Compound In Broccoli Could Boost Immune System, Says Study

This is just a test-tube and mice study so far but further exploration is clearly warranted. The fact that the compound worked only when eaten (not when injected) suggests that understanding of it is still at an early stage. Possible harmful effects have also not been explored

A compound found in broccoli and related vegetables may have more health-boosting tricks up its sleeves, according to a new study led by researchers at the University of California, Berkeley. Veggie fans can already point to some cancer-fighting properties of 3,3'-diindolylmethane (DIM), a chemical produced from the compound indole-3-carbinol when Brassica vegetables such as broccoli, cabbage and kale are chewed and digested. Animal studies have shown that DIM can actually stop the growth of certain cancer cells.

This new study in mice, published online Monday, Aug. 20 in the Journal of Nutritional Biochemistry, shows that DIM may help boost the immune system as well. "We provide clear evidence that DIM is effective in augmenting the immune response for the mice in the study, and we know that the immune system is important in defending the body against infections of many kinds and cancer," said Leonard Bjeldanes, UC Berkeley professor of toxicology and principal investigator of the study. "This finding bodes well for DIM as a protective agent against major human maladies."

Previous studies led by Bjeldanes and Gary Firestone, UC Berkeley professor of molecular and cell biology, have shown that DIM halts the division of breast cancer cells and inhibits testosterone, the male hormone needed for growth of prostate cancer cells. In the new study, the researchers found increased blood levels of cytokines, proteins which help regulate the cells of the immune system, in mice that had been fed solutions containing doses of DIM at a concentration of 30 milligrams per kilogram. Specifically, DIM led to a jump in levels of four types of cytokines: interleukin 6, granulocyte colony-stimulating factor, interleukin 12 and interferon-gamma. "As far as we know, this is the first report to show an immune stimulating effect for DIM," said study lead author Ling Xue, who was a Ph.D. student in Bjeldanes' lab at the time of the study and is now a post-doctoral researcher in molecular and cell biology at UC Berkeley.

In cell cultures, the researchers also found that, compared with a control sample, a 10 micromolar dose of DIM doubled the number of white blood cells, or lymphocytes, which help the body fight infections by killing or engulfing pathogens. (A large plateful of broccoli can yield a 5-10 micromolar dose of DIM.). When DIM was combined with other agents known to induce the proliferation of lymphocytes, the effects were even greater than any one agent acting alone, with a three- to sixfold increase in the number of white blood cells in the culture. "It is well-known that the immune system can seek out and destroy tumor cells, and even prevent tumor growth," said Xue. "An important type of T cell, called a T killer cell, can directly kill certain tumor cells, virally infected cells and sometimes parasites. This study provides strong evidence that could help explain how DIM blocks tumor growth in animals."

DIM was also able to induce higher levels of reactive oxygen species (ROS), substances which must be released by macrophages in order to kill some types of bacteria as well as tumor cells. The induction of ROS - three times that of a control culture - after DIM was added to the cell culture signaled the activation of macrophages, the researchers said. "The effects of DIM were transient, with cytokine and lymphocyte levels going up and then down, which is what you'd expect with an immune response," said Bjeldanes. "Interestingly, to obtain the effects on the immune response, DIM must be given orally, not injected. It could be that the metabolism of the compound changes when it is injected instead of eaten."

To examine the anti-viral properties of DIM, the researchers infected mice with reoviruses, which live in the intestines but are not life-threatening. Mice that had been given oral doses of DIM were significantly more efficient in clearing the virus from their gut - as measured by the level of viruses excreted in their feces - than mice that had not been fed DIM. "This means that DIM is augmenting the body's ability to defend itself by inhibiting the proliferation of the virus," said Bjeldanes. "Future studies will determine whether DIM has similar effects on pathogenic viruses and bacteria, including those that cause diarrhea."

The discovery of DIM's effects on the immune system helps bolster its reputation as a formidable cancer-fighter, the researchers said. "This study shows that there is a whole new universe of cancer regulation related to DIM," said Firestone, who also co-authored the new study. "There are virtually no other agents known that can both directly shut down the growth of cancer cells and enhance the function of the immune system at the same time."

Two co-authors of the study are from Michigan State University's Department of Food Science and Human Nutrition - James Pestka, professor of food science, and Maoxiang Li, a visiting research associate. DIM is currently under investigation in government-funded clinical trials as a treatment for prostate and cervical cancer. The University of California has filed patent applications on the use of DIM and its derivatives for immune modulation. Berkeley BioSciences, Inc., a company co-founded by Bjeldanes and Firestone, has licensed the related patent applications from the University of California and is researching and developing immune-enhancing nutritional supplements and therapeutics based on this discovery.

Source. Journal abstract here. The title of the original article is: "3,3'-Diindolylmethane stimulates murine immune function in vitro and in vivo"






New booster vaccine for TB

One of the most feared diseases in the world is making an alarming comeback in the UK. Cases of tuberculosis increased by 10 per cent in 2005, with 8,494 cases, and are set to continue rising, as the bug becomes increasingly resistant to drugs, and international travel extends its global reach. TB kills about 1.6 million people a year, largely in developing countries, and experts believe that its global resurgence goes hand in hand with the Aids pandemic. However, Helen McShane, a British scientist, announced today that a groundbreaking new vaccine - the first in 80 years, which has taken ten years to develop - is being tested in human clinical trials for the first time.

The areas most affected by the disease in Britain are cities such as London, Birmingham and Leicester, with immigrant communities from areas where the disease is still common: Pakistan, Bangladesh and parts of Africa. One in five cases of TB is found in new arrivals into the country. However, the disease is not something you could simply catch on a train; only frequent or prolonged contact with someone with TB puts a person at risk (hence why it's passed within families), and it can be treated with antibiotics if diagnosed quickly. Nevertheless, the Government is so concerned at the growing number of people with TB that it is considering screening visitors to the UK from countries such as China and India, it was revealed this week.

If the new TB vaccine passes its trials, as it is expected to do, it could be available in your GP's practice by 2015, when it would work as a booster for the childhood BCG injection (now given only to children in high-risk groups), conferring long-lasting immunity on all adults and thus preventing the spread of this disease.

Symptoms include a persistent cough, weight loss and fever. Before the First World War there were more than 100,000 UK cases a year, but numbers have fallen steadily since the BCG vaccination was introduced in 1953.

Dr McShane, the scientist behind this latest booster vaccine, is a 40-year-old medical doctor-turned-vaccinologist. It's impossible not to share her excitement, particularly when she describes the day in her Oxford University laboratory when she realised she was on to something. "It was a little tense," says Dr McShane, who was then 35 and five years into a project that she had started as a PhD student in 1997. "I went into the lab to check blood tests taken the day before, looked at the plates and couldn't believe my eyes. The results were excellent. We knew the vaccine would stimulate the production of some antibodies but there were ten times the number we had predicted. I ran down the corridor to show my professor immediately." Dr McShane knew she had created a vaccine that could potentially save two million lives a year worldwide. The Wellcome Trust will today announce her project as the first new vaccine for TB in 80 years.

There are two main reasons why a new vaccine has taken so long to develop. The first is that it's a difficult bug to vaccinate against as it disguises itself efficiently in the body. There are different strains of the bug, but Dr McShane believes that they are similar enough for the vaccine to be effective against them all. The other reason for the delay, according to the charity TB Alert, is that there wasn't any funding. Until recently TB was prevalent only in the developing world and so drug companies were reluctant to plough money into a vaccine.

A potential vaccine is an achievement that Dr McShane would not have dared to imagine when she first joined Professor Adrian Hill at the Nuffield Department of Medicine in Oxford to begin a PhD. "Most students were working on a malaria project; no one was looking at a TB vaccine, so I thought it would be a good idea," she says. Dr McShane had first started to study the tuberculosis bacterium when, as a young doctor, she was working in an HIV clinic in London. The two diseases often present hand-in-hand because TB is an opportunistic infection and finds the weakened immune system of an HIV-infected person an easy way in. Dr McShane says she found it frustrating that she could offer the latest antiretrovirals for the HIV infection but she had nothing to prescribe except traditional antibiotics for the TB. She could see that as different strains of TB bacteria became resistant to these drugs, her armoury was looking more and more depleted. Surely something could be done?

She decided to take her curiosity into the laboratory. Most contagious diseases can be vaccinated against by priming the immune system to recognise the pathogen and building armies of immune cells to attack it if it invades the body. A vaccine against measles, for example, introduces a highly weakened strain of the disease into the body. This allows the immune system to target the responsible bacteria, deal with them, and prepare defences for attacks in the future.

But TB is more complicated as it is able to hide inside cells and avoid normal antibodies. Instead it requires a subgroup of white blood cells, called T cells, to be activated, which are better at seeking out the bug to destroy it. Immunologists have begun to use recombinant viruses to teach the body how to recognise TB bacteria and prepare its T cells correspondingly. These are modified viruses that carry cloned genes containing a simple protein, harvested from the disease to be fought. The "tweaked" virus is harmless to human beings. It arrives in the body, unloads the cloned protein, and dies. The protein, however, is spotted by the immune system, which prepares T cells for attack. Afterwards, the patient's body is left ready for further invasion.

Dr McShane found that her vaccine worked particularly well at boosting the weak immune response primed by the traditional BCG. "It would be fantastic if this vaccine was proven to work and became available," she says. "It's been a huge team effort with units in The Gambia and South Africa and Oxford working to a common end. The real challenges now are to see if it really does stop people getting TB, and if it does, to make sure that it gets to the people who need it."

Source

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Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

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