I stumbled upon Seneff’s latest paper on sulfate and EZ water and, as expected of her it’s a real eye-opener! She already discussed the importance of sulfate on a number of occasions and in this study she goes into more detail in terms of the mechanisms that the body uses to obtain sulfate when there’s a lack of Vitamin B12, that is essential to generate EZ water.
I had to read it several times before understanding even the basics, so here’s my attempt at laying out some of the information presented.
Sulfate’s Critical Role for Maintaining Exclusion Zone Water: Dietary Factors Leading to Deficiencies
Overview
Exclusion Zone (EZ) water has been described by Pollack as the fourth phase of water (beyond solid, liquid and gas) and is the dominant phase found in the human body. EZ water yields a gel that is negatively charged that interfaces with the positively charged bulk water. It also has a higher degree of organisation compared to bulk water that has positive polarity and is less structured. The gelled water induces charge separation which forms a battery that supplies energy to tissues. For example, cancerous tissue has a lower degree of organisation, and pathology is generally associated with loss of water structure.
Sulfate plays a key role in providing the negative charge necessary to build and maintain the EZ water lining the blood vessels and in maintaining the proper viscosity of the circulating blood. eNOS, red blood cells (RBCs) Cobalamin (vitamin B12) are involved in sulfate production and regulation.
External factors such as metformin and glyphosate as well as a vegan diet reduce sulfate production and hence narrow the EZ layer, while certain nutrients have the opposite effect of thickening the EZ layer.
eNOS
eNOS is an enzyme that synthesises nitric oxide (NO) in the vascular endothelium lining the interior surface of blood vessels (see image below). eNOS is therefore essential for ensuring a healthy cardiovascular system.
Kosmotropes are ions that structure water (form a gel) while chaotropes instead are ions that desctructure water (maintain a liquid phase). Sulfate is a kosmotrope and has a gelling effect, thereby increasing blood viscosity, while nitrate is a chaotrope and decreases blood viscosity, maintaining adequate blood flow. Both sulfate and nitrate are regulated and maintained in balance to keep blood viscosity in check.
eNOS is generally accepted as being the enzyme that produces nitric oxide (NO) in the endothelium. Seneff proposes that eNOS in RBCs is also involved in production of sulfate and is therefore involved in regulating the balance between sulfate and nitrate in the blood. RBCs use membrane-bound eNOS (i.e. eNOS found on the surface of RBCs) to synthesise sulfur (SO2) rather than NO. eNOS synthesis of SO2 is catalysed by sunlight where eNOS responds to blue light by emitting the electrons needed to oxidise sulfur to produce SO2. Infrared light also provides energy for the formation of EZ water, hence why sunlight is essential to this whole process.
She hints at
intelligent design when describing the exquisite external control mechanism that utilises the eNOS enzyme to keep blood viscosity within narrow limits by regulating the production of the two ions.
RBCs and Cholesterol Sulfate
Sulfate is synthesised both in the skin and in RBCs using the energy from sunlight. Sulfate is then combined with cholesterol to make Cholesterol Sulfate (CS). Cholesterol sulfate supplies oxygen, sulfur, cholesterol and negative charge to all tissues.
Cholesterol is fatty molecule that helps the body make cell membranes, hormones as well as vitamin D. Cholesterol is hydrophobic, meaning that it doesn’t dissolve well in water, and hence isn’t able to flow in the blood. For this reason, it is packaged inside lipoproteins (e.g. HDL, LDL) that carry it around and distribute it to cells and tissues. When the cholesterol is sulfated, however, the resulting molecule is both water soluble and fat soluble so it doesn’t need to be packaged up inside a lipoprotein to be transported to organs and tissues. It is instead released onto the surface of lipoproteins rather than inside them. Additionally, HDL particles are able to use CS molecules to create a negatively charged field that acts as a shell to protect it from oxidation and glycation damage.
RBCs also use CS on the membrane to maintain an EZ water layer on the surface. RBCs obtain CS by conjugating (i.e. forming a stable link) sulfate with cholesterol. RBCs carry the sulfated cholesterol molecules in the membrane, with the sulfate part sticking out giving the RBC membrane negative charge. As the RBCs move through the blood vessel, they then shed the CS molecules that hop to the endothelial cells, providing them with both cholesterol and sulfate, along with oxygen and negative charge (see image below).
According to Seneff, this demonstrates two things:
- Due to the sheer number of RBCs in the blood, they contribute to the overall viscosity of the blood flow given the negatively charged gelled layer around their surface, which is dependent on CS supply.
- RBCs store CS only temporarily in their membranes before releasing them to both endothelial cells as well as tissues and organs where they decompose into cholesterol and sulfate.
CS also plays an important role in cases of high serum cholesterol (e.g. high LDL particles). High LDL is associated with heart disease and is the reason so many people are administered statin drugs. CS serves the purpose of distributing both cholesterol and sulfate to all the tissues, which are essential elements to the wellbeing of cells. When the artery wall is depleted of sulfate, it doesn’t work properly and that’s when the body ends up producing cardiovascular plaques since there is not enough sulfate in the artery wall and this causes the plaque to build up.
Seneff goes on to claim that a lack of cholesterol and sulfate supplies are the main factors that drive many of today’s modern diseases, the reason being that the system attacks its own body in order to obtain the sulfate it needs to deliver to the blood so that it can flow properly. The organs are basically “sacrificed” in order to produce the necessary sulfate and this is the main cause behind disease such as Rheumatoid arthritis, Alzheimer’s and autism among others. This is described in detail below.
Colabamin (Vitamin B12)
eNOS depends on several ions and cofactors in order to function properly, including iron, sulfur, zinc, oxygen, glutathione and sunlight. Seneff shows how Cobalamin (Vitamin B12) is one such ion that plays a critical role in the synthesis of sulfate by eNOS enzymes. Cobalamin conjugates with glutathione and the resultant molecule binds to eNOS via a cavity in the latter that matches the cobalamin molecule (imagine a puzzle piece fitting with another piece). This subsequently secures a sulfane-sulfur atom which gets oxidised to SO2 from an ambient hydrogen sulfite atom, thus generating the necessary sulfate required by the cell.
However, there are 3 exogenous factors that can disrupt the supply of cobalamin, hence affecting this mechanism of sulfate synthesis:
- Vegan Diet: plants don’t need cobalamin, nor produce it, hence a strict vegetarian/vegan diet doesn’t bring the necessary levels of dietary vitamin B12 needed for the body to produce sulfate.
- Metformin: the drug widely used to control blood sugar levels has the effect of disrupting cobalamin absorption in the gut.
- Glyphosate: Cobalamin is usually absorbed by binding to intrinsic factor, which is produced by parietal cells in the stomach. Now, Vitamin B12 degrades in acidic environments and the stomach has an extremely low (acidic) pH of 1.5 to 3.5. Since glyphosate is able to penetrate a cell plasma membrane in an acidic environment (the more acidic the better it can penetrate the medium), one can predict that the parietal cells will be very susceptible to dietary glyphosate in the stomach, and won’t be able to produce the intrinsic factor necessary to absorb the cobalamin. Moreover, cobalamin depends on cobalt as a cofactor and studies have shown that cows exposed to glyphosate have very low levels of cobalt and manganese.
Because of these factors affecting the absorption of cobalamin, the body needs to find other ways to procure this vitamin in order to generate sulfate. Seneff shows that, when faced with a cobalamin deficiency, our body is able to generate sulfate via alternate means to compensate for low cobalamin and ultimately maintain adequate EZ water within tissue and blood stream, which can only happen when sulfate is in sufficient supply. These alternate mechanisms, however, lead to side effects that are associated with many of today’s modern diseases (numbering is mine):
1. A cobalamin deficiency leads to reduced eNOS synthesis of sulfate. One of the responses to compensate for the loss of sulfate via the eNOS molecules happens in 2 ways:
- Bacteria converts sulfur to H2S in the gut to help eNOS generate SO2
- Taurine is released from the brain and heart and binds to bile salts in the liver to convert to sulfate
Symptoms of these adaptations include: dysbiosis, SIBO, inflammatory bowel disease (eg. Crohn’s) ulcerative colitis, hypotension, concentration and memory impairment, rheumatic conditions, severe neuropathy, dementia, thrombosis and cardiovascular disease.
2. Lower cobalamin leads to an unhealthy accumulation of homocysteine. This induces an inflammatory cascade in the artery wall releasing superoxide to oxidate sulfur in homocysteine to sulfate, thus compensating for eNOS-derived sulfate.
The inflammation involved in this process of generating sulfate drives cardiovascular disease.
3. Lower cobalamin increases cholesterol in artery walls (hence increased BMI, triglycerides and total cholesterol). Seneff proposes that the increase of cholesterol in fat cells within cardiovascular arteries provides a ready supply of cholesterol to convert to cholesterol sulfate once sulfate becomes available. Strokes are actually generated by the body as a mechanism to produce adequate amounts of cholesterol sulfate
4. Lower cobalamin suppresses the ability to use methyl groups derived from glycine to synthesise choline. The subsequent excess of glycine bioavailability helps in heme synthesis which is itself needed for eNOS and sulfite oxidase to synthesise sulfate from H2S.
However, choline deficiency leads to severe fatty liver disease, including non-alcoholic fatty liver disease which affects nearly one in three people. This could be especially relevant in a vegan diet.
5. Lower cobalamin leads to a reduction in glucose synthesis from glycogen stores. Tissues are then less able to store the glucose due to sulfate deficiency, which makes the glucose more glycating. This also makes lipid particles and RBCs more susceptible to glycation damage since their shield of gelled (EZ) water will not be adequate, due to the lack of sulfate. Glycation is known to be linked to multiple inflammatory diseases.
6. Cobalamin is involved in the reaction necessary to produce ATP. However, a lack of cobalamin leads to a blockage of this reaction which leads to ammonia and glutamate to accumulate to toxic levels. Now, since ammonia has a high pKa, it can substitute for taurine to support the high pH of the mitochondrial matrix. This enables the release of taurine which is transported to the gut microbes that can oxidise the taurine (which is conjugated to bile acids in the liver) to sulfate. Additionally, the e-coli enzyme that oxidises taurine to sulfite depends on glutarate. The increased availability of glutamate therefore facilities e-coli’s task. However, study has also shown that glyphosate down-regulates proteins involved in taurine transport.
Adverse effects on the brain due to excessive levels of ammonia and glutamate include chronic encephalopathy and neurotoxicity. Also, bile acids conjugated by taurine may explain the link between a high animal-based food diet and colon cancer (this in the context of cobalamin deficiency, not necessarily in a general sense of following a high-meat diet).
7. Lower cobalamin leads to increase in levels of propionate, malonate and ammonia. These are known to be disruptors of myelin sheaths that surround nerve fibres. Due to the insufficient sulfate caused by lower cobalamin levels, the gelled water surrounding the sheath destructures and makes the myelin more prone to immune attack. Seneff hypothesises that myelin sheath is actually attacked to retrieve the sulfate found in the sulfatide, to help restore sulfate levels.
Degradation of myelin sheath could be the factor that links cobalamin deficiency with Alzheimer’s disease. In fact, a study found that 93% of Alzheimer’s patients saw sulfatide levels plummet in the early stages of the disease. Cobalamin deficiency is also linked to other neurological diseases, including myelopathy as well as peripheral and optic neuropathy.
Conclusion
Seneff concludes by stressing the importance of sulfate as the source of negative charge necessary for forming EZ water in our bodies and how several diseases have a common origin as a compensatory mechanism to produce sufficient levels of sulfate when cobalamin is low.
She also outlines the factors that can be used to increase the size of EZ water:
- CoQ10, which enhances energy production as well as being an essential cofactor in the activity of sulfate as well as
- Nutrients including Vitaminc C, Vitamin D, curcumin and resveratrol that play a role in sulfate distribution
- Infrared Light increases the size of EZ water, with the greatest impact reported at a wavelength of 3000nm.
