Highlight HEALTH

With all the recent discussion and debate by the presidential candidates regarding healthcare issues, I thought a study published last month in CA: A Cancer Journal for Clinicians was quite timely. The study, titled Association of Insurance with Cancer Care Utilization and Outcomes, presents evidence that lack of adequate health insurance coverage is associated with reduced access to care and poorer outcomes for cancer patients [1]. The article further presents data on the association between health insurance status and screening, stage at diagnosis and survival for breast and colorectal cancer.

American Cancer Society (ACS) researchers analyzed over half-a-million patient cases using data from the National Cancer Data Base as well as data from the 2005 and 2006 National Health Interview Survey conducted by the National Center for Health Statistics and the Centers for Disease Control and Prevention (CDC). Perhaps not surprisingly, the results show that uninsured individuals are (1) less likely to receive cancer screening, (2) more likely to be diagnosed at an advanced disease stage and (3) less likely to survive than privately insured individuals.

National health survey and healthcare

People who are uninsured or insured by government programs may face significant obstacles obtaining healthcare. Indeed, some physicians do not accept new patients without private insurance or uninsured individuals who are not able to pay the full cost at the time of visit. A recent national survey found that while 96% of office-based physicians were currently accepting new patients, 40.3% indicated they would not accept new charity cases, 25.5% did not accept new Medicaid cases and 13.9% did not accept new Medicare cases [2]. This lack of access to healthcare can have adverse affects on preventive care and management for chronic conditions.

In the present ACS study, analyses of the 2006 National Health Interview Survey showed that 53.6% of uninsured people aged 18 to 64 years had no usual source of healthcare compared to just 9.9% of privately insured and 10.8% of individuals with Medicaid insurance. People who are uninsured were much more likely to report no healthcare visits in the past year than people who are privately- or Medicaid-insured. Compared to insured individuals, people who were uninsured were more likely to report that they did not get care due to cost, delayed care due to cost, did not get prescription drugs due to cost and had no healthcare visits in the past 12 months due to cost.

National health survey and cancer prevention

Up to two-thirds of cancers may be prevented through healthy lifestyle changes. Healthcare visits provide an opportunity for health providers to counsel people on smoking cessation and weight loss. However, uninsured individuals are much more likely to report no healthcare visits in the past 12 months than people who are Medicaid- or privately-insured and are thus much less likely to be advised to quit smoking or to lose weight. Further, analyses of the 2006 National Health Interview Survey showed that the likelihood of receiving recommended cancer screening tests varied by insurance status. Privately-insured women were most likely to have had a mammogram or Pap test, followed by Medicaid-insured women. Similarly, privately-insured men were most likely to have had a test for prostate cancer, followed by Medicaid-insured men. Further, both men and women who were privately insured were most likely to have had a colorectal cancer screening test. In all cases, uninsured individuals were least likely to have had any type of cancer screening.

Health insurance status is associated with other sociodemographic characteristics (e.g. race, level of education). However, when the data was analyzed by race, at every level of education, individuals with health insurance were about twice as likely as those without to have had mammography or colorectal cancer screening. Thus, having health insurance is an important predictor of cancer screening.

Insurance status, cancer stage at diagnosis and survival

ACS researchers also analyzed data from the National Cancer Data Base to investigate the relationship between insurance status, cancer stage at diagnosis and survival. In analyses of cancer survival for all cancers, uninsured individuals and Medicaid-insured individuals were 1.6 times more likely to die in 5 years than those with private insurance. Specifically, 35% of uninsured patients died in five years compared with 23% of privately insured patients. Since cancer screening tests are key to diagnosing and treating cancer in its early stages, not surprisingly people with health insurance were more likely to be diagnosed with early stage disease than individuals without insurance.

These results are consistent with previous studies showing that people who are uninsured or have Medicaid insurance are more likely to be diagnosed with late-stage cancer (breast and cancer of the mouth or throat, respectively) than people who are privately insured [3-4].

According to Dr. Otis Brawley, chief medical officer of the American Cancer Society [5]:

This report clearly suggests that insurance and cost-related barriers to care are critical to address if we want to ensure that all Americans are able to share in the progress we have achieved by having access to high-quality cancer prevention, early detection, and treatment services.

Research has shown that healthy lifestyle changes can prevent cancer. Additionally, advances in cancer detection and treatment have resulted in a decline in US cancer deaths in 2003 and 2004, the first decrease seen since 1930.

The American Cancer Society launched the Access to Care campaign in 2007. Access to Care is a national initiative dedicated to raising awareness about the predicament of uninsured and underinsured people in the United States. The campaign encourages Americans to find ways to fix the problem and make access to healthcare a national priority.

What are your thoughts? How can we reasonably and responsibly make healthcare accessible to everyone?

References

1. Ward et al. Association of insurance with cancer care utilization and outcomes. CA Cancer J Clin. 2008 Jan-Feb;58(1):9-31. Epub 2007 Dec 20.
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2. Hing and Burt. Characteristics of office-based physicians and their practices: United States, 2003–04. Series 13, No. 164. Hyattsville, MD: National Center for Health Statistics. 2007.
3. Halpern et al. Insurance status and stage of cancer at diagnosis among women with breast cancer. Cancer. 2007 Jul 15;110(2):403-11.
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4. Chen et al. The impact of health insurance status on stage at diagnosis of oropharyngeal cancer. Cancer. 2007 Jul 15;110(2):395-402.
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5. Report Links Health Insurance Status With Cancer Care. American Cancer Society News Center. 2007 Dec 20.

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It’s been three months since an article on dichloroacetate (DCA), the chemotherapeutic agent that selectively inhibits cancer cell growth in lung, breast and brain tumor cells grown in culture and lung tumors grown in immunocompromised rats, was published on Highlight HEALTH. Since then, thousands of people have read the article. Indeed, the blogosphere has been buzzing about DCA, unfortunately focusing on a conspiracy theory accusing big pharma of suppressing a cure for cancer instead of recognizing the study for what it is — a preliminary study in cell culture and rats that cannot be translated to humans without further research and clinical trials.

Safe alternative to DCA?

I was curious to see if there were any new developments regarding DCA use in either cancer prevention or the treatment of cancer. A Google search for “dichloroacetate” returned 340,000 pages, but before I had a chance to start browsing, one of the Sponsored Links at the top of the page caught my eye. In addition to a site where you can buy DCA, another site advertised a “safe alternative” to dichloroacetate.

Intrigued, I clicked on the link. The alternative is a “new flavonoid cancer treatment protocol”, which involves nothing more than dissolving 1000 mg of vitamin C in 0.5 L of water and adding the contents of 1 — 2 quercetin (pronounced “kwer-see-tin”) capsules (500 mg — 1000 mg).

Quercetin

A polyphenol, quercetin is one of a number of water-soluble plant pigments called flavonoids (meaning class of plant secondary metabolites known for their antioxidant activity) and is largely responsible for the color of many flowers, fruits and vegetables. High concentrations of quercetin are found in apples, onions, tea and red wine [1]. Quercetin and other flavonoids (also referred to as bioflavonoids) cannot be produced in the human body.

Quercetin is a powerful antioxidant; from a range of dietary flavonoids, quercetin was found to be the most effective inhibitor of oxidative damage to LDL (bad) cholesterol in vitro [2]. In contrast, another study found that quercetin had mostly prooxidant effects [3]. However, when mixed with other phenolic compounds, significant antioxidant capacity was identified, indicating a synergistic effect.

A number of research studies have demonstrated that quercetin is a natural antihistamine and anti-inflammatory [4-6]. Indeed, quercetin is unique in its ability to inhibit TNF-alpha (a cytokine involved in systemic inflammation) gene expression [7]. Studies have also shown that quercetin exhibits anticancer effects [8].

Clinical trials

A number of phase I clinical trials have been performed with quercetin evaluating pharmacokinetics [9] and adenoma regression [10]. A combination of curcumin and quercetin was evaluated to regress adenomas in patients with familialadenomatous polyposis (FAP), an autosomal-dominant disorder characterized by the development of colorectal adenomas and eventual colorectal cancer. The study found that the combination appeared to decreased polyp number and size from baseline after 6 months of treatment [10].

Epidemiologic data indicates that reduction in colorectal cancer risk associated with the highest 25% of data vs. the lowest 25% was largest for quercetin and catechin [11]. Overall, flavonoids showed strong and linear inverse associations with colorectal cancer risk. Large-scale genomic studies in colon cancer cells suggest that quercetin affects the expression of genes involved in cell cycle control [12-13]. Flavonoids also modulate cell cycle progression in prostate cancer cells [14-15].

Antioxidants and cancer

In September 2005, an article published in CA: A Cancer Journal for Clinicians warned against the use of antioxidants in combination with radiotherapy and chemotherapy [16]. Indeed, quercetin may alter the effects of chemotherapy medications used to treat cancer [17]. However, this position has been refuted by others [18] and a recent meta-analysis suggests that antioxidant supplementation does not interfere with therapeutic modalities for cancer and instead enhances the killing of therapeutic cancer agents, decreases modality side effects and protects normal tissue [19-20]. Another meta-analysis reviewing the evidence from randomized controlled trials on the impact of antioxidant supplementation on chemotherapeutic efficacy, although limited by lack of statistical power, found that many of the studies indicated that antioxidant supplementation resulted in either increased survival times, increased tumor responses or both, as well as fewer toxicities than controls [21].

A recent review assessing the contribution of dietary flavonoids to the total antioxidant capacity of plasma in humans concluded that the large increase in plasma total antioxidant capacity observed after the consumption of flavonoid-rich foods is not caused by the flavonoids themselves, but is likely the consequence of increased uric acid levels [22]. A potent antioxidant, uric acid is a normal constituent of the body and is the end product of purine (meaning the nucleotides adenine and guanine, two of the four building blocks of RNA and DNA) metabolism. Because the increased plasma concentration of uric acid is much greater than the concentration of flavonoids, the change in uric acid levels is thought to be responsible for the relatively large increase in plasma total antioxidant capacity after consumption of flavonoid-rich foods. Most uric acid produced in the body is excreted by the kidneys. However, it has been proposed that renal uric acid clearance is regulated by an unknown signal that is issued in response to the level of oxidative stress [23], allowing the kidneys to reabsorb the potent antioxidant when needed.

Flavonoids have been shown to induce detoxifying Phase II enzymes [24-25], indicating that they are recognized by the body as foreign compounds. Thus, it has been proposed that the ability of flavonoids to induce detoxifying enzymes may be a major mechanism by which flavonoids protect against mutagens and carcinogens, and act as cancer chemopreventive agents [22].

References

1. Sampson et al. Flavonol and flavone intakes in US health professionals. J Am Diet Assoc. 2002 Oct;102(10):1414-20.
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2. O’Reilly et al. Flavonoids protect against oxidative damage to LDL in vitro: use in selection of a flavonoid rich diet and relevance to LDL oxidation resistance ex vivo? Free Radic Res. 2000 Oct;33(4):419-26.
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3. Cirico and Omaye. Additive or synergetic effects of phenolic compounds on human low density lipoprotein oxidation. Food Chem Toxicol. 2006 Apr;44(4):510-6. Epub 2005 Oct 10.
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4. Middleton and Drzewiecki. Flavonoid inhibition of human basophil histamine release stimulated by various agents. Biochem Pharmacol. 1984 Nov 1;33(21):3333-8.
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5. Taguchi et al. Pharmacological studies of Houttuyniae herba: the anti-inflammatory effect of quercitrin. Yakugaku Zasshi. 1993 Apr;113(4):327-33.
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6. Loggia Della et al. Anti-inflammatory Activity of Benzopyrones that are Inhibitors of Cyclo- and Lipo-oxygenase. Pharmacol Res Commun. 1988 Dec;20 Suppl 5:91-4.
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7. Wadsworth et al. Effects of Ginkgo biloba extract (EGb 761) and quercetin on lipopolysaccharide-induced signaling pathways involved in the release of tumor necrosis factor-alpha. Biochem Pharmacol. 2001 Oct 1;62(7):963-74.
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8. Morrow et al. Dietary supplementation with the anti-tumour promoter quercetin: its effects on matrix metalloproteinase gene regulation. Mutat Res. 2001 Sep 1;480-481:269-76.
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9. Ferry et al. Phase I clinical trial of the flavonoid quercetin: pharmacokinetics and evidence for in vivo tyrosine kinase inhibition. Clin Cancer Res. 1996 Apr;2(4):659-68.
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10. Cruz-Correa et al. Combination treatment with curcumin and quercetin of adenomas in familial adenomatous polyposis. Clin Gastroenterol Hepatol. 2006 Aug;4(8):1035-8. Epub 2006 Jun 6.
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11. Theodoratou et al. Dietary flavonoids and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):684-93.
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12. van Erk et al. Integrated assessment by multiple gene expression analysis of quercetin bioactivity on anticancer-related mechanisms in colon cancer cells in vitro. Eur J Nutr. 2005 Mar;44(3):143-56. Epub 2004 Apr 30.
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13. Murtaza et al. A preliminary investigation demonstrating the effect of quercetin on the expression of genes related to cell-cycle arrest, apoptosis and xenobiotic metabolism in human CO115 colon-adenocarcinoma cells using DNA microarray. Biotechnol Appl Biochem. 2006 Jul;45(Pt 1):29-36.
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14. Kobayashi et al. Effect of flavonoids on cell cycle progression in prostate cancer cells. Cancer Lett. 2002 Feb 8;176(1):17-23.
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15. Knowles et al. Flavonoids suppress androgen-independent human prostate tumor proliferation. Nutr Cancer. 2000;38(1):116-22.
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16. D’Andrea GM. Use of antioxidants during chemotherapy and radiotherapy should be avoided. CA Cancer J Clin. 2005 Sep-Oct;55(5):319-21.
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17. Desai et al. Human liver microsomal metabolism of paclitaxel and drug interactions. Eur J Drug Metab Pharmacokinet. 1998 Jul-Sep;23(3):417-24.
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18. Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther. 2006 Mar;5(1):63-82.
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19. Simone et al. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, part 1. Altern Ther Health Med. 2007 Jan-Feb;13(1):22-8.
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20. Simone et al. Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2. Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.
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21. Block et al. Impact of antioxidant supplementation on chemotherapeutic efficacy: A systematic review of the evidence from randomized controlled trials. Cancer Treat Rev. 2007 Mar 14; [Epub ahead of print].
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22. Lotito and Frei. Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: cause, consequence, or epiphenomenon? Free Radic Biol Med. 2006 Dec 15;41(12):1727-46. Epub 2006 Jun 3.
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23. Kirschbaum B. Renal regulation of plasma total antioxidant capacity. Med Hypotheses. 2001 Jun;56(6):625-9.
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24. Kong et al. Induction of xenobiotic enzymes by the MAP kinase pathway and the antioxidant or electrophile response element (ARE/EpRE). Drug Metab Rev. 2001 Aug-Nov;33(3-4):255-71.
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25. Walle and Walle. Induction of human UDP-glucuronosyltransferase UGT1A1 by flavonoids-structural requirements. Drug Metab Dispos. 2002 May;30(5):564-9.
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The goal of the annual National Colorectal Cancer Awareness Month is to make people aware of colorectal cancer and to encourage people to learn more about how to reduce their risk of colorectal cancer (CRC) through regular screening and a healthy lifestyle. The results of the National Health Interview Survey (NHIS) administered to 32,374 adults 18 years of age or older in 2000 showed that colorectal cancer screening is underused [1]. Just over 60% of adults had ever had colorectal cancer testing. Only 44% of men and 37% of women greater than 75 years of age were current for testing. Colorectal cancer screening is very important. If colorectal cancer is allowed to metastasize (meaning to spread to other parts of the body), the 5-year survival rate is less than 10%. However, if colorectal cancer is found early, the 5-year survival rate is greater than 90% [2].

Colorectal cancer can be prevented. Colorectal cancer starts in the digestive system and begins as a polyp. Polyps are small growths of tissue that start in the lining and grow in to the center of the colon or rectum. A specific type of polyp, an adenoma, can become cancerous. Screening for colorectal cancer can identify polyps and they can be removed to prevent cancer from ever occurring. Starting at age 50, men and women who are at average risk for colorectal cancer should get screened. Men and women who have a higher risk of the disease may need to be tested earlier and should talk to their health care professional about when. Colorectal cancer incidence rates are also increasing among people younger that 50 years of age. Indeed, colorectal cancer is ranked among the top 10 cancers occurring in males and females aged 20-49 years regardless of race [3]. No matter what your age, know the risk factors, the symptoms and your family history.

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