Cholesterol sulfate boosts the electrical charge
that makes blood flow
This is the theory of Stephanie Senoff that I summarize here.
Cholesterol sulfate--Ch-S--is not only for circulation but electrons are also for mitochondria, which means total body energy (net negative charge of the cells) for every cell, organ, function and symptom.
Observable signs of a deficiency of Ch-S are: inflammation, pain, blood pressure either way, fatigue, arteriosclerosis, and more. Or, just about anything more indirectly since it has to do with total body energy.
“High” levels of things like cholesterol and homocysteine (with sulfur in it), indicate a lack of cofactor nutrients to utilize those nutrients, and especially sulfur to make cholesterol sulfate, to complete the job.
Inflammation is not the enemy but is a healing process that needs nutrients to be completed.
The pain associated with inflammation is a good metric to track progress that can respond immediately when the causes in nutrient deficiencies are addressed.
First, we need to see the big picture in the new theory of circulation:
1. The way blood circulates is that it is primarily pulled by an electrical charge from the capillaries, not just from the heart as a pump. (the new cardiology, Thomas Cowan)
2. The strength of the pull is relative to lack of friction between blood vessels and cells, in three ways:
3. Much of the electrical charge comes from the water of the blood, the 4th phase or exclusion zone water.
Ch-S helps hold electrons for a continuous flow from the sun on the skin where blood is charged with electrons to reach every cell of the body, involving intracellular and extracellular fluids. (Exclusion zone, 4th phase of water theory)
I should contrast this with the existing common over-simplified understanding before going into detail:
Nitric Oxide dilates the vessels for circulation.
NO does much more than that:
eNOS, endothelial nitric oxide synthesase is essential to making cholesterol sulfate.
A common perception is that arterial plaque or deposits of cholesterol is bad by obstructing circulation in a simple manner under the assumption you just ate too much cholesterol.
There are problems with these plaques, but cholesterol is not the issue.
These are an unfinished healing process due to deficiency of cholesterol sulfate.
Cholesterol is not bad. It may be useless until it joins sulfur, so it may accumulate in waiting.
There is no good and bad cholesterol, only utilized and unutilized.
Don’t ask me about your numbers: they do not have any definite meaning.
It’s important to get the cholesterol bogey man out of the brain to receive the new information.
So how do cholesterol sulfate and electrons come together?
A good example of how cholesterol and sulfur are synthesized is a bit off point but easier to remember to start:
Cholesterol and sulfur form vitamin D on the skin in the presence of sunlight with UVB rays.
Cholesterol at the skin donates an electron to prevent damage from UV rays and sunburn.
The remaining oxidized cholesterol can then join with sulfur to make vitamin/hormone D sulfate or cholesterol sulfate, which have a similarity.
D sulfate is water soluble, unlike supplements that are fat soluble and cannot do nearly as much.
Cholesterol sulfate in the cell membranes is both fat and water soluble: fat soluble as membranes are made of fat soluble cholesterol and water soluble to be transported easily through the blood and interface with the blood by presenting their negatively charged (having electrons) toward the blood to help keep it charged and flowing.
Sunlight is also turned into electrons as EZ water is created in the blood.
This is through Einstein’s photo electric effect.
There are other ways that cholesterol sulfate is created by blood and vessel cells.
This is an introduction for people who cannot understand Senoff’s highest level scientific article all by itself, so I am not posting the link, anyone can find it:
“A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome.”
Now for Senoff’s words.
I don’t have time to untangle all the terminology and assumptions in these quotes so you will have to put it together and connect to what I said above, but it’s still a lot simpler than reading the whole article.
On Electrical charge:
“….vascular flow is critically dependent on the negative charge provided by sulfate ions attached to the glycosaminoglycans in the capillary wall and to cholesterol in the plasma membrane of red blood cells. Electrostatic repulsion prevents RBCs from adhering to the capillary wall, and the encasement of the glycocalyx within structured water, formed in response to the kosmotropic properties of sulfate, provides a smooth surface further protecting from adhesion. The RBCs are propelled toward the venous end of the capillary by the electromagnetic field induced by the voltage drop across the capillary. The RBCs themselves act as moving charged particles that create a circular magnetic force around the capillary wall. This force induces nitric oxide release from the endothelial cells, which promotes vascular relaxation and increases flow.
…..properties of the endothelial surface in capillaries, likely reflected as near frictionless flow or squeezing of RBCs through capillaries whose internal diameters of ca. 4–9 μm are nearly the same or even smaller than the average RBC diameter of ca. 7.8 μm.”
“As noted above, atherosclerosis is increasingly regarded as an inflammatory condition. In earlier reviews, Davidson and Seneff have proposed exogenous interfacial water stress (EIWS) – the disruption of normal interfacial tension between water and biomacromolecules in vivo by exogenous agents such as the aluminum aquo cation -- as the earliest step in the pathogenesis of inflammation and disease.”
“… we propose that Ch-S acts as the key biosurfactant enabling healthy blood flow in the microvasculature.”
While the cardiovascular complications of diabetes are often attributed to loss of nitric-oxide-mediated vasodilation, an alternative pathophysiology was suggested, involving impaired microvascular perfusion due to (a) decreased fluidity and deformability of the RBC membrane related to biosulfate deficiency in the endothelial glycocalyx layer (EGL); and (b) increased capillary endothelial interfacial (surface) tension.
“As mentioned above, we previously proposed an eNOS- and sunlight-catalyzed mechanism as a normal route for sulfate biosynthesis.”
One way the body grabs sulfur:
“DHEA sulfate, but not DHEA, inhibits NF-κB synthesis, suggesting that sulfate deficiency is a driver of inflammation.”
“We propose that this cholesterol is accumulated as a reserve supply, which will be conjugated with sulfate to form Ch-S as soon as sulfate becomes available.”
“We propose a novel theory that atherosclerosis can best be explained as being due to cholesterol sulfate deficiency. Furthermore, atheromatous plaques replenish the supply of cholesterol and sulfate to the microvasculature, by exploiting the inflammatory agent superoxide to derive sulfate from homocysteine and other sulfur sources. We argue that the sulfate anions attached to the glycosaminoglycans in the glycocalyx are essential in maintaining the structured water that is crucial for vascular endothelial health and erythrocyte mobility through capillaries.”
“atherosclerosis results from a deficiency in a critical nutrient, cholesterol sulfate (Ch-S), and that the atheroma is a locale where endothelial cells, macrophages, and platelets collaborate to produce Ch-S from homocysteine and oxidized LDL.”
…it was proposed that the protein endothelial nitric oxide synthase (eNOS), along with sunlight, catalyzes sulfate production in erythrocytes, endothelial cells, platelets and keratinocytes in the skin. Thus, eNOS is a dual-purpose enzyme, producing sulfate when it is membrane–bound and producing nitric oxide when it is free in the cytoplasm.”
“Ch-S produced in erythrocytes and the endothelial wall is essential for distributing both cholesterol and sulfate to the tissues.”
“The contribution of sGAGs to cardiovascular health rests on their ability to maintain specially-structured water zones in the blood vessels.”
“The most commonly used GAGs in clinical practice are heparin, chondroitin sulfate, and keratin sulfate.”
Inflammation occurs for a good reason:
“While the view that atherosclerosis is an inflammatory disease is gaining in popularity today, anti-inflammatory pharmaceutical drugs increase the risk to heart disease. Elevated homocysteine is a strong risk factor for atherosclerosis, yet attempts to correct it have met with failure. Administration of B vitamin supplements in an attempt to reduce serum homocysteine has been effective, but did not result in any clinical improvement in cardiac disease risk. All of these seemingly contradictory results can be explained if we assume the point of view that the
inflammation is needed to induce superoxide production, which will allow sulfate production with homocysteine, H2S, and superoxide as substrates. Any attempt to reduce either the superoxide or the homocysteine levels will further impair the supply of sulfate to the capillary glycocalyx.”
“We have argued here that the inflammation renews sulfate supplies and the thrombosis reduces viscosity. Vascular flow is improved, and this leads to nitric oxide production, mediated by EVSP. Nitric oxide reaction products break down and redistribute locally-produced sGAGs.”
“A recent experiment showed that 25-hydroxycholesterol sulfate (25HCS) activated PPARγ in macrophages, resulting in the suppression of NF-κB and the subsequent inflammatory response.”
“While the cardiovascular complications of diabetes are often attributed to loss of nitric-oxide-mediated vasodilation, an alternative pathophysiology was suggested, involving impaired microvascular perfusion due to (a) decreased fluidity and deformability of the RBC membrane related to biosulfate deficiency in the endothelial glycocalyx layer (EGL); and (b) increased capillary endothelial interfacial (surface) tension.”
Toxicity disrupts nutrition by displacement and stealing electrons when toxins are free radicals:
“…..the aluminum found in high-SPF sunscreens as an emulsifier actively disrupts eNOS’ function….
….eNOS is an orphan cytochrome P450 (CYP) enzyme, and aluminum is a known disruptor of CYP enzyme function through its displacement of the iron in the heme group. Many other environmental toxicants also disrupt CYP enzymes, including mercury, arsenic, cadmium, glyphosate, and lead.”
Senoff is also an expert on glyphosate and has a whole book on it.
I would add that free radical toxins steal electrons as they float through the blood.
Toxicity raises nutritional requirements, and thus creates nutritional deficiencies, as more nutrients are needed to detoxify and supply electrons. Antioxidants are electron donors.
Thus, nutrition and toxic load are relative and the two main root causes to address first.
Infections are toxins that fight back and is more complicated.
Everyone has unique nutritional needs.
The most important nutrient is the one you lack the most.
All nutritional deficiencies must be addressed because we are only as strong as our weakest links.
I approach sulfur intolerance in terms of cofactor nutrient deficiencies for all these reasons. There are direct known cofactors for sulfur, but any missing nutrient can be an indirect cofactor as the system breaks down in a general, unpredictable way. There can lead to multiple sensitivities that people automatically assume are histamines, mca, etc, which may be part of the truth, but it’s often more complicated.
Cholesterol sulfate--Ch-S--is not only for circulation but electrons are also for mitochondria, which means total body energy (net negative charge of the cells) for every cell, organ, function and symptom.
Observable signs of a deficiency of Ch-S are: inflammation, pain, blood pressure either way, fatigue, arteriosclerosis, and more. Or, just about anything more indirectly since it has to do with total body energy.
“High” levels of things like cholesterol and homocysteine (with sulfur in it), indicate a lack of cofactor nutrients to utilize those nutrients, and especially sulfur to make cholesterol sulfate, to complete the job.
Inflammation is not the enemy but is a healing process that needs nutrients to be completed.
The pain associated with inflammation is a good metric to track progress that can respond immediately when the causes in nutrient deficiencies are addressed.
First, we need to see the big picture in the new theory of circulation:
1. The way blood circulates is that it is primarily pulled by an electrical charge from the capillaries, not just from the heart as a pump. (the new cardiology, Thomas Cowan)
2. The strength of the pull is relative to lack of friction between blood vessels and cells, in three ways:
- Electrical charge between blood cells to repel each other so they don’t clump: this is called Zeta potential, natural blood thinning.
- Electrical charge of cells that helps repel against vessel walls.
- Electrical charge of the vessel walls to repel blood cells.
3. Much of the electrical charge comes from the water of the blood, the 4th phase or exclusion zone water.
Ch-S helps hold electrons for a continuous flow from the sun on the skin where blood is charged with electrons to reach every cell of the body, involving intracellular and extracellular fluids. (Exclusion zone, 4th phase of water theory)
I should contrast this with the existing common over-simplified understanding before going into detail:
Nitric Oxide dilates the vessels for circulation.
NO does much more than that:
eNOS, endothelial nitric oxide synthesase is essential to making cholesterol sulfate.
A common perception is that arterial plaque or deposits of cholesterol is bad by obstructing circulation in a simple manner under the assumption you just ate too much cholesterol.
There are problems with these plaques, but cholesterol is not the issue.
These are an unfinished healing process due to deficiency of cholesterol sulfate.
Cholesterol is not bad. It may be useless until it joins sulfur, so it may accumulate in waiting.
There is no good and bad cholesterol, only utilized and unutilized.
Don’t ask me about your numbers: they do not have any definite meaning.
It’s important to get the cholesterol bogey man out of the brain to receive the new information.
So how do cholesterol sulfate and electrons come together?
A good example of how cholesterol and sulfur are synthesized is a bit off point but easier to remember to start:
Cholesterol and sulfur form vitamin D on the skin in the presence of sunlight with UVB rays.
Cholesterol at the skin donates an electron to prevent damage from UV rays and sunburn.
The remaining oxidized cholesterol can then join with sulfur to make vitamin/hormone D sulfate or cholesterol sulfate, which have a similarity.
D sulfate is water soluble, unlike supplements that are fat soluble and cannot do nearly as much.
Cholesterol sulfate in the cell membranes is both fat and water soluble: fat soluble as membranes are made of fat soluble cholesterol and water soluble to be transported easily through the blood and interface with the blood by presenting their negatively charged (having electrons) toward the blood to help keep it charged and flowing.
Sunlight is also turned into electrons as EZ water is created in the blood.
This is through Einstein’s photo electric effect.
There are other ways that cholesterol sulfate is created by blood and vessel cells.
This is an introduction for people who cannot understand Senoff’s highest level scientific article all by itself, so I am not posting the link, anyone can find it:
“A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome.”
Now for Senoff’s words.
I don’t have time to untangle all the terminology and assumptions in these quotes so you will have to put it together and connect to what I said above, but it’s still a lot simpler than reading the whole article.
On Electrical charge:
“….vascular flow is critically dependent on the negative charge provided by sulfate ions attached to the glycosaminoglycans in the capillary wall and to cholesterol in the plasma membrane of red blood cells. Electrostatic repulsion prevents RBCs from adhering to the capillary wall, and the encasement of the glycocalyx within structured water, formed in response to the kosmotropic properties of sulfate, provides a smooth surface further protecting from adhesion. The RBCs are propelled toward the venous end of the capillary by the electromagnetic field induced by the voltage drop across the capillary. The RBCs themselves act as moving charged particles that create a circular magnetic force around the capillary wall. This force induces nitric oxide release from the endothelial cells, which promotes vascular relaxation and increases flow.
…..properties of the endothelial surface in capillaries, likely reflected as near frictionless flow or squeezing of RBCs through capillaries whose internal diameters of ca. 4–9 μm are nearly the same or even smaller than the average RBC diameter of ca. 7.8 μm.”
“As noted above, atherosclerosis is increasingly regarded as an inflammatory condition. In earlier reviews, Davidson and Seneff have proposed exogenous interfacial water stress (EIWS) – the disruption of normal interfacial tension between water and biomacromolecules in vivo by exogenous agents such as the aluminum aquo cation -- as the earliest step in the pathogenesis of inflammation and disease.”
“… we propose that Ch-S acts as the key biosurfactant enabling healthy blood flow in the microvasculature.”
While the cardiovascular complications of diabetes are often attributed to loss of nitric-oxide-mediated vasodilation, an alternative pathophysiology was suggested, involving impaired microvascular perfusion due to (a) decreased fluidity and deformability of the RBC membrane related to biosulfate deficiency in the endothelial glycocalyx layer (EGL); and (b) increased capillary endothelial interfacial (surface) tension.
“As mentioned above, we previously proposed an eNOS- and sunlight-catalyzed mechanism as a normal route for sulfate biosynthesis.”
One way the body grabs sulfur:
“DHEA sulfate, but not DHEA, inhibits NF-κB synthesis, suggesting that sulfate deficiency is a driver of inflammation.”
“We propose that this cholesterol is accumulated as a reserve supply, which will be conjugated with sulfate to form Ch-S as soon as sulfate becomes available.”
“We propose a novel theory that atherosclerosis can best be explained as being due to cholesterol sulfate deficiency. Furthermore, atheromatous plaques replenish the supply of cholesterol and sulfate to the microvasculature, by exploiting the inflammatory agent superoxide to derive sulfate from homocysteine and other sulfur sources. We argue that the sulfate anions attached to the glycosaminoglycans in the glycocalyx are essential in maintaining the structured water that is crucial for vascular endothelial health and erythrocyte mobility through capillaries.”
“atherosclerosis results from a deficiency in a critical nutrient, cholesterol sulfate (Ch-S), and that the atheroma is a locale where endothelial cells, macrophages, and platelets collaborate to produce Ch-S from homocysteine and oxidized LDL.”
…it was proposed that the protein endothelial nitric oxide synthase (eNOS), along with sunlight, catalyzes sulfate production in erythrocytes, endothelial cells, platelets and keratinocytes in the skin. Thus, eNOS is a dual-purpose enzyme, producing sulfate when it is membrane–bound and producing nitric oxide when it is free in the cytoplasm.”
“Ch-S produced in erythrocytes and the endothelial wall is essential for distributing both cholesterol and sulfate to the tissues.”
“The contribution of sGAGs to cardiovascular health rests on their ability to maintain specially-structured water zones in the blood vessels.”
“The most commonly used GAGs in clinical practice are heparin, chondroitin sulfate, and keratin sulfate.”
Inflammation occurs for a good reason:
“While the view that atherosclerosis is an inflammatory disease is gaining in popularity today, anti-inflammatory pharmaceutical drugs increase the risk to heart disease. Elevated homocysteine is a strong risk factor for atherosclerosis, yet attempts to correct it have met with failure. Administration of B vitamin supplements in an attempt to reduce serum homocysteine has been effective, but did not result in any clinical improvement in cardiac disease risk. All of these seemingly contradictory results can be explained if we assume the point of view that the
inflammation is needed to induce superoxide production, which will allow sulfate production with homocysteine, H2S, and superoxide as substrates. Any attempt to reduce either the superoxide or the homocysteine levels will further impair the supply of sulfate to the capillary glycocalyx.”
“We have argued here that the inflammation renews sulfate supplies and the thrombosis reduces viscosity. Vascular flow is improved, and this leads to nitric oxide production, mediated by EVSP. Nitric oxide reaction products break down and redistribute locally-produced sGAGs.”
“A recent experiment showed that 25-hydroxycholesterol sulfate (25HCS) activated PPARγ in macrophages, resulting in the suppression of NF-κB and the subsequent inflammatory response.”
“While the cardiovascular complications of diabetes are often attributed to loss of nitric-oxide-mediated vasodilation, an alternative pathophysiology was suggested, involving impaired microvascular perfusion due to (a) decreased fluidity and deformability of the RBC membrane related to biosulfate deficiency in the endothelial glycocalyx layer (EGL); and (b) increased capillary endothelial interfacial (surface) tension.”
Toxicity disrupts nutrition by displacement and stealing electrons when toxins are free radicals:
“…..the aluminum found in high-SPF sunscreens as an emulsifier actively disrupts eNOS’ function….
….eNOS is an orphan cytochrome P450 (CYP) enzyme, and aluminum is a known disruptor of CYP enzyme function through its displacement of the iron in the heme group. Many other environmental toxicants also disrupt CYP enzymes, including mercury, arsenic, cadmium, glyphosate, and lead.”
Senoff is also an expert on glyphosate and has a whole book on it.
I would add that free radical toxins steal electrons as they float through the blood.
Toxicity raises nutritional requirements, and thus creates nutritional deficiencies, as more nutrients are needed to detoxify and supply electrons. Antioxidants are electron donors.
Thus, nutrition and toxic load are relative and the two main root causes to address first.
Infections are toxins that fight back and is more complicated.
Everyone has unique nutritional needs.
The most important nutrient is the one you lack the most.
All nutritional deficiencies must be addressed because we are only as strong as our weakest links.
I approach sulfur intolerance in terms of cofactor nutrient deficiencies for all these reasons. There are direct known cofactors for sulfur, but any missing nutrient can be an indirect cofactor as the system breaks down in a general, unpredictable way. There can lead to multiple sensitivities that people automatically assume are histamines, mca, etc, which may be part of the truth, but it’s often more complicated.
Eat to energize, detoxify & immunize.
Move to circulate, align, & relax.
Primal Rejuvenation Health Coaching
Find out what you get in a
Free Assessment
See how I support you fully in
Health Coaching Steps
I work over video: Facebook, Zoom, Google, from Michigan, USA
[email protected]
Follow me on FACEBOOK:
choose “See First” to get all notifications. blog posts
INSTAGRAM
Primal Rejuvenation
Systematic
enough to make a difference
Simple
enough to implement
Sensitive
to individual needs
Eat to energize, detoxify & immunize.
Move to circulate, align, & relax.
Primal Rejuvenation Health Coaching
Find out what you get in a
Free Assessment
See how I support you fully in
Health Coaching Steps
I work over video: Facebook, Zoom, Google, from Michigan, USA
[email protected]
Follow me on FACEBOOK:
choose “See First” to get all notifications. blog posts
Primal Rejuvenation
Systematic
enough to make a difference
Simple
enough to implement
Sensitive
to individual needs
