21 August 2007

Viruses, Fat, and Obesity

My research indicates that there are dozens of viruses stored in the fatty tissue of everyone, particularly in the gut. There are at least nine different variations of altered cells caused by each virus, along with a dozen or more other components that are side effects of virus construction and replication.

These altered cells are difficult to eliminate in the abdomen and certain viruses like the one below cause them to proliferate. Once the viruses are eliminated by frequencies, many burn off immediately, fat redistributes normally in the body, and diet and exercise appear to burn off fat normally.

Scientists Say Common Virus Could Cause Obesity
Medical News Today - Featured Article
21 Aug 2007 - 3:00 PDT

Scientists at the 234th national meeting of the American Chemical Society in Boston, Massachusetts this week presented the results of a study that suggests a common virus could be partly responsible for the obesity epidemic that is sweeping across America and other nations. They hope their findings will develop antiviral medication to treat "viral obesity".

According to the National Institutes of Health (NIH), some 97 million adult Americans are obese. Obesity increases risk of many illnesses, including type 2 diabetes, heart disease, stroke, and osteoarthritis.

So far scientists have shown that genetic predisposition increases risk of obesity, as do other contributory factors including over-eating, eating foods high in fat, lack of physical exercise, genetics, and some medications.

In this latest study, researchers used lab experiments to show that infection with a common virus that causes respiratory and eye infections in humans, called human adenovirus-36 (Ad-36) turns adult stem cells retrieved from fat tissue into fat cells. But stem cells that were not exposed to Ad-36 did not turn into fat cells.

The scientists have also discovered that a specific gene in the virus causes the transformation from stem cells into fat cells.

Presenting the results of the study was Dr Magdalena Pasarica, obesity researcher at the Pennington Biomedical Research Center, part of Louisiana State University:

"We're not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections."

Pasarica explained that:

"Not all infected people will develop obesity. We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it."

Pasarica and colleagues took adult stem cells from the fatty tissue of a range of patients who had undergone liposuction. They exposed half of the stem cells to Ad-36, but not the other half.

After a week, most of the virus infected stem cells had transformed into fat cells, but the ones that were not infected had not changed.

Pasarica was involved in an earlier study led by Dr Nikhil Dhurandhar, now associate professor at Pennington Biomedical Research Center. The study showed that Ad-36 caused fat accumulation in animals infected with the virus. The research team then carried out an epidemiological study that showed 30 per cent of obese people were infected with Ad-36, compared with only 11 per cent of lean people.

It was not until this latest study that they were able to show how the virus actually increases fat in humans, according to the researchers.

The research team has also identified a gene in the Ad-36 virus, called E4Orfl, that seems to play a key role in switching on the fat accumulation process in infected animals. The gene could be a target for a range of human therapies, including vaccines and anti-virals, to treat obesity, said Pasarica.

04 August 2007

Ginger causes ovarian cancer cells to die

Ginger causes ovarian cancer cells to die, U-M researchers find

ANN ARBOR, MI – Ginger is known to ease nausea and control inflammation. But researchers at the University of Michigan Comprehensive Cancer Center are investigating a new use for this age-old remedy: treating ovarian cancer.

J. Rebecca Liu, M.D.In laboratory studies, researchers found ginger caused ovarian cancer cells to die. Further, the way in which the cells died suggests ginger may avoid the problem common in ovarian cancer of cells becoming resistant to standard treatments.

The researchers are presenting their results in a poster session at the American Association for Cancer Research annual meeting.

Researchers used ginger powder, similar to what is sold at grocery stores, only a standardized research grade. The ginger powder was dissolved in solution and applied to ovarian cancer cell cultures. Ginger induced cell death in all the ovarian cancer cell lines tested.

Moreover, the researchers found that ginger caused two types of cell death. One type, known as apoptosis, results from cancer cells essentially committing suicide. The other type of cell death, called autophagy, results from cells digesting or attacking themselves.

Chemotherapy: High Cost for Marginal Benefit

The emperor's new clothes - can chemotherapy survive?
Eva Segelov, Medical Oncologist, St Vincent's Clinical School, Sydney
(Aust Prescr 2006;29:2-3)

'An Australian study suggests that the benefits of chemotherapy have been oversold … Why has it been oversold? Are you suggesting that medical oncologists in Australia are just sort of marketing shysters or what?' These were some of the questions posed by Dr Norman Swan when he presented the Health Report on ABC Radio National on 18 April 2005. Dr Swan was quizzing Associate Professor Graeme Morgan, the lead author of a controversial article entitled 'The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies'. This article reported that chemotherapy has improved survival by less than 3% in adults with cancer.

These provocative figures were derived from a literature search of all randomised clinical trials reporting a five-year survival benefit attributable solely to cytotoxic chemotherapy in 22 major adult malignancies. The common malignancies of bowel, lung, breast and prostate were included. The total number of newly diagnosed cancer patients for each malignancy in 1998 was determined from cancer registry data in Australia and the USA. The absolute number to benefit was the product of the total number of patients with that malignancy, the proportion or sub-group(s) with that malignancy showing a benefit, and the percentage increase in five-year survival due solely to cytotoxic chemotherapy. The overall contribution was the sum total of the absolute numbers of patients showing a five-year survival benefit expressed as a percentage of the total number for the 22 malignancies.

Overall cancer survival, following all kinds of treatment, is approximately 63%. Based on the calculations in the study the contribution of chemotherapy to adult survival from cancer was estimated to be 2.3% in Australia and 2.1% in the USA. The authors, two of whom are radiation oncologists, but one of whom is a practicing professor of medical oncology, concluded that 'chemotherapy only makes a minor contribution to cancer survival' and 'to justify the continued funding and availability of drugs used in cytotoxic chemotherapy, a rigorous evaluation of the cost-effectiveness and impact on quality of life is urgently required'.