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April 2008 HCV Advocate

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No Viral Reservoir
Alan Franciscus, Editor-in-Chief

OraQuick Rapid HCV Test – Update
Alan Franciscus, Editor-in-Chief

Oxidative Stress and the Liver
Liz Highleyman

Healthwise: Another April Fools’ Column
Lucinda Porter, RN

Extrahepatic Manifestations: Scleroderma
Alan Franciscus, Editor-in-Chief

Disability & Benefits: Fighting Working With Social Security
Jacques Chambers, CLU

Exercise and Aging
Alan Franciscus, Editor-in-Chief

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No Viral Reservoir
Alan Franciscus, Editor-in-Chief

About 50% of people who are treated with current HCV medications (pegylated interferon plus ribavirin) are able to achieve a sustained virological response (SVR) which means that the presence of HCV RNA (viral load) is undetectable 6 months after treatment stops.  In addition some people who contract acute hepatitis C are able to spontaneously resolve or rid the body of the hepatitis C virus.  But does achieving an SVR or spontaneous clearance mean that the hepatitis C virus can be completely eradicated from the body?   This has been a very hotly debated topic, but results from a new study add some credibility to the notion that perhaps hepatitis C can be cured!

Peripheral blood mononuclear cells (PBMC) are blood cells with one nucleus; the term PBMC generally refers to lymphocytes and macrophages (immune system cells).  PBMCs are the most likely cells where a virus could hide out; they may act as a reservoir for viral particles from where infection could potentially rekindle and spread throughout the entire body – at least that’s the theory.   

Some previous studies have found that within these cells there were detectable hepatitis C viral particles.  However, the HCV RNA viral load tests in previous studies were not as sensitive as today’s tests so there could have been small amounts of the hepatitis C virus circulating in the bloodstream that the older tests were not picking up.  These previous study results are now being challenged by a study that detects lower levels of HCV RNA than the tests used in the earlier studies.   

In the March 2008 issue of Hepatology, Bernardin and colleagues released the results from a study titled “Clearance of hepatitis C virus RNA from the peripheral blood mononuclear cells of blood donors who spontaneously or therapeutically control their plasma viremia.”  In their study the authors tried to determine whether the hepatitis C virus (HCV) RNA or, a viral load, could be detected in peripheral blood mononuclear cells (PBMC) in people who had acquired HCV (acute infection) but who were able to resolve or clear the infection (spontaneous clearing) and in people who had achieved an SVR with HCV medications.

The study population was broken into two groups:

 • Group A:  63 patients who spontaneously cleared the virus and  6 patients who had achieved an SVR. (Aviremic group)

 • Group B:  the control group of 56 patients who tested positive for the hepatitis C virus.  (Viremic group)

The authors reported that in Group A there was no hepatitis C virus found in the PBMC’s.   In Group B, 43 of the donors tested positive for the hepatitis C virus; in the remaining 13, who did not have detectable hepatitis C virus, viral load levels were very low, which may mean that low levels of HCV RNA are not present in PBMC’s.  

Conflicting Results
So why have previous studies found low levels of the hepatitis C virus in PBMC’s and this study didn’t?  One explanation that the authors offered up was that viral load tests can now detect HCV viral load at a much lower level than in the previous studies using larger volumes of blood samples, suggesting that when an SVR is achieved it is more likely that the HCV virus has been completely eradicated from the body.  As a result, it could be theorized that there were also low levels of the virus in PBMC’s

The authors concluded that “Our results indicate that PBMC are unlikely to serve as a long-lived reservoir of HCV in aviremic subjects.” 

This is very encouraging news that basically tells us that, whether by natural or spontaneous clearance of acute HCV or by successful drug treatment (SVR), the hepatitis C virus can be completely eradicated from the body.  However, given the low number of patients in this study, larger studies are needed to confirm these results. 

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OraQuick Rapid HCV Test – Update
Alan Franciscus, Editor-in-Chief

In 2007 Orasure, the makers of the OraQuick Advance rapid HIV-1/2 antibody test, began clinical trials on its prototype OraQuick rapid HCV antibody test using the same technology that is used for their HIV antibody test.  The pre-clinical study results reported mid-2007 found that the performance of the HCV antibody test was equivalent to or better than results obtained from finger-stick, whole blood, venous whole blood, and serum plasma samples.  It was also found that the results had a sensitivity and specificity greater than 99%. 

Recently it was announced that Schering-Plough and OraSure Technologies were expanding their collaboration internationally on the HCV antibody test.  The agreement allows for payments to cover certain costs incurred by OraSure in the development of the HCV oral antibody test.  In addition, Schering-Plough will help provide promotional support for the HCV test internationally. 

The clinical trial is on-going and the company expects to seek and get marketing approval sometime in the first or second quarter of 2009. 

How It Works
There are three substances that are part of the test:

 • HCV antibodies – substances produced by the body to help fight or control an infection. 

 • HCV antigens – certain proteins of HCV that antibodies bind to in order to fight off infection

 • An enzyme that binds the HCV antibodies to the antigens. 

The test looks for the presence of HCV antibodies only – not the hepatitis C virus – in a fluid called oral mucosal transudate that is obtained from the cheeks and gums (upper and lower) inside the mouth.

The Kit Is in Two Parts
 • A device that holds a test strip (to swab the gums/cheeks), and

 • A plastic casing that contains the substance that will react to the fluid sample if the sample contains HCV antibodies.   

First, fluid is collected from the gums/cheeks using the test strip.  Once the fluid is collected, the test strip is inserted into the plastic casing that contains the binding enzyme.  In about 20 minutes the results will be reported in the result window on the plastic casing.  

An important piece of information to know is that a positive antibody test does not mean that a person is currently infected with hepatitis C.  An HCV RNA (viral load) test will need to be performed as a follow-up measure to confirm active hepatitis C virus infection. 

The introduction of an oral rapid HCV antibody test could be a huge advancement in HCV awareness and care by making it easier to test and identify the estimated 75% of people who are infected with hepatitis C but don’t know it.

refers to the proportion of people in a population that will be correctly identified when given a test that is designed to detect a certain disease. 

refers to the probability that an individual who does not have the particular disease that is being tested for will be identified as having a negative test result.

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Oxidative Stress and the Liver
Liz Highleyman

Oxidative stress – the build-up of highly reactive forms of oxygen and other so-called “free radicals” in the body – has been linked to a wide range of detrimental effects, including liver damage.

A growing body of research indicates that oxidative stress is a major mechanism underlying drug-induced liver toxicity and alcoholic liver disease. Oxidative damage also contributes to steatosis (fat buildup in the liver), fibrosis, and liver cancer. Hepatitis C virus (HCV) itself promotes oxidative stress, and this effect is magnified in people coinfected with HIV. Oxidative stress, in turn, facilitates HCV replication.

What Is Oxidative Stress?
It is well known that oxygen is essential for life, and oxygen molecules are among the thousands that naturally exist within the body. As a result of normal metabolism, however, atoms and molecules can acquire an extra electron, becoming free radicals. Because they have an unpaired electron, radicals easily form bonds with other molecules, “stealing” their electrons and setting off a chemical chain reaction. Highly reactive forms of oxygen are known as reactive oxygen species; reactive nitrogen is also involved.

Free radical production rises when the body is under physiological stress, for example due to chronic infection, consumption of a high-fat diet, or exposure to environmental hazards such as pollution or radiation. Impairment of mitochondria – the tiny “power plants” within cells – can cause increased release of free radicals due to less efficient energy production.

Oxidative stress occurs when production of free radicals exceeds the body’s natural antioxidant defense mechanisms. The interaction between oxygen radicals and other molecules can alter proteins and fats, damage cell structures, and disrupt various cellular processes. Oxidative stress can damage cell membranes and DNA, causing mutations in a cell’s genetic code. It interferes with cytokine production and cell signaling, and appears to play a role in apoptosis (programmed cell death); chronic conditions such as atherosclerosis, neurodegenerative diseases, and cancer; and the overall aging process.

But reactive oxygen forms are not purely detrimental; they also play crucial roles in cell signaling, immune defense against pathogens, and recruitment of blood platelets to sites of injury.

Liver Damage Due to Oxidative Stress
Some of the chemicals that cause liver toxicity promote oxidative stress when they are processed in the liver. Acetaminophen, for example, is toxic at high doses because it is broken down into a chemical that causes oxidative damage in the liver. N-acetyl-cysteine, a precursor of the natural antioxidant glutathione, is used as an antidote. The breakdown of alcohol, especially after heavy or prolonged drinking, can produce harmful oxygen radicals that contribute to cirrhosis and other adverse outcomes.

Several studies have found that people with chronic hepatitis C have a higher degree of oxidative stress and decreased glutathione levels. A recent Italian study of more than 100 hepatitis C patients reported in the March 2008 Journal of Hepatology, for example, found that 61% had evidence of oxidative stress regardless of age, sex, HCV viral load, genotype, body mass index, or severity of liver inflammation.

HCV infection itself can worsen oxidative stress in the liver, but how it does so is not fully understood. Laboratory studies have shown that HCV proteins directly induce production of reactive oxygen species in hepatocytes; the virus also promotes oxidative damage in the liver due to chronic inflammation. Interestingly, hepatitis B virus does not seem to have a similar effect on oxidative stress. Excess iron in the liver also plays a role, probably by depleting glutathione stores.

Oxidative stress, in turn, disrupts interferon signaling pathways, blunting the antiviral effect of natural interferon alpha and potentially reducing response to interferon-based treatment. It encourages lipid peroxidation, a process whereby free radicals break down fats by taking their electrons, producing byproducts that contribute to liver steatosis. Oxygen radicals and lipid peroxidation byproducts also stimulate release of pro-inflammatory cytokines and promote hepatic stellate cell activity leading to fibrosis progression.

The June 2007 Journal of Gastroenterology and Hepatology included a review of studies showing that oxidative stress and the resulting activation of the body’s antioxidant mechanisms promotes development of hepatocellular carcinoma. Systemic oxidative stress contributes to some of the metabolic complications and other extrahepatic manifestations commonly seen in people with chronic hepatitis C. Free radicals, for example, are known to affect insulin sensitivity; the aforementioned Italian study found that among individuals with HCV genotypes other than 3, those with oxidative stress were more likely to have insulin resistance, steatosis, and fibrosis.

Some studies have shown that oxidative stress improves with successful interferon-based therapy. But treatment itself can cause some forms of oxidative damage, such as red blood cell destruction associated with ribavirin. Further, HCV itself contributes to mitochondrial dysfunction, which may be worsened by drugs that cause mitochondrial toxicity – including ribavirin, especially in combination with certain antiretroviral medications used to treat HIV.

HCV, steatosis, alcohol use, drug toxicity and other factors associated with oxidative liver damage can interact and have an additive or “multi-hit” effect, which helps explain why people with chronic viral hepatitis are more susceptible to liver damage due to heavy alcohol use or hepatotoxic medications – and why experts recommended that people with chronic hepatitis C drink little or no alcohol and exercise extra caution when using drugs that could potentially harm the liver.

Managing Oxidative Stress
Antioxidants are agents that act as “scavengers,” binding with – and thereby neutralizing  – free radicals. The body produces its own antioxidants including glutathione and superoxide dismutase to “mop up” radicals generated during normal metabolism. Imbalances can occur, however, due to either increased free radical production or decreased antioxidant levels, as often happens when faced with environmental stressors or chronic disease.

Antioxidants are also available in many foods and dietary supplements, for example vitamins C and E. Other supplements, including alpha-lipoic acid, N-acetyl-cysteine, and coenzyme Q10 are used in the production of natural antioxidants in the body. Trace minerals such as selenium and zinc enable the activity of antioxidant enzymes. Good food sources of antioxidants include the polyphenols, flavonoids, and carotenoids found in berries, citrus fruit, pomegranates, tomatoes, carrots, cabbage, broccoli, olive oil, dark chocolate, walnuts, red wine, coffee, and tea.

Because oxidative stress plays a role in many types of cell damage, antioxidants have been widely studied for the prevention and treatment of disease. Several large epidemiological studies have shown an association between a diet high in plant antioxidants and decreased risk of cardiovascular disease and cancer.

But while animal and human research indicates that a shortage of natural antioxidants is detrimental, the benefits of supplemental antioxidants are less clear. A few studies have shown that consuming large doses of antioxidant supplements (for example vitamin E) may actually be harmful, possibly because some antioxidants can exert a pro-oxidant effect at high levels.

Antioxidants have been studied for liver diseases including chronic hepatitis C. The benefits of many complementary and alternative therapies – such as silymarin (derived from milk thistle), glycyrrhizin (derived from licorice root), and ursodeoxycholic acid (found in bear bile) – may be largely due to their antioxidant effects, potentially both retarding HCV replication and reducing liver inflammation and fibrosis related to oxidative damage.

An Israeli study of 50 chronic hepatitis C patients, for example, found that using a preparation of 11 oral and injected antioxidants (including herbs, vitamins C and E, lipoic acid, and L-glutathione) for 20 weeks was associated with ALT normalization, decreased HCV RNA, and histological improvement. But several other studies of N-acetyl-cysteine, L-glutathione, and other antioxidants in people with hepatitis C and other types of chronic liver disease have produced conflicting data.

While research on isolated supplements remains mixed, however, there is little controversy about the benefits of consuming antioxidants as part of a healthy, balanced, low-fat diet rich in fruits, vegetables, and whole grains.


Choi, J. and Ou, J. Mechanisms of liver injury. III. Oxidative stress in the pathogenesis of hepatitis C virus. American Journal Physiol Gastrointes Liver Physiol 290(5): G847-851. May 2006.

Koike, K. Hepatitis C virus contributes to hepatocarcinogenesis by modulating metabolic and intracellular signaling pathways. Journal of Gastroenterology & Hepatology 22(Suppl 1):S108-S111. June 2007.

Levent, G. et al., Oxidative stress and antioxidant defense in patients with chronic hepatitis C before and after pegylated interferon alfa-2b plus ribavirin therapy. Journal of Translational Medicine 4:25. June 2006.

Mantena, S. et al. Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases. Free Radical Biology & Medicine. January 3, 2008 (Epub ahead of print).

Melhem, A. et al. Treatment of chronic hepatitis C virus infection via antioxidants: results of a phase I clinical trial. Journal of Clinical Gastroenterology. 39(8): 737-742. September 2005.

Vidali, M. et al. Interplay between oxidative stress and hepatic steatosis in the progression of chronic hepatitis C. Journal of Hepatology 48(3): 399-406. March 2008.

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HealthWise: Another April Fools’ Column
Lucinda Porter, RN

In honor of April Fools’ Day, my monthly column usually focuses on some aspect of humor. I believe that laughter is beneficial to the body, mind and spirit. I am able to endure just about anything if I can find a reason to laugh. Naturally, there needs to be restraint. After the tragedy on Sept. 11, humor briefly disappeared while we grieved. A week later, David Letterman and Jon Stewart returned and our nation began to heal. Laughter enabled us to endure the tragedy.

The same process works with health issues. All of us face serious illnesses, loss and death. At first it feels horrible. After awhile, the ache is relieved by a something such as a joke, a fond memory, a sunrise, religious consolation or the kindness of others. Even a brief interruption reminds us that pain is temporary.

I may be leading you astray. My opening paragraph mentions my April tradition of writing a column about humor. However, this year is different. I can’t think of anything funny to say. Why, you might ask? Because I have not been getting enough sleep. And why is that? Because, I have been seduced by Brain Age2™

Brain Age2™ is a game that is supposed to help sharpen my brain. However, I like it so much, that I am foolishly playing it past my usual bedtime.  This is counterproductive. When I am tired my brain function decreases. Instead of becoming sharper, I am becoming duller. So dull, that I can’t think of anything funny to say.

Regular Healthwise readers are probably rolling their eyes. How many times have I written that sufficient sleep is the cornerstone of good health? So many times, I should know better. Instead, I lured myself into this bad habit under the guise of enhancing my mental skills. This is not rational thinking.

This may seem like it has nothing to do with hepatitis C (HCV), but it has everything to do with it. Two common complaints from those living with HCV are fatigue and mental fogginess. People ask me if HCV is the cause for their being so tired and forgetful. When asked if they are getting sufficient sleep, the answer is usually no. Those with HCV are not alone – every week more than half of us have a few nights of insomnia.

Insufficient sleep does more than make us feel tired and give us bags under the eyes. Sleep deprivation may have contributed to the Exxon Valdez oil spill, the space shuttle Challenger’s explosion, and the Three-Mile Island accident. There are more than 100,000 motor vehicle accidents every year because of it. Drowsy drivers are as dangerous as someone with a blood alcohol level of 0.05% (0.08% is legally drunk). Cardiovascular diseases, type 2 diabetes, and obesity are some of the serious disorders associated with inadequate sleep.

The National Sleep Foundation recommends 7 to 9 hours of sleep on a daily basis for adults. Some people need more, some less. If you are fatigued, assess whether you are getting sufficient quality sleep. If the answer is no, then find out why. If it is because you are staying up to play computer games, this is easy to fix. If it is because of Restless Leg Syndrome, allergies, sleep apnea, or other medical conditions, seek medical attention.

Sleep aids, such as supplements, prescription and non-prescription drugs should only be used under medical supervision. Each has some risks, such as dependence. The choices of sleep medications are getting better and the newest ones have minimal risks. The herb valerian may be effective but those with liver disease should avoid it. There is not enough melatonin research to make recommendations for or against it. Short-term use of melatonin is most likely safe, but learn how to use it and how much to take. 

The best way to promote sleep does not involve any pills. It is learning how to break the cycle of sleeplessness. Research shows that cognitive-behavioral therapy (CBT) is the most effective way to improve sleep. CBT uses biofeedback, relaxation techniques, and sleep hygiene education. Your medical provider may be able to refer you to a sleep clinic or psychotherapist who is trained in this area.

If your sleep problems are minimal, you may be able to restore good sleep habits yourself. There are some excellent suggestions on the websites listed at the end of this article. Here are a few tips:

 • Go to bed at the same time every night. If you stay up an hour or more past your regular bedtime playing computer games, you may reset your internal clock. If your wake-up time is not extended, you will be sleeping less. The next day you will be grumpy and irritate everyone around you.

 • Sleep in a dark, quiet, cool room. If you need to, wear a face mask, ear plugs, use white noise and or a fan. If your clock glows, put a mask over it.

 • If you share the bed with a snorer, strongly advise him or her to seek help. In the meantime, do everything you can to block out the noise. If you are considering suffocating him with a pillow, maybe one of you should sleep on the couch.

 • If you are awake for 30 minutes, get up and do something relaxing. Do not do anything stimulating, particularly if it is a computer game. Try reading the U.S. tax code or James Joyce’s Ulysses.

 • After lunch, skip the triple espresso and the caffeine craver’s cola.

 • Before bedtime, don’t fill your belly with food and your bladder with liquids. Food makes it hard to sleep. So does an ever-filling bladder.

 • Leave your worries out of the bedroom. If something is bothering you, write it down. Tomorrow there will be plenty of time to fret.

Take a look at your sleep pattern and if you can honestly say that you are getting enough sleep but are still tired, there are plenty of medical causes for fatigue other than HCV.  Rule these out before assuming HCV is the cause. If after ruling everything out, you still feel that HCV is the cause, then learn to laugh. Life can still be fun in a horizontal position.

 • American Academy of Sleep Medicine www.sleepeducation.com

 • Hepatitis C Support Project www.hcvadvocate.org/hepatitis

 • National Institutes of Health links health.nih.gov/result.asp/601

 • National Sleep Foundation



It is easy to have opinions about health policy, but when it comes to their own health, politicians don’t necessarily walk the talk. How important is it that the President of the United States is in good health? Do you know if your favorite candidate exercises? Eats well? He or she is probably sleep deprived. Does age matter? How about weight? How many of us would choose a fit president over one with good ideas to mend the economy? These are complicated questions because they play into our prejudices. Think about why you prefer one candidate over another.

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Extrahepatic Manifestations: Scleroderma
Alan Franciscus, Editor-in-Chief

The hepatitis C virus (HCV) and the medications used to treat hepatitis C – interferon and ribavirin – are known to induce or exacerbate underlying autoimmune diseases. The incidence of scleroderma in the general population is very low (200-300 per million Americans) and is believed to be even more uncommon in people with hepatitis C.  The link between hepatitis C and scleroderma has not been established.  In fact, there have only been a handful of studies that have looked at the relationship between HCV and scleroderma.  However, since hepatitis C and the medication to treat hepatitis C are known to cause other types of autoimmune conditions some researchers believe that there may be a link. 

Scleroderma is an autoimmune disease characterized by excessive deposits of collagen that most often affects the skin, but it can also affect blood vessels and internal organs.  The most common visible symptoms of scleroderma is hardening and scarring of the skin.  Scleroderma symptoms and disease progression vary widely among people with the condition.  Some people have few symptoms and slow or no disease progression while for some others it can be life-threatening.  There are three types of scleroderma:

 • Diffuse scleroderma – the most severe form of the condition is characterized by widespread hardening of the skin and internal organs (lungs, digestive tract, kidneys). 

 • Limited scleroderma/CREST syndrome – a milder form of scleroderma usually preceded by Raynaud’s phenomenon, and usually limited to the fingers.  CREST is an acronym for Calicosis (calcium deposits on the skin usually seen on the elbows, knees or other joints), Raynaud’s phenomenon, Espohageal dysmotility (nausea, fullness, acid reflux or heartburn), Sclerodactyly (localized thickening of the skin of the fingers), and Telangiectasia (spider veins). 

 • Morphea/linear scleroderma – generally seen as isolated patches of hardened skin and does not generally affect the internal organs. 
The diagnosis of scleroderma is based upon a combination of the presence of autoimmune antibodies, physical exam, x-rays and biopsy.  Up to 90% of people with scleroderma test positive for anti-nuclear antibodies, which is common blood marker of autoimmune disease.   About 80% of people with scleroderma also have Raynaud’s phenomenon – a condition that is an HCV-related extrahepatic manifestation (see the HCSP Factsheet: Raynaud’s Phenomenon,in this series).  The American College of Rheumatology has established criteria for the diagnosis of scleroderma – www.rheumatology.org.

There are no drugs that can cure scleroderma, but there are a variety of treatments and self-help strategies that can treat and lessen the symptoms.  Treatment of scleroderma is usually a multi-pronged approach that is supervised by a rheumatologist.  There are drugs used to help dilate blood vessels that will help in managing Raynaud’s phenomenon.  Proton pump inhibitors can be used to treat the symptoms of heartburn.    If the kidneys are involved the use of blood pressure medication can help protect them.  If the lungs are involved there are medications to treat pulmonary hypertension and control the damage caused by scleroderma.  Immunosuppressive therapy can also be given for any muscle pain and disease caused by scleroderma.

Self-help strategies include:
 • Keep the hands and toes warm to help with Raynaud’s phenomenon
 • To reduce the incidence of heartburn make sure that the head is elevated while lying down
 • Seek professional and peer-support to deal with the emotional toll of having the visible signs and symptoms of scleroderma
 • Physical therapy, exercise, and being physically active will help to reduce the damage scleroderma causes to muscle and joints 

For more information:

The Scleroderma Foundation

HCSP Factsheet:
Extrahepatic Manifestations: Raynaud’s Phenomenon

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Disability & Benefits: Fighting Working With Social Security
Jacques Chambers, CLU

The majority of people, who file for Social Security Disability benefits, either SSDI or SSI, complete the requested paperwork, submit it and wait, sometimes for months, without hearing a word – then they start worrying.  Part of this is fear that any contact with Social Security is a bad thing. Part of this is not being sure who to contact and how to talk with them.

Many people are under the impression that Social Security staff are dedicated to finding ways to deny every claim they can. This is frequently heard by attorneys and on many of the newsgroups and bulletin boards that deal with Social Security and disability.

One urban myth is that attorneys have an incentive to get people to believe that “all claims are denied the first time around,” WHICH IS NOT TRUE.  Sixty per cent of initial claims are declined, which means 40% of the claims are approved the first time around. However, the less time a person spends on the initial claim the greater the chance an attorney will be needed for an Administrative Law Judge and the retrospective payment will have grown so that the attorney receives the maximum fee of $5,300.00.

The sites on the internet that exchange information and assistance on Social Security Disability issues can be very helpful. They give a lot of good background on how Social Security does things and how people have handled their own claims. However, those sites can also be very scary. Spend much time on those sites, and you will come away convinced that every morning the staff will meet to discuss new ideas on denying claims.

If you choose to use these sites, and they can be very informative, keep in mind that most of the people on those sites are there because they have also had problems with their claims. The 40% whose claims were approved at the first application have little need to visit the sites, so only the problems are discussed.

It has been my experience from helping hundreds of people file for disability benefits that Social Security has no agenda to keep people off benefits. It is just not true that the Social Security Administration is “out to deny your claim.” The people that decide whether or not you qualify for benefits would just as soon approve your claim as deny it. It’s not their money; they’re happy for you to get it; they really don’t have time to care if you don’t. The problem they have is the small amount of time they can spend on each claim.

The people reviewing disability claims work in a huge bureaucracy. That bureaucracy, in its attempt to decide claims in the same manner in all offices, requires that specific information and documents must be in the file before a claim can be approved. A Claims Service Representative or a Claims Analyst’s performance is measured by how quickly and thoroughly they can complete and close their claim files. Because of all the rules they must follow and the performance standards they are under they really focus on whether the information in the claim file provides enough information to decide the claim. If they can “check the right boxes in their checklist” the claim is approved; if not, the claim is denied. Because of the workload and pressure for uniformity that they are under, a denial doesn’t mean you are not disabled, it might just mean that the right “boxes didn’t get checked.”

Their workload is such that they can’t follow up and track down everything they need or have requested. If they don’t have enough information to approve your claim and if they do not receive the medical records they need after a few requests, they will simply deny the claim. You can prevent that by staying in touch with the people handling your claim. They will appreciate any help you can give them.

To help get your claim approved initially, you should learn about the process before making an appointment to file your initial claim. Know what information is going to be asked. Visit the Social Security website; visit other sites that offer information on the process. Be prepared for the questions they will be asking.

The Claim Representative you meet at the initial interview is not the person who will be reviewing your medical records. Once a disability file is opened at Social Security, they will send your file to the local state office that examines all disability claims in your state and determines if you meet Social Security’s definition of disability. A Claims Analyst in that office will be assigned to your claim and will order the medical records from your doctors, send you and your doctors questionnaires to complete, decide whether you need to see a Social Security doctor, and finally decide whether or not you are eligible for benefits. You can provide invaluable help to the Analyst through the process.

When you have your initial interview, ask the Claims Representative how long it will take to assign a Claims Analyst. Following the timeline recommended by the Social Security Representative, and call back to get the name and phone number of Analyst assigned to your claim.

Call the Analyst. Introduce yourself. Usually she (the Analyst may be a “he” but many are women) will need your name and Social Security number to locate your file. Ask her for the Case or File Number. This is an internal number that the Disability Evaluations Department assigns to each application. Using that number during future calls will help the Analyst find your file faster. Let her know that you are calling simply to offer your help in obtaining all the information needed to make a determination.

When talking to the Analyst (or the Social Security Representative), stay helpful and empathetic to her workload. While you want to make each contact as pleasant as possible, don’t expect her to have the time to “visit” with you. Keep your contact brief and to the point.

A good way to avoid calling too often and becoming a “pest” is, at the end of each conversation, to tell the Analyst, “I don’t want to bother you but I want to stay on top of my claim. When would be a good time to check back with you? In a week?” That lets the Analyst stay “in control” of your contacts. She won’t feel so intruded upon if you call back after an interval that she has already agreed to. 

Also remember that your contacts are to help the Analyst perform her job. Trying to persuade her to approve your claim is no help. Focus on getting her what she needs to decide your claim. Arguing with her is downright harmful.

Ask her to let you know when she sends out requests (if she hasn’t already) to your doctors for medical records, unless you actually take them in yourself. Ask her to send you copies of the requests so you can follow up with each doctor to make sure the records are sent promptly.

Once you know which doctors she is sending requests to, you should contact each doctor’s office, advise the office staff that the request is coming, and ask them to send the information as quickly as possible. Once you have confirmed the date that the records were sent to the Analyst, allow for mail time, then call the Analyst to make sure she got them. You may have to go back and forth between the various doctors and the Analyst several times. Do not be impatient, and don’t blame either the Analyst or the doctor’s office staff. Be patient, but persistent. Just keep calling and asking and checking.

An Analyst may send you a questionnaire to complete, and she usually wants it back within ten days. However, if you call the Analyst, she will always allow you extra time to complete and submit it.

There are some things that an Analyst will not do, however, so it is better not to ask. They will not help you fill out the questionnaires they send. These are for you and your advocate to do.

Also, they are not allowed to tell you whether your claim has been approved or denied. However, you may get a clue to the decision by what happens next. The Analyst sends out the denial letters, but acceptances must be sent from the Social Security Administration.

Once all the information is in, if you don’t receive a denial fairly quickly, that’s usually a good sign. However, the Analyst’s decision is reviewed by an in-house physician who may or may not feel more information is needed, which can slow down the process.

Occasionally, a claim is sent to the Regional office for a “quality review,” before being returned to the SSA office. The good news there is that most claims sent for quality review are approved claims.

One final note: some Analysts never answer their phones and rely on voicemail for client contact or only take calls at certain times. Don’t let that deter you. Conduct your business by voicemail, just as if you are talking to her. Offer to help; ask for the doctors she is contacting; offer to follow up. It is the rare Analyst that won’t take advantage of your offer. Your assistance makes it easier for her to do her job. 

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Exercise and Aging
Alan Franciscus, Editor-in-Chief

In the January 2008 issue of the Archives of Internal Medicine results from a study of more than 2,400 twins (2,152 women; 249 men) on the effect of exercise on aging was released.  In this study the affect of exercise was evaluated on LTL or leukocyte telomere Length (sequences of DNA that protect chromosomes from degrading) – as we age telomeres become shorter, which is a signal that our body is aging.  The study looked at physical activity and leisure time over a 12 month period. 

What the study found was that in those who averaged at least 30 minutes of exercise daily, the telomeres were longer than in those who were the least physically active participants.  This finding remained significant even after factoring in “age, sex, body mass index, smoking, socioeconomic status, and physical activity at work.”

The authors concluded that “A sedentary lifestyle (in addition to smoking, high body mass index, and low socioeconomic status) has an affect on LTL and may accelerate the aging process.”

Although this study is not about exercise and hepatitis C it does strengthen the message that exercise can have a dramatic effect on the health and well-being of healthy individuals.  It appears (from this study) that exercise can have a remarkable affect on the aging process and that exercise should be a part of everyone’s health maintenance including those of us who are living with hepatitis C. 

“The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length.” Cherkas et. al. Arch. Intern. Med. 168: 154, 2008.

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