Can Bacteria Help Us Metabolize Sulfur and Rescue Us from Crisis?

Over the past year or so, I have been furiously reading the research literature, while simultaneously brainstorming on a fanciful story about how the human body might maintain good health in the face of severe deficiencies. I am going to try to piece certain parts of this story together here, in the hopes that someone else who knows more about biology than I do will pick up on it. I admit that what I write here is full of speculation, so please take it with a grain of salt. But if I am right about even some of what I say, I think it is very important for my message to get out to the world, because it means that the way we currently go about treating illness is all wrong.

In the 1800’s, Louis Pasteur framed illness in terms of infectious diseases, and his message has dictated how we treat disease today. Our aggressive administration of vaccines has greatly reduced the incidence of childhood diseases like measles and chicken pox, but at what cost? We need to seriously ask ourselves whether the alarming increases in autism, Tourette’s syndrome, ADHD, asthma, allergies, and childhood depression are a fair bargain in return. Antibiotics are clearly reaching the end of the line, with runaway MRSA (methicillin-resistant Staphylococcus aureus) leaving people terrified to spend time in a hospital, and no clear path towards new antibiotics in the pipeline to rescue us from disaster.

A little-known contemporary of Louis Pasteur, Antoine Béchamp, had an opposing point of view on the driver behind all disease, and I think he got it more right than Pasteur did. His focus was on the stability of the blood [1], and he felt that diseased states came about when the blood was chemically imbalanced. Béchamp’s most well known quote is probably, “The primary cause of disease is in us, always in us.” Certainly this seems to be more and more true over time, as modern noninfectious diseases like diabetes and Alzheimer’s replace the infectious diseases of yesteryear.

My studies, beginning with autism, have led me to the bold hypothesis that cholesterol sulfate deficiency is the most significant factor in modern diseases, ranging from arthritis to GERD (gastrointestinal reflux disease) to heart disease and Alzheimer’s. As I have discussed in previous posts, the troubles begin in many cases in the womb, where the mother’s deficiencies in the supply of cholesterol sulfate to the fetus predispose that child to future autism. Postnatally, the child continues to be deprived of dietary cholesterol, fat, sulfur, zinc and magnesium. In parallel, overexuberant application of sunscreen containing both aluminum and vitamin A leads to a direct suppression of cholesterol sulfate synthesis in the skin, an effect which may well continue even after the sunscreen has been washed off.

The dangers of insufficient cholesterol sulfate supply are manifested most poignantly in the blood stream. Without enough sulfate, the glycocalyx, which is the term used to describe the complex mesh of glycosaminoglycans (GAGs) lining the walls of the blood vessels, becomes incompetent in its function of maintaining low viscosity/surface tension in the capillaries. While this may sound unimportant, it is absolutely crucial for the ability of blood to flow smoothly through the capillary. A fascinating paper [2] has shown, using physical arguments, how a capillary will flush all of its blood out towards both the arteries and the veins, whenever its pressure is greater than the pressure in the arteries and veins. Since pressure is inversely related to the diameter of the vessel, the pressure in capillaries will automatically be higher than that in arteries, unless the capillaries maintain a very low viscosity to offset the smaller radius. This viscocity trick will work because pressure is directly related to viscosity.

I propose that the capillary achieves this goal through populating its glycocalyx with sulfate anions. This has the effect of creating a ’gel-like’ region along the interior of the capillary wall, which encloses all the dangling proteins and sugar molecules that are attached to the endothelial cells in the wall. Thus, a smooth “frictionless” surface, like the surface of jello, surrounds the interior of the capillary, preventing turbulent flow, and therefore lowering the viscosity. Due to their anionic kosmotropic property, the sulfate ions each surround themselves with a field of structured water, an exclusion zone of nearly pure water that behaves almost like a crystalline solid; i.e., that stays in place and does not join the flowing water in the middle of the capillary [3].

If there isn’t enough sulfate in the capillary wall, then the gel will turn into mush, and the viscosity will go up, as this part of the stream starts to participate in the flow. A crisis will be reached if the pressure in the capillary gets too high. This may well be the key reason why people develop hypertension – the arterial pressure must necessarily be raised through vasoconstriction of the artery wall in order to keep the pressure there higher than the pressure in the capillary. Otherwise the capillary will collapse. An alternative solution is to lower the viscosity in the capillary by depolymerizing the glycocalyx [4, 5]. Depolymerization (breaking down into smaller sized units) will significantly decrease the viscosity as well, and this can be achieved by attacking the wall with reactive oxygen species (ROS), a characteristic feature of heart disease. Thus the glycocalyx will be stripped away into little pieces, and the effective capillary diameter will grow. However, ROS can do a lot of collateral damage to the neighboring cells, which is why such inflammation is in general a bad idea. And the exposed capillary wall is now highly vulnerable to attack by things like maurauding microbes.

When the capillaries are in a fragile state due to inadequate sulfation, any disruption of the status quo could lead to a crisis, where the capillaries collapse and the affected organs are no longer supplied with oxygen. In my opinion, this could be a precipitating cause of both sudden infant death syndrome (SIDS) and sudden adult death syndrome (SADS), both of which are alarmingly on the rise. Since the aluminum in vaccines is known to deplete sulfate, vaccines would only increase a vulnerable child’s susceptibility. And endotoxin, which is the active ingredient in vaccines, is known to cause the heparan sulfate in the glycocalyx to erode [6].

The body responds to such a crisis with a remarkable reaction cascade that attempts to avert disaster, which I believe explains the extreme adverse reactions ot vaccines that result in anaphylactic shock and encephalitis, which I have previously discussed. A new insight that I have developed concerning encephalitis is the possible role that bacteria play in renewing critical nutrients, especially sulfate. It is very interesting to me that, in encephalitis, bacteria are literally invited into the brain. And I hypothesize that this is because they are useful to the brain in some way. Encephalitis is characterized by a leaky blood brain barrier [7], and this allows microbes to gain easy access to the brain. Heparan sulfate has been shown to be essential to maintain the epithelial barrier in the intestines [8], which is also known to be impaired in autism. So the bacteria can easily cross the gut wall as well as the BBB.

I have found a paper that describes how many bacteria, including E. coli, a common source of infection, can produce sulfate from taurine, using an enzyme called taurine alpha-ketoglutarate dioxygenase (TauD) [9]. The reaction also converts alpha-ketoglutarate to succinate, and converts oxygen to carbon dioxide. I am now thinking that this could be the key reason why bacteria are allowed into the brain during an acute crisis of the blood. In encephalitis, alpha ketoglutarate would likely be abundantly available, as it is easily derived from glutamate, which is known to be released by astroyctes in response to the swelling associated with encephalitis [10]. Astrocytes routinely store an abundance of taurine, which is also released along with glutamate [11]. And the neutrophils that follow the bacteria into the brain and that will eventually kill them also harbor taurine. So all the ducks are lined up to allow the bacteria to save the blood stream by resupplying the glycocalyx with sulfate derived from taurine.

The carbon dioxide that is produced by the bacteria as a by-product could be the key trigger of the hyperventilation and coma that often appear with acute encephalitis. Excess carbon dioxide in the blood leads to an acidosis condition that can easily be fatal if left unchecked. The brain stem responds by producing serotonin, which triggers a cascade reaction inducing spontaneous hyperventilation, associated with general anxiety [12]. By breathing faster and deeper than normal, the excess carbon dioxide could be expelled, thus averting the crisis. Rett syndrome, a rare condition affecting exclusively girls but with many similarities to autism [13], is associated with a charateristic hyperventilation behavior that highly suggests excess serotonin in the brain stem [14]. And the anxiety associated with autism [15] can be explained the same way, as the serotonin induces a state of anxiety and high alertness appropriate for the impending crisis. This idea is further supported by the fact that the serotonin system appears to be disturbed in autism [16]. A subsequent coma arises if the condition becomes so acute that the brain must shut down in order to rescue itself from potential extensive brain damage due to rampant exposure to carbon dioxide and to neuroexcitatory agents like glutamate.

Acidosis is a serious problem, since an increase in the blood concentration of free protons by as little as 0.1 M is fatal. It has been proposed that a defective serotonergic system might explain increased susceptibility to sudden infant death as well as panic disorders and the anxiety associated with autism [17]. I propose that such an impairment could arise due to a chronic exposure to excess carbon dioxide in the brain from the reaction carried out by the bacteria to extract sulfate from taurine. If true, this shows the critical importance of sulfate to the health of the blood system.

Now I want to abruptly change the topic to talk about algae, and you will soon see why this is relevant to the larger picture I am painting. A must-read book written by Elizabeth Plourde, called “Sunscreen Biohazard” [18] has a lot to say about the dangers of sunscreen, not just to us but to the fish, algae and coral in the sea. One of the key topics she covers is the destruction of coral reefs by sunscreen. Think of all the visitors who douse themselves in sunscreen before going snorkling over the coral reef. It turns out that sunscreen is extremely toxic to the algae that live in symbiosis with the coral and that supply the coral with critical nutrients for its survival.

I have dug up an article on algae that might explain not only how sunscreen destroys algae but at the same time how it interferes with the sulfur cycle in humans. In other words, the biochemical method that algae use to metabolize sulfate, in the presence of sunlight, may well be happening in human skin as well. It’s even possible that we exploit bacteria residing in our skin to provide critical enzymes to help us perform this feat, since common bacteria, such as E. coli, can also metabolize sulfate. And the sunscreen applied to the skin could be interfering with the process in the bacteria on the surface of the skin. According to the article [19], algae, when exposed to light, can extract sulfate from a molecule called APS (similar to PAPS that humans use as an activated form of sulfate), and reduce it to sulfide. It may be a long shot to propose that sunscreen interferes with the same process in algae and in humans, which is the reduction of sulfate to sulfide, but it would be remarkable if this were true. And it would mean that we have a complete sulfur cycle functioning in our bodies, utilizing sunlight as a source of energy.

References

[1] A. Béchamp, “The Blood and its Third Element,” Paperback edition, Review Press, 2012.

[2] I.A. Sherman, “Interfacial tension effects in the microvasculature,” Microvascular Research 22(3) Nov 1981, 296-307.

[3] G.H. Pollack, X. Figueroa and Q. Zhao, “Molecules, Water, and Radiant Energy: New Clues for the Origin of Life,” Int. J. Mol. Sci. 10:1419-1429, 2009.

[4] M.S. Baker, S.P. Green, and D.A. Lowther, “Changes in the Viscosity of Hyaluronic Acid after Exposure to a Myeloperoxidase-Derived Oxidant,” Arthritis & Rheumatism, 32(4):461467, Apr 1989.

[5] F.E. Lennon and P.A. Singleton, “Hyaluronan regulation of vascular integrity,” Am J Cardiovasc Dis 2011;1(3):200-213.

[6] P. Colburn, E. Kobayashi, and V. Buonassisi, “Depleted level of heparan sulfate proteoglycan in the extracellular matrix of endothelial cell cultures exposed to endotoxin,” J Cell Physiol 159: 121130, 1994.

[7] H.E. De Vries, J. Kuiper, A.G. De Boer, T.J.C. Van Berkel and D.D. Breimer, “The Blood-Brain Barrier in Neuroinflammatory Diseases,” Pharmacological Reviews 49(2):143-155, 1997.

[8] L. Bode, C. Salvestrin, P.W. Park, J.-P. Li, J.D. Esko, Y. Yamaguchi, S. Murch, and H.H. Freeze, “Heparan sulfate and syndecan-1 are essential in maintaining murine and human intestinal epithelial barrier function,” J. Clin. Investig. 118(1):229-238, Jan. 2008.

[9] K.P. McCusker and J.P. Klinman, “Facile synthesis of 1,1-[2H2]-2-methylaminoethane-1-sulfonic acid as a substrate for taurine a ketoglutarate dioxygenase (TauD),” Tetrahedron Letters 50:611-613, 2009.

[10] V. Parpura, T.A. Basarsky, F. Liu, K. Jeftinija, S. Jeftinija and P.G. Haydon, “Glutamate-mediated astrocyteneuron signalling,” Nature 369:744-747, Jun 30, 1994.

[11] H.K. Kimelberg, S.K. Goderie, S. Higman, S. Pang, and R.A. Waniewski, “Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures,” J Neurosci. 1990 May;10(5):1583-91.

[12] Brashear, R.E., “Hyperventilation syndrome,” Lung 161(1) 257-273, 1983.

[13] B. Olsson and A. Rett, “Autism and Rett syndrome: behavioural investigations and differential diagnosis,” Dev Med Child Neurol 29:429-441, 1987.

[14] D.P. Southall, A.M. Kerr, E. Tirosh et al, “Hyperventilation in the awake state: potentially treatable component of Rett syndrome,” Arch Dis Child 63:1039-48, 1988.

[15] J.A. Kim, P. Szatmari, S.E. Bryson, D.L. Streiner, and F.J. Wilson, “The Prevalence of Anxiety and Mood Problems among Children with Autism and Asperger Syndrome,” Autism 4(2):117-132, Jun. 2000.

[16] E.H. Cook and B.L. Leventhal, “The serotonin system in autism.” Curr Opin Pediatr. 8(4):348-54, Aug. 1996.

[17] G.B. Richerson, “Serotonergic Neurons as Carbon Dioxide Sensors that Maintain pH Homeostasis,” Nature Reviews 5:449-461, 2004.

[18] E. Plourde, “Sunscreens Biohazard: Treat as Hazardous Waste,” New Voice Publications, 2012.

[19] A. Schmidt, “On the mechanism of photosynthetic sulfate reduction,” Archives of Microbiology 84(1) (1972), 77-86.