Research & Treatment News
January 19, 2009
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Physicians are finding an increasing correlation with HCV infection and clinical depression. Learn about the four possible mechanisms linking depression with Hepatitis C, as well as the role standard combination therapy may play in this relationship.
by Nicole Cutler, L.Ac.
As the most common blood borne viral infection today, the Hepatitis C virus (HCV) is a major cause of chronic liver disease and affects an estimated 180 million people worldwide. For many living with HCV, the standard therapy of peginterferon-alfa and ribavirin is either not an option or it was unsuccessful. Whether an HCV-infected person has not attempted standard therapy or is a non-responder, physicians are finding an increasing correlation with HCV infection and clinical depression. Being aware of depression’s prevalence among this population and its potential mechanisms will encourage both patients and their physicians to take depression seriously.
Defining Depression
According to the Diagnostic and Statistical Manual for Mental Disorders (DSM-IV), major depressive disorder is characterized by a period of depressed mood or anhedonia (inability to experience pleasure from normally pleasurable life events such as eating, exercise, social or sexual interaction) occurring for at least two consecutive weeks. Depressed mood or anhedonia must also be accompanied by at least four of the following:
· Overwhelming sadness or emptiness
· Lack of interest or pleasure in daily activities
· Appetite or weight changes
· Disturbed sleep patterns
· Changes in psychomotor activity
· Fatigue or loss of energy
· Feelings of guilt or worthlessness
· Difficulty focusing, concentrating or making decisions
· Recurrent thoughts of death or suicidal ideation
A result of inconsistent measures of depression, calculating the actual prevalence of depression among patients with chronic HCV infection is challenging. Nevertheless, most researchers and physicians agree that the prevalence of depressive disorders is significantly higher among HCV-infected patients compared with the general population. According to the DSM-IV criteria, reported prevalence rates for major depressive disorder are higher in those with HCV:
· Ranging from 24 to 70 percent with chronic Hepatitis C infection
· Ranging from 6 to 10 percent in the general population
HCV Treatment
Hepatitis C’s current standard of treatment consists of combination therapy with peginterferon-alfa and ribavirin for 24 or 48 weeks depending on viral genotype. Although the treatment response rates are favorable for those able to complete this therapy, many must abandon the treatment protocol due to combination therapy’s severe side effects. Some studies indicate that chemically-induced depression occurs in approximately 20 to 40 percent of treated patients. Administering physicians have observed that depression associated with HCV therapy reduces the likelihood of eliminating the virus with peginterferon-alfa and ribavirin, due to patient non-compliance or even premature discontinuation.
Possible Mechanisms
The various factors contributing to major depressive disorder makes it difficult to establish a causative relationship between HCV infection and depression. The origins of depression with Hepatitis C are most likely a combination of physiological characteristics of the virus, emotional and physical health of the individual, the extent of a person’s social support network, personal beliefs and available treatment options. Following are four potential mechanisms connecting chronic HCV infection and depression:
1. Pre-Existing Condition – This theory suggests that having a psychiatric disorder, such as depression or posttraumatic stress disorder, can lead to high-risk behaviors increasing the probability for HCV infection, such as intravenous drug use or unprotected sexual practices. According to this premise, HCV itself is not the causative agent for depression, but there is a high prevalence of depression in individuals who engage in risky behaviors. Several studies have found higher incidences of drug use and unsafe sexual practices among patients with major depressive disorder or other depressive symptoms.
2. Psychological Impact of HCV – This theory suggests that depression related to HCV infection is due to the psychological burden and distress associated with this chronic disease. Foster and colleagues demonstrated that in a sample of HCV-infected patients without cirrhosis, quality of life scores were reduced, particularly regarding mental health and physical function, when compared with a control group. Many health experts are recognizing that chronic Hepatitis C virus infection alone leads to physical symptoms capable of reducing a person’s quality of life, the springboard for depression.
3. Biological Result of HCV – This theory describes the potential for the Hepatitis C virus to negatively affect the central nervous system bringing about depression. Although not directly proven, this hypothesis is supported by studies demonstrating that HCV directly causes fatigue and other neuro-cognitive symptoms. Adair and colleagues used gene expression analysis to evaluate gene expression in HCV-infected patients and a control group. The researchers found a difference in the expression of 29 genes, including those involved in brain oxidative and energy metabolism. These findings support a biological basis for the link between HCV infection and depression. Additionally, Hepatitis C viral particles noted to cause chemical changes that could initiate depressive symptoms have been found in the central nervous system.
4. Psycho-Spiritual Perception – Best-selling author and motivational speaker, Esther Hicks, describes depression as a location on one extreme edge of an emotional scale. On one end of this scale, good feelings are likened to the perception of freedom; on the other end bad feelings are likened to the perception of bondage. Bondage, otherwise felt as lack of freedom or control, embodies the empty sensation of depression. According to this psycho-spiritual theory, Hepatitis C is often associated with depression, because many affected feel that their ability to recover from this illness is beyond their control. Such feelings of hopelessness in those with Hepatitis C may occur when those affected:
· Are informed their disease is incurable
· Feel doubtful about ridding themselves of Hepatitis C
· Experience severe side effects from standard therapy, causing the perception that their condition is worsening – further confirming a loss of control over their health
By accumulating hopefulness about a Hepatitis C diagnosis, a person will naturally progress on the emotional scale away from fear, and thus away from depression.
Patients and their physicians must be aware of the simultaneous presentation of HCV and depression, the role combination therapy may play in this relationship and the four possible mechanisms linking depression with Hepatitis C. Armed with this knowledge, we can be proactive in addressing major depressive disorder as affiliated with chronic Hepatitis C infection.
References:
http://clinicaloptions.com, Risks and Mechanisms of Depression in HCV, Michael R. Krauss, MD, PhD, Depression Associated With HCV Infection and Its Therapy: Impact on Patient Management, Clinical Care Options, LLC, March 2007.
http://jac.oxfordjournals.org, Interferon-induced depression in chronic hepatitis C, Y. Horsmans, Journal of Antimicrobial Chemotherapy, September 2006.
www.abraham-hicks.com, It’s All About Vibrational Relativity, Abraham-Hicks Publications, 2007.
www.natap.org, Chronic Hepatitis C, Depression and Interferon, Journal of Hepatology, June 2005.
www.psychiatrictimes.com, Depression as Co-Pilot: Clinical Implications of Hepatitis C and Interferon/Ribavirin Treatment, James A. Bourgeois, MD, OD, Lorenzo Rossaro, MD, and Robert D. Canning, PhD, Psychiatric Times, April 2005.
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By targeting p7, a protein that helps Hepatitis C spread, British researchers believe that combination therapies will be more effective at defeating the virus.
Hepatitis C virus: Combination therapies may be effective against hepatitis C virus
Researchers at the University of Leeds have found that combination therapies similar to those used for HIV patients may be the best way of treating hepatitis C virus (HCV).
A study of a protein called p7, has shown that differences in the genetic coding of the protein between virus strains - known as genotypes - alter the sensitivity of the virus to drugs that block its function.
The p7 protein assists the spread of HCV around the body and is a promising target for new drug treatments for the virus.
This role of the protein was discovered in 2003 by Dr Steve Griffin with Professors Mark Harris and Dave Rowlands of the University’s Faculty of Biological Sciences.
And their study has shown that inhibiting p7 with drugs can prevent the spread of HCV.
“One of the challenges in finding treatments for viruses is their ability to constantly change their genetic makeup. Our research shows there can’t be a one-size-fits-all approach to treating HCV with p7 inhibitors in the future. We believe combination treatments will work much more efficiently, as they take into account the variability of the p7 protein,” Harris said.
The researchers examined the response of HCV to a panel of compounds including the well-known anti-viral drug, rimantadine, which targets a similar protein in the flu virus.
They found that the drug’s effectiveness was altered depending on the genetic makeup of the p7 protein.
Dr Griffin said: “We ‘borrowed’ rimantadine to test its effects because p7 behaves similarly to a protein found in the flu virus. Although rimantadine works well in the laboratory, we now need to develop new drugs specifically targeted against p7 that we can take forward for future therapies.” (ANI)
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URL for Article Source:
http://www.entertainmentandshowbiz.com/hepatitis-c-virus-combination
-therapies-may-be-effective-against-hepatitis-c-virus-200901119123
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Once again, ethnicity appears to be a factor in the effectiveness of Hepatitis C treatment. Sponsored by Roche, a recent study shows that Latinos have a lower response rate to standard treatment with peginterferon alfa-2a and ribavirin than non-Latinos.
HCV Therapy Less Effective in Latinos
By Michael Smith, North American Correspondent, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine.
SAN JUAN, Puerto Rico, Jan. 14 -- Latino whites with chronic hepatitis C virus infection respond poorly to therapy, compared with non-Latino Caucasians, researchers here said.
The finding, from a prospective but non-randomized study, adds ethnicity to the factors that predict outcomes to standard therapy for chronic HCV, according to Maribel Rodriguez-Torres, M.D., of the Fundacion de Investigacion de Diego, and colleagues.
And because the U.S. Latino population is growing, it may also highlight an important public health issue, Dr. Rodriguez-Torres and colleagues said in the Jan. 15 issue of the New England Journal of Medicine.
Previous studies have shown that blacks have a reduced response to standard treatment with peginterferon alfa-2a (Pegasys) and ribavirin (Copegus), the researchers noted, possibly because of a reduced sensitivity to interferon or diminished HCV-specific immunity.
At the same time, more limited data have hinted that a similar effect is present among Latinos, but because Latinos are often under-represented in clinical trials, the findings were not considered conclusive evidence that ethnicity plays a role in response, the researchers said.
To fill the gap, they enrolled 269 Latino and 300 non-Latino whites with chronic HCV genotype 1 infection, who had not previously been treated, for an open-label, non-randomized study.
They were given peginterferon alfa-2a at 180 mcg a week and ribavirin at 1,000 or 1,200 mg daily (depending on body weight) for 48 weeks and followed for another 24 weeks.
The primary endpoint of the study was sustained virologic response -- defined as undetectable HCV RNA level -- less than 28 IU/mL -- 24 weeks after the end of treatment.
The researchers also looked at secondary endpoints such as responses during treatment, rapid responses, and relapses.
Analysis showed:
* Baseline characteristics were similar, although more Latino patients were 40 or younger, had a body mass index of more than 27 or more than 30, and had cirrhosis.
* The rate of sustained virologic response was 49% among non-Latino whites compared with 34% among Latinos, a difference that was significant at P<0.001).
* Non-Latinos were significantly more likely (at P=0.045) to have undetectable HCV RNA in serum at week four and the advantage continued at all subsequent time points (P<0.001 for other comparisons.
* In an analysis adjusted for baseline differences in body mass index, cirrhosis, and other characteristics, non-Latinos were almost seven times more likely to have a sustained virologic response. The odds ratio was 6.93, significant at P<0.001.
* In both groups, a lower baseline HCV RNA level predicted a sustained virologic response.
* Adherence did not differ significantly between the two groups.
* And the number of patients with adverse events and dose modifications was similar, but fewer Latino patients stopped treatment owing to adverse events.
The findings "add to a growing body of evidence of differences in treatment responses among ethnic groups," Dr. Rodriguez-Torres and colleagues concluded.
They added that better treatment strategies are needed to improve the rate of sustained virologic response among Latinos with chronic HCV genotype 1.
They suggested that "Latinos should be considered for clinical trials involving specifically targeted antiviral therapies for hepatitis C to determine whether the addition of investigational agents to standard therapy improves the rate of response in this difficult-to-treat population."
The study was supported by Roche. Dr. Rodriguez-Torres reported financial links with Roche, Abbott Laboratories, Anadys, Pharmasset, Vertex, Glaxo-SmithKline, Bristol-Myers Squibb, Valeant, Novartis, Wyeth, Virochem Pharma, Idera, Intarcia, sanofi-aventis, Human Genome Sciences, Idenix, Pfizer, Gilead, Tibotec, and Merck.
Primary source: New England Journal of Medicine
Source reference:
Rodriguez-Torres M, et al "Peginterferon alfa-2a and ribavirin in Latino and non-Latino whites with hepatitis C" N Engl J Med 2009; 360: 257-67.
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URL for Article Source: http://www.medpagetoday.com/Gastroenterology/Hepatitis/12451
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January 14, 2009
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Biologists have known for a long time that the mitochondria in human cells are where energy is made. However, scientists are just now becoming aware of how living with Hepatitis C damages the mitochondria and why this causes fatigue. Fortunately, this understanding offers a unique solution to the exhaustion caused by Hepatitis C.
by Nicole Cutler, L.Ac.
The most commonly encountered symptom in clinical healthcare settings is fatigue, a problem that plagues a majority of people living with chronic disease. While many mechanisms may be responsible for the fatigue characteristic of the Hepatitis C virus (HCV), one burgeoning theory may have a simple remedy. Possibly due to the medications used to treat it or a direct impact from the virus, chronic HCV is believed to damage the cell’s mitochondria.
Remembering back to high school biology, mitochondria are known as the cell’s power centers. Containing hundreds to thousands of mitochondria in each cell, these organelles are responsible for creating adenosine triphosphate (ATP), molecules that release energy. Scientists believe that a breakdown of the mitochondria’s membrane is a significant factor in mitochondrial damage. Occurring with aging and chronic disease, the breakdown of this membrane directly correlates with a decline in energy levels.
Some of the factors capable of causing damage to the mitochondria include:
· Toxic substances
· Oxidative stress from free radicals
· Viruses that attack membranes
When it comes to living with the Hepatitis C virus, two reasons stand out for causing mitochondrial membrane damage and, therefore, fatigue:
1. Drugs used for treatment
2. The Hepatitis C virus itself
Drugs: Mitochondrial Toxicity
When medications cause damage to the mitochondria, it is known as mitochondrial toxicity. Used for standard HCV combination therapy, ribavirin is known to be toxic to mitochondria. Ribavirin is a nucleoside analog drug, a class of medications particularly likely to cause mitochondrial damage.
When viruses replicate, a process that involves building new chains of genetic material, viral enzymes may mistakenly add a nucleoside or nucleotide analog onto the chain instead of a normal nucleotide. This mistake causes the viral replication process to grind to a halt. Nucleoside analog drugs can act similarly, interfering with the production of DNA in mitochondria. Unlike other locations for DNA, mitochondria have no mechanism for detecting and fixing such an error. Although potentially able to stop HCV from replicating, nucleoside analogs can also stop the mitochondria from maintaining its longevity.
While severe mitochondrial toxicity is uncommon among those only taking ribavirin, simultaneously taking two or more drugs that can potentially injure the mitochondria poses a much greater risk. People co-infected with HIV/HCV who take ribavirin in combination with anti-retroviral drugs have exhibited more damage to this valuable cell organelle. Some other drugs in use or in development for Hepatitis C that are also nucleoside analogs include:
· Taribavirin (Viramidine) – this drug is a pro-drug of ribavirin, which is converted to ribavirin.
· Polymerase Inhibitors – while not all polymerase inhibitors are nucleoside analogs, valopicitabine (NM283), R-1626 and MK-0608 are.
Viral Damage
It has been suggested that the actual Hepatitis C virus itself may contribute to mitochondrial dysfunction. In addition to the potential mitochondrial damage from therapeutic drugs, several studies have suggested that the Hepatitis C virus contributes to this organelle’s deterioration:
· According to a study published in the July 2006 edition of Journal of Virology, researchers reported that HCV infection causes cellular DNA damage and mutations. This injury was confirmed to be mediated by nitric oxide (NO), a substance known to damage mitochondria.
· A recent study found an inverse relationship between HCV viral load and the amount of mitochondrial DNA in peripheral blood mononuclear cells. This means that a rise in HCV viral particles in a person’s system corresponds with fewer functional mitochondria.
· According to a study published in the September 2005 Journal of Biological Chemistry, a Hepatitis C viral protein directly affects mitochondria. By looking at the oxidative stress caused by free radicals, researchers concluded that antioxidant therapy may defend against some of HCV’s damage to mitochondria.
Lipid Replacement Therapy
Preventing mitochondrial cell membrane damage and loss of membrane integrity are important for averting the loss of cellular energy. One popular method that has been used to replace damaged components of the mitochondrial membrane is replacement therapy. By replacing the damaged lipids with phospholipids and fatty acids essential to the structure and function of biological membranes, restoration of the mitochondria’s boundaries is possible.
The first outward sign of mitochondrial membrane deterioration is likely to be fatigue. Damage to the mitochondrial membrane results in the following cascade of events:
1. Its phospholipid structure loses fluidity which leads to…
2. An increasingly porous membrane which leads to…
3. A reduction in the membrane’s electrical potential which leads to…
4. A decreased capability of making cellular energy.
Using lipid replacement therapy, the innovation of NT Factor® has been successful in repairing the mitochondrial membrane and restoring people’s energy levels. Shown in clinical studies to increase participant’s energy by up to 40 percent, NT Factor® has helped many people combat the mitochondrial membrane’s decline. With the ability to strengthen this important membrane, the mitochondria become more resilient to nucleoside analogs and virally-induced damage – thus preserving a person’s energy.
Affecting between 65 and 75 percent of people with HCV, profound fatigue is a likely result of a deficiency in the mitochondria. Helping to sustain the fluidity of cell’s mitochondrial membranes has the direct result of maintaining youthful vigor. Whether due to aging, medications or a result of HCV, consider lipid replacement therapy as a means to energize your mitochondria and abandon excessive tiredness.
References:
Agadjanyan, Michael, PhD, Garth L. Nicholson, PhD, et al., Nutritional Supplement (NT Factor™) Restores Mitochondrial Function and Reduces Moderately Severe Fatigue in Aged Subjects, Journal of Chronic Fatigue Syndrome, 2003.
Machida K., et al., Hepatitis C virus triggers mitochondrial permeability transition with production of reactive oxygen species, leading to DNA damage and STAT3 activation, Journal of Virology, July 2006.
Masaaki Korenaga, et al., Hepatitis C virus core protein inhibits mitochondrial electron transport and increases ROS production, Journal of Biological Chemistry, September 2005.
Okuda M., et al., Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein, Gastroenterology, February 2002.
www.hcvadvocate.org, Mitochondrial Toxicity, Liz Highleyman, Hepatitis C Support Project, August 2007.
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January 6, 2009
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Discover why alcoholic hepatitis, pathological gambling and alcoholism can all benefit from supplementing with a well-known amino acid.
by Nicole Cutler, L.Ac.
Although alcoholism is not a prerequisite to alcoholic hepatitis or pathological gambling, all three of these predicaments are entangled in a web of similarities. Alcoholism is a chronic disease where a person is dependent on alcohol; alcoholic hepatitis is a condition that progressively harms the liver as more alcohol is consumed; and pathological gambling is an inability to stop gambling even when one recognizes that it is causing serious life problems. Each of their respective definitions makes them entities onto themselves. However, one single supplement can help all three of these problems.
Several of the facts supporting their intertwined web are:
· At their core, alcoholism and pathological gambling are both serious addictions.
· Abusing alcohol is the most straightforward path towards developing alcoholic hepatitis.
· As a treatment approach, supplementing with N-Acetyl Cysteine (NAC) has been shown to help alcoholism, alcoholic hepatitis and pathological gambling.
N-Acetyl Cysteine
Glutathione is a powerful antioxidant found within every one of the body’s cells. Known to defend the cell it inhabits against damage, glutathione is often depleted with repeated exposure to toxins, increasing age and chronic disease. Rapidly metabolized to glutathione by the body, NAC is an amino acid supplement. Thus, it is used by many healthcare professionals to protect people’s cells from the universal cause of declining health, cellular damage.
Alcoholism
According to a study published in the Archives of General Psychiatry, approximately thirty percent of U.S. adults have experienced alcohol abuse or alcoholism. Alcohol abuse involves engaging in excessive drinking that causes health or social problems without a full loss of control or dependence on alcohol. Alcoholism, or alcohol dependence, is a disease that includes these four symptoms:
1. Craving alcohol
2. Loss of control – not being able to stop drinking
3. Physical dependence – experiencing withdrawal symptoms such as nausea, sweating, shakiness and anxiety after stopping drinking
4. Tolerance – the need to drink greater amounts of alcohol to get high
With full commitment and support, alcoholism is considered to be treatable. Medications, counseling and self-help groups are among the therapies that can help an alcoholic recover. While taking NAC is not advised as part of this recovery, it can help protect the liver from alcohol’s damage. This is because of the following:
· Responsible for alcohol-induced liver damage, acetaldehyde is a toxic byproduct of alcohol consumption.
· N-Acetyl Cysteine binds to acetaldehyde, thus preventing its damaging effects.
Alcoholic Hepatitis
Inflammation of the liver caused by alcohol consumption, alcoholic hepatitis does not necessarily result from an alcohol addiction. However, alcoholic hepatitis is more likely to develop in heavy drinkers than those who rarely or moderately indulge.
In those unable or unwilling to abstain from drinking alcohol, alcoholic hepatitis can easily progress to cirrhosis and liver failure. Unfortunately, it might be extremely difficult for those with an addiction to alcohol to quit – putting them most in danger of this fate.
Taking a supplement is not a substitute for alcohol abstinence. However, NAC can help the liver of someone with alcoholic hepatitis much in the same way that it may benefit an alcoholic. Because it can replenish depleted glutathione levels, those with all kinds of liver inflammatory diseases could benefit from NAC supplementation.
Pathological Gambling
Although there is no substance that a person swallows, snorts, injects or smokes, pathological gambling is a problematic addiction. Compulsive gambling parallels alcohol and drug addiction in many ways, including losing control over one’s behavior and commonly lying and cheating in order to continue one’s addiction. Problematic gambling is more common among those who abuse or are dependent on alcohol than in those without an alcohol use disorder.
The action that compulsive gamblers crave is an aroused, euphoric state comparable to the high sought by drug users. This aroused state is accompanied by changes in brain chemistry similar to those caused by alcohol or drugs. Those with an addiction typically develop a tolerance to gambling much like alcoholics develop a tolerance to alcohol. In order to create the same amount of excitement, pathological gamblers often increase the size of their bets or the odds against them.
By the time most pathological gamblers seek help, they are in enormous debt and their relationships with friends and family members have been destroyed. Statistics show that about 80 percent of pathological gamblers seriously consider suicide, and 13 to 20 percent actually attempt it or kill themselves.
The gravity of this problem drove researchers at the University of Minnesota to look for unconventional solutions to pathological gambling. They discovered that supplementing with NAC might help curb pathological gamblers’ addiction. Published in the September 2007 edition of Biological Psychiatry, the researchers believe this has to do with NAC’s impact on brain chemistry. Because NAC affects glutamate, a chemical in the brain frequently associated with reward, NAC may help to control various types of addictions – including pathological gambling.
N-Acetyl Cysteine is far from a panacea for addictions or diseases characterized by liver inflammation. However, the more it is studied, the greater range of conditions it proves to aid. By replenishing depleted glutathione levels, protecting liver cells from damaging toxins and affecting the brain to reduce an addict’s need for reward, NAC possesses enormous healing potential. Until this amino acid’s full value is realized, supplementing with N-Acetyl Cysteine could help support those battling alcoholism, alcoholic hepatitis or pathological gambling.
References:
Grant JE, et al, N-acetyl cysteine, a glutamate-modulating agent, in the treatment of pathological gambling: a pilot study, Biological Psychiatry, September 2007.
http://findarticles.com/p/articles/mi_6839/is_2008_Jan/ai_n28493756, N-acetyl cysteine may curb gambling addiction, Life Extension, Dayna Dye, Retrieved December 22, 2008, Life Extension, January 2008, CBS Interactive Inc., 2008.
http://pubs.niaaa.nih.gov/publications/arh26-2/143-150.pdf, Pathological Gambling and Alcohol Use Disorder, Jon E. Grant MD, et al, Retrieved December 22, 2008, Alcohol Research and Health, 2002; 143-50.
http://rf-web.tamu.edu/security/SECGUIDE/Eap/Gamble.htm, Compulsive Gambling, Retrieved December 22, 2008, Texas A&M Research Foundation, 2008.
http://www.lifeextensionvitamins.com/ananwihe.html, Anti-Alcohol Antioxidants with Hepatoprotection, Retrieved December 25, 2008, Life Extension Vitamin Supplies and Life Extension Institute, Inc., 2008.
http://www.mayoclinic.com/health/alcoholism/DS00340, Alcoholism, Retrieved December 25, 2008, Mayo Foundation for Medical Education and Research, 2008.
http://www.medicalnewstoday.com/articles/82240.php, Pathological Gamblers Addiction Targeted By Health Food Supplement, Retrieved December 22, 2008, MediLexicon International Ltd, September 2007.
http://www.webmd.com/mental-health/alcohol-abuse/news/20070702/
alcohol-abuse-alcoholism-common, Alcohol Abuse, Alcoholism Common, Miranda Hitti, Retrieved December 25, 2008, WebMD LLC, 2008.
http://www1.umn.edu/umnnews/Feature_Stories/Curbing_gambling_
addiction_with_food_supplements.html#, Curbing gambling addiction with food supplements, Retrieved December 22, 2008, Regents of the University of Minnesota, September 2007.
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January 5, 2009
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Learn about the potential connection between Hepatitis C and fibromyalgia, and find out why it is possible that Hepatitis C infection may act as a trigger for fibromyalgia syndrome. If you suspect having both conditions, awareness of this link can lead you to seek the expert evaluation and care that may help reduce your symptoms of pain and fatigue.
by Nicole Cutler, L.Ac.
Due to overwhelming empirical evidence, some medical circles believe that the symptoms and presenting patterns shared between Hepatitis C and fibromyalgia are beyond coincidental. While Hepatitis C is known to be transmitted through infected blood, authorities are still debating how fibromyalgia is acquired. Due to similarities in manifestation and physiology, there is a possibility that Hepatitis C infection may be one of fibromyalgia syndrome’s triggers. If you suspect having both conditions, awareness of this link can lead you to seek the specialized evaluation and care that may improve your most frustrating symptoms.
Prevalence
Estimates of disease prevalence in the United States approximate the number of people living with fibromyalgia to be around 6 million people, while the number of people known to be living with Hepatitis C hovers just above 4 million. While accurate statistics of the number of people affected by both diagnoses are not currently available, a surprising number of people dually diagnosed with Hepatitis C and fibromyalgia are emerging. However, one study did find the prevalence of fibromyalgia in people with Hepatitis C (15 to 19 percent) to be much higher than the occurrence of fibromyalgia in the general American population (2 percent).
Fibromyalgia
Fibromyalgia is a syndrome causing widespread muscle pain, extreme fatigue and multiple tender points in specific parts of the body. With pain characterized as aching, burning, stabbing and throbbing, its severity can vary widely. While fibromyalgia is a chronic condition, it is not a progressive disease. However, this condition can greatly reduce the quality of life of those affected.
Experts do not agree on what causes fibromyalgia. When trying to determine the etiology of this complex syndrome, it is challenging to discern between cause and effect. The endless cycle of pain, inactivity, insomnia, fatigue and depression typical of fibromyalgia complicates the isolation needed to trace this syndrome’s origins. Although researchers have identified several possible reasons for fibromyalgia, it remains unclear if they are a cause, or part of the problem. Some of the leading contenders for what triggers fibromyalgia include:
· Hormone Imbalance
· Infectious Disease
· Immune System Malfunction
· Sleep Disorder
· Traumatic Event
· Muscle Abnormality
The Hepatitis C Connection
Although not yet confirmed, many experts believe that Hepatitis C may act as a trigger to the onset of fibromyalgia. The documented links between the two conditions include:
· Symptom Specificity – Fibromyalgia and chronic Hepatitis C infection share many clinical features including musculoskeletal pain and fatigue. While the two conditions do not always accompany each other, some symptoms may be unique when a person has both fibromyalgia and Hepatitis C. One study found that people dually diagnosed with fibromyalgia and Hepatitis C exhibit symptoms such as inflammation around a joint, bursa and/or tendon, and vasculitis (blood or lymph vessel inflammation) that are not seen in Hepatitis C negative people with fibromyalgia.
· Immune Proteins – Cytokines are proteins that regulate immune response. Interleukins are a specific type of cytokine that cause a person to feel pain. Several interleukins have been found to be dramatically elevated in fibromyalgia patients. Harvard researchers found those same interleukins increased in production when exposed to the Hepatitis C virus.
· Hepatitis C and Pain – Many people infected with Hepatitis C virus infection complain of myalgias, arthritis and widespread pain. When compared to other liver diseases, the frequency of musculoskeletal pain clearly favors Hepatitis C. The frequencies of musculoskeletal pain for the following isolated conditions are as follows: Alcoholic liver disease = 48 percent, Hepatitis B = 59 percent and Hepatitis C = 91 percent. As fibromyalgia’s most prominent symptom, it is not surprising that musculoskeletal pain may represent the link to Hepatitis C.
Infectious Cause
Certain infections, notably viruses, often occur in the histories of people with fibromyalgia. As these infectious organisms invade the body, scientists think they may cause damage at a cellular level. While fibromyalgia is considered to be non-contagious, it is possible that it may be a manifestation of a viral disease such as Hepatitis C, which is contagious. While many infectious microorganisms have been tied to fibromyalgia, the link with Hepatitis C is becoming increasingly suspect. At this point, there is sufficient evidence linking infectious diseases and fibromyalgia together, but it is unknown if any of these microorganisms are fibromyalgia’s origin, a simultaneous condition or a result.
Why it Is Important
A high prevalence of fibromyalgia has been found in patients infected with Hepatitis C, especially women. According to Israeli researchers, recognizing fibromyalgia in people with Hepatitis C will prevent misinterpretation of fibromyalgia symptoms as part of the liver disease and enable physicians to correctly focus on alleviating these symptoms.
A doctor well versed in fibromyalgia should be consulted if this syndrome is suspected. Because its diagnosis is not simple and symptoms often overlap with other conditions, a proper evaluation will test for fibromyalgia while ruling out other diseases. Doctors who are familiar with fibromyalgia typically make a diagnosis based on criteria established by the American College of Rheumatology (ACR). Those criteria are:
1. Widespread pain (right and left side body pain, above and below the waist) that lasts for more than 3 months.
2. Eleven or more tender points present at 18 specific sites on the body.
Whenever there is a profound crossover in a disease’s symptoms, we can learn from their parallels. Although many questions shroud the connection between fibromyalgia and Hepatitis C, their relationship exists in many people with either condition. With their comparable symptoms, similar immune biochemistry and irrefutable statistics of simultaneous presentation, exposure to the Hepatitis C virus may be one of fibromyalgia’s triggers.
Understanding this connection may prompt a person with fibromyalgia to get tested for Hepatitis C or it may help a person with Hepatitis C seek evaluation for fibromyalgia. If you think you might be burdened with both conditions, discuss your thoughts with your primary healthcare provider. By taking this proactive stance, you may open yourself up to new ways of reducing Hepatitis C’s challenging symptoms of pain and fatigue.
References:
www.archinte.ama-assn.org, Fibromyalgia in hepatitis C virus infection. Another infectious disease relationship, Buskila D., et al, Archives of Internal Medicine, November 1997.
www.cdc.gov, Viral Hepatitis C Fact Sheet, US Department of Health and Human Services, 2007.
www.hcvadvocate.org, Extrahepatic Manifestations: Hepatitis C and Fibromyalgia, Alan Franciscus, HCV Advocate, July 2006, Hepatitis C Support Project, 2007.
www.ihop-net.org, Fibromyalgia, hepatitis C infection and the Cytokine connection, Thompson ME, Barkhuizen A, Current Pain and Headache Reports, 2003.
www.medscape.com, Fibromyalgia Pain: Do We Know the Source?, Roland Staud, Current Opinion In Rheumatology, April 2004.
www.rheumatology-oxfordjournals.org, Fibromyalgia-associated hepatitis C virus infection, Rivera J, et al., The British Journal of Rheumatology, 1997.
www.vir.sgmjournals.org, Structural proteins of Hepatitis C virus induce interleukin 8 production and apoptosis in human endothelial cells, Anuradha Balasubramanian,, et al., Journal of General Virology, 2005.
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