Monthly Archives: July 2016


Enhancing the Function of Cartilage

Cartilage consists of dense, semi-opaque gray or white flexible connective tissue produced by a matrix of cells called Chondrocytes. Cartilage does not contain blood vessels or nerves.

Cartilage is found in:

  • Bronchial tubes
  • Ear
  • Intervertebral discs
  • Joints between bones
  • Nose
  • Rib cage

Cartilage is classified in three types:

  • Elastic cartilage
  • Fibrocartilage
  • Hyaline cartilage


Chondrocytes are responsible for the formation of new and the breaking down of old cartilage.

Specialized cells called chondrocytes produce ground substance that is rich in proteoglycan and elastin fibers. Ground substance is primarily composed of:

  • Water
  • Glycosaminoglycans (hyaluronan)
  • Proteoglycans
  • Glycoproteins

There are certain substances that may damage cartilage, especially if taken in excess.

Table: Substances that May Damage Cartilage

Damaged Cartilage










Excessive Interlukin 1 (IL-1 beta)



Excessive Tumor Necrosis Factor (TNF-alpha)






Prostaglandin E2






COX-2 Inhibitors (long term use)



Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)


There are certain substances that may enhance the function of cartilage.

Table:  Nutraceuticals that Enhance the Function of Cartilage







Amino Acids




S-Adenosylmethionine (SAMe)






Chondroitin Sulfate (CSA)



Glucosamine Sulfate









Silicon (orthosilicic acid)








Sulfuric Compounds




Methylsulfonylmethane (MSM)






Vitamin C



Vitamin D



Vitamin E


Informational Reference:

Cartilage Health

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The Power of Raw Watercress

Watercress is a plant species with the botanical name Nasturtium officinale. Garden cress, which is known as Lepidium sativum, is related to but a different plant than watercress.

Raw watercress contains two very important and well researched compounds:

  • Phenethyl isothiocyanate (PEITC) (a glucosinolate derivative)
  • Gluconasturtiin (phenethylglucosinolate)(a glucosinolate and a precursor of PEITC)

PEITC has the ability to modulate and turn on genes that suppress cancer by acting as a potent inducer of phase II enzymes. [i]

It is important to note that consumption of watercress should be as raw uncooked watercress. This is because when watercress is cooked, the heat will likely destroy the enzyme myrosinase. PEITC is produced from gluconasturtiin by the action of the enzyme myrosinase.

Table:  Health Benefits of Watercress



















Watercress may prevent various types of cancers



Breast Cancer





Watercress may prevent breast cancer.  watercress and broccoli-derived compounds were also shown to suppress a highly invasive breast cancer cell line



Lung Cancer





Watercress may prevent lung cancer



Prostate Cancer





Watercress may prevent prostate cancer.  When human prostate cancer cells were exposed to PEITC, both proliferation (multiplication of cells) and tumorigenesis (production of tumors) were inhibited



Colon Cancer





Watercress extract was “significantly protective” against three stages of the carcinogenic process in human colon cancer cells. The stages investigated were initiation, proliferation, and metastasis (spread of cancer)








Watercress isothiocyanates restrained certain pro-inflammatory compounds that are associated with chronic inflammation and cancer.












Nicotine-derived nitrosamine ketone (NNK), also known as 4-(methylnitro-samino)-1-(3-pyridyl)-1-butanone is one of the key tobacco-specific nitrosamines which play an important role in carcinogenesis Watercress may inhibit(4-(methylnitro-samino)-1-(3-pyridyl)-1-butanone, the primary carcinogenic compound in tobacco that is the underlying cause of Tobacco-

induced Lung Cancer.

  7 8 9

Nucleic Compounds










Watercress may help to prevent damage to the body’s Deoxyribonucleic Acid (DNA). Watercress supplementation in diet reduces lymphocyte DNA damage and alters blood antioxidant status in healthy adults



[i]Rose P, Faulkner K, Williamson G, Mithen R. 7-Methylsulfinylheptyl and 8-methylsulfinyloctyl isothiocyanates from watercress are potent inducers of phase II enzymes. Carcinogenesis. 2000 Nov;21(11):1983-8.

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Alkaloid from Curry Leaf Inhibits the growth of Liver and Lung Cancer

The curry tree (Murraya koenigii or Bergera koenigii) is a tropical to sub-tropical tree in the family Rutaceae which is native to India and Sri Lanka. 

Curry tree and leafs are not to be confused with Curry Powder.


Curry Tree

There are a number of alkaloids found in the curry tree leaves, stems, and seeds:  1

  • 2-methoxy-3-methyl-carbazole
  • girinimbine
  • isomahanine
  • koenimbine
  • mahanine
  • Mahanimbine
  • Undecalactone

A study published in the Journal Molecules on August 23, 2011 found that the alkaloid girinimbine islolated in curry leafs inhibited the growth and induced apoptosis in human hepatocellular carcinoma, HepG2 cells in vitro.  2



Hepatocellular carcinoma is the most common type of liver cancer.

The authors of the study indicated that:  “Girinimbine-treated HepG2 cells showed typical morphological features of apoptosis, as observed from normal inverted microscopy and Hoechst 33342 assay.

Together, these results demonstrated for the first time that girinimbine could effectively induce programmed cell death in HepG2 cells and suggests the importance of conducting further investigations in preclinical human hepatocellular carcinoma models, especially on in vivo efficacy, to promote girinimbine for use as an anticancer agent against hepatocellular carcinoma.”

Another subsequent study from February 2013 published in Evidence-Based Complementary and Alternative Medicine investigated the anticancer effects of girinimbine, a carbazole alkaloid isolated from Murraya koenigii Spreng, on A549 lung cancer cells in relation to apoptotic mechanistic pathway. 

“After 24 h treatment with 19.01 μM of girinimbine, decrease in the nuclear area and increase in mitochondrial membrane potential and plasma membrane permeability were readily visible. Moreover the translocation of cytochrome c also was observed. Girinimbine mediates its antiproliferative and apoptotic effects through up- and downregulation of apoptotic and antiapoptotic proteins.

There was a significant involvement of both intrinsic and extrinsic pathways. Moreover, the upregulation of p53 as well as the cell proliferation repressor proteins, p27 and p21, and the significant role of insulin/IGF-1 signaling were also identified. Moreover the caspases 3 and 8 were found to be significantly activated. Our results taken together indicated that girinimbine may be a potential agent for anticancer drug development.”  3


Supplement – Curry Leaf & Black Seed Capsules

Fresh or dried Curry leafs can be purchased at most Indian markets or grocery stores

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The Importance of Apoptosis

Apoptosis, a form of programmed cell death, is a genetically regulated cell-suicide mechanism that is essential for our well-being. In this process, cells acquire the means of their own destruction in the form of an arsenal of deadly proteins, which they turn upon themselves. Usually apoptosis is for the good of the organism.

It is required in biological processes such as embryogenesis and homeostasis (maintenance of a stable body). It also destroys cells, which may present a risk to our health, such as cells, which have undergone DNA damage.

Its importance is shown by considering the serious consequences of reduced apoptosis. Tumors often form because of cancer cells developing the ability to suppress apoptosis, making them immortal and very dangerous.

The other extreme, when too much apoptosis occurs, is thought to play a role in the development of diseases such as Alzheimer’s and in the massive destruction of lymphocytes in AIDS and in the adverse consequences of heart attacks.

Accumulations of damaged cells is undesirable and apoptosis is the body’s mechanism for disposing of dead cells.

The aging process is associated with a failure of damaged cells to “kill themselves” via the process of apoptosis, increased (abnormal) apoptosis of non-damaged cells, increased resitance of (damaged) senescent cells to (normal) Apoptosis and failure of (normal) apoptosis to kill cancer cells. [1]

Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.


Figure: Apoptosis Process

There are three degrees of apoptosis that the body produces:

  • Inhibited Apoptosis
    • Allows cancer cells to survive. Permits cells damaged through aging to accumulate (clog the body).
  • Normal Apoptosis
    • Removes damaged, deformed Cells – e.g. aged cells, cancer cells. Normal apoptosis unfortunately does not discriminate – some healthy cells are forced to die.
  • Excessive Apoptosis
    • Kills and removes some non-damaged cells.

The goal is to maximise normal apoptosis within the body and to counteract excessive apoptosis.

Table: Nootropics/Nutraceuticals/Foods/Herbs/Spices that Counteract Excessive Apoptosis

Excessive Apoptosis











Coenzyme Q10




Vitamin B3

Niacinamide [4]



Korean Ginseng


Table: Nootropics/Nutraceuticals/Foods/Herbs/Spices that Facilitate Normal Apoptosis

Normal Apoptosis    







Saffron [6]






Perillyl Alcohol











Ellagic Acid











Sulfuric Compounds






Vitamin C




Green Tea



Saw Palmetto














[1] Higami, Y., et al. Apoptosis in the aging process. Cell Tissue Res. 301(1):125-132, 2000.


[3] Kagan, T., et al. Coenzyme Q10 can in some circumstances block apoptosis, and this effect is mediated through mitochondria. Annals of the New York Academy of Sciences USA. 887:31-47, 1999.

[4] Klaidman, L. K., et al. Nicotinamide as a precursor for NAD+ prevents apoptosis in the mouse brain induced by tertiary-butylhydroperoxide. Neurosci Lett. 206(1):5-8, 1996.

[5] Thatte, U., et al. Modulation of programmed cell death by medicinal plants. Cell Mol Biol. 46:199-214, 2000.

[6] Thatte, U., et al. Modulation of programmed cell death by medicinal plants. Cell Mol Biol. 46:199-214, 2000.

[7] Monograph: fish oil. Alternative Medicine Review. 5(6), 2000.

[8] Mills, J. J., et al. Induction of apoptosis in liver tumors by the monoterpene perillyl alcohol. Cancer Res. 55(5):979-983, 1995.

[9] Mills, J. J., et al. Induction of apoptosis in liver tumors by the monoterpene perillyl alcohol. Cancer Res. 55(5):979-983, 1995.

[10] Pearson, D., et al. The best calcium? Life Enhancement. May 1998:15-17.

[11] Narayanan, B. A., et al. p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest and apoptosis in ellagic acid treated cancer cells. Cancer Letters. 136(2):215-221, 1999.

[12] Jiang, M. C., et al. Curcumin induces apoptosis in immortalized NIH 3T3 and malignant cancer cell lines. Nutrition and Cancer. 26(1):111-120, 1996.

[13] Ahmad, N., et al. Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells. Journal of the National Cancer Institute. 89(24):1881-1886, 1997.

[14] Siler-Marsiglio, K. I., et al. Pycnogenol and vitamin E inhibit ethanol-induced apoptosis in rat cerebellar granule cells. J Neurobiol. 59(3):261-271, 2004.

[15] Thatte, U., et al. Modulation of programmed cell death by medicinal plants. Cell Mol Biol. 46:199-214, 2000.

[16] Sakagami, H., et al. Apoptosis-inducing activity of vitamin C and vitamin K. Cell Mol Biol. 46:129-143, 2000.

[17] Ahmad, N., et al. Green tea constituent epigallocatechin-3-gallate and induction of apoptosis and cell cycle arrest in human carcinoma cells. Journal of the National Cancer Institute. 89(24):1881-1886, 1997.

[18] Iguchi, K., et al. Myristoleic acid, a cytotoxic component in the extract from Serenoa repens, induces apoptosis and necrosis in human prostatic LNCaP cells. Prostate. 47(1):59-65, 2001.

[19] Thatte, U., et al. Modulation of programmed cell death by medicinal plants. Cell Mol Biol. 46:199-214, 2000.

[20] Jiang, M. C., et al. Curcumin induces apoptosis in immortalized NIH 3T3 and malignant cancer cell lines. Nutrition and Cancer. 26(1):111-120, 1996.

Ashwagandha induces significant regeneration of neurites and reconstructs pre- and postsynapses in neurons

A neurite refers to the projection from the cell body of a neuron, which is either an axon or a dendrite. 


Anatomy of a neuron

An axon is the slender projection of a neuron that conducts electrical impulses away from the neuron’s cell body.  The function of the axon is to transmit information to different neurons, muscles and glands.

Axons are insulated with myelin which is a fatty substance formed by two types of glial cells:

  • Schwann cells – ensheathing peripheral neurons and
  • Oligodendrocytes – insulating neurons of the central nervous system

Dendrites are the branched projections of a neuron that act to propagate the electrochemical stimulation received from other neural cells to the cell body, or soma. The electrochemical stimulation onto the dendrites are carried via the synapses located on the end of the dendrites. 

A synapse is a structure that permits a neuron to pass the electrochemical stimulation signal to another neuron.  At a synapse, the presynaptic neuron, via the presynaptic membrane, which is located on the axon, comes into close apposition with the postsynaptic neuron, via the postsynaptic membrane, which is located on a dendrite or soma.


Diagram of Synapses

Many neurodegenerative diseases and cognitive impairment are caused by:  1

  • Neuritic atrophy
  • Synaptic loss

The atrophy of neurites and synaptic loss has been observed in the following neurodegenerative diseases:

  • Alzheimer’s disease
    • Neurite atrophy  2  3
    • Synaptic loss  4
  • Parkinson’s disease  5
  • Huntington’s disease  6
  • Creutzfeldt–Jakob disease   7

Scientists at the Uehara Memorial Foundation explored compounds that would facilitate the regeneration of neurites and the reconstruction of synapses, even in severely damaged neurons, and to show evidence of the effects in vivo as well as in vitro

Their analysis and results were published in the British Journal of Pharmacology in April 2005.  The article, entitled Neuritic regeneration and synaptic reconstruction induced by withanolide A, investigated the effects of withanolide A (WL-A), isolated from the Indian herbal compound Ashwagandha (root of Withania somnifera), on neuritic regeneration and synaptic reconstruction in cultured neurons damaged by Aβ(25–35) and cognitive-deficient mice by Aβ(25–35)-injection.  8

The authors hypothesized that reconstructing neuronal networks in the injured brain would be the most necessary step in the fundamental recovery of brain function. In order to reconstruct neuronal networks, neuritic regeneration and synaptic reconstruction must take place in the damaged brain.  9

Withania somnifera, known commonly as ashwagandha, is a plant in the Solanaceae or nightshade family. It is widely used as a medicinal herb in Ayurvedic medicine.  The leaves contain the steroidal lactones withanolides.


Ashwagandha roots

Amyloid β and Aβ(25–35) is a major pathological cause of Alzheimer’s disease which forms deposits in the brain, and subsequently induces:

  • Neuronal cell death 10
  • Neuritic atrophy  11
  • Synaptic loss  12

In the study, treatment with withanolide A (WL-A) (Ashwagandha) induced significant regeneration of both axons and dendrites, in addition to the reconstruction of pre- and postsynapses in the neurons.  WL-A could also ameliorate the memory deficit in mice, and could generate neurites and synapses in the cerebral cortex and the hippocampus.  13

The authors concluded:

“WL-A is therefore an important candidate for the therapeutic treatment of neurodegenerative diseases, as it is able to reconstruct neuronal networks.”  14


Gaia Herbs – Ashwagandha root extract (capsule)

Ojio – Ashwagandha Extract (powder)

Herb Pharma – Ashwagandha Extract (liquid tincture)

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Nexrutine®: Huáng bǎi (黄栢 or 黃栢 ) or Huáng bò (黄檗): Chemoprotective and Chemopreventive Herb from the Amur Cork Tree

Huáng bǎi (黄栢 or 黃栢 ) or Huáng bò (黄檗), also known as Cortex Phellodendri, is the bark of one of two species of Phellodendron tree: Phellodendron amurense or Phellodendron chinense.  Phellodendron amurense Rupr. is a species of tree in the family Rutaceae, commonly called the Amur cork tree.


Amur Cork Tree bark

A large number of active molecules have been identified and found in the bark.  They include:

(Source:  Wikipedia – Huáng bǎi)

Nexrutine® is a patented compound extracted from Phellodendron amurense trees.  Next Pharmaceuticals, a research and development company is the formulator of Nexrutine®.

A number of scientific studies have shown the extensive chemoprotective capabilities of Nexrutine®, specifically in the following cancers:

Nexrutine® has been shown to inhibit cancer cell growth as a consequence of mitochondrial damage and mitophagy.  One study revealed that autophagy plays an important role in the inhibition of cancer cell proliferation by Nexrutine®.  1

Breast Cancer

In this study we investigated the anticancer effects of Nexrutine on ER negative breast cancer cell lines that are positive or negative for HER-2. Nexrutine decreased the activities of 2 potential targets of breast cancer, cyclooxygenase (COX)-2, and peroxisome proliferators activated receptor gamma (PPARγ). The antiinflammatory effects of Nexrutine were evident with decreased prostaglandin (PG)E2 production, protein expression of microsomal PGE2 synthase (mPGES), and PPARγ. Nexrutine decreased cell survival and induced a G1 cell cycle arrest in SkBr3 and MDA-MB 231 cells, which were associated with reduced protein expression of Cyclin D1 and cdk2 along with increased protein expression of p21 and p27. The growth-inhibitory effect of Nexrutine was associated with apoptosis in SkBr3 cells and autophagy in MDA-MB231 cells. Based on these findings, we propose that Nexrutine may provide a novel approach for protection against breast cancer.  2

Colon Cancer

Here, we explored the mechanism of chemopreventive/chemotherapeutic efficacy of Nexrutine (NX) against colon cancer. We found that dietary exposure of Nexrutine (NX) significantly reduced the number of azoxymethane (AOM)-induced aberrant crypt foci (ACF) in rats. In addition, significant inhibition in AOM-induced cell proliferation and reduced expression of the inflammatory markers COX-2, iNOS as well as the proliferative markers PCNA and cyclin D1 were also seen. Moreover, Nexrutine (Nexrutine (NX)) exposure significantly enhanced apoptosis in the colon of AOM treated rats.  Based on these in vivo and in vitro findings, we suggest that Nexrutine (NX) could be useful candidate agent for colon cancer chemoprevention and treatment.   3

Pancreatic Cancer

Recent studies from our laboratory have shown that Nexrutine® (Nx), a bark extract from Phellodendron amurense exhibits excellent anticancer activity in human pancreatic cancer cells through inhibition of inflammatory signaling via STAT3/NFκB/Cox-2. Given the apparent high oxidative stress and autophagic activity in pancreatic tumors, we investigated the potential of Nx to modulate autophagy, reactive oxygen species (ROS), and their crosstalk. Our results show that Nx inhibits autophagy and decreases ROS generation.  Overall, our findings reveal an important role for STAT3/LC3/ROS in Nx-mediated anti-pancreatic cancer effects.  4

Prostate Cancer

The current standard of care for prostate cancer includes hormone therapy, radiation therapy and radical prostatectomy, each with its own set of undesirable side effects. In this regard there is an unmet need to develop strategies that can prevent or delay the development of clinical prostate cancer. One potential area involves the use of natural compounds involving botanicals. Along these lines we have found that Nexrutine®, a dietary supplement derived from Phellodendron amurense bark extract, has prostate cancer prevention activity.   5

Skin Cancer

In the present investigation, we explored the mechanism of chemopreventive/chemotherapeutic efficacy of NX against skin cancer. Single application of NX (1.0mg/mouse) prior to 12-O-tetradecanoylphorbol 13-acetate (TPA) application significantly inhibited TPA-induced skin edema, hyperplasia, thymidine incorporation and ornithine decarboxylase (ODC) activity; expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS); phosphorylation of extracellular signal-regulated kinases (ERK) 1/2, p38 and c-jun N-terminal kinase (JNK) mitogen-activated protein kinases (MAPKs); and activation of I kappa B kinase (IKK), IκBα and nuclear factor-kappa B (NF-κB) in mouse skin.  Based on our in vivo and in vitro studies, NX could be useful in the management (chemoprevention as well as chemotherapy) of skin cancer.  6


Swanson Health Products – Nexrutine


Huang Bai, Extract Powder Phellodendron Amurense Bark,黃柏濃縮粉,100 g/bt



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Maintaining the Integrity and Overall Health of the Large Intestine

The large intestine or colon is the last section of the digestive system and is about 1.5 metres (4.9 ft) long, which is about one-fifth of the whole length of the gastrointestinal tract.

The main functions of the large intestine is to:

  • Extract water and salt from solid wastes before they are eliminated from the body through the rectum
  • Provide a site for bacterial fermentation of unabsorbed food material

The large intestine does not play a role in the absorption of foods and nutrients, which is the role of the small intestine.

In order to maintain the overall health of the large intestine, there are three very important substances that need to be supplied or produced endogenously by the large intestine.  These three substances include:

  • Glutamine
  • Short Chain Fatty Acids
  • Beneficial Bacteria


Glutamine is an α-amino acid that is used in the biosynthesis of proteins.  In human blood, glutamine is the most abundant free amino acid, with a concentration of about 500–900 µmol/l.

Glutamine is essential for the health of the cells that line the wall of the large intestine.  Glutamine also increases blood circulation to the large intestine.

The dietary sources of glutamine include:

  • Brussels Sprouts   
  • Papaya
  • Carrots
  • Celery
  • Parsley
  • Spinach
  • Cabbage
  • Dandelion Greens
  • Lettuce

Short-chain fatty acids (SCFAs)

Short-chain fatty acids (SCFAs), also referred to as volatile fatty acids (VFAs), are fatty acids with less than six carbon atoms.  They are normally manufactured endogenously when dietary fiber is fermented in the large intestine.  Some SCFA’s can be consumed by diet.

The three most important SCFA’s for the large intestine include:

  • Acetate  (50% to 60% of the total SCFA’s)
  • Butyrate (15% to 20% of the total SCFA’s)
  • Propionate  (20% to 25% of the total SCFA’s)

SCFA’s are produced when dietary fiber and resistant starch are fermented in the large intestine.  The rate and amount of SCFA production depends on the species and amounts of microflora present in the large intestine. 

Acetate enters the peripheral circulation to be metabolized by peripheral tissues.  Acetate is the principal SCFA in the colon, and after absorption it has been shown to increase cholesterol synthesis.

The following foods/substances enhance the production of Acetate in the large intestine:

  • Pectins   (Apple and/or Grapefruit Pectin)
  • Galactooligosaccharides
  • Psyllium
  • Oat Bran

Propionate is largely taken up by the liver.  Propionate, a gluconeogenerator, has been shown to inhibit cholesterol synthesis.

The following foods/substances enhance the production of Propionate in the large intestine:

  • Larch Arabinogalactan
  • Psyllium
  • Rhamnose

Dietary Butyrate is the major energy source for colonocytes.  Butyrate has been studied for its role in nourishing the colonic mucosa and in the prevention of cancer of the colon, by promoting cell differentiation, cell-cycle arrest and apoptosis of transformed colonocytes; inhibiting the enzyme histone deacetylase and decreasing the transformation of primary to secondary bile acids as a result of colonic acidification.   Without butyrates for energy, colon cells undergo autophagy (self digestion) and die.   1

The following foods/substances enhance the production of Butyrate in the large intestine:

  • Inulin
  • Resistant Starch (Amylose) (Banana Flour is superior form of resistant starch)  2
  • Fructooligosaccharides (FOS)
  • Larch Arabinogalactan
  • Psyllium
  • Wheat Bran

Butyrate can also be taken as a supplement in the following forms:

  • Calcium/Magnesium Butyrate
  • Sodium Butyrate

Specific SCFA may reduce the risk of developing gastrointestinal disorders, cancer, and cardiovascular disease.  Therefore, a greater increase in SCFA production and potentially a greater delivery of SCFA, specifically butyrate, to the distal colon may result in a protective effect.  3  4  5  

Beneficial Bacteria

The beneficial bacterial of the glut flora is health-enhancing and serves to prevent the overgrowth of potentially harmful bacteria in the gut. There is always a competition for resources (space and food) in the large intestine between beneficial and detrimental bacteria.  A ratio of 80-85% beneficial to 15–20% potentially detrimental bacteria generally is considered normal within the intestines.



Butyrate (Supplement)

Resistant Starch  (Banana Flour)

Apple Pectin


Beneficial bacteria (there are are a wide selection)

The Dangers of Heterocyclic Aromatic Amines

“Heterocyclic amines are a group of 20 chemical compounds formed during cooking. They are found in meats that are cooked to the well done stage, in pan drippings, and in meat surfaces that show a crispy brown crust. Epidemiological studies show associations between intakes of heterocyclic amines and cancers of the colon, rectum, breast, prostate, pancreas, lung, stomach, and esophagus, and animal feeding experiments support a causal relationship. The U.S. Department of Health and Human Services Public Health Service labeled several heterocyclic amines as likely to be carcinogenic to humans in its most recent Report on Carcinogens.”


The most common types of Heterocyclic Aromatic Amines (HAA’s) include:

  • 4,8-DiMelQx 2-Amino-3,4,8-Trimethylimidazo [4,5-f]Quinoxaline
  • 8-MelQx 2-Amino-3,8-Dimethylimidazo [4,5-f]Quinoxaline
  • IQ 2-Amino-3-Methylimidazo [4,5-f]Quinoline
  • MelQ 2-Amino-3,4-Dimethylimidazo [4,5-f]Quinoline
  • PhIP 2-Amino-1-Methyl-6-Phenylimidazo [4,5,b]Pyridine
  • TMIP 2-Amino-N,N,N-Trimethylimidazopyridine

HAAs form when Amino Acids and Creatine present in muscle Meats react at high temperatures (above 100° C). Temperature is the most important factor in formation of HAAs. Frying, Grilling, and Barbecuing produce the largest amounts of HAAs because the Meats are cooked at very high temperatures. Roasting and Baking are done at lower temperatures, so lower levels of HAAs are likely. Microwaving, Stewing, Boiling, or Poaching are done at or below 100° and cooking at this low temperature creates negligible amounts of HAAs.

The following substances have been studied and research for their ability to counteract the toxic effects of HAA’s:


Guo, D., et al. Protection by chlorophyllin and indole-3-carbinol against 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced DNA adducts and colonic aberrant crypts in the F344 rat. Carcinogenesis. 16(12):2931-2937, 1995

Caffeic Acid

Mitchell, T. Barbequer beware. Life Extension. 6(11), 2000


Shishu, et al. Inhibitory effect of curcumin and its natural analogues on genotoxicity of heterocyclic amines from cooked food. Indian J Exp Biol. 40(12):1365-1372, 2003

Epigallo-Catechin-Gallate (EGCG)

Dashwood, R. H., et al. Cancer chemopreventive mechanisms of tea against heterocyclic amine mutagens from cooked meat. Proc Soc Exp Biol Med. 220(4):239-243, 1999


Mitchell, T. Barbequer beware. Life Extension. 6(11), 2000


Ciolino, H. P., et al. Dietary flavonols quercetin and kaempferol are ligands of the aryl hydrocarbon receptor that affect CYP1A1 transcription differentially. Biochem J. 340(Part 3):715-722, 1999


Ziegler, J. It’s not easy being green: Chlorophyll being tested Journal of the National Cancer Institute. 87(1):11, 1995

Guo, D., et al. Protection by chlorophyllin and indole-3-carbinol against 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced DNA adducts and colonic aberrant crypts in the F344 rat. Carcinogenesis. 16(12):2931-2937, 1995


Rajendran, R., et al. Binding activity of natto (a fermented food) and Bacillus natto isolates to mutagenic-carcinogenic heterocyclic amines. Can J Microbiol. 47(10):935-942, 2001


Puangsombat, K., et al. Inhibition of heterocyclic amine formation in beef patties by ethanolic extracts of rosemary. J Food Sci. 75(2):T40-T47, 2010


Walters, D. G., et al. Cruciferous vegetable consumption alters the metabolism of the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in humans. Carcinogenesis. 2004

Brussels Sprouts

Hoelzl, C., et al. Consumption of Brussels sprouts protects peripheral human lymphocytes against 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and oxidative DNA-damage: results of a controlled human intervention trial. Mol Nutr Food Res. 2008


Knize, M. G., et al. Analysis of cooked muscle meats for heterocyclic aromatic amine carcinogens. Mutation Research. 376(1-2):129-134, 1997

Sugimura,T.(1997). Overview of carcinogenic heterocyclic amines. Mutation Research, 376, 211-219

Chemicals in Meat Cooked at High Temperatures and Cancer Risk

A Review on the Formation of Carcinogenic/Mutagenic Heterocyclic Aromatic Amines

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Creatine significantly lowers accumulation of Lipofuscin

Lipofuscin is a fine granular yellow-brown pigment composed of lipid containing residues of lysosomal (waste) digestion. 

Lipofuscin is normally found in the following organs:

  • Kidney
  • Heart
  • Liver
  • Retina
  • Skin
  • Adrenals
  • Neurons
  • Ganglion cells

The accumulation of lipofuscin is considered a “marker of aging”.

A study published in Amino Acids in May 2011 concluded that:

“In brains of creatine-treated mice, there was a trend toward a reduction of reactive oxygen species and significantly lower accumulation of the “aging pigment” lipofuscin.”

The authors further state that:

“These data showed that creatine improves health and longevity in mice. Creatine may, therefore, be a promising food supplement to promote healthy human aging. However, the strong neuroprotective effects in animal studies of creatine have not been reproduced in human clinical trials (that have been conducted in Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis).”


Klopstock T, Elstner M, Bender A. Creatine in mouse models of neurodegeneration and aging. Amino Acids. 2011 May;40(5):1297-303.

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Uridine: The Neurological Benefits

Uridine is one of five nucleosides which make up nucleic acids and is found in RNA but not DNA.

Uridine is present in many foods in the form of RNA. The following foods contain trace amounts of uridine:

§  Tomatoes

§  Brewer’s yeast

§  Beer

§  Broccoli

§  Baker’s Yeast

§  Mushrooms

§  Oats

§  Chinese Cabbage, Spinach, and Cauliflower

§  Parsley

However, uridine in RNA is not bioavailable, since it is almost entirely destroyed in the liver and gastrointestinal tract.  The only studied exception to this is beer. Yet no food, when consumed, has ever been reliably shown to elevate blood uridine levels.

Uridine is found in two forms:

§  Uridine-5′-Monophosphate Disodium (UMP)

§  Triacetyluridine (TAU)

Uridine-5′-Monophosphate Disodium (UMP)

Uridine 5′-monophosphate disodium salt is a nucleotide that is a major component of ribonucleic acid. It is found in dietary supplements as well as natural RNA rich foods as well as the milk of most mammals, including human mother’s milk.

Uridine monophosphate (UMP) is water soluble, and can be taken sublingually to drastically increase the amount that gets to your brain.

Triacetyluridine (TAU)

Triacetyluridine (TAU) is a prodrug of uridine, and thus is a more bio available form of uridine.  TAU is also fat soluble whereas UMP is water soluble. TAU has 7-fold greater bioavailability than an equimolar amount of Uridine and is rapidly converted within the body to Uridine.


Table 1.1 Neurological Benefits of Uridine



















Uridine may be useful for the treatment of Alzheimer’s Disease.








Uridine may stimulate the outgrowth of Axons.








Uridine may useful in alleviating depression when combining uridine and omega-3 fatty acids



Huntington’s Disease





Uridine may be useful for the treatment of Huntington’s Disease








Uridine may help in the improvement of memory



Parkinson’s Disease





Uridine may be a useful treatment of Parkinson’s Disease








Uridine enhances the neurite outgrowth produced by nerve growth factor (NGF)

The TAU form of uridine is able to enhance nerve growth factor (NGF) by activating P2Y2 receptors within the brain, thus increasing neuron growth.








Uridine may stimulate the release of dopamine in the Brain



Choline synthesis





Exogenous uridine was shown to elevate intracellular CDP-choline levels, by promoting the synthesis of uridine triphosphate (UTP), which was partly converted to CTP



Cell Membrane phospholipids





Short-term administration of uridine increases brain membrane phospholipid precursors in healthy adults



[1] Agnati, L. F., et al.  Intravenous uridine treatment antagonizes hypoglycaemia-induced reduction in brain somatostatin-like immunoreactivity.  Acta Physiol Scand.  126(4):525-531, 1986.


Wurtman, R. J., et al.  Synapse formation is enhanced by oral administration of uridine and dha, the circulating precursors of brain phosphatides.  J Nutr Health Aging.  13(3):189-197, 2009.


[2] Wang, L., et al.  Dietary uridine-5′-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.  J Mol Neurosci.  27(1):137-145, 2005.


[4] Saydoff, J. A., et al.  Oral uridine pro-drug PN401 decreases neurodegeneration, behavioral impairment, weight loss and mortality in the 3-nitropropionic acid mitochondrial toxin model of Huntington’s disease.  Brain Research.  994(1):44-54, 2003.


[5] Drago, F., et al.  Memory deficits of aged male rats can be improved by pyrimidine nucleosides and N-acetyl-glutamine.  Clin Neuropharmacol.  13(4):290-296, 1990.


Holguin, S., et al.  Chronic administration of DHA and UMP improves the impaired memory of environmentally impoverished rats.  Behav Brain Res.  2008.


[6]Kilvenyi, P., et al.  Neuroprotective effects of oral administration of triacetyluridine against MPTP neurotoxicity.  Neuromolecular Medicine.  6(2-3):87-92, 2004.


[7] Wang, L., et al.  Dietary uridine-5′-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.  J Mol Neurosci.  27(1):137-145, 2005.


[8] Wang, L., et al.  Dietary uridine-5′-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.  J Mol Neurosci.  27(1):137-145, 2005.


[9] Wang, L., et al.  Dietary uridine-5′-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.  J Mol Neurosci.  27(1):137-145, 2005.