Amazing Food Facts: Red grapes produce resveratrol as a defense against fungal invasion

 

NaturalNews) You may have heard of resveratrol, a miracle antioxidant found in grape skins (and many other foods) that’s linked to a lower risk of heart disease and enhanced longevity. Unlike other antioxidants such as anthocyanins, which give blueberries their color and are an integral part of the fruit, plants produce resveratrol only in response to fungal or bacterial attack. That’s right — resveratrol is a natural antibiotic and fungicide that’s intelligently synthesized by the grape plant in order to survive a biological attack!

This means that the more natural fungi and bacteria a plant is exposed to, the more resveratrol it will produce. That’s why if a grape plant is repeatedly sprayed with synthetic fungicides — and grapes are among the most pesticide-intensive crops cultivated — the resveratrol content in the fruit will be lower. Conventionally-grown grapes, in other words, contain relatively low levels of resveratrol. Wild grapes, on the other hand, contain enormous quantities of resveratrol (because that’s how they survive in the wild).

That alone may be incentive enough to buy organic grapes and wines, because resveratrol may also help maintain “healthy programmed cell death,” which means a process by which cancer cells commit “suicide” and kill themselves. (This helps prevent cancer from growing.) Studies have also shown that resveratrol can make chemotherapy more effective, weaken viruses including influenza and HIV, counter the effects of a high-fat diet and increase physical endurance. Perhaps most miraculously, resveratrol supplements appear to extend the lifespan of yeast, worms and even fish.

NaturalNews recently published a downloadable resveratrol report that contains a wealth of well-cited research about the astonishing health benefits of resveratrol.

Click here to download that report right now (FREE).

Sources for this article include:
 

Source: 25 Amazing Facts About Food, authored by Mike Adams and David Guiterrez. This report reveals surprising things about where your food comes from and what’s really in it! Download the full report (FREE) by clicking here. Inside, you’ll learn 24 more amazing but true facts about foods, beverages and food ingredients. Instant download of the complete PDF. All 25 facts are documented and true

Learn more: http://www.naturalnews.com/033349_red_grapes_resveratrol.html#ixzz1VNFukO3W

Blocking Cancer Cell’s Energy ‘generator’ Could Lead to New Targeted Treatments

ScienceDaily (Aug. 17, 2011) — Cancer Research UK scientists have found that blocking the pathway used by some kidney cancer cells to generate energy can kill the cancer cells, sparing the healthy ones.

The research is published in the journal Nature.

Cells need energy to grow and divide. This energy is generated through a process called the TCA cycle (also known as the Krebs cycle), which is supported by a range of cellular catalysts called enzymes. Without these enzymes the cycle grinds to a halt, causing the cells to die.

But, in the rare genetic condition ‘hereditary leiomyomatosis and renal cell cancer*’ (or HLRCC, found in around 200 families worldwide), which can lead to a very aggressive form of kidney cancer, one of these enzymes, fumarate hydratase (FH), is missing and yet the kidney cancer cells are able to survive.

The researchers found that these cells were able to get around the loss of the TCA cycle by switching to a pathway that builds and breaks down a molecule called haem, an important by-product of the TCA cycle. By blocking the action of a key enzyme called Haem Oxygenase, the researchers were able to specifically target the fumarate hydratase deficient cancer cells while leaving normal kidney cells unaffected.

Professor Eyal Gottlieb, lead researcher at Cancer Research UK’s Beatson Institute in Glasgow, said: “By using the latest chemistry and computer technologies we were able to look at every energy generating reaction taking place in the cell and predict the effect of blocking these pathways. Armed with this knowledge we now need to confirm our findings in HLRCC patients and ultimately develop targeted drugs that selectively kill kidney cancer cells.

“We also want to use our approach to find other pathways and expose weaknesses in cancer cells that could be exploited, suggesting a whole new range of drugs to kill cancer cells.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “Ten years ago, Cancer Research UK scientists found that faults in the gene for fumarate hydratase lead to the condition HLRCC. These latest results show us that the adaptation that the cancer cells use to survive could also be exploited as a weakness, and potentially lead to the design of new treatments.

“Recent research has found that levels of fumarate hydratase are also reduced in other types of kidney cancer, suggesting that if they are using the same pathway to generate energy then a drug to block this process could be used to treat a wider range of people with kidney cancer.”

ells Derived from Pluripotent Stem Cells Are Developmentally Immature

ells Derived from Pluripotent Stem Cells Are Developmentally Immature

ScienceDaily (Aug. 16, 2011) — Stem cell researchers at UCLA have discovered that three types of cells derived from human embryonic stem cells and induced pluripotent stem cells are similar to each other, but are much more developmentally immature than previously thought when compared to those same cell types taken directly from human tissue.

The researchers, from the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, found that the progeny of the human embryonic stem cells and induced pluripotent stem cells (iPS) were more similar to cells found within the first two months of fetal development than anything later. This could have implications both clinically and for disease modeling, said William Lowry, senior author of the study and an assistant professor of molecular, cell and developmental biology in the Life Sciences.

The two-year study was published August 17 in the peer-reviewed journal Cell Research.

“Once we found that the human embryonic stem cell- and the iPS-derived progeny were similar, we wanted to understand how similar the progeny were to the same cells taken directly from human tissue,” Lowry said. “What we found, looking at gene expression, was that the cells we derived were similar to cells found in early fetal development and were functionally much more immature than cells taken from human tissue. This finding may lead to exciting new ways to study early human development, but it also may present a challenge for transplantation, because the cells you end up with are not something that’s indicative of a cell you’d find in an adult or even in a newborn baby.”

There might also be challenges in disease modeling, unless you’re modeling diseases that occur within the first two months of development, Lowry said.

Employing the most commonly used methods for deriving cells from embryonic stem cells and iPS cells, Lowry and his team differentiated these human pluripotent stem cells into neural progenitor cells, which create neurons and glia, hepatocytes, the main tissue found in the liver, and fibroblasts, common to the skin. They selected those cell types because they are easy to identify and are among the most commonly differentiated cells made from pluripotent stem cells. They also represent cell types found in the three germ layers, the endoderm, mesoderm and ectoderm, where the first cell fate decisions are made, Lowry said.

The progeny of the human pluripotent stem cells were compared to each other using their gene expression patterns, functionality and appearance. There was essentially little or no difference between them, Lowry said. Then the work began to compare them to equivalent cell types found in humans.

“One important reason to do this is to ensure that the cells we are creating in the Petri dish and potentially using for transplantation are truly analogous to the cells originally found in humans,” said Michaela Patterson, first author of the study and a graduate student researcher. “Ideally, they should be a similar as possible.”

What the team found was that while the progeny were alike, they bore striking differences from the same cells found in humans when analyzing their gene expression. A significant number of genes, about 100, were differentially expressed in the cell types made from pluripotent stem cells, Lowry said.

About half of those differentially expressed genes are normally thought to be strictly expressed in pluripotent stem cells, which have the potential to differentiate into any cell of the three germ layers. Those genes had not been turned off even after the cell had differentiated into either a neural progenitor cell, hepatocyte or a fibroblast, Patterson said.

“Previously, we assumed that all pluripotency genes get shut off right away, after the fetus begins developing,” Patterson said. “We found that this is not the case, and in fact some of these genes remain expressed.”

The differences in gene expression could be problematic, Lowry said, because some of these same differentially expressed genes in the progeny are genes that are expressed during cancer development. Also worrisome was their developmental maturity — would they work correctly when transplanted into humans? As part of their study, the team left the differentiating cells in culture about a month longer to see if they would further mature, and there was some modest but statistically significant maturation. However, genetic discrepancies remained.

These discrepancies could be critical, Patterson said, particularly in the hepatocytes. During fetal development, these cells express proteins that aid the metabolism of the fetus, a role they don’t play later in adults.

“The roles these cells play in the fetus and the adult are inherently different,” she said. “It may be that the progeny, if transplanted into a human, would mature to the same levels as those found in the adult liver. We don’t know.”

The team then compared the progeny to cells from humans that were closer to the progeny’s developmental maturity and found that the two types of cells were indeed becoming more similar in gene expression and functionality, Lowry said.

The UCLA team is not the first to suggest that the progeny of human pluripotent stem cells reflect an early developmental immaturity. However, these data put a more precise window on their developmental age.

Going forward, Lowry and his team are going to study the 100 genes being differentially expressed in the progeny to see if manipulating some or all of them results in the maturation of the cells.

“These findings provide support for the idea that human pluripotent stem cells can serve as useful in vitro models of early human development, but also raise important issues for disease modeling and the clinical applications of their derivatives,” the study states.

The study was funded in part by a seed grant and training grants from the California Institute of Regenerative Medicine, the Basil O’Connor Started Scholar Award and the Fuller Foundation

Maternal Fat Has Negative Impact On Embryo Development

ScienceDaily (Aug. 17, 2011) — Exposing eggs to high levels of saturated fatty acids — as commonly found in the ovaries of obese women and those with Type II diabetes — compromises the development of the embryo, according to new research published in PLoS ONE.

The study — by researchers from Antwerp, Hull, and Madrid — found that embryos resulting from cattle eggs exposed to high levels of fatty acids had fewer cells, altered gene expression and altered metabolic activity, all indicators of reduced viability.

Although the work was carried out using eggs from cows, the findings could help to explain why women suffering from metabolic disorders like obesity and diabetes struggle to conceive. Patients in this group tend to metabolise more of their stored fat, resulting in higher levels of fatty acids being present within the ovary, which research has already shown to be toxic for the growing eggs before ovulation.

Lead researcher, Professor Jo Leroy from the University of Antwerp, says: “In cows we can induce very similar metabolic disorders leading to reduced fertility in these animals and compromised egg quality in particular. This is one of the reasons that bovine eggs are a very interesting model for human reproductive research.”

Co-researcher, Dr Roger Sturmey, from the University of Hull and Hull York Medical School, says: “Our findings add further weight to the public health recommendations which emphasise the importance of women being a healthy weight before starting a pregnancy.”

Professor Leroy adds: “We know from our previous research that high levels of fatty acids can affect the development of eggs in the ovary, but this is the first time we’ve been able to follow through to show a negative impact on the surviving embryo.”

University of Antwerp PhD student, Veerle Van Hoeck, funded by FWO-Flanders and the EU Cost Gemini Action FA0702, tested the embryos eight days after fertilisation, when they had developed into what are known as blastocysts, containing around 70 to 100 cells. One of the key indicators of embryo viability is metabolic activity, calculated through analysis of what the embryo consumes from its environment and what it releases back out.

“The most viable embryos, those most likely to result in a successful pregnancy, have a ‘quieter’, less active metabolism, particularly in relation to amino acids,” explains Dr Sturmey. “Where eggs were exposed to high levels of fatty acids, the resulting embryos showed increased amino acid metabolism and altered consumption of oxygen, glucose and lactate — all of which indicates impaired metabolic regulation and reduced viability.”

“These embryos also showed increased expression of specific genes which are linked to cellular stress,” adds Professor Leroy. “And although the higher fatty acid levels didn’t stop eggs developing to the two-cell stage, there was a notable reduction in those able to develop into blastocysts.”

The researchers are now applying for further funding to take their findings into a clinical setting and to investigate whether exposing eggs to high levels of fatty acids can also lead to post natal effects.

Antioxidant vitamins may cut mortality risk: EPIC data

Related topics: Research, Antioxidants, carotenoids, Minerals, Vitamins & premixes, Cancer risk reduction, Cardiovascular health

Users of antioxidant vitamin supplements may be at reduced risk of cancer mortality, as well as premature death in general, suggests data from the European Prospective Investigation into Cancer and Nutrition.

 

Antioxidant vitamin supplement use at the start of the study was associated with a 48 percent reduction in the risk of cancer mortality over 11 years of study, according to findings published in the European Journal of Nutrition .

In addition, the risk of all-cause mortality was reduced by 42 percent in people who were supplement users at the start of the study, report scientists from the German Cancer Research Centre and the University of Zurich.

‘Sick-user effect’?

General multivitamin/mineral supplementation, however, was not associated with any impact on mortality risks.

And on the flip side, the EPIC researchers note that people who started taking supplements after the start of the study were at a higher risk of cancer mortality and so-called all-cause mortality, said the researchers.

“The significantly increased risks of cancer and all-cause mortality among baseline non-users who started taking supplements during follow-up may suggest a ‘sick-user effect’, which researchers should be cautious of in future observational studies,” they wrote.

Methodological challenges

Commenting independently on the research, Professor Jeff Blumberg, director of the Antioxidants Research Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, said he agreed that based on a “small number of users of antioxidant vitamin supplements and lack of detailed information on dose, contents, and durations of use,” there appears to be a statistically modest reduction in cancer and all-cause mortality.

“Some other studies are consistent with this finding and others are not. Why? Because the methodological challenge of conducting observational studies on the effect of dietary supplements is great and fraught with serious confounding variables (including the difficulty of accurately assessing the product[s] and their use),” he observed.

Controversial

An attempt to bring together the science was made in 2007, with the publication of a meta-analysis by Goran Bjelakovic et al. and from the Copenhagen Trial Unit at the Copenhagen University Hospital in Denmark in the Journal of the American Medical Association (Vol. 297, pp. 842-857).

The meta-analysis concluded that vitamins A and E, and beta-carotene may increase mortality risk by up to 16 per cent.

On the other hand, vitamin C did not have an effect on mortality and the antioxidant mineral selenium was associated with a nine per cent decrease in all-cause mortality.

Following publication of the Bjelakovic paper, numerous scientists and dietary supplement trade associations questioned the methodology, particularly the exclusion of over 400 clinical trials from the data set because no deaths were reported.

Revisiting old data

Recently, a team of internationally renowned antioxidant scientists, including Prof Blumberg, re-analysed the data used by Bjelakovic et al., and arrived at a different set of conclusions.

This re-analysis, published in Nutrients , found that 36 percent of the trials showed a positive outcome or that the antioxidant supplements were beneficial, 60 percent had a null outcome, while only four percent found negative outcome.

New data

The EPIC scientists based their findings on analysis of intakes of 23,943 people, all free of cancer and heart disease at the start of the study.

After 11 years of data collection, the researchers had documented 1,101 deaths, of which 513 were from cancer and 264 from cardiovascular conditions.

Data analysis showed that users of antioxidant vitamin supplements at the start of the study had a significantly reduced risk of both cancer mortality and all-cause mortality, while people who started taking supplements after the study had started had significantly increased risks.

“Based on limited numbers of users and cases, this study suggests that supplementation of antioxidant vitamins might possibly reduce cancer and all-cause mortality,” they concluded.

Compliance

Prof Blumberg added that an issue he has always found interesting is the definition of ‘regular use’ of a dietary supplement.

“In this study, which is not unlike others, using a supplement as little as 25 percent of the typical indication counts as regular use. In other words, for 5 doses or one week of use per month when the label states ‘take daily’,” he said.

“If this was a study of a drug and adherence was this poor, a null outcome would be dismissed as meaningless due to non-compliance.”

Source: European Journal of Nutrition
Published online ahead of print, doi: 10.1007/s00394-011-0224-1
“Vitamin/mineral supplementation and cancer, cardiovascular, and all-cause mortality in a German prospective cohort (EPIC-Heidelberg)”
Authors: K. Li, R. Kaaks, J. Linseisen, S. Rohrmann

New Non-Invasive Technology Shows Promise in Shrinking Liver Tumors

ScienceDaily (Aug. 14, 2011) — A potential new option is beginning to emerge for patients with the fastest growing form of cancer in the United States, according to researchers at the University of Alabama at Birmingham.

In a phase II study, 41 patients with hepatocellular carcinoma (HCC), a liver cancer that often does not respond well to chemotherapy, were treated with very low levels of an electromagnetic field emitting from a spoon-like device placed in the patients’ mouths.

After six months, the tumors in 14 patients had stabilized after each received three one-hour treatments per day each day; the therapy created no significant side effects. The most successful tumor shrinkage occurred in a female patient who has received regular therapy since August 2006; her tumor continues to shrink without serious side effects.

Boris Pasche, M.D., Ph.D., director of the UAB Division of Hematology and Oncology in the Department of Medicine, and collaborators reported their findings Aug. 9, 2011, in the online version of the British Journal of Cancer.

“The very appealing advantage of this novel therapy is its capability to shrink tumors without collateral damage. This method literally finds cancer cells in the body and blocks their growth without affecting the growth of normal cells,” says Pasche, senior author of the study.

To date, other treatment options have been limited. The U.S. Food and Drug Administration has only approved one drug, sorafenib, in 20 years. Pasche says this drug does prolong life an average of three months, but it doesn’t make the patient feel better.

“With our treatment, seven of the 11 patients who reported pain prior to the start of their treatment reported either a complete disappearance of pain or decreased amounts,” says Pasche. Preliminary evidence also indicates that the treatment not only affected the primary cancer, but also its metastases.

The small battery-driven “radio frequency electromagnetic field generator” has an attached spoon-shaped mouthpiece. The device is programmed and the patient pushes a button to start treatment. It is like a watch in that it emits low levels of amplitude-modulated radio frequency, resulting in the delivery of doses 100 to 1,000 times less than those generated from a cell phone.

“When you take the mouthpiece and put it in your mouth the body becomes an antenna — the whole body receives a tiny but fairly homogenous amount of radio-frequency,” Pasche says.

In a 2009 study, Pasche and research partners Alexandre Barbault in France and Frederico Costa at the University of Sao Paulo in Brazil identified tumor-specific frequencies and tested the feasibility of administering such frequencies to patients with advanced cancer. They then decided to determine whether these frequencies had an effect on the growth of tumors.

Pasche believes this a promising therapy that could become a standard of care in the near future. The therapy is ready for an FDA-registration study and randomized trials, which will be initiated at UAB upon funding being secured for the project.

The technology also is in the beginning stages of being studied in breast cancer patients, by Pasche together with UAB collaborators Andres Forero, M.D., and John Carpenter, M.D.

“Although liver transplant is the most effective treatment, that option will be available for only a fraction of patients. Better therapies are sorely needed for the larger number of HCC patients,” Pasche says

Higher Estrogen Production in the Breast Could Confer Greater Cancer Risk Than Thought

ScienceDaily (Aug. 14, 2011) — Could some women who naturally produce excess aromatase in their breasts have an increased risk of developing breast cancer? Results of a new animal study suggests that may be the case, say researchers at Georgetown Lombardi Comprehensive Cancer Center, a part of Georgetown University Medical Center.

In the issue of August 15 Cancer Research, the investigators say their mice study shows that overproduction of aromatase, which converts testosterone into estrogen, in breast tissue is even more important in pushing breast cancer development than excess production of the estrogen receptor that the hormone uses to activate mammary cells. In addition, the researchers found that aromatase over-expressing mice also expressed more estrogen receptors on the breast cells.

While current breast cancer therapies target both of those processes — inhibition of aromatase and inactivation of the estrogen receptor — the researchers say this study suggests that aromatase inhibitors may prove to be a more potent choice for cancer prevention in postmenopausal women. Tamoxifen and other drugs that block the estrogen receptor have long been used to prevent breast cancer and deter recurrence, while aromatase inhibitors are only now being studied as a protectant.

“We know that estrogen is the fuel that most breast tumors use to grow, and this study shows us that making more estrogen in the breast, right next to cells that can use the hormone as fuel, appears to be a key trigger of early breast cancer,” says the study’s senior investigator, Priscilla Furth, M.D., professor of oncology and medicine at Georgetown Lombardi.

The study also reached another important conclusion, says Edgar Díaz-Cruz, Ph.D., a postdoctoral researcher working in the Furth laboratory and first author of the study.

“This study appears to help inform a longstanding controversy about whether it is systemic estrogen or estrogen produced in the breast that is the primary risk factor for breast cancer,” he says. “With our animal models, we’ve demonstrated that local production of estrogen in mammary tissue is potent enough to spur development of breast cancer, and does not require estrogen from the ovaries or produced from fat tissue, as had been hypothesized.”

Their study set out to achieve two goals: to look at whether production of estrogen or production of estrogen receptors in the breast was more potent in breast cancer development, and to find more answers to the controversy alluded to by Díaz-Cruz.

To address these issues, the researchers developed the first “conditional” mouse model of aromatase production in mammary tissue. That means they inserted a gene into mice that expresses human aromatase in the animal’s mammary tissue — a gene the researchers can turn on or off.

They compared this new mouse model to one they had developed several years ago — a conditional mouse model in which a gene that produces estrogen receptors (ER) could also be turned on and off.

While they study found that both mouse models experienced the earliest stages of tumor formation, known as preneoplasia, the aromatase over-expressing mice model exhibited both increased preneoplasia and outright development of cancer. These mice also expressed proteins that are tightly linked to cancer, Furth says.

The researchers also found, to their surprise, that aromatase over-expressing mice expressed more estrogen receptors than did the ER-conditional mice. “Increased aromatase produced both more estrogen and the receptors that the hormone needs to enter breast cells,” says Díaz-Cruz. “This is obviously a greater risk for development of breast cancer than just over-expression of estrogen receptors.”

“In our conditional mice, aromatase provides a double whammy — more estrogen and more estrogen receptors,” Furth notes.

These mice also over-expressed progesterone receptors, downstream targets of estrogen receptors that can be cancer-promoting in some settings, as shown in this study in the context of aromatase over-expression.

Furth notes that the amount of aromatase and estrogen receptors produced in these mice is high, but not higher than would be expressed in a woman with breast cancer. “These were not super large amounts. Comparable levels can be measured in women.”

Finally, they tested the effect of local versus systemic estrogen on development of preneoplasia. The researchers made three comparisons: between mice in which the ER was over-expressed; mice that had excess estrogen due to aromatase; and mice that were given more estrogen systemically. “If we give extra systemic estrogen, we don’t see any increased risk of breast cancer, but the risk increases with extra expression of ER, and is higher still with local production of aromatase,” says Díaz-Cruz. “That suggests that estrogen production in the breast is an important risk factor for development of breast cancer.”

What these results suggest for women is that if females vary in the amount of aromatase they naturally produce, as some studies suggest, then women with higher aromatase levels may be more susceptible to breast cancer, Furth says.

“Some day we may have a test available that can determine individual aromatase levels in postmenopausal women so that a preventive aromatase inhibitor can be prescribed to women at higher risk for breast cancer,” she says.

The research was funded by the National Cancer Institute and a Susan G. Komen for the Cure Postdoctoral Fellowship grant awarded to Díaz-Cruz.

Co-authors include G. Ian Gallicano, Ph.D., director of the Transgenic Core Facility at GUMC, and Yasuro Sugimoto Ph.D. and Robert W. Brueggemeier Ph.D. from the College of Pharmacy at The Ohio State University.

Monsanto preys on popularity of omega-3s by developing GMO soybean that produces fake fish oil

NaturalNews) Leave it to Monsanto to take a good thing and corrupt it for financial gain. According to a recent report in Forbes, the multinational biotechnology-slash-agriculture-manipulating monolith has developed a new genetically-modified (GM) soybean that artificially produces stearidonic acid, a type of omega-3 fatty acid — and the US Food and Drug Administration (FDA) is expected to approve the “frankenbean” sometime this year.

Monsanto appears to be introducing the omega-3 enhanced GM soybean oil, called Soymega or “stearidonic acid soybean oil” (SDA oil), at a craftily strategic time when much of the world is still reeling from the Fukushima Daiichi mega-disaster, which left ocean waters ridden with radioactive isotopes. And since omega-3s just happen to be most readily found in fatty ocean fish, the perpetual fear over radioactive and other poisons that may be lurking in such fish could drive many to embrace Monsanto’s fake fish oil instead.

According to an FDA letter responding to Monsanto’s request to have SDA oil approved for use as a food additive and acknowledged as being “generally recognized as safe” (GRAS), the FDA noted that Monsanto intends to use its omega-3-enhanced oil in a variety of food applications. These include baked goods, breakfast cereals, fish products, frozen dairy desserts, cheeses, grains and pastas, gravies, nuts, poultry, fruit juices, processed vegetable products, and soups — yes, basically every processed food product in existence.

Monsanto created its GM soybean oil by injecting two specific enzymes into soybean genes. One came from Primula juliae, a type of flower, and the other from Neurospora crass, a type of red mold that grows on bread. As a result, the beans produce SDA oil and gamma-linolenic acid, two compounds not normally found in soybeans.

In its original request letter, Monsanto claims that its company-funded trials prove that SDA oil is safe for animal and human consumption, and that “no toxicologically significant effects were observed.” However, the data does not specifically highlight the long-term effects of the oil in animals or in humans — it merely alleges that nothing bad was observed during the 16-week trial period, which is hardly enough reassurance that the product is undeniably safe for consumption.

Nevertheless, the FDA has already granted Soymega GRAS status, which means that the agency acknowledges Monsanto’s safety claims, and essentially has no problems with or objections to them. And if the FDA grants full approval for Soymega, you can expect to see it turning up in all sorts of consumer food products.

Have all the ocean disasters in recent years been a catalyst for forcing people over to artificial, patented varieties of omega-3s?

Between BP’s “Deepwater Horizon” oil disaster in the Gulf of Mexico in April 2010, and the earthquake and tsunami that ravaged the Fukushima Daiichi nuclear facility in March 2011, many of the world’s oceans, and corresponding fish stocks, have been severely tainted. Add in perpetual mercury poisoning and other pollution that has been afflicting ocean life for many decades, and seafood appears less and less enticing as a safe and healthy source of omega-3s.

Enter Monsanto. By positing its omega-3 GM soybean variety as a safer, healthier alternative to natural seafood and sea-based fish oils, the company stands to gain an incredible amount of profit while ultimately steering public preference away from natural sources of omega-3s, and towards its own patented varieties of omega-3s.

The same Forbes article that announced the advent of Monsanto’s Soymega also mentions that sea-based fish oils can be contaminated with toxins, and also suggests that fish-derived omega-3s are responsible for depleting fish stocks and damaging the environment. Do you see where this is all going?

It is all too convenient that as omega-3s become more popular than ever, Monsanto, in conjunction with the FDA and the mainstream media, is coordinating a leveraged attack against natural sources of omega-3s in order to brainwash the public into accepting its “safer” variety. And by getting SDA oil laced throughout the food supply, the public will ultimately have little choice in avoiding it., and will probably just accept it as beneficial.

Monsanto is clearly dead set on capturing the omega-3 market through its new soybean oil. After all, soybean oil has become a staple in most American processed foods, and by “enriching” everything from breads and cereals to vegetable dishes and quick dinners with Soymega, the general public will be less prone to purchase fish for its health benefits. And the end result will be more control of the food supply handed over to Monsanto, and less availability of natural omega-3s on the market.

Sources for this story include:

http://blogs.forbes.com/jeffmcmahon…

http://www.fda.gov/Food/FoodIngredi…

Learn more: http://www.naturalnews.com/033305_GMO_soybeans_fish_oil.html#ixzz1V5ixeHN2

The death cry of a carrot – If carrots are not dead when you pick them out of the ground, when are they dead

NaturalNews) When do carrots die? Apparently not in the way most of us thought. Carrots don’t die when you pull them out of the ground, but in fact only die when ingested in the stomach, cooked to 60c in hot water or left out to rot. This startling discovery has serious consequences not only for vegetarians, but also for everyone who is concerned about their health. In the light of the raw milk scandal, it takes on an even greater significance.

In his ground breaking new book, Blinded by Science, www.blindedbyscience.co.uk author Matthew Silverstone provides impressive scientific evidence that supports these ideas and uncovers new information that shows many other unknown aspects of plants will completely alter the way that you look at life around you. Vegetables turn out not to be the simple objects that we thought they were but are in fact as sophisticated as animals and 100% behaviorally the same as humans.

Silverstone shows using many different scientific experiments, some dating back as far as 1910, that at the point of death, carrots (and all vegetables, milk and meat) give out an electrical charge, equivalent to what we could poetically refer to as its final death cry.

This is very important information that has serious consequences for our health. Eating raw vegetables is not only healthier because they contain more minerals and vitamins, but is also better for our digestive system as they emit an electrical output into our digestive tract as well. A single pea emits 0.5v, so these electrical stimulations are very significant and can provide extra ammunition for those people who promote raw vegetables as offering a means to a healthier life.

How does the electrical output of a vegetable improve our health? If our bodies have been developed to expect to eat raw food all of the time, then our stomachs and our digestive tract would evolve methods to absorb the electrical output every time food was digested. The stomachs bacteria would be the first to receive it and would react in a negative way. Some have argued that the electrical stimulation can kill off the bad bacteria and stimulate the good bacteria. Could it just be a coincidence that as we are eating less and less raw food, the levels of stomach related illnesses has risen exponentially. Almost everyone now suffers from candida, a fungus that lives in our stomachs, which can be treated successfully with a diet of raw food. Scientists at Oxford University found that vegetarians were a third less likely to suffer from common bowel disorders, which they believe is caused by eating too little fibre, but might, as Silverstone suggests, instead be caused by an absence of an electrical charge from the raw vegetables.

Does the electrical charge give the body extra energy by adding an additional stimulation to our blood? Sadly there is absolutely no research that has been conducted in this area that can offer up any ideas.

Why not? These are fundamental health issues that seem to have been clearly overlooked by every nutritionist , doctor and health advisor.

Not only does this knowledge affect our attitude to eating raw food but this information should make us question our method of cooking and its relationship to the health benefits of a carrot and other vegetables. Should we eat it alive or dead? Also many of us, especially vegetarians, steam our vegetables. So should we cook them to a temperature of under 60c in order for them to stay alive? There are simply too many questions raised with this information and very little in the way of answers.

It’s the raw foodists that seem to gain the most in the way of health benefits here. Perhaps their diet really is the healthiest and they are getting the most out of their vegetables. For vegetarians though, the question is whether it is better to roast, steam or boil their vegetables. The method in which they cook their vegetables may be very important health-wise in order for them to gain the most nutrients from the main component of their diet. Vegetarians may also need to think about what length of time they would have to be cooked and within which temperature range is important too.

If you have been reading about the argument on naturalnews.com recently regarding the issues over raw milk, another factor that is over looked by the governments scientists who have chosen to ban raw milk is that as milk is a living organism, it not only contains lots of healthy bacteria but also a healthy electrical charge as well. Even more of an argument to support the view that raw food is incredibly good for all of us

If after reading Silverstone’s book, Blinded by Science, www.blindedbyscience.co.uk I guarantee you that when eating your next meal, you will not look at the plate of food in front of you in the same way ever again.

About the author:
Matthew Silverstone is the author of Blinded by science, www.blindedbyscience.co.uk a book that will completely change your attitude to your health.

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Blocking Receptor in Key Hormone Fires Up Enzyme to Kill Pancreatic Cancer Cells

ScienceDaily (Aug. 10, 2011) — Pancreatic cancer researchers at Thomas Jefferson University have shown, for the first time, that blocking a receptor of a key hormone in the renin-angiotensin system (RAS) reduces cancer cell growth by activating the enzyme AMPK to inhibit fatty acid synthase, the ingredients to support cell division.

angiotensin II type 2 receptor — never before thought to play a role in tumor growth — could be developed to help treat one of the fastest-moving cancers that has a 5-year survival rate of only 5 percent.

Hwyda Arafat, M.D., Ph.D., associate professor of Surgery at Jefferson Medical College of Thomas Jefferson University and the co-director of the Jefferson Pancreatic, Biliary and Related Cancers Center, and her fellow researchers, including the chair of the Department of Surgery at Jefferson, Charles J. Yeo, M.D., FACS, present their findings in the August issue of Surgery.

Angiotensin II (AngII) is the principal hormone in the RAS that regulates our blood pressure and water balance; it has two receptors: type 1 and type 2. AngII is also generated actively in the pancreas and has been shown to be involved in tumor angiogenesis.

Previous studies have pointed to the hormone’s type 1 receptor as the culprit in cancer cell proliferation and tumor inflammation; however, the idea that type 2 had any effect was never entertained.

By looking at pancreatic ductal adenocarcinoma (PDA) cells in vitro, Jefferson researchers discovered that the type 2 receptor, not just type 1, mediates the production of fatty acid synthase (FAS), which has been shown to supply the cell wall ingredients necessary for cancer cells to multiply.

FAS was previously identified as a possible oncogene in the 1980s. It is up-regulated in breast cancers and is indicator of poor prognosis, and thus believed to be a worthwhile chemopreventive target.

“AngII is not just involved in cell inflammation and angiogenesis; it’s involved in tumor metabolism as well,” said Dr. Arafat, a member of the Kimmel Cancer Center at Jefferson. “It promotes FAS with both receptors, which makes the tumor grow.”

“Blocking the type 2 receptor reduces PDA cell growth with the activation of AMPK, revealing a new mechanism by which chemoprevention can exploit,” she added. “In fact, maybe combined blocking of the two receptors would be more efficient than just blocking one receptor.”

AMPK, or adenosine monophosphate-activated protein kinase, is the focus of several agents today, including ones for diabetes and related metabolic diseases. It is a master metabolic regulator for cells that is activated in times of reduced energy availability, like starvation. Activation of AMPK has been shown to improve energy homeostasis, lipid profile and blood pressure. The enzyme also activates a well-known tumor suppressor, p53.

“The main thing is activation of AMPK in tumor cells,” said Dr. Arafat. “AMPK is the perfect candidate as it regulates multiple targets that both halt tumor cell division and activate programmed cell death. Although it is yet to be determined how the type 2 receptor imposes deregulation of AMPK activity, identification of the type 2 receptor as a novel target for therapy is very exciting”

Next, Dr. Arafat and fellow researchers are proposing to take this research into animal studies. They hope to target the receptors early on in the disease to better understand its prevention capabilities and also study its treatment potential. Considering pancreatic cancer is typically detected in later stages, finding better ways to treat cases that have progressed further along would be of great benefit to patients.