Research Articles
Journal of Hepatology: December 2011 (Volume 55, Issue 6)
Viral Hepatitis
Impact of insulin resistance on sustained response in HCV patients treated with pegylated interferon and ribavirin: A meta-analysis
Pierre Deltenre, Alexandre Louvet, Maud Lemoine, Abbas Mourad, Laetitia Fartoux, Christophe Moreno, Jean Henrion, Philippe Mathurin, Lawrence Serfaty
Background & Aims
Recent studies suggested that SVR rates might be lower in HCV patients with insulin resistance (IR) than in patients without IR, but the extent of the impact of IR on treatment response has not been established. We aimed to confirm the role of IR assessed by the homoeostasis model assessment (HOMA-IR) on SVR and to determine its magnitude.
Methods
We performed meta-analysis of studies evaluating the impact of IR in HCV patients treated with pegylated interferon and ribavirin.
Results
Fourteen studies involving 2732 patients were included. SVR was less frequent in patients with IR than in patients without IR (mean difference: −19.6%, 95% CI: −29.9% to −9.4%, p
<0.001). In sensitivity analyses according to HCV-1 patients, patients with IR also less frequently attained a SVR than patients without IR (mean difference: −13.0%, 95% CI: −22.6% to −3.4%, p=0.008). In addition, the baseline HOMA-IR index was lower in responders than in non-responders (mean difference: −0.92, 95% CI: −1.53 to −0.32, p<0.001). In sensitivity analyses restricted to HCV-1 patients, the baseline HOMA-IR index remained lower in responders than in non-responders (mean difference: −0.63, 95% CI: −1.13 to −0.14, p<0.001).
Conclusions
HCV patients with IR have a 20% lower SVR than patients without IR. The baseline HOMA-IR index is a major determinant of SVR.
Beneficial IL28B genotype associated with lower frequency of hepatic steatosis in patients with chronic hepatitis C
Hans L. Tillmann, Keyur Patel, Andrew J. Muir, Cynthia D. Guy, Josephine H. Li, Xiang Qian Lao, Alexander Thompson, Paul J. Clark, Stephen D. Gardner, John G. McHutchison, Jeanette J. McCarthy
Background & Aims
IL28B polymorphisms have been associated with both treatment induced and spontaneous clearance of hepatitis C virus (HCV). We previously found that LDL cholesterol levels were higher in chronic hepatitis C (CHC) patients with the CC genotype at the rs12979860 polymorphism, located proximal to the IL28 gene. Here we analyzed the association of steatosis with IL28B genotype in treatment naïve patients with CHC.
Methods
Two independent cohorts of 145 genotype 1 infected patients from an antifibrotic study and 180 genotype 1 patients from Duke were analyzed for the presence and severity of steatosis in relation to the rs12979860 polymorphism at the IL28B locus. TaqMan assay based genotyping classified three groups CC, CT, and TT.
Results
CC genotype was associated with a lower prevalence of steatosis. In the antifibrotic study, steatosis was found in 47.6% (50/105) of IL28B non-CC vs. 22.5% (9/40; p=0.008) in CC patients. Similarly, steatosis was found in 67.4% (89/132) of non-CC patients compared to only 39.6% (19/48; p=0.001) of CC patients in the Duke cohort.
Conclusions
IL28B CC genotype is associated with less pronounced disturbances of lipid metabolism, as reflected both in serum lipoprotein levels and hepatic steatosis, in HCV infection.
The predictive value of IL28B gene polymorphism for spontaneous clearance in a single source outbreak cohort is limited in patients carrying the CCR5Δ32 mutation
Jacob Nattermann, Jörg Timm, Hans Dieter Nischalke, Anne Olbrich, Monika Michalk, Hans L. Tillmann, Thomas Berg, Heiner Wedemeyer, Hannelore Tenckhoff, Manfred Wiese, Ulrike Kullig, Uwe Göbel, Emanuela Capka, Ingolf Schiefke, Wolfgang Güthof, Kurt Grüngreiff, Ingrid König, Michael Roggendorf, Tilman Sauerbruch, Ulrich Spengler, for the East German HCV Study Group
Background & Aims
The CCR5Δ32 mutation has been suspected to adversely affect outcomes of HCV infection, although reports have remained controversial. Here, we investigated the relative genetic contributions of the CCR5Δ32 deletion and the IL28B rs12979860 polymorphisms to spontaneous clearance of hepatitis C in a single-source outbreak.
Methods
We retrieved 396 Caucasian women (119 women with spontaneous HCV clearance) who had been infected with HCV genotype 1-contaminated anti-D immunoglobulin in 1978, and determined their IL28B and CCR5 alleles.
Results
IL28B CC, CT, and TT genotypes were found in 35.4%, 50%, and 14.6% of patients and corresponded to spontaneous clearance rates of 50%, 21.2%, and 12.1% (Chi2=38.7, p=5.0×10−10), respectively. CCR5 WT/WT, WT/Δ32, and Δ32/Δ32 genotypes were observed in 76%, 22.7%, and 1.3% of patients and corresponded to clearance rates of 33.2%, 21.2%, and 0% (Chi2=6.9, p=0.009), respectively. In a stepwise forward-conditional multivariate regression model both CCR5 (OR 2.1, p=0.01 for WT/WT) and IL28B genetic variants (OR 4.3, p=4.6×10−10 for the C/C genotype) were identified as independent predictors of spontaneous HCV clearance. Importantly, favorable response rates were associated with the IL28B CC genotype only in CCR5 wild-type homozygous women, while HCV clearance in CCR5Δ32 carriers remained poor even in patients with the rs12979860 CC genotype.
Conclusions
Both IL28B rs1297860 and CCR5Δ32 allelic variants are independent genetic determinants of spontaneous HCV clearance. The variable relative distribution between IL28B rs1297860 and CCR5Δ32 allelic variants in different populations may have masked the role of the CCR5Δ32 mutation in some studies.
Click Here For All Abstracts @This Months Journal of Hepatology
Hepatology. 2011 Nov 16. doi: 10.1002/hep.24791. [Epub ahead of print]
Division of Antiviral Products, Office of Antimicrobial Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, MD 20993. Patrick.Harrington@fda.hhs.gov.
Abstract
Boceprevir- and telaprevir-based treatments for chronic hepatitis C virus (HCV) infection use specific response-guided therapy (RGT) guidelines. Eligibility for shortened treatment duration is based on achieving Undetectable HCV RNA early during treatment.
It is unclear whether a detected HCV RNA level that is below the assay lower limit of quantitation (Detectable/BLOQ) is comparable to an Undetectable HCV RNA level, particularly regarding RGT decision making.
We analyzed data from boceprevir and telaprevir clinical trials to obtain a comprehensive understanding of the frequency and clinical relevance of Detectable/BLOQ HCV RNA measurements. In Phase 3 trials P05216 (boceprevir), C216 (telaprevir) and 108 (telaprevir), Detectable/BLOQ levels were reported for approximately 10-20% of all on-treatment HCV RNA measurements. In P05216 and C216, subjects with Detectable/BLOQ HCV RNA, on average, had a reduced sustained virologic response (SVR) rate compared to subjects with Undetectable HCV RNA at the same on-treatment timepoint. At key RGT timepoints (Week 8 for boceprevir, Week 4 for telaprevir), subjects with Detectable/BLOQ HCV RNA had an approximately 20% lower SVR rate compared to subjects with Undetectable HCV RNA, and this difference widened for later on-treatment timepoints. A similar trend was observed for Study 108, but the differences in SVR rates were more modest, which may be explained by a higher frequency of reported Detectable/BLOQ results. Analyses of Phase 2 boceprevir and telaprevir trials indicated subjects with Detectable/BLOQ HCV RNA at RGT timepoints benefited from extended treatment duration.
CONCLUSIONS: During boceprevir- and telaprevir-based treatment, subjects with Detectable/BLOQ HCV RNA had a reduced virologic response compared to subjects with Undetectable HCV RNA. Eligibility for shortened treatment duration should be based on patients achieving Undetectable HCV RNA at RGT decision timepoints. (HEPATOLOGY 2011.).
Copyright © 2011 American Association for the Study of Liver Diseases.
Video:
From the Upper GI to the Lower GI: A Recap of ACG 2011
Dr. David Johnson offers his perspective on some of the key scientific presentations from this year's American College of Gastroenterology meeting.
Medscape Gastroenterology, November 2011
Report: Bee Gees' Robin Gibb fighting liver cancer
Following a couple of health scares this year, Robin Gibb is in the fight of his life.
The Bee Gees star has reportedly been diagnosed with liver cancer, according to the Daily Mail — a condition he became aware of several months ago.
MORE: Bee Gee Robin Gibb Back Home After Health Scare
The 61-year-old "Stayin' Alive" singer, who has become noticeably thinner in recent months, has had to cancel several appearances recently due to issues with severe abdominal pain.
Most recently, Gibb was rushed to the hospital Tuesday, following an emergency call from his home. He was released later that day.
News of Gibb's diagnosis comes on the heels of another hospitalization in October, due to severe abdominal pain.
Hepatitis BLiving with HBV and Dealing with “Itchy” Skin
The previous Hepbtalk blog discussed skin manifestations associated with hepatitis B and liver disease. This is a follow-up with some suggestions on dealing with rashes and pruritus (itchy) skin. Unfortunately, I have experience with this.
Most people living with HBV have episodes with rashes that itch, or with an itch without the rash. Rashes can be caused by all kinds of things, but the skin truly does let us know when there is something going on with our body. We may not be able to eliminate the itch, but we can work on providing the body with a little relief, and to be sure we do not do anything to make the persistent itching worse.
First, consider the root of the problem. It is possible that your rash and itching are unrelated to the current status of your HBV infection. Unless you have serious liver disease, this might be difficult to pin down since many living with chronic HBV have compensated livers that perform all of the necessary liver functions required for life. That does not mean you aren’t going crazy with itchy skin, but it is important to look at other factors that may be contributing to your pruritus.
- Are you currently being treated with IFN or PEG for your HBV?
- Have you recently started a new medication?
- Do you have allergies, seasonal, food or otherwise?
- Do you have other symptoms that might relate to another virus or infection?
- Have you recently switched laundry detergents or rinses?
- Have you recently switched any of your personal care items – shampoo, soap, creams, deodorant, etc.
Try to determine if there is a pattern associated with your skin problems. Any of the above can cause rashes or pruritus without the added complication of HBV or advanced liver disease from HBV. I was convinced that HBV was the root of all skin problems, but I was wrong. That’s why it’s good to look at other possible sources so you can at least eliminate the things you have control over.
Here are some simple things you can do to help reduce the degree of pruritus:
- Choose products that are unscented including laundry detergent and dryer sheets, along with shampoos, conditioners, creams and other personal care items. Unscented products are better for you liver, anyway. Everyone in my house is clean, but there is no fresh, clean smell.
- Avoid soaps and use gentle skin cleansers like Cetaphil (another favorite in our house).
- Use moisturizers that contain a minimum of alcohol, since alcohol is drying. There is sometimes a balance with thick vs. thinner creams. We bounce back and forth between Cetphil and Eucerin, but you might have to test a few of them before you find the one that works best for you.
- Take tepid rather than hot showers and baths, but be sure to bathe daily.
- Wean your kids out of the tub ASAP. This broke my heart, but the extra time in the bath is drying. (However, oatmeal baths are recommended, even though this didn’t work for us). Don’t spend too long in the shower. Learn to take a 5 minute shower.
- When you come out of the shower, do not completely dry yourself, and immediately apply gentle cream or lotion from head to toe to lock in the moisture.
- Use topical steroids in order to combat affected skin patches. For kids we found the ointment, though a little messier, was more effective. Take care when topicals are used for extended periods of time. It thins the skin, which can be especially problematic in the summer. Don’t forget sunscreen, too!
- Keep nails cut short to avoid the temptation. We even tried gloves and socks at night. Try to avoid scratching with sharp objects, but be sure to properly sanitize them if they are used inappropriately. We often had concerns with “weepy” skin and needed to keep it covered in public.
- If you choose to add humidity during the winter months be careful to balance that with possible dust mite allergies. We initially used warm mist humidifiers and that was a big mistake, even though it feels great. Unfortunately it took us a while to make that link. As it turns out, a more moderate temperature is better – that and additional circulation with a ceiling fan.
- Stay hydrated by drinking plenty of water
- After swimming in a chlorinated pool, be sure to rinse immediately and apply moisturizer.
- Pruritus is worse at night, so take an anti-histamine like Benedryl or prescription Atarax to help with the itching. Atarax is effective for a longer period of time, so it’s a favorite in our house.
Although the “itching” in our house brought many tearful nights, and nasty looking skin patches that persisted for years, it did get better over time, with changes. It is important to note that is was much worse during treatment with interferon. Pruritus truly is a horrible, sometimes unrelenting symptom for those with more advanced liver disease. Although the above ideas are worth investigating, it is important that you discuss severe pruritus with your doctor. There are more potent prescriptions available that might help reduce the relentless itching.
Got any tips for reducing the itch? Feel free to comment and share your ideas with others living with HBV.
HIVNo HIV Disease Progression in Transplant Recipients
Sandra Yin
November 18, 2011 (Bethesda, Maryland) — Now that people infected with HIV are living longer, physicians are seeing a growing number who need kidney or liver transplants because of comorbid conditions. But what happens when you take patients in an immunosuppressed population, give them new organs, and further immunosuppress them with drugs to prevent rejection of those organs?
HIV does not progress in HIV-positive transplant recipients, according to findings from a study titled "Opportunistic Infections and Neoplasms Following Liver and Kidney Transplantation in the HIV Infected Recipient," which was presented at the 13th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI) here at the National Institutes of Health (NIH).
But there is a much higher incidence of organ rejection, indicating a dysregulated immune system rather than an absence of immunity, investigators said.
"The take-home message is that HIV is not the issue," Peter Stock, MD, PhD, professor of surgery at the University of California at San Francisco. He was the principal investigator of a multicenter trial in patients with HIV who received liver or kidney transplants.
"It's the comorbidities that are the issue. In other words, we did not see progression of HIV in any of the transplantations. Nor did we see an increase in the incidence of AIDS-related malignancies."
The aim of the trial was to evaluate the effect of HIV infection on graft function and survival, study the effect of transplantation and post-transplant immunosuppression on HIV progression and markers of immune function and activity, and describe the pharmacokinetic interactions between immunosuppressive agents and antiretroviral agents.
The NIH-funded trial involved 150 kidney and 125 liver transplants at 18 centers across the United States, with 3- to 4-year follow up. Patients selected for the study had CD4+ T-cell counts greater than 200 cells/mm3 for kidney recipients and greater than 100 cells/mm3 for liver recipients. For kidney patients, the HIV viral load had to be undetectable while the patients were receiving a stable antiviral regimen. A detectable HIV viral load was permitted in liver recipients as long as the HIV providers said that the virus could be suppressed after transplantation. Researchers excluded patients with opportunistic infections that could not be treated, such as cryptosporidiosis and visceral Kaposi's sarcoma. Post-treatment management included prophylaxis against opportunistic infections, immunosuppression, management of rejection, and antiretroviral therapy.
Of 150 kidney transplant recipients, 20% were co-infected with hepatitis C virus (HCV) at baseline. The median follow-up was 3.6 years. One in 4 patients had a history of opportunistic infections before transplantation.
For the 150 kidney transplant recipients, researchers reported that HIV generally remained suppressed and CD4 counts remained relatively stable. When they used antithymocyte globulin, patients' CD4 counts were wiped out for a year and they still saw minimal opportunistic infections in the year it took for the CD4 counts to come back. The investigators did see a higher incidence of serious bacterial infections, about 2-fold greater, in the patients whose CD4+ counts were deleted. Both patient and graft survival were similar to that in the general population at 1 and 3 years.
The main problem, Dr. Stock said, was a high incidence of organ rejection, 2- to 3-fold higher than what they saw in HIV-negative patients. Research is underway to explore the mechanism behind the high rate of rejection. "But it is real," he said. "It clarifies to me that this is not the absence of an immune system, it is the presence of a very dysregulated immune system."
Among 125 liver transplant recipients, 69% at baseline were co-infected with HCV, 36% had hepatocellular carcinoma, and 12% had a history of opportunistic infections before transplantation. Median duration of follow-up was 4 years.
Compared with patients mono-infected with hepatitis B virus (HBV), HIV-positive liver transplant recipients co-infected with HBV did just as well with their transplants 5 years out. "I think this is the proof that HIV is not the problem," said Dr. Stock. "It's the co-pathogens that are the problem after transplantation. We do a pretty good job of controlling HIV."
HCV was a different story, he said. The 3-year survival rate for the HCV-HIV co-infected group was 64%, compared with 75% for the group with HCV infection only.
Not surprisingly, many centers are balking at transplantations for co-infected patients with HCV, but not those with HBV, because the low survival rate is affecting center-specific results, Dr. Stock said. Those rates could endanger Medicare funding and scare third-party payer referrals away.
Graft survival in co-infected patients at 3 years was 59%, compared with 67% in the mono-infected controls.
The incidence of rejection in the HIV-HCV co-infected patients was 2-fold higher, and 50% of those rejection episodes happened early on.
Treating those rejections is problematic because rejection becomes an independent predictor of graft loss and severe HCV recurrence, Dr. Stock said. Control over the virus and the co-pathogen is lost when these patients are immunosuppressed. "That begs the question of what we're doing to all the viruses that may be associated with cancer," he observed.
"I think the striking thing about the cancer risk in those patients, which is what Dr. Stock was presenting, is that it's not a lot higher than what he observed," Eric Engels, MD, MPH, senior investigator at the National Cancer Institute's Division of Cancer Epidemiology and Genetics, told Medscape Medical News.
There certainly are some cancers, but no more than you would probably expect in a transplant population that did not have HIV infection, Dr. Engels said.
13th International Conference on Malignancies in AIDS and Other Acquired Immunodeficiencies (ICMAOI); Abstract #P6. Presented November 8, 2011.
FDA
FDA drug approvals bode well for nation
Recent reports of the demise of the development pipeline for new medications in the United States appear to have been greatly exaggerated. Reversing a recent multiyear trend of reduced numbers of Food and Drug Administration approvals, 2011 was a very good year.
Thirty-five new medications were approved during the FDA’s 2011 fiscal year, the second-highest number in a decade. New medications on the market include seven treatments for various types of cancer, the first new drug for lupus in more than 50 years, an antibiotic for drug-resistant bacteria and two drugs for hepatitis C.
As a gastroenterologist, I have closely watched development of the two drugs approved for treatment of hepatitis C. These medications are “protease inhibitors,” conceptually similar to those now used to successfully treat HIV.
Hepatitis C is a chronic viral infection of the liver that affects more than 170 million people worldwide. Left untreated, liver disease caused by the virus can lead to poor health and early death. It is the leading cause for liver transplantation worldwide.
Until this year, approved treatments for hepatitis C were effective in only about 50 percent of cases. The two newly approved protease inhibitors increase the cure rate to 70 percent to 80 percent, a major advance.
The story of these drugs is as typical as the approval process is long.
It took nearly 15 years of work — first by university scientists funded from government dollars and later by pharmaceutical companies willing to risk the investment — to develop these drugs.
Why so long? The hepatitis C virus was discovered in 1989. Its genetic make-up was then described in detail throughout the early 1990s by hundreds of scientists all over the world.
The clock really started in 1996, when the hepatitis C virus protein NS3-4A protease was discovered. This suggested that protease inhibitors might prove useful.
It took chemists about four years to develop an active protease inhibitor. It was finally tested in humans in 2004.
Several full-scale clinical trials followed. Because the effects of hepatitis C on the liver are slowly progressive, these trials took several years to accurately judge effectiveness. New drug applications were filed with the FDA in 2010, and approvals were granted this year.
This saga is not unusual. The average time from discovery to the marketplace for new drugs is 10 to 15 years. The majority of drugs fail because of lack of benefit or unacceptable side effects.
To me, the approval of 35 new drugs by the FDA in 2011 makes for a fantastic and optimistic story.
The power of today’s discovery science, increasingly productive interactions between universities and industry and the FDA’s ability to move more quickly on regulatory approvals are remarkable.
And I am certain it will only get better.
If you or a loved one has newly diagnosed hepatitis C, the prospects for a cure are far better this year than last.
Dr. John Barnard is president of the Research Institute at Nationwide Children's Hospital.
Big Pharma
Gilead Sciences agrees to pay $11 billion for hepatitis C drug developer Pharmasset
By Associated Press, Updated: Monday, November 21, 8:13 AM
FOSTER CITY, Calif. — Gilead Sciences Inc. said Monday that it has agreed to pay about $11 billion for drug developer Pharmasset Inc. in a huge bet on its experimental hepatitis C treatments. The offer is an 89 percent premium over the stock’s latest closing price.
Pharmasset, based in Princeton, N.J., currently has no products on the market but is developing potential treatments for a disease that is expected to become a larger public health problem as baby boomers get older.
Hepatitis C is spread through the blood. That can happen through needle sharing or having sex with an infected person. The disease could also be picked up from blood transfusions before 1992, when testing of the blood supply for the virus began.
Gilead said it will pay $137 per share in cash for each Pharmasset share. The stock closed at $72.67 on Friday, and climbed $62.33, or 86 percent, to $136 in pre-market trading on Monday. Gilead shares dropped $1.98, or 5 percent, to $37.90.
The Pharmasset board unanimously approved the deal, which will be made in the form of a tender offer for the stock.
Schaefer Price, president and CEO of Pharmasset, said Gilead’s “established expertise and leadership in the field of antiviral drug development and commercialization” makes it a good match for Pharmasset.
Pharmasset shares climbed earlier this month after the company said it had started late-stage clinical testing of an experimental hepatitis C drug labeled PSI-7977. The company will run a 12-week study that treats hepatitis C with a combination of PSI-7977 and ribavirin, both of which are given orally.
Pharmasset plans to start two other late-stage trials in 2012 and hopes to file for marketing approval of PSI-7977 in the United States and European Union in the second half of 2013.
Pharmasset’s regimen could become a preferred option for hepatitis C if studies show it works as well as drug cocktails containing the intravenous drug interferon. Dosing the drug would be more convenient, and it could have fewer side effects because it does not include interferon.
Gilead, which is based in Foster City, Calif., said it will pay for the deal with cash on hand, bank debt and senior unsecured notes. It expects the acquisition to close in next year’s first quarter.
Copyright 2011 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
Troubled Boehringer Unit Suspends Manufacturing
As we previously reported, the FDA issued a 483 inspection report last May, and inspectors found numerous problems, many of which Ben Venue failed to properly investigate. These included metallic particles or flakes in some medicines, which inspectors suggested came from scrapes on metal doors or window frames; rain water leaking through a ceiling; operators were using gloves that were not sterile and shedding fibrous materials; bacterial contamination in some batches of medicines and mold in classified areas, including manufacturing areas
Without Consent: How Drugs Companies Exploit Indian 'Guinea Pigs'
(The Independent, London, November 14, 2011)
"Western pharmaceutical companies have seized on India over the past five years as a testing ground for drugs -- making the most of a huge population and loose regulations which help dramatically cut research costs for lucrative products to be sold in the West…Globally, it is estimated around 120,000 trials are taking place in 178 countries...China, Indonesia and Thailand are among the countries which have also seen the incidence of trials soar in recent years. A quarter of all clinical data submitted to European drug regulators to secure market approval for a new drug has been obtained from trials in low- and middle-income countries. Confidential data from drug companies suggests this has recently increased to closer to 50 per cent…[regulations aside] India is…attractive…for researchers…because of the…genetic diversity of the 1.2 billion population and because of the variety of conditions to treat. Added to this, almost all doctors speak some English. The infrastructure for such trials, often in the form of government hospitals, is widely available....
Off The Cuff
Canada: In Medicine, Sometimes It's Better to Do Nothing
(The Globe and Mail, Toronto, November 14, 2011)
"That Latin maxim roughly translated as 'above all, do no harm' is a key element of the Hippocratic Oath. One of the foundational elements of medical ethics is non-maleficence, the notion that when treating a patient, it may be preferable to not do something, or even do nothing at all, if the intervention risks causing more harm than good. Yet, in our modern era, with its dizzying technological innovation, ready access to a cornucopia of drugs and impatience driven by the jolts-per-minute pace of daily life, the guiding maxim has become: 'Do something. Do anything.' You see it every day in medical practice…We seem -- in medicine as in life -- to have lost the precious ability to ponder. To wait. To utter the three magic words 'I don’t know.' To wisely do nothing until we do know more, or until nature takes its course. The result is an epidemic of overtreatment that is both financially costly and physically harmful...
Social Media
The Director of the Mayo Clinic Center for Social Media recently visited Australia and talks about how social media has the potential to improve patients' health.
Healthy You
The Fiber Brigade
Food companies are adding fiber to almost everything, for better or worse
If you’re not keen on foods that are naturally high in fiber—such as oatmeal, lentils, broccoli and peas—you may be tempted to choose fiber-fortified foods as a way to get your “roughage.” Manufacturers are putting isolated (“functional”) fibers in foods such as yogurt, ice cream, sugary cereals, energy bars, even juices and water, in order to make “high-fiber” claims. Dietary fiber, found in plant foods, promotes good bowel function and lowers blood sugar and cholesterol, among other benefits. The general recommendation is to get 14 grams of fiber for every 1,000 calories you consume. But are fiber-fortified foods as good as those that contain intact, naturally occurring fiber?
Teasing apart the fibers
Isolated fibers are either extracted from foods or chemically synthesized. They include inulin (from chicory root), pectin, polydextrose, methylcellulose and maltodextrin. If you see a highly refined food (such as white bread) or a food that normally contains no fiber at all (such as yogurt) that lists a fair amount of fiber on the nutrition label, chances are you’ll find one or more of these isolated fibers in the ingredients list. In contrast, if you see wheat bran, corn bran or oats on the ingredients list, for instance, you’re getting natural intact fiber.
Food companies also use small amounts of isolated fibers for a variety of reasons other than their fiber—for instance, to replace fat and sugar in salad dressings, dairy foods and frozen desserts; thicken puddings; prevent separation in chocolate milk; or add crispness to pizza crust.
Faux fiber vs. the real thing
Isolated fibers have health benefits on their own (see page 2). But there’s not much evidence that adding fiber to food has the same effects as eating foods that are naturally high in fiber. The research on isolated fibers is inconsistent, and much of it is funded by manufacturers. Often, the amount of fiber added is too little to matter.
Moreover, different dietary fibers have different physiological effects, and many fiber-fortified foods contain only one type of fiber, not the range found in naturally high-fiber foods. Keep in mind, too, that it’s not even clear whether all or most of the benefits of a high-fiber diet, such as de--creased risk of heart disease, come from the fiber itself or from the vitamins, minerals and other plant compounds that accompany the fiber.
Cases in point:
• Not all isolated fibers do much to keep you “regular”—a prime reason why people seek out high-fiber foods. Some, like cellulose and pea or oat hull fiber, help constipation, says Dr. Wendy Joanne Dahl, assistant professor of food science at the University of Florida, while others, such as maltodextrin, won’t help much.
• Many isolated fibers lack the “gumminess” that natural soluble fibers have, which is what’s key in their ability to help control blood sugar and cholesterol levels. Polydextrose and maltodextrin, for example, are not gummy (who wants gummy orange juice?) and thus won’t have these benefits. And it’s unclear how much of an effect inulin has on blood cholesterol.
• When consumed in large amounts, isolated fibers—such as oligofructose, polydextrose and inulin—can cause gas and bloating and have a laxative effect. And it’s easy to overconsume ice cream and other tempting foods that have fiber added to them, compared to foods that naturally contain fiber, such as broccoli.
BOTTOM LINE: Fiber-fortified foods can help boost your overall fiber intake, but they tend to be foods that are not very nutritious in other ways. You’re better off eating fiber-rich unprocessed foods—whole grains, legumes (beans, peas, lentils), vegetables and fruit—which contain a range of natural fibers, as well as nutrients and other beneficial substances. An English muffin made of refined flour with some fiber added back in, for example, is not the same as one made from whole grains, which retain all the healthful components of the grain.
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