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27th Annual Convention (7/25/08)        Convention Lecture
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TWO NEW Convention Colors For ANMA Polo Shirts

ANMA Photo I.D. Membership Cards

Healthy Help Through Enzymes

Benefits of a Special Sea Cucumber Extract in Anti-angiogenic Therapy
& RTK Inhibition For Cancer

Bring A Friend To The ANMA Convention

A Call For Validated Research Papers

To advertise in the ANMA Monitor or ANMA MONITOR ONLINE
Call: Julie Morgan at (702) 897-7053

Please take the time to look over our sponsors!

INSIDE THIS ISSUE:

The  President's  Corner

By: Jane Carter for Dr. Curtis

Come one, come all, it’s that time again. It’s time to enjoy yourself while increasing your knowledge by attending ANMA’s Annual Convention at the Riviera Hotel in Las Vegas, NV July 29, 30, 31. Enthusiasm is high, and we look forward to seeing you.

All attendees will have the chance to win hundreds of dollars worth of prizes donated by our fine merchants for the "Super Raffle". ANMA will also hold a raffle with prizes including a weekend stay at the Riviera Hotel, Dinner and Show Tickets. Fun for all!

Again this year we have invited political representatives who have an interest in natural health care. We will have the heads of legislative advocacy groups such as Coalition for Natural Health, and Health Keepers Alliance. There will be discussions on current licensing laws, commitment, and practice guidelines.

We highly recommend you maintain an active interest in your future. Non-involvement and non-interest in tracking legislation in your state can be disastrous to your practice. We recommend web site www.statelocalgov.net to monitor such bills. Once you are familiar with the site, it takes only a few moments of your time daily to protect your practice or future practice. If you have any questions please contact us.

We wish to clarify that even though a law was recently passed that we did not support, we will continue to support the Coalition for Natural Health, and Health Keepers Alliance. Even though our position will remain as follows: we do not support any naturopathic bill that differentiates between distant learning and resident school learning. We believe these two organizations attempt to act in your best interest.

On a final note, if you are interested in expressing an opinion regarding the profession, or ANMA, to be published in the Editors column please send to the Monitor at address provided. Each editorial will be considered, however ANMA reserves the right to accept or not accept any editorial submitted.

If you haven’t already made your plans to attend the convention, you should do it today. ANMA Board of Directors will be there to meet each and everyone of you. See you soon!

INSIDE THIS ISSUE:

The Canola Oil 'Urban Legend'

By: Steven Brynoff

INSIDE THIS ISSUE:

Prostate Problems & Elevated Estrogen

By: Mike Menkes, BA, LMT

Men over the age of 45 are surprised to learn that estrogen, a 'female' hormone, is also present in their bodies. Male estrogen is produced in very small quantities, as a by-product of the testosterone conversion process. This process is regulated by an enzyme called aromatase.

Balanced levels of estrogen encourage a healthy libido, improve brain function, protect the heart and strengthen the bones. Oestradiol is the most potent oestrogen of a group of steroids which includes oestrone and oestriol. Excessive oestradiol levels can lead to the suppression and

reduced activity of testosterone. Typically, men's oestrogen levels increase with age, and it is not uncommon for a 59 year-old man to have more oestrogen than a 54 year-old woman.

Obesity, pesticides, nutritional deficiencies, prescription medicines and excessive alcohol intake can all raise a man's estrogen levels. When this happens, men frequently lose muscle tone and gain body fat. The end results of high oestrogen for men can include obesity, an enlarged prostate, diabetes and a higher incidence of heart disease and cancer.

"…studies have shown a strong correlation between consumption of cruciferous vegetables and a lower risk of prostate cancer. These vegetables contain glucosinolates, which during metabolism give rise to several breakdown products, mainly Indole-3-Carbinol (I3C)…"1

"It is time to revamp the prostate cancer hypothesis. Orchiectomy [removal of the testicles] provided a prostate cancer benefit not because it removed testicular testosterone but because it lowered estradiol levels.

"The two most important factors in the underlying metabolic imbalance prostate (and all hormone-dependent cancers) are oestrogen dominance and nutritional imbalance. Prevent these two factors and you will prevent the cancer. If the cancer is already underway, correcting the estrogen dominance will slow the cancer growth and prolong life.2

1. "In the current study, we investigated whether I3C had any effect against prostate cancer cells and, if so, attempts were made to identify the potential molecular mechanism(s) by which I3C elicits its biological effects on prostate cancer cells. Here we report for the first time that I3C inhibits the growth of PC-3 prostate cancer cells.

Induction of apoptosis was also observed in this cell line when treated with I3C, as measured by DNA laddering and poly (ADP-ribose) polymersae (PARP) cleavage.

From these results, we conclude that I3C inhibits the growth of PC-3 prostate cancer cells by inducing G1 cell cycle arrest leading to apoptosis,

and regulates the expression of apoptosis-related genes. These findings suggest that I3C may be an effective chemopreventive or therapeutic agent against prostate cancer."3

2. "We have previously shown that 3,3'-diindolylmethane (DIM – a metabolite of I3C) has a suppressive effect on the growth of human breast and PC cell lines. The objective of this study was examination of the potential therapeutic effects of DIM in an in vivo model. METHODS: TRAMP-C2, a mouse PC cell line, was injected into the flank of male C57BL/6 mice. When tumors appeared, mice were injected intraperitoneally with either corn oil (vehicle) or DIM (2.5, 5, or 10 mg per kg body weight) three times a week, for three weeks, and tumor volumes were measured bi-weekly with calibermeters. Later, the tumors were removed, their final weights and volumes were measured, and tumor sections were tested for histological studies. RESULTS: DIM had a significant inhibitory effect, caused by diminished tumor growth.

CONCLUSIONS: The inhibitory action of DIM on tumor growth was demonstrated in vivo. Hence, this compound at the concentrations tested may offer an effective and non toxic therapeutic means against tumour growth in rodents, and may serve as a potential natural anti-carcinogenic compound in humans.4

PSA Levels Not A Good Indicator of Cancer

"PSA level was also found to be not an especially good indicator of prostate cancer. If only PSA levels were used, 82 (17.3%) of the 473 cancers found by TRUS would have remained undetected. Moreover, among men with cancer and a PSA level of less than four ng/ml (usually considered a safe level), 42% of the cancers were termed minimal, 42% termed moderate, and 16% were advanced."5

"Orchiectomy: This is surgical removal of the testicles, removing the source of male hormones. Prostate cancers typically shrink after removal of the testes. However, over time, the cancer inevitably returns. Luteinizing hormone-releasing hormone (LHRH) agonists: These medications reduce the amount of testosterone the testicles make. These injectable drugs can decrease the amount of testosterone produced by a man's testicles. The two available in the United States are leuprolide and goserelin. Antiandrogens: Orchiectomy and LHRH agonists do not fully block the production of androgens. Antiandrogens block the effects of those residual androgens, and are often used in combination with Orchiectomy and LHRH agonists in a process called total androgen blockade. The antiandrogens available in the United States are flutamide, nilutamide, and bicalutamide. Female hormones: Di-ethyl stilbesterol (DES) is a synthetic oestrogen often used in prostate cancer."6

Serum vs. Saliva Testing

"For reasons that escape rational thinking, conventional medicine persists in using serum tests rather than saliva tests. The results have been disastrous. When using hormone creams or gels, the hormone is absorbed through the skin and into the blood without first passing through the liver. Thus, they are essentially all absorbed in the 'free' form. When given orally, they pass first through the liver and 90% of them become protein-bound. For this reason, transdermal dosing is at least ten times more efficient than oral dosing.

"If one uses serum testing to measure the blood levels achieved by transdermal dosing, the test will fail to measure all the hormone carried by red blood cells. As a consequence, physicians are apt to greatly overdose their patients.

"When using saliva testing, it is found that the transdermal dose of testosterone when treating someone with testosterone deficiency is only 0.25-0.5 mg in women, and one to two mg in men. As the New Yorker article indicated, the transdermal doses of testosterone ranged from five mg to 100 mg a day. The same is observed in estrogen replacement therapy – the doses are generally all greatly excessive. The same hormone that brought good health without side effects when in normal endogenous levels will bring on very bad side effects when given in grossly excessive doses. The problem is not the hormone, per se, the problem is the dosing."7

Prior to enhancement with female hormones, surgery, or radiation, reduction of confirmed elevated estradiol levels, via saliva testing, appears to be the more logical choice from prostate cancer treatment options. Indole-3-Carbinol has shown to be a safe, effective and inexpensive non-prescriptive course of action.

Mike Menkes - PresidentHealth Science Solutions • 4401 Sheridan Street, Hollywood, FL 33021 • 800 432-2254 (954) 252-3962 http://www.naturalproductsinsider.com/ibg/ibg.aspx?li=32763&st=All+Natural+FMG+Inc.

REFERENCES

INSIDE THIS ISSUE:

TWO NEW Convention Colors For ANMA
Embroidered Polo Shirts

If you have any questions or want to place an order, e-mail me at: webmaster@anma.com or call Julie Morgan at (702) 897-7053 or mail to ANMA, P.O. Box 96273, Las Vegas, NV 89193.

NOTE: BE SURE TO ORDER NOW BEFORE THE CONVENTION TO GET THE SIZE AND QUANTITY YOU WANT. THE BURGUNDY AND FOREST GREEN POLOS WILL DEFINITELY BE VERY LIMITED OR EVEN SOLD OUT AFTER THE CONVENTION.

INSIDE THIS ISSUE:

ANMA Photo I.D. Membership Cards

ANMA for the fist time, offers a remarkably new Photo I.D. Membership Card. The fresh new card will be in full color (including picture) and double sided. The front side will have the ANMA insignia, photograph, membership type, member I.D. number, and date joined. The back side of the card is bestowed with ANMA’s Code of Ethics. In addition, the Photo I.D. card is laminated for long lasting durability. The new Photo I.D. Membership Card cost is $15.00 and shipping is free of charge. For more information or to place an order, please call 702-897-7053 or e-mail us at webmaster@anma.com.

INSIDE THIS ISSUE:

Healthy Help Through Enzymes

 By: Donna Werner, D.C.

The 20th century saw remarkable gains in wiping out the nutritional scourges of the past, such as scurvy, pellagra and rickets. Certain advancements in the last century also brought about an explosion of chronic, degenerative disorders, including cancer, cardiovascular disease and type-2 diabetes.

Research has proven that many of these conditions can be directly attributed to our modern diets.

Nature endowed us with remarkable digestive mechanisms, many of which are now failing us at an early age. Nature doesn’t typically make mistakes, so why is this happening?

What nature didn’t anticipate was humankind’s increasing reliance upon a diet of cooked and processed food as the primary source of nutrition.

Enzymes for digestion essentially come from two sources: internally from our own digestive organs (digestive enzymes) and externally from the food we eat (food enzymes).

Food enzymes, however, are present in raw food only. Cooking or processing food at temperatures greater than 118 F destroys all of its enzymes and places the entire burden for digestion on the body. The impact of this destruction of food enzymes has been largely overlooked in allopathic medicine.

The pioneering work of Dr. Edward Howell in the 1920s and 1930s led to the current practice of enzyme supplementation.

His research indicated that people were suffering from various chronic diseases, because their bodies were expending so much energy digesting their food, it left them little energy for important metabolic functions. His premise was this: If enzymes that are lost during the cooking and processing of food could be replaced; the body would be spared some of the energy-intensive process of digestion and could devote more of its resources towards maintaining optimum health.

Today, healthcare practitioners in many different disciplines are beginning to recommend enzyme supplements and are noticing improvements in the health of their patients and, subsequently, the profitability of their practices.

In his book, Enzyme Nutrition: The Food Enzyme Concept, Howell states: "The length of life is inversely proportional to the rate of exhaustion of the enzyme potential of an organism. The increased use of food enzymes promotes a decreased rate of exhaustion of the enzyme potential." Howell believed the number of enzymes the body is capable of producing is finite and their depletion leads to chronic conditions and eventually the loss of life.

Based on our current knowledge of genetic predisposition and the effect of stress on organ function in the body, Howell’s premise has merit. The lack of naturally occurring enzymes in food puts undue stress on the pancreas and other enzyme-producing digestive organs to produce all of the enzymes needed for complete digestion of food.

It is well documented that continuous stress on an organ or system of the body will eventually result in diminished functioning of that organ or system.

Since a top priority of the body is obtaining nutrition through digestion, the body’s resources are readily made available to complete this function. If an excessive amount of these resources are constantly used for digestion, the other metabolic functions in the body will suffer.

Therefore, the goal of enzyme supplementation is to relieve the digestive organs of unnecessary stress and allow the body to allocate its valuable resources to maintaining healthier metabolic function.

In order to accomplish this goal, the right enzyme supplements must be used. Enzymes from animal sources, such as pancreatin, are most active in the more alkaline environment of the small intestine (approximate pH 6.0 – 8.0) after the body has already produced enzymes to complete digestion.

This means animal enzyme supplements do nothing to spare the pancreas and other digestive organs from producing excess enzymes.

Vegetarian enzymes, on the other hand, are active over a broad pH range (pH 2.0 to 11.0) so they are able to begin digesting food immediately after entering the stomach.

The presence of digested food in the stomach signals the body to produce fewer enzymes for the digestive process. Vegetarian enzymes, therefore, are a better choice because they relieve the body of some of the burden of digestion.

While nutritional enzyme supplements are available to the consumer at health-food stores, on the Internet and even in the neighborhood pharmacy, the most therapeutically effective supplements are those available only through healthcare practitioners.

These enzymes contain higher potency and are full-spectrum. They would not be appropriate for a self-diagnosing consumer.

Healthcare practitioners, however, are able to assess each patient’s health status and tailor an individualized enzyme supplementation program.

To recommend enzyme supplementation to your patients, follow these guidelines:

• Select vegetarian enzymes. Animal enzymes (pancreatin) and basic plant enzymes (bromelain and papain) concentrate their digestive activity on breaking down protein.

But, vegetarian enzymes from safe, mycological sources provide a full spectrum of enzymes for more complete digestion.

• Include four common enzymes. When selecting an enzyme supplement to recommend, be certain at least the four primary types are present to assure digestion of the main food components.

These enzymes include amylase (starch digestion), cellulase (fibrous foods breakdown), lipase (fatty acid splitting) and protease (protein digestion).

• Consider other enzymes. Many other enzymes, such as glucoamylase, sucrase, lactase, alpha-galactosidase, phytase and peptidase, to name a few, ensure further digestion of all food groups.

• Recommend systemic supplementation. In addition to adding an enzyme supplement to assist with digestion, recommend taking enzyme supplements between meals to reduce inflammation, boost immune function, maintain cardiovascular health, maximize endocrine effectiveness, detoxify and promote normal respiratory function.

This type of enzyme supplementation is referred to as "systemic" and typically uses proteolytic enzymes (proteases).

The 20th century provided medical advancements at a rate unprecedented throughout history. What will the 21st century hold for the health of mankind, and what role will nutritional enzyme supplementation play?

Based on the exceptional clinical results seen thus far, the future of enzyme supplementation proves extremely promising.

INSIDE THIS ISSUE:

Benefits of a Special Sea Cucumber Extract in
Anti-angiogenic Therapy & RTK Inhibition For Cancer

Angiogenesis, or the growth of new blood vessels, is involved in such vital processes as wound healing, restoration of blood flow to tissues after injury, and menstruation1-2. However, when the body is unable to control angiogenesis, diseases such as age-related macular degeneration, rheumatoid arthritis, or psoriasis can result3. But more importantly, angiogenesis is central to tumor growth, proliferation, invasion, and metastasis.

When normal tissues are diseased or injured, such as in tumors, different growth factors or proteins are released into the nearby tissues to stimulate angiogenesis. The growth factors subsequently bind to their corresponding receptor tyrosine kinases (RTKs) within endothelial cells in the blood vessels. This receptor binding results in the activation of the otherwise dormant endothelial cells, causing them to divide and migrate towards the diseased tissues or, in this case, the tumor cells. Adhesion molecules help the growing new blood vessels to sprout forward. These sprouting endothelial cells roll up to form new blood vessel tubes. Ultimately these tubes form a network of new blood vessels that can circulate blood4. With the new blood vessels now feeding it, the tumor can continually grow in size, invade other tissues and facilitate the spread of the cancer to other organs.

Inhibiting angiogenesis at some point in the process is obviously essential to stopping tumor growth. Normally, the body has naturally-occurring angiogenesis inhibitors that try to counter the potentially abnormal effect of growth factors. However, when a tumor reaches a size of about 2 mm in diameter, growth factors are produced in overwhelming amounts and the effect of natural angiogenesis inhibitors is overpowered4. As a result, a cascading process of new blood vessel formation is initiated. One aspect of cancer therapy research, called RTK inhibition, concentrates not necessarily on stopping the overproduction of angiogenesis-related growth factors but in blocking these from binding to their receptors in order to stop the signaling that launches the process of new blood vessel formation.

For more than three decades now, cancer therapy research has tried to find resources-- natural or otherwise-- that can block the angiogenesis process. Researchers have since developed synthetic angiogenesis inhibitors, but they have also found potential angiogenesis inhibitors in natural marine resources, most especially sea cucumbers. Sea cucumbers are delicacies in the South China seas and are known to be rich in nutritional compounds such as polysaccharides5 and lactones6. In the 1990s, scientists have uncovered that sea cucumbers are active inhibitors of angiogenesis as well (U.S. Patent No. 5,985,330). This comes as no surprise to people living in the South China seas. For centuries, sea cucumbers have been considered as an integral part in Chinese folk medicine, primarily used as treatment for stomach ulcer and stomach cancer. The discovery that these natural resources are angiogenesis inhibitors only reinforces their centuries-old history of traditional use. More recently, a research team in China published more concrete evidence that philinopside A (chemical formula C55O22H85SO3Na), extracted from a special sea cucumber species, is not only able to suppress new blood vessel formation but also inhibit RTK binding of growth factors7.

Results of studies by the research team in China revealed that due to philinopside A's significant inhibition of three important stages of angiogenesis (endothelial cell proliferation, migration and tube formation), the formation of new blood vessels was greatly reduced. It was observed that, at various doses, philinopside A inhibited proliferation of human microvascular endothelial cells (HMECs) at rates of up to 98.7%. Using the same doses, HMEC migration was also inhibited by as much as 94.1%. Figures 1 and 2 illustrate the sprouting of microvessels in cultured rat aortas before and after treatment with philinopside A. After addition of philinopside A, the outgrowth is visibly reduced, indicating that it did block blood vessel formation. In more specific tests, philinopside A was found to inhibit proliferation in several cancer cell lines, including MKN-28 (gastric cancer), SPC-4A (colorectal cancer), HL-60 (leukemia), A-549 (lung tumor), BEL-7402 (liver cancer), MCF-7 (breast cancer), HCT-116 (colorectal cancer) and HO-8910 (ovarian cancer)7.

In subsequent studies, philinopside A produced a more potent anti-angiogenic effect than Suramin, a synthetic angiogenesis inhibitor manufactured by Parke-Davis, requiring only a minimal dosage to produce the same effect as Suramin. A comparable result, in terms of dosages, was obtained when philinopside A was compared against 5-Fluorouracil (5-FU), a popular chemotherapeutic agent7.

Further studies revealed that philinopside A is able to shrink mouse sarcoma 180 tumor tissues by inducing apoptosis, or cell death. It produced a 10-fold increase in apoptopic endothelial cells and a 9-fold increase in apoptopic tumor cells compared to the untreated tissues. A similar degree of tumor shrinkage was observed using 5-FU but a much higher concentration (at least 12 times more than philinopside A) was needed. In addition, both compounds operate through different modalities: philinopside A through apoptosis of tumor and endothelial cells and 5-FU through cytotoxicity of tumor cells7. The method by which it reduces tumor size is what sets philinopside A, and other angiogenesis inhibitors, apart from other cancer treatments. By inducing apoptosis of tumor and endothelial cells, treatment is localized and damage to the surrounding healthy cells is minimized. Chemotherapeutic agents and/or radiation, on the other hand, directly kills both healthy and cancer cells (cytotoxicity) and generates more physiological side effects.

Perhaps the most novel function of philinopside A is its ability to inhibit RTK binding. It has been previously mentioned that shutting off the switch close to the source can effectively stop the angiogenesis process. To achieve this, growth factors must be prevented from attaching to their receptors.

There are at least 20 known growth factors associated with angiogenesis, each with its own corresponding receptor(s)8. Some of these growth factors include the vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF) and epidermal growth factor (EGF). The type of growth factors produced and their degree of responsiveness to receptors can vary from tumor to tumor. For example, VEGF is highly expressed in solid tumors-- such as in breast cancer, gliomas, and gastrointestinal cancer-- and attaches to the receptor fetal liver kinase-1 (Flk-1), among other receptors. By interfering with the stimuli at the receptor site, VEGF-RTK inhibitors can stop further tumor growth in these types of cancer.

The studies on Philinopside A determined that it is able to stop the signaling caused by the binding of VEGF, FGF, PDGF and EGF to their corresponding receptors (Flk-1, FGFR-1, PDGFR-b, and EGFR, respectively). Two other angiogenesis inhibitors, PD153035 and SU5416, were also tested. Results indicate that PD153035 inhibits the EGF receptor (EGFR) alone. Similarly, SU5416, manufactured by Pfizer, only inhibits the Flk-1 tyrosine kinase. It was concluded that because growth factors tend to critically overlap, inhibition of one RTK alone might not be enough to sufficiently block RTK signaling. Philinopside A, with its inhibition of all four tested RTKs, might possibly prove to be a more effective RTK inhibitor than other compounds. And with a lethal dose (LD50) of 625 mg/kg orally in mice, it might also be a safer alternative than chemotherapy and/or radiation7.

The inhibition of angiogenesis now seems like the most logical and valuable tool in the fight against cancer. Yet when it was first hypothesized in 1971 by Dr. Judah Folkman that tumor growth depends on new blood vessel formation, it was considered heresy by scientists9. Through continuing research by him and others who believed in his hypothesis, angiogenesis inhibition has been firmly established as an innovative cancer therapy and has led to the development of angiogenesis and RTK inhibitor drugs-- collectively known as targeted therapies-- by various pharmaceutical companies worldwide.

In 2004, the first angiogenesis inhibitor drug was approved for use in the United States. Although not the first targeted therapy drug approved, Avastin (bevacizumab), is the first drug proven to actually delay tumor growth by targeting the VEGF tyrosine kinase, which is mainly responsible for vascular growth. Manufactured by Genentech, Avastin works in combination with standard chemotherapy drugs like the Saltz regimen (a combination of three drugs: irinotecan, 5-FU and leucovorin). Patients who received both Avastin and the Saltz regimen were found to survive 5 months longer than those who received the Saltz regimen alone10.

Although Avastin is technically the first angiogenesis inhibitor, there are other drugs that belong to a class called tyrosine kinase inhibitors (or RTK inhibitors). Unlike Avastin, these drugs have not been shown to starve tumors and induce apoptosis. Rather they interfere with the growth factor-to-receptor signaling that facilitates the proliferation of the cancer. In a way, they indirectly influence angiogenesis inhibition. Gleevec (imatinib mesylate) is a drug manufactured by Novartis used to chronic myeloid leukemia (CML) by blocking the Bcr-Abl tyrosine. In studies, patients have a 76% response rate to Gleevec compared to interferon, the standard CML treatment, which has a 12% response rate. Gleevec also works as a PDGFR inhibitor for the treatment of gastrointestinal stromal tumors (GIST), a rare form of stomach cancer. Additional studies have found that within two years of using Gleevec, GIST patients develop a 75% resistance to it11.

Three other RTK inhibitor drugs, Tarceva (erlotinib), Iressa (gefitinib) and Erbitux (cetuximab), block the EGF tyrosine kinase. The first two are used to treat non small cell lung carcinoma (NSCLC) while Erbitux is indicated for advanced colorectal cancer. Tarceva, manufactured by OSI Pharmaceuticals, was found to have an overall survival of 6.7 months12. Both Iressa, manufactured by AstraZeneca, and Erbitux, manufactured by Imclone Systems, have not been shown to prolong survival although some patients have responded to the treatment. In clinical trials, Iressa caused significant tumor shrinkage in about 10% of lung cancer patients13. Erbitux produced a 10.8% tumor response rate among colorectal cancer patients14.

These are just examples of a growing class of drugs that can be collectively called "smart bombs" -- a reference to the selective way these drugs target cancer cells and minimize damage to healthy cells15. And now this term not only refers to synthetic drugs but to naturally occurring compounds like philinopside A in special sea cucumbers as well. Based on evidence just presented, philinopside A may be a more relevant cancer therapeutic agent than the enumerated drugs because of its dual role as an anti-angiogenic agent and RTK inhibitor.

In its function as an angiogenesis inhibitor, philinopside A has been shown to inhibit cell proliferation, cell migration and tube formation -- three of the most important stages in angiogenesis. Evidence also suggests that treatment with philinopside A caused tumor shrinkage and apoptosis without any effect on normal cells. This is the very essence of targeted therapy: confining the treatment to the diseased area.

Philinopside A's broad range of RTK inhibitory effect is an important factor that makes it potentially more effective than Gleevec, Iressa, Erbitux or Tarceva. Angiogenesis is a complex process that likely involves multiple RTK signaling pathways. Inhibition of one RTK, therefore, may not be able to fully suppress angiogenesis. A concrete example to illustrate this point is the inhibitory effect of Gleevec on GIST patients. In approximately 10% of GIST cases that are attributed to abnormal PDGF tyrosine kinase signaling, Gleevec has been shown to have favorable results. More recent studies, however, have found that after a year or two of treatment, these GIST patients develop resistance to it. There may be other factors that lead to the drug resistance but a prevailing theory is that inhibiting PDGFR alone may not be enough to stop the tumor from growing. A Pfizer drug, Sutent (also known as SU11248), currently in clinical trials, has been shown to benefit 65% of GIST patients resistant to Gleevec. Although Gleevec and Sutent are both RTK inhibitors, Sutent targets several more RTKs than Gleevec: VEGFR, PDGFR-µ and PDGFR-b, Flt3 and C-kit16. This suggests that therapies that target a wide range of RTKs will provide more effective and long-term anti-angiogenic effects than those that target a limited number of growth factor receptors.

Similarly, philinopside A's inhibition of four different RTKs (Flk-1 or the VEGF receptor, FGFR-1, PDGFR-b , and EGFR) puts it in a very viable position as a more robust RTK inhibitor than drugs of a similar function. And with strong evidence of philinopside A's inhibition of angiogenesis and induction of apoptosis, sea cucumbers are a very promising natural cancer therapy alternative to current conventional cancer treatments-- able to potentially block all five important processes involved in cancer: angiogenesis, apoptosis inhibition, proliferation, invasion and metastasis.

REFERENCES

INSIDE THIS ISSUE:

Friday, Saturday, Sunday July 29, 30, & 31, 2005

INSIDE THIS ISSUE:

A Call For Validated Research Papers
Dealing With Alternative/Naturopathic Health Care 

? Are you a Natural Health Care Professional with a Research paper or Article that you would like to publish?

? Are you a Naturopathic or Natural Health Care student with an excellent class project / or thesis?

? Are you an instructor teaching the most current natural healthcare skills?

The ANMA Monitor is a widely distributed newsletter to healthcare professionals and naturopathic students. If you would like to submit an article, or know of someone that would be interested, now is the time to do so!

You are invited to submit an article or case study to be featured in the ANMA Monitor.

The ANMA Monitor is published quarterly by ANMA, P.O. Box 96273, Las Vegas, Nevada 89193 (702) 897-7053. Deadlines for articles and advertisements are November 20, March 20, June 20, and September 20 . Please submit articles on a IBM compatible 3.5" disk or by e-mail to webmaster@anma.com, clearly identified as an article for the ANMA Monitor. The editor reserves the right to edit any portion of an article before publishing. The editor also reserves the right to refuse articles which he deems inappropriate for this publication.

We appreciate those who have already sent in articles.

Take advantage of this opportunity to be in print!