Archive for the ‘Nutrition and Cancer’ Category

Substance in greens shrinks cancer again

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Posted 19 May 2012 — by James Street
Category apigenin, Breast Cancer

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A University of Missouri researcher has once again found that a natural substance extracted from celery and parsley can shrink a type of aggressive breast cancer.

A year ago, Salman Hyder, a professor of biomedical sciences, discovered that rats exposed to the substance, apigenin, experienced significant delays in tumor formation compared to those that weren’t exposed.

This time around, his study used human cells that were injected into mice.

In the study, Hyder and his research team implanted cells of a deadly fast-growing breast cancer and then treated some of the mice with a common hormone therapy that’s known to cause cancer cells to grow more aggressively. Among that group, some mice were then given apigenin.

Cancerous tumors grew rapidly in mice that did not receive apigenin, but those treated with the substance saw cancer growth drop to the same rate of the control group that never received the hormone treatment.

“We don’t know exactly how apigenin does this on a chemical level,” Hyder said in a statement. “We do know that apigenin slowed the progression of human breast cancer cells in three ways: by inducing cell death, by inhibiting cell proliferation, and by reducing expression of a gene associated with cancer growth. Blood vessels responsible for feeding cancer cells also had smaller diameters in apigenin-treated mice compared to untreated mice. Smaller vessels mean restricted nutrient flow to the tumors and may have served to starve the cancer as well as limiting its ability to spread.”

In the future, apigenin injections could be a safe alternative to chemotherapy, he said. But Hyder fears funding for clinical testing in humans could be difficult: Because the substance is easy to extract from plants, pharmaceutical companies don’t stand to profit from the treatment.

Reach Janese Silvey at 573-815-1705 or e-mail jsilvey@columbiatribune.com.

Beehive remedy may slow prostate cancer

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Posted 09 May 2012 — by James Street
Category propolis, propolis, propolis, Prostate Cancer

U. CHICAGO (US) — An over-the-counter remedy derived from honeybee hives stalls the growth of prostate cancer cells in mice.

Caffeic acid phenethyl ester, or CAPE, is a compound isolated from honeybee hive propolis, the resin used by bees to patch up holes in hives.

Propolis has been used for centuries as a natural remedy for conditions ranging from sore throats and allergies to burns and cancer. But the compound has not gained acceptance in the clinic due to scientific questions about its effect on cells.

In a paper published in Cancer Prevention Research, researchers from the University of Chicago combined traditional cancer research methods with cutting-edge proteomics to find that CAPE arrests early-stage prostate cancer by shutting down the tumor cells’ system for detecting sources of nutrition.

“If you feed CAPE to mice daily, their tumors will stop growing. After several weeks, if you stop the treatment, the tumors will begin to grow again at their original pace,” says Richard B. Jones, assistant professor in the Ben May Department for Cancer Research and Institute for Genomics and Systems Biology and senior author of the study.

“So it doesn’t kill the cancer, but it basically will indefinitely stop prostate cancer proliferation.”

Natural remedies isolated from plant and animal products are often marketed as cure-alls for a variety of maladies, usually based on vague antioxidant and anti-inflammatory claims.

While substances such as ginseng or green tea have been occasionally tested in laboratories for their medicinal properties, scientific evidence is commonly lacking on the full biological effects of these over-the-counter compounds.

“It’s only recently that people have examined the mechanism by which some of these herbal remedies work,” Jones says. “Our knowledge about what these things are actually doing is a bit of a disconnected hodge-podge of tests and labs and conditions. In the end, you’re left with a broad, disconnected story about what exactly these things are doing and whether or not they would be useful for treating disease.”

To study the purported anti-cancer properties of CAPE, first author Chih-Pin Chuu (now at the National Health Research Institutes in Taiwan) tested the compound on a series of cancer cell lines. Even at the low concentrations expected after oral administration, CAPE successfully slowed the proliferation of cultured cells isolated from human prostate tumors.

CAPE was also effective at slowing the growth of human prostate tumors grafted into mice. Six weeks of treatment with the compound decreased tumor volume growth rate by half, but when CAPE treatment was stopped, tumor growth resumed its prior rate. The results suggested that CAPE stopped cell division rather than killing cancerous cells.

To determine the cellular changes that mediated this effect, the researchers then used an innovative proteomics technique invented by Jones and colleagues called the “micro-western array.”

Western blots are a common laboratory tool used to measure the changes in protein levels and activity under different conditions. But whereas only one or a few proteins at a time can be monitored with Western blots, micro-western arrays allow researchers to survey hundreds of proteins at once from many samples.

Chuu, Jones, and their colleagues ran micro-western arrays to assess the impact of CAPE treatment on the proteins of cellular pathways involved in cell growth—experiments that would have been prohibitively expensive without the new technique.

“What this allowed us to do is screen about a hundred different proteins across a broad spectrum of signaling pathways that are associated with all sorts of different outcomes. You can pick up all the pathways that are affected and get a global landscape view, and that’s never been possible before,” Jones says.

“It would have taken hundreds of Westerns, hundreds of technicians, and a very large amount of money for antibodies.”

The micro-western array results allowed researchers to quickly build a new model of CAPE’s cellular effects, significantly expanding on previous work that studied the compound’s mechanisms.

Treatment with CAPE at the concentrations that arrested cancer cell growth suppressed the activity of proteins in the p70S6 kinase and Akt pathways, which are important sensors of sufficient nutrition that can trigger cell proliferation.

“It appears that CAPE basically stops the ability of prostate cancer cells to sense that there’s nutrition available,” Jones says. “They stop all of the molecular signatures that would suggest that nutrition exists, and the cells no longer have that proliferative response to nutrition.”

The ability of CAPE to freeze cancer cell proliferation could make it a promising co-treatment alongside chemotherapies intended to kill tumor cells. Jones cautioned that clinical trials would be necessary before CAPE could be proven effective and safe for this purpose in humans. But the CAPE experiments offer a precedent to unlock the biological mechanisms of other natural remedies as well, perhaps allowing these compounds to cross over to the clinic.

“A typical problem in bringing some of these herbal remedies into the clinic is that nobody knows how they act, nobody knows the mechanism, and therefore researchers are typically very hesitant to add them to any pharmaceutical treatment strategy,” Jones says.

“Now we’ll actually be able to systematically demonstrate the parts of cell physiology that are affected by these compounds.”

Research was supported by grants from the Cancer Research Foundation, American Cancer Society, National Institutes of Health, U.S. Department of Health, and National Science Council.

More news from the University of Chicago: http://news.uchicago.edu/

Obama betrays the left; cheers continued expansion of drug war, criminalization of plant-based medicine

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Posted 16 Apr 2012 — by James Street
Category Finance and Politics of cancer research and treatment, Legal, Marijuana

 

 

(NaturalNews) If you happen to need even more evidence that President Obama has gutted his campaign promises and betrayed not only the left but also African Americans who enthusiastically supported his election, he has just gone public with his support for the continued war on drugs. Keeping marijuana criminalized, it seems — and keeping more African Americans in prison — is a top priority for the Obama administration.

This means Obama supports the midnight DEA raids on our citizenry; the filling of prisons with small-time pot smokers; the disproportionately punitive sentences handed down to black men and women across America who aren’t really criminals at all… they merely suffer from a chemical addiction that would more rightly be considered a medical issue.

Nearly every country in Latin America has now openly and publicize recognized that the so-called “war on drugs” is a complete and total failure. But Obama thinks it’s just great! Fill the prisons! Prosecute more blacks! Buy more guns and night vision gear for the DEA! That’s what Obama’s America stands for, it seems.

“I personally and my administration’s position is that legalization is not the answer,” Obama said just hours before the meeting of Latin American leaders at the Convention Centre in Cartagena, Colombia, for the Americas Summit (http://www.bbc.co.uk/news/world-latin-america-17716926). Meanwhile, Obama’s top Secret Service agents and military commanders were banging Colombian whores in the background, then refusing to pay them their $47 prostitution fee. (http://www.naturalnews.com/035580_Secret_Service_Colombia_prostitutes…) Obama had “no comment” on that particular issue.

Let’s get real about all this. Marijuana prohibition simply doesn’t work. At least not for reducing crime and drug addiction. Anyone who thinks prohibition works is completely delusional. But it does work for certain special interests. What are those special interests, anyway?

Who BENEFITS from the continued criminalization of marijuana?

If you really want to know why prohibition remains in place with marijuana, it’s simple to find out why. Just ask yourself “Who benefits?”

• The DEA. Without a drug “problem,” the DEA won’t get hundreds of millions of dollars worth of increases in operating budgets from the federal purse strings. If drugs were decriminalized, the DEA would have to be sharply downsized (which would be a great thing for liberty and safety but a terrible thing for the DEA honchos).

• Private prisons. Thanks to illegal agreements between prison operators and state governments, prisons can put prisoners to work at slave labor wages — just a few cents an hour — manufacturing goods that the corporate prison owners sell for pure profit. If you thought the Nike sweatshops in Asia were bad, go visit a prison in the USA some time and watch the slave labor taking place right here at home.

• Local police. The “drug war” is the excuse that local police departments use to receive more grant money for weapons, assault gear and now even armored assault vehicles to be used against the citizens. Without the drug war excuse, all this grant money disappears and these cops have to go back to actually serving the community instead of bashing in doors like a bunch of cocaine cowboys.

• The government drug runners! It’s now a well-known fact that the ATF, DEA and other government agencies are all heavily involved in running drugs across America. Just Google any of these terms if you want to check it out for yourself. The ATF is even engaged in money laundering through the globalist banks. This is why government crackdowns on drugs are highly selectively — drug raids are really just a way to eliminate the competition so that the biggest drug dealer of all — the government itself — can continue to rake in the maximum profits. Legalizing drugs would obviously cause street prices to collapse, sucking all the profits out of the government-run drug business.

• Local District Attorneys and prosecutors. Without the drug war to give them a juicy field of easy targets to prosecute, their careers would take a huge hit. It’s so much harder to arrest real criminals than to go after pot smokers and raw milk farmers, isn’t it? Gee, imagine the difficulty of actually fighting REAL crime for a change?

• Big Government. The entire government benefits from the continued criminalization of drugs. For starters, it establishes the outrageous precedent that government can outlaw a native plant — even a plant that has grown wild across North America for hundreds of years. This alone is an outrageous encroachment on fundamental human freedom. Beyond that, the government can always point to “drug violence” as another excuse to squash our freedoms and put in place a tyrannical police state. It’s all “for your own good,” of course. Isn’t it always?

• Big Pharma and the hospital industry. Because recreational drugs are illegal, they’re often cut with dangerous chemicals that cause liver damage and kidney damage. This results in yet more repeat business for hospitals and the drug industry. If street drugs were legalized, they would be standardized and regulated, and adulteration of those products would be extremely rare. They would be safer to use, in other words, which is exactly what the pharmaceutical industry is dead set against. They only make money when people are damaged or sick from using street drugs concocted in somebody’s trailer.

Who LOSES from the drug war? You!

So we’ve covered the beneficiaries of the drug war, but who loses from it? You do, of course: Your liberties, freedoms, tax dollars and personal safety are all threatened by the existence of the war on drugs. Decriminalizing and regulating these drugs would have an enormously positive impact on you and your life.

If drugs were decriminalized, here’s what would happen:

• Drug gangs would vanish as their source of revenues (illegal drugs at black market prices) dry up.

• Drug-related crime would sharply fall.

• State revenues would skyrocket from the regulated sale of legalized marijuana.

• The corrupt prison industry would collapse to perhaps only 25% of its current size.

• Your personal safety and security would be greatly enhanced due to the lack of drug violence, shootings, home invasions and more.

• Mexican drug gangs would lose their power base, resulting in a sharp drop in crime along the border.

• Former “criminal” pot smokers would once again become taxpaying members of the workforce, contributing to the financial upkeep of society rather than draining it as prisoners.

• The happiness index across society would sharply rise.

Even the Red Cross says decriminalize marijuana

It’s all pure economics, my friends. Cause and effect. Legalize recreational drugs and you end the violence, the crime, the prison system overload and the entire underground market for the stuff.

It’s all so obvious that even the Red Cross has called for decriminalization (http://copssaylegalize.blogspot.com/2012/03/red-cross-calls-for-drug….).

At the same time, countless members of the FBI, DEA and active-duty police organizations are also openly calling for decriminalization (http://www.leap.cc/).

The rational argument for ending prohibition is further detailed at www.Norml.org

There are no rational reasons for keeping marijuana criminalized. There are only political reasons for doing so. That’s why Obama continues to support the irrational war on drugs — because it’s a political issue.

Obama, the betrayer of the political left

Obama, of course, is a teleprompter-reading puppet of the global elite. He does what they tell him to do, and right now they’re telling him to keep pushing Drug War propaganda because it’s a highly effective way to expand the police state and keep people living in fear while denying them access to plant-based medicine.

Obama, it turns out, has betrayed the left so many times I can hardly keep count: He supports the GMO industry, he signed the NDAA which expands secret arrests and secret Gitmo-style prisons, he’s an opponent of farm and food freedom (http://www.naturalnews.com/035301_Obama_executive_orders_food_supply….) and he has proven himself to be nothing more than a big business operative who defends the status quo while preaching “hope and change” that he never delivers.

Obama has assaulted free speech, due process (http://www.naturalnews.com/034537_NDAA_Bill_of_Rights_Obama.html), medical freedom and parental rights. In doing so, he has betrayed many of the top priorities of the very people who once put him into office.

He wants to keep marijuana criminalized because that’s what the police state fascist system of corporate control wants.

Of course, this doesn’t mean the alternatives we’re given are going to be any better. This is not some pitch for Romney, for God’s sake. That guy is just as much of a corporate sellout as Obama (and Bush before him). Elections are created to present the illusion that the People have a choice when, in reality, all they’re voting for is which color of puppet they want to see on television while we’re all being imprisoned, exploited, enslaved and oppressed by a growing fascist state.

Care to guess which candidate would have decriminalized marijuana from the get-go? His name is Ron Paul, and the ideas of freedom and liberty that he espouses are the real answer for the future of our nation. No matter who shows up in the ballot box this November, Ron Paul is my President, because he’s the only candidate who is deeply committed to legalizing freedom in America.

Folate Receptor-Targeted Antioxidant Therapy Ameliorates Renal Ischemia-Reperfusion Injury.

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Posted 16 Mar 2012 — by James Street
Category Antioxidants, Hypoxia, Kidney
J Am Soc Nephrol. 2012 Jan 26. [Epub ahead of print]

Source

*Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;

Abstract

Antioxidant therapy can protect against ischemic injury, but the inability to selectively target the kidney would require extremely high doses to achieve effective local concentrations of drug. Here, we developed a directed therapeutic that specifically targets an antioxidant to renal proximal tubule cells via the folate receptor. Because a local increase in superoxide contributes to renal ischemic injury, we created the folate-antioxidant conjugate 4-hydroxy-Tempo (tempol)-folate to target folate receptors, which are highly expressed in the proximal tubule. Dihydroethidium high-performance liquid chromatography demonstrated that conjugated tempol retained its efficacy to scavenge superoxide in proximal tubule cells. In a mouse model of renal ischemia-reperfusion injury, tempol-folate reduced renal superoxide levels more effectively than tempol alone. Furthermore, electron spin resonance revealed the successful targeting of the tempol-folate conjugate to the kidney and other tissues expressing folate receptors. Administration of tempol-folate protected the renal function of mice after ischemia-reperfusion injury and inhibited infiltration of macrophages. In conclusion, kidney-specific targeting of an antioxidant has therapeutic potential to prevent renal ischemic injury. Conjugation of other pharmaceuticals to folate may also facilitate the development of treatments for other kidney diseases.

Woman with brain tumor says she was kicked out of hospital for using medical marijuana

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Posted 14 Mar 2012 — by James Street
Category Cannabis, Ethics of Physicians, Ethics of Science, Finance and Politics of cancer research and treatment, Legal

View more videos at: http://nbcbayarea.com.

By Cheryl Hurd, NBCBayArea.com

SAN FRANCISCO — A medical marijuana celebrity with a brain condition said a local hospital kicked her out after she attempted to use medical marijuana inside.

Angel Raich, who fought for the right to use medical cannabis in a case that went to the U.S. Supreme Court in 2004 and 2005, talked to us outside of UCSF Medical Center in San Francisco moments after she said they booted her out.

“The pharmacist says ‘you’re not allowed to have cannabis in this hospital,’” Raich said. “‘And if you’re gonna try to have cannabis in this hospital we’re going to call the feds.’”

Raich said she checked into the hospital Monday morning for doctor-ordered tests on her brain. She suffers from chronic pain and seizures from an inoperable brain tumor and doctors didn’t give her very long to live, she said.

“You’re basically saying if I stay it’s like giving me a death sentence ’cause I’d have to be without my cannabis,’” Raich said she told a hospital employee.

Raich said she had no choice but to leave the hospital.

“I’m in a state university hospital in the state of California,” Raich said. “I have the right to have the same medical care as any other patient does.”

UCSF Medical Center released the following statement:

“UCSF is a smoke-free campus and this includes medical marijuana. Several members of the media have asked if UCSF allows the use of a vaporized form of marijuana. It does not. Even a vaporized form of medical marijuana releases particles in the air that are damaging to the lung. Any particles from vapor and odor could have an impact on other patients and hospital employees.

Under federal and state law, a physician is at legal risk related to any activity that could be construed as prescribing medical marijuana to a patient.”

During our interview with Raich, she appeared to have a seizure. When the fire department and paramedics arrived, Raich refused to return to UCSF. Instead, they took her to St. Mary’s Hospital.

Modified Citrus Pectin

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Posted 13 Mar 2012 — by James Street
Category Modified Citrus Pectin (MCP)
Inhibition of Cancer Cell Growth and Metastases 

By Jim English and Ward Dean, MD

Pectin is a complex carbohydrate (polysaccharide) found in virtually all plants. Pectin helps to bind cells together and provides a structural framework for maintaining the shape and integrity of cell membranes. Recently, a modified form of citrus pectin derived from the pulp and peel of citrus fruits has been shown to attach to cancer cells to prevent them from spreading throughout the body, pointing the way to a potentially safe approach for preventing or reducing cancer metastases.

Spreading Metastases

Conventional cancer treatment involves surgery to remove primary tumors, followed by chemotherapy, radiation, or a combination of treatments designed to eradicate all remaining traces of cancer. This follow-up therapy is critical for addressing the biggest threat from cancer – the formation of secondary cancers, or metastases. Metastases are not new or different cancers, but new cancer colonies started from cells that have migrated to new sites. Sites where metastases commonly occur include the bones, lungs, prostate, kidney, liver, thyroid and brain. Left unchecked, metastases can quickly overwhelm the body’s defenses. In fact, it is metastases, not primary tumors that are responsible for most cancer deaths.

Halting Metastases

Over the last two decades, research into controlling or halting cancer metastases has led to two promising new strategies. The first, antiangiogenesis, targets the growth of new blood vessels (angiogenesis) that are required for tumor growth. Originally pioneered by noted cancer researcher Dr. Judah Folkman, antiangiogenesis grew from his observation that tumors cannot grow without access to a constant supply of new blood vessels. Folkman theorized that cancer cells actively communicate with surrounding tissues to trigger the growth of new blood vessels (neovascularization) needed to supply nutrients and remove waste products. Once neovascularization is initiated, hundreds of new capillaries converge on the tumor site and are quickly coated with new layers of rapidly dividing tumor cells.

Folkman also theorized that, just as certain chemical messengers can initiate new capillary formation, other signals could inhibit neovascularization. This insight led to the development of antiangiogenic therapy, which, in contrast to other cancer treatments, doesn’t directly destroy tumors, but aims to limit their blood supply, causing tumors to shrink. By 1997 researchers were excited by promising results from several antiangiogenic drugs. Speaking of one early angiogenesis inhibitor called TNP470, in 1997 Folkman commented on the results of early clinical human trials, stating, “We’ve not seen a tumor that we cannot regress (shrink).” Currently TNP470 and several other angiogenesis inhibitors are in clinical trials, and other promising compounds are under study in university laboratories and in some 30 pharmaceutical and biotechnology companies around the world. For more information on nutritional compounds that have been shown to help inhibit new capillary growth and reduce angiogenesis refer to “Nutritional Support for Cellular Mutagenic Concerns”.

Intercepting Cancer Cells

The second strategy for controlling metastases works by intercepting migrating cancer cells before they have a chance to establish new tumors. This approach targets a family of carbohydrate-binding proteins called lectins. Lectins are attracted to sugar molecules found on the surface of almost all cells. Lectins help cancer cells stick together to form multi-celled clusters that are believed to be necessary for metastases formation. Lectins also enable cancer cells to communicate with each other, as well as with other types of cells (cell-to-cell communication) to trigger cellular transformations that assist the spread of cancer. One class of lectin – called galectins (for galactoside-binding lectins) – possesses an especially strong affinity for galactose, a simple sugar located on the surface of cells lining blood vessels.

A number of cancer researchers have focused on a particular galectin – galectin-3 – that has been found to be directly involved in the progression and spread of several types of cancers, including breast, prostate and colon cancer. Serum levels of galectin-3 correlate closely with the spread of cancer, and may serve as a biological marker to help physicians and patients monitor the efficacy of anti-cancer therapies.

The Protein-Sugar Connection

The powerful attraction between galectins and galactose plays a pivotal role in how cancers spread in the body. After a cancer cell has broken free from its primary tumor (or is accidentally dislodged during surgery) it floats freely through the blood and lymph systems until it eventually becomes trapped in a small blood vessel (microcapillary). Firmly lodged in the microcapillary, galectins on the surface of the cancer cell start to bind to galactose receptors on endothelial cells (the cells that form the inside lining of blood vessels). After securely attaching to the endothelium the cancer cells penetrate through the blood vessel walls. The final step after invading the vessel involves the release of chemical signals that trigger new blood vessel growth (angiogenesis), and a new tumor colony is firmly established.

Modified Citrus Pectin

Modified citrus pectin (MCP) is a unique dietary fiber that is produced by processing natural citrus pectin by altering its pH and splitting the carbohydrate chains to form a low molecular-weight, water-soluble fiber that is rich in the sugar, galactose. It is this presence of particularly high amounts of galactose that led researchers to wonder if MCP might bind with proteins (lectins) on cancer cells to inhibit their ability to bind with other tissues.

Early test tube studies revealed that MCP did indeed bind to galectins from numerous human cancer cell lines to inhibit their ability to adhere to other cells. Researchers found that as little as a 1.0 percent solution of MCP inhibited attachment of 1) human prostate adenocarcinoma cells, 2) human breast carcinoma cells, 3) human melanoma cells, and 4) human laryngeal epidermoid carcinoma cells to human endothelial cells. (Naik H, et al.)

In 1992, Platt and colleagues demonstrated that MCP was effective at reducing metastases in mice injected with live melanoma cells. One group of mice was injected with normal melanoma cells, while a second group received melanoma cells that had been incubated in a solution containing MCP. Seventeen days after being injected, the mice receiving untreated melanoma cells were found to have, on average, 33 new tumors (metastases) in their lungs, while the mice receiving the MCP-treated cells had virtually no lung tumors. The researchers hypothesized that MCP had successfully attached to the lectin sites on the cancer cells, blocking the receptors and rendering them incapable of attaching to other cells.

In a second study conducted in 1995, Pienta and colleagues demonstrated that adding MCP to drinking water was an effective delivery route for reducing experimental metastases in rats. Four days after injecting rats with live prostate cancer cells, the animals were divided into three groups. Two groups of rats were treated with MCP added to their drinking water in amounts of 0.1% and 1.0%. The animals in the third group, the control, received no MCP. Thirty days after being injected with one million active prostate cancer cells, 15 out of 16 rats in the control (untreated) group had cancer metastases in their lungs, compared with 7 of 14 rats in the 0.1% group, and 9 of 16 in the 1.0% group. Importantly, the 1.0% group had, on average, only one tumor per animal, versus an average of nine tumors in the lungs of the control group. Commenting on the results of the study the researchers noted that oral intake of modified citrus pectin acts as a “potent inhibitor of spontaneous prostate cancer metastasis…”

MCP Exhibits Antiangiogenesis Activity

A paper published in the December 2002 issue of the Journal of the National Cancer Institute found, as with earlier studies, that MCP significantly reduced both the incidence and the size of tumors in rats injected with human breast cancer and colon cancer cells (Fig. 1). Additionally, in vitro experiments demonstrated that MCP inhibited formation of capillaries, demonstrating that MCP possesses antiangiogenic properties. Of their findings, the researchers concluded that, “MCP, given orally, inhibits carbohydrate-mediated tumor growth, angiogenesis, and metastasis in vivo, presumably via its effect on galectin-3 function. These data stress the importance of dietary carbohydrate compounds as agents for the prevention and/or treatment of cancer.”

Conclusion and Dosage Recommendations

There are unfortunately no clinical studies that we are aware of to confirm the efficacy of Modified Citrus Pectin as an anti-cancer substance in humans. Nevertheless, we believe that because of its absolute lack of toxicity in any amount, its demonstrated efficacy in reducing the incidence and size of tumors in experimental animals, and its potential anti-cancer mechanisms as demonstrated in a number of in vitro models, Modified Citrus Pectin should be considered as a key part in any preventive or therapeutic regimen for any type of cancer. Dosage is also speculative, but based on the animal studies, we believe that a dosage of five grams per day may provide significant preventive or therapeutic benefits.

References

1. Al-Mehdi AB, et al. Intravascular origin of metastasis from the proliferation of endothelium-attached tumor cells: a new model for metastasis. Nat Med 2000;6:100–2.
2. Beuth J, et al.. Inhibition of liver tumor cell colonization in two animal tumor models by lectin blocking with D-galactose or arabinogalactan. Clin Exp Metastasis 1988;6:115–20.
3. Hartwell DW, Butterfield CE, Frenette PS, Kenyon BM, Hynes RO, Folkman J, et al. Angiogenesis in P- and E-selectin-deficient mice. Microcirculation 1998;5:173–8.
4. Hayashi A, Gillen AC, Lott JR. Effects of daily oral administration of quercetin chalcone and modified citrus pectin. Altern Med Rev 2000;5:546–52.
5. Hensel A, Meier K. Pectins and xyloglucans exhibit antimutagenic activities against nitroaromatic compounds. Planta Med 1999;65:395–9.
6. Hsieh TC, Wu JM. Biochem Mol Biol Int 1995;37:833–41.
7. Inohara H, Raz A. Effects of natural complex carbohydrate (citrus pectin) on murine melanoma cell properties related to galectin-3 functions. Glycoconj J 1994;11:527–32.
8. Inufusa H, Nakamura M, Adachi T, Aga M, Kurimoto M, Nakatani Y, et al. Role of galectin-3 in adenocarcinoma liver metastasis. Int J Oncol 2001;19:913–9.
9. Meromsky L, Lotan R, Raz A. Cancer Res 1986;46:5270–5.
10. Naik H, et al. Proc Annu Meet Am Assoc Cancer Res; 36:A377 1995.)
11. Nangia-Makker P, Baccarini S, Raz A. Carbohydrate-recognition and angiogenesis. Cancer Metastasis Rev 2000;19:51–7.
12. Nangia-Makker P, et al. Galectin-3 induces endothelial cell morphogenesis and angiogenesis. Am J Pathol 2000;156:899–909.
13. Nangia-Makker P, et al. The role of galectin-3 in tumor metastasis. In: Lectins and pathology. London (U.K.): Taylor & Francis, Inc.; 2000.
14. Pienta KJ, Naik H, Akhtar A, Yamazaki K, Replogle TS, Lehr J, et al. Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. J Natl Cancer Inst 1995;87:348–53.
15. Platt D, Raz A. Modulation of the lung colonization of B16-F1 melanoma cells by citrus pectin. J Natl Cancer Inst 1992;84:438–42.
16. Pratima Nangia-Makker, Victor Hogan, Yuichiro Honjo, Sara Baccarini, Larry Tait, Robert Bresalier, Avraham Raz. Inhibition of Human Cancer Cell Growth and Metastasis in Nude Mice by Oral Intake of Modified Citrus Pectin. J Natl Cancer Inst, Vol. 94, No. 24, December 18, 2002
17. Raz, A., & Lotan, R. “Endogenous galactoside-binding lectins: A new class of functional tumor cell surface molecules related to metastasis,” Cancer Metastasis Rev, 6: 433-52, 1987.
18. Smith-Barbaro P, Hanson D, Reddy BS. Carcinogen binding to various types of dietary fiber. J Natl Cancer Inst 1981;67:495–7.
19. Taper HS, Delzenne NM, Roberfroid MB. Growth inhibition of transplantable mouse tumors by non-digestible carbohydrates. Int J Cancer 1997;71:1109–12.
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Breakthrough Cancer Research Presented at Naturopathic Oncology Conference

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Posted 11 Mar 2012 — by James Street
Category Galectin, Honokiol, Modified Citrus Pectin (MCP)

press release

March 6, 2012, 5:13 a.m. EST

CAREFREE, Ariz., Mar 6, 2012 (GlobeNewswire via COMTEX) — Isaac Eliaz, M.D., M.S., L.Ac., distinguished medical doctor and researcher, presents Galectin-3 as a breakthrough biomarker for numerous life-threatening diseases. He also shared new research on the critical role of Modified Citrus Pectin (MCP) as the foremost Galectin-3 blocker. Dr. Eliaz’s latest presentation was given to hundreds of integrative oncologists during the Oncology Association of Naturopathic Physician’s 2012 Convention (OncANP).

OncANP is one of the largest naturopathic organizations with members who specialize in the treatment of cancer. A major focus of the association’s mission is to provide advanced training in the practice of naturopathic oncology for its membership and by doing so to improve the quality of care and patient outcome.

“It’s truly rewarding to share cutting edge research with the medical community, demonstrating Modified Citrus Pectin’s ability to promote health and prevent disease,” says Dr. Eliaz. Modified Citrus Pectin offers remarkable health benefits, which includes binding and blocking excess Galectin-3 molecules throughout the body.

Role of Galectin-3 Molecules

Galectin-3 is produced naturally by our bodies, but new research proves that elevated levels can lead to serious health conditions like heart disease, fibrosis and metastatic cancer. By binding to and blocking excess Galectin-3 molecules, Modified Citrus Pectin prevents Galectin-3 from wreaking havoc on our bodies. A new blood test that measures circulating levels of Galectin-3 as a risk factor in progressive heart failure is now approved by the FDA and covered by most health insurance. This test can also help to determine risks of damage in other organs, including the liver, lungs, brain, kidneys, and others, as well as the progression of cancer.

Versatile Health Benefits of MCP

Recent studies also demonstrate that Modified Citrus Pectin enhances immune function, and reduces galectin-3 expression and disease severity in kidney injury. MCP is also proven to remove lead, mercury, arsenic and cadmium, without reducing essential minerals. “When the toxic burden is high, I recommend a gentle, yet highly effective heavy metal detoxification program using Modified Citrus Pectin,” says Dr. Eliaz.

In addition, groundbreaking new research proves Modified Citrus Pectin (MCP) works synergistically to inhibit aggressive cancer cell behavior, when combined with two of Dr. Eliaz’s advanced poly-botanical formulas: one for breast health and one for prostate health. This study was presented at the last Experimental Biology meeting and is presently in press for publication.

“The findings are extremely promising! Researchers have shown that MCP, in combination with either the breast or prostate formula, significantly further inhibits the metastatic processes of adhesion and migration of breast and prostate cancer cells, in a dose dependant manner,” says Dr. Eliaz.

Honokiol For Cancer, Antioxidant and Anxiety Support

Research presented during Dr. Eliaz’s lecture shows Honokiol has multiple health benefits ranging from anti-cancer and anti-oxidant, to a calming effect. Honokiol is extracted from the bark of the Magnolia tree and is safe to use with conventional cancer therapies. It also works synergistically with Modified Citrus Pectin for increased anti-cancer support.

The new discoveries give Modified Citrus Pectin greater potential in the prevention and treatment of many serious health conditions for which there are currently limited or no treatments available. For more information on Modified Citrus Pectin and the Poly-Botanical Formulas, contact (707) 583-8622 or e-mail info@betterhealthpublishing.com.

About Better Health Publishing

Better Health Publishing (BHP) focuses on the publication of key works promoting health and wellness. BHP believes that education and accessible information are the core components of a healthy and sustainable society.

For Media Questions/Interviews with Dr. Isaac Eliaz, Contact:

Amy Pellegrini Communications Specialist Better Health Publishing amy@dreliaz.org (707) 583-8622

This news release was distributed by GlobeNewswire, www.globenewswire.com

SOURCE: Better Health Publishing

This information was brought to you by Cision http://www.cisionwire.com http://www.cisionwire.com/better-health-publishing/r/breakthrough-cancer-research-presented-at-naturopathic-oncology-conference ,c9227939

Fundraiser planned for unexpected cancer survivor

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Posted 11 Mar 2012 — by James Street
Category Complementary and Alternative Medicine, Gerson Diet, Gerson Diet, Local Recurrence, Lung Metastases, Metastases, Osteosarcoma
by Kelli Easterling

16-year-old Jonathan Hernandez has been battling metastic osteosarcoma, bone cancer that doctors said had spread to his lungs, for about two years.

When he was diagnosed, doctors told his parents that the cancer was in an advanced stage and that the prognosis was typically very poor, according to his mother, Diana Janica, a Spanish teacher at Richmond Senior High School.

“The doctors told us that if he received chemotherapy treatment, he would maybe live for two years,” said Janica. “After that, it was likely his kidneys and liver would shut down.”

Janica’s husband, Pablo Hernandez, discovered a unique treatment option when talking to his sister, a doctor in Columbia, South America.

She told the frantic parents about the Gerson Institute. The Institute uses a whole-body approach to healing that supposedly boosts the body’s immune system, and other defenses, to cure cancer, arthritis, heart disease and allergies.

Since their son had only a small chance of surviving the chemo treatments, the couple decided they had to go out on a limb and try something different than they were being offered at the hospitals.

“They were basically telling me he was going to die, but that he should do chemotherapy anyway,” said Janica.

The Gerson Diet is high in vitamins, minerals and fluids, and low in sodium and fats. The typical daily diet consists of three full vegetarian meals and 10-13 glasses of fresh raw juice. All ingredients must be organic, fresh and washed in distilled water, to avoid excess fluoride exposure. The diet is supplemented with things like niacin, potassium compound and flax seed oil. The strictest form of this diet will continue for two to four years.

It is a very demanding program to stick with. On top of the sometimes outrageous costs of purchasing fresh, organic produce, the juice has to be made fresh, every hour from 8 a.m.-7 p.m. This means his father stays home with him during the day, and works at night once his mother is home from school.

Today, Jonathan’s mother is happy to report that Jonathan’s cancer is officially shrinking.

“We went to Chapel Hill December 29 and the oncologists said the lesions in his lungs are getting smaller,” said Janica. “His bone cancer is regressing. They told me when he was diagnosed that he should be dead by now! We are so happy. This type of cancer does not usually get smaller – this is amazing. For the first time, the oncologist did not mention chemotherapy.”

Jonathan reported that he has been seeing his doctor every three months, but now the doctors have told him his appointments can be scheduled six months apart.

“That means I’m doing really good,” he said. “My breathing is at 100 percent now. And I’ve gotten a lot taller – I’m almost six feet tall now.”

Jonathan is home schooled because he has a weaker immune system and can’t take the risk of being exposed to germs.

“I miss school a lot because I have to figure out a lot of the work on my own,” he said. “I’d like other kids to know that they’re lucky to be able to go to class and have their teachers there.”

While health insurance would help with the costs of conventional cancer therapy, it doesn’t acknowledge this type of treatment. The burden of paying about $2,500 a month in supplies fell squarely on the family – until community members stepped in.

Richmond Senior High faculty, staff and students have been there for the family, spreading the word and helping any way they can. Churches and neighbors soon found out about the unique situation and have also been helping along the way.

A new fund raising committee has formed, and is planning an all-day event and barbecue fundraiser for the the boy at Pat’s Kitchen, in Rockingham.

“I’m their neighbor, and this is their only child,” said committee member, Susanne McInnis. “My heart just goes out to them. They were brought here as missionaries from their home, and when Jonathan was diagnosed they had no family here to turn to. The community is their family now.”

Pat’s Kitchen hosted a fundraiser for Jonathan last year, and raised $9,700 for Nature’s Own, the supplier of Jonathan’s organic fruits and vegetables.

“We’ve put too much into Jonathan getting better to give up on him now,” said Marshall Berry, co-owner of Pat’s Kitchen. “We’ve been hosting benefits here since we opened for business, and the Lord has blessed us tremendously. We are happy to be able to give back.”

“We’re excited about Jonathan’s progress,” said McInnis. “At one time, he couldn’t breath very good, but recently he was able to play the flute at church.”

Encouraged by Jonathan’s progress over the past two years, McInnis teamed with Sandra Parker, Pam Dillman, Betty Brigman, Debbie Webb, Lisa Britt and Pat Britt to plan another event at Pat’s Kitchen to help pay for Jonathan’s food.

On Saturday, March 24 from 11 a.m. – 5 p.m., Pat’s Kitchen will host a pork barbecue and fried chicken plate sale – dine in or carry out – for $7 per plate.

Delivery is available for orders of five or more.

“Marshall won the Kansas City Cook-off with his barbecue, and his fried chicken won a blue ribbon at the State Fair,” said McInnis.

There will be live entertainers at the restaurant all day, including original member of beach music group O’Kaysions, Ed Dement, singing “I’m a Girl Watcher,” a self-proclaimed cousin of Elvis Presley, doing spot-on impersonations, Brookes and Dunn impersonators, other country music impersonators, gospel singers and beach tunes.

There will be an auction at 5 p.m., hosted by Iron Horse Auction.

Plate tickets are available for sale now at Pat’s Kitchen, or plates can be purchased the day of the event.

Raffle tickets are also available now for $1. A 32” flat-screen television from R.W. Goodman Co. and neighbors and a gas grill will be raffled off March 24 at the event.

“So many businesses have donated for the auction, I can’t even thank them all,” said McInnis.

For more information about the event, or to donate auction items or funding to Jonathan’s cause, contact 910-895-1009, 910-206-1009 or 910-895-0683.

“The Lord is good,” said Janica. “The Lord is teaching us to live by faith, this is an adventure! We are trying to enjoy this time while we are seeing what the Lord has next for Jonathan. This has helped Jonathan to focus on the future and what the Lord has for him in the following hours, days and years. He can really enjoy little details in life as miracles for him now since he did not expect to live this long.”

— Staff Writer Kelli Easterling can be reached at 910-997-3111, ext. 18, or by email at keasterling@heartlandpublications.com.

Curcumin May Support Body’s Ability to Slow Prostate Tumor Growth

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Posted 18 Feb 2012 — by James Street
Category Androgren Deprivation, CPB, CURCUMIN, p300, Prostate Cancer

ProHealth.com
February 11, 2012
Source: Thomas Jefferson University news release, Feb 10, 2012

Curcumin, an active component of the Indian curry spice turmeric, may help the body slow tumor growth in prostate cancer patients whose cancers become resistant to androgen deprivation therapy (ADT), a study by researchers at Thomas Jefferson University suggests.

The situation in these patients is that, over time, prostate cancer cells can start to become resistant to hormonal therapies designed to block the release and/or uptake of androgen (testosterone), which is an important male hormone in the development and progression of prostate cancer: Two known nuclear receptor activators, p300 and CPB (or CREB1-binding protein), have been shown to work against androgen deprivation therapy, and with their help, sophisticated tumor cells sometimes bypass the therapy (become ADT resistant).

But the TJU team, led by cancer biologist Karen Knudsen, PhD, have observed in a pre-clinical (animal) study that supplementation with curcumin may support suppression of p300 and CPB.

As described in their report, published in the February issue of Cancer Research, they began by studying prostate cancer cells subjected to hormone deprivation – both without curcumin and with curcumin in doses that were “physiologically attainable.” (Previous studies, which found similar results, had involved doses that were not realistic.)

They found that the curcumin supported greater ADT results, and reduced cell numbers compared with ADT alone. Moreover, the curcumin was found to be a potent inhibitor of both cell cycle and survival in prostate cancer cells.

Next, the researchers investigated curcumin supplementation in a study involving mice that were castrated to mimic ADT. They were randomized into two cohorts: curcumin and control. Tumor growth and mass were significantly reduced in the mice supplemented with curcumin, the researchers report.

These data demonstrate for the first time that curcumin helps the body to both hamper the transition of ADT-sensitive disease to castration-resistance, and block the growth of established castrate-resistant prostate tumors, the researchers say. And “It also has implications beyond prostate cancer, since p300 and CBP are important in other malignancies, like breast cancer.”

Note: This information has not been evaluated by the FDA. It is general information and is not meant to prevent, diagnose, treat or cure any illness, condition or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

How cancer cells get by on a starvation diet

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Posted 09 Feb 2012 — by James Street
Category Glucose, Glutamine, Hypoxia

MIT researchers have found that when deprived of oxygen, cancer cells can engage an alternate metabolic pathway that allows them to use glutamine (seen above) as the starting material for synthesizing lipids.
New study shows that tumor cells, deprived of glucose, alter their metabolism to use other sources of sustenance.
Anne Trafton, MIT News Office

November 21, 2011

Cancer cells usually live in an environment with limited supplies of the nutrients they need to proliferate — most notably, oxygen and glucose. However, they are still able to divide uncontrollably, producing new cancer cells.

A new study from researchers at MIT and the Massachusetts General Hospital (MGH) Cancer Center helps to explain how this is possible. The researchers found that when deprived of oxygen, cancer cells (and many other mammalian cells) can engage an alternate metabolic pathway that allows them to use glutamine, a plentiful amino acid, as the starting material for synthesizing fatty molecules known as lipids. These lipids are essential components of many cell structures, including cell membranes.

The finding, reported in the Nov. 20 online edition of Nature, challenges the long-held belief that cells synthesize most of their lipids from glucose, and raises the possibility of developing drugs that starve tumor cells by cutting off this alternate pathway.

Lead author of the paper is Christian Metallo, a former postdoc in the lab of Gregory Stephanopoulos, the William Henry Dow Professor of Chemical Engineering and Biotechnology at MIT and a corresponding author of the paper. Othon Iliopoulos, an assistant professor of medicine at Harvard Medical School and MGH, is the paper’s other corresponding author.

Alternate pathways

Much of the body’s supply of oxygen and glucose is carried in the bloodstream, but blood vessels often do not penetrate far into the body of tumors, so most cancer cells are deficient in those nutrients. This means they can’t produce fatty acids using the normal lipid-synthesis pathway that depends mostly on glucose.

In prior work, Stephanopoulos’ lab identified a metabolic pathway that uses glutamine instead of glucose to produce lipids; the new paper shows that this alternate pathway is much more commonly used than originally thought. The researchers found that in both normal and cancerous cells, lack of oxygen — a state known as hypoxia — provokes a switch to the alternate pathway.

In a normal oxygen environment, 80 percent of a cell’s new lipids come from glucose, and 20 percent from glutamine. That ratio is reversed in a hypoxic environment, Stephanopoulos says.

“We saw, for the first time, cancer cells using substrates other than glucose to produce lipids, which they need very much for their rapid growth,” Iliopoulos explains. “This is the first step to answering the question of how new cell mass is synthesized during hypoxia, which is a hallmark of human malignancies.”

The glutamine may come from within the cell or from neighboring cells, or the extracellular fluid that surrounds cells.

“There’s protein everywhere,” says Matthew Vander Heiden, the Howard S. and Linda B. Stern Career Development Assistant Professor of Biology at MIT and a co-author of the Nature paper. “The new pathway allows cells to conserve what glucose they do have, perhaps to make RNA and DNA, and then co-opt the new pathway to make lipids so they can grow under low oxygen.”

The switch from glucose to glutamine is triggered by low oxygen and allows cancer cells to thrive and proliferate in an environment with minimal glucose, though it is not clear how this is done. “Elucidating the molecular mechanism regulating this switch would be important in understanding regulation of cancer metabolism,” Stephanopoulos says. “This could be important not only for cancer cells but also other cells growing in hypoxic environments, such as stem cells, placenta and during embryonic development.”

New insights into old models

The researchers are now looking into what other unexpected sources might be diverted into lipid-synthesis pathways under low oxygen. “We had to revise models of metabolism that had been established over the past 50 years. This opens up the possibility for more exciting discoveries in this field that may impact strategies of therapy,” Metallo says.

A better understanding of metabolic pathways and their regulation raises the possibility of developing new drugs that could selectively disrupt key metabolic pathways for cancer cell survival and growth. One possible target is the enzyme isocitrate dehydrogenase, which performs a critical step in the transformation of glutamine to acetyl CoA, a lipid precursor.

“While this target is not new, our findings point to a new function and, hence, generate new ideas for drug development,” Iliopoulos says. “The better we understand the molecular basis of these phenomena, the more optimistic we can be about efforts to translate these basic results into effective treatments of cancer.”

“We’ve been looking, as a field, for almost 90 years for a metabolic pathway that could truly be used to differentiate malignant tumors from normal tissues,” says Ralph DeBerardinis, an assistant professor of pediatrics and genetics at the University of Texas Southwestern Medical Center, who was not involved in this research. He adds that more study is needed, but “if this could be exploited, that could have significant therapeutic potential.”

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