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.

A variety of compounds are found in soy products, so naturally Hogervorst and other researchers are intent on discovering which specific compounds, or group of compounds found in soy might contribute to impaired health, such as memory loss among the elderly.

Hogervorst and team seem to be leaning towards the hypothesis that phytoestrogens – micronutients found in soy that partially mimic the hormone oestrogen – may be to blame for the mental damage observed in their study subjects. According to Rebecca Wood of the Alzhemier’s Research Trust (which funded the study), oestrogens tend to promote growth among cells. Could there be something about faster growing cells that could be detrimental to the elderly brain?

Without much evidence at hand to prove the above hypothesis correct, Hogervost and team have also considered the possibility that high levels of oestrogens might allow cells to be damaged more frequently by free radicals, yet the mechanisms behind such a hypothesis also remain cloudy.

Finally, the researchers have hypothesized that the observed mental decline in the Indonesian subjects might not have been caused by the tofu, but by formaldehyde, which is sometimes used in Indonesia as a preservative. Yet the fact that previous research has also linked high tofu consumption to an increased risk of dementia in older Japanese American males, and Amercian soy products do not contain formaldehyde, renders the hypothesis rather dubious as well.

So how would one explain this evidence? Hogervost and his research team seem to have their share of hypotheses, but here’s another: the reason why soy is harmful for older adults is that the primary isoflavone found in soy, Genistein, is immunosuppressive. Dr. Marshall has shown that Genistein actually dysregulates the innate immune response by binding and inactivating the vitamin D receptor. Just like exogenous vitamin D (known as 25-D), chlorogenic acid (found especially in coffee), or other compounds that negatively affect VDR activity, high levels of Genistein are able to slow the innate immune response (which is controlled by the VDR). As innate immune system activity decreases, less of the chronic bacteria implicated in causing a plethora of physical and cognitive symptoms are killed. The result is a temporary decrease in the inflammation generated when the pathogens die and a feeling of temporary palliation.

Dr. Hogervost may not know it, but his data is consistent with that of Dr. Martha Payne. In 2007, Payne and her team showed that vitamin D intake in older adults correlated with higher total volume of brain lesions. What’s the common thread between these two studies? In both cases, the elderly subjects are consuming foods (or supplements in the case of vitamin D) that slow the VDR. The resulting immunosuppression allows numerous bacteria-driven chronic diseases, including Alzheimer’s and dementia– to develop with greater ease -and within the time parameters defined by the study. Younger, and presumably healthier subjects, will likely suffer from the same detrimental effects if given a longer window of time.

Dr. Hogervorst has stated that there is some evidence that soy may “protect” the brains of younger and middle-aged people from damage but its effects on the aging brain are less clear. The statement directly supports the hypothesis that soy is immunodulatory. The periods of “protection” Hogervorst refers to are almost certainly periods of immunosuppression which ultimately allow enough bacterial spread in the brain so that elderly patients present as symptomatic.

Since the Th1 pathogens are picked up over the course of a lifetime, elderly people also generally have higher bacterial loads than their younger counterparts. Since many of the Th1 pathogens likely create ligands that also block the VDR, elderly patients are more susceptible to compounds like Genistein that contribute to VDR dysregulation. Because their VDRs have already been rendered largely inactive by the pathogens they harbor, smaller amounts of a compound like soy can more easily push the elderly “over the edge” into a state where they are strongly immunosuppressed.

Unfortunately the great majority of mainstream researchers remain unaware of Genistein’s negative effects on the VDR. And because the same researchers also fail to factor chronic bacteria into the pathogenesis of mental disorders such as Alzheimer’s and dementia, they are continually confused by other anomalies in their study data. For example, a different study recently found that eating tempe, a fermented soy product made from the whole soy bean, is associated with better memory. Huh?

Again, it is only when the new study is viewed through the lens of the Marshall Pathogenesis that the mental “improvements” observed in subjects can be better understood. Tempe is not only high in soy but also high in folic acid – a compound that bacteria use to their advantage. Upon consumption, folic acid is enzymatically converted into a form that the body can use to produce the nucleic acids that make up our DNA. However, if a person consumes extra folic acid, the Th1 pathogens are able to use the substance to generate their own nucleic acids and replicate and create their own DNA.

The result is that the Th1 pathogens find it easier to survive in a folate-rich environment, so high levels of the substance again prevent the immune system from effectively killing the chronic pathogens implicated in causing memory loss and dementia. By temporarily keeping many these pathogens at bay, folic acid also prevents the rise in inflammation associated with their deaths, and mistakenly, at least in the short-term, gives the impression of “wellness.”

When will the difference between palliation and true wellness become commonly understood? We know enough now to realize that the feel good effects of food simply can’t be taken at face value.

In the meantime, there’s no need to be obsessive about avoiding soy or folic acid. Marshall recommends that soy product in the diet be kept to a minimum (particularly among those patients on the MP). And because it’s excess folic acid that tends to most greatly benefit the bacteria we harbor, he recommends eating only those foods which naturally contain the substance. So products with extra folic acid, particularly white bread products, should be avoided.

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.”

This suggests that Genistein interferes with the operation of the VDR, as well as with the operation of two other receptors (PPAR-gamma and PPAR-alpha), all of which are key to the immune system.

Huh? If I just lost you on the last few sentences, they boil down to the following: Marshall’s model shows that Genistein binds and activates the VDR. Yet it appears to modulate its activity, and the activity of several nearby receptors, in a way that can dysregulate the activity of the immune system.

But the above conclusion is based on a molecular model. “How much faith can we put into molecular modeling research?” some skeptics might ask.

A study published this week by researchers at Department of Biological Sciences at University of Notre Dame in Indiana suggests that molecular modeling software, when used effectively, can be pretty darn accurate.

In a paper published in the Journal of steroid biochemistry and molecular biology, the team confirmed that Genistein does indeed bind and adjust the activity of the VDR.

The Notre Dame researchers had previously characterized an area in the human VDR gene (called a promoter), that, when bound by certain substances, adjusts the activity of the Vitamin D Receptor. When the team treated this promoter region with Genistein, they found that the substance up-regulated the transcription of proteins produced by the VDR. They verified these results with a second molecular technique called Western blot analysis.

Now that the ability of Genistein to affect the VDR has also been confirmed by a variety of molecular approaches, Marshall’s message that soy intake should be restricted rings louder and clearer then ever. This is particularly true for people with Th1 disease, who are extra sensitive to substances that dysregulate VDR activity. These people also need the receptor to function optimally in order to help the immune system target the Th1 pathogens.

According to Marshall, problems with soy are dose-dependent. Anything up above the cited “20 grams of roasted soybeans,” or 40mg of isoflavones, is likely to be a problem.

Because L-form bacteria grow so slowly, few researchers have made the connection between acute infection and chronic symptoms that rear their heads decades down the road. However, several research teams have finally taken note of the fact that food poisoning victims, who at one point suffered from a severe acute infection, are much more likely to develop chronic symptoms later in life.

“It’s a dirty little secret of food poisoning,” says Lauren Neergaard of Yahoo News. “E. coli and certain other foodborne illnesses can sometimes trigger serious health problems months or years after patients survived that initial bout. Scientists only now are unraveling a legacy that has largely gone unnoticed.”

In a recent interview with the Associated Press, researchers at the University of Utah described how many survivors of severe E. coli infections as children are suffering from severe kidney issues later in life. The research team, which has long tracked children with E. coli, found that about 10 percent of E. coli sufferers develop a life-threatening complication called hemolytic uremic syndrome, or HUS, where their kidneys and other organs fail.

Ten to 20 years after they recover, between 30 percent and half of HUS survivors will have some kidney-caused problem, says Dr. Andrew Pavia, the university’s pediatric infectious diseases chief. That includes high blood pressure caused by scarred kidneys, slowly failing kidneys, even end-stage kidney failure that requires dialysis.

“Folks often assume once you’re over the acute illness, that’s it, you’re back to normal and that’s the end of it,” said Dr. Robert Tauxe of the Centers for Disease Control and Prevention. “The long-term consequences are an important but relatively poorly documented, poorly studied area of foodborne illness.”

Donna Rosenbaum of the consumer advocacy group STOP (Safe Tables Our Priority) told the Associated Press that every week, her group hears from patients with health complaints that they suspect or have been told are related to food poisoning years earlier. One woman to contact the group survived severe E. coli at 8 only to have her colon removed in her 20s. Other people report developing diabetes after a bout of food poisoning that inflamed the pancreas. Then, there are children who survived food poisoning dialysis as toddlers and are now suffering from learning problems.

“There’s nobody to refer them to for an answer,” says Rosenbaum.

So STOP this month is beginning the first national registry of food-poisoning survivors with long-term health problems — people willing to share their medical histories with scientists in hopes of boosting much-needed research.

One person to share her story is Alyssa Chrobuck of Seattle, who at age 5 was hospitalized as part of the Jack-in-the-Box hamburger outbreak 15 years ago that resulted after several people ate meat infected with a dangerous form of E. coli.

Today she’s a successful college student but ticks off a list of health problems unusual for a 20-year-old: High blood pressure, recurring hospitalizations for colon inflammation, a hiatal hernia, thyroid removal, endometriosis.

“I can’t eat fatty foods. I can’t eat things that are fried, never been able to eat ice cream or milkshakes,” says Chrobuck. “Would I have this many medical problems if I hadn’t had the E. coli? Definitely not. But there’s no way to tie it definitely back.”

Further evidence connecting acute infection to chronic illness later in life comes from studies which have shown that about 1 in 1,000 sufferers of campylobacter, a diarrhea-causing infection spread by raw poultry, develop far more serious Guillain-Barre syndrome a month or so later. Their body attacks their nerves, causing paralysis that usually requires intensive care and a ventilator to breathe. About a third of the nation’s Guillain-Barre cases have been linked to previous campylobacter, even if the diarrhea was very mild, and they typically suffer a more severe case than patients who never had food poisoning.

Similarly, a small number of people develop what’s called reactive arthritis six months or longer after a bout of salmonella. It causes joint pain, eye inflammation, sometimes painful urination, and can lead to chronic arthritis. Certain strains of shigella and yersinia bacteria, far more common abroad than in the U.S., trigger this reactive arthritis, too, Tauxe says.

It remains to be seen how long it will take Tauxe and other researchers to connect these chronic infections of L-form bacteria. But when the connection is finally made, the medical community will become aware of the fact that persistent L-form infection is affecting the entire population, not just food poisoning victims. As biomedical researcher Trevor Marshall describes, the chronic illnesses that all people develop are a direct result of the “peasoup” of L-form bacteria and other pathogens they have collected over a lifetime.

The implications of this situation are clear: when a person develops an infection, treatment must be administered that kills both the classical and L-form bacteria. Happily, the Marshall Protocol works effectively to kill L-form bacteria. This means that people can now do a short course of the Marshall Protocol after developing an acute infection, allowing them to get rid of any L-form bacteria that have formed, and saving them from a host of chronic symptoms later in life.

However recent research has revealed that over the past decade, rates of colorectal cancer in the United States have risen for inexplicable reasons, even as regular colonoscopy check-ups have become more common. In Canada, where folic acid supplementation was introduced a bit later, the same trend has been observed.

Two recent commentaries appearing in Nutrition Reviews address these findings and provide an overview of the existing evidence on folic acid fortification and the associated policy issues.

Dr. Solomons, author of one of the commentaries, “Food Fortification with Folic Acid: Has the Other Shoe Dropped?” advises that a careful reconsideration of the fortification program is needed stating, “One size of dietary folic acid exposure does not fit all. It can be beneficial to some and detrimental to others at the same time.”

Since the risk-benefit value of fortification varies according to age, Solomons suggests a reevaluation of the manner in which folic acid to prevent birth defects is delivered to the public. Among other things, Solomon feels that folic acid supplementation could be targeted in a different manner to women of reproductive age. Then, in order to protect the rest of the population, reducing folic acid levels in foods for which fortification is optional (such as ready-to-eat cereals and commercial drinks), would be worthy of consideration.

“Folic acid supplementation wields a double-edged sword,” remarks Dr. Young-In Kim, author of Folic Acid Fortification and Supplementation—Good for Some but Not So Good for Others,” the other commentary review published in the November issue. According to Kim, “It may be beneficial or harmful, depending on the timing of intervention.” Exposure to high intakes of folic acid in early life and young adulthood may provide life-long protection from the tendency for cancer formation in different organs, such as the large intestines, whereas such exposures later in life, when cell damage has occurred, can spur on the advance of the tumor.

These results should come as no surprise to people on the Marshall Protocol who realize that L-form bacteria at the root of most chronic disease use extra folic acid to their own advantage. If a person consumes too much folic acid, L-form bacteria will use it to generate their own nucleic acids, facilitating their ability to replicate and create their DNA.

Similarly, researchers in the UK are arguing against a measure that would require an increase in the amount of folic acid added to food products in England. Their concerns stem from the results of a recent study by the Institute of Food Research in the United Kingdom, which found that the liver could easily become saturated by folic acid at the levels the English government plans to add to the food supply (levels that would equal those mandated by the American government).

Writing in the British Journal of Nutrition, the researchers warn this could lead to unmetabolized folic acid entering the blood, which could damage health. “With doses of half the amount being proposed for fortification in the UK, the liver becomes saturated and unmetabolised folic acid floats around the blood stream,” reports Dr. Sian Astley of the research team.

“This can cause problems for people being treated for leukemia and arthritis, women being treated for ectopic pregnancies, men with a family history of bowel cancer, people with blocked arteries being treated with a stent and elderly people with poor vitamin B status.”

“For women undergoing in-vitro fertilization, it can also increase the likelihood of conceiving multiple embryos, with all the associated risks for the mother and babies.”

Studies have confirmed that unmetabolized folic acid accelerates cognitive decline in the elderly with low levels of vitamin B12. It may also increase the incidence of breast cancer in postmenopausal women.

However, since the 1980s a consensus formed that folic acid is metabolized in the small intestine in a similar way to naturally-occuring folates.

“We challenge the underlying scientific premise behind this consensus,” states Astley, who also warned it could take 20 years for any potential harmful effects of unmetabolized folic acid to become apparent.

These studies are proof positive of the fact that adding artificial levels of a substance to the food chain can have serious, unintended, and detrimental effects on much of the population. While government efforts to help the public obtain substances such as folic acid have been in good faith, the simplistic notion that a large, diverse, population should all be given the same level of a substance has run its course.

In the case of vitamin D, mandatory fortification has resulted In disastrous consequences. Armed with the understanding that “vitamin” D obtained from supplements (25-D) is not a vitamin, but a potent secosteroid that represses the innate immune system and the transcription of thousands of genes, it is of utmost importance to re-evaluate the vitamin D dietary guidelines. Molecular research implies that when it comes to folic acid as well as vitamin D, we should be much less cavalier in our eagerness to fortify the food supply.

Bacteria can glean iron from the host and use it to grow

Our bodies require iron in order to function, but numerous studies have shown that bacteria also use iron to grow. In fact, bacteria consume large quantities of iron, leaving little free iron available to the host organism.

This may explain why many people who suffer from certain chronic diseases and obesity, which are now hypotesized to be caused or affected by bacteria, display low levels of iron and are considered to be deficient in the substance. Deficiency reflects the fact that bacteria are using the host’s iron to their own advantage.

Not surprisingly, researchers at the University of Texas found that overweight U.S. children run an alarmingly high risk of iron deficiency. They were able to detect an association between obesity and iron deficiency in children as young as one year old. Dr. Jane Brotanek, the study’s lead author stated, “A key finding of this study is the alarmingly high prevalence of iron deficiency among overweight toddlers.”

Although the researchers hypothesized that the deficiency might be due to “excessive milk or juice intake, prolonged bottle-feeding, snacking and junk food intake”, a more likely explanation is that the obese toddlers had higher loads of bacteria.

The methods that bacteria use to acquire iron have been elucidated by a different team of researchers, also at the University of Texas. According to the researchers, the ability of a particular species of bacteria to glean iron from its host is often a good indicator of its virulence.

The biochemistry of a siderophore.

The team, under the guidance of Professor Shelley M. Payne, has published widely on the genetics and iron acquisition methods of bacteria such as Vibrio and Shigella. Shigella and Vibrio are able to secrete iron binding complexes that have a high affinity for the proteins inside the host. These complexes are called siderophores. Siderophores remove iron from host proteins, making it available for use by the bacteria.

The bacterial species Vibrio produces a variety of siderophores. When deprived of iron, Vibrio bacteria create five proteins on the surface of their bodies. Some of the proteins serve as receptors that allow them to bind and attach siderophores to their bodies. Others serve as receptors for heme, large molecules made up of iron atoms contained in the center of a ring.

The Shigella species of bacteria have at least three different iron transport systems. Two of these, called the aerobactin and the enterobactin systems, consist of siderophores and receptors that will allow the bacteria to bind the siderophores once they have removed iron from the host. The third pathway allows Shigella to transport and utilize iron in the form of heme. By culturing mutated species of Shigella bacteria, Payne and team were able to determine that siderophores provide iron to bacteria in the environment outside the cells of the host, and that the heme transport pathways are used by bacteria when they are growing inside the cells.

The team also discovered that the bacteria S. flexneri create a protein that not only allow it to bind large amounts of heme, but facilitate its attachment to the host cells it will parasitize. The protein is encoded on a large plasmid, a circular molecule of DNA that can replicate independently of a pathogen’s other genetic material.

In order to fully understand the mechanisms of iron acquisition and transport mentioned above, Payne is carefully analyzing the bacterial genes involved in each process. By using cloning techniques to create multiple copies of each gene, Payne has been able to test and measure the expression of various genes under different environmental conditions, such as changes in temperature and pH. According to Payne, “These studies will allow us to determine the molecular mechanisms of iron acquisition and ultimately to assess the roles of these systems in bacterial infection.”

There is no need to remove iron from a healthy, well-balanced diet, but iron supplements should be avoided, as the extra iron will likely be used by bacteria rather than the host. People with chronic disease who are deficient in iron should understand that the low level of the substance is the consequence of bacterial infection.

Sources of dietary iron include red meat, fish, poultry, lentils, beans, leaf vegetables, tofu, chickpeas, black-eyed peas, potatoes with skin, bread made from completely whole-grain flour, molasses, teff and farina. Iron in meat is more easily absorbed than iron in vegetables.

Folic Acid can help bacteria replicate their DNA

Another substance that bacteria use to their own advantage is folic acid. An enzyme called DiHydro-Folate Reductase (DHFR), converts folic acid into a form that the body can use to produce the nucleic acids essential for life. Nucleic acids are building blocks that our bodies use to create DNA. However, if a person consumes too much folic acid, L-form bacteria will use it to generate their own nucleic acids and replicate and create their own DNA.

Enriched white flour products should be avoided.

Folic acid is found naturally in food such as leafy vegetables, dried beans and peas. But it has also been artificially added to “enriched” flour products including white flour, white bread, and a variety of pastas and nutrition bars. Because excess folic acid can be used by L-form bacteria, these enriched products should be avoided.

A conventional treatment for the lung disease sarcoidosis confirms that folic acid does indeed affect the activity of bacteria. Some patients with sarcoidosis are told to take Methotrexate (MTX), a drug that temporarily slows progression of the disease by blocking the activity of folic acid, and subsequently the activity of DHFR. Another drug that blocks the activity of DHFR is the antibiotic Trimethoprim, which is used to create the drug Bactrim.

A team of researchers at the Institute of Food Research in the UK has shown that when people consume foods that are supplemented with folic acid, the liver can easily become saturated with the substance. Writing in the British Journal of Nutrition, the researchers warn this could lead to unmetabolised folic acid entering the blood, which could damage health.

“This can cause problems for people being treated for leukemia and arthritis, women being treated for ectopic pregnancies, men with a family history of bowel cancer, people with blocked arteries being treated with a stent and elderly people with poor vitamin B status,” states british researcher Dr. Sian Astley.

“For women undergoing in-vitro fertilization, it can also increase the likelihood of conceiving multiple embryos, with all the associated risks for the mother and babies.”

Since high levels of folic acid enable chronic bacteria to thrive, it’s also not surprising that two recent commentaries appearing in Nutrition Reviews found that the introduction of flour fortified with folic acid into common foods was followed by an increase in colon cancer diagnoses in the U.S. and Canada. Extra folic acid may also increase the incidence of breast cancer in postmenopausal women.

Some people are told to supplement with folic acid because it lowers levels of homocysteine, a chemical that has been linked to heart disease. However a recent meta analysis on folic acid and cardiovascular disease by researchers at the Tulane University School of Public Health found that folic acid had no beneficial effect on the study subjects, despite the fact that it does lower homocysteine.

The team to concluded, “Folic acid supplementation has not been shown to reduce risk of cardiovascular diseases or all-cause mortality among participants with prior history of vascular disease.”

It should be emphasized that the negative consequences observed in these studies were the result of folic acid supplementation, meaning that these results do not pertain to normal levels of folic acid obtained through a healthy diet.

Carbohydrates provide bacteria with an easy source of energy

A sugar molecule. Both humans and bacteria use sugar as a source of energy.

Our bodies use carbohydrates as a source of energy, but carbohydrates are also a source of fuel for bacteria. The body breaks down both carbohydrates and sugar into the exact same sugar molecules, so a diet high in carbohydrates will produce the same fuel for bacteria as a diet high in refined sugar.

The human body extracts the nutrients in food through a biological process known as the Krebs Cycle. The Krebs Cycle is part of a metabolic pathway that converts carbohydrates, fats and proteins into a form of energy that can be used by the body. The cycle uses sugar to generate molecules of NADPH, which humans are able to use as a source of energy. But bacteria such as Borrelia, Treponema, and possibly other bacteria, do not have proteins in their genomes that allow them to use NADPH as an energy source. Instead, they obtain energy directly from sugar. This means that while humans must wait until sugar is broken down in order to put it to use, some bacteria can use it right away. Consequently, extra sugar inevitably ends up benefiting the pathogen rather than the host.

Furthermore, sugar has been shown to affect the immune system in ways not yet completely understood. Sugars in the body often bind to proteins, a process called glycosylation. Once attached to a protein, sugars adjust the protein’s ability to react with other molecules. T-shaped molecules of the immune system called immunoglobulins have a location at the center of their structure which has a high affinity for sugar. Sugars are attracted to this region and once attached, stay bonded for long periods of time. It is not yet known what changes sugars induce when bound to immunoglobulins, but their ability to bind these molecules does suggest that sugar can modulate the immune response.

Consequently, it’s important that sugar and carbohydrates be eaten in moderation. Depending on metabolism and activity level, some people may want to consider eating a diet low in carbohydrates and sugar, such as the South Beach Diet or Atkins diet.

Some researchers, such as Loren Cordain, who has written several books on diet, argue that humans are meant to eat a diet low in carbohydrates. Cordain argues that the healthiest human diet is that which was eaten during the longest period of our evolution, which was prior to agriculture. Although not all experts agree on exactly what percentage of meat and vegetables were eaten by our ancient ancestors, they all agree that grains, sugar and legumes were not consumed to any significant degree by ancient, pre-agricultural man.

Cordain and others have noted that there was a decline in health, indicated by examination of skeletal evidence, after agriculture took hold. Agriculture permitted large civilizations to develop through grain cultivation, but Cordain argues that the widespread switch to cereals and grains has been a two-edged sword, and he has even linked it to diseases like multiple sclerosis, autism and schizophrenia.

Foods that slow the immune system

Molecular modeling research has shown that the Vitamin D Receptor (VDR), a fundamental receptor of the body, controls the activity of the innate immune system. The medication Benicar binds and activates the Vitamin D Receptor.

Foods high in vitamin D should be avoided.

A wide variety of compounds can also bind the receptor and adjust its level of activity. Some of the substances found in food bind and inactivate the Vitamin D Receptor, causing the activity of the immune system to slow down. These substances are called VDR antagonists. When the immune system slows down, some people report feeling better. These people are most likely infected with chronic disease-causing bacteria.

Chronic bacteria have evolved mechanisms that allow them to live for long periods of time within the cells, and when alive, generally persist without generating too many symptoms. It is when bacteria die that they begin to cause a major increase in symptoms for the host, since as they die they release a large amount of toxins and cytokines, proteins that generate pain and fatigue. Additionally, as bacteria die, the cell that they have parasitized dies as well, and cellular debris is released into the bloodstream.

Many people infected with L-form. biofilm, and other chronic bacterial forms unknowingly eat foods with substances that deactivate the VDR, which temporarily slows the release of cytokines and toxins. Unaware that this reaction is taking place, people often attribute a small boost in “wellness” to the idea that the foods with VDR-blocking substances are somehow beneficial. Often they try to maintain the feeling of “wellness” by eating increased quantities of these foods. But over the long term, eating high amounts of foods with substances that block the VDR only allow the chronic pathogens they harbor to spread and proliferate as the person’s immune system becomes increasingly deactivated.

Some people even find they are addicted to foods with substances that block the VDR. If they stop eating these foods, their immune systems begin to kill more L-form/biofilm bacteria and they feel worse. Unable to tolerate the rise in symptoms, they continue to crave and consume the foods high in VDR-blocking substances.

According to recent molecular models, the steroid 25-D is a VDR antagonist – it binds the Vitamin D Receptor and decreases the activity of the receptor, causing the innate immune system to slow down and shut off. This effect gradually increases with higher concentrations of 25-D, and reaches full blockage of the VDR at around 40 ng/ml.

It is critical that people consume only moderate amounts of vitamin D, so that the level of the steroid does not rise to the point at which it becomes immunosuppressive. People who are infected with chronic disease-causing bacteria should completely remove vitamin D from their diets. This is because certain forms of biofilm bacteria create proteins that bind and deactivate the VDR in a manner similar to 25-D. Extra 25-D only exacerbates the problem by further shutting off the receptor.

Furthermore, the low level of 25-D observed in many people with chronic diseases is not a sign of “deficiency” but a result of hormonal adjustments that occur naturally as part of the disease process.

According to biomedical researcher Trevor Marshall of Autoimmunity Research Foundation, “There is a big problem with the assumption that ‘Food makes the man.’ It doesn’t. In fact, when the body starts down-regulating hormones and metabolites the body is usually doing that for a reason. The whole concept of ‘replacement’ or ‘supplementation’ is fraught with non-sequiturs and risks.

“You should not assume that just because your body is ‘low’ in something that you should be adding a supplement. In the presence of a controlled metabolite, ‘deficiency’ can be a non-sequitur. You have to know more about the underlying metabolite,” says Marshall.

Vitamin D is found in seafood, egg yolks, sunflower seeds, pumpkins seeds, flaxseeds and a variety of other foods. Supplements such as fish oils (Cod liver oil, Omega 3 oil, primrose oil), and mushroom supplements all contain vitamin D. Many herbal supplements may contain vitamin D that is not listed in the ingredients on the bottle. Consequently, it is wise to avoid all supplements unless they are absolutely necessary.

Coffee is high in chlorogenic acid.

According to molecular modeling research, another substance that negatively effects the activity of the VDR is chlorogenic acid. Chlorogenic acid is an antioxidant found in foods such as coffee, tea, apples, pears, tobacco, pomegranate, potatoes and eggplant.

It’s fine to eat these foods in moderation, but eating excessive quantities of any one food high in chlorogenic acid might have an impact on the immune system. In particular, juicing, which greatly concentrates substances in fruits, should be avoided. In order to ensure that the immune system can kill L-form bacteria as effectively as possible, some people on antibiotic therapy to kill L-form bacteria may want to avoid foods high in chlorogenic acid.

Coffee is very high in chlorogenic acid (both caffeinated and decaffeinated). Some people find they are addicted to coffee or require a cup of coffee in the morning in order to function. Although some of this “pick me up” effect may be due to caffeine, it may also be due in part to the action of high levels of chlorogenic acid on the immune system.

Carnosic acid will displace 1,25-D (and Benicar) from the VDR in a concentration-dependent manner.

Some people who suffer from sensitivity reactions to certain foods find that they are sensitive to chlorogenic acid. Researcher Joyce Waterhouse PhD argues that sensitivity to chlorogenic acid might also cause a person to become sensitive to other substances that bind the VDR such as Benicar. This is because all molecules that bind the VDR have very similar structures and the body may confuse one for another. Thus, in the rare case that a patient on the MP becomes sensitive to Benicar, reducing chlorogenic acid in the diet may stop the body from reacting to VDR binding substances, allowing the patient to effectively tolerate the medication.

Molecular modeling research has also revealed that a substance called carnosic acid also binds and deactivates the VDR. In fact, it is a total antagonist of the VDR. Herbs such as rosemary and sage are high in carnosic acid. The calculated affinity of carnosic acid for the Vitamin D Receptor is Ki = 54 nanomolar. In simple terms, that means that only tens of milligrams of the substance can affect the immune system.

It’s okay to enjoy small amounts of carnosic acid in foods seasoned with rosemary and sage, but carnosic acid is also found in a variety of over-the-counter supplements. Consequently, although herbal supplements can seem harmless, they may have unintended effects on the immune system, especially since carnosic acid is only one of the many immunosuppressive substances often found in supplements.

Soy also contains a VDR antagonist. Soy products contain antioxidants called isoflavones. The primary isoflavone found in soy is called Genistein. Molecular models have revealed that Genistein interferes with the operation of the VDR, and also negatively affects two other receptors that control the immune system.

A picture of 1,25-D and Genistein as they dock into the VDR.

A study by researchers at the Rowett Research Institute in Scotland implies that 40mg of isoflavones a day is likely to produce concentrations capable of affecting the VDR (about 500 nanomolar). This amount is equivalent to about 20 grams of roasted soyabeans. It is wise to keep soy content in the diet below this level.

Green tea contains low levels of genistein. According to Marshall, those who choose to drink green tea should allow the tea bag to steep for only 30 seconds or less in order to ensure that the level of genistein in the beverage remains low. Black tea also contains genistein but is processed in a manner that is supposed to remove most of the substance. However, the amount of genistein actually removed by this process is disputed, so black tea should be made weakly as well.

The medication Benicar can counteract the immunosuppresive effects of Vitamin D Receptor blocking substances. Benicar binds and activates the Vitamin D Receptor, reversing to some degree the effects of substances that turn it off. However, even people taking Benicar should limit foods with VDR blocking substances in order to ensure that the immune system works at maximum capacity.

Everything in moderation

At the moment, a large part of the American public seems to feel that maintaining good health involves taking extra supplements. Often people don’t realize all the substances in the supplements they are taking. Taking extra supplements becomes a dangerous habit when many compounds found in these products can affect the activity of the immune system and foster the growth of chronic, disease-causing bacteria.

It seems that the best way to stay healthy is to avoid unnecessary supplements and to eat most foods in moderation. Problems arise when people try to consume an unnaturally high amount of a particular food or substance. It’s also important to have a good understanding of chronic disease and the actions of harmful bacteria when making decisions about diet. Just because a food or supplement makes a person feel better does not necessarily mean that it is improving their health. It may simply be slowing the activity of the immune system. Similarly, just because a person displays a low level of a substance like iron does not necessarily mean that they should supplement with large amounts of the substance. It’s important to realize that the nutrients we consume can also be used by bacteria. Eating a well-rounded and natural diet, while at the same time avoiding supplements unless they are absolutely necessary, will help to ensure that our bodies, and not the pathogens we harbor, get adequate nutrition.