicobacter Pylori treatment (gastric cancer is

increasingly being thought to be

initiated by H.Pylori infection, not antioxidant deficiency). All

three interventions produced

highly significantly improvements, causing substantial regression of

gastric cancer. The authors

conclude " dietary supplementation with antioxidant micronutrients may

interfere with the precancerous

process, mostly by increasing the rate of regression of cancer

precursor lesions, and may be an

effective strategy to prevent gastric carcinoma. " (see abstract below).

 

So, how could this study bias the results towards increased mortality?

For the simple reason that

six people out of 368 treated with antioxidants died, many of whom

were smokers, compared to none

out of 117 people treated with anti- H.Pylori treatment died! The most

logical explanation for

this finding is that, by virtue of participating in this trial, these

patients were excluded from

taking anti- H.Pylori treatment, which is highly recommended for

gastric cancer. It is highly

unlikely that the antioxidants had anything to do with it. The authors

of this study make no reference to

the possibility of antioxidants increasing mortality risk, instead

concluding that both

beta-carotene and vitamin C reduce risk.

 

A review of the Lancet study (also published in the Lancet) by David

Forman and Douglas Altman of

the Centre for Epidemiology and Biostatistics says " The mortality

analysis in this review does not

offer convincing proof of hazard. " In my opinion this is the most

atrocious piece of biased number

crunching, and I'm surprised that the Lancet published it. The funding

source for this trial

should be seriously investigated, just to check it is not as biased as

the rhetoric. Drug companies

have a lot to gain by discrediting nutritional treatments and I have

no doubt that there is an

orchestrated campaign under way to do just this. I certainly won't be

stopping my daily antioxidant

supplement, although I wouldn't advise heavy smokers to supplement

beta-carotene on its own. I would

advise people wanting to reduce their cancer risk to supplement 50 to

150mcg of selenium, together

with other antioxidant nutrients. "

 

Patrick Holford.

 

References

 

1 Baron, J et al., 'Neoplastic and antineoplastic effects of

beta-carotene on volorectal adenoma',

J Natl Cancer Inst. 95, 10, pp. 717-22 (2003).

 

2 Correa P et al., 'Chemoprevention of gastric dysplasia:randomised

trial of antioxidant

supplements and anti-helicobacter pylori therapapy', J Natl Cancer

Inst. 2000 Dec 6;92(23):1881-8.

 

ABSTRACT OF THE CRITICAL STUDY

 

J Natl Cancer Inst. 2000 Dec 6;92(23):1881-8. Chemoprevention of

gastric dysplasia: randomized

trial of antioxidant supplements and anti-helicobacter pylori therapy.

Correa P, Fontham ET, Bravo JC, Bravo LE, Ruiz B, Zarama G, Realpe JL,

Malcom GT, Li D, Johnson

WD, Mera R.Department of Pathology, Louisiana State University Health

Sciences Center, New Orleans,

LA 70112-1393, USA.

 

BACKGROUND: Previous research has identified a high risk of gastric

carcinoma as well as a high

prevalence of cancer precursor lesions in rural populations living in

the province of Narino,

Colombia, in the Andes Mountains. METHODS: A randomized, controlled

chemoprevention trial was conducted

in subjects with confirmed histologic diagnoses of multifocal

nonmetaplastic atrophy and/or

intestinal metaplasia, two precancerous lesions. Individuals were

assigned to receive anti-Helicobacter

pylori triple therapy and/or dietary supplementation with ascorbic

acid, beta-carotene, or their

corresponding placebos. Gastric biopsy specimens taken at baseline

were compared with those taken

at 72 months. Relative risks of progression, no change, and regression

from multifocal

nonmetaplastic atrophy and intestinal metaplasia were analyzed with

multivariate polytomous logistic

regression models to estimate treatment effects. All statistical tests

were two-sided. RESULTS: All three

basic interventions resulted in statistically significant increases in

the rates of regression:

Relative risks were 4.8 (95% confidence interval [CI] = 1.6-14.2) for

anti-H. pylori treatment, 5. 1

(95% CI = 1.7-15.0) for beta-carotene treatment, and 5.0 (95% CI =

1.7-14.4) for ascorbic acid

treatment in subjects with atrophy. Corresponding relative risks of

regression in subjects with

intestinal metaplasia were 3.1 (95% CI = 1.0-9.3), 3.4 (95% CI =

1.1-9.8), and 3.3 (95% CI = 1.1-9.5).

Combinations of treatments did not statistically significantly

increase the regression rates.

Curing the H. pylori infection (which occurred in 74% of the treated

subjects) produced a marked and

statistically significant increase in the rate of regression of the

precursor lesions (relative

risks = 8.7 [95% CI = 2.7-28.2] for subjects with atrophy and 5.4 [95%

CI = 1.7-17.6] for subjects

with intestinal metaplasia). CONCLUSIONS: In the very high-risk

population studied, effective

anti-H. pylori treatment and dietary supplementation with antioxidant

micronutrients may interfere with

the precancerous process, mostly by increasing the rate of regression

of cancer precursor lesions,

and may be an effective strategy to prevent gastric carcinoma

 

1. Baron, J et al., 'Neoplastic and antineoplastic effects of

beta-carotene on volorectal

adenoma', Journal of the National Cancer Institute 95, 10, pp. 717-22

(2003).