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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A few days ago, I was glad to read the following study which supports the hypothesis I plan to present at the upcoming Days of Molecular Medicine Conference in Sweden.

In a study published this month in the Journal of Clinical Psychiatry, researchers at the University of Salt Lake City in Utah, reported that although boys with attention-deficit hyperactivity disorder (ADHD) appear to be more impulsive and troubled than their female counterparts, in adulthood the condition seems to have more impact in women than in men.

“We found that adult women with ADHD frequently have high levels of emotional symptoms as well as the cognitive problems found in ADHD,” Dr. Frederick W. Reimherr, head of the study, told Reuters Health.

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Why do some people develop reactions in response to immune system challenges while others don’t?

This week, in a study published in the New England Journal of Medicine, Dr. Thomas Platts-Mills of the University of Virginia and colleagues looked at reports of patients who experienced what they believe are severe allergic reactions to the cancer drug Erbitux. The drug, which is widely used — it had global sales of $1.1 billion in 2006 for use in treating colon, head and neck cancers — is a monoclonal antibody, a genetically engineered immune system compound designed to home in specifically on cancer cells.

The team tested 538 people, including 76 cancer patients who got Erbitux in Tennessee, Arkansas and North Carolina and healthy volunteers from Tennessee, California and Boston in order to gauge their reaction to the drug. Of the 76 cancer patients, 25 developed what were labelled “hypersensitivity reactions.”

Data revealed that the number of patients to develop a reaction to Erbitux varied depending on location. Platts- Mills and team found that as 22 percent of patients treated with Erbitux in Tennessee and North Carolina reported some kind of reaction, including anaphylaxis, which can rapidly lead to difficulty breathing, shock or fainting. Some of the reactions were described as life threatening. Even higher rates were reported from parts of Arkansas, Missouri and Virginia. But fewer than 1 percent of patients treated in the Northeast reported any reactions.

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As a greater number of research teams begin to use molecular technology rather than standard cultivation mechanisms to detect bacteria in their samples, it is becoming increasingly obvious why doctors and researchers are unaware that their patients with chronic inflammatory disease are infected with large quantities of L-form and biofilm bacteria – the techniques they are using to look for bacteria prove rather useless in actually identifying the pathogens.

This month yet another paper was published whose results confirm that the Petri dish is a thing of the past. The study, which was published in BMC Microbiology, used a series of molecular techniques to identify the species of biofilm bacteria present inside several different kinds of wounds.

Bioflims are formed when a complex and varied group of bacteria aggregate together inside a protective and adhesive protein matrix. The bacteria inside a biofilm cooperate to promote their own survival and the chronic nature of an infection. While dentists have long realized that bacteria in the mouth often reside inside biofilms – they form much of the goo that they remove from teeth – researchers are just starting to investigate bioflim communities that form in other areas of the body.

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It’s not unusual for people, especially those with Th1 disease, to find that soy doesn’t always work well in their diet.

But the reason why soy appears to cause problems in many people with Th1 disease remained largely speculative until several month ago, when biomedical researcher Trevor Marshall used molecular modeling software to observe the way that the primary soy isoflavone (or antioxidant), called Genistein, interacts with the Vitamin D Receptor.

Marshall’s model of 1,25-D and Genistein as they dock into the VDR.

His models revealed that Genistein is a partial agonist (activator) of the VDR, and that the substance forms hydrogen bonds with several of the same residues as the vitamin D metabolite 1,25-D (which also activates the VDR).

But, Marshall warned, there’s a catch. Genistein doesn’t have the “tail” of Vitamin D or Benicar, meaning that it cannot transcribe certain genes “which need co-activators requiring helix 12 to be stabilized.”

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Several months ago, I reported on two studies published in the medical journal Nature by Jeff Gordon, a Washington University Scientist intent on investigating correlations between gut bacteria and weight.

Among Gordon’s findings was the fact that his obese and lean volunteers had substantially different compositions of bacteria in their guts. Obese volunteers had 20 percent more of a bacterial species called firmicutes in their gut, but harbored almost 90 percent less of another bacterial species called bacteroidetes than lean volunteers.

Interestingly, when obese subjects were put on a low-carb, low-fat diet, the composition of the bacteria in their guts started to adjust to more closely resemble the ratios of bacteria seen in their lean counterparts.

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A week ago, yet another study was published that casts serious doubt on a long-standing consensus among mainstream doctors and researchers – namely the idea if people are given extra vitamin D they will absorb more calcium, thus strengthening their bones.

In a paper published in the Journal of Bone Mineral Research titled “Disease or No Disease?” researchers tested the effects of extra vitamin D on calcium absorption in a group of postmenopausal women. The women had been diagnosed with “vitamin D insufficiency” – a label given to those people mainstream medicine contends to have a “low” level of the secosteroid 25-D.

The researchers put the consensus to the test by tracking the amount of calcium absorbed (called fractional calcium absorption) after subjects were administered 50,000 IU of vitamin D daily (a ridiculously high amount!) for 15 days. During the study, subjects also consumed their typical diet along with (44)Ca– the number 44 refers to the isotope of Calcium being consumed– orally with breakfast and (42)Ca administered intravenously each day.

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What’s the latest news among people taking statins, or drugs that are marketed as cholesterol lowering agents? Pfizer Inc.’s Lipitor, the world’s best-selling statin, with revenues of $12.6 billion in 2007, causes some women to experience what researchers are referring to as serious cognitive side effects, reports reports The Wall Street Journal.

“This drug makes women stupid,” Orli Etingin, vice chairman of medicine at NewYork-Presbyterian Hospital, declared at a recent luncheon discussion sponsored by Project A.L.S. to raise awareness of gender issues and the brain. Dr. Etingin, who is also founder and director of the Iris Cantor Women’s Health Center in New York, told those present about a typical patient in her 40s, who after taking Lipitor was unable to concentrate or recall words. Tests found nothing amiss, but when the woman stopped taking Lipitor, the symptoms vanished. When she resumed taking Lipitor, they returned.

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Several recent reports have made it abundantly clear that until drug companies understand the infectious pathogenesis of chronic disease, they will continue to churn out dangerous drugs with numerous side effects – drugs that only offer “Band–Aids” for symptoms at the cost of billions of dollars to the consumer.

A few days ago, researchers at Stanford University released the results of a study that tracked the effects of a drug called Sutent on patients with kidney cancer or gastrointestinal stromal tumor (GIST). Sutent, which is widely being tested for the treatment of several other cancers, works by starving tumors — stopping them from growing blood vessels to feed themselves.

Fifteen percent of study subjects taking Sutent developed heart failure, a chronic condition in which the heart loses its ability to pump blood properly. Sutent, made under the generic name sunitinib by Pfizer, has also been shown to damage heart cells.

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