Monthly Archives: January 2016


Maintaining the Integrity of and Repairing the Glycocalyx: The Endothelial Gatekeeper

Examining the Human Blood Vessels

The human circulatory system consists of blood vessels that transport blood throughout the body. There are three major types of blood vessels:

  • Arteries (Arteries carry the blood away from the heart)
  • Veins (Veins carry blood from the capillaries back toward the heart)
  • Capillaries (Capillaries allow the exchange of water and chemicals between the blood and the tissues)

Figure 1:  Comparison of Arteries, Capillaries and Veins

The tunicae (a membranous sheath enveloping or lining an organ) of blood vessels, specifically the arteries and veins, contain three layers:

  • Inner layer (the tunica intima)
    • This is the thinnest layer of squamous endothelial cells glued by a polysaccharide intercellular matrix
  • Middle layer (the tunica media)
    • This is the thickest layer in the arteries of circularly arranged elastic fiber and connective tissue.  It is prominent in vascular smooth muscle.
  • Outer layer (the tunica adventitia)
    • This is the thickest layer in the veins made of entirely connective tissue composed of collagen.  The collagen serves to anchor the blood vessel to nearby organs, giving it stability.  Nerves are contained in the tunica adventitia.

The Capillaries consist of a layer of endothelium and connective tissue.

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Figure 2:  Structure of the Artery Wall

Introduction to the Glycocalyx in General

The glycocalyx is a glycoprotein-polysaccharide coating that surrounds the cell membranes of some epithelia and other cells.  The epithelia is a form of tissue that lines the cavities and surfaces of blood vessels and organs throughout the body.

The glycocalyx surrounding the cell membrane consist of a fuzzy-like coat and provide backbone molecules for support.  The polysaccharide portion of the glycocalyx molecule assists the molecule in:  1

  • cell-cell recognition
  • communication
  • intercellular adhesion

The body utilizes the glycocalyx as a mechanism to distinguish between its own healthy cells and transplanted tissues, diseased cells, or invading organisms.

The major role of the glycocalyx is in the regulation of  the endothelial vascular tissue through the endothelial glycocalyx.  2   

Introduction to the Endothelial Glycocalyx

The endothelial glycocalyx is a very thin (approximately 1 μm magnitude or .001 millimeters or 0.00003937007874 inches) 3 hydrated gel-like layer on the luminal surface of the vascular endothelium. The thickness of the glycocalyx increases with vascular diameter, at least in the arterial system, ranging from 2 to 3 μm in small arteries 4 to 4.5 μm in carotid arteries.  5

It is commonly referred to as the endothelial glycocalyx layer (EGL) or endothelial surface layer (ESL).  6  7  The glycocalyx is located on the apical surface of vascular endothelial cells which line the lumen.

The endothelial glycocalyx was already visualized some 40 years ago by JH Luft using electron microscopy.  8   The importance and validity of the endothelial glycocalyx as a vital factor in vascular physiology and pathology has increased over the years.  9  10 

Figure 3:  High-powered electron microscope photograph of the endothelial glycocalyx  (Source)

The name “glycocalyx” means “sweet husk” or “sugar coat”, referring to its high polysaccharide content. The term was initially applied to the polysaccharide matrix coating epithelial cells which is a delicate gel lining inside our arteries.

The glycocalyx is a gel-like coating that acts as a shield for the endothelium and forms the interface between the vessel wall and moving blood. The glycocalyx is held in place to the arterial wall by protein hair-like fibers.  The composition of the glycocalyx is not static as there is a balance between biosynthesis and shedding of glycocalyx components.

The glycocalyx is composed of a negatively charged network of proteoglycans, glycoproteins, and glycolipids.  11   Located between the blood stream and the endothelium, the endothelial glycocalyx is an important determinant of vascular permeability.  12  It is able to limit access of certain molecules to the endothelial cell membrane.  A dynamic equilibrium exists between the glycocalyx and the flowing blood, continuously affecting composition and thickness of the glycocalyx.   In fact, the shear stress applied from blood flow patterns provide the stimulus for the synthesis of the glycosaminoglycans present in the glycocalyx. As would be expected, the more turbulent blood flow patterns around vessel bifurcations and curvatures result in an inherently thinner glycocalyx, which explains the vulnerability of these areas to clot formation.

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Figure 4:  Schematic representation of the endothelial glycocalyx, showing its main components. Left: The endothelial glycocalyx can be observed in vivo as a red blood cell exclusion zone, located on the luminal side of the vascular endothelium. It consists of membrane-bound and soluble molecules. Right: Components of the endothelial glycocalyx. Bound to the endothelial membrane are proteoglycans, with long unbranched glycosaminoglycan side-chains (GAG-chain) and glycoproteins, with short branched carbohydrate side-chains.  (Source:  The endothelial glycocalyx: composition, functions, and visualization, flugers Arch. 2007 Jun; 454(3): 345–359., Published online 2007 Jan 26. doi:  10.1007/s00424-007-0212-8)

The major components of the endothelial glycocalyx layer are:  13  14

  • Glycoproteins
    • selectins
    • integrins
  • Glycosaminoglycans
    • heparin sulfate
    • chondroitin sulfate
    • hyaluronic acid
  • Proteoglycans
    • syndecans
    • glypicans


Figure 5: Structure of glycocalyx: the backbone molecules, glycoproteins and proteoglycans; GAG chains linked to core proteins; soluble molecules derived from plasma or endothelium bound to proteoglycans; intertwined HA molecules; sheltered adhesive molecules.  (Source:  Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions, Mediators of Inflammation, Volume 2014 (2014), Article ID 694312, 17 pages)

The molecular components of the endothelial glycocalyx are characterized by a polyanionic charge which helps repel circulating platelets. The exact composition varies greatly according to the local microenvironment.

At any given time, it also contains constituents of the routine molecular traffic which passes through it or lodges within it, such as:

  • Plasma proteins
  • Enzymes and enzyme inhibitors
  • Growth factors
  • Cytokines
  • Amino acids
  • Cations
  • Water
    • The glycocalyx is comprised of 95% water.

The endothelial glycocalyx also consists of a wide range of enzymes and proteins that regulate leukocyte and thrombocyte adherence, since its principal role in the vasculature is to maintain plasma and vessel wall homeostasis.

These enzymes and proteins include:

  • Extracellular superoxide dismutase (SOD3)
  • Angiotensin converting enzyme
  • Antithrombin-III
  • Lipoprotein lipase
  • Apolipoproteins
  • Growth factors
  • Chemokines

Biological Function of the Endothelial Glycocalyx

The endothelial glycocalyx plays a major role in the regulation of endothelial vascular tissue and thus has a variety of biological functions.

They include:

  • Vascular permeability
    • Glycocalyx regulates vascular permeability and fluid balance due to the large size and negative charge of glycosaminoglycans.  15  16
  • Impenetrable layer
    • Glycocalyx serves as a slippery layer to prevent things such as oxidized LDL cholesterol and white blood cells from sticking to the endothelial cells.  Once endothelial cells are exposed, then cholesterol plaque may develop.
  • Exclusion zone
    • Acts as the exclusion zone between blood cells and the endothelium.
  • Physical barrier
    • Provides a physical barrier against inadvertent adhesion of platelets and leukocytes to the vascular wall.  17
  • Modulates red blood cell volume
    • Modulation of red blood cell volume in capillaries  18
  • Barrier against leakage of certain molecules
    • Acts as a barrier against leakage of fluid, proteins and lipids across the vascular wall.
  • Dynamic interaction
    • Interacts dynamically with blood constituents.
  • Natural coagulant regulator
    • Regulates coagulation under normal physiological condition  19
  • Modulation of adhesion
    • Modulates adhesion of inflammatory cells and platelets to the endothelial surface.
  • Sensor and mechanotransducer
    • Functions as a sensor and mechanotransducer of the fluid shear forces to which the endothelium is exposed.
  • Protective enzymes
    • Retains protective enzymes (eg. superoxide dismutase).
  • Protection of cell membrane
    • Cushions the plasma (cell) membrane and protects it from chemical injury.
  • Inflammation regulation
    • Glycocalyx coating on endothelial walls in blood vessels prevents leukocytes from rolling/binding in healthy states.  20
  • Filtration of interstitial fluid
    • Affects the filtration of interstitial fluid from capillaries into the interstitial space.  21
  • Binding site
    • Serves as a significant binding site for antithrombin III (ATIII), tissue factor pathway inhibitor, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and lipoprotein lipase.  22

Damage to the Endothelial Glycocalyx

The glycocalyx is fragile and subject to damage.  Damage to the glycocalyx is the result of either:

  • Thinning of the glycocalyx layer, and/or
  • Shedding of the glycocalyx layer

The major common factors that contribute to the damage and disruption of the glycocalyx are:

  • Aging
  • Lack of moderate exercise.
    • Note that excessive or strenuous exercise or over training can also damage the glycocalyx.
  • Smoking
  • Poor diet
  • Single high sugar meal
    • Frequent and repeated meals consisting of sugars eventually wears the glycocalyx down into a thinner, less healthy layer.  High blood sugar is the most damaging cause of the glycocalyx

Despite the factors that contribute to a damaged glycocalyx, it has the ability to restore itself and is self-repairing.  A study found that the glycocalyx’s ability to restore itself can take up to 6 to 8 hours under normal and healthy circumstances.  The problem is that before it has time to repair itself, it my be assaulted repeatedly through smoking, poor diet or a high sugar meal.

Thinning of the glycocalyx layer

The thinning of the glycocalyx layer is caused by the following pathological processes:

  • Hyperglycemia (a condition in which an excessive amount of glucose circulates in the blood plasma.  Diabetes mellitus and metabolic syndrome (insulin resistance))
    • Individuals with hyperglycemia and diabetes are known to have less endothelial glycocalyx.
  • Hyperlipidemia (involves abnormally elevated levels of any or all lipids and/or lipoproteins in the blood)
    • The glycocalyx can also be reduced in thickness when subjected to oxidized LDL cholesterol.  23
  • Smoking

The pathological processes are known to cause atheroma formation, which is an accumulation of degenerative material in the tunica intima (inner layer) of artery walls. 24

Shedding of the glycocalyx layer

The second major cause of glycocalyx damage derives from enzymatic or shear-induced shedding. 

Fig 1

Figure 6:  Example of a healthy glycocalyx and a shedding glycocalyx  (Source:  Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy, Br. J. Anaesth. (2012) doi: 10.1093/bja/aer515)

Shedding of the glycocalyx layer can be caused by:

  • Inflammatory mediators  (when systemic inflammation is present and at raised levels)
    • Tumor Necrosis Factor alpha (TNFα) 25
    • C-reactive protein 26
    • A3 adenosine receptor stimulation  27
    • Bradykinin  28 
    • Mast cell tryptase  29
  • Ischaemia-reperfusion injury (which halts the endothelial synthesis of glycosaminoglycans) 30
  • Hypervolemia (medical condition where there is too much fluid in the blood)  31
  • Major vascular surgery  32
  • Major abdominal surgery (significant flaking of the endothelial glycocalix occurred in patients with sepsis, and to a lesser extent in patients after major abdominal surgery)  33
  • Sepsis  (Sepsis is a whole-body inflammatory response to an infection)  34

Whatever the stimulus, shedding of the glycocalyx leads to a drastic increase in vascular permeability.  35  When the glycocalyx is damaged, the vasculoprotective properties of the blood vessels are lost.  36

Adverse Biological Effects of Glycocalyx Damage and Disruption

The modulation of glycocalyx structure is seen under systemic inflammatory conditions and the possible consequences for pathogenesis of selected diseases and medical conditions.  The damage to the endothelial glycocalyx is due primarily to many inflammation-based pathological states.

Figure 7:  The glycocalyx in a healthy physiological state versus a state of Ischemia or Inflammation

Many studies have demonstrated that the degree of glycocalyx shedding depends on the extent of the systemic inflammatory state.  There exists a correlation between the severity of a disease and the level of glycocalyx components in the blood.  37  38  39 


Figure 8:  Overview of alternated glycocalyx functions as a result of its shedding which could lead to pathological states connected with various diseases. Matrix metalloproteinases (MMPs), reactive oxygen and nitrogen species (ROSs/RNSs), and tumor necrosis factor α (TNF-α).  (Source:  Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions, Mediators of Inflammation, Volume 2014 (2014), Article ID 694312, 17 pages)

Damaged and impaired endothelial glycocalyx is also demonstrated in the patients with:

  • Coronary heart disease  40 
  • Renal diseases  41 
  • Lacunar stroke (a small vessel disease)  42
  • Severe trauma  43 
  • Hypoglycemia/Diabetes 44 
  • Ischemia/reperfusion 45 
  • Atherosclerosis  46 
  • Local hypercoagulability  47
  • Global autoheparinisation (especially during trauma)  48
  • Impaired microcirculatory oxygen distribution  49
  • Loss of vascular responsiveness  50
  • Increased platelet aggregation  51
  • Increased leucocyte-endothelium interaction  52
  • Pulmonary Edema and Acute Lung Injury (Pulmonary endothelial dysfunction plays a major role in lung injury via alterations in barrier permeability, thus promoting pulmonary edema formation; the adjoining glycocalyx has recently emerged as a major endothelial element involved in the regulation of vascular integrity and fluid homeostasis.  A glycocalyx mechanotransduction-mediated lung injury model predicts that activation of pressure- or flow-induced signals during pulmonary resection may lead to augmentation in endothelial cell hydraulic conductivity, i.e., capillary permeability, involved in the formation of pulmonary edema).   53

General Maintenance of the Glycocalyx

Maintaining the integrity of the glycocalyx demands the practice of a healthy lifestyle.  In order to accomplish this, the daily positive habits should be practiced:

  • Obtain a proper nights sleep
  • Reduce daily stress or stressors
  • Engage in moderate exercise daily or at least 6 times per week
  • Eat real natural foods with no consumption of processed foods

In addition, the following negative habits should be avoided:

  • High sugar diet.  When dietary sugars are consumed, the glycocalyx is damaged and destroyed wherein the body then begins to re-build the glycocalyx.
  • Smoking

Managing chronic (systemic) inflammation is also important to avoiding damaged glycocalyx. 

Beyond practicing the positive daily habits and avoiding the negative daily habits, there are subsequent therapeutic strategies that can be followed to assure that the integrity of the glycocalyx is maintained.  These strategies are discussed in the next two sections. 

Certain Experimental Strategies to Regenerate and Repair the Glycocalyx

There are only handful of studies examining the strategies to regenerate and repair the glycocalyx.   Most of the agents suggested for the repair or regeneration of the glycocalyx is pharmaceutical based, and thus require the administration from a licensed physician, if at all possible.

The following experimental strategies to repair the glycocalyx have been researched are are contained in the scientific literature:   54

  • Adenosine A2A receptor agonists  55
    • Adenosine A2A receptors are believed to play a role in regulating myocardial oxygen consumption and coronary blood flow.
  • Nitric oxide  56
    • Nitric oxide is a cardiovascular signaling molecule and a powerful vasodilator with a short half-life of a few seconds in the blood.
  • TNF-α inhibitors  57
    • A TNF-alpha inhibitor is a substance or drug that suppresses the physiologic response to tumor necrosis factor (TNF), which is part of the inflammatory response.  TNF-alpha or its effects are inhibited by several natural compounds, including curcumin (a compound present in turmeric), and catechins (in green tea).
  • Allopurinol  58
    • Allopurinol is a medication used primarily to treat excess uric acid in the blood.
  • Sulodexide
    • Sulodexide, a mixture of glycocalyx GAG precursors consisting of heparin sulphate (80%) and dermatan sulphate (20%), can be included among compounds suggested as a possible treatment of dysfunctional glycocalyx.  59 
  • Albumin Plasma Proteins
    • A suggested way to protect the glycocalyx is to maintain a sufficiently high concentration of plasma proteins  60  
    • The protective effect of the albumin supplementation on glycocalyx preservation in a model of transplantation-induced ischemia/reperfusion glycocalyx damage was presented by Jacob et al.  61
  • N-acetyl cysteine (NAC)
    • In human research, NAC prevented the hyperglycemia-induced reduction of glycocalyx.  62  It is important to note that in this study NAC was infused into the blood stream 15 minutes before and then continuously with glucose infusion at a very a large dose. Such a protocol is good for research but has a very limited application in a real life situation. In another words, oral supplementation of NAC is unlikely to achieve this effect in hyperglycemic individuals.  
  • Chondroitin sulphate and hyaluronic acid 
    • Infusion of a mixture of hyaluronan and chondroitin sulfate after enzyme treatment reconstituted the glycocalyx, although treatment with either molecule separately had no effect.  63

Other than N-acetyl cysteine, chondroitin sulphate and hyaluronic acid, which are easy to obtain from a health store or online, the other strategies, such as Sulodexide and Allopurinol, require a prescription and supervision from a health professional. 

An Alternative (Natural) Approach to Regenerating and Repairing the Glycocalyx

Scientists have spent years researching ways to regenerate and repair the endothelial glycocalyx in a simple effective manner.  The answer to repairing the endothelial glycocalyx may lie in the consumption of sulphated polysaccharides.

Sulphated Polysaccharides

Seaweeds (algal) are known as sources of sulfated polysaccharides.  Green algal polysaccharides, or sulphated polysaccharides have emerged as rich and important sources of bioactive natural compounds with a wide range of physiological and biological activities.  64  65  These physiological activities include:

  • anticoagulant
  • anti-inflammation
  • antioxidant
  • antitumor
  • immunomodulation


Figure 9:  Many sea vegetables contain sulphated polysaccharides

Researchers discovered that sulphated polysaccharides from marine algae had heparin-like anticoagulant activities.  66 67   The sulphated polysaccharides from marine green algae show higher anticoagulant activities than sulphated polysaccharides from red and brown seaweeds.  68

A highly investigated green seaweed that produce anticoagulant sulphated polysaccharides belong to the genus Monostroma. Researchers found that there were high anticoagulant activities derived from extracts from Monostroma nitidum seaweed, which contains a high amount of sulphated polysaccharides . In Monostroma nitidum, the active polysaccharide was purified by chromatography to yield an approximately six fold higher activity than standard heparin.  69  

In addition to the high anticoagulant activity of Monostroma nitidum, researchers also found that it possessed excellent anti-inflammatory activities.  The following inflammation markers were suppressed with Monostroma nitidum:  70

  • inducible NO synthase (iNOS)
  • tumor necrosis factor-α (TNF-α)
  • interleukin-6 (IL-6)
  • interleukin-8 (IL-8)

Figure 10:  Monostroma nitidum

Rhamnan sulfate

Rhamnan sulfate is a sulphated polysaccharide in which more than one type of monosaccharide are present. Rhamnose is the major monosaccharide found in rhamnan sulfate and hence gives the polysaccharide its name.

Monostroma nitidum is rich in rhamnan sulfate, a negatively charged polysaccharide, and has been shown to exhibit the following health benefits:

  • anticoagulant  71  
  • antithrombotic  72  
  • antiviral  73 
  • antitumor  74
  • immunomodulator  75 
  • lowers total and LDL cholesterol in borderline or mild hypercholesterolemia human subjects  76 
  • reduces blood glucose level compared to the control animals  77 


Figure 11:  Rhamnan sulphate from Monostroma nitidum

A study from 2015 investigated the use of Rhamnan sulphate obtained from Monostroma nitidum and its effect on endothelial cells and vascular smooth muscle cells.  78   The results show that Rhamnan sulphate has the potential to be used in the treatment of cardiovascular diseases.

Rhamnan sulfate has a remarkably similar chemical structure to heparan sulfate.  Heparan sulphate is found abundantly in the endothelial glycocalyx.  Because of this similarity, Rhamnan sulphate may act by repairing and regenerating the glycocalyx.

A 2013 study corroborated the ability of Rhamnan sulphate to repair the glycocalyx.  The researchers reported that rhamnan sulfate enhances the endothelial glycocalyx and decreases the LDL permeability of human coronary artery endothelial cells in vitro.  79   This again is due to the fact that Rhamnan sulfate has a similar chemical structure to heparan sulfate.


Arterosil® is a product marketed by Calroy Health Sciences, and is the only dietary supplement that helps maintain optimal endothelial function through regeneration of the vascular endothelial glycocalyx.

Calroy Health Science focuses on developing original science-based solutions to major health challenges through a scientific research program led by Chief Scientific Officer Dr. Chen Chen.   Dr. Chen Chen is a widely respected scientist and entrepreneur. With a PhD in nutritional science, he has conducted pioneering research in the field of food and nutrition for over 30 years.  While championing healthy lipids, Dr. Chen has conducted extensive studies on functional carbohydrates and participated in the research and development of some of the most innovative products on the market, such as Arterosil®.

The primary active ingredient of Arterosil® is rhamnan sulfate, derived from Monostroma nitidum. The beneficial effects of Arterosil® on endothelial glycocalyx and its mediated endothelial functions are backed up by many years of research. In fact, an randomized double blind clinical study was conducted to evaluate the effectiveness of ArterosilHP® on endothelial function.

The study consisted of 20 healthy human subjects that were placed on ArterosilHP® for 4 weeks. At the beginning and the end of the study, the subjects were challenged with a high fat/high sugar meal in the morning and then followed up for 8 hours at the clinic.

The endothelial glycocalyx thickness was estimated by the measurement of sublingual capillary blood flow as described by Nieuwdorp et al.  80  Endothelial function is evaluated by reactive hyperemia index (RHI).

At the beginning of the study, the subjects experienced a compromised glycocalyx at 1.5 hours after consumption of the high fat/high sugar meal. With 4 weeks of ArterosilHP® supplementation, the same subjects showed a significantly improved glycocalyx at 1.5 hours after the high fat high sugar meal. In both visits, the glycocalyx recovered back close to normal 8 hours after the meal.

Similar trend was also observed with RHI in the subjects (see Figure 12 below). Before ArterosilHP® supplementation (blue baseline), subjects experienced a dramatic drop of RHI 1.5 hours following the high fat/high sugar meal. After 4 weeks on ArterosilHP® supplementation (red ArterosilHP®), the drop of RHI for the same subjects 1.5 hours after the high fat/high sugar meal was significantly reduced. Again RHI showed significant recovery after 8 hours in both visits.

Figure 12:  Reactive hyperemia index (RHI) study results

These results clearly demonstrate that ArterosilHP® supplementation ameliorates the damage of endothelial glycocalyx and the loss of endothelial function caused by a high fat/high sugar meal in the healthy human subjects.

Arterosil®  comes in two (2) product versions:
  • Arterosil® has been shown to support a healthy endothelial glycocalyx, the inner lining of every blood vessel in the human body.
  • ArterosilHP® is the high potency version of Arterosil with twice the active ingredients per capsule.


Informational References:

White Paper:  CALROY HEALTH SCIENCES Nutritional Support for the Endothelial Glycocalyx:  ArterosilHP

Video:  Arterosil Helps to Strengthen The Glycocalyx from Arterosil HP

Website:   Arterosil®



To purchase Arterosil®, click on the link(s) below:




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Strategies for Detoxifying and Ameliorating the Toxic Effects of Lead Poisoning

Lead has no known beneficial function in human metabolism.

The leading sources of human lead exposure are the following:

  • Lead-containing paint
  • Food stored in lead can liners
  • Food stored in ceramic jars
  • Contaminated water (pipes cast in lead or soldered using lead solder)

In addition to direct ingestion of lead, studies also suggest that lead can be absorbed through the skin.  Once lead is in the human body, it has the ability of cross the blood brain barrier.

Children absorb lead up to 8-times more efficiently than adults.  1

Lead can be excreted from the body through feces or urine.  2  

The toxicological effect of lead can be reviewed at the website Agency for Toxic Substances and Disease Registry.

The main focus of this article is to examine the different strategies to detoxify lead from the body and to ameliorate the toxicological effects of lead poisoning.

Detoxification Strategies for Lead Poisoning

Chelation Therapy

Chelation therapy is a medical procedure that involves the administration of chelating agents to remove heavy metals from the body. 

Chelation therapy is used as a treatment for metal poisoning, including acute metal poisoning by:

  • arsenic
  • iron
  • lead
  • mercury
  • plutonium
  • uranium

The chelating agent used for detoxification of metal poisoning is administered either:

  • intravenously
  • intramuscularly
  • orally

Chelation therapy is performed under the supervision of a licensed health care professional.  Patients should seek the advise and counsel from a licensed health care professional when considering chelation therapies.  Patients can contact the The American College for Advancement in Medicine (ACAM) for a U.S. national directory of physicians that practice and are licensed as chelation therapists.

There are 4 common chelating agents that are used (in the United States) for chelating lead poisoning:



Used in
Dimercaprol (British anti-Lewisite; BAL) Intravenous lead poisoning
Dimercaptosuccinic acid (DMSA) Oral lead poisoning
Penicillamine Oral lead poisoning
Ethylenediamine tetraacetic acid (calcium disodium versante) (CaNa2-EDTA) Intravenous lead poisoning

Two other candidates for chelating lead include:

  • Polygamma-glutamic acid-coated superparamagnetic nanoparticles.  These nanoparticles have been shown to have a high removal level of lead from the gastrointestinal fluid at 147.71 mg per gram.  3 
  • Magnetic chitosan/graphene oxide composites.  A 2013 study found that magnetic chitosan/graphene oxide composites had highly selective adsorption of lead ions at 76.94 mg per gram.  4 

Natural Substances (Nutraceuticals, Foods and Herbs) that Detoxify and Ameliorate the Effects of Lead Poisoning

In addition to the more aggressive chelation therapies administered and supervised by a licensed health care professional, there are certain natural substances that have been studied for their ability to either detoxify lead poisoning and/or ameliorate the toxic effects of lead poisoning.

The Table below lists these various natural substances and their scientific references:

Nutraceuticals, Foods and Herbs that Detoxify and Ameliorate the Effects of Lead Poisoning

Spirulina1 2
Amino acids
N-Acetyl-Cystiene (NAC)3 4 5
Taurine6 7 8 9
Modified Citrus Pectin10
Poly(gamma-glutamic acid) from Japanese Natto11
Coriander14 15
Green Tea16
Melatonin17 18 19
Fish Oil (DHA and EPA)20
Curcumin24 25
Alpha Lipoic Acid27
Vitamin B128
Vitamin C29 30 31 32

Informational References:

Lead and children:  Clinical management for family physicians

Agency for Toxic Substances and Disease Registry:  Toxicological Profile For Lead. 2007b;:1–582



N-Acetyl-Cysteine (NAC)


Modified Citrus Pectin




Green Tea


Fish Oil (DHA and EPA)






Alpha Lipoic Acid

Vitamin B1

Vitamin C

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Earthing : Grounded in Science?

Earthing is connecting to the Earth’s natural, negative surface charge by being barefoot outside or in bare skin contact with conductive systems indoors while you sleep, relax, or work.

With Earthing, the apparent impact on the physiology of the human body is profound. As modern science is learning, the human body is a complex structure of electrical circuitry and Earthing restores the electric potential to the body and which initiates self-healing mechanisms. In particular these mechanisms facilitate antioxidant potential through negatively charged free electrons into the body which produces anti-inflammation effects.

There have been many scientific and anecdotal benefits of Earthing, such as: *

  • improvement or elimination of the symptoms of many inflammation-related disorders
  • reduction or elimination of chronic pain
  • better sleep and faster to sleep
  • increased energy
  • lowered stress, more calmness by cooling down the nervous system and stress hormones
  • normalization of the body’s biological rhythms
  • thinner blood, improved blood pressure and flow
  • muscle tension and headache relief
  • lessened hormonal and menstrual symptoms
  • dramatically faster healing and reduction/prevention of bedsores
  • reduction/elimination of jet lag
  • protection against potentially health-disturbing environmental electromagnetic fields (EMFs)
  • accelerated recovery from intense athletic activity


Changes in Pulse Rate, Respiratory Rate, Blood Oxygenation, Perfusion Index, Skin Conductance, and Their Variability Induced During and After Grounding Human Subjects for 40 Minutes

Chevalier G et al. Earthing produces unique electrical function in brain and muscles. Euro Biol Bioelectromag. 2006;600–621.

Does Grounding the Human Body to Earth Reduce Chronic Inflammation and Related Chronic Pain?

Earthing (Grounding) the Human Body Reduces Blood Viscosity—a Major Factor in Cardiovascular Disease

Earthing the Human Body Influences Physiologic Processes

Chronic Disease: Are We Missing Something? (Editorial)

Earthing: Health Implications of Reconnecting the Human Body to the Earth’s Surface Electrons

Earthing: Restoring Health From the Ground Up

Earthing: The Most Important Health Discovery Ever?

Emotional Stress, Heart Rate Variability, Grounding, and Improved Autonomic Tone: Clinical Applications

Gaetan Chevalier, Ph.D., The Earth’s Electrical Surface Potential A summary of present understanding

Is our disconnection from the earth endangering our health?

James Oschman, Ph.D., Perspective: Assume a spherical cow: The role of free or mobile electrons in bodywork, energetic and movement therapies

Medical Thermography Case Studies

Method of treating inflammation and autoimmune diseases (U.S. Patent)

Oschman JL. Can electrons act as antioxidants? A review and commentary J Alt Comp Med 2007;13(9):955–967.

Our Place in Nature: Reconnecting with the Earth

Our Place in Nature: Reconnecting with the Earth for Better Sleep

Pilot Study on the Effect of Grounding on Delayed-Onset Muscle Soreness

Sleeping grounded normalizes cortisol level and improves sleep. Ghaly M, Teplitz D. J Alt Comp Med. 2004;10(5)767–776

The Biologic Effects of Grounding the Human Body During Sleep as Measured by Cortisol Levels and Subjective Reporting of Sleep, Pain, and Stress


The Effect Of Earthing On Human Physiology, Part 1

The Effect Of Earthing On Human Physiology, Part 2

The Effectiveness of a Conductive Patch and a Conductive Bed Pad in Reducing Induced Human Body Voltage Via the Application of Earth Ground

The neuromodulative role of earthing

Informational References:

For additional Information on Earthing visit The Earthing Institute


Dr. Stephen Sinatra talks about Bioenergetics, Earthing and Grounding


Where to purchase Earthing products:

Book: Earthing by: Clinton Ober, Stephen Sinatra, and Martin Zucker

*  The statements on this Post have not been evaluated by the Food and Drug Administration. Any products referred to on this Post are not intended to diagnose, treat, cure, or prevent any disease.

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Repairing the Cell Membrane

The human cell membrane separates the interior of all cells from the outside environment of the cell called the extracellular matrix.

The fundamental building blocks of all cell membranes are phospholipids.


Phospholipids are a class of lipids that are a major component of all cell membranes. They can form lipid bilayers because of their amphiphilic characteristic. The structure of the phospholipid molecule generally consists of two hydrophobic fatty acid “tails” and a hydrophilic “head”, joined together by a glycerol molecule.

About 50% of the mass of most cell membranes are composed of phospholipids.

They include:

  • Phosphatidyl-choline (PC)
  • Phosphatidyl-ethanolamine (PE)
  • Phosphatidyl-glycerol(PG) (precursor to Cardiolipin)
  • Phosphatidyl-inositol (PI)
  • Phosphatidyl-serine (PS)

Forty percent of the total lipid content of the cell membrane consists of glycolipids and cholesterol. The glycolipids include:

  • Digalactosyldiacylglyceride (DGDG)
  • Monogalactosyldiacylglycerol (MGDG)

Adequate intake of phospholipids and glycolipids is important for the integrity of the cell membranes. A therapy called Lipid Replacement Therapy (LRT®) consists of replacing the appropriate lipids and glycolipids by oral supplementation. [i]

Lecithin contains a balanced amount of phospholipids and glycolipids. Lecithin consists of phospholipids such as phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, Phosphatidic acid, other minor phospholipids and glycolipids.

The substances in the Table below have been researched for their ability to maintain and repair the cell membrane.

Table:  Nutraceuticals/Foods/Herbs that Enhance the Function of and Repair the Cell Membrane

Cell Membrane






Amino Acids













Ginko Biloba






Phosphatidyl-choline (PC)



Phosphatidyl-ethanolamine (PE)



Phosphatidyl-glycerol(PG) (precursor to Cardiolipin)



Phosphatidyl-inositol (PI)



Phosphatidyl-serine (PS)



Digalactosyldiacylglyceride (DGDG)



Monoglactosyldiacylglyceride (MGDG)



Omega 3 Fatty Acids






Calcium 2-AEP



Chromium Picolinate



Germanium (Ge-132)









Dimethylaminoethanol (DMAE)






Alpha-GPC (Choline)



Vitamin E


A mitochondrion contains outer and inner membranes composed of phospholipid bilayers and proteins.

The inner and outer mitochondrial membrane contains the major classes of phospholipids found in all cell membranes:

  • Phosphatidylcholine (PC)
  • Phosphatidylethanolamine (PE)
  • Phosphatidylinositol (PI)
  • Phosphatidylserine (PS)
  • Phosphatidic acid (PA)
  • Phosphatidylglycerol (PG), the precursor for Cardiolipin (CL)

The inner mitochondrial membrane can be subject to oxidative damage due to the presence of a very oxidation-sensitive phospholipid named Cardiolipin which represents 20% of the total lipid composition of the inner mitochondrial membrane.

Cardiolipin is functionally required for the electron transport system, and it is synthesized inside the mitochondria from two phosphatidylglyerol molecules.

The inner mitochondrial membrane can become damaged and altered due to an increasingly “leaky” membrane. This is caused when Cardiolipin is damaged by oxidation.

Once the Cardiolipin in the inner mitochondrial membrane becomes oxidized, the membrane become compromised and no longer form a tight ionic/electrical “seal” or barrier. With the loss of this ionic/electrical barrier the mitochondria losses electron transport and cellular energy. Ultimately this could result in cell death.

The substances in the Table below have been researched for their ability to enhance the function of Cardiolipin.

Table: Nutraceuticals that Enhance the Function of Cardiolipin







Amino Acids




Acetyl-L-Carnitine (ALCAR)













 14 15


[i] Nicolson GL, Ellithrope R. Lipid replacement and antioxidant nutritional therapy for restoring mitochondrial function and reducing fatigue in chronic fatigue syndrome and other fatiguing illnesses. J. Chronic Fatigue Syndr. 2006;13(1): 57-68. 

Ellithorpe RA, Settineri R, Mitchell CA, Jacques B, Ellithorpe E, Nicolson GL. Lipid replacement therapy drink containing a glycophospholipid formulation rapidly and significantly reduces fatigue while improving energy and mental clarity. Funct Food Health Dis. 2011;1(8): 245-254.

Nicolson GL, Ellithorpe R, Ayson-Mitchell C, Jacques B, Settineri R. Lipid Replacement Therapy with a Glycophospholipid-Antioxidant-Vitamin Formulation Significantly Reduces Fatigue Within One Week. J Am Nutraceut Assoc. 2010;13(1):10-14.

Piper BF, Dibble SL, Dodd MJ, Weiss MC, Slaughter RE, Paul SM. The revised Piper Fatigue Scale: psychometric evaluation in women with breast cancer. Oncol Nurs Forum. 1998;25(4):677-684.

Agadjanyan M, Vasilevko V, Ghochikyan A, Berns P, Kesslak P, Settineri R, Nicolson GL. Nutritional supplement (NTFactor) restores mitochondrial function and reduces moderately severe fatigue in aged subjects. J Chronic Fatigue Syndr 2003;11(3):23-26.


Allergy Research Group – NTFactor® EnergyLipids Chewables

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Celery Seeds provides Multiple Health Benefits

Celery (Apium graveolens) is a cultivated plant commonly used as a vegetable. Celery is also grown exclusively to produce celery seeds, which are used as a spice in some parts of the world.  Celery seeds are also used to manufacture nutraceuticals that contain the main active ingredient, 3-n-butylphthalide.


Celery plant

The active compounds in celery seeds are:

  • Butylphthalide (3-n-butylphthalide or NBP or 3nB) 
  • Sedanolide
  • Apiin and
  • Apigenin
  • d-limonene,
  • p-mentha-2,8-dien–ol, p-mentha-8(9)-en-1,2-diol

The 3nB extract of celery seeds have been studied and recognized for its treatment of hypertension.  Animal and lab studies reveal that 3nB-rich extracts of celery seeds produce blood pressure reductions of up to 38 mm Hg in hypertensive rats (this effect was not seen in those with normal blood pressures).

In 2004, a synthetic form of 3nB was approved in China for the treatment of cerebral ischemia and mild cognitive impairment as well as for the prevention of Alzheimer’s disease.

The health benefits of celery seeds go well beyond the cardiovascular benefits.  The Table below lists some of the other health benefits of celery seeds.

Table:  Health Benefits of Celery Seeds

Celery Seeds


















Celery seeds may lower blood pressure



Blood circulation





Celery seed may improve blood circulation due to 3-n-Butyl-Phthalide



Antiplatelet and Antithrombotic





Antiplatelet and antithrombotic activity of L-3-n-butylphthalide in rats.








Vasodilatory action mechanisms of apigenin isolated from Apium graveolens in rat thoracic aorta.


Immune System














Celery seed extract having anti-inflammatory activity



Helicobacter pylori





May kill helicobacter pylori



Liver cancer





May help to prevent liver cancer








Chemoprevention of benzo[a]pyrene-induced stomach cancer.  The data indicating that 3-n-butyl phthalide and sedanolide were both active in tumor inhibition and GST assays suggested a correlation between the inhibitory activity and the GST-inducing ability


Musculoskeletal System










May alleviate gout








May alleviate rheumatism












Dl-3-n-butylphthalide (NBP), first isolated from the seeds of celery, showed efficacy in animal models of stroke

 [10]  [11]


Vascular Dementia





Protective effects of dl-3-n-butylphthalide on changes of regional cerebral blood flow and blood-brain barrier damage following experimental subarachnoid hemorrhage



Cerebral hypoperfusion





l-3-n-Butylphthalide improves cognitive impairment induced by chronic cerebral hypoperfusion in rats.



Tau phosphorylation





L-3-n-butylphthalide reduces tau phosphorylation and improves cognitive deficits in AbetaPP/PS1-Alzheimer’s transgenic mice.



Amyotrophic lateral sclerosis





“Dl-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis”.



Brain ischemia





3-n-butylphthalide (NBP) attenuated neuronal autophagy and amyloid-beta expression in diabetic mice subjected to brain ischemia



Parkinson’s disease





Dl-3-n-butylphthalide, a natural antioxidant, protects dopamine neurons in rotenone models for Parkinson’s disease




Heyen BJ, Alsheikh MK, Smith EA, Torvik CF, Seals DF, Randall SK. The calcium-binding activity of a vacuole-associated, dehydrin-like protein is regulated by phosphorylation. Plant Physiol. 2002 Oct;130(2):675-87.Moghadam MH, Imenshahidi M, Mohajeri SA. Antihypertensive effect of celery seed on rat blood pressure in chronic administration. J Med Food. 2013 Jun;16(6):558-63.

[2] Peng Y, Zeng X, Feng Y, Wang X. Antiplatelet and antithrombotic activity of L-3-n-butylphthalide in rats. J Cardiovasc Pharmacol. 2004 Jun;43(6):876-81.

[3] Ko FN, Huang TF, Teng CM. Vasodilatory action mechanisms of apigenin isolated from Apium graveolens in rat thoracic aorta. Biochim Biophys Acta.  1991 Nov 14;1115(1):69-74.

[4] Powanda MC, Rainsford KD. A toxicological investigation of a celery seed extract having anti-inflammatory activity. Inflammopharmacology. 2011 Aug;19(4):227-33.

[5] Zhou, Y., et al.  A novel compound from celery seed with a bactericidal effect against Helicobacter pylori.  J Pharm Pharmacol.  61(8):1067-1077, 2009.

[6] Sultana, S., et al.  Inhibitory effect of celery seeds extract on chemically induced hepatocarcinogenesis: modulation of cell proliferation, metabolism and altered hepatic foci development.  Cancer Letters.  221(1):11-20, 2005.

[7] Zheng, G. Q., et al.  Chemoprevention of benzo[a]pyrene-induced forestomach cancer in mice by natural phthalides from celery seed oil.  Nutrition & Cancer.  19(1):77-86, 1993.

[8]Soundararajan, S., et al.  Pilot biomedical study for pain relief in rheumatic pain.  School of Medicine, The University of Queensland, Brisbane, Queensland, Australia, 1991-92.

Venkat, S., et al.  Use of Ayurvedic medicine in the treatment of rheumatic illness. Department of Orthopaedics, Kovai Medical Center and Hospitals, Coimbatore, India, 1995.

[9] Soundararajan, S., et al.  Pilot biomedical study for pain relief in rheumatic pain.  School of Medicine, The University of Queensland, Brisbane, Queensland, Australia, 1991-92.

Venkat, S., et al.  Use of Ayurvedic medicine in the treatment of rheumatic illness. Department of Orthopaedics, Kovai Medical Center and Hospitals, Coimbatore, India, 1995.

[10] Zhang L, Yu WH, Wang YX, et al. DL-3-n-Butylphthalide, an anti-oxidant agent, prevents neurological deficits and cerebral injury following stroke per functional analysis, magnetic resonance imaging and histological assessment. Curr Neurovasc Res. 2012 Aug;9(3):167-75.

[11]Ninety-day administration of dl-3-n-butylphthalide for acute ischemic stroke: a randomized, double-blind trial.

[12] Peng Y, Sun J, Hon S, et al. L-3-n-butylphthalide improves cognitive impairment and reduces amyloid-beta in a transgenic model of Alzheimer’s disease. J Neurosci. 2010 Jun 16;30(24):8180-9.

Chong Z, Feng Y. Protective effects of dl-3-n-butylphthalide on changes of regional cerebral blood flow and blood-brain barrier damage following experimental subarachnoid hemorrhage. Chin Med J (Engl). 1998 Sep;111(9):858-60.

[13] Peng Y, Xu S, Chen G, Wang L, Feng Y, Wang X. l-3-n-Butylphthalide improves cognitive impairment induced by chronic cerebral hypoperfusion in rats. J Pharmacol Exp Ther. 2007 Jun;321(3):902-10.

[14] Peng Y, Hu Y, Xu S, et al. L-3-n-butylphthalide reduces tau phosphorylation and improves cognitive deficits in AbetaPP/PS1-Alzheimer’s transgenic mice. J Alzheimers Dis. 2012;29(2):379-91.

[15] Feng, X; Peng, Y; Liu, M; Cui, L (2011). “Dl-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis”. Neuropharmacology 62 (2): 1004–10. doi:10.1016/j.neuropharm.2011.10.009. PMID 22056419. 

[16] Zhang, T; Yan, W; Li, Q; Fu, J; Liu, K; Jia, W; Sun, X; Liu, X (2011). “3-n-butylphthalide (NBP) attenuated neuronal autophagy and amyloid-beta expression in diabetic mice subjected to brain ischemia”. Neurological research 33 (4): 396–404. doi:10.1179/1743132810Y.0000000006.

[17]Xiong, N; Huang, J; Chen, C; Zhao, Y; Zhang, Z; Jia, M; Zhang, Z; Hou, L; Yang, H; Cao, Xuebing; Liang, Zhihou; Zhang, Yongxue; Sun, Shenggang; Lin, Zhicheng; Wang, Tao (2011). “Dl-3-n-butylphthalide, a natural antioxidant, protects dopamine neurons in rotenone models for Parkinson’s disease”. Neurobiology of Aging 33 (8): 1777. doi:10.1016/j.neurobiolaging.2011.03.007. PMID 21524431.


Natural Factors – Celery Seed Standardized Extract (85% 3nB)

Spice Jungle – Celery Seeds (Bulk)

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Lactobacillus frementum ME-3: A Probiotic with Antioxidant Activities

Lactobacillus fermentum is a Gram-positive species of bacterium in the genus Lactobacillus. IT is a normal inhabitant of the human intestinal tract.

There are two known commercialized strains of Lactobacillus fermentum:

Lactobacillus fermentum

  • Lactobacillus fermentum VRI-003 PCC®
  • Lactobacillus fermentum strain ME-3 DSM-14241

Lactobacillus fermentus ME-3 was discovered in 1994 when joint research between The University of Linkoping initiated a scientific cooperative agreement between the Department of Pediatrics and the Department of Microbiology of the University of Tartu. The agreement aimed to find associations between allergies and intestinal microbiota.

Professor Marika Mikelsaar of the The University of Tartu led the joint research project since her and her team had long-lasting experience in research into microbial ecology and the lactobacilli of the human organism.

Their discovery of L. fermentum showed that it had double functional properties:

  • Antimicrobial activity against intestinal pathogens
  • High total antioxidative activity (TAA) and total antioxidative status (TAS) characterized by a complete glutathione system of synthesis, uptake and redox turnover.

In April 2009, Marika Mikelsaar, published in Microbial Ecology in Health and Disease an article entitled, Lactobacillus fermentum ME-3 – an antimicrobial and antioxidative probiotic.

They demonstrated that Lactobacillus fermentum ME-3 was able to lower the level of oxidized LDL cholesterol and thus improve cardiovascular disease.

Figure 7 from the article illustrates the balance of oxidative stressor (pro-oxidants) and antioxidant defense systems. The verbiage underneath the diagram is reproduced below:

“A net of prooxidants and the potency of antioxidant defence system normally balanced in the human body. (a) A summary effect of oxidative stressors and potency of antioxidant defence system of the human body are normally balanced. An imbalance leads to oxidative stress. PUFA, polyunsaturated fatty acids; SOD, superoxide dismutase; GSHPx, glutathione peroxidase; CAT, catalase; HO1, haem oxygenase; GSH, reduced glutathione. (b) Oxidative stress causes the production of oxidized LDL (oxLDL), which is a potent atherogenic and inflammatory agent. Strain ME-3 lowers the level of oxLDL. LDL, low-density lipoprotein; CVD, cardiovascular diseases.” (Source)



The authors started to check the antioxidant charecteristics of Lactobacillus fermentum ME-3. Table IV (from the article) lists the antioxidative properties of L. fermentum ME-3:

Table IV

Antioxidativity-related properties and effects of strain ME-3.

Property/effect Experimental (ES), animal (AS), human (HS) study (reference nos)
Expression of Mn-SOD, prolonged survival time in presence of high H2O2, scavenging of superoxide and hydroxyl radicals ES (156)
Characterized by high TAA and TAS values ES (156,157)
Containing of GSH and related antioxidative enzymes ES (157,158)
Working as natural antioxidant in soft cheese spreads with different fats ES (159)
Maintaining its high TAA during production of probiotic cheese ES (136)
Removal effect of metals (prooxidants) from environment ES (160)
Elevation of blood TAS or TAA and TAA in the gut mucosa HS, AS (100,102,157,161,162)
Elevation of oxyresistance of LDL HS (100,157,162)
Lowering level of oxLDL HS (100,102,162)
Lowering level of isoprostanes HS (100,162,163)
Lowering the glutathione redox ratio in blood, in the gut mucosa, in skin HS, AS (100,102,157,161,164)
Lowering lipid peroxidation in the gut mucosa AS (161,164)
Lowering level of BCD-LDL HS (100,162,167)
Positive effects on post-prandial status of OxS, blood lipoprotein status and urine isoprostanes HS (162,163)

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“BCD-LDL, baseline diene conjugates in low-density lipoprotein; GSH, reduced glutathione; H2O2, hydrogen peroxide; LDL, low-density lipoprotein; Mn-SOD, manganese superoxide dismutase; oxLDL, oxidized low-density lipoprotein; OxS, oxidative stress; TAA, total antioxidative activity; TAS, total antioxidative status. (Source)

In 2010 an article in Prikladnaja biohimija i mikrobiologija apperaed by the authors Kullisaar T, Songisepp E, Aunapuu M, Kilk K, Arend A, Mikelsaar M, Rehema A, Zilmer M. The title of the article is Complete glutathione system in probiotic Lactobacillus fermentum ME-3.

The abstract of the article demonstrates a complete glutathione system with Lactobacillus fermentum ME-3:

“Results of this study show that probiotic L. fermentum ME-3 contains both glutathione peroxidase and glutathione reductase. We also present that L. fermentum ME-3 can transport GSH from environment and synthesize GSH. This means that it is characterized by a complete glutathione system: synthesis, uptake and redox turnover ability that makes L. fermentum ME-3 a perfect protector against oxidative stress.” (Source)

On August 4, 2004, U.S. Patent US20040151708 A1 was published with the U.S. Patent and Trademark Office. The inventors were Marika Mikelsaar, Mikhel Zilmer, Tiiu Kullisaaar, Heidi Annuk, Epp Songisepp and was entitled Strain of micro-organism lactobacillus fermentum me-3 as novel anti-microbial and anti-oxidative probiotic.

On July 3, 2014, inventors Marika Mikelsaar, Mikhel Zilmer, Tiiu Kullisaaar, Heidi Annuk, Epp Songisepp through the applicant University of Tartu, U.S. Patent WO2014102692 A1 was published. It is entitled Method of treatment using lactobacillus fermentum me-3.

In the U.S., Lactobacillus fermentum ME-3 is marketed by Essential Formulas Incorporated under the trademark name Reg’Activ.

Lactobacillus fermentum ME-3 can also be found in the Hellus product line of foods. Hellus is a Estonian food manufacturer an their products are sold mainly in Europe.

Another product called Reg’Activ Cholesterol exists primarily in Europe.

“The product Reg’Activ Cholesterol has been specially formulated for cardiovascular health. This innovative formulation combines L. fermentum ME-3 with functional ingredients, exerting a triple effect on cholesterol levels, protection against oxidative stress, and metabolism of homocysteine.” (Source)


Reg’Activ – Essential Formulas

Hellus products (Estonia)

Reg’Activ Cholesterol (Europe)

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Soil-Based Organisms: What’s the Dirt on these Probiotics?

Soil-Based Organisms (SBO’s) or Hemostatic Soil Organism (HSO) are a form of probiotics that can be obtained when one has eaten:

  • Soil
  • Food fermented with SBO’s, or
  • Soil-covered vegetables and fruits.

SBO’s are bacteria that are naturally found in soil. There was a time in the not too distant past that SBOs were present in abundance in our food chain. Now with modern farming techniques, most natural food grown in soil is sterilized.

There are over a hundred strains and species of SBOs. The most common strain comes from the Bacillus genus.

One of the main distinctions between SBO’s and Lactobacillus and Bifidobacterium strains is that SBO’s are spore forming. Spore forming means that it is able to replicate its DNA and then pinch its plasma membranes off between the two sets of chromosomes, to create an external spore.

SBO’s have some unique characteristics from other probiotic strains:

  • SBO’s are resistant to the harsh acid environment of the stomach
  • SBOs reach the small and large intestine intact and complete due to the fact that they are very stable and do not require any coatings for protection.

The scientific research on SBO’s is very limited. There is virtually no scientific evidence (not found at time of publication) regarding the safety of SBOs.

In the Bittner et. Al. studies, the authors used Prescript-Assist SBO and their end result was that the three main symptoms of IBS: nausea, indigestion/flatulence and colitis pain were all reduced by a statistically significant amount in the probiotic group during the time of the study.

There appears to be a debate in the health industry regarding SBO’s. The pro-SBO’s group consists of the main manufactures and distributors of the SBO probiotic formulations. There are four main manufactures of SBO probiotics:

There are also a number of anti-SBO advocates. They have written articles regarding their position. Three of these articles follow:

Following is list of the strains and species of SBO’s (and other bacterial genus) in the four main SBO probiotic formulas:

Prescript-Assist: (29 strains)

  • Arthrobacter agilis,
  • Arthrobacter citreus,
  • Arthrobacter globiformis,
  • Arthrobacter luteus,
  • Arthrobacter simplex,
  • Acinetobacter calcoaceticus,
  • Azotobacter chroococcum,
  • Azotobacter paspali,
  • Azospirillum brasiliense,
  • Azospirillum lipoferum,
  • Bacillus brevis,
  • Bacillus marcerans,
  • Bacillus pumilus,
  • Bacillus polymyxa,
  • Bacillus subtilis,
  • Bacteroides lipolyticum,
  • Bacteriodes succinogenes,
  • Brevibacterium lipolyticum,
  • Brevibacterium stationis,
  • Kurthia zopfii,
  • Myrothecium verrucaria,
  • Pseudomonas calcis,
  • Pseudomonas dentrificans,
  • Pseudomonas fluorescens,
  • Pseudomonas glathei,
  • Phanerochaete chrysosporium,
  • Streptomyces fradiae,
  • Streptomyces cellulosae,
  • Streptomyces griseoflavus

Primal Defense (Garden of Life – Homeostatic® Soil Organisms) (12 strains)

(Note: Only 1 strain is considered a SBO: Bacillus subtilli. The other 11 strains are from the genus Lactobacillus and the Bifidobacterium genus).

  • Bacillus subtilis
  • Bifidobacterium bifidum
  • Bifidobacterium breve
  • Bifidobacterium lactis
  • Bifidobacterium longum
  • Lactobacillus acidophilus
  • Lactobacillus brevis
  • Lactobacillus casei
  • Lactobacillus paracasei
  • Lactobacillus plantarum
  • Lactobacillus rhamnosus
  • Lactobacillus salivarius

Megasporebiotic: (5 strains)

  • Bacillus Clausii
  • Bacillus coagulans
  • Bacillus indicus HU36
  • Bacillus lichenformis
  • Bacillus subtilis HU58

BioKult: (14 strains)

(Note: Only 1 strain is considered a SBO: Bacillus subtilli PXN 21).

  • Bacillus subtilis PXN 21
  • Bifidobacterium bifidum PXN 23
  • Bifidobacterium breve PXN 25
  • Bifidobacterium infantis PXN 27
  • Bifidobacterium longum PXN 30
  • Lactobacillus acidophilus PXN 35
  • Lactobacillus delbrueckii ssp. bulgaricus PXN 39
  • Lactobacillus casei PXN 37
  • Lactobacillus plantarum PXN 47
  • Lactobacillus rhamnosus PXN 54
  • Lactobacillus helveticus PXN 45
  • Lactobacillus salivarius PXN 57
  • Lactococcus lactis ssp. lactis PXN 63
  • Streptococcus thermophilus PXN 66

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Broccoli Sprouts and the Health Benefits of Sulforphane

When raw or lightly steamed broccoli or raw broccoli sprouts are chewed, glucoraphanin and the enzyme myrosinase is released.  The function of the myrosinase enzyme is to catalyze the hydrolysis of a class of compounds called glucosinolates. Glucoraphanin is a glucosinolate.  Myrosinase transforms the glucoraphanin into sulforaphane, the active compound that exhibits anti-cancer and antimicrobial properties in experimental models.

Nature has designed myrosinase and its natural substrate, glucosinolate, to be part of the plant’s defense response. When the plant is attacked by pathogens, insects, or other herbivore, the plant uses myrosinase to convert glucosinolates, which are otherwise-benign, into toxic products like isothiocyanates, thiocyanates, and nitriles.

There are a number of plants in nature that use the myrosinase-glucosinolate defense system.  They include:

  • Bok choy
  • Broccoli
  • Broccoli Sprouts
  • Cabbage
  • Cauliflower
  • Daikon (Raphanus sativus)
  • Daikon Sprouts
  • Garden cress (Lepidium sativum)
  • Kale
  • Rape seed (Brassica napus)
  • Wasabi (Wasabia japonica)
  • White mustard (Sinapis alba)
  • Yellow mustard (Brassica juncea)

In 1994, scientists discovered that three-to-four-day-old broccoli sprouts had 20 times the concentration of glucoraphanin than full grown broccoli. 

Specifically, there is 73 mg of glucoraphanin for broccoli sprouts versus v. 11 mg of glucoraphanin for broccoli per serving.  This results in one ounce of broccoli sprouts containing as much glucoraphanin as over 1.25 pounds (20 ounces) of broccoli.

The presence of myrosinase in the plant is needed to convert glucoraphanin into sulforaphane, otherwise glucoraphanin provides zero protective effects.

FigureX_GR Hydrolysis

The raw plant obviously contains the enzyme myrosinase.  However, myrosinase will be denatured at high temperatures and thus lose its activity when cooked. 

Cooking broccoli or other myrosinase/glucorphanin plants by boiling or microwave may destroy the myrosinase.  Reserachers compared boiled, microwaved and steamed broccoli, and found that steaming broccoli for up to five minutes was the best way to retain its myrosinase. Boiling and microwaving broccoli for one minute or less destroyed the majority of the enzyme, according to Elizabeth Jeffery, a researcher at University of Illinois at Urbana-Champaign.

Broccoli sprouts or Daikon sprouts are often eaten raw and therefore contain the myrosinase enzyme intact.

An alternative to eating broccoli spouts is consuming broccoli sprout powders and/or capsules.  However, many of these products are produced from myrosinase-inactive sprout or seed extracts.  It becomes difficult to determine which broccoli sprout powder or capsule contain the essential precursor glucoraphanin as well as the active myrosinase enzyme. Without the myrosinase enzyme intact, there is no conversion of the glucoraphanin to sulforaphane.

The potential problem with broccoli sprout powders or capsule is in the extraction process used by the manufacturer.  It is believed that this extraction process often destroys and renders the myrosinase enzyme inactive.

The safest way to insure that you are consuming glucorahanin and myrosinase together is to eat fresh broccoli sprouts.  Broccoli seeds and sprouting jars can be purchased at a health food store or online. 

A further option is to eat broccoli sprouts with daikon sprouts.  Daikon and its sprouts are known to contain myrosinase.

If cruciferous vegetables are cooked via boiling or microwave, another option to insure sulforaphane production is to eat some myrosinase-rich raw daikon radish with the meal.


An article appeared in The British Journal of Nutrition in May 2012 written by Cramer JM, Teran-Garcia M, and Jeffery EH in which they used air-dried broccoli sprouts to provide the myrosinase enzyme in this study.

Their studies indicated that about 4/5 of the glucorophanine in the broccoli sprouts is converted into sulforaphane during eating and digestion because the sprouts contain active enzyme. Combining broccoli sprout powder with enzyme-empty broccoli powder allowed the enzymes from the sprouts to convert about half of the glucoraphanin in the inert powder into sulforaphane.

Only about one-fifth of the glucoraphanin was converted into sulforaphane when just broccoli powder was consumed.

The abstract of this important study follows:

“Sulforaphane (SF) is a chemopreventive isothiocyanate (ITC) derived from the myrosinase-catalyzed hydrolysis of glucoraphanin, a thioglucoside present in broccoli. Broccoli supplements often contain glucoraphanin but lack myrosinase, putting in question their ability to provide dietary SF. This study compared the relative absorption of SF from air-dried broccoli sprouts rich in myrosinase and a glucoraphanin-rich broccoli powder lacking myrosinase, individually and in combination. Subjects (n = 4) each consumed 4 meals consisting of dry cereal and yogurt with 2 g sprouts, 2 g powder, both, or neither. Blood and urine were analyzed for SF metabolites. The 24 h urinary SF recovery was 74%, 49%, and 19% of the dose ingested from broccoli sprouts, combination, and broccoli powder meals, respectively. Urinary and plasma ITC appearance was delayed from the broccoli powder compared to the sprouts and combination. A liver function panel indicated no toxicity from any treatment at 24 h. These data indicate a delayed appearance in plasma and urine of SF from the broccoli powder relative to SF from myrosinase-rich sprouts. Combining broccoli sprouts with the broccoli powder enhanced SF absorption from broccoli powder, offering the potential for development of foods that modify the health impact of broccoli products.”  [1]  [2]

The following table is a representation of the epidemiological evidence of cancer prevention by cruciferous vegetables.

Epidemiological Evidence of Cancer Prevention by Cruciferous Vegetables

Site of cancer

Amount of crucifers eaten

RR – relative risk OR-odds ratio (P value)



>5 servings/week

RR 0.49 (0.008)

Michaud et al. (1999)


>5 servings/week

RR 0.67 (0.03)

Zhang et al. (2000)


5 servings/week

OR 0.61 (0.006)

Kolonel et al. (2000)


>3 servings/week

OR 0.50 (0.02)

Cohen et al. (2000)

Colon (men)

Top 20%

RR 0.76 (0.011)

Voorips et al. (2000)

Colon (women)

Top 20%

RR 0.51 (0.004)

Voorips et al. (2000)


Top 25%

OR 0.05 (0.01)

Fowke et al. (2003)


Top 25%

OR 0.53 (0.001)

Yuan et al. (1998)

Source: E.H. Jeffery, Phytochemical Review, 2008.


Table:  Health Benefits of Broccoli Sprouts (Sulforaphane)

Broccoli Sprouts (Sulforaphane)













Chemo protective





Sulforaphane is a promising chemo preventive agent that exerts its effect by strong induction of phase 2 enzymes via activation of Nrf2



Cervical Cancer





Sulforaphane may stimulate the apoptosis (cell death) of Cervical Cancer cells








Sulforaphane may help to prevent Leukemia



Liver Cancer





Sulforaphane may stimulate the apoptosis (cell death) of Liver Cancer cells



Lung Cancer





Sulforaphane may help to prevent Lung Cancer








Sulforaphane may help to prevent Melanoma



Mouth Cancer





Sulforaphane may help to prevent Mouth Cancer



Ovarian Cancer





Sulforaphane may stimulate the apoptosis (cell death) of Ovarian Cancer cells



Pancreatic Cancer





Sulforaphane may help to prevent and treat Pancreatic Cancer



Tongue Cancer





Sulforphane may help to prevent Tongue Cancer



Helicobacter pylori





Broccoli Sprouts may facilitate the eradication of Helicobacter pylori.








CUR + SFN and PEITC + SFN combinations could be more effective than used alone in preventing inflammation and possibly its associated diseases including cancer.



Skin Tumors





Mice were exposed to damaging levels of UV light for 20 weeks in a study conducted at Johns Hopkins Medical School. Following the exposure, application of sulforaphane resulted in a 50% reduction in the number of mice with tumors.



Breast Cancer





Study results revealed the women who had eaten higher levels of Brassica vegetables—broccoli, cabbage, cauliflower and kale—all of which contain glucoraphanin and related compounds—were 50% less likely to be diagnosed with breast cancer.



Prostate Cancer





Human prostate cancer cells responded to treatment with sulforaphane in the form of broccoli sprout extracts, showing dramatic increases in their Phase 2 protective enzymes.



Colon Cancer





Ability of sulforaphane and broccoli sprouts extracts to inhibit cancer in vitro in human colon cancer cells.



Bladder Cancer





Studies have also shown sulforaphane and broccoli sprout extract can induce apoptosis and cell cycle arrest in human bladder cancer cells in vitro



Stomach Cancer





Dual actions of sulforaphane in inhibiting Helicobacter infections and blocking gastric tumor formation offer hope that these mechanisms might function synergistically to provide diet-based protection against gastric cancer in humans












Sulforaphane-induced Phase 2 enzymes from broccoli sprouts improved cardiovascular health by decreasing inflammation and improving heart, artery and kidney function








Delayed administration (15 min) of a single dose of SUL significantly decreased cerebral infarct volume following focal ischemia












Broccoli Sprouts may lower total serum Cholesterol levels



Glucose metabolism





Sulforaphane promotes lipolysis via hormone sensitive lipase activation mediated by decreasing AMPK signal activation in adipocytes.








Results suggest sulforaphane from broccoli may help reverse the damaging effects of diabetes-linked vascular disease







Macular Degeneration





Ability of sulforaphane to protect retinal pigment epithelial cells from damage by chemical carcinogens and by ultraviolet light


Musculo- Skeletal System










Sulforaphane may be useful for the treatment of Rheumatoid Arthritis







Phase II Enzyme inducer





Study identified sulforaphane as a very potent phase II enzyme inducer in brocooli and noted that sulforaphane induces both quinone reductase and glutathione transferase activities in several mouse tissues








Oral sulforaphane safely and effectively induces mucosal Phase II enzyme expression in the upper airway of human subjects








Broccoli sprouts are an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens.



Nrf2 Activation





Activates a transcription factor, Nrf2 in the cell












Sulforaphane Shows Promise in Autism Spectrum Disorder



[3] Hecht, S. S.  Chemoprevention of cancer by isothiocyanates, modifiers of carcinogen metabolism.  Journal of Nutrition.  129:768-774, 1999.

Misiewicz, I., et al.  Sulforaphane and 2-oxohexyl isothiocyanate induce cell growth arrest and apoptosis in L-1210 leukemia and ME-18 melanoma cells.  Oncol Rep.  10(6):2045-2050, 2003.

Nestle, M.  Broccoli sprouts in cancer prevention.  Nutrition Reviews.  46(4 Part I):127, 1998.

Thimmulappa, R. K., et al.  Identification of Nrf2-regulated genes induced by the chemopreventive agent sulforaphane by oligonucleotide microarray.  Cancer Research.  62(18):5196-5203, 2002.

Zhang, Y., et al.  A major inducer of anticarcinogenic protective enzymes from broccoli:  isolation and elucidations of structure.  Proceedings of the National Academy of Sciences USA.  89:2399-2403, 1992.

[4] Park, S. Y., et al.  Induction of apoptosis by isothiocyanate sulforaphane in human cervical carcinoma HeLa and hepatocarcinoma HepG2 cells through activation of caspase-3.  Oncol Rep.  18(1):181-187, 2007.

[5] Misiewicz, I., et al.  Sulforaphane and 2-oxohexyl isothiocyanate induce cell growth arrest and apoptosis in L-1210 leukemia and ME-18 melanoma cells.  Oncol Rep.  10(6):2045-2050, 2003.

[6] Park, S. Y., et al.  Induction of apoptosis by isothiocyanate sulforaphane in human cervical carcinoma HeLa and hepatocarcinoma HepG2 cells through activation of caspase-3.  Oncol Rep.  18(1):181-187, 2007.

[7] Liang, H., et al.  Sulforaphane induces cell-cycle arrest and apoptosis in cultured human lung adenocarcinoma LTEP-A2 cells and retards growth of LTEP-A2 xenografts in vivo.  Journal of Natural Products.  2008.

[8] Misiewicz, I., et al.  Sulforaphane and 2-oxohexyl isothiocyanate induce cell growth arrest and apoptosis in L-1210 leukemia and ME-18 melanoma cells.  Oncol Rep.  10(6):2045-2050, 2003.

[9] Kim, J. H., et al.  Sulforaphane increases cyclin-dependent kinase inhibitor, p21 protein in human oral carcinoma cells and nude mouse animal model to induce G(2)/M cell cycle arrest.  J Clin Biochem Nutr.  46(1):60-67, 2010.

[10]Bryant, C. S., et al.  Sulforaphane induces cell cycle arrest by protecting RB-E2F-1 complex in epithelial ovarian cancer cells.  Mol Cancer.  9:47, 2010.

[11] Pham, N. A., et al.  The dietary isothiocyanate sulforaphane targets pathways of apoptosis, cell cycle arrest, and oxidative stress in human pancreatic cancer cells and inhibits tumor growth in severe combined immunodeficient mice.  Mol Cancer Ther.  3(10):1239-1248, 2004.

[12] Yao, H., et al.  Sulforaphane inhibited expression of hypoxia-inducible factor-1alpha in human tongue squamous cancer cells and prostate cancer cells.  Int J Cancer.  2008.

[13] Galan, M. V., et al.  Oral broccoli sprouts for the treatment of Helicobacter pylori infection:  a preliminary report.  Dig Dis Sci.  49(7-8):1088-1090, 2004.

[15] Cancer Epidemiology, Biomarkers & Prevention, 2005, 14(11).

Cancer Letters, 2006, 240:243–252.

Cancer Research, 2006, 66:8293–8296

Proc. Natl. Acad. Sci., USA, 2007, 104(44):17500-5.

[20] Fahey, J. W., t al.  Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors.  Proc Natl Acad Sci USA.  99(11):7610-7615, 2002.

[22] Zhao, J., et al.  Sulforaphane reduces infarct volume following focal cerebral ischemia in rodents.  Neurosci Lett.  393(2-3):108-112, 2006.

[23] Murashima, M., et al.  Phase 1 study of multiple biomarkers for metabolism and oxidative stress after one-week intake of broccoli sprouts.  Biofactors.  22(1-4):271-275, 2004.

[27] Kong, J. S., et al.  Inhibition of synovial hyperplasia, rheumatoid T cell activation, and experimental arthritis in mice by sulforaphane, a naturally occurring isothiocyanate.  Arthritis Rheum.  62(1):159-170, 2010.

[28] Prochaska, H. J., et al.  Rapid detection of inducers of enzymes that protect against carcinogens.  Proceedings of the National Academy of Sciences USA.  89:2394-2398, 1992.

·Zhang, Y., et al.  A major inducer of anticarcinogenic protective enzymes from broccoli:  isolation and elucidations of structure.  Proceedings of the National Academy of Sciences USA.  89:2399-2403, 1992.

[29] Riedl, M. A., et al.  Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway.  Clinical Immunology.  130(3):244-251, 2009.


West African Pepper: High Piperine Content

Piper guineense is a West African species of Piper; the spice derived from its dried fruit is known as West African pepper, Ashanti pepper, Benin pepper, false cubeb, Guinea cubeb, uziza pepper or (ambiguously) “Guinea pepper”, and called locally kale, kukauabe, masoro, sasema and soro wisa.

It is a close relative of cubeb pepper and a relative of black pepper and long pepper. Unlike cubeb pepper, which is large and spherical in shape, Ashanti peppers are prolate spheroids, smaller and smoother than Cubeb pepper in appearance and generally bear a reddish tinge.

Ashanti peppers contain 5-8% of the chemical piperine which gives them their ‘heat’.


West African Pepper plant

West African Pepper contains the following active compounds:

West African Pepper Compounds

West African Pepper 

The Table list the recognized and researched studies on the health benefit of West African Pepper:

West African Pepper Health Benefits

West African Pepper  
Lipid Peroxidation
Piper guineense inhibits
Fe2+- Induced Lipid Peroxidation
Beta-caryophyllene was shown to be selective agonist of cannabinoid receptor type-2 (CB2) and to exert significant neuroprotective effects.2
Results suggest that inhalation of P. guineense essential oil might induce a mild tranquilizing effect.3
Results indicate that the extract of P. guineense has prolonged anticonvulsant activity at doses which do not cause significant CNS depression.4

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Cheonggukjang: Korean Superfood

Cheonggukjang (CGJ) (청국장) is a fermented soybean paste used in Korean cuisine. It contains whole as well as ground soybeans.  Traditionally prepared Cheonggukjang was manufactured at Midari Farm (Yeongwol county, Kangwon-Do, Korea). Cooked soybeans were fermented with Bacillus subtilis at 30°C for 43 h and then freeze-dried and powered for adding into the diet.

Cheonggukjang contains abundant levels of Vitamin K2 in the MK-7 form, similar to Japanese natto.  When cheonggukjang is fermented by using Bacillus amyloliquefaciens KCTC11712BP, the content of menaquinone (MK) can reach as high as 12.47 μg/g, which was about 4-fold higher than that of commercial cheonggukjang and natto products.  1

The Table below lists the recognized and researched studies on the use and consumption of Cheonggukjang and its respective health benefits:

Health Benefits of Cheonggukjang

Diabetes (Insulin resistance)8 week consumption of the fermented soybean food, chungkookjang (20% of the diet), increases β-cell function and mass and attenuates insulin resistance in type 2 diabetic ratsA
Chungkookjang fermented with B. lichemiformis retains the anti-diabetic properties of the most efficacious traditional chungkookjang and it may be even more effective for improving insulin function than traditionally prepared chungkookjangB
Long-term consumption of fermented soybean-derived Chungkookjang attenuates hepatic insulin resistance in 90% pancreatectomized diabetic ratsC
AntioxidantChungkookjang has a much stronger antioxidant activity than unfermented steamed soybeans, probably due to its increased aglycone isoflavone and malonylglycoside isoflavone which resulted from fermentation as well as total polyphenol contentsD
Cognitive function (Beta-Amyloid)Standardized chungkookjang, short-term fermented soybeans with Bacillus lichemiformis, improves cognitive function and insulin resistance in β-amyloid-infused diabetic rats E
Hyperlipidemia (lipid-lowering effects)Study investigated the lipid-lowering effects of fermented soybean-derived chungkookjang (CKJ) in hyperlipidemic Bio F1B hamstersF
Antimutagenic (Chemoprotective)Antimutagenic effects of chungkookjang prepared with the different fermentation periods and ingredient ratio were studied against aflatoxin B1 (AFB1) using Ames test and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) using SOS chromotestG
Anticancer activity Chungkookjang showed a strong inhibitory effect on cancer cell growth in vitro, as well as a more preventive effect against chemically induced mammary tumorigenesis in vivo. These results suggest that Chungkookjang acquire its anticancer activity through the fermentation process.
Anti-obesitySaponin compounds in cheonggukjang, a traditional Korean fermented soy food, were quantitatively evaluated, and their antiobesity effect was studied. Two saponin groups, i.e., soyasapogenol A and B, were isolated from cheonggukjang. AMPK activation was stimulated more by soyasapogenol B than by soyasapogenol A. Therefore, cheonggukjang saponin may be a potential antiobesity agent.I
NeuroprotectiveResults demonstrate that cheonggukjang fermented by mixed culture of B. subtilis and L. sakei could exert a wide range of beneficial activities for neurodegenerative diseases, including Alzheimer, Parkinson, and Huntington disease.J
Serum lipid profiles and fatty acid oxidationCheonggukjang supplement leads to increased mRNA expressions of enzymes and protein involved in fatty acid oxidation in liver, reduced accumulation of body fat and improvement of serum lipids in high fat diet fed mice.K
OsteoporosisResults suggest that administration of CGJ containing abundant levels of MK-7 may be a promising approach for the treatment and prevention of osteoporosis.L
ImmunityCheonggukjang (PSCJ) have immunostimulatory activities in RAW 264.7 macrophages and primary cultured splenocytes. These results suggest that the cheonggukjang could be utilized as an effective immunostimulatory agent.M
Growth hormone measurementsResults indicate that cheonggukjang extract may increase the thickness of the epiphyseal growth plate and the compact bone of the femur, elevate GH secretion, and stimulate regulation of the GH receptor downstream signaling pathway in the liver and muscle tissues of SD rats. N
AsthmaFindings demonstrated that cheonggukjang can be used as an antiasthmatic dietary supplements candidate for histamine-mediated asthma.O
Anti-inflammatoryKorean traditional soybean fermented products, especially CGJ, suppress the generation of reactive species, NF-κB activity, and NF-κB-related inflammatory genes.P


Cheonggukjang can be purchased at Asian markets and/or Korean markets

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