Exploring chronic disease
23 Apr 2008
Need proof that consuming high levels of vitamin D can curb your lifespan? Look no farther then a study published this month in theAmerican 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.
Although the study did not examine what about the eggs might affect the risk of death, the results of the study can almost certainly be explained by the fact that egg yolks are very high in vitamin D – a secosteroid with immunosuppressive properties when elevated. Molecular modeling data, that is supported by a large amount of clinical data from the Marshall Protocol study site, has confirmed that 25-D – the form of vitamin D obtained from foods such as egg yolks – binds and blocks the Vitamin D Receptor (VDR). The VDR is fundamental receptor of the body that controls the activity of the innate immune system, the production of many families of antimicrobial peptides, and the transcriptions of hundreds and possibly thousands of genes.
Since, diabetes has now been linked to bacteria, blockage of the Vitamin D Receptor results in decreased immune function that allows the L-form and biofilm bacteria (collectively called the Th1 pathogens) that cause diabetes to spread with much greater ease. 25-D starts to cause immunosuppression via the VDR at levels at around 20 ng/ml, an amount that can be easily be obtained by eating only a moderate amounts of vitamin D.
It goes with out saying then, that physicians consuming a high number of eggs over a twenty year period would easily accumulate enough “vitamin” D to substantially block their VDRs.
Actually though, the extent to which 25-D blocks the VDR is related to another important factor – a person’s bacterial load. Biomedical research Trevor Marshall has used molecular modeling to show that at least one of the Th1 pathogens can create a substance that binds and blocks the VDR. Because slowing the VDR is such a logical survival mechanism for any form of pathogen, it’s almost certain that other species of the Th1 pathogens also create substances that block the receptor.
In the Harvard study, the physicians with diabetes no doubt had high bacterial loads. Subsequently their VDRs were already substantially blocked by bacterial substances. Since their VDRs were already blocked, it’s clear that even a small amount of 25-D from egg consumption easily exacerbated the existing blockage. Not surprisingly then, even moderate egg consumption in these men increased VDR blockage to a point where the subsequent decrease in immune function more then doubled their risk of death.
If the extent of VDR blockage generated by bacterial ligands is an important variable in determining how quickly 25-D contributes to VDR blockage, then healthy subjects with lower bacterial loads should not have been as negatively impacted by the immunosuppressive properties of the secosteroid. Indeed, the Harvard team found that healthy physicians without diabetes could eat up to six eggs a week with no extra risk of death.
Yet even among healthy physicians, risk of death increased by 23% among those who consumed seven or more eggs a week. This suggests that healthy men have more leeway when it comes to consuming vitamin D because of the fact that their VDRs are not yet significantly blocked by bacterial substances. Yet, even among healthy subjects, eating a sufficiently high level of vitamin D (over six eggs) did allow 25-D to rise above 20 ng/ml – to a point where they also began to suffer from negative consequences of decreased immune function.
The message is clear. Most healthy people are probably able to tolerate some vitamin D – moderate amounts of the substance that are found in non-fortified foods. Yet once a person develops symptoms of an inflammatory disease and their bacterial load starts to rise, consuming the secosteroid will only hinder immune function and exacerbate VDR blockage. Hence the Marshall Protocol guidelines, which state that patients on the treatment must remove all forms of vitamin D from their diet as they recover.
As for the rest of the the medical community, how long will it take before they connect the consumption of egg yolks to vitamin D – the real villan at the scene of the crime? As of today, they appear to be largely oblivious.
Take, for example, researchers in Finland, who recently discovered that the vitamin D content of an egg can be raised sevenfold by tripling the vitamin D in chicken feed, the hope being that such eggs could allow the public to consume ever higher amounts of vitamin D on a daily basis. The study was published in the Oct. 18 issue of the Journal of Agricultural and Food Chemistry.
Sevenfold? I’m literally getting shivers down my spine, and clearly not the good kind. If the amount of vitamin D in a natural egg doubles the rate of death for the average diabetic male physician, then imagine how quickly consuming eggs with a seven-fold increase in vitamin D will send them to the grave? And this trend applies to the entire population.
We are living in the midst of an epidemic of chronic disease that is fostered by nothing less then an epidemic of vitamin D delusion.
Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.
Amy has spoken at several international conferences and authored several peer-reviewed papers on the intersection of bacteria and chronic disease.
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