Vitamin E may lower liver cancer risk

ScienceDaily (July 18, 2012) — High consumption of vitamin E either from diet or vitamin supplements may lower the risk of liver cancer, according to a study published July 17 in the Journal of the National Cancer Institute.

See Also:Health & MedicineLiver DiseaseCancerBreast CancerProstate CancerColon CancerVitamin DReferenceB vitaminsHealth benefits of teaVitamin DRickets

Vitamin E is a fat-soluble vitamin which is considered an antioxidant and numerous experimental studies have suggested that vitamin E may prevent DNA damage.

Liver cancer is the third most common cause of cancer mortality in the world, the fifth most common cancer found in men and the seventh most common in women. Approximately 85 percent of liver cancers occur in developing nations, with 54 percent in China alone.

To determine the relationship between vitamin E intake and liver cancer risk, Wei Zhang, M.D., MPH., Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, and colleagues analyzed data from a total of 132,837 individuals in China who were enrolled in the Shanghai Women’s Health Study (SWHS) from 1997-2000 or the Shanghai Men’s Health Study (SMHS) from 2002-2006, two population-based cohort studies jointly conducted by the Shanghai Cancer Institute and Vanderbilt University.

Using validated food-frequency questionnaires, the researchers conducted in-person interviews to gather data on study participants’ dietary habits. Participants were asked how often they ate some of the most commonly consumed foods in urban Shanghai and whether they took vitamin supplements.

The investigators then compared liver cancer risk among participants who had high intake of vitamin E with those who had low intake.

The analysis included 267 liver cancer patients (118 women and 149 men) who were diagnosed between two years after study enrollment and an average of 10.9 (SWHS) or 5.5 (SMHS) years of follow-up. Vitamin E intake from diet and vitamin E supplement use were both associated with a lower risk of liver cancer. This association was consistent among participants with and without self-reported liver disease or a family history of liver cancer.

“We found a clear, inverse dose-response relation between vitamin E intake and liver cancer risk,” the authors write, noting a small difference between men and women in the risk estimate, which is likely attributable to fewer liver cancer cases having occurred among male participants due to the shorter follow-up period.

“Overall, the take home message is that high intake of vitamin E either from diet or supplements was related to lower risk of liver cancer in middle-aged or older people from China,” said Xiao Ou Shu, M.D., Ph.D., professor of Medicine at the Vanderbilt Epidemiology Center.

Conversely, participants who had the highest vitamin C intake from supplements and who had a family history of liver cancer or self-reported liver disease were more likely to develop liver cancer. There was no link to liver cancer among participants who had the highest levels of vitamin C or other vitamins from food.

Other investigators involved with the study included Honglan Li, M.D., M.Ph., Jing Gao, M.D., Yong-Bing Xiang, M.D., M.Ph., and Yu-Tang Gao, M.D., Shanghai Cancer Institute; Gong Yang, M.D., MPH, Hui Cai, M.D., Ph.D., and Wei Zheng, M.D., Ph.D., Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center; and Bu-Tian Ji, M.D., Dr.PH, National Cancer Institute.

Funding for the study was supported by grants from the National Cancer Institute, a division of the National Institutes of Health (R37 CA070867 and R01 CA082729), the State Key Project Specialized for Infectious Diseases of China (2008ZX10002-015 and 2012ZX10002008-002), and a training grant from the Fogarty International Center (D43 TW008313).

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New animal model may lead to treatments for common liver disease

ScienceDaily (July 3, 2012) — Scientists at Texas Biomed have developed the laboratory opossum as a new animal model to study the most common liver disease in the nation -- afflicting up to 15 million Americans -- and for which there is no cure.

See Also:Health & MedicineLiver DiseaseCholesterolDiseases and ConditionsPlants & AnimalsExtreme SurvivalEndangered PlantsMiceReferenceHepatitisLiver transplantationKetone bodiesGallstone

The condition, nonalcoholic steatohepatitis (NASH), resembles alcoholic liver disease, but occurs in people who drink little or no alcohol. The major feature of NASH is accumulation of fat in the liver, along with inflammation and functional damage. Most people with NASH feel well and are not aware that they have a liver problem. Nevertheless, NASH can progress to cirrhosis, in which the liver is permanently damaged and no longer able to work properly. NASH-related cirrhosis is the fourth most common indication for liver transplantation in the U.S.

NASH affects 2 to 5 percent of Americans -- roughly six million to 15 million people. An additional 15 to 30 percent of Americans have excess fat in their livers, but no inflammation or liver damage, a condition called "fatty liver" or the non-progressive form of nonalcoholic fatty liver disease (NAFLD).

The study, published in the July issue of the American Journal of Physiology-Gastrointestinal and Liver Physiology, was supported by the National Institutes of Health and the Robert J. Kleberg, Jr., and Helen C. Kleberg Foundation.

"This is the type of model in which to develop mechanism-based therapies," writes Geoffrey C Farrell, M.D., of the Australian National University Medical School in Canberra, in a journal editorial.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity and its important health complications, type 2 diabetes, high blood cholesterol levels, high blood pressure and other risk factors for heart attack and stroke. In the past 10 years, the prevalence of obesity has doubled in adults and tripled in children. It was previously reported by other scientists that the prevalence of NAFLD and NASH in a cohort of middle-aged patients in San Antonio is 46 percent and 12 percent, respectively.

"It now seems likely that genetic factors, such as those important for diabetes and high cholesterol levels, are what determines why a small proportion of those with fatty liver develop NASH and its complications of cirrhosis and liver cancer," said Farrell.

In the new study, high responding opossums developed elevated cholesterol and fatty liver disease when fed a high cholesterol and high fat diet, whereas low responding opossums did not. High responders carry a mutated ABCB4 gene, which affects their ability to secrete excess cholesterol from the liver into bile which, in turn, transports the cholesterol to the intestines for excretion from the body. As a consequence, opossums with the mutated gene accumulate cholesterol in the liver and ultimately in the blood.

"We showed that the fatty livers of high responders contain a tremendous amount of cholesterol," said first author Jeannie Chan, Ph.D., of Texas Biomed. "The opossum is a new animal model for investigating the mechanism by which cholesterol mediates liver injury, which will lead to a better understanding of the role of dietary cholesterol in the development of NASH."

Co-authors on the study included Rampratap S. Kushwaha, Ph.D., Jane F. VandeBerg, and John L. VandeBerg, Ph.D., all of Texas Biomed; and Francis E. Sharkey, M.D., of the UT Health Science Center San Antonio.

Texas Biomed, formerly the Southwest Foundation for Biomedical Research, is one of the world's leading independent biomedical research institutions dedicated to advancing health worldwide through innovative biomedical research. Located on a 200-acre campus on the northwest side of San Antonio, Texas, the Institute partners with hundreds of researchers and institutions around the world, targeting advances in the fight against AIDS, hepatitis, malaria, parasitic infections and a host of other infectious diseases, as well as cardiovascular disease, diabetes, obesity, cancer, psychiatric disorders, and problems of pregnancy.

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Japan raw liver lovers lament new food ban

Reuters – 2 hrs 14 mins ago TOKYO (Reuters) - Japan, the home of raw fish, has banned the serving of raw liver after a series of food poisoning cases last year in which five people died and 24 became seriously ill after consuming the dish at a major restaurant chain.

The dish, raw beef liver cut into bite-sized chunks and served with onions and sauce, was taken off restaurant menus indefinitely from July 1 by Japan's Health Ministry.

"When you actually cook liver it's a bit rough, but raw it's very easy to eat," said Yoshiko Miki, a 38-year-old who rushed to Kintan, a downtown Tokyo restaurant that specialized in the dish, before the ban came into effect.

"Especially the liver here is very nice and delicious. So when I think about the fact that I can't eat it anymore, it's quite sad."

Food analyst Chiharu Saito, a member of the Japan Food Analyst Association, said there were a number of well-liked raw meat items on sale, but beef liver was the most popular.

"In terms of what has the most chance of causing food poisoning, I believe that's why they chose to ban beef liver," she said.

"It can be a star product for restaurants, and if they are suddenly unable to sell that then it will indeed affect sales and profits."

Yuichi Kamata, management chief at Edge, the company that oversees the Kintan restaurant chain, said that probably 90 percent of customers had been coming specifically to eat raw liver, with a plate going for around 1,800 yen ($23).

But despite the ban, it's still far too early to count out the restaurant chain - or its star product. Kintan said it was looking into developing new products to circumvent the ban, including one in which the liver is partly cooked.

(Reporting by Chris Meyers; Editing by Elaine Lies and Eric Meijer)

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High Fructose Death Syrup Causes Low Energy and Fatty Liver

It is a testament to Pavlov and his dogs that the average American is dumb enough to consume 35 pounds of high fructose death syrup every year.  The Corn Refiners Association loves to say that their death syrup is no different than any other sugar.  Two recent studies prove that is not true and also prove that the death syrup uniquely causes fatty liver disease, which is a key marker of metabolic malfunction.  Even the FDA is onto the charade, denying a petition from the Corn Refiners Association to change food labels from “high fructose corn syrup” to innocent sounding “corn sugar.”

The public has a great deal of confusion on this topic because fructose is also the sugar naturally contained in fruit.  The new information helps explain why excess consumption of high fructose corn syrup creates metabolic problems; it turns one’s liver fatty and increases the risk for becoming a “metabolic cripple” when higher levels of fructose intake continue as problems are occurring.

Clearly, the preferred intake of fructose is from fruit (never high levels of fruit juice).  Fruit is a comprehensive nutritional package that also contains flavonoid antioxidants, magnesium, potassium, vitamin C, and fiber – along with a modest amount of fructose.  In comparison, most manufactured products containing large amounts of high fructose corn syrup have little nutritional value. Instead, they contain a branded flavor that is full of addictive chemical stimulants.  The goal for manufacturers is to create brand addiction, resulting in the powerful subconscious urge to consume more of their brand, which leads to massive overconsumption of fructose. 

The interesting thing about fructose is that unlike other sugar molecules it actually requires ATP (energy) to be metabolized.  At the same time the fructose molecule could potentially become energy as it is metabolized, leading to increased ATP synthesis.  When healthy people eat fruit, this happens.  Unfortunately, consuming high fructose corn syrup in excess is like flooding your engine with gas.  Your liver simply conks out.  Energy is actually depleted.  And enzymes are activated that turn on fat buildup in the liver while elevating uric acid to a point that it causes free radical damage and inflammation.  This is a fast path to obesity, fatty liver disease, type 2 diabetes, and cardiovascular disease.

Two studies show the results of high fructose corn syrup intake.  The first is an animal study that analyzed how fructose is metabolized.  It shows that fructose is first acted upon by the fructokinase enzyme, which adds energy (ATP) to the fructose molecule so that it can proceed in metabolism.  As it turns out there are two forms of this enzyme, fructokinase A and C.  Fructokinase A operates around the body and has a low affinity for fructose, meaning that when eaten in moderation this enzyme will slowly and steadily help metabolize the fructose.  Fructokinase C is highly concentrated in the liver and loves fructose.

These researchers showed that if both enzymes were knocked out in mice then they couldn’t develop metabolic syndrome from any amount of fructose metabolism because none of the fructose was metabolized.  Then they showed that mice lacking the A form rapidly developed insulin resistance, fatty liver, and metabolic syndrome.  They went on to show that the A form balances and protects against the potential adverse effects of the C form, but only at moderate intake.  At high intake the A form, which has low affinity for fructose, is no longer able to maintain balance and the C form goes wild.  This study is extremely important as it is the first to show this precise mechanism explaining why high intake of fructose is problematic.

The next study involved human type 2 diabetic patients and their ability to metabolize fructose.  The researchers used less than 15 grams of fructose per day to define low and more than 15 grams per day to define high fructose intake.  Please note that the average American consumes about 42 grams per day to get to 35 pounds a year. 

Diabetic patients who consumed more than 15 grams of fructose had lower stores of liver ATP, meaning liver energy function was compromised as predicted by the above animal study mechanism.  Furthermore, a fructose challenge resulted in further decreased energy production, meaning that the people were metabolic cripples when it now came to the fructose they were consuming in high amounts.  The degree of the fructose metabolism problem predicted fatty liver disease and its severity, as well as higher than normal levels of uric acid, which is highly inflammatory to the liver and general circulation. 

High fructose corn syrup is the fastest way to get large and excess amounts of fructose into your body.  It is clear that this compromises your liver’s energetic function, which will take its toll sooner or later.  The first sign of a problem is weight gain.  If not corrected, liver damage and malfunction follow, locking in metabolic disease.  This is not a pretty picture.

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Arthritis Treatment Linked to Liver Problems in Study

HealthDay – 4 hrs ago MONDAY, June 18 (HealthDay News) -- A "medical food" called Limbrel, which doctors prescribe to treat osteoarthritis of the knee, was linked to several cases of liver disease in a small study, but the effects so far seem to be rare and easily reversible.

Still, patients who take Limbrel, also known as flavocoxid, should be aware of the potential for liver problems, said study lead author Dr. Naga Chalasani, director of the division of gastroenterology and hepatology at Indiana University School of Medicine, in Indianapolis.

Patients should not assume that "medical foods," such as Limbrel, are 100 percent safe, he added.

In the United States, medical foods are not subjected to the clinical trials required of prescription drugs before coming to market.

According to Primus Pharmaceuticals, Inc., maker of Limbrel, the main ingredients of the pills are plant elements known as bioflavonoids, specifically baicalin and catechins. The company says Limbrel helps improve mobility and relieve joint discomfort and stiffness related to arthritis.

For the new study, Chalasani and colleagues analyzed 877 cases of liver injury and found four linked with Limbrel. The researchers said it's "highly likely" that the product caused the liver problems in three of the patients and possible in the other one.

Symptoms included nausea, fatigue and yellow skin, Chalasani said. The four patients were women between 57 and 68 years old who showed signs of liver illness between one and three months after taking Limbrel.

They recovered within weeks of discontinuing the drug.

"Our report provides convincing evidence that flavocoxid is capable of causing clinically apparent, acute liver injury," the study authors wrote. They also noted that the pharmaceutical company has discovered 31 possible cases of liver problems among more than 284,000 users since the drug was brought to market in 2004.

It's not clear why Limbrel might cause liver problems, although the researchers suspect one of its chemicals may be at fault, Chalasani said.

According to Dr. Robert Levy, director of clinical development for Primus Pharmaceuticals, "Limbrel is, by far, the safest anti-inflammatory on the market."

Limbrel has an "extraordinary safety profile," he added. He said medical foods must be prescribed and used under the direction of a physician, adding that physicians should monitor the livers of patients who take the drugs.

"Because the liver is the site of metabolism of most drugs and foreign chemicals, a great many drugs, including all anti-inflammatory agents, are known to have some liver toxicity," Levy said.

Painkillers, another common treatment for osteoarthritis, only provide limited relief and are also associated with adverse events, the study authors said.

About 20 million Americans suffer from osteoarthritis, which is the leading cause of disability in the United States, according to the U.S. National Institutes of Health.

Study lead author Chalasani said patients and physicians should be aware that medical food products haven't gone through the same kind of review as regular prescription drugs.

"I'll bet most people who prescribe Limbrel think it's gone through the typical review process," he said. "If a physician chooses to prescribe Limbrel, he or she should be aware that it can cause this toxicity." If patients develop symptoms of liver damage, they should stop taking Limbrel, he added.

The study appears in the June 19 issue of the Annals of Internal Medicine.

The authors of an accompanying journal editorial said that the current policy of allowing medical foods to come to market without rigorous testing may need to be reconsidered, given their popularity and potential for damage.

More information

The U.S. Food and Drug Administration has more about medical foods.

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Liver fat gets a wake-up call that maintains blood sugar levels

ScienceDaily (May 6, 2012) — A Penn research team, led by Mitchell Lazar, MD, PhD, director of the Institute for Diabetes, Obesity, and Metabolism at the Perelman School of Medicine, University of Pennsylvania, reports in Nature Medicine that mice in which an enzyme called histone deacetylase 3 (HDAC3) was deleted had massively fatty livers, but lower blood sugar, and were thus protected from glucose intolerance and insulin resistance, the hallmark of diabetes.

See Also:Health & MedicineDiabetesObesityDiet and Weight LossLiver DiseaseCholesterolFitnessReferenceBlood sugarDiabetes mellitus type 2Ketone bodiesHyperglycemia

Insulin resistance occurs when the body does a poor job of lowering blood sugars. Typically, patients with obesity and type 2 diabetes have fatty livers, and the dogma in the field, says Lazar, is that the fatty livers contribute to the insulin resistance and diabetes in a vicious cycle. These findings are "a clear counterexample to this thinking," he says.

The researchers observed that the extra fat in the liver did not cause insulin resistance because it was sequestered in tiny lipid droplets inside individual liver cells, coated by a specific protein. The metabolites that would otherwise be used by the body to make glucose were re-routed to make fat, leading to reduced glucose in the bloodstream. The advantage of the lower blood sugar is tempered by the excess liver fat, which can lead to problems of its own, including liver failure.

Cells of high-fat-diet-induced fatty livers in wild-type mice were characterized by larger lipid droplets, but liver-specific HDAC3 knockout mice on a high-fat diet were characterized by smaller lipid droplets, even though the total lipid content increased versus the wild-type mice.

Why would the body have this re-routing process in the first place? The team looked to the circadian rhythm of the nocturnal mice for answers. When inactive during the day, mouse HDAC3 migrates to genes to turn off fat synthesis. This allows metabolites to make glucose for fueling the sleeping body. When waking, during the night, the mouse body makes a metabolic switch, anticipating the intake of food, and turns on fat synthesis for energy storage. The on-and-off cycle of HDAC3 is directly regulated by the internal circadian clock, and the system falls apart when HDAC3 is deleted.

The findings suggest that the cordoning off of lipids of the liver in many, tiny coated droplets helps to manage insulin resistance in the body. And, the findings cement the fact that HDAC3 is pivotal in integrating signals from the internal body clock to coordinate metabolism, especially in the liver, notes the first author Zheng Sun, PhD, postdoctoral fellow in the Lazar lab.

The findings demonstrate that fat itself is not necessarily all bad. "It matters a lot how fat is handled and stored," notes Lazar. "It also highlights the importance of complying with our internal circadian clock. For example, since our body does not anticipate food at night and is preparing to generate more glucose, night-time eating is likely to shoot up blood sugar and thus may contribute to diabetes."

The work was funded in part by National Institute of Diabetes and Digestive and Kidney Diseases (R37 DK43806; P01 DK49210; R01 DK40936; R01 DK075017); the Cox Institute of Medical Research; and the JPB Foundation.

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Childhood Obesity May Raise Odds of Adult Liver Cancer

HealthDay – 13 mins ago FRIDAY, April 20 (HealthDay News) -- Adults who were obese as children are at increased risk for liver cancer, a new study suggests.

Researchers looked at the birth weight and body-mass index (a measurement of body fat based on height and weight commonly called BMI) of more than 165,000 men and 160,000 women in Denmark born between 1930 and 1989.

Of those participants, 252 developed hepatocellular carcinoma, the most common form of liver cancer in adulthood.

The study authors calculated that at age 7, the risk of developing hepatocellular carcinoma increased by 12 percent for every one-point increase in BMI. By age 13, that risk increased to 25 percent. Therefore, as units of BMI increased into adulthood, so did the risk of developing hepatocellular carcinoma. This was consistently similar across both genders and all ages.

Other factors associated with liver cancer include alcoholism, infection by hepatitis B and C, and other liver diseases. But the study results did not change when participants with these factors were removed from the study, which indicates that childhood obesity was the major factor in the development of hepatocellular carcinoma, the researchers said.

The study was slated for presentation Thursday at the International Liver Congress in Barcelona.

"Childhood obesity not only leads to the development of many adverse metabolic conditions -- such as type 2 diabetes and heart disease -- but also fatty liver disease, which may subsequently result in liver cancer," Dr. Frank Lammert, a scientific committee member of the European Association for the Study of the Liver, said in an association news release.

"The importance of maintaining a healthy childhood BMI cannot be underestimated," Lammert said in the release. "These alarming study results point to a potential correlation between childhood obesity and development of liver cancer in adulthood."

Data and conclusions presented at meetings should be considered preliminary until published in a peer-reviewed medical journal.

More information

The American Liver Foundation has more about liver cancer.

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