August 2003

Vol. 2     No. 8  

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Lower Cholesterol for Improved Cancer Survival
 

More than 30 years of medical practice have left me with many impressions concerning the treatment of diseases.  I have hesitated to share some of these views because they have yet to be fully established as beneficial by proper scientific research.  Even so, I feel the time has now come to discuss the topic of cholesterol for cancer patients. Fully realizing there is still much research to be done; I leave open the option for me to modify my opinion on this subject in the future. 

Cholesterol in the diet and the cholesterol in the body (as reflected by the blood cholesterol) seem to be tied to the development and progression of cancer.1-5  Some research suggests high blood cholesterol levels may also be tied to a poor prognosis.2,4,5  Over the years, I have noticed that too many of my cancer patients have had high cholesterol levels.  More concerning, too many times I have also observed these elevated levels are resistant to the cholesterol-lowering benefits of a low-fat, no-cholesterol diet.  These observations and evolving scientific research has caused me to become more aggressive when treating my cancer patients – similar to the way I treat my heart patients.  (See my September 2002 Newsletter).

Early Research Shows Diet-Cancer Connection

The first published connection between a high-fat diet and cancer was made in 1930 by Watson and Mellanby in their paper which appeared in the British Journal of Experimental Pathology.6   A diet high in butter fed was found to accelerate the growth of skin cancer in mice treated with cancer-causing tar.  Subsequently, many scientific studies have shown the cancer-promoting effects of excess calories, fat, and cholesterol – hallmarks of the American diet.7

One of the first studies to show the benefits of lowering cholesterol for cancer was also performed on mice.  In 1966 Littman published his work in the journal Cancer Chemotherapy Reports.8  A cholesterol-free, fat-free diet retarded the growth of cancers (sarcomas and carcinomas) and prolonged the survival of these mice with cancer.  The diet cut the tumor growth rate in half (compared to controls) and survival time was often doubled.  The benefits from the diet were attributed to the cholesterol-lowering effects of the cholesterol-free, fat-free diet (rather than the accompanying weight loss).  Also, the absence of cholesterol in the diet appeared to be more important than the absence of fat, because adding cholesterol back to the diet completely reversed the growth inhibition of this approach.  The use of cholesterol lowering agents along with a cholesterol-free diet caused even further tumor inhibition.

How Does Lower Cholesterol Benefit Cancer Patients? 

Cholesterol is required for the growth and survival of cells.9  There is evidence that cancer cells have even higher demands for cholesterol than normal cells. Furthermore, growing cancer cells lose their capacity to synthesize cholesterol, and therefore become dependent upon outside sources of cholesterol – sources such as the diet.  Deprivation of abundant sources of cholesterol slows growth of the tumor, reduces the spread of cancer (metastasis), and prolongs survival of the animal.10

In practical terms, the overall nutritional qualities of a no-cholesterol diet have a major impact on health.  Plant foods have no cholesterol – so by definition in the real world this means a diet that looks a lot like the McDougall diet.

Practical Experience of Cancer Diet Therapy

Worldwide, the intake of cholesterol in the diet correlates directly with the population risks of developing common cancers – like breast, colon and prostate cancer.1  Furthermore, worldwide, people with cancer who follow diets lower in fat and cholesterol and higher in plant foods have a better survival than those on richer diets, loaded with these harmful ingredients.11,12  Multiple studies have been published on the benefits of low-fat, low-cholesterol, high-plant food diets on various kinds of cancers.13-17  Many so called “alternative therapies” for cancer have as their basic treatment a low-fat, low-cholesterol diet. These include the Macrobiotic diet, the Gerson Therapy, the Livingston-Wheeler treatment and the Ornish Diet for prostate cancer.18-20

In most cases when cancer is in an advanced stage it is fatal; however, a patient should never give up hope.  There have been cases where otherwise terminal patients have had a miraculous recovery – described in the medical business as a “spontaneous remission.”21-24  Logically, a patient’s chance of such a miracle happening would be more likely to occur if he or she were in good health and well nourished, than not.

Cholesterol Intervention with Medications

Recommending a healthy low-fat, low-cholesterol diet to patients, even those with serious diseases, like cancer, should be done routinely by doctors.  After all, if you believe diet causes, or at least contributes to the cause of, common cancers, then it makes no sense to “throw gasoline on a fire.” At the very least the patient with cancer will be healthier – and no harm is done.  

However, when it comes to medications then there are always side (undesirable) effects and costs; hopefully, along with real benefits.  Therefore, I have hesitated until now to make recommendations about cholesterol-lowering medications to my patients with cancer.  Let me explain some of the evidence causing me to now act otherwise.

Cholesterol binding resins:

One class of cholesterol-lowering medications works by binding cholesterol and cholesterol precursors (bile acids) in the intestine, preventing their absorption into the body and causing their elimination with the stool.  One of these medications, called cholestyramine (Questran), has been reported to cause regression of prostate cancer in 3 men.25

During a large study of patients for heart disease treatment, the cholestyramine and placebo groups had similar 13.4-year mortality rates from cancer, other medical causes, and trauma and similar cancer incidence rates.26 However, the incidences of benign colorectal tumors (50 vs 34), cancer of the buccal cavity and pharynx (eight vs. two), gallbladder disease (68 vs. 53), and gallbladder surgery (58 vs. 40) were non- significantly increased in the cholestyramine group.  Therefore, this agent is not without risks and would be best used by patients with cancers not related to the gastrointestinal tract.

Statins:

Statins (Mevacor, Lipitor, Pravachol, Zocor, and Lescol for example) lower cholesterol by inhibiting production in the liver.  These medications have been shown to lower cholesterol by 20 to 60% and also reduce the risk of death from heart disease and stroke.27,28 I prescribe these kinds of medications often for my patients at high risk of heart disease (see my September 2002 Newsletter).  They have a record of being quite safe with few side effects.  Pravachol is currently my favorite statin because – even though all statins lower cholesterol -- this kind of medication appears to be most effective at lowering the risk of heart disease.29  It also poses less risk of serious complications such as muscle damage.  There is good evidence that people on these kinds of medications should also be taking a dietary supplement called Co-enzyme Q 10 (ubiquinone 60 mg qid) to help prevent muscle damage.30

In animal studies, Mevacor (lovastatin) has been found to inhibit tumor growth and spread (metastasis) in mice with breast, lung, and melanoma cancers.30-32  Cancer growth inhibition has also been seen with human cancer cells studied in a laboratory.33 Although large studies on heart disease patients have failed to show a reduction in risk of cancer, there is one very encouraging study of patients with liver cancer treated with Pravachol 40 mg/day.34   Survival was doubled. 

My Recommendations

The decision to treat is based on a risk versus benefit calculation.  All cancer patients should be on a low-fat, no-cholesterol, plant-based diet.*  There are numerous qualities of this kind of diet that prevent and slow the growth of cancer (See the McDougall Program for Women book). They should also exercise and give up bad habits like smoking.  A healthy diet and lifestyle provide all benefit at no risk.  All other treatments, such as surgery, radiation, and chemotherapy, must be decided upon based on their own merits.  I strongly encourage you to do research at the National Library of Medicine at www.nlm.nih.gov (free).  I have also discussed many of these treatment issues in my books and newsletter articles – especially the McDougall Program for Women.

I believe people with cancer should make all reasonable and necessary steps to lower their cholesterol levels to 150 mg/dl or lower – the same ideal value I have encouraged for people in general, and especially those interested in heart disease, prevention and treatment. If with diet alone a cancer patient fails to reach this goal, then cholesterol-lowering medications – like statins and/or cholestyramine – should be the next step.  I believe the benefits outweigh the risks for most patients.

Someone diagnosed with cancer has every reason to be as healthy as possible and this means taking the best care of himself – and never giving up.  I believe, based on my experience and what the scientific literature tells, that most cancer patients can prolong their lives dramatically by making the right decisions.  By slowing tumor growth my hope is that recurrences for all my patients can be staved off until their 90th birthdays.

* One word of caution if you change to a healthy diet.  Weight loss often becomes an issue for cancer patients.  Doctors caution against cancer patients losing weight, because in the doctor’s mind weight loss means the terminal days have arrived.  However, this is not the case when weight loss is due to becoming healthier with a plant-based diet and exercise.  Be prepared and guard against this confusion. 

References:

1)  Sidney S.  Cholesterol, cancer, and public health policy. Am J Med. 1983 Sep;75(3):494-508.

2)  Abu-Bedair FA.  Serum lipids and tissue DNA content in Egyptian female breast cancer patients. Jpn J Clin Oncol. 2003 Jun;33(6):278-82.

3)  Mady EA.  Association between estradiol, estrogen receptors, total lipids, triglycerides, and cholesterol in patients with benign and malignant breast tumors. J Steroid Biochem Mol Biol. 2000 Dec 31;75(4-5):323-8.

4) Tartter PI.  Cholesterol and obesity as prognostic factors in breast cancer.  Cancer. 1981 May 1;47(9):2222-7.

5)  Cruse P.  Dietary cholesterol is co-carcinogenic for human colon cancer.  Lancet. 1979 Apr 7;1(8119):752-5.

6)  Watson AF.  Tar cancer in mice. II.  The condition of the skin when modified by external treatment or diet, as a factor in influencing the cancerous reaction.  Br J Exp Pathol.1930; 11:311-328.

7)  Ip C.  Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary carcinogenesis in animals.  Am J Clin Nutr. 1997 Dec;66(6 Suppl):1523S-1529S.

8)  Littman ML.  Effect of cholesterol-free, fat-free diet and hypocholesteremic agents on growth of transplantable animal tumors.  Cancer Chemother Rep. 1966 Jan-Feb;50(1):25-45.

9)  Chen HW. The role of cholesterol in malignancy.  Prog Exp Tumor Res. 1978;22:275-316.

10)  Cruse JP.  Dietary cholesterol deprivation improves survival and reduces incidence of metastatic colon cancer in dimethylhydrazine-pretreated rats. Gut. 1982 Jul;23(7):594-9.

11)  Morrison AS.  Some international differences in treatment and survival in breast cancer.  Int J Cancer. 1976 Sep 15;18(3):269-73.

12)  Chlebowski RT.  Adjuvant dietary fat intake reduction in postmenopausal breast cancer patient management. The Women's Intervention Nutrition Study (WINS).  Breast Cancer Res Treat. 1992 Jan;20(2):73-84.

13)  Rock CL.  Responsiveness of carotenoids to a high vegetable diet intervention designed to prevent breast cancer recurrence.  Cancer Epidemiol Biomarkers Prev. 1997 Aug;6(8):617-23.

14)  Zhang S.  Better breast cancer survival for postmenopausal women who are less overweight and eat less fat. The Iowa Women's Health Study.  Cancer. 1995 Jul 15;76(2):275-83.

15)  Saxe GA.  Diet and risk for breast cancer recurrence and survival.  Breast Cancer Res Treat. 1999 Feb;53(3):241-53.

16)  McDougall JA.  The McDougall Program for Women. Plume 2000.

17)  Cohen LA.  A rationale for dietary intervention in postmenopausal breast cancer patients: an update.  Nutr Cancer. 1993;19(1):1-10.

18)  Kushi LH.  The macrobiotic diet in cancer.  J Nutr. 2001 Nov;131(11 Suppl):3056S-64S.

19)  Weitzman S.  Alternative nutritional cancer therapies.  Int J Cancer Suppl. 1998;11:69-72.

20)  Ornish D.  Dietary trial in prostate cancer: Early experience and implications for clinical trial design.  Urology. 2001 Apr;57(4 Suppl 1):200-1.

21)  Cole WH.  Spontaneous regression of cancer: the metabolic triumph of the host?
Ann N Y Acad Sci. 1974;230:111-41.

22)  Glasser M.  Widespread adenocarcinoma of the colon with survival of 28 years.  JAMA. 1979 Jun 8;241(23):2542-3.

23)  Sperduto P.  Spontaneous regression of squamous cell lung carcinoma with adrenal metastasis.  Chest. 1988 Oct;94(4):887-9.

24)  McDermott WV.  Clear cell carcinoma of the liver with spontaneous regression of metastases.  J Surg Oncol. 1994 Nov;57(3):206-9.

25)  Addleman W.  Cancer, cholesterol and cholestyramine.  N Engl J Med. 1972 Nov 16;287(20):1047.

26)  The Lipid Research Clinics Coronary Primary Prevention Trial. Results of 6 years of post-trial follow-up. The Lipid Research Clinics Investigators.  Arch Intern Med. 1992 Jul;152(7):1399-410.

27)  Hunt D.  Benefits of pravastatin on cardiovascular events and mortality in older patients with coronary heart disease are equal to or exceed those seen in younger patients: Results from the LIPID trial.  Ann Intern Med. 2001 May 15;134(10):931-40.

28)  Sandercock P.   Statins for stroke prevention?  Lancet. 2001 May 19;357(9268):1548-9.

29)  Ichihara K .  Disparity between angiographic regression and clinical event rates with hydrophobic statins.  Lancet. 2002 Jun 22;359(9324):2195-8.

30)  Chan KK.  The statins as anticancer agents.  Clin Cancer Res. 2003 Jan;9(1):10-9.

31)  Brower V.  Of cancer and cholesterol: studies elucidate anticancer mechanisms of statins. J Natl Cancer Inst. 2003 Jun 18;95(12):844-6.

32)  Shibata MA.  Comparative effects of lovastatin on mammary and prostate oncogenesis in transgenic mouse models.  Carcinogenesis. 2003 Mar;24(3):453-9.

33)  Holstein SA.  Synergistic interaction of lovastatin and paclitaxel in human cancer cells.  Mol Cancer Ther. 2001 Dec;1(2):141-9.

34)  Kawata S.  Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial. Br J Cancer. 2001 Apr 6;84(7):886-91.

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