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In This Issue:
Dramatic Increase in U.S. Liver Cancer Rates
Alan Franciscus, Editor-in-Chief
Disability & Benefits:
Government Plans Updated for 2009
Jacques Chambers, CLU
HealthWise: Depression and Hepatitis C
Lucinda Porter, RN
New Insights into HBV/HCV Coinfection
Omega-3ís Protect Liver
Alan Franciscus, Editor-in-Chief
HCV Advocate Eblast
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Dramatic Increase in U.S. Liver Cancer Rates
Alan Franciscus, Editor-in-Chief
The incidence of hepatocellular carcinoma (HCC or liver cancer) in the United States has seen a dramatic increase between 1975 and 2005, according to a recent study. However, as the rates of HCC have been rising, the same study found that people with HCC are living longer.
HCC is the third leading cause of cancer deaths worldwide with the highest incidence reported in East Asia. In the United States the incidence of HCC has been historically lower, but it is now increasing dramatically.
Hepatocellular Carcinoma Incidence, Mortality, and Survival Trends
In the Journal of Clinical Oncology a study titled “Hepatocellular Carcinoma Incidence, Mortality, and Survival Trends in the United States from 1975 to 2005,” by Alterkruse and colleagues, analyzed data from the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) registries.
The study found that between 1975 to 2005 the rates of HCC tripled from 1.6 per 100,000 people to 4.9 per 100,000. But deaths due to HCC actually declined between 1992 and 2004 – the 2-to 4-year HCC survival rates actually doubled. The authors noted that this was most likely due to earlier diagnosis and treatment of HCC.
The study did not factor in the causes of HCC, but it was speculated that the increase was probably due to the higher incidence of chronic hepatitis B and chronic hepatitis C. Asian Pacific Islanders and Hispanics were found to have a higher rate of liver cancer and death caused by HCC, but, similar to the overall findings, there was a decrease in deaths related to HCC.
A separate analysis of birthplace was also conducted – information was available for 81% of persons diagnosed between 2000 and 2005. Thirty-one percent were found to have been born outside the U.S. Of those, 80% were Asian Pacific Islanders and 40% were Hispanic. In the same analysis, it was found there was a noticeable increase in the rates of liver cancer among Hispanic, black, and white middle-aged men that the authors believed is related to the hepatitis C epidemic during the 1960’s.
The authors concluded:“This report provides reason for optimism that, with more HCC screening of high-risk groups and treatment of low-stage disease, the burden of HCC can be lessened.”
J Clin Oncol 27:1485-1491. March 20, 2009
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Disability & Benefits:
Government Plans Updated for 2009
Jacques Chambers, CLU
Social Security and Medicare revise their benefits at the beginning of each year to update the programs for inflation. Some numbers are based on the Federal Poverty Level table which does not come out until April of each year.
For 2009, they have applied an inflation factor of 5.8%. which is the highest in several years. Those of you who are collecting Social Security benefits, either disability, retirement or spouse & children benefits should have already received a letter announcing the amount of your benefit for 2009. There are other numbers that change as well due to this inflation adjustment. Below is a quick rundown of the numbers affecting people on or considering Social Security Disability or Retirement:
One-Time Economic Stimulus Payment: As part of the recently passed Economic Stimulus Package, all persons receiving a Social Security benefit, either retirement, disability or other monthly payment will receive an additional payment of $250 sometime during May, 2009.
Social Security Benefits
Supplemental Security Income (SSI): The federal contribution for SSI, the needs based benefits for aged (65+) and disabled, is increased to $674 for an individual and $1,011 for a couple. Note that this is only the federal portion of SSI payments.
Many states including California and New York supplement the federal SSI payment with an additional payment, called SSP. However, with many states having budget problems this year, look for some changes in your state’s contribution. For example, in California, the state benefit has been reduced by the amount of the federal Cost of Living Increase so there is effectively no increase in SSI/SSP payments in California.
The Resource Limit remains at $2,000 for an individual and $3,000 for a couple.
Working Disabled: For persons collecting Social Security Disability (SSD) benefits, the minimum monthly amount they must earn for the month to count as a Trial Work Month is $700 per month. There are nine Trial Work Months in a Trial Work Period during which a beneficiary can earn unlimited amounts without affecting the Disability Benefit amount.
The Substantial Gainful Activity (SGA) amount for 2009 is $980 per month for a disabled person and $1,640 for a blind beneficiary. Social Security disability benefits will continue after the Trial Work Period if the earnings remain below the SGA.
The amount that students can earn without affecting their SSI benefit is $1,640 per month up to $6,600 per year. This allows students collecting SSI to earn more money during school breaks.
As part of the Medicare Modernization Act, many of the numbers used in Medicare are also tied to inflation.
Medicare Premiums for 2009
Part A: (Hospital Insurance) Premium
Most people do not pay a monthly Part A premium because either they or a spouse has 40 or more quarters of Medicare-covered employment.
For persons age 65 and over or for disabled persons who have returned to work and continued their Medicare for the maximum 93 months after the Trial Work Period, premiums may be charged based on the number of quarters/credits they earned while working:
- The Part A premium is $244.00 for people having 30-39 quarters of Medicare-covered employment.
- The Part A premium is $443.00 per month for people who are not otherwise eligible for premium-free hospital insurance and have less than 30 quarters of Medicare-covered employment.
Part B: (Medical Insurance) Premium
$96.40 per month which is normally taken out of your Social Security benefit payment. HOWEVER, Medicare is now tying the premium for Part B to the beneficiary’s total income. If your income is less than $80,000 (single) or $160,000 (married couple), then your Medicare Part B premium will be $96.40 per month.
If Your Yearly Income Is
$85,000 or less
$170,000 or less
If You Are Married but You File a Separate Tax Return from Your Spouse and Your Yearly Income Is
$85,000 or less
Medicare Deductible and Coinsurance Amounts for 2009
Part A: (pays for inpatient hospital, skilled nursing facility, and some home health care) For each benefit period Medicare pays all covered costs except the Medicare Part A deductible (2009 = $1,068) during the first 60 days and coinsurance amounts for hospital stays that last beyond 60 days and no more than 150 days.
For each benefit period you pay:
- A total of $1,068 for a hospital stay of 1-60 days.
- $267 per day for days 61-90 of a hospital stay.
- $534 per day for days 91-150 of a hospital stay (Lifetime Reserve Days).
- All costs for each day beyond 150 days
Skilled Nursing Facility Coinsurance
- $133.50 per day for days 21 through 100 each benefit period.
Part B – Medical Insurance: (covers Medicare eligible physician services, outpatient hospital services, certain home health services, durable medical equipment)
- Calendar Year Deductible - $135.00 per year. (Note: You pay 20% of the Medicare-approved amount for services after you meet the $135.00 deductible.)
- Coinsurance remains generally at 80% of the Medicare allowable amount
Part D – Prescription Drug Coverage: The regular enrollment period just closed on 01-01-09. Only people just becoming eligible for Medicare or persons who qualify for the Special Enrollment Period may enroll in a Part D plan before the next open enrollment which begins on 11-15-09 for a January 1, 2010 effective date.
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Depression and HCV
—Lucinda Porter, RN
May is Mental Health Month. In the U.S., roughly one in five experience some sort of mental illness. Depression is the most widespread psychiatric condition. Those with chronic hepatitis C virus infection (HCV) frequently experience depression.
Depression is common in the general public, with sources reporting from 5% to 20%. That number increases for those living below the poverty level. Women, non-Hispanic blacks and those ages 40-59 have higher depression rates. The World Health Organization reports that depression is the leading cause of disability worldwide.
The number of people with depression and HCV is, quite frankly, depressing. Sources report numbers ranging from 25% to 70%. Additionally, as many as 3 out of 4 patients who undergo HCV treatment may experience neuropsychiatric problems. These are astonishing figures, but fortunately researchers are gaining insight into depression related to HCV and its treatment.
HCV may affect brain function by interfering with several neurochemical activities. These interferences may explain depression as well as cognitive problems such as impaired concentration or memory. Interferon, one of the major components of HCV therapy, also affects the brain and nervous system. Preliminary studies are looking at the possibility of a genetic marker that may predispose some to HCV treatment-induced depression.
The jury is still out on whether a history of depression increases the risk of interferon-related depression. Some studies say yes; others say no. Ditto for higher doses. There is no apparent difference for depression risk between peginterferon and unmodified interferon.
Seek immediate professional help if you have thoughts of suicide or hurting yourself or others.
Here is what we do know:
- Depression increases with longer treatment durations.
- There is an increased risk for interferon-induced depression when there is a previous history of depression caused by HCV therapy.
- Depression risk does not seem to increase with past history of chemical dependency as long as patients refrain from substance use during treatment.
- Having mild-to-moderate depression at baseline is a major risk factor for severe depression during HCV treatment. This does not mean that a patient with mild-to-moderate depression cannot be treated, but these patients do need to be monitored very closely by a psychiatrist as well as their liver specialist.
- HCV medication-related depression tends to show up around 3 months after starting treatment, leveling off around 6 months.
The impact of ribavirin on depression is not well-studied, making it impossible to draw conclusions at this time. Higher incidences of anxiety and irritability may be associated with ribavirin.
Symptoms of Depression
In Darkness Visible, author William Styron described depression as “the gray drizzle of horror.” Less poetically, depression presents itself in many ways, such as persistent sadness, anxiety, irritability or decreased energy. The notion of persistence is important when defining depression because all humans occasionally feel sad or irritable.
Feelings of anxiety or sadness that last for more than a few weeks may signal depression. HCV-related depression may have features of hypomania or mania. The National Institute of Mental Health publication Depression liststhe following common symptoms of depression:
- Feeling sad or “empty”
- Fits of crying with no reasonable explanation
- Feeling hopeless or pessimistic
- Feelings of guilt, worthlessness, or helplessness
- Feeling anxious, irritable, or restless
- Loss of interest or enjoyment in hobbies, social activities, or sex
- Fatigue or decreased energy
- Poor memory, difficulty concentrating, and decision-making problems
- Insomnia or other sleep-related problems
- Appetite loss and/or weight loss
- Overeating and/or weight gain
- Thoughts of death or suicide; suicide attempts
Men may experience depression differently than women do. Men report fatigue, irritability, sleep problems and loss of interest in areas that used to provide pleasure. They are more likely to use substances such as alcohol or drugs or throw themselves into their work. When depressed, men may be easily frustrated, angry, or abusive. Women are more likely to feel sad, worthless or excessively guilty. Women are more likely to attempt suicide but men are more likely to die by that means. In the general population women are at higher risk for depression. However with HCV treatment-induced depression, the risk is the same for both sexes.
Even though science shows a connection between depression and HCV and its treatment, it is vital that we don’t automatically assume that HCV is the cause of our depression. There are many risk factors for it, such as socioeconomic circumstances, medical causes and the various situations that life presents us. HCV may be another risk factor, but it isn’t the only one.
Depression Prevention and Treatment
Let’s start with what we know. Patients with a previous history of HCV treatment-induced depression are strongly encouraged to start antidepressant medications at least 2 weeks prior to retreatment. What we don’t know is whether to recommend prophylactic antidepressant use for everyone.
Since depression might not occur, it makes sense to wait and see. Fortunately, when depression is induced by HCV treatment, antidepressant medication seems to work fairly quickly (1 to 2 weeks versus 4 or more weeks for nontreatment-related depression). However, those who have concerns about depression may feel strongly about the need to use antidepressants even without a known risk. Your medical provider should be able to help you decide which course to take.
There are a number of antidepressants on the market. Generally, medications known as selective serotonin reuptake inhibitors (SSRIs) are prescribed. SSRIs have slightly different features, and recommendations will be made based on your medical history. Nefazodone carries a liver failure risk. Duloxetine has a risk of liver toxicity and steatosis, or fatty liver. Bupropion may be associated with an increased risk of interferon-related seizures. Mirtazapine may decrease white blood cell count, which is already an HCV treatment risk.
Antidepressants have potential side effects. If you have specific concerns about a particular antidepressant, read the product information and discuss these concerns with your medical provider. A pharmacist is also a good resource. Links to information about SSRIs and depression are provided at the end of this article.
Never stop antidepressant medications on your own. Sometimes patients have a hard time stopping them after HCV-treatment has ended. Some clinicians suggest staying on antidepressants for 3 to 6 months after treatment ends. Some patients may need to continue antidepressant medication for a year.
There are no proven non-drug or alternative treatments for interferon-related depression.
Social support may reduce depression risk. Activities which stimulate positive neurochemicals may also help.
Here are some suggestions to help yourself during treatment. These are not substitutes for medical treatment, but ways that might make a difference in how you feel.
- Join an HCV support group
- Seek support from your family and friends
- Avoid or reduce stress
- Try to be physically active a little bit every day
- Get at least 8 hours of sleep every night
- Avoid alcohol and non-prescribed substances
- Eat healthy foods
- Find ways to laugh and amuse yourself
- Avoid isolation
- Balance rest and activity
- Practice positive thinking
Depression is a medical condition. It can be treated. You don’t snap out of it merely by positive thinking. If we could, we would. If you think you may be depressed, talk to a professional. Life is too short to suffer unnecessarily.
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New Insights into HBV/HCV Coinfection
Due to similar transmission routes, many people are exposed to both hepatitis B virus (HBV) and hepatitis C virus (HCV). Some people acquire both viruses at the same time, while others become infected sequentially (superinfection).
While about 75% of people with acute hepatitis C go on to develop chronic infection, most adults with acute hepatitis B (unlike children) spontaneously clear the virus. It is estimated that as many as 20% of people with chronic hepatitis B may be coinfected with HCV and up to 10% of individuals with hepatitis C also have hepatitis B, though the latter figure is likely considerably higher if “occult” HBV (low-level HBV DNA despite undetectable hepatitis B antigens) is included.
Dual infection with HBV and HCV can lead to more rapid liver disease progression, but treatment can be a challenge since suppressing one virus can lead to enhanced activation of the other.
Numerous studies have shown that HBV and HCV interact in such a way that each virus inhibits the other’s replication.
Among participants in the REVEAL-HBV trial in Taiwan, coinfected hepatitis B patients were significantly less likely than HBV monoinfected people to have detectable HBV viral load, and serum HBV DNA levels rose as HCV RNA levels fell. Coinfected people are also more likely to experience spontaneous HBV surface antigen (HBsAg) and “e” antigen (HBeAg) seroconversion than those with HBV alone.
Active HBV replication also has an inhibitory effect on HCV. In an Italian study described in the April 2009 issue of Hepatology, E. Sagnelli and colleagues found that among 24 chronic hepatitis C patients with long-term follow-up, all became HCV RNA negative during acute HBV superinfection, 71% still had undetectable HCV RNA after one year, and 25% were still undetectable after 3-6 years. Interestingly, coinfected patients were five times more likely than those without HCV to experience severe liver disease during acute HBV infection.
How HBV and HCV influence one other is not fully understood. Several studies have suggested a direct effect; for example, the hepatitis C core protein (especially of HCV genotype 1) appears to suppress HBV replication by interfering with gene expression and transcription.
While Spanish researchers found HBV and HCV coexisting in hepatocytes from liver biopsies of coinfected patients, with dually infected cells having lower levels of both HBV DNA and HCV RNA, a Swiss-German team recently showed that HBV and HCV could multiply in the same cells in an in vitro cell culture, and inhibition of one virus did not affect the replication or gene expression of the other. The investigators concluded, therefore, that the viral interference observed in coinfected patients is “probably due to indirect mechanisms” mediated by host immune responses.
Although HBV and HCV inhibit one another, dual infection is associated with more aggressive liver disease progression, and several studies have shown that HBV/HCV coinfected individuals have higher rates of both liver-related and all-cause mortality than people with either virus alone.
Simultaneous acute infection, or acute superinfection with a second virus, can lead to life-threatening fulminant hepatitis. In a Taiwan study of patients superinfected with HCV after HBV, for example, Y.F. Liaw and colleagues found that 11% experienced rapid liver failure and 10% died.
HBV/HCV coinfected individuals more often experience ALT elevation, indicating liver inflammation. In addition, they may have altered immune cytokines—including higher levels of tumor necrosis factor-alpha, transforming growth factor-beta, and interleukin 1, 6, and 8 than monoinfected individuals—which may help explain differences in viral replication and disease progression.
Untreated patients with chronic dual HBV/HCV infection are more likely to develop advanced fibrosis, and do so more rapidly than people with either virus alone. In Liaw’s study, about half of coinfected patients developed cirrhosis over 10 years of follow-up. In a U.S. study by National Institutes of Health researchers, 44% of coinfected patients developed cirrhosis compared with 21% of HBV monoinfected individuals; among cirrhotic patients, those with dual infection were disproportionately likely to progress to liver decompensation (24% vs. 6%, respectively).
Likewise, HCC is also more common in HBV/HCV coinfected people than HBV or HCV monoinfected individuals. In Liaw’s study, 14% of coinfected patients developed HCC after 10 years of follow-up, and 32% did so after 20 years. An Italian study found that over a decade, HBV/HCV coinfected patients had a cumulative HCC risk of 45%, compared with 16% for HBV monoinfected individuals and 28% for those with HCV alone.
Even past HBV infection increases the risk of liver disease progression in people with chronic hepatitis C. Occult HBV has been linked to more severe liver inflammation, more rapid fibrosis progression, and higher HCC risk, though some studies have observed little or no effect.
Treating HCV/HBV Coinfected Patients
Since HBV/HCV coinfected individuals are at greater risk for disease progression, patients with detectable HBV DNA and/or HCV RNA should be considered for treatment.
With regard to hepatitis B, U.S., European, and Asian guidelines recommend treatment for people with moderate to severe liver inflammation or fibrosis. While there are no specific guidelines for HBV/HCV coinfection, many experts use the same criteria. Since interferon is an immune modulator used to treat both HBV and HCV—unlike the directly targeted anti-HBV nucleoside/nucleotide analogs—it may be particularly beneficial for coinfected patients.
Turning to hepatitis C, HBV/HCV coinfected patients respond best to pegylated (vs. conventional) interferon and to combination therapy that includes ribavirin. Several studies have found lower sustained virological response (SVR) rates in coinfected patients compared with HCV monoinfected individuals, but others have seen little difference. Interferon-based therapy may lead to HBV DNA clearance and HBsAg loss, but in other cases it can cause HBV reactivation (“flares”) as HCV is cleared.
As reported in the November 2008 Journal of Hepatology, the German HEP-NET B/C Coinfection Study Group assessed the safety and efficacy of pegylated interferon alfa-2b (PegIntron) plus weight-adjusted ribavirin for 48 weeks in 19 coinfected patients (10 with HCV genotype 1). In an intent-to-treat analysis, 74% achieved SVR and 63% experienced biochemical response; among adherent patients, sustained response rates rose to 86% for genotype 1 and 100% for genotype 2 or 3.
Among participants with available data, two of the five individuals who started the study with detectable HBV viral load achieved undetectable HBV DNA, but four of the five with initially undetectable HBV viral load became HBV DNA positive. “HBV replication may increase after the clearance of HCV, and thus close monitoring for both the viruses is recommended,” the investigators concluded.
In the largest HBV/HCV coinfection treatment trial to date, reported in the February 2009 Gastroenterology, C.J. Liu and colleagues evaluated interferon-based therapy in 321 patients in Taiwan with active chronic hepatitis C patients, half of whom were also HBsAg positive; in addition, 6% of HBsAg negative patients were found to have occult HBV. Participants received 180 mcg/week pegylated interferon alfa-2a (Pegasys) plus 1,000-1,200 mg/day weight-adjusted ribavirin for 48 weeks (genotype 1) or 800 mg/day ribavirin for 24 weeks (genotype 2 or 3).
In an intent-to-treat analysis, SVR rates were similar in the HBV/HCV coinfected and HCV monoinfected groups (72% vs. 77%, respectively, for genotype 1; 83% vs. 84% for genotype 2 or 3). These rates are higher than those typically seen in studies of Caucasians and African-Americans, but not unusual for studies of Asians.
In contrast with some prior research, Liu and colleagues found that HBV/HCV dually infected patients “clear HCV equally as well as HCV monoinfected individuals,” Stuart Gordon and Kenneth Sherman wrote in an editorial accompanying the report, “but a dark side of this therapy was also exposed.”
Looking at hepatitis B markers, 11% of coinfected participants achieved HBsAg clearance and 44% experienced anti-HBs seroconversion by the end of follow-up. However, about one-quarter of coinfected patients still had persistent ALT elevation after achieving SVR, and 76% of this group were found to have detectable HBV DNA.
Among patients with detectable HBV viral load prior to treatment, 56% achieved HBV DNA suppression by the end of follow-up. But 36% of individuals who did not have detectable HBV DNA at baseline did so after treatment. HBV reactivation was not associated with large ALT increases or clinical symptoms during the study period, but it remains to be seen whether it will lead to accelerated disease progression over the long term.
Adding an anti-HBV nucleoside/nucleotide analog may be an effective approach for treating patients with dual active HCV and HBV, as well as reducing the risk of HBV reactivation in people with undetectable pre-treatment HBV viral load.
A few studies have shown that adding lamivudine (Epivir-HBV) to conventional or pegylated interferon contributed to HBV DNA clearance and ALT normalization in people with dual active viruses. More recently, French researchers described an HBV/HCV coinfected patient treated with interferon-based therapy plus adefovir who did not experience HBV reactivation after HCV clearance.
If liver disease progresses to an advanced stage before or despite treatment, HBV/HCV coinfected patients may actually fare better and survive longer after liver transplantation than those with hepatitis B or C alone, according to two recent studies.
In summary, although HBV and HCV can interact, with each virus suppressing the other, dually infected individuals are nevertheless prone to more rapid and severe liver disease progression. Because they have an elevated risk of cirrhosis and HCC, coinfected patients should receive regular liver function monitoring and cancer screening.
While there are no established guidelines for treating HBV/HCV coinfected people, studies indicate that standard hepatitis B and C therapies are effective for this population. Caution is necessary, however, since hepatitis C treatment can lead to HBV reactivation when the suppressive effect of HCV is lost; though there is less evidence, the reverse may also occur.
In their Gastroenterology editorial, Gordon and Sherman offered more questions than answers. As we enter a “new HCV antiviral era” that may include HCV protease or polymerase inhibitors, they asked “how will these new agents interact with HBV in the coinfected population?”
- P. Bellecave, et al. Hepatitis B and C virus coinfection: A novel model system reveals the absence of direct viral interference. Hepatology. March 16, 2009 (Epub ahead of print).
- S.D. Crockett and E.B. Keeffe. Natural history and treatment of hepatitis B virus and hepatitis C virus coinfection. Annals of Clinical Microbiology and Antimicrobials 4: 13. September 13, 2005.
- S.C. Gordon and K.E. Sherman. Treatment of HBV/HCV Coinfection: Releasing the Enemy Within. Gastroenterology 136(2): 393-396. February 2009.
- C.J. Liu et al. Peginterferon alfa-2a plus ribavirin for the treatment of dual chronic infection with hepatitis B and C viruses. Gastroenterology 136(2): 496-504. February 2009.
- Potthoff, et al. The HEP-NET B/C co-infection trial: A prospective multicenter study to investigate the efficacy of pegylated interferon-alfa2b and ribavirin in patients with HBV/HCV co-infection. Journal of Hepatology 49(5): 688-694. November 2008.
- E. Sagnelli, et al. HBV superinfection in HCV chronic carriers: A disease that is frequently severe but associated with the eradication of HCV. Hepatology 49(4): 1090-1097. April 2009.
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Omega-3’s Protect Liver
Alan Franciscus, Editor-in-Chief
In the last few years omega-3 fatty acids have been in the news as the next best thing to help manage and treat a wide variety of health-related issues. Usually when this type of hype builds up on anything it is difficult to separate fact from fiction. But omega-3’s just might buck this trend because there is a good amount of scientific data that is confirming some of the claims made in the last few years. For instance, omega-3 fatty acids have been found to improve the overall health of the heart by lowering unhealthy cholesterol and blood pressure. Some research has also found that omega-3’s may even help to lower the risk of stroke. In this article I will explore some of the facts of omega 3’s and how these relate to the liver – namely fatty liver disease and insulin resistance, two factors that greatly affect HCV disease progression and treatment outcome.
On February 15, 2009 a report was published about the potential benefits of omega-3 fatty acids on fatty liver disease and insulin resistance – at least in mice. In the study, A. Gonzalez-Periz and colleagues tested the effect of omega-3 fatty acids on obesity and fatty liver disease in mice. What they found out is that two types of lipids found in omega-3 fatty acids – protectrins and resolvins may reduce the effects of certain complications of obesity, namely fatty liver and insulin resistance. Although the study has not yet been conducted in humans it does lend some evidence to the growing body of literature showing the benefits of omega-3 fatty acids. This study clearly shows that the next step would be to study omega-3’s in humans and hopefully in people with HCV. There is a real need for new approaches to counter some of the negative effects of obesity in people with hepatitis C since fatty liver and insulin resistance clearly have a dramatic effect on HCV disease progression and treatment outcome.
Discussed below is a simple overview of omega-3 fatty acids – what they are, and potential benefits and risk, both in the general population and for people with liver disease.
Omega-3 fatty acids are a family of unsaturated fatty acids consisting of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) that are essential to overall human health. Omega-3 fatty acids are not made by the body so they must be obtained from food or supplements. The best sources of omega-3’s are fatty fish such as mackerel, lake trout, herring, sardines, albacore tuna and salmon. Alpha-linolenic acid (LNA) is another source – when LNA is eaten the body converts LNA to EPA and DHA. Sources of LNA from plant sources include soybeans, canola, walnut and flaxseed and the oils made from these plants.
In September 8, 2004 the Food and Drug Administration (FDA) issued a statement on the health claims of omega-3 fatty acids. The language of the announcement is below:
The Food and Drug Administration (FDA) today announced the availability of a qualified health claim for reduced risk of coronary heart disease (CHD) on conventional foods that contain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) omega-3 fatty acids.
Typically, EPA and DHA omega-3 fatty acids are contained in oily fish, such as salmon, lake trout, tuna and herring. These fatty acids are not essential to the diet; however, scientific evidence indicates that these fatty acids may be beneficial in reducing CHD.
“Coronary heart disease is a significant health problem that causes 500,000 deaths annually in the United States,” said Dr. Lester M. Crawford, Acting FDA Commissioner. “This new qualified health claim for omega-3 fatty acids should help consumers as they work to improve their health by identifying foods that contain these important compounds.”
A qualified health claim on a conventional food must be supported by credible scientific evidence. Based on a systematic evaluation of the available scientific data, as outlined in FDA’s “Interim Procedures for Qualified Health Claims in the Labeling of Conventional Human Food and Human Dietary Supplements”, FDA is announcing a qualified health claim for EPA and DHA omega-3 fatty acids. While this research is not conclusive, the FDA intends to exercise its enforcement discretion with respect to the following qualified health claim:
“Supportive but not conclusive research shows that consumption of EPA and DHA omega-3 fatty acids may reduce the risk of coronary heart disease. One serving of [name of food] provides [x] grams of EPA and DHA omega-3 fatty acids. [See nutrition information for total fat, saturated fat and cholesterol content.]
In 2000, FDA announced a similar qualified health claim for dietary supplements containing EPA and DHA omega-3 fatty acids and the reduced risk of CHD. FDA recommends that consumers not exceed more than a total of 3 grams per day of EPA and DHA omega-3 fatty acids, with no more than 2 grams per day from a dietary supplement.
The EPA and DHA omega-3 fatty acid qualified health claim is the second qualified health claim that FDA has announced for conventional food. For additional information about QHC visit: www.fda.gov/NewsEvents/Newsroom/
Studies suggest that certain inflammatory conditions could benefit from the use of omega-3’s – most evidence comes from studies using omega-3 fatty acids to treat diseases associated with the heart, such as high cholesterol, high blood pressure and heart disease in general, and it may lower the risk of stroke. Other conditions that omega-3’s may be useful in treating include obesity, arthritis, osteoporosis, various psychiatric disorders (depression, bipolar disease), some cancers, and psoriasis, but the evidence isn’t as strong as the evidence for heart disease.
As stated above you can get your omega-3’s from certain fish and plants. In regards to fish, there has been a lot of news about the potential for mercury poisoning from eating too much fish so you want to make sure that you do not eat a lot of one particular variety of fish or eat too much fish too often.
Fish oil can interfere with blood clotting and it may raise the level of vitamin A and D in your body. Although the risk is low there is a risk for worsening of diabetes, cholesterol and bleeding. You should be careful using fish oil if you have bipolar disease, diabetes, and low blood pressure. In people with liver disease fish oil can raise liver enzymes.
The most common side effect of omega-3’s include fishy aftertaste, gastrointestinal upset and rash.
Another way to make sure you get enough omega-3’s is by supplementing what you receive from fish with plant sources and concentrated pills or capsules of fish oil – just make sure that the fish oil has been distilled or purified. Start with low doses of omega-3’s and slowly work your way up to the recommended dose.
If you are sensitive to omega 3 supplements there are a couple of options including gel capsules, enteric/film coated capsules and caplets (released in the lower intestines) and a flavored paste formulation manufactured by Coromega, Inc.
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