Life Extension Magazine®

Issue: Nov 2002

In The News

Aspirin fights cancer; watch out for low antioxidant levels.

Scientifically reviewed by: Dr. Gary Gonzalez, MD, in January 2021. Written by: Life Extension Editorial Staff.

Aspirin fights colon, prostate and pancreatic cancer

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Earlier this year, the U.S. Preventive Services Task Force recommended aspirin for the prevention of heart attack and stroke. Further, it may not be long before doctors are officially told to start advising patients with an elevated risk of certain cancers to take aspirin daily, thanks to recent findings.

Research from Dartmouth Medical School presented at this year’s meeting of the American Association for Cancer Research, in San Francisco, showed that a daily dose of baby aspirin lowered the risk of recurrent colon polyps. Of men and women who had polyps removed, results from a follow-up screening three years later demonstrated that new polyps had developed in only 38% of low-dose aspirin users versus 45% of those taking full-dose aspirin and 47% of a placebo group. Meanwhile, The Mayo Clinic found that NSAIDs (non-steroidal anti-inflammatory drugs), including aspirin and ibuprofen, could reduce prostate cancer risk in men over age 60 by two-thirds [Mayo Clin Proc. 2002;77:219-225]. After tracking more than 1300 men for 5.5 years, researchers found that only 23 NSAID users developed prostate cancer compared to 68 non-users; the benefit also increased with age. The latest findings, from the University of Minnesota, reveal that aspirin may also reduce the risk of pancreatic cancer [JNCI 2002 Aug 7;94(15):1168-1171]. Researchers analyzed aspirin and other NSAID use in over 28,000 postmenopausal women, and discovered that aspirin users had a 43% lower rate of pancreatic cancer than non-users, and that risk reduction increased proportionally to frequency of use. Researchers, however, will contain their enthusiasm about aspirin for cancer prevention, until they weigh all the benefits and risks related to regular aspirin use.

—Angela Pirisi

Low antioxidant levels may contribute to hepatitis C

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It is believed that oxidative stress may play a role in the pathogenesis of viral hepatitis C. Higher rates of lipid peroxidation and lower antioxidant levels, as measured in blood and urine samples, have been noted in the advanced stages of this disease. However, some findings now suggest that damaging oxidative stress may occur much sooner than when disease complications appear (i.e. cirrhosis), and may actually contribute to them. A recent UK study of 42 chronic hepatitis C patients, for example, showed that a lipid peroxidation marker (8-isoprostane) and the ratio of oxidized to reduced glutathione were significantly elevated in both cirrhotic and non-cirrhotic patients [J Hepatol 2002 Jun;36(6):805-11]. Furthermore, antioxidants, including glutathione, selenium and vitamins A, C and E, were significantly decreased compared to controls. The authors concluded that, “Antioxidant therapy may therefore have a role in slowing disease progression to cirrhosis.”

Other researchers have demonstrated a high rate of glutathione turnover in the lymphocytes of hepatitis C patients, which may alter lymphocyte function and facilitate chronic infection [J Hepatol 1999 Nov;31(5):808-14]. Some have found that children with chronic viral hepatitis B and C have significantly lower catalase (CAT) and superoxide dismutase (SOD) activity, and higher glutathione peroxidase (GSH-Px) activity than non-infected children, hinting at compromised antioxidant defenses [Med Sci Monit 2000 Jul-Aug;6(4):713-8]. One theory is that hepatitis C viral proteins (i.e. NS5A) may be what induce oxidative stress [Proc Natl Acad Sci USA 2001 Aug 14;98 (17):9599-604], by upsetting intracellular calcium, thus triggering a jump in reactive oxygen species (ROS) in mitochondria, and activating NF-kappaB and STAT-3 transcription factors.


Heart disease risk and abdominal fat

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Abdominal fat, or visceral fat, has been associated with hypertension, diabetes and cardiovascular disease. Now a new study that looked at a European sample of middle-aged men confirms that abdominal fat is an independent risk factor for heart attack. Body measurements were taken from 1346 healthy Finnish men, aged 42 to 60, to assess their waist-to-hip ratio. Results revealed that, over a 10-year period, those with the highest ratio had nearly three times the risk of heart attack or related coronary events than men with lower ratios [European Heart Journal 2002;23:706-713].

Earlier studies had shown this to be true in men and women [Int J Obes Relat Metab Disord 1999 Jan;23(1):90-7]. In Paris, investigators found that, among 552 men and 160 women at risk for cardiovascular disease, aged 30 to 74, the risks of a coronary event over the next 10 years and a heart attack over the next six years was highest in those with the highest waist-hip-ratio. Meanwhile, data from the Nurses’ Health Study [JAMA 1998 Dec 2;280(21):1843-8] showed that a higher waist-to-hip ratio and waist circumference were independently and strongly related to heart disease risk, even among women with a body mass index of 25 kg/m2 or less.

Other research has shown that visceral fat breeds insulin resistance, which can lead to type 2 diabetes. As study results presented at the this year’s American Diabetes Association’s annual meeting suggest, abdominal fat may be responsible for creating abnormal glucose metabolism by releasing fatty acids into the bloodstream, which then overstimulate the liver’s production of glucose. Abdominal fat has also been associated with increasing vascular stiffness, leading to high blood pressure and its complications, such as heart disease [Hypertension 2001 Sep;38(3):429-33].


Pain killer or cancer treatment?

What a pleasant surprise it was when scientists established that the humble pain killer, aspirin, can be used as a potent weapon against heart attack, stroke and some forms of cancer. Now a related type of painkiller, cyclooxygenase (COX-2) inhibitors—nonsteroidal anti-inflammatory drugs that block the COX-2 enzyme—have joined the ranks of disease-fighting drugs.

The latest evidence points to COX-2 inhibitors to help treat an aggressive form of lung cancer in its early stages. Findings from Cornell University scientists presented at the American Society of Clinical Oncology meeting in Orlando, Florida in May were that administering 400 mg of a COX-2 inhibitor called Celebrex twice daily along with chemotherapy treatment for six weeks helped fight raging lung cancer. Among 16 patients treated, the cancer virtually disappeared in five of them, tumors shrank in five patients, and the disease stabilized in four others. In a third of the patients, they found cancer cell death when their lung tissue was examined under a microscope. The authors suggest, however, that a larger placebo-controlled study will be needed to compare the effects of chemotherapy plus Celebrex to chemotherapy alone.

COX-2 produces an inflammatory, hormone-like byproduct called prostaglandin, which is part of the body’s natural response to injury. In cancer cells, COX-2 is often overexpressed, which leads to the overproduction of prostaglandins. The latter supply blood to cancer cells for growth, keep the immune system from attacking them, and reduce the rate of cancer cell death by setting their internal killer switch to off. COX-2 inhibitors and NSAIDs in general have already been eyed for the prevention of certain cancers, such as colon and breast. Life Extension has recommended COX-2 inhibitors for cancer treatment since 1996.