By this point, people familiar with the Marshall pathogenesis realize that the Vitamin D Receptor plays an extremely important role in activating immune function and keeping the chronic, intraphagocytic bacteria that cause inflammatory disease under control.

But when the vitamin D feedback pathways fleshed out by Marshall in a recent BioEssays paper are examined, another important receptor enters the picture. It goes by the name of the Pregane X Receptor (PXR), and like the VDR, the PXR is also a nuclear receptor. Mainstream researchers generally understand that the PXR plays an important role in regulating the metabolism, transport, and excretion of exogenous compounds, steroid hormones, vitamins, bile salts, and xenobiotics (chemicals that are foreign to the body). However, they are only recently beginning to understand that the receptor is also intricately connected to VDR function, vitamin D metabolism, and proper regulation of the vitamin D metabolites.

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Chickens beware. Your meat, and that of other animals, may soon be in higher demand. The problem is that tofu, a soy product often used to replace meat, has once again been tied to negative health consequences - in this case, memory loss and dementia.

Researchers at Loughborough University in England recently published two studies — in the journal Dementias and in Geriatric Cognitive Disorders - which found that eating high levels of some soy products may raise the risk of memory loss.

The research team, led by Professor Ef Hogervorst, tracked soy intake and subsequent memory function in 719 elderly Indonesians living in urban and rural regions of the island of Java. They found high tofu consumption - at least once a day - was associated with worse memory, particularly among subjects over 68 years of age.

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For several years now, studies have emerged showing that breastfed babies often perform better on standardized tests and display higher overall levels of intelligence than their formula-fed counterparts. And since baby formula possesses, at least according to a number of mainstream researchers, many of the same basic characteristics as breast milk, the reality that breastfed babies tend to display higher levels of intelligence currently presents a conundrum for the medical community.

Of course, theories have been proposed. One such theory is that women who breastfeed their babies possess different personality traits than those women who chose to feed their infants formula. It’s been postulated that women who take the time to feed their babies from their own breasts are smarter. Perhaps the fact that such women harbor the desire to breastfeed also indicates that they are more invested in the future of their infant. And if they are more invested their baby, then it could be proposed that they interact more closely with the baby and initiate a greater number of activities to foster its intelligence.

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Biomedical researcher Trevor Marshall is currently at the “Understanding Aging” conference in UCLA where, in his talk, he will bring up an increasingly plausible possibility - namely that our stem cells can become infected with bacteria that contribute to the aging process. Serendipitously, a study released this week by a group of researchers at Ohio State University College of Medicine in Columbus provides evidence that Marshall is on the right track. At a June 2nd meeting of the American Society of Clinical Oncology the team, under the direction of Sanford Barsky PhD, reported that data obtained from a study on organ transplant donors/recipients supports the hypothesis that many, if not all cancers, are caused when stem cells somehow go bad.

Stem cells allow our organs renew themselves over the course of time. As described by a recent article in the Economist, every organ and tissue in the body has its own collection of stem cells. When these cells divide, they produce two very different daughter cells. One resembles the parent stem cell and thus allows the process of regeneration in the same organ to continue. The progeny of the other differentiate into mature cells within the skin, kidney, lung or what have you. In a healthy organ, the stem cells divide only when needed—usually in response to injury or when other cells have died.

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The Indian sub-continent is situated between 8.4 degree N and 37.6 degree N latitude and has adequate sunshine throughout the year. So say researchers at the Apollo Hospital in New Delhi India. In fact, in their introduction to a recent study on vitamin D, the team postulated further, stating that “it has been presumed that Indians have ’sufficient’ levels of vitamin D.”

And who wouldn’t presume such a thing? Considering that the average temperature in India is quite high, it’s doubtful that natives would be deficient in a substance that is easily obtained from the sun. Nevertheless, with growing concerns of what mainstream medicine calls vitamin D “deficiency” at hand, the team set out to confirm that the staff from a hospital in north India did indeed possess levels of vitamin D (25-D) that the medical community has deemed healthy - specifically 25-D level between 35-50 ng/ml. Using a machine called dual energy X-ray absorptiometer, the Apollo Hospital team were able to measure the staff’s serum 25-D and 1, 25-D levels.

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This week’s pharmaceutical fiasco? Federal regulators are investigating whether a group of best-selling arthritis drugs made by Abbott Laboratories, Schering-Plough Corp. and other companies heighten the risk of cancer in youngsters.

The drug etanercept binds to TNF-alpha to block its action on the immune system.

The drugs under review are called tumor necrosis factor blockers (TNF-alpha blockers) and include Enbrel, Humira, and Remicade. The current uproar over the medications began after the Food and Drug Administration received 30 reports of children and young adults developing cancer while taking the drugs over the last 10 years. Roughly half the cases were lymphomas, a type of immune system cancer. Others reported were leukemia, melanoma and cancers of various organs. The fact that a possible association between TNF-alpha blockers and some cancers has been recognized for years in adults has only heightened the FDA’s concern.

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For the last century, the medical community has largely assumed that the bacteria that inhabit our bodies and natural surroundings have been accurately characterized and documented.

Yet according to Penn State researcher Jennifer Loveland-Curtze, “Microbes comprise up to one-third or more of the Earth’s biomass, yet fewer than 8,000 microbes have been described out of the approximately 3,000,000 that are presumed to exist,”

The statistic may be mind-boggling to some, yet, in reality, should come as no surprise. Considering the fact that bacteria are notoriously adept at evolving crafty survival mechanisms and have had eons in which to do so, the amount of research over the previous decades aimed at characterizing new bacteria and their survival adaptations has actually been minimal.

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A century ago, Alois Alzheimer and his colleagues suggested that microorganisms likely contribute to the generation of senile plaques in patients with the disease that now bears his name. Apparently few people listened, as over the past decades, research on Alzheimer’s disease has focused almost soley on searching for a genetic cause of the illness. As reported by Science Daily, “The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection [in Alzheimer's] has received little attention in the past, despite the fact that during infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression.”

However, since those scientists fixated on finding a genetic cause for Alzheimer’s have yet to correlate particular genes with the disease, an increasing number of other research teams are beginning to search for alternative causes of the illness. Happily, this new streak of research focuses on the role of bacteria in causing the Alzheimer’s.

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This month, researchers from several institutions including the University of Oulu in Finland and the Imperial College in London reported the results of a study which found an association between high-dose vitamin D supplementation in infancy and an increased risk of atopy, allergic rhinitis, and asthma later in life. Atopy, or atopic syndrome, is an allergic hypersensitivity affecting parts of the body not in direct contact with an allergen. It may involve eczema (inflammation of the upper skin layers), allergic conjunctivitis, allergic rhinitis and asthma.

The team started collecting data in 1967. That year, every mother in the two most northern provinces of Finland - a group of mothers referred to as the Northern Finland Birth Cohort (NFBC) - who had given birth to a child during the previous year was required to report the level of vitamin D they were giving their infant. At the time, Finnish government recommendations stated that mothers should supplement their infants with 50 ug of vitamin D. Mothers were asked to report if they were giving their infant the recommended dose of vitamin D, no vitamin D, or an irregular dose of vitamin D. An irregular dose of vitamin D usually reflected the fact that the infant was given high levels of vitamin D rich cod liver oil.

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There is little doubt about it: blockage of the Vitamin D Receptor severely impairs human health. Since the Th1 pathogens create substances that block the receptor, they are easily able to create an environment that is conducive to their survival but quite detrimental to the host. If a person acquires enough of the Th1 pathogens, their VDRs likely become blocked by so many bacterial substances that the activity of the receptor decreases to a point where it is essentially off.

Since having a Vitamin D Receptor with no activity is analogous to having no VDR at all, studies on VDR knockout mice can be extremely informative. VDR knockout mice are rodents that have been grown in the lab under conditions that cause them to develop without Vitamin D Receptors. Their receptors are missing, or have been “knocked out.”

This week, a team of researchers at the University of Chicago examined the effects of inducing colitis on VDR knockout mice. Their goal: to investigate the role of the VDR in mucosal barrier homeostasis. The mucosal barrier allows the intestines to retain the proper pH and structure. The team used a substance called dextran sulfate sodium (DSS) in order to create an environment in the rodents’ intestines that resembles that of people with bowel disease.

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In another sign pointing to the fact that autism is almost certainly a Th1 disease, a study released on last week found that having a schizophrenic parent or a mother with psychiatric problems roughly doubled a child’s risk of becoming autistic.

“Our research shows that mothers and fathers diagnosed with schizophrenia were about twice as likely to have a child diagnosed with autism,” said Julie Daniels of the University of North Carolina, Chapel Hill, who worked on the study. The teams research has also been confirmed by earlier studies on the same topic.

“We also saw higher rates of depression and personality disorders among mothers, but not fathers,” she said in a statement.

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According to The Independent, a mood of deep pessimism has spread among the international community of AIDS scientists after the trial of a promising vaccine failed at the end of last year. It was the latest in a series of setbacks in a 25-year struggle to develop an HIV vaccine.

In fact, according to a poll conducted by the The Independent, most scientists involved in AIDS research believe that a vaccine against HIV is further away than ever and some have admitted that effective immunization against the virus may never be possible.
What went wrong?

It turns out that one of the major realizations to emerge from the failed clinical trial - which involved the most promising prototype HIV vaccine - was that an important animal model used for more than a decade does not work. The model involves testing possible vaccines on monkeys before they are used on humans.

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Last week biologists announced that several studies have solidified that fact that most cases of bad breath are caused by bacteria. Shocking? Not for anyone who understands the Marshall pathogenesis for chronic disease in which nearly all conditions can be attributed to the presence of L-form bacteria, biofilm bacteria, or other persistent forms of bacteria (collectively called the Th1 pathogens).

The culprit behind bad breath - Solobacterium moorei, which uses the tongue as a base on which to brew its halitosis-provoking fatty acids and malodorous compounds.

Two studies helped researchers confirm the findings. One, by the Buffalo School of Dental Medicine, probed 21 people with chronic bad breath and 36 without and found S. moorei in every patient that had halitosis. S. moorei was found in four of the comparison group, and while they were not yet polluting the air with foul emissions, all had periodontitis, an infection of the gums that can also lead to chronically bad breath. The biologists presented their findings at the annual meeting of the American Association for Dental Research in Dallas.

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Need proof that consuming high levels of vitamin D can curb your lifespan? Look no farther then a study published this month in the American Journal of Clinical Nutrition which found that middle-aged men who ate seven or more eggs a week had a higher risk of earlier death from diabetes.

More specifically, Dr. Luc Djousse and Dr. J. Michael Gaziano of Brigham and Women’s Hospital at Harvard Medical School found that men with diabetes who ate any eggs at all doubled their risk of death during a 20-year study period. The team studied 21,327 men taking part in the much larger Physicians’ Health Study, which has been watching doctors since 1981 who have agreed to report regularly on their health and lifestyle habits.

“More egg on our faces? It’s really hard to say at this point, but it still seems, if you’re a middle-aged male physician and enjoy eggs more than once a day, then having some of the egg left on your face may be better than having it go down your gullet,” said Dr. Robert Eckel of the University of Colorado and a former president of the American Heart Association.

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How many times have you been told that you can control your weight simply by adjusting your diet and making time for exercise? The idea that we are able to completely control our weight through willpower and food intake has been seared into our thinking so frequently by friends, family, the media, and even or our doctors, that most people still blame MacDonalds for the country’s weight problems.

Yet, this week another study was published which strongly suggests that our weight is not, by any means, soley governed by what we eat. Rather, it is mediated by factors out of our control, one of them being the balance of chemicals in our bodies.

In a recent paper, published in the Annals of the New York Academy of Sciences, researchers at the Institute of Molecular and Cellular Biosciences Institute at the University of Tokyo in Japan explain two molecular pathways that directly affect the formation of adipocytes, another name for fat cells. At the center of both pathways is the nuclear receptor PPAR-gamma, a receptor that is also at the heart of the immune response.

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