Monthly Archives: August 2015


Terminalia chebula: Effective Glycation Inhibitor

Terminalia chebula is a medium to large deciduous tree growing to 30-metre (98 ft) tall, is a species of Terminalia, native to South Asia from India and Nepal east to Southwest China (Yunnan), and south to Sri Lanka, Malaysia and Vietnam.

In Ayuryedic medicine, Terminalia checula is known as Haritaki and is one of three herbs in a combination formula called Triphala, which means “three fruits” in Hindi/Sanskirt. The three fruits in Triphala are Amalaki (Emblica officinalis), Bibhitaki (Terminalia bellirica), and Haritaki (Terminalia chebula).

Chebulic acid is a phenolic compound isolated from the ripe fruits of Terminalia chebula. Chebulic acid has been studied for its ability to neutralizes free radicals and reduce AGE formation.

The research on Terminalia chebula and chebulic acid indicates that it is seven times more effective at reducing glycation than the well-known glycation inhibitor aminoguanidine.

Chebulic acid demonstates the ability to break the bond existing between abnormally cross-linked proteins.


Lee HS, Koo YC, Suh HJ, Kim KY, Lee KW. Preventive effects of chebulic acid isolated from Terminalia chebula on advanced glycation endproduct-induced endothelial cell dysfunction. J Ethnopharmacol. 2010;131(3):567-74.

Lee HS, Cho HY, Park KW, et al. Inhibitory effects of Terminalia chebula extract on glycation and endothelial cell adhesion. Planta Med. 2011 Jul;77(10):1060-7.

Lee JY, Oh JG, Kim JS, Lee KW. Effects of chebulic acid on advanced glycation end products-induced collagen cross-links. Biol Pharm Bull. 2014 Apr 24.



Banyan Botanticals (Powder)


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Magnesium-L-Threonate: High Brain Bioavailability

Magnesiun-l-threonate consists of magnesium bonded to the organic acid, threonic acid, and is denoted by the chemical formula Mg(C4H7O5)2.  

Magnesiun-l-threonate has high brain bioavailability. It is the only magnesium compound that has been shown to effectively raise the brain’s magnesium levels.

In pre-clinical models, L-threonate contained in Magnesiun-l-threonate boosted magnesium levels in spinal fluid by an impressive 15% compared to no increase with conventional magnesium.  [1]

Research on Magnesiun-l-threonate has been led by the biopharmaceutical company Magceutics of Hayward, California.  They tradmarked the product named Magtein(TM).  They began testing Magtein,’s(TM) ability to boost magnesium ion (Mg2+) levels in the brain in 2012 and the results have been impressive.   [2]


Gao Sheng-Li;Yang Xu-Wu;Chen San-Ping;Ju Zhan-Feng (2002). “Synthesis and Standard Enthalpy of Formation of Magnesium L-Threonate”. Acta Phys. -Chim. Sin. 18 (11): 994–997. 

Magnesium Supplement Helps Boost Brainpower, Science Daily, Feb. 2, 2010

Inna Slutsky, Nashat Abumaria, Long-Jun Wu, Chao Huang, Ling Zhang, Bo Li, Xiang Zhao, Arvind Govindarajan, Ming-Gao Zhao, Min Zhuo, Susumu Tonegawa, and Guosong Liu (2010). “Enhancement of Learning and Memory by Elevating Brain Magnesium”. Neuron 65 (2): 165–177. doi: 10.1016/j.neuron.2009.12.026. PMID 20152124


Toxin Toxout

A new book that is highly recommended is Toxin Toxout, published in 2013 and 2014.  It is a well researched text on the subject of the toxins that humans are exposed to and recommended therapies to remove such toxins.

From the Toxin Toxout website:

“Bruce Lourie and Rick Smith, two of Canada’s environmental leaders, have been asked this question on an almost daily basis since the publication of their runaway international bestseller, Slow Death by Rubber Duck: How the Toxic Chemistry of Everyday Life Affects Our Health. Their answer? It’s not as simple as we’d like, and it’s not as easy as we’d hope. But it’s too important to ignore.

In Toxin Toxout, Lourie and Smith give practical and often surprising advice for removing toxic chemicals from our bodies and homes. There are over 80,000 synthetic chemicals in commerce today, and the authors use their outrageous experiments (they and their brave volunteers are the guinea pigs) to prove how easily our bodies absorb these chemicals. With trademark humour, they give us the good news about what is in our control, the steps we can take to help our bodies remove our toxic burden—and what we can do to avoid it in the first place. Furthermore, Lourie and Smith investigate the truth behind organic foods, which detox methods actually work, if indoor air quality is improving, how we dispose of waste (where do those chemicals go?), and the ins and outs of a greener economy. The result is nothing short of a prescription for a healthier life.”


Toxin Toxout website

Amazon – Toxin Toxout

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Idebenone: Synthetic Derivative of Ubiquinone

Idebenone (full structural name of 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone and codename of-2619[1]) is a synthetic derivative of ubiquinone (reduced CoQ10). [1]

COQ10 is a long chained compound while Idebenone is a short chained compound. This means that idebenone has a much higher level of bioavailability than CoQ10.

Like its parent compound, it is a powerful antioxidant with additional nootropic benefits including improving memory, learning, and symptoms of age related memory loss. Idebenone is also able to increase adenosine triphosphate (ATP) production. [2]

It also provides a basic level of neuroprotection and is a mood booster since it is able to boost dopamine levels within the brain. [3]



Powder City

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The 6 Detoxification Organs and Systems of the Human Body

There are 6 main detoxification organs or systems in the human body:

  • Liver (processes and packages toxins) (70% of detoxification)
  • Lungs (gas exchange of oxygen and carbon dioxide)
  • Gastrointestinal Tract (excretes waste)
  • Skin (sweat)
  • Kidneys (urination)
  • Endothelial cells of the blood brain barrier (protects brain from neurotoxins)


Biotransformation enzymes exist in the smooth endoplasmic reticulum, cystosol (intracellular fluid) and to a lesser degree in the membranes of the mitochondria, nuclei and lysosomes (small spherical organelles) of the liver’s hepatocytes.

The kidneys and lungs are the next major biotransformation sites, but only at 10 – 30% of the livers capacity.

The skin, nasal mucosa and intestinal mucosa also have some biotransformation capacity.

Other sites of detoxification metabolism include epithelial cells of the gastrointestinal tract, lungs, kidneys, and the skin. These sites are usually responsible for localized toxicity reactions.

Once an unwanted compound has been completely bio-transformed and removed from the cell, it will then be eliminated from the body via – kidneys, bowels, breath, sweat, saliva or hair – completing the detoxification process.

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Nutrients that Support Phase II Detoxification Pathways

During phase II detoxification, activated substances from phase I, which are known as intermediates are conjugated and altered further before expulsion from the body.

Six different major biochemical reactions occur in this phase, known as:

  • Glutathione conjugation
  • Amino acid conjugation
  • Methylation
  • Sulfation
  • Acetylation
  • Glucuronidation

Each of these reactions works on specific types of intermediates and needs specific nutrients in order to proceed to successful completion.

The nutrients required for phase II fall into two categories. The first are the amino acids, which donate molecules that are attached to phase I intermediates. These include the sulfur donors, among which are the amino acids methionine, taurine, cysteine, and N-acetylcysteine. Other, non-sulfur-containing amino acids are also required: glycine, taurine, glutamine, ornithine, and arginine.


Table: Nutrients needed by Phase II Detoxification Enzymes

Nutrients Phase II

Phase II System


Glutathione conjugation


Vitamin B6

Glutathione Precursors (Cysteine, Glycine, NAC)

Essential Fatty Acids

Vitamin B6

Amino acid conjugation


Folic Acid, Manganese, B-2, B-6/P-5-P






S-adenosyl-methionine (SAMe)


Folic Acid

Vitamin B12

Betaine (TMG)





Vitamin B12

Folic Acid





Acetyl CoA



Niacinamide (B3)

Vitamin B2


Glucuronic acid



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The Effects of Dehydration on the Brain

“Dehydration increases the osmolality of extracellular fluid in the body and decreases blood volume [Costill et al., 1976]. Both are processes that could reduce total brain volume and lead to a corresponding increase in CSF volume. Increased concentrations of solutes in extracellular fluid cause water to move from inside cells to the extracellular fluid along the osmotic gradient, causing cellular shrinkage [Gullans and Verbalis, 1993]. However, cells prevent large increases and decreases in volume by actively regulating their intracellular solute (particularly potassium ions), which is of vital importance in the brain because of the fixed volume of the cranium [Stricker and Verbalis, 2003]. Indeed, if such homeostatic processes were not active we might expect to see larger changes in brain structure following dehydration. As brain volume decreases, the empty space is filled by CSF; this may come from an increase in production or a decrease in absorption of CSF, or from the CSF filled spinal dural sack which unlike the cranium, can change its volume in response to intracranial pressure [Lee et al., 2001; Lofgren and Zwetnow, 1973].”

From Effects of acute dehydration on brain morphology in healthy humans, Matthew J. Kempton1,2,*, Ulrich Ettinger1, Anne Schmechtig1, Edward M. Winter3, Luke Smith4, Terry McMorris4, Iain D. Wilkinson5, Steven C.R. Williams1 and Marcus S. Smith4. Human Brain Mapping

Neurons store water in tiny balloon-like structures called vacuoles. Vacuoles are essentially enclosed compartments which are filled with water containing inorganic and organic molecules including enzymes in solution, though in certain cases they may contain solids which have been engulfed.

Water is essential for optimal brain health and function. Water is necessary to maintain the tone of membranes for normal neurotransmission. It enhances circulation and aids in removing wastes.

Microtubules in the neuron is filled with water. [1] Microtubules are tiny sub-components of cells. They are prominent aspects of the skeleton of all eukaryotic cells and are the structural and dynamical basis of the cells. They may participate in important quantum mechanical phenomena involving water ordering in their interior.

Microtubules contribute to the structural integrity of neurons as they maintain the semi-rigidity of neurons.

There are various substances that may interfere with microtubules:

  • Acetaldehyde may inhibit the ability of tubulin to assemble into microtubules. [2]
  • Mercury may disrupt the structural integrity of neuronal microtubules. [3]


The Toxic Effects of Organochlorines

Organochlorines are compounds that contain carbon, chlorine, and hydrogen. Their chlorine-carbon bonds are very strong which means that they do not break down easily. They are highly insoluble in water, but are attracted to fats.

Since they resist metabolism and are readily stored in fatty tissue of any animal ingesting them, they accumulate in animals in higher trophic levels. This may occur when birds eat fish that have been exposed to the contaminant.

Organochlorines are some of the chemicals found most often in the hundreds of tests of human body tissue – blood, adipose tissue, breastmilk – that have been conducted around the world. Because of their chemical structure, organochlorines break down slowly, build up in fatty tissues, and remain in our bodies for a long time.

Pesticide residues on food are a major source of organochlorine exposure.

Table:  Nutraceuticals/Herbs that may reduce the toxic effects of Organochlorines






Phospholipid Exchange






Green Tea



[2] Crinnion, W. J. Chlorinated pesticides: threats to health and importance of detection. Altern Med Rev. 14(4):347-359, 2009.

Chlorophyll and chlorophyll-containing foods have been shown to increase excretion of fat-soluble persistent toxins (including organochlorines) via the feces. Increasing chlorophyll-containing foods or daily supplementation with chlorophyll can slowly increase the excretion of these compounds.

[3] Umemura, T., et al. Prevention of dual promoting effects of pentachlorophenol, an environmental pollutant, on diethylnitrosamine-induced hepato- and cholangiocarcinogenesis in mice by green tea infusion. Carcinogenesis. 24(6):1105-1109, 2003. Division of Pathology, National Institute of Health Sciences, Setagaya-ku, Tokyo, Japan.


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Activating Adenosine monophosphate-activated protein kinase (AMPK)

Adenosine monophosphate-activated protein kinase (AMPK) is found in every cell in our body. It serves as the body’s “master regulating switch” that fends off degenerative factors by revitalizing aging cells.

AMPK is involved in reducing fat storage, regulating glucose uptake, creating new mitochondria, and eliminating cellular garbage that accumulates inside aging cells.


An important property of AMPK is that it induces multiple longevity factors, which have been shown to increase stress-resistance and extend life span in many organisms.

With reduced AMPK signaling, a range of damaging conditions begins to take over a previously healthy body, often leading to an early death. These damaging conditions include:


Table: Nutraceuticals/Foods/Herbs that Activate AMPK

Activating AMPK









Amino Acids


Acetyl-L-Carnitine (ALCAR)











Bitter Melon




Gynostemma pentaphyllum

Jiaogulan [6]


Rose Hips

Trans- tiliroside [7]






Queen Bee Acid (Royal Jelly)


























Coenzyme Q10




Alpha Lipoic Acid



Vitamin E




Gauhar R, Hwang SL, Jeong SS, et al. Heat-processed Gynostemma pentaphyllum extract improves obesity in ob/ob mice by activating AMP-activated protein kinase. Biotechnol Lett. 2012 Sep;34(9):1607-16.

Nguyen PH, Gauhar R, Hwang SL, et al. New dammarane-type glucosides as potential activators of AMP-activated protein kinase (AMPK) from Gynostemma pentaphyllum. Bioorg Med Chem. 2011 Nov 1;19(21):6254-60.

Lobo SN, Qi YQ, Liu QZ. The effect of Gynostemma pentaphyllum extract on mouse dermal fibroblasts. ISRN Dermatol. 2014 Mar 4.

Muller C, Gardemann A, Keilhoff G, Peter D, Wiswedel I, Schild L. Prevention of free fatty acid-induced lipid accumulation, oxidative stress, and cell death in primary hepatocyte cultures by a Gynostemma pentaphyllum extract. Phytomedicine. 2012 Mar 15;19(5):395-401.

[7] Nagatomo A, Nishida N, Matsuura Y, Shibata N. Rosehip Extract Inhibits Lipid Accumulation in White Adipose Tissue by Suppressing the Expression of Peroxisome Proliferator-activated Receptor Gamma. Prev Nutr Food Sci. 2013 Jun;18(2):85-91

Goto T, Teraminami A, Lee JY, et al. Tiliroside, a glycosidic flavonoid, ameliorates obesity-induced metabolic disorders via activation of adiponectin signaling followed by enhancement of fatty acid oxidation in liver and skeletal muscle in obese-diabetic mice. J Nutr Biochem. 2012 Jul;23(7):768-76.

Shi L, Qin N, Hu L, Liu L, Duan H, Niu W. Tiliroside-derivatives enhance GLUT4 translocation via AMPK in muscle cells. Diabetes Res Clin Pract. 2011 May;92(2):e41-6.

Neurotoxic Effects of High Levels of Homocysteine

Homocysteine is an endogenous amino acid derivative which damages the endothelial cells that line the inside of blood vessels and contributes to the pathogenesis of atherosclerosis and vascular dysfunction.

A high level of homocysteine in the blood (hyperhomocysteinemia) makes a person more prone to endothelial cell injury, which leads to inflammation in the blood vessels, which in turn may lead to atherogenesis, which can result in ischemic injury.


Figure: Homocysteine Metabolic Pathways

The remethylation pathway requires vitamin B12, folate, and the enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR). In kidney and liver, homocysteine is also remethylated by the enzyme betaine homocysteine methyltransferase (BHMT), which transfers a methyl group to homocysteine via the demethylation of betaine to dimethylglycine (DMG). The transsulfuration pathway requires the enzyme cystathionine-synthase (CBS) and vitamin B6 (pyridoxal-5’-phosphate). Once formed from cystathionine, cysteine can be utilized in protein synthesis and glutathione (GSH) production. Figure taken from:

It is recommended that an optimal homocysteine level is <8µmol/L. One comprehensive review showed that every 2.5 µmol/L increase above this optimal level is associated with about a 20% increase in stroke risk. [1]

Elevated homocysteine levels is a result of a faulty and defective methylatio n process in the body the high levels of homocysteine in the bloodstream is not being remethylated When you have poor methylation your body’s levels of homocysteine will elevate.

A variety of extrinsic and intrinsic factors including stress, nutritional deficits, certain disease states, and genetics can contribute to insufficient methylation.

Homocysteine is metabolized through two pathways: remethylation and transsulfuration.

Remethylation requires folate and B12 coenzymes.

Transsulfuration requires pyridoxal-5’-phosphate, the B6 coenzyme.

Table: Neurotoxic Effects of High Levels of Homocysteine

Toxic Effects of Homocysteine




Blood Flow

Homocysteine has been associated with reduced blood flow to the brain



Homocysteine can impair memory


Cognitive function

Homocysteine can result in poorer global cognitive function


Brain volume

Homocysteine results in smaller overall brain volume


Brain infarcts

Homocysteine is associated with increased silent brain infarcts (subclinical stroke-like blood vessel occlusions in the brain).



Elevated homocysteine may cause dementia in the elderly

[7] [8]


Elevated Homocysteine may cause Depression


Neurons and mylein sheath

Homocysteine may kill Neurons and the Myelin Sheaths that surround Neurons.



Elevated Homocysteine levels may cause Schizophrenia



Elevated Homocysteine levels may cause Aggressiveness.



Homocysteine may stimulate the death of Astrocytes.



[1] Homocysteine Studies Collaboration. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA. 2002 Oct 23-30;288(16):2015-22.

[2] Kumar M et al. Homocysteine decreases blood flow to the brain due to vascular resistance in carotid artery. Neurochem Int. 2008 Dec;53(6-8):214-9.

[3] Matte C et al. Acute homocysteine administration impairs memory consolidation on inhibitory avoidance task and decreases hippocampal brain-derived neurotrophic factor immunocontent: prevention by folic acid treatment. Neuroscience. 2009 Nov 10;163(4):1039-45.

[4] Siuda J et al. From mild cognitive impairment to Alzheimer’s disease – influence of homocysteine, vitamin B12 and folate on cognition over time: results from one-year follow-up. Neurol Neurochir Pol. 2009 Jul-Aug;43(4):321-9.

[5] Seshadri S et al. Association of plasma total homocysteine levels with subclinical brain injury: cerebral volumes, white matter hyperintensity, and silent brain infarcts at volumetric magnetic resonance imaging in the Framingham Offspring Study. Arch Neurol. 2008 May;65(5):642-9.

[6] Seshadri S et al. Association of plasma total homocysteine levels with subclinical brain injury: cerebral volumes, white matter hyperintensity, and silent brain infarcts at volumetric magnetic resonance imaging in the Framingham Offspring Study. Arch Neurol. 2008 May;65(5):642-9.

[7] Leblhuber F., et al. Hyperhomocysteinemia in dementia. J Neural Transm. 107(12):1469-1474, 2000. Department of Gerontology, Landesnervenklinik Wagner Jauregg, Linz, Austria.

Kessler, H., et al. [Homocysteine and dementia.] Fortschr Neurol Psychiatr. 71(3):150-156, 2003.


[9] Bjelland, I., et al. Folate, vitamin B12, homocysteine, and the MTHFR 677C->T polymorphism in anxiety and depression: the Hordaland Homocysteine Study. Arch Gen Psychiatry. 60(6):618-626, 2003. Department of Public Health and Primary Health Care, Locus for Homocysteine and Related Vitamins, University of Bergen, Norway.

[10] Firshein, R. The Nutraceutical Revolution. Riverhead Books via Penguin Putnam Inc., New York, USA. 1998:147.

[11] Haidemenos, A., et al. Plasma homocysteine, folate and B12 in chronic schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry. 2007. 8th Psychiatric Department, Psychiatric Hospital of Attica, Athens, Greece.

[12] Stoney, et al. Plasma homocysteine concentrations are positively associated with hostility and anger. Life Sciences. 66(23):2267-2275, 2000.

[13] Maler, J. M., et al. Homocysteine induces cell death of rat astrocytes in vitro. Neurosci Lett. 347(2):85-88, 2003. Department of Psychiatry and Psychotherapy, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany

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