Good Morning Folks,The beginning of the week brings us a few HCV headlines and important research updates.
Monday Research And News
Experts Offer Guidance on Use of DAAs for Difficult-To-Treat Hep C Patients
ISSUE: MAY 2012 | VOLUME: 63:5
by Christina Frangou
San Francisco—For several months, it has been one of the most pressing questions among clinicians who treat patients with hepatitis C: How well do the two FDA-approved direct-acting antivirals (DAAs) perform in the patients who are most in need of a new form of therapy?
The answer, based on evidence presented at The Liver Meeting 2011, appears to be that these therapies improve sustained viral response (SVR) rates in hepatitis C patients with cirrhosis and those who have previously failed standard therapy, but these patients still lag far behind others, with SVR rates that dip below the 50% mark. Two factors—previous response to treatment and fibrosis stage—appear to be the most important predictors of achieving SVR. But experts have yet to reach a consensus on the best treatment for difficult-to-treat patients.
In a crowded plenary session called “HCV: Refining the Use of Direct-Acting Antivirals,” researchers presented three new subanalyses from the Phase III trials that led to the approval of boceprevir and telaprevir. Overall, the new reports revealed the following:
The answer, based on evidence presented at The Liver Meeting 2011, appears to be that these therapies improve sustained viral response (SVR) rates in hepatitis C patients with cirrhosis and those who have previously failed standard therapy, but these patients still lag far behind others, with SVR rates that dip below the 50% mark. Two factors—previous response to treatment and fibrosis stage—appear to be the most important predictors of achieving SVR. But experts have yet to reach a consensus on the best treatment for difficult-to-treat patients.
In a crowded plenary session called “HCV: Refining the Use of Direct-Acting Antivirals,” researchers presented three new subanalyses from the Phase III trials that led to the approval of boceprevir and telaprevir. Overall, the new reports revealed the following:
- Cirrhotic patients who previously received the standard two-drug therapy and then received telaprevir in combination with pegylated interferon (Peg-IFN) and ribavirin had improved SVR compared with patients who received Peg-IFN and ribavirin alone. However, among those with cirrhosis, SVR rates peaked at 47% in previous responders and were lower for previous null responders. The study also found that cirrhotic patients with several baseline factors—high baseline alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels—were more likely to achieve SVR following telaprevir triple therapy.
- HCV genotype 1–infected patients who previously failed Peg-IFN and ribavirin treatment had significant improvements in SVR rates when telaprevir was added to their therapy. But the strongest predictor of achieving SVR with a telaprevir-based regimen was the patient’s previous response to Peg-IFN and ribavirin. In other words, patients who did not respond to standard therapy had a reduced likelihood of responding to telaprevir. Prior relapsers had the greatest chance of achieving SVR, followed by previous partial responders. The lowest SVR rates were among previous null responders. Patients’ baseline factors also changed the odds for achieving SVR, particularly baseline low-density lipoprotein (LDL) levels and fibrosis stage.
- Among poor IFN responders who received boceprevir in Phase III trials, 28% to 34% achieved SVR compared with 0% to 4% of those who received Peg-IFN and ribavirin alone. Poor IFN responders were much more likely to achieve SVR if they were infected with HCV subtype 1b rather than subtype 1a, and had fibrosis stages 0 to 2 rather than 3 to 4.
That leaves many questions about who should be treated with these new therapies, said session moderator Anna Lok, MD, professor in the Department of Internal Medicine and Alice Lohrman Andrews Research Professor in Liver Disease, University of Michigan, Ann Arbor.
“You can tell these patients that they have a 30% chance of responding. But, there’s the flip side to that—a 70% chance of resistance. All of a sudden, the equation becomes very different,” she said.
Telaprevir-based Regimen: Patients With Cirrhosis
In the first study presented during the session, Stanislas Pol, MD, PhD, professor of hepatology at Université Paris V (René Descartes), and head of the Hepatology Unit at Cochin Hospital, Paris, and colleagues conducted a subanalysis of the Phase III REALIZE (Re-treatment of Patients with Telaprevir-based Regimen to Optimize Outcomes) trial (presentation 31). The study was designed to gauge the effect of triple therapy including telaprevir on patients with Child class A cirrhosis who previously responded poorly to the Peg-IFN and ribavirin regimen.
The REALIZE study compared telaprevir in combination with Peg-IFN and ribavirin in patients with HCV genotype 1 who had a previous null or partial response or who relapsed after treatment with Peg-IFN and ribavirin. The study included one treatment arm of Peg-IFN and ribavirin alone and two telaprevir treatment arms, which were pooled together for this analysis.
Of 662 randomized patients, 578 with complete baseline information were included in the study. There were 169 patients with cirrhosis and 493 without. Cirrhotic patients were slightly older and more likely to be prior null responders but, otherwise, the two groups were similar in demographics.
Results showed that SVR was achieved in 75% of patients who underwent triple therapy and had no, minimum or intermediate fibrosis. However, the SVR rate decreased to 67% in patients with bridging fibrosis and dropped to 47% in cirrhotics. SVR rates were even lower among cirrhotics who were previous partial responders, at 34%, and cirrhotics who were previous null responders, who had the lowest SVR rate reported, at 14%.
Previous response to Peg-IFN and ribavirin therapy was a key predictive factor for all patients. Even among non-cirrhotic patients who had previously not responded to Peg-IFN and ribavirin, the SVR was low, at only 41%. The rate was similarly low (42%) among previous null responders with mild fibrosis.
The study showed that a relationship exists between fibrosis stage, prior response and SVR but the association with fibrosis stage is not singularly incremental. Patients who relapsed after prior Peg-IFN and ribavirin therapy still achieved high rapid viral response rates and low virologic failure rates, irrespective of the fibrosis stage. However, for prior null and partial responders, fibrosis stage had a significant impact on SVR.
Rash, pruritus and anemia (hemoglobin <10 g/dL) were more frequent in cirrhotic patients receiving triple therapy (43%, 55% and 44%, respectively) than in those who received Peg-IFN and ribavirin alone (27%, 35% and 27%, respectively). Adverse events led to telaprevir discontinuation in 15% of cirrhotic patients compared with 11% of non-cirrhotics. Anemia and neutropenia were significantly more common in cirrhotics (42% and 25%) than non-cirrhotics (34% and 27%).
After hearing the study presentation, Paul Pockros, MD, division head of gastroenterology/hepatology and director of the Center for Liver Diseases at Scripps Clinic in La Jolla, Calif., said that many of his cirrhotic patients become anemic “rather rapidly,” a finding not borne out in Dr. Pol’s study of Child class A patients. The condition is difficult to manage because it begins soon after DAA treatment is initiated. Making it worse, according to FDA recommendations, cirrhotic patients are required to undergo a 48-week course of therapy and are not eligible for a shortened course of therapy.
Dr. Pol noted that anemia occurs in approximately 50% of patients in his group’s unpublished experience with more advanced cirrhotics and “indeed” appears very early. However, he cautioned that, for the moment, the recommendation remains to treat cirrhotics with 48 weeks of treatment, irrespective of extended rapid viral response.
Logistic regression analysis defined the predictors of response to the telaprevir-based regimen in cirrhotic patients. The only factors that were significantly associated with SVR across all groups were low baseline AST levels and prior relapse following Peg-IFN and ribavirin therapy.
Telaprevir-based Regimen: Patients With HCV Genotype 1
In a second study, researchers again analyzed data from the Phase III REALIZE study (Berg T et al, presentation 32). This time, they focused on the predictors of SVR in HCV genotype 1 patients with prior Peg-IFN and ribavirin treatment failure. And again, the study showed that patients’ prior response to treatment predicted their response to DAA therapy.
The study, presented by Thomas Berg, MD, professor of medicine, University Hospital, Leipzig, Germany, included 578 patients of the 662 who were originally randomized. Of these, 28% were prior null responders, 19% were partial responders and 53% were prior relapsers. For the entire cohort, median age was 51 years, 69% were male, 88% had HCV RNA levels of 800,000 IU/mL or less and 25% had cirrhosis.
On multivariate analysis, the following factors were independent predictors of treatment outcome: patients’ prior response to standard Peg-IFN and ribavirin therapy, high LDL concentration, HCV subtype 1b and maximum AST/ALT. A patient’s viral load and stage of fibrosis had only borderline value in predicting SVR. Of all factors, prior response to therapy was the most significant.
There was one other valuable clue as to a patient’s odds of achieving SVR, the researchers found. The on-treatment response—or viral detectability at weeks 4 and 12—was a strong predictor of SVR (odds ratio, 7.8).
“In summary, prior response and on-treatment response appear to be the main predictive factors in terms of likelihood of response. Other baseline parameters, although statistically significant, do not appear to add much prognostic value,” said Dr. Berg. “Further investigation is needed to examine how baseline LDL is associated with treatment response.”
Boceprevir-based Regimen: Prior Poor Responders
In a third study, investigators looked at factors that appear to increase the chance of SVR in patients who are poor IFN responders and then received boceprevir (Bacon BR et al, presentation 33). In this study, patients’ HCV genotype and fibrosis stage appeared to carry the greatest weight in predicting patients who will attain SVR after a poor response to the Peg-IFN and ribavirin lead-in.
Investigators studied boceprevir-treatment outcomes in patients who were poorly responsive to interferon during the four-week Peg-IFN and ribavirin lead-in during the RESPOND-2 (Retreatment with HCV Serine Protease Inhibitor Boceprevir and PegIntron/Rebetol 2) and SPRINT-2 (Serine Protease Inhibitor Therapy 2) Phase III trials (Bacon BR et al. N Engl J Med 2011;364:1207-1217 and Poordad F. N Engl J Med 2011;364:1195-1206, respectively). Of the more than 1,000 patients in the two trials, 28% to 34% responded poorly to IFN, and patients’ response to the lead-in was the strongest predictor of SVR response.
In the follow-up study, investigators focused on 282 poor IFN responders. Of these, 93 patients achieved an SVR. Analysis showed that the baseline factors that were associated with SVR were HCV subtype 1b not 1a, minimal not advanced fibrosis and a low baseline viral load, defined as HCV RNA less than 400,000 IU/mL.
“HCV subtype and fibrosis level may differentiate between responders and nonresponders in poorly interferon-responsive patients,” said Bruce R. Bacon, MD, the study’s lead author and the James F. King Endowed Chair in Gastroenterology, Saint Louis University School of Medicine, St. Louis.
Viral load decline after eight weeks of treatment with boceprevir also was shown to be highly predictive of SVR. No patient studied who had a less than 3 log10 decline in HCV RNA levels after eight weeks of boceprevir went on to achieve SVR.
Still No Consensus
It’s still unclear what these findings mean in terms of best treatment practice for poorly responsive patients. Dr. Lok questioned whether patients should be stopped on boceprevir after eight weeks if they don’t have a significant early response. But, Dr. Bacon replied that there is no well-defined course of action other than detailed conversation with patients.
“If your patient wasn’t doing very well, it’s reasonable to consider stopping,” Dr. Bacon said. “Still, it’s a relatively small group of patients and it hasn’t been prospectively vetted. With those caveats, nonetheless, the data are pretty strong.”
But should patients who have poor baseline predictions even be started on a DAA regimen?
“That’s a good question,” Dr. Bacon said. “And one that has been batted about in multiple conversations that I’ve been in over the last couple of days. I don’t think we have an answer.”
Dr. Bacon noted that new medications are in the pipeline, although they are still several years away. It’s important to consider, too, that any patient who is started on a DAA is at risk for developing resistance. In some groups of patients—cirrhotics and poor IFN responders, specifically—that risk comes without a strong likelihood of a SVR, he said.
Physicians and patients must discuss all these issues.
“Each practitioner and their patients are going to have to address that question. You have to know the data and you have to present it to your patients and let them participate in the decision,” Dr. Bacon said.
“For some people, a 30% chance is valid. That’s the best thing they’ve heard in years. For others, it just isn’t good enough.”
Source:gastroendonews.com
.From Journal of Viral Hepatitis
Association of Hepatitis C With Insulin Resistance and Type 2 Diabetes in US General Population
The Impact of the Epidemic of Obesity
M. Stepanova; B. Lam; Y. Younossi; M. K Srishord; Z. M. Younossi
Introduction Only
Full Text Available @ Medscape
Hepatitis C viral (HCV) infection has been suspected to affect glucose metabolism and predispose HCV-infected individuals to insulin resistance (IR) and type 2 diabetes diabetes mellitus (DM).[1,2] Although not entirely clear, the proposed mechanisms for HCV-related IR/DM may include direct pancreatic β-cell destruction, autoimmune β-cell injury and other mechanisms.[3–6] To support these hypotheses, one study has linked HCV core protein levels with IR as measured by increasing HOMA score values and decreasing the expression of insulin receptor substrate (IRS)-1 and IRS-2.[7] Findings of this study suggest that HCV can upregulate proteosomal degradation of IRS-1 and IRS-2, directly contributing to the development of insulin resistance.
In addition to the molecular mechanism for the interaction between HCV and IR/DM, there are clinical and epidemiological studies providing support for this association. Nevertheless, the clinical and the epidemiological data linking HCV with IR and DM come from both tertiary care medical centres and from population-based studies. In one such study, the prevalence of anti-HCV positivity in DM was 4.39-fold higher than in the matched blood donor controls.[8] In another study involving 1117 HCV and HBV patients, the prevalence of DM was 21% in HCV and 12% in HBV patients.[3] These results were subsequently supported by the Atherosclerosis Risk in Communities (ARIC) study reporting that HCV-infected individuals who were at risk for DM were 11 times more likely than those without HCV to develop overt DM.[9] Finally, a decade ago, a study analysing the data from the Third National Health and Nutrition Examination Survey (NHANES) (1988–1994) suggested that HCV infection in those aged ≥40 years was associated with 3.77-fold increased risk for DM.[10]
It is important to note that the findings from population-based studies reporting association between DM and HCV infection were based on the data collected in the 1980s and 1990s.[10,11] Given the rapid increase in the rate of obesity and DM in the US population in the recent decades, our understanding of the interaction between DM and HCV may benefit from re-examination of this population-based data. In this study, we use the recent NHANES data collections to assess association of HCV infection with IR and DM.....Continue Reading
Cirrhosis and mortality risks of biopsy-verified alcoholic steatohepatitis
The most recent issue of Alimentary Pharmacology & Therapeutics exmines cirrhosis and mortality risks of biopsy-verified alcoholic pure steatosis and steatohepatitis.
Alcoholic fatty liver disease comprises alcoholic pure steatosis and alcoholic steatohepatitis. These diseases are prevalent, but their prognostic outcome is uncertain, particularly regarding the impact of hepatic inflammation.
The paucity of data based on liver biopsy diagnoses contributes to this uncertainty.
Dr Deleuran and colleagues from Denmark examined the cirrhosis and mortality risks of Danish men and women with biopsy-verified alcoholic pure steatosis or steatohepatitis.
In this registry-based historical cohort study, the researchers combined liver biopsy diagnoses with hospital discharge diagnoses from nationwide healthcare registries to identify all Danish citizens with alcoholic pure steatosis or alcoholic steatohepatitis during 1997–2008.
The researchers enrolled a reference cohort of 100 gender- and age-matched persons from the general population for each patient and compared cirrhosis and mortality risks through 2010.
The 5-year mortality risk was 4%
Alimentary Pharmacology & Therapeutics
The team found that the 5-year cirrhosis risks were 7% for patients with alcoholic pure steatosis, and 16% for patients with alcoholic steatohepatitis, their 5-year mortality risks were 17%, and 25%, respectively.
Patients with steatohepatitis had a higher liver-related mortality than patients with pure steatosis.
In the reference cohort, the team found that the 5-year cirrhosis and mortality risks were 0.3% and 4%, respectively
Dr Deleuran's team concluded, "Patients with alcoholic fatty liver disease had markedly increased cirrhosis and mortality risks compared with a matched reference cohort."
"The cirrhosis risk was more than twice as high for the patients with steatohepatitis than for those with pure steatosis, and was higher for women than for men."
Aliment Pharmacol Ther 2012: 35(11): 1336–1342
14 May 2012
Source:GastroHep
New at NATAP
EASL 2012: HEPATITIS C VIRUS REINFECTION FOLLOWING SUSTAINED VIROLOGICAL RESPONSE IN INTRAVENOUS DRUG USERS
The majority of intravenous drug users (IVDUs) are infected with the hepatitis C virus (HCV) and they may be the source of infection of many other subjects due to their risky behavior. Despite the fact that the majority of IVDUs in Greece are infected with HCV genotype 3 and have similar response rates to non-IVDU patients, only a minority of them start antiviral treatment. The risk of reinfection following therapy is one of the main reasons for not initiating antiviral treatment. We evaluated the rate of HCV reinfection in past - current IVDUs following sustained virological response (SVR) having received anti viral treatment in a multidisciplinary program.
EASL Video Highlights
View Two EASL abstracts from ViralEds "Expert Poster Review and Discussion" presentation.
1-Dual Oral Therapy with the NS5A Inhibitor (BMS-790052) and NS3 PI (BMS-650032) in HCV Genotype 1B-infected Null Responder or Ineligible/Intolerant to Peginterferon/Ribavirin
2-PSI-7977 PROTON and ELECTRON: 100% Concordance of SVR4 with SVR24 in HCV GT1, GT2, and GT
View Video Abstract
Standardization of Terminology of Virological Response in the Treatment of Chronic Hepatitis C
Over the past decade, the standard of care for the treatment of infection with HCV – 48 weeks of peginterferon alfa-2a or 2b plus ribavirin – yielded overall sustained virological response (SVR) rates of 42–46%.[1,2] The recent approval of direct-acting antiviral agents (DAA), such as the protease inhibitors telaprevir and boceprevir, represent a new standard of care for treatment-naïve and experienced patients. Many other DAAs are in development as well.
Not unexpectedly, these new agents have brought with them novel study designs, patient categorizations and treatment paradigms, which has led to some confusion over the terminology used at scientific meetings and in published articles, especially for terms relating to on-treatment virological response.
Continue Reading.........
Triple Therapy for Hepatitis C-Maximizing Opportunities and Avoiding Mistakes
A special supplementary issue of Gastroenterology with full text viral hepatitis review articles and commentaries available through open access.
Click here to view an index of articles.
News
Calculating life
Our church is praying for a liver.
That is, we’re praying for a liver to be successfully transplanted into one of our members who contracted Hepatitis C (and other complications) through a bad blood transfusion back in the early 1980s. This brother (I’ll call him “Jim”) shouldn’t even be alive, according to any law of averages—he’s been near death several times, most recently in March. But alive he is, even though time is running out.
His body is now in desperate balance between the other organs, which are gamely struggling on, and his liver, which is rapidly giving up. The protocols for getting on a transplant list are daunting; once on, even more so. His position on the list (No. 1 being first in line) is determined by a rubric called Model for End-Stage Liver Disease (MELD). Even though I have Jim’s explanation in writing, I won’t try to explain. But the formula looks like this:
Jim has finally moved up to No. 1 on the list, so he and his wife are staying in a hotel close to the hospital. (Anyone have Marriott points they’d like to donate?) They expect a call any day now. Any day, any hour … all the months and years of anxious waiting are collapsing in a single moment of incredible density. He’ll live, or he’ll die.
But for him to live, someone else has to die. The donor liver has to be whole and healthy, and preferably young, taken from a life cut short, from someone walking around this moment, perhaps, with no idea that his time is almost up. Jim’s focus is a constant readjustment of scores and blood and fluid and medical terminology, and right now it depends on a single person whose dominant thoughts may be buying a speedboat or planning the twins’ next birthday party. Who lives, who dies? Hospitals, insurance companies, and government agencies pare lives down to formulas, because they have to. But we belong to One who knows all factors, and needs no formulas.
God doesn’t calculate: He died; we live. That’s what Jim can count on, whatever the next month may hold. The ultimate decision is not ours, and that’s ultimately a comfort.
Source
That is, we’re praying for a liver to be successfully transplanted into one of our members who contracted Hepatitis C (and other complications) through a bad blood transfusion back in the early 1980s. This brother (I’ll call him “Jim”) shouldn’t even be alive, according to any law of averages—he’s been near death several times, most recently in March. But alive he is, even though time is running out.
His body is now in desperate balance between the other organs, which are gamely struggling on, and his liver, which is rapidly giving up. The protocols for getting on a transplant list are daunting; once on, even more so. His position on the list (No. 1 being first in line) is determined by a rubric called Model for End-Stage Liver Disease (MELD). Even though I have Jim’s explanation in writing, I won’t try to explain. But the formula looks like this:
MELD = 3.78 [Ln bilirubin (mg/dL)] + 11.2 [Ln INR] + 9.57 [Ln creatinine (mg/dL)] + 6.43Pretty impressive. But the bracketed letters and numbers don’t cover all the physical factors of liver disease, as we learned in March when Jim’s near-death episode did not alter his MELD score. It doesn’t make sense that a person has to be in such bad shape that radical surgery is risky before he receives the nod for radical surgery. Steve Jobs received a liver transplant only a year and a half before he died of pancreatic cancer—shouldn’t that liver have—theoretically, anyway—gone to Jim, who isn’t 41 yet and shows no signs of cancer? How are these things really determined?
Jim has finally moved up to No. 1 on the list, so he and his wife are staying in a hotel close to the hospital. (Anyone have Marriott points they’d like to donate?) They expect a call any day now. Any day, any hour … all the months and years of anxious waiting are collapsing in a single moment of incredible density. He’ll live, or he’ll die.
But for him to live, someone else has to die. The donor liver has to be whole and healthy, and preferably young, taken from a life cut short, from someone walking around this moment, perhaps, with no idea that his time is almost up. Jim’s focus is a constant readjustment of scores and blood and fluid and medical terminology, and right now it depends on a single person whose dominant thoughts may be buying a speedboat or planning the twins’ next birthday party. Who lives, who dies? Hospitals, insurance companies, and government agencies pare lives down to formulas, because they have to. But we belong to One who knows all factors, and needs no formulas.
God doesn’t calculate: He died; we live. That’s what Jim can count on, whatever the next month may hold. The ultimate decision is not ours, and that’s ultimately a comfort.
Source
FDA
By Emily P. Walker, Washington Correspondent
FDA Panel Endorses Two HIV Drugs
The FDA's Antiviral Drugs Advisory committee voted 19-3 Thursday that an anti-HIV combination pill should be approved to prevent HIV infection in healthy people.
The combination of emtricitabine and tenofovir (Truvada), made by Gilead Sciences, is safe and well tolerated, the committee decided, and helps prevent HIV infection when used daily by people at high risk, including men who have sex with men and heterosexuals without HIV who have a partner that is HIV-positive.
The vote marks a departure in the battle to control the HIV/AIDS pandemic – HIV drugs until now have always been approved for therapy, rather than for so-called pre-exposure prophylaxis.
The following day the panel turned to another medication by Gilead Sciences -- a new single-pill, once-daily treatment for use in treatment-naïve HIV patients or in those previously treated but without resistance to any of the components.
The committee voted 13-1 to recommend approval of the "quad" pill, which contains four drugs -- two are widely used anti-HIV drugs, emtricitabine and tenofovir, and the other two, elvitegravir and cobicistat, are investigational...Read More @ Medpage Today
Pharmaceuticals
Opioids & An Overdue Senate Probe : Kolodny Explains
By Ed Silverman- May 14th, 2012
Last week, the US Senate Finance Committee is investigating drugmakers that sell prescription painkillers and their ties to several patient advocacy groups and various physicians due to “an epidemic of accidental deaths and addiction resulting from the increased sale and use of powerful narcotic painkillers
We spoke with him about the event that led to these developments and what should be done..Read more @ Pharmalot
HCV Awareness
3Peaks4HCV - Reaching The Summit For Hepatitis C Awareness
Hepatitis C is a life changing disease peppered with life altering moments; both good and bad.
For Peter Moore, like so many people with HCV, the virus silently took up residence in his liver for 10 years before his diagnosis.
Peter is embarking on a HCV awareness campaign unlike any other; he will be spreading the word from atop three peaks spread across the British Isles.
Read More @ HCV New Drugs
Healthy You
Hep C Bulletin: Medication Management
Editors at Hepatitis-Central.com
To assist with drug safety in the presence of Hepatitis C infection, patients are urged to take an active role in managing their medications.
Good healthcare tends to costs a bundle, and not all Americans have it. While this administration's political agenda includes expanding access to healthcare for everyone, the system remains far from perfect. Even those who have health insurance are not guaranteed personalized, detail-oriented, medical attention. As such, everyone is encouraged to know what medications could be harmful to their health. Since the livers of people with Hepatitis C are especially vulnerable to toxicity from medications, these individuals must be particularly knowledgeable about every drug they put in their body....Continue Reading @ Hepatitis Central
UC Berkeley Wellness Letter, June 2012
Vitamin D
Ask the Experts
June 2012
Q: Is it necessary to have some fat in a meal for the body to absorb fat-soluble nutrients such as vitamin D?
A: Probably just a small amount of fat, though the research is not clear and many variables are involved.
The key difference between fat-soluble vitamins (A, D, E, K) and water-soluble ones (C and the Bs) is that the former are stored in the liver and fatty tissues and are eliminated much more slowly than the latter, which need to be consumed more regularly.
A small recent Brazilian study did find that high-dose vitamin D supplements were better absorbed with a very-high-fat meal than a very-low-fat meal. However, some other studies have not found a difference in the vitamin’s absorption.
The evidence is somewhat clearer for beta carotene, a precursor to vitamin A. Studies have found, for instance, that beta carotene in a salad is much better absorbed when regular dressing is used instead of nonfat dressing.
Keep in mind, many factors affect the “bioavailability” of nutrients, notably other nutrients and compounds in the food or meal, what you ate earlier, whether the vitamin is in a food or pill, and your body’s needs.
If you have a varied, nutritious diet, none of this should be a concern, unless you have a medical condition that affects nutrient absorption. As for supplements, we generally don’t recommend them (with the exception of calcium and vitamin D for many people). Supplements are usually overkill anyway—supplying 100 percent or more of the RDA of nutrients—so it hardly matters if absorption is reduced.
Read More @ UC Berkeley
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