Risk Of Developing Liver Cancer After HCV Treatment

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Thursday, February 16, 2012

News Ticker: Fake Drugs - All At a Pharmacy Near You!

The Newspaper Boy - Christian Krohg


New On The Blog 

New On The Web Site
 In The News
Henry I. Miller, Contributor
 The FDA has increased the number of its investigations of domestic counterfeiting (which can involve ingredients from abroad) several-fold during the past decade. The perpetrators include not only greedy businessmen trying to increase their profit margins, but also big-time organized crime entities, such as the Russian mafia, Chinese triads and Columbian drug cartels, as well as terrorist groups such as Hezbollah, the Irish Republican Army and Spain’s separatist organization ETA.
Some products, such as the fake “generic Tamiflu,” are completely bogus. In dozens of drugs in the United States — including anti-HIV medicines, cholesterol-lowering agents, and anti-arthritis medications — dangerous substances have been substituted for the active ingredient.
 Continue Reading Here
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Specialty Pharmacy Reveals Early Incivek, Victrelis Data:

‘It’s Looking Good’ for Many
 Reprinted from SPECIALTY PHARMACY NEWS, a monthly newsletter designed to help health plans, PBMs, providers and employers contain costs and improve outcomes related to high-cost specialty products.
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By Angela Maas, Managing Editor - February 2012Volume 9 Issue 2
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When the FDA approved Incivek (telaprevir) and Victrelis (boceprevir) for the treatment of hepatitis C last May, many in the industry hailed them as game-changers. Not only are Merck & Co., Inc.’s Victrelis and Vertex Pharmaceuticals Inc.’s Incivek the first oral hepatitis C therapies and the first protease inhibitors approved for the condition (SPN 5/11, p. 1), but new data just released echo the clinical trials data that indicate the drugs also show much more promise than the previous regimen of pegylated interferon and ribavirin did of actually clearing the virus.

The drugs could cut the current 48-week treatment time down to 24 weeks for certain patients if they achieve an early viral response. However, both drugs are used with pegylated interferon and ribavirin to create a triple therapy that is fairly complicated (SPN 9/11, p. 1). People taking Incivek stop that treatment after the initial 12 weeks and continue the regimen only with pegylated interferon and ribavirin, while people on Victrelis do not take it for the initial four weeks of treatment.

Patient adherence to the rigid treatment regimen is critical to the drugs’ success, and many people are expected to clear the virus, meaning they are essentially cured. Compliance with the regimen also can have a huge impact on health plans’ bottom lines. Merck set Victrelis’ weekly price at $1,100, or $26,400 to $48,400 for a course of treatment. Vertex gave Incivek a price tag of $49,200 for a 12-week regimen. Those prices mean that treatment costs for the condition have basically doubled.

Steve Burman, CEO of Burman’s Medical Supplies and Specialty Pharmacy and president of Burman’s Pharmacy, points to a study that shows each patient in which an early viral response is identified “can save the health system a minimum of $16,200 via shortened duration of treatment. With approximately 400,000 naïve/relapsed patients in the U.S., that represents the potential of reducing the cost burden to the health system by over $4 billion.

Additional saving opportunities exist when you consider identifying those less-fortunate patients by applying the FDA futility rules,” which apply when patients are not responding, and the FDA recommends halting the therapy.

With patients who were among the first to be dosed recently hitting the 24-week mark in their regimens, Burman has shared exclusive data with SPN on what his specialty pharmacy has seen so far among about 700 people it has treated with Incivek and Victrelis.

Among the people taking Incivek, “50% of referrals were for patients who were naïve” to previous hepatitis C treatment, which is exactly what Vertex had estimated, he notes. Nineteen percent were relapsers, 17% were partial responders to prior therapy, and the rest were nonresponders.
Among those taking Victrelis, “63% of the patients were naïve,” with the remainder of the patients equally divided among the other three demographic groups.

Within the naïve patient population on Victrelis, “66% achieved an early viral response; therefore, they have the opportunity for response-guided therapy,” meaning the shortened duration of treatment.
Among a sample of 77 patients taking Incivek, 75% of the naïve patients were eligible for response-guided therapy, a percentage that is “actually a little bit better than controlled studies,” he says. And 91% of prior relapsers were eligible for response-guided therapy, which is “pretty much what’s expected. Relapsers have a really great chance of clearing the virus. The only thing we can do now is compare ourselves to the clinical trials data.”

With Incivek, “if people were partial or nonresponders to previous therapy, they are not eligible for response-guided therapy and instead need to go for 48 weeks of treatment.” However, says Burman, “there are some patients who are partial responders who qualify for response-guided therapy with Victrelis.”

People treated for hepatitis C with the previous two-drug regimen have always been at risk of stopping treatment because of the dreadful flu-like symptoms they cause. Adherence is even more at risk with the addition of Incivek and Victrelis, though, which bring additional side effects.
Among those people who discontinued therapy, 30% of them discontinued Incivek due to not responding to the drug, while 44% of those patients halted therapy because they were “unable to tolerate the side effects.”

In addition, “twice as many discontinued from Victrelis due to severe anemia than Incivek,” says Burman, adding that “this is what we expected.”

“We haven’t seen any problems with patient compliance on Victrelis,” which “was an industry concern because it’s a complicated regimen,” he tells SPN.

In an interesting twist, the drugs’ rigid regimens may work in favor of patient compliance. People need to go in for lab work four weeks after starting therapy. Burman’s keeps track of the date patients start their therapy — which often may not be the same day they receive their medications — through direct communication with patients. They also have certified counselors on staff who are experts on drug and alcohol recovery for patients with a history of abuse to help them stay adherent. Then through calls, emails or text messages, the company makes sure patients come back for their four-week labs on schedule.

Following the lab results, “at four weeks, at eight weeks, they’ll have a good idea of if they will clear the virus.” Bolstered with positive results, these patients “are motivated to finish therapy.”
With clinical trials data available for only the approved regimens, some of Burman’s patients have detoured from those paths slightly but are still on the triple therapy, so he’s curious to see their final outcomes.

For example, “even though we consulted with all of the patients before they started the regimen, there were a few patients who skipped the four-week lead-in with Victrelis and started right away, but their physicians kept them on the regimen,” he says. Burman says he thinks there were two patients who did this, both naïve to prior therapy. “One was negative for the virus after four weeks,” and he is unsure of the other patient’s status.

The specialty pharmacy also had “one patient who basically had cleared the virus, and he had to go in for emergency surgery that was unrelated to the hepatitis C, which meant he had to go off the medications for one week. His doctor started him back up [on Victrelis], so it will be interesting to see what happens.”

As far as side effects of the drugs, “we have slightly more anemia with Victrelis, which was expected,” Burman says. “In most of these cases, we’ve seen physicians use ribavirin dose reductions to treat the anemia.” Ultimately, though, his specialty pharmacy has seen “a little more anemia but not as many side effects with Victrelis.”

Among people taking Incivek, “a very low percentage — less than 1% of patients — were discontinued because of a rash, although we have seen a rash on quite a few of these patients.”
One troubling trend that Burman has noticed is that “about 5% of our patients are getting triple therapy from two pharmacies.” He says he’s been told by larger PBMs that “You fill the ribavirin and interferon, and we’ll fill Incivek” — which can be $17,000 for each fill, he notes.
This kind of situation, though, can cause a “continuity of care issue,” he contends. “It doesn’t seem to be cost-effective,…and it’s disruptive to the patient.”

Burman explains that “about 25% to 30% of patients we set up and trained switched to mail order after one or two months of the six-month therapy.” But within that “complicated” six-month treatment, “there’s no room for error.”

However, some patients almost have had their adherence impacted through no fault of their own, says Burman. He tells SPN that he’s gotten calls from patients who are receiving their drugs from other PBMs through mail order but haven’t gotten their next dose as scheduled, so they’re trying to find a pharmacy that can help. Because patients cannot miss a dose, his company has driven medications to patients an hour or so away to make sure they stay compliant.

Burman expects to have final outcomes for initial patients in May or June. “The first batch of patients just finished therapy. We need to wait six months to retest them, and if they’ve still cleared the virus, we’ll consider them cured. It’s looking good for a lot of patients.…This is a new lease on life for some of these people.”
Source-Specialty Pharmacy

We usually think of Hepatitis C as a virus that is passed from person to person. However, most infections occur via an intermediary, inanimate object. Thus, determining the length of time Hepatitis C can survive outside the body is crucial to prevent transmission of this virus. 


Cancer

New Defense Mechanism Against Viruses and Cancer Identified

ScienceDaily (Feb. 15, 2012) —
A team of scientists from the Charité and German Rheumatism Research Center Berlin and the University of Geneva has found a fundamentally new mechanism how our defense system is ramped up when facing a viral intruder. Exploitation of this mechanism in vaccines sparks new hope for better prevention and therapy of infectious diseases and cancer.
"T killer cells" (CD8 T cells) represent an important element of our body's defense system. They have the capacity to specifically identify and kill cells, which harbor viruses and bacteria or form a cancer. T killer cells would therefore represent an important component of yet unavailable vaccines against infections like HIV/AIDS, hepatitis C virus and malaria, and also for the treatment of cancer.
It has been a longstanding observation that there is no match to the overwhelming T killer cell armada, which is triggered when a viral infection invades our body. Scientists had generally accredited this observation to "pathogen-associated molecular patterns" (PAMPs) on viruses and other microbes. PAMPs, i.e. the "foreign look" of viruses, alert so-called "dendritic cells," which serve as policemen coordinating the T killer cell response.

In a report now published in the journal Science, researchers led by Prof. Max Löhning (Charité-University Medicine & DRFZ Berlin) and Prof. Daniel Pinschewer (University of Geneva) describe an additional general mechanism by which viral infection triggers potent T killer cells: "Dying virus-infected cells themselves ring the alarm bells to T killer cells.," Löhning says. Viruses cause infected cells to die, resulting in the release of cell components, which normally are not be visible to the outside -- analogous to an injured individual loosing blood. Such substances, heralding injury when released, are referred to as "alarmins." The scientists found that T killer cells can sense an alarmin called "interleukin 33" (IL-33). IL-33 is contained in cells, which form the scaffold of the T killer cells' home, the spleen and lymph nodes, and is released when such scaffold cells die.

Mice lacking the gene encoding IL-33 failed to form a large T killer cell army upon viral infection. The few remaining cells had very poor fighting skills. Such mice were therefore exquisitely sensitive to several types of viral infections. Conversely, IL-33 could be used to artificially increase the T killer cell army, which was generated in response to vaccination. As Max Löhning and Daniel Pinschewer explain, PAMPs and alarmins apparently have complementary and non-redundant functions in shaping our T killer cell defense: "The "foreign look" of viruses (PAMPs) activates the "dendritic cell" policemen to engage T killer cells. T killer cells, however, remain lousy fighters unless alerted by a cell death in their neighborhood (alarmins)." These new findings could provide a key to effective vaccination against infectious diseases and cancer.

Organ Donation

Lack of donor organs and poor access to treatment mean mortality rates for liver disease destined to rise
Source-TORONTO, Feb. 16, 2012 /CNW/ -
When you ignore a health issue, it only tends to get worse. Liver disease has been lurking in the dark gaining strength while individuals and governments devote their attention elsewhere. Reports from Statistics Canada and most recently the Canadian Institutes for Health Information (CIHI) however are revealing glimpses of what the future may hold for liver disease patients if action is not taken soon. With rising liver cancer rates and shortages of donor organs, that future looks bleak.

"The most common forms of liver disease - hepatitis B and C, liver cancer and fatty liver disease - are chronic conditions that move slowly and may have few symptoms," says Dr. Morris Sherman, Canadian Liver Foundation Chairman and practicing hepatologist. "In some cases these diseases may not be discovered until they reach an advanced stage when a transplant is the only option. What is more disturbing however is when diseases like hepatitis B or C are diagnosed at an early stage, patients cannot access the treatment they need to avoid the need for a transplant."

According to the CIHI report on organ transplantation released this week, hepatitis C remains the leading cause of liver transplants in Canada, followed by cholestatic liver disease. Liver cancer has taken over the number 3 spot from alcoholic cirrhosis - an indication that lack of diagnosis and intervention is allowing other forms of liver disease such as hepatitis B to progress to liver cancer.
"When the country is facing a chronic shortage of donor organs, we should be looking at ways to reduce the numbers of people who need them," says Dr. Sherman. "Livers are the second most frequently transplanted organ and in 2010 74 people died on the waiting list. This is almost as many as died waiting for kidneys despite the fact that there are six times as many people waiting for kidneys. Patients with failing livers do not have an option for dialysis."

The Canadian Liver Foundation believes that improving organ donor rates is only part of the solution for liver disease patients. "We have the means to significantly reduce the demand for liver transplants," says Dr. Sherman. "We have treatments for hepatitis B that can effectively control, and in some cases cure, hepatitis B before it turns into liver cancer but in many provinces, these treatments are not accessible to patients. In the case of hepatitis C, many people are still not diagnosed. For those that are, new treatment options are available but once again it comes down to accessibility. If governments do not cover the costs of these drugs, only patients with the financial means or independent coverage will be able to afford them."

The CIHI report is further evidence that now is the time to address liver disease in Canada. "There are an estimated 600,000 Canadians living with chronic hepatitis B or C. If there are not enough donor organs now, we should be doing everything we can to keep these people off the transplant list in the future. We hope that these statistics will motivate governments to implement policies regarding screening and treatment that will not only benefit patients but help reduce the demand for liver transplants."

For more information on hepatitis or the Canadian Liver Foundation's positions on liver-related issues, visit www.liver.ca
For further information: Melanie Kearns
Canadian Liver Foundation
416-491-3353 ext. 4923
mkearns@liver.ca
 

Living donor liver transplant varies with availability of deceased donor liver transplants
2/16/2012 GastroHep.com News
The most recent issue of Liver Transplantation reports that living donor liver transplantation varies with the availability of deceased donor liver transplantation.


HIV

AIDS Coalition Protests Merck Laboratories
By Dan Dou, CRIMSON STAFF WRITER
Published: Thursday, February 16, 2012

The Harvard College Global Health and AIDS Coalition put a Valentine’s Day spin on the group’s campaign demanding that pharmaceutical company Merck’s increase access to its AIDS drug raltegravir in poor nations.

A group of 20 people—primarily members of the Coalition and several Medical School students—protested outside Merck’s research laboratories adjacent to Harvard Medical School on Monday afternoon.

The demonstration included pink, red, and white balloons—a play on Valentine’s Day colors with a symbolic message, Coalition member Nathan T. Georgette ’13 said.
“The implication [of the theme] is that their current policies are breaking the hearts of the millions of people who can’t afford their life-saving AIDS drugs,” Georgette said.



Non-alcoholic fatty liver disease (NAFLD)

Released: 2/16/2012 10:10 AM EST
Source: Johns Hopkins Medicine
Newswise — Menopausal women with non-alcoholic fatty liver disease (NAFLD) who don't consume enough of the essential nutrient choline appear to be at higher risk for liver scarring, according to research led by scientists at Johns Hopkins Children's Center.

The findings of a multicenter study, which compared liver damage and choline consumption among 664 children and adults with NAFLD, were published online Feb. 15 in The American Journal of Clinical Nutrition.

Choline-rich foods include dairy, eggs, cod, broccoli, peanut butter, lean beef, chicken breast, chicken liver, seed oils, leafy greens, cauliflower and legumes, such as peas, beans and lentils. Low choline intake was not linked to worse damage in children, women of childbearing age and men with NAFLD, a finding that underscores the existence of important age and gender differences in disease progression, the research team reports.

The scientists caution that the exact link behind low choline and liver damage remains unclear and emphasize that adding choline to one's diet may not halt disease progression.

Researchers speculate that one possible explanation behind the worse scarring seen among post-menopausal women is that estrogen may affect a subset of genes that regulate choline synthesis, and that declining levels of estrogen after menopause may interfere with this process.
Complicating the picture, they note, is that NAFLD has many causes and develops differently from patient to patient. However, the researchers say, the new findings do point to choline as one possible catalyst that may hasten liver damage in certain patients.

Because choline needs vary by age and gender, the Institute of Medicine recommends 425 mg daily choline consumption for non-pregnant, non-breastfeeding women and 550 mg daily for men. Teens should consume 400 mg daily and pre-teens 375 mg daily.

Children between ages 4 and 8 should get 250 mg per day, and children between ages 1 and 3 should consume 200 mg daily. Infants less than 1 year of age should receive between 125 and 150 mg daily via formula or breast milk.
"Physicians have long been fascinated by the unpredictable nature of fatty liver disease and the reasons some patients progress quickly to advanced stages of liver scarring while others have little to no inflammation for many years," says lead investigator Anthony Guerrerio, M.D., Ph.D., a pediatric gastroenterologist at the Johns Hopkins Children's Center.

"Our research illuminates one potential mechanism of liver scarring that portends worse outcomes in some but not all patients," he adds.

NAFLD affects one in three Americans, researchers estimate, and is marked by fatty build-up in the liver, with or without inflammation.

In its advanced form, known as non-alcoholic steatohepatitis, the disease causes cell death, irreversible scarring and liver failure. 

Physicians do not know why some patients develop the more severe forms of the disease fairly quickly while others remain relatively healthy, but nutrition, body weight, genes and environment are all believed to play a role in disease progression. Recent research shows that more children and adults are developing fatty livers, likely due to growing obesity rates, the investigators say.

In the current study, the researchers analyzed liver biopsy results and choline consumption, obtained from patient food diaries. None of the patients met the daily recommended intake, but only those eating less than half the recommended doses were deemed choline-deficient. 

Controlling for other risk factors, like body weight and alcohol consumption, menopausal women who consumed less than half the recommended daily choline had greater degrees of liver scarring, the researchers found. Advanced liver scarring was found in nearly half of the 63 postmenopausal women in the group with choline-deficient diets, compared with 30 percent of the 131 post-menopausal women with non-deficient diets. Differences were far less pronounced among men, children and women of child-bearing age. Advanced liver scarring was found in 18 percent of choline-deficient women of childbearing age and in 10 percent of those with non-deficient diets. Eighteen percent of choline-deficient males 14 years of age and older had advanced liver scarring compared with 16 percent among their non-deficient counterparts. Advanced liver fibrosis was seen in 10 percent of choline deficient children ages 9 through 13, while 17 percent of non-deficient ones had the same degree of liver scarring.

Other Johns Hopkins co-investigators on the study included Amy Schwartz, R.D., C.N.S.D., L.D.; Michael Torbenson, M.D.; and Ryan Colvin. Ann Scheimann, M.D., M.B.A., of Johns Hopkins was principal investigator.

Other institutions participating in the study included Indiana University School of Medicine, Seattle Children's Hospital, Duke University Medical Center, Children's National Medical Center, Washington, D.C., University of California-San Diego and Columbia University.
The research was funded by the National Institutes of Health.
Related links:

The American Journal of Clinical Nutrition
http://www.ajcn.org/content/early/recent
Institute of Medicine
http://www.iom.edu


Founded in 1912 as the children's hospital at The Johns Hopkins Hospital, the Johns Hopkins Children's Center offers one of the most comprehensive pediatric medical programs in the country, treating more than 90,000 children each year. Hopkins Children's is consistently ranked among the top children's hospitals in the nation.
Hopkins Children's is Maryland's largest children's hospital and the only state-designated Trauma Service and Burn Unit for pediatric patients. It has recognized Centers of Excellence in dozens of pediatric subspecialties, including allergy, cardiology, cystic fibrosis, gastroenterology, nephrology, neurology, neurosurgery, oncology, pulmonary, and transplant. For more information, please visit www.hopkinschildrens.org


Healthy You

COLUMBUS, Ohio --
According to a new study, smoking causes the body to turn against its own helpful bacteria, leaving smokers more vulnerable to disease.

Despite the daily disturbance of brushing and flossing, the mouth of a healthy person contains a stable ecosystem of healthy bacteria. New research shows that the mouth of a smoker is a much more chaotic, diverse ecosystem—and is much more susceptible to invasion by harmful bacteria.

As a group, smokers suffer from higher rates of oral diseases -- especially gum disease -- than do nonsmokers, which is a challenge for dentists, according to PurnimaKumar, assistant professor of periodontology at Ohio State University. She and her colleagues are involved in a multi-study investigation of the role the body’s microbial communities play in preventing oral disease.

“The smoker’s mouth kicks out the good bacteria, and the pathogens are called in,” said Kumar. “So they’re allowed to proliferate much more quickly than they would in a non-smoking environment.”

The results suggest that dentists may have to offer more aggressive treatment for smokers and would have good reason to suggest quitting smoking, Kumar said.

“A few hours after you’re born, bacteria start forming communities called biofilms in your mouth,” said Kumar. “Your body learns to live with them, because for most people, healthy biofilms keep the bad bacteria away.”

She likens a healthy biofilm to a lush, green lawn of grass. “When you change the dynamics of what goes into the lawn, like too much water or too little fertilizer,” she said, “you get some of the grass dying, and weeds moving in.” For smokers, the “weeds” are problem bacteria known to cause disease.

In a new study, Kumar’s team looked at how these bacterial ecosystems regrow after being wiped away. For 15 healthy nonsmokers and 15 healthy smokers, the researchers took samples of oral biofilms one, two, four and seven days after professional cleaning.

The researchers were looking for two things when they swabbed subjects’ gums. First, they wanted to see which bacteria were present by analyzing DNA signatures found in dental plaque. They also monitored whether the subjects’ bodies were treating the bacteria as a threat. If so, the swab would show higher levels of cytokines, compounds the body produces to fight infection.

“Smokers' mouths start getting colonized by pathogens—bacteria that we know are harmful—within 24 hours. It takes longer for smokers to form a stable microbial community, and when they do, it’s a pathogen-rich community.”

The results of the study were published in the journal Infection and Immunity.

“When you compare a smoker and nonsmoker, there’s a distinct difference,” said Kumar. “The first thing you notice is that the basic ‘lawn,’ which would normally contain thriving populations made of a just few types of helpful bacteria, is absent in smokers.”

The team found that for nonsmokers, bacterial communities regain a similar balance of species to the communities that were scraped away during cleaning. Disease-associated bacteria are largely absent, and low levels of cytokines show that the body is not treating the helpful biofilms as a threat.

“By contrast,” said Kumar, “smokers start getting colonized by pathogens—bacteria that we know are harmful—within 24 hours. It takes longer for smokers to form a stable microbial community, and when they do, it’s a pathogen-rich community.”

Smokers also have higher levels of cytokines, indicating that the body is mounting defenses against infection. Clinically, this immune response takes the form of red, swollen gums—called gingivitis—that can lead to the irreversible bone loss of periodontitis.

In smokers, however, the body is not just trying to fight off harmful bacteria. The types of cytokines in smokers’ gum swabs showed the researchers that smokers’ bodies were treating even healthy bacteria as threatening.

Although they do not yet understand the mechanisms behind these results, Kumar and her team suspect that smoking is confusing the normal communication that goes on between healthy bacterial communities and their human hosts.

Practically speaking, these findings have clear implications for patient care, according to Kumar.

“It has to drive how we treat the smoking population,” she said. “They need a more aggressive form of treatment, because even after a professional cleaning, they’re still at a very high risk for getting these pathogens back in their mouths right away.

“Dentists don’t often talk to their patients about smoking cessation,” she continued. “These results show that dentists should take a really active role in helping patients to get the support they need to quit.”

For Kumar, who is a practicing periodontist as well as a teaching professor, doing research has changed how she treats her patients. “I tell them about our studies, about the bacteria and the host response, and I say, ‘Hey—I’m really scared for you.’ Patients have been more willing to listen, and two actually quit.”

Kumar’s collaborators include Chad Matthews and Vinayak Joshi of Ohio State’s College of Dentistry as well as Marko de Jager and Marcelo Aspiras of Philips Oral Healthcare. The research was sponsored by a grant from Philips Oral Healthcare.

Contact: Purnima Kumar, (614) 247-4532; Kumar.83@osu.edu

Media Contact: Pam Frost Gorder, (614) 292-9475; Gorder.1@osu.edu

Written by Maureen Langlois.


Behind The Headlines

Behind the Headlines provides an unbiased and evidence-based analysis of health stories that make the news.

How our system works
  • Each day the NHS Choices team selects health stories that are making headlines.
  • These, along with the scientific articles behind the stories, are sent to Bazian, a leading provider of evidence-based healthcare information.
  • Bazian's clinicians and scientists analyse the research and produce impartial evidence-based assessments, which are edited and published by NHS Choices.

Does a daily dose of dhal dispel dementia?
The Daily Mail reported today that “eating a curry once (or twice) a week could stave off dementia.”
Sadly, this mouth-watering headline is not a good representation of the research. The study in question tested the effects of curcumin (a chemical found in the spice turmeric) on fruit flies. It found that curcumin improved lifespan and activity in some genetically engineered fruit fly models of Alzheimer’s disease. However, some other fruit flies, including the normal fruit flies, those eating actually died more quickly.

This type of study is essential for the initial testing of chemicals that may be of some benefit to humans. Chemicals showing beneficial effects and sufficient safety in animal studies need to be tested in humans before we can know what their true effects on a disease are. However, the promising effects of many chemicals seen in animals are not replicated in humans.
Despite what the papers say, this study cannot tell us whether a weekly curry will stave off Alzheimer’s disease or other forms of dementia.

Where did the story come from?
The study was carried out by researchers from Linköping University in Sweden and was funded by The Knut and Alice Wallenberg foundation, Alice and Georg Olsson, the Swedish Foundation for Strategic Research, ‘Hjärnfonden’ (the Brain Foundation), the Swedish Research Council, the Gustaf V Foundation, and the European Union FP-7 Health project LUPAS.
The study was published in the peer-reviewed scientific journal Public Library of Science One.
The Daily Mail reported that the study was in fruit flies (Drosophila melanogaster) and used the chemical curcumin. However, its headline suggesting that eating a curry one or twice a week may stave off dementia is not representative of this research.

What kind of research was this?This was an animal study looking at the effect of the chemical curcumin on fruit fly models of Alzheimer’s disease. Curcumin is found in turmeric, a spice commonly used in curry recipes such as korma and jalfrezi. Previous studies have suggested that curcumin may be able to help reduce the build-up of toxic amyloid beta that occurs in the brain of people with Alzheimer’s disease.

Animal models of human diseases are used in the initial testing of chemicals that may be beneficial to humans. It is easier and safer to do these early tests in animals in the laboratory than in humans. These models replicate specific aspects of the disease in question, but due to differences between species, do not fully represent the human condition.

As fruit flies are not mammals like humans, any chemicals found to show promise would then also need to be tested in a mammal species such as mice. Although certain chemicals may be effective and safe when tested on mammals, they then need to be tested in humans to see if they are really beneficial to us and safe to use.

What did the research involve?
The researchers used fruit flies that had been genetically engineered to replicate (to a certain extent) what happens in the brains of people with Alzheimer’s disease. They used five different types of fruit flies engineered to produce different sections of the protein amyloid beta or another protein called tau. Both of these proteins build up and form abnormal insoluble deposits called plaques and tangles in the brains of people with Alzheimer’s disease. These fruit flies are less active than normal ones of the same age, and have a shortened lifespan.

The researchers carried out various experiments where they fed the genetically engineered and normal fruit flies different amounts of curcumin. They looked at the effect of the curcumin on the fruit flies’ activity and lifespan compared to the same types of flies not fed curcumin. They also looked at how curcumin affected the build-up of amyloid beta in the brains of the flies.

What were the basic results?
The researchers found that the effect of curcumin on lifespan depended on the concentration of curcumin used and the type of fly being tested:
  • increasing concentrations of curcumin reduced lifespan in normal (control) fruit flies
  • two of the five Alzheimer’s model fly strains also died sooner with high curcumin dose
  • three of the Alzheimer’s model fly strains lived longer with the low and intermediate doses of curcumin, although this was still shorter than the lifespan of the normal untreated flies
The greatest effect of curcumin observed was a 75% increase in lifespan with an intermediate dose of curcumin – from fewer than 10 days to more than 15 days on average, in one of the Alzheimer’s fruit fly models.

As all the different types of flies got older they became less active. Again, the effect of curcumin depended on the type of fruit fly tested:
  • curcumin reduced activity slightly in normal flies
  • curcumin had no effect on the activity one of the Alzheimer’s model fly strains
  • the other four Alzheimer’s model fly strains all showed some increase in activity with curcumin, but the extent of the increase varied
The Alzheimer’s model fruit fly strain that showed the greatest increase in lifespan did not show the greatest increase in activity.

The researchers found that curcumin did not decrease the build up of insoluble deposits of amyloid beta in the brains of the fruit flies. However, curcumin sped up the soluble beta amyloid sticking together to form larger bundles called ‘fibrils’.

How did the researchers interpret the results?
The researchers concluded that curcumin reduces the toxic effects of amyloid beta or tau protein in the brains of genetically engineered fruit fly models of Alzheimer’s disease.

Conclusion
Curcumin is found in the bright yellow spice turmeric, which is commonly used in curries. This study has shown that curcumin can improve lifespan and activity in some genetically engineered fruit fly models of Alzheimer’s disease. It is worth noting that this effect was not seen in all of the genetically engineered fruit fly models of Alzheimer’s disease, and that some fruit flies, including the normal ones, actually showed reduced lifespan with curcumin.

Chemicals showing beneficial effects and sufficient safety in animal studies need to be tested in humans before we can know what their true effects on a disease are. Sadly, the promising effects of many chemicals seen in animals are not replicated in humans.
Despite what the papers have reported, this study cannot tell us whether a weekly curry will stave off Alzheimer’s or other forms of dementia. However, it is worth noting that a high-fat diet is associated with some forms of dementia.
Analysis by Bazian.

Links to the headlinesHot new tip... eating a curry once (or twice) a week could stave off dementia, say scientists.
Daily Mail, February 16 2012
Having a curry could help ward off dementia.
The Daily Telegraph, February 16 2012

Links to the scienceCaesar I, Jonson M, Nilsson KPR, et al. Curcumin Promotes A-beta Fibrillation and Reduces Neurotoxicity in Transgenic Drosophila. Public Library of Science One. Published online February 13 2012

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