The year was 2005. Under the guidance of Mary H. Schweitzer, researchers from North Carolina State University reported a groundbreaking finding. The team had, according to its members, discovered bona-fide dinosaur tissue inside a femur bone that had once belonged to Tyrannosaurus Rex. The discovery was reported after Schweitzer’s team, working at a remote dig site in Montana, was forced to break the femur into chunks small enough to be transported by helicopter. Inside were pieces of rubbery material that looked like blood vessels and bone marrow. Eureka?

Although several scientists voiced skepticism of the possibility that what appeared to be soft, organic matter could have survived intact for over 70 million years, such concerns were set aside and the find was received as one of the year’s most stunning scientific discoveries.

Schweitzer and team continued to receive accolades from the scientific community until a team of scientists at the Burke Museum of Natural History and Culture at the University of Washington decided to examine a fossilized turtle toe in the hopes of finding even more dinosaur tissue.

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The actor and comedian Bernie Mac died today, and it was because of sarcoidosis. Preliminary news reports say otherwise. A statement by Mac’s publicist, who very likely got it on authority from his doctors, said that it was the “complications due to pneumonia” which ended his life. Mac had suffered from the disease sarcoidosis for 20 some years.

Pneumonia is a lung disease, and the lungs of a patient with sarcoidosis are greatly weakened by the chronic intraphagocytic metagenomic bacteria that cause the illness. Though it is truly a deadly disease, Mac expressed little concern, publicly at least, about sarcoidosis. Mac was likely convinced by his doctors that sarcoidosis could be successfully kept at bay by high doses of immunosuppressants. In one statement, Mac said his sarcoidosis had “gone into remission” around 2005.

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How are the pathogens that cause Th1 disease passed from parent to child? For one thing, it’s quite probable that the pathogens are able to survive in the sperm and egg. It’s equally true that the pathogens are simply passed among people in close contact, and infants and their parents are together quite often.

But the results of a recent study show it’s also likely that some of the chronic bacterial species that cause inflammatory disease can remain alive in breast milk and thus be passed from mother to child by breast feeding. While the study, conducted by researchers at the University of Turku in Finland, indicates that a virus can be passed in breast milk during feeding, the fact that the Th1 pathogens have evolved so many survival mechanisms and are such persistent pathogens strongly suggests that at least some of them possess the same capability.

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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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