Has Big Pharma Gone Bonkers?

Big Pharma has gone bonkers! That is the only way I can explain the most recent developments in the quest to destroy cholesterol synthesis in the body. The recent FDA mandate to label every statin prescription with warnings of increased risk to diabetes and cognitive impairment has not phased them in the least! With their extraordinary marketing schemes, the industry has managed to convince the doctors, the media, and the general public that there is no number below which LDL becomes pathologically low; no number above which HDL becomes pathologically high. If you happen to fall outside of a strict range, you have no doubt that you are sick – you need to take at least one drug for the rest of your life to whip those numbers into shape. Never mind that you feel just fine. Never mind that you are a child with a maturing brain or a young woman about to start a family. In fact, some are now suggesting that anyone over 50 years old should be automatically put on a statin, without even bothering to check their cholesterol levels [1].

The industry has now decided that it is not enough to offer an HMG coenzyme A reductase inhibitor (statin) that interferes with the mevalonate pathway at its root – a pathway that is essential to the survival of the cell. Now they are scheming with two new drug classes, one of which promises to knock your LDL cholesterol down by 75%, and the other of which promises to drive your HDL sky high, to levels never seen in nature. Can they be serious? Can they have any credibility left after the fiasco that will surely develop once these new toxins are widely disseminated?

NARC-1 Inhibitors

It turns out that, if you take a statin drug, your body tries desperately to get around the toxic effect of the statin by greatly increasing the synthesis of the enzyme, HMG Coenzyme A reductase, that the statin drug inhibits. This alone ought to tell us that the body needs this enzyme! But furthermore, your body will also increase its synthesis of an extraordinarily powerful high level controlling element, called NARC-1 (also known as PCSK9), one of only a handful of so-called protein convertases, which are still today poorly understood, but which surely have far reaching implications for the homeostasis of the body. NARC-1 is unusual among the protein convertases in that, unlike all the others, it does not require calcium uptake to be activated [2]. Furthermore, it is sulfated at two highly conserved tyrosine residues as it leaves the ER ready for prime time. I find both of these observations highly significant in light of the research I have been conducting on the importance of sulfate and the pathology associated with calcium uptake.

One of the known effects of NARC-1 is to decrease the reuptake of LDL by the liver, which is a good idea in order to allow the LDL (now in scarce supply) to linger longer in the blood so that it can deliver its goods (triglycerides, antioxidants, fat-soluble vitamins, and cholesterol) to the tissues. The industry, in all its wisdom, has now come up with a new injectable drug which interferes with the synthesis of NARC-1 [3], and the hope is that people who are not happy with their LDL numbers even after statin therapy can use this drug to drive their LDL down to as close to zero as possible. The two people who won the Nobel prize for their research on cholesterol back in the 1980’s are now working for one of the companies that is marketing a version of this new drug. These agents apparently can get your LDL down to levels you won’t see even if you’re taking the highest dosage of a statin drug [4, 5].

What NARC-1 stands for is “neural apoptosis-regulated convertase 1,” which is, to say the least, a confusing name, but with the word “neural” in there you ought to be worried about the concept of an inhibitor of this protein. Studies on zebrafish have shown that NARC-1 is expressed in neurons in the cerbral cortex and in the cerebellum in association with neurogenesis. Suffice it to say that, if you render NARC-1 inactive in a zebrafish embryo, the embryo dies after just 3 to 4 days of development with its midbrain and hindbrain blended together in a confusing array of disorganized neurons [6]. This is not a protein that I would care to mess with! Yet the industry is currently getting its rocks off thinking about the kachink of the cash register if it can successfully market this drug, as a way to further reduce your LDL number beyond the already too-low values achievable through statin therapy.

CETP Inhibitors

The other new drug, Torcetrapib, that had everybody excited [7] until the phase III trial results came in, is in a class called “CETP” (cholesterol ester transferase) inhibitors, and it works by inhibiting a protein that allows all the various lipoproteins (HDL, LDL, IDL, VLDL) to equilibrate their supplies of cholesterol and fatty acids by making trades. A quote from a recently published article on a phase III trial involving 15,000 people sums up the current situation: “Hopes have been running high that treatments aimed at raising HDL levels would soon help to reduce the large burden of cardiovascular disease that remains in patients at high risk of CHD who are now treated with statins. The unexpected and premature termination of the ILLUMINATE study has dashed those hopes.” [8] p. 257.

After 82 people died in the treatment group, as against only 51 in the placebo group, they called an early halt to the trial, and scrambled to regroup. As well as a substantially increased death rate, increases were observed in the treatment group in heart failure, angina, and revascularization procedures [8].

Why they could possibly think this drug was a good idea is beyond me! CETP is critically important for getting the fatty acids from the factory to the table. In diabetes, the skeletal muscles are insulin resistant, which means that they don’t like glucose as a fuel. The fat cells have assumed an awesome responsibility in maintaining fat stores that can be delivered to the muscles to keep them well fed. The delivery mechanism is interesting – kind of like the truck taking the goods to the dock where they’re piled into a containiner that’s loaded onto the cargo ship for long-distance transport. The HDL particle is the truck, and the VLDL particle is the ship. HDL takes up the fatty acids from the fat cell, and, as a consequence of now having a cargo load, it picks up an apo signature called “apo-CIII” which tells the liver not to recycle this particular particle (because it still has valuable goods to deliver). What it’s supposed to do next is to hand over its goods to a VLDL particle, along with the apo-CIII sign, and to pick up more cholesterol in return, so that it can now support a new load of fatty acids (the fatty acids need adequate cholesterol to wrap them and protect them from oxidative damage during transport). But with a CETP inhibitor at work, this exchange of goods can’t take place, so the HDL particle is stuck with a load it can’t deliver. The muscle cells don’t get fed, and the HDL particle is essentially converted into an LDL particle that can never be recycled. Your HDL numbers are high, but you should be thinking of them as LDL numbers! HDL containing apo-A1 is the healthy kind of HDL, but these fat-laden HDL particles can no longer reconvert themselves into apo-A1 versions, due to the fact that CETP isn’t working. In an in vitro study, it was shown that apo-CIII is handed over along with fatty acids when the exchange takes place. And HDL particles containing apo-CIII, i.e., burdened with fatty acids, are even worse than LDL containing an apo-CIII signature in terms of cytotoxicity to cells [9].

People with metabolic syndrome or diabetes tend to have an excess of free triglycerides in their blood, which have been released by fat cells to supply fatty acids to skeletal muscle cells for fuel. So their HDL particles are often overloaded in fatty acids relative to their cholesterol content, particularly in the context of a statin drug which has assured that cholesterol is in short supply. The CETP inhibitor prevents them from trading their excess triglycerides for some cholesterol with a VLDL particle, and therefore they are stuck with a situation where they can’t protect the fats they’re carrying from attack by oxidizing agents, and they can’t unload them. So, when you take this drug, you end up with a wonderfully high number of HDL particles in your blood, laden with dangerous undeliverable goods, because these oxidized fatty acids will launch a reaction cascade to create further damage to any biologically important molecules that intersect their path.

Statin Drugs

Now I want to reexamine the effects of statin drugs on muscle cells, in the light of some new information I have recently uncovered from the literature. It appears to me that statins offer the possibility of a nasty reaction cascade that would lead to an escalating pile of toxic cell debris accumulating in the skeletal muscles. This would go a long ways towards explaining all the muscle pain and weakness associated with statin therapy. As I’ve said before, statins interfere with the mevalonate pathway at its root. What I have come to realize lately is that, despite the fact that cholesterol is vitally important to the cell’s well-being, it may be the effect that statins have on another branch of the mevalonate pathway that is even more significant. This is because this other branch, involving G-proteins, is critical to the ability of the cell to communicate with other cells [10], something that is particularly important when the cell is distressed. Such communication turns out to be essential in order for the cell to die graciously. Why might the cell be distressed? Well, with insufficient cholesterol in its membrane, it’s going to be subjected to excess ion leaks, as I’ve discussed before. To solve this problem, it will switch from potassium to calcium (a bigger molecule) as a positively charged electrolyte to help it maintain its ion buffering and its charge balance. Having switched to calcium, it also has to switch its eNOS molecules from producing sulfate to producing nitric oxide. If the cell is a muscle cell, it depends on calcium transport between cellular compartments to generate the contractions that will support mobility. However, excess calcium in the cytoplasm provides background noise that weakens the signal and therefore the contraction strength. Furthermore, nitric oxide nitrosylates a critical protein that pumps calcium back into the sarcoplasmic reticulum to restore initial conditions after the contraction has completed [11]. So the cell becomes less and less able to perform its function, and at some point the best option is to die.

In such a situation, ordinarily a cell would send out a signal using G-proteins and this would draw the attention of a nearby neutrophil, which would arrive on the scene, ready and waiting to clean up the debris left behind after the cell dies with dignity. The neutrophil actually sends a reply signal that initiates a programmed cell death process called apoptosis, such that the cell can die in an orderly fashion, much like initiating a controlled computer “shutdown” rather than just pressing the power button [12, 13]. The SOS signal is called ”Fas” and the neutrophil’s response signal is called “Fasl.” The complex response initiated in the cell is aptly named a “death-inducing signaling complex” (DISC).

But with statins suppressing the mevalonate pathway, both the cell in trouble and the neutrophil are depleted in G-proteins [14] and are thus impaired in their ability to initiate the Fas-Fasl signaling that would allow the cell to shut down gracefully. Neither one can carry out its half of the signaling handshake, so instead the cell dies a messy unorchestrated death by necrosis, spilling its guts out into the intercellular space. One of the really toxic substances that shows up as debris when a cell dies an “unnatural” death is D-ribose, a glycating agent that is much worse than fructose, which in turn is much worse than glucose. So now we have a reaction cascade taking place where neighboring cells also die untimely deaths as a consequence of the toxicity of D-ribose, and a necrotic pile of cell debris accumulates. I would imagine that an accumulation of necrotic cell debris would also show up in the atherosclerotic plaque, because neutrophils are unable to respond to SOS signals sent out by distressed cells in the plaque. Indeed, what you typically see in statin therapy is a decrease in the overall number of heart attacks (and I think this may also be attributable to the shutdown of cell-cell communication channels), but an increase in the number and size of big heart attacks that are much more likely to kill you.

But the bigger problem, in my view, with these necrotic deaths, is that it has the effect of globally increasing the body’s cells’ exposure to advanced glycation end products (AGEs). Some have argued that AGEs should be equated with aging: that aging can best be defined as the accumulation over time of more and more AGE products. These AGEs are the biggest health problem associated with diabetes. They cause impaired function for all cells and blood proteins that come in contact with them. This accumulation of D-ribose from debris from dead cells is, in fact, I think, the key reason why statin drugs accelerate the rate at which you grow old. And I think that is the best way to characterize statin drugs.

An Exciting New Book

Finally, I want to shamelessly promote a book that has just been released called, “How Statin Drugs Really Lower Cholesterol and Kill You One Cell at a Time.” I just got a copy of this book [15], and I have been devouring it! The technique the authors use of showing snippets from papers written by the major players in the early promotion of statin drugs is stunning. If you do nothing else this summer, read this book! It will change forever your view of the medical establishment and the FDA.

Here, I just want to talk about one key paper referenced in the book [16]. This paper, written in 1980, discusses the core problem with statins addressed by the book, namely, that they interfere with the cell cycle and therefore prevent cells from being able to replicate their DNA. It’s another branch of the mevalonate pathway besides the cholesterol branch that leads to the key enzyme that is necessary for cell replication, and this is why statins interfere with the cell’s ability to multiply. Many cell types depend upon such cloning to maintain healthy tissues, such as in the skin, and most certainly a fetus, which probably explains why they’re labelled class X for pregnancy. But the really disturbing thing, to me, that this paper points out is that tumor cells exhibit a near universal pathology which is uncontrolled, unregulated, synthesis of mevalonate, the precursor to the reaction that is blocked by statin drugs. Since stressors induce tumorigenesis, and since the mevalonate pathway is highly stressed when a cell is bathed in statin drugs, I would expect that statins would be highly tumorigenic. But the key reason why they don’t actually lead to tumor growth is that statins interfere with the new tumor cell’s ability to clone itself. My prediction is that, when people who have been taking a statin for a long time go off of it (which they will surely do in droves if they read this book!), they will be primed for runaway cancer, because the statins are probably causing many cells to become malignant, but these cells have been trapped in a limbo state because of the suppression of DNA replication by statins.

References

[1] R. Smith, “All over 50s should be taking statins,“ The Telegraph, May 17, 2012. Accessed May 17, 2012.

[2] S. Benjannet, D. Rhainds, R. Essalmani, J. Mayne, L. Wickham, et al., “NARC-1/PCSK9 and Its Natural Mutants: Zymogen Cleavage and Effects on the Low Density Lipoprotein (LDL) Receptor and LDL Cholesterol,” J. Biol Chem 279(47) Nov. 19, 2004.

[3] R. Huijgen, S. M. Boekholdt, B.J. Arsenault, W. Bao, et al., “Plasma PCSK9 Levels and Clinical Outcomes in the TNT (Treating to New Targets) Trial A Nested Case-Control Study,” J Amer Coll Cardiol 59(20):1778-1784, 2012.

[4] D. Holmes, “Hopes soar as cholesterol plummets with new drug class,” http://www.nature.com/nm/journal/v18/n5/full/nm0512-633.html; accessed May 13, 2012.

[5] R.A. Vogel, “PCSK9 Inhibition: The Next Statin?” J. American College of Cardiology 59(25), 1-2, 2012.

[6] S. Poirier, A. Prat, E. Marcinkiewicz, J. Paquin, B.P. Chitramuthu, D. Baranowski, B. Cadieux, H.P. J. Bennett, and N.G. Seidah, “Implication of the proprotein convertase NARC-1/PCSK9 in the development of the nervous system,” J. Neurochem. 98:838850, 2006.

[7] M.E. Brousseau, E.J. Schaefer, M.L. Wolfe, L.T. Bloedon, A.G. Digenio, R.W. Clark, J.P. Mancuso, and D.J. Rader, M.D., “Effects of an Inhibitor of Cholesteryl Ester Transfer Protein on HDL Cholesterol,” New England Journal of Medicine 350(15):1505-1515, Apr. 8, 2004.

[8] The Failure of Torcetrapib : Was it the Molecule or the Mechanism? Alan R. Tall, Laurent Yvan-Charvet and Nan Wang Arterioscler Thromb Vasc Biol 2007, 27:257-260

[9] M.K. Jensen, E.B. Rimm, J.D. Furtado and F.M. Sacks, “Apolipoprotein C-III as a Potential Modulator of the Association Between HDL-Cholesterol and Incident Coronary Heart Disease,” J Am Heart Assoc 1:1-10, 2012.

[10] N. Wettschureck and S. Offermanns, “Mammalian G Proteins and Their Cell Type Specific Functions,” Physiol Rev 85:1159-1204, 2005.

[11] R.I. Viner, T.D. Williams, and C. Schöneich, “Nitric Oxide-Dependent Modification of the Sarcoplasmic Reticulum Ca-ATPase: Localization of Cysteine Target Sites,” Free Radical Biology and Medicine 29(6):489-496, 2000.

[12] M.-C. Lee, G.-R. Wee, and J.-H. Kim, “Apoptosis of Skeletal Muscle on Steroid-Induced Myopathy in Rats,” J Nutr.135(7):1806S-1808S, Jul. 2005.

[13] M. Bennett, K. Macdonald, S.-W. Chan, J.P. Luzio, R.Simari and P. Weissberg, “Cell Surface Trafficking of Fas: A Rapid Mechanism of p53-Mediated Apoptosis,” Science 282(5387):290-293, Oct. 9, 1998.

[14] L.M. Blanco-Colio, B. Muñoz-García, J.L. Martín-Ventura, C. Lorz, C. Díaz, G. Hernández and J. Egido, “3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors Decrease Fas Ligand Expression and Cytotoxicity in Activated Human T Lymphocytes,” Circulation 108:1506-1513, 2003.

[15] G.B. 14]Yoseph an H.Y. Yoseph, How Statin Drugs Really Lower Your Cholesterol and Kill You One Cell at a Time. Hannah Yoseph, Publisher, March 12, 2012.

[16] V.Q. Huneeus, M. H. Wiley, and M.D. Siperstein, “Isopentenyladenine as a mediator of mevalonate-regulated DNA replication,” Proc. Natl. Acad. Sci. 77(10) 5842-5846,Oct. 1980.

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.