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Letters to the Editor Issue 153

by Letters(more info)

listed in letters to the editor, originally published in issue 153 - December 2008

Lancet Homeopathy Reviews Seriously Flawed

Two new studies conclude that a review which claimed that homeopathy is just a placebo, published in The Lancet, was seriously flawed.

George Lewith, Professor of Health Research at Southampton University comments: 'The review gave no indication of which trials were analysed nor of the various vital assumptions made about the data. This is not usual scientific practice. If we presume that homeopathy works for some conditions but not others, or change the definition of a 'larger trial', the conclusions change. This indicates a fundamental weakness in the conclusions: they are NOT reliable.'

The background to the ongoing debate is as follows:

In August 2005, The Lancet published an editorial entitled The End of Homeopathy, prompted by a review comparing clinical trials of homeopathy with trials of conventional medicine. The claim that homeopathic medicines are just placebo was based on 6 clinical trials of conventional medicine and 8 studies of homeopathy, but did not reveal the identity of these trials. The review was criticized for its opacity as it gave no indication of which trials were analysed and the various assumptions made about the data.

Sufficient detail to enable a reconstruction was eventually published, and two recently published scientific papers based on such a reconstruction challenge the Lancet review, showing that:
  • Analysis of all high-quality trials of homeopathy yields a positive conclusion;
  • The 8 larger higher-quality trials of homeopathy were all for different conditions; if homeopathy works for some of these but not others the result changes, implying that it is not placebo;
  • The comparison with conventional medicine was meaningless;
  • Doubts remain about the opaque, unpublished criteria used in the review, including the definition of higher quality.
The Lancet review, led by Prof Matthias Egger of the Department of Social and Preventive Medicine at the University of Berne, started with 110 matched clinical trials of homeopathy and conventional medicine, reduced these to 'higher-quality trials' and then to 8 and 6 respectively 'larger higher-quality trials'. Based on these 14 studies, the review concluded that there is "weak evidence for a specific effect of homoeopathic remedies, but strong evidence for specific effects of conventional interventions".

There are a limited number of homeopathic studies, so it is quite possible to interpret these data selectively and unfavourably, which is what appears to have been done in the Lancet paper. If we assume that homeopathy does not work for just one condition (Arnica for post-exercise muscle stiffness), or alter the definition of 'larger trial', the results are positive. The comparison with conventional medicine was meaningless: the original 110 trials were matched, but matching was lost after they were reduced to 8 and 6. But the quality of homeopathic trials was better than conventional trials.

This reconstruction casts serious doubts on the review, showing that it was based on a series of hidden judgments unfavourable to homeopathy. An open assessment of the current evidence suggests that homeopathy is probably effective for a number of conditions including allergies, upper respiratory tract infections and flu, but more research is urgently needed.

Prof Egger has declined to comment on these findings.

References

Lüdtke R, Rutten ALB. The conclusion on the effectiveness of homeopathy highly depend on the set of analysed trials. Journal of Clinical Epidemiology. doi: 10.1016/j.jclinepi.2008.06.015. 2008.
Rutten ALB, Stolper CF. The 2005 meta-analysis of homeopathy: analysis of post-publication data. Homeopathy. doi:10.1016/j.homp.2008.09.008. 2008.

Further Information

Prof George Lewith, Tel: 0044 (0)7970 067884  gl3@soton.ac.uk
Rainer Lüdtke, Tel: 0049 201 5630516  r.luedtke@carstens-stiftung.de
Dr Lex Rutten, Tel: 0031 765 227340  lexrtn@concepts.nl

Source

Healthcare News  news@massmediadistribution.com
Mass Media Distribution LLC, Naples FL 34113 USA.
 

Vitamin C Slows Cancer Down and Can Reverse It as Well

The BBC recently reported(1) that "Vitamin C 'slows cancer growth.' An injection of a high dose of vitamin C may be able to hold back the advance of cancers, US scientists claim. The vitamin may start a destructive chain reaction within the cancer cell." The injection "halved the size" of tumours, and was reported in the Proceedings of the National Academy of Sciences.
 
The study authors themselves said that daily, high-dose vitamin C treatment "significantly decreased growth rates" of ovarian, pancreatic, and malignant brain tumours in mice. Such high, cancer-stopping levels of vitamin C can be "readily achieved in humans given ascorbate intravenously."(2)

"Readily achieved"? Then this is important, absolutely vital news for millions fighting or fearing cancer.

So what do major cancer organizations have to say? Not much. That is disappointing, but hardly surprising. Both the American Cancer Society and Cancer Research UK have downplayed or flatly ignored decades of physician reports and controlled clinical studies indicating that vitamin C stops cancer. What's worse, each of these supposedly comprehensive cancer research and education organizations continues to actively discourage people from using vitamin C against cancer.

Look for yourself and see. The American Cancer Society's vitamin C webpage(3) specifically states: "Although high does of vitamin C have been suggested as a cancer treatment, the available evidence from clinical trials has not shown any benefit." And Cancer Research UK states that "There is currently no evidence from clinical trials in humans that injecting or consuming vitamin C is an effective way to treat cancer."(1)

"No benefit," they say. "No evidence," they say.

Both organizations are wrong. Neither statement is true.
  • In 2008, Korean doctors reported that intravenous vitamin C "plays a crucial role in the suppression of proliferation of several types of cancer," notably melanoma.(4)
  • In 2006, Canadian doctors reported on the effectiveness of intravenous vitamin C in treating cancer. (5)
  • In 2004, doctors in America and Puerto Rico published clinical cases of vitamin C successes against cancer.(6)
  • In 1990, American doctors published their results successfully using vitamin C to treat kidney cancer(7). In 1995 and 1996, other cancers.(8) Using 30,000 mg of intravenous vitamin C twice per week, they found that "metastatic lesions in the lung and liver of a man with a primary renal cell carcinoma disappeared in a matter of weeks. . . We subsequently reported a case of resolution of bone metastases in a patient with primary breast cancer [1A] using infusions of 100 grams, once or twice per week."(9)
  • In 1982, Japanese doctors showed that vitamin C greatly prolonged the lives of terminal cancer patients.(10)
  • And as early as 1976, over two decades ago, physicians in Scotland showed that intravenous vitamin C improved quality and length of life in terminal cancer patients.(11)
Why are ACS and Cancer Research UK oblivious to the weight of evidence? All these previous clinical reports were published in peer-reviewed medical journals. One may bear in mind that both ACS and Cancer UK made their restrictive statements August 2008. Yes, 2008. In spite of increasingly compelling evidence for 22 years, both the American Cancer Society and Cancer Research UK are dragging their feet. Foot-dragging costs lives. Hundreds of thousands of people have died from cancer that could have been helped with ascorbate therapy. But for decades, their three advocated cancer treatments have been "cut, zap, and drug" - surgery, radiation and chemotherapy. The use of high doses of vitamins has been thoroughly excluded.

Indeed, ACS still says: "If a supplement is taken, the best choice for most people is a balanced multivitamin/mineral supplement that contains no more than 100% of the 'Daily Value' of most nutrients."(3) That is harmful advice. Many well designed clinical studies show that large doses of vitamin C and other nutrients improve both quality and length of life for cancer patients. The key is the use of sufficiently high quantities, appropriately administered. More orange juice just won't do it.

Cancer Research UK even maintains(1) that vitamin C "can make cancer treatment less effective, reducing the benefits of radiotherapy and chemotherapy." That statement is untrue.(12,13) Oncologists routinely administer antioxidant drugs along with chemotherapy with no diminution of effect.(14) ACS and Cancer Research UK say that there is "no evidence from clinical trials" that vitamin C is any good against cancer. They should start reading the medical literature. They are way behind the times. And they are wrong. Dead wrong.

References:

(1) BBC NEWS:  http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/7540822.stm Published: Aug 4, 2008.
(2) Chen Q, Espey MG, Sun AY, Pooput C, Kirk KL, Krishna MC, Khosh DB, Drisko J, Levine M. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci U S A. 2008 Aug 4.
(3) www.cancer.org/docroot/ETO/content/ETO_5_3X_Vitamin_C.asp (accessed Aug 12, 2008)
(4) Padayatty et al. Intravenously administered vitamin C as cancer therapy: three cases. Canadian Medical Association Journal, 2006. 174(7), March 28, p 937-942.  www.cmaj.ca/cgi/reprint/174/7/937
(5) Lee SK, Kang JS, Jung da J et al. Vitamin C suppresses proliferation of the human melanoma cell SK-MEL-2 through the inhibition of cyclooxygenase-2 (COX-2) expression and the modulation of insulin-like growth factor II (IGF-II) production. J Cell Physiol. 2008 Jul;216(1):180-8.
(6) Riordan HD, Riordan NH, Jackson JA, Casciari, J.J., Hunninghake, R, Gonzalez MJ, Mora, E.M., Miranda-Massari, J.R., Rosario, N., Rivera, A.: Intravenous Vitamin C as a Chemotherapy Agent: a Report on Clinical Cases. Puerto Rico Health Sciences J, June 2004, 23(2): 115-118.
(7) Riordan HD, Jackson JA, 'Schultz M. Case study: high-dose intravenous vitamin C in the treatment of a patient with adenocarcinoma of the kidney. J Ortho Med 1990; 5: 5-7.
(8) Riordan N, Jackson JA, Riordan HD. Intravenous vitamin C in a terminal cancer patient. J Ortho Med 1996; 11: 80-82. Also: Riordan, N. H., et al. (1995) Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. Medical Hypotheses, 44(3). p 207-213, March.
(9) Riordan NH, Riordan HD, Hunninghake RE. Intravenous ascorbate as a chemotherapeutic and biologic response modifying agentwww.doctoryourself.com/riordan1.html and  www.canceraction.org.gg/recnac.htm . Additional papers may be read at  http://brightspot.org/cresearch/index.shtml .
(10) Murata A, Morishige F and Yamaguchi H. (1982) Prolongation of survival times of terminal cancer patients by administration of large doses of ascorbate. International Journal of Vitamin and Nutrition Research Suppl., 23, 1982, p. 103-113. Also in Hanck, A., ed. (1982) Vitamin C: New Clinical Applications. Bern: Huber, 103-113).
(11) Cameron E and Pauling L. (1976) Supplemental ascorbate in the supportive treatment of cancer: prolongation of survival times in terminal human cancer. Proceedings of the National Academy of Sciences USA. 73:3685-3689. Also: Cameron E and Pauling L. (1978) Supplemental ascorbate in the supportive treatment of cancer: Reevaluation of prolongation of survival times in terminal human cancer. Proceedings of the National Academy of Sciences USA. 75:4538-4542. And: Cameron E and Pauling L. (1981) Survival times of terminal lung cancer patients treated with ascorbate. J. Intern. Acad. Prev. Med. 6: 21-27.
(12) Hoffer A. High doses of antioxidants including vitamin C do not decrease the efficacy of chemotherapy. Townsend Letter for Doctors and Patientswww.doctoryourself.com/chemo.html
(13) Chemotherapy Doesn't Work, So Blame Vitamin C. Orthomolecular Medicine News Service, October 7, 2008.  http://orthomolecular.org/resources/omns/v04n12.shtml
(14) Moss RW. Antioxidants against Cancer. Equinox Press Inc. Brooklyn NY, 2000. ISBN-10: 1881025284; ISBN-13: 978-1881025283. Also: Moss RW. Questioning Chemotherapy. Equinox Press, Brooklyn NY, 1995. ISBN-10: 188102525X; ISBN-13: 978-1881025252.

For more information:

Intravenous vitamin C protocols for cancer treatment are posted at:
 www.doctoryourself.com/riordan1.html
 www.canceraction.org.gg/recnac.htm
 www.doctoryourself.com/cameron.html
Cameron E and Pauling L. Cancer and Vitamin C, revised edition. Philadelphia: Camino Books. ISBN-10: 094015921X; ISBN-13: 978-0940159211. 1993.
Hoffer A and Pauling L. Vitamin C and Cancer: Discovery, Recovery, Controversy. Quarry Press, Kingston, ON. ISBN 1-55082-078-8 Reviewed at  www.doctoryourself.com/hoffer_vitc_can.html 1999.
Riordan HD, Hunninghake, R.E., Riordan NH, Jackson, J.J., Meng, X.L., Taylor, P., Casciari, J.J., Gonzalez MJ, Miranda-Massari, J.R., Mora, E.M., Norberto, R, Rivera, A. Intravenous Ascorbic Acid: Protocol for its Application and Use. Puerto Rico Health Sciences Journal: 22:3. September 2003.

Further Information

Andrew W Saul PhD Editor omns@orthomolecular.org   www.orthomolecular.org

Claims that Statins Lower Heart Attack Risk Misleading

A recent study suggested that statins might be used to avoid the effects of nutritional deficiency. Writing in the New England Journal of Medicine, the Jupiter group described a study of statin drugs in people with high C-reactive protein and low cholesterol.(1) High C-reactive protein levels are associated with inflammation and heart disease/stroke. The authors concluded that, in apparently healthy persons with elevated C-reactive protein levels, rosuvastatin (Crestor) significantly reduced the incidence of major cardiovascular events.

Their much-publicized claim, that this statin lowers the risk of heart attack by approximately one half, is technically correct though highly misleading. The reported annual incidence of coronary events was 37 people in 10,000 (controls) and 17 people in 10,000 (treated). Similar results were reported for risk of stroke. When expressed as a proportion, a 46% improvement (17/37) sounds large. However, an improvement of 20 events (37-17) in 10,000 people known to be at risk is less impressive. Such an improvement means that 500 people (10,000/20) with this increased risk would need to take the tablet daily for a year, to prevent one person suffering an event.

The paper does not explicitly report deaths. One reason for this may be that if a person on statins suffered a heart attack, that person was about three times more likely to die than a control who was not on statins.

The cost of rosuvastatin per person is approximately $1000 per year. So, treating enough people to prevent one heart attack costs $500,000 per year. Since about 70% of the heart attacks were not fatal, prevention of a single death from heart attack would cost even more, approximately $1,700,000. Giving the benefit of the doubt, we may allow for a similar reduction in stroke and say that 'only' $250,000 is needed to protect one person from a stroke or heart attack. It is hardly surprising that Astra Zeneca's share price increased by $1.3 billion dollars on release of this paper and the corresponding media hype.(2)

The media suggested millions of healthy people could cut their risk of heart disease by taking statins.(3) They also claimed that statins could cut the risk of heart attack for "everyone".(4) This is inaccurate and incorrect. The study did not include normal healthy people, only a sample of a relatively small number of people suffering from inflammation (increased C-reactive protein) - a known cause of heart disease and stroke. Out of 89,890 people considered for inclusion, 17,802 people (19.8%) met the specific criteria of poor health for the study. Widespread prescription of statins to healthy people is not supported by these findings.

The fact that statins produce a modest improvement is unsurprising, since they are known to lower inflammation, as do many nutritional supplements. As Bill Sardi has pointed out, Crestor lowered C-reactive protein by 37%, but vitamin E lowers it by 32%,(5) and vitamin C by 25.3%.(6,7) These effects are similar to those of statins and would be expected to provide comparable benefits, without side effects and at a lower cost.

Crestor and other statin drugs have serious side effects. The incidence of established side-effects, such as rhabdomyolysis [the breakdown of muscle fibres resulting in the release of muscle fibre contents (myoglobin) into the bloodstream] (0.3 per 10,000 per year), myopathy (1.1 per 10,000) and peripheral neuropathy (1.2 per 10,000 per year) seems low,(8) but may be underestimated as it takes time to establish long-term side-effects. (The depletion of coenzyme Q10 by statins is a particular concern.) The figures imply that for every ten people who avoid a cardiovascular event, at least one previously healthy person will suffer a non-trivial side effect of the statin drug.

The doctors reported a statistically significant increase (270) in diabetes in the statin group compared to the placebo group (216). Over the course of the study, this corresponds to an increased risk of approximately 61 in 10,000 people. So, the number of people on statins reported to become diabetic was greater than the number that avoided a heart attack! These people might have shorter lives and be at greater risk of heart disease in the long term.

Notably, the Jupiter study was stopped early, which the authors admit prevents assessment of how side-effects might outweigh reported benefits in the longer term. The study was to last 3-5 years and the criteria for stopping were not included in the original published design.(9) The paper claims that when the study was stopped "these [diabetic] events were not adjudicated by the end-point committee". The committee either knew about the diabetes in which case it was considered, or it did not and the committee was not doing its job properly.

The Jupiter name stands for Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin; the reader might think this "justification" sounds more like a marketing plan than a scientific endeavour. The researchers did not address the underlying cause of the inflammation and increased C-reactive protein: they simply treated the condition with drugs. In many cases, raised C-reactive protein is a result of nutritional deficiency.(10)

It is worth mentioning that several nutritional supplements inhibit inflammation and lower C-reactive protein, without causing known side effects. Deficiency in vitamins A,(11) B6, C, E, A, folate, carotenoids and lycopene,(12) and selenium (for example) is associated with raised C-reactive protein.(13,14,15) We suggest that the $250,000 cost of preventing a single cardiovascular event with rosuvastatin might be better spent funding a study of such inexpensive alternatives the deficiency of which may be the cause of the problem.

The people at risk could be encouraged to supplement their diet and restore their health without using these expensive drugs to conceal their underlying sickness.

Stick with the supplements!

References:

(1) Ridker P.M. Danielson E. Fonseca F.A.H. Genest J. Gotto A.M. Kastelein J.J.P. Koenig W. Libby P. Lorenzatti A.J. MacFadyen J.G. Nordestgaard B.G. Shepherd J. Willerson J.T. Glynn R.J. for the JUPITER Study Group (2008) Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein, NEJM, 359(21), 2195-2207.
(2) Mail Online (2008) Crestor news helps AstraZeneca market value leap by more than £1.3bn, 9:25 PM, 10th Nov.
(3) Smith R. (2008) Millions could cut heart attack risk by taking statins, study finds, telegraph.co.uk, 7:55AM GMT, 10 Nov.
(4) Hope J. (2008) The new statin drug that cuts the risk of heart attacks and strokes for EVERYONE, Daily Mail, 11th Nov.
(5) Devaraj S. Tang R. Adams-Huet B. Harris A. Seenivasan T. de Lemos J.A. Jialal I. (2007) Effect of high-dose alpha-tocopherol supplementation on biomarkers of oxidative stress and inflammation and carotid atherosclerosis in patients with coronary artery disease, Am J Clin Nutr, 86(5), 1392-1398.
(6) Block G. Jensen C.D. Dalvi T.B. Norkus E.P. Hudes M. Crawford P.B. Holland N. Fung E.B. Schumacher L. Harmatz P. (2008) Vitamin C treatment reduces elevated C-reactive protein, Free Radic Biol Med, Oct 10. [Epub]
(7) Sardi B. (2008) The Headline You Should Be Reading: Statin Drugs Don't Save Lives And May Increase Your Risk For Diabetes, Knowledge of Health Report, Nov 11.
(8) Law M. Rudnicka A.R. Statin Safety: A Systematic Review, The American Journal of Cardiology, 97(8), Suppl 1, S52-S60.
(9) Ridker P.M. JUPITER Study Group (2003) Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial, Circulation, 108(19), 2292-2297.
(10) Ford E.S. Liu S. Mannino D.M. Giles W.H. Smith S.J. (2003) C-reactive protein concentration and concentrations of blood vitamins, carotenoids, and selenium among United States adults, European Journal of Clinical Nutrition, 57, 1157-1163.
(11) Root M.M. Hu J. Stephenson L.S. Parker R.S. Campbell T.C. (1999) Determinants of plasma retinol concentrations of middle-aged women in rural China. Nutrition, 15, 101-107.
(12) Boosalis M.G. Snowdon D.A. Tully C.L. Gross M.D. (1996): Acute phase response and plasma carotenoid concentrations in older women: findings from the nun study, Nutrition, 12, 475-478.
(13) Friso S. Jacques P.F. Wilson P.W. Rosenberg I.H. Selhub J.(2001) Low circulating vitamin B(6) is associated with elevation of the inflammation marker C-reactive protein independently of plasma homocysteine levels, Circulation, 103(23), 2788-2791.
(14) Devaraja S. Jialal I. (2000) Alpha tocopherol supplementation decreases serum C-reactive protein and monocyte interleukin-6 levels in normal volunteers and type 2 diabetic patients, Free Radical Biology and Medicine, 29(8), 790-792.
(15) Upritchard J.E. Sutherland W.H. Mann J.I. (2000): Effect of supplementation with tomato juice, vitamin E, and vitamin C on LDL oxidation and products of inflammatory activity in type 2 diabetes, Diabetes Care, 23, 733-738.

Further Information

Andrew W Saul PhD, Editor  omns@orthomolecular.org  www.orthomolecular.org/subscribe.html

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