In 1999 Jerry Brunetti was diagnosed with Non-Hodgkin’s Lymphoma and given 6 months to live. He did not submit to chemotherapy, but rather, developed his own unique dietary approach to enhance his immune system. In this informative video, Jerry shares his personal experiences and provides his recipe for healthy living. You will learn about the crucial importance of minerals, which foods to choose for your best health requirements and what to avoid. After viewing this video you’ll realize the remarkable value of food in building good foundations, and providing buffers, to keep your body healthy.
Topics of the first video include:
- Why we are losing the ‘war’ on Cancer
- Metastasis kills 90% of the cancer patients; 50% die of cachexia (wasting disease).
- The virtue of the immune system in combating disease, including cancer.
- Chemotherapy agents MOP and CHOP are derivatives of WWI mustard gas.
- Angiogenesis and why cutting out the primary tumor is bad.
- Obesity, diabetes and the sugar consumption explosion.
- The greatest of health threats called Iatrogenic disease – illness caused by modern medicine.
- The superficiality of regular medicine with regards to the US cancer patient.
- Negative synergy of cocktails of different toxins.
- Why Prunes and Eggs are healthy foods.
- Selenium the antidote to mercury.
- The benefits of resveratrol.
- The benefits of Blueberries, Strawberries, Raspberries, Cranberries, Apples, Elderberries, Black Cherries, Lycopene, Pumpkins.
- How foods barely contain minerals in the US.
- Vegetables of the cross/cruciferous vegetables – “nr 1 vegetables in protecting against cancer”.
- Why antacids are not the answer to your stomach troubles.
Check out the accompanying resources page for slides and food advice.
Researchers point out that people live a lot longer than they used to, and since cancer becomes more prevalent with age, it’s unfair to look just at the raw numbers when assessing progress. So when they calculate the mortality rate, they adjust it to compare cancer fatalities by age group over time. But even using this analysis (in which the proportion of elderly is dialed back to what it was during the Nixon administration), the percentage of Americans dying from cancer is about the same as in 1970 … and in 1950. The figures are all the more jarring when compared with those for heart disease and stroke–other ailments that strike mostly older Americans. Age-adjusted death rates for those diseases have been slashed by an extraordinary 59% and 69%, respectively, during the same half-century.
Researchers also say more people are surviving longer with cancer than ever. Yet here, too, the complete picture is more disappointing. Survival gains for the more common forms of cancer are measured in additional months of life, not years. The few dramatic increases in cure rates and patient longevity have come in a handful of less common malignancies–including Hodgkin’s, some leukemias, carcinomas of the thyroid and testes, and most childhood cancers. (It’s worth noting that many of these successes came in the early days of the War on Cancer.) Thirty-three years ago, fully half of cancer patients survived five years or more after diagnosis. The figure has crept up to about 63% today.
Yet very little of this modest gain is the result of exciting new compounds discovered by the NCI labs or the big cancer research centers–where nearly all the public’s money goes. Instead, simple behavioral changes such as quitting smoking have helped lower the incidence of deadly lung cancer. More important, with the help of breast self-exams and mammography, PSA tests for prostate cancer, and other testing, we’re catching more tumors earlier. Ruth Etzioni, a biostatistician at Seattle’s Fred Hutchinson Cancer Research Center, points out that when you break down the Big Four cancers (lung, colon and rectal, breast, and prostate) by stage–that is, how far the malignant cells have spread–long-term survival for advanced cancer has barely budged since the 1970s (see charts opposite).
When you add it all up, Americans have spent, through taxes, donations, and private R&D, close to $200 billion, in inflation-adjusted dollars, since 1971. What has that national investment netted so far?
Without question, the money has bought us an enormous amount of knowledge, just as Varmus says. Researchers have mapped the human cell’s intricate inner circuitry in extraordinary detail, identifying dozens of molecular chains of communication, or “signaling pathways,” among various proteins, phosphates, and lipids made by the body. In short, scientists now know (or think they know) nearly all the biochemical steps that a healthy cell uses to multiply, to shut down its growth, and to sense internal damage and die at the right time–as well as many of the genes that encode for these processes. What’s more, by extension, they know how these same gene-induced mechanisms go haywire in a cancer cell.
According to PubMed, the NCI’s online database, the cancer research community has published 1.56 million papers–that’s right: 1.56 million!–largely on this circuitry and its related genes in hundreds of journals over the years. Many of the findings are shared at the 100-plus international congresses, symposiums, and conventions held each year.
Yet somehow, along the way, something important has gotten lost. The search for knowledge has become an end unto itself rather than the means to an end. And the research has become increasingly narrow, so much so that physician-scientists who want to think systemically about cancer or the organism as a whole–or who might have completely new approaches–often can’t get funding.
Take, for instance, the NCI’s chief funding mechanism, something called an RO1 grant. The grants are generous, averaging $338,000 apiece in 2003. And they are one of the easiest sweepstakes to win: One in three applications is accepted. But the money goes almost entirely to researchers who focus on very specific genetic or molecular mechanisms within the cancer cell or other tissue. The narrower the research niche, it sometimes seems, the greater the rewards the researcher is likely to attain. “The incentives are not aligned with the goals,” says Leonard Zwelling, vice president for research administration at M.D. Anderson, voicing the feeling of many. “If the goal is to cure cancer, you don’t incentivize people to have little publications.”
Jean-Pierre Issa, a colleague of Zwelling’s who studies leukemias, is equally frustrated by the community’s mindset. Still, he admits, the system’s lure is powerful. “You get a paper where you change one gene ever so slightly and you have a drastic effect of cancer in the mouse, and that paper gets published in Science or Nature, and in your best journals. That makes your reputation. Then you start getting grants based on that,” he says. “Open any major journal and 80% of it is mice or drosophila [fruit flies] or nematodes [worms]. When do you get human studies in there?”
Indeed, the cancer community has published an extraordinary 150,855 experimental studies on mice, according to a search of the PubMed database. Guess how many of them have led to treatments for cancer? Very, very few. In fact, if you want to understand where the War on Cancer has gone wrong, the mouse is a pretty good place to start.
Says Weinberg: “A fundamental problem which remains to be solved in the whole cancer research effort, in terms of therapies, is that the preclinical models of human cancer, in large part, stink.”
A few miles away, Bruce Chabner also finds the models lacking. A professor of medicine at Harvard and clinical director at the Massachusetts General Hospital Cancer Center, he explains that for a variety of biological reasons the “instant tumors” that researchers cause in mice simply can’t mimic human cancer’s most critical and maddening trait, its quick-changing DNA. That characteristic, as we’ve said, leads to staggering complexity in the most deadly tumors.
“If you find a compound that cures hypertension in a mouse, it’s going to work in people. We don’t know how toxic it will be, but it will probably work,” says Chabner, who for many years ran the cancer-treatment division at the NCI. So researchers routinely try the same approach with cancer, “knocking out” (neutralizing) this gene or knocking in that one in a mouse and causing a tumor to appear. “Then they say, ‘I’ve got a model for lung cancer!’ Well, it ain’t a model for lung cancer, because lung cancer in humans has a hundred mutations,” he says. “It looks like the most complicated thing you’ve ever seen, genetically.”
Homer Pearce, who once ran cancer research and clinical investigation at Eli Lilly and is now research fellow at the drug company, agrees that mouse models are “woefully inadequate” for determining whether a drug will work in humans. “If you look at the millions and millions and millions of mice that have been cured, and you compare that to the relative success, or lack thereof, that we’ve achieved in the treatment of metastatic disease clinically,” he says, “you realize that there just has to be something wrong with those models.”
Vishva Dixit, a vice president for research in molecular oncology at Genentech in South San Francisco, is even more horrified that “99% of investigators in industry and in academia use xenografts.” Why is the mouse model so heavily used? Simple. “It is very convenient, easily manipulated,” Dixit explains. “You can assess tumor size just by looking at it.”
Although drug companies clearly recognize the problem, they haven’t fixed it. And they’d better, says Weinberg, “if for no other reason than [that] hundreds of millions of dollars are being wasted every year by drug companies using these models.”
Even more depressing is the very real possibility that reliance on this flawed model has caused researchers to pass over drugs that would work in humans. After all, if so many promising drugs that clobbered mouse cancers failed in man, the reverse is also likely: More than a few of the hundreds of thousands of compounds discarded over the past 20 years might have been truly effective agents. Roy Herbst, who divides his time between bench and bedside at M.D. Anderson and who has run big trials on Iressa and other targeted therapies for lung cancer, is sure that happens often. “It’s something that bothers me a lot,” he says. “We probably lose a lot of things that either don’t have activity on their own, or we haven’t tried in the right setting, or you don’t identify the right target.”
If everyone understands there’s a problem, why isn’t anything being done? Two reasons, says Weinberg. First, there’s no other model with which to replace that poor mouse. Second, he says, “is that the FDA has created inertia because it continues to recognize these [models] as the gold standard for predicting the utility of drugs.”
In the end, it is not localized tumors that kill people with cancer; it is the process of metastasis–an incredible 90% of the time. Aggressive cells spread to the bones, liver, lungs, brain, or other vital areas, wreaking havoc.
So you’d think that cancer researchers would have been bearing down on this insidious phenomenon for years, intently studying the intricate mechanisms of invasion. Hardly. According to a FORTUNE examination of NCI grants going back to 1972, less than 0.5% of study proposals focused primarily on metastasis–trying to understand, for instance, its role in a specific cancer (e.g., breast, prostate) or just the process itself. Of nearly 8,900 NCI grant proposals awarded last year, 92% didn’t even mention the word metastasis.
That is also the devastating conclusion of a major study published last August in the British Medical Journal. Two Italian pharmacologists pored over the results of trials of 12 new anticancer drugs that had been approved for the European market from 1995 to 2000, and compared them with standard treatments for their respective diseases. The researchers could find no substantial advantages–no improved survival, no better quality of life, no added safety–with any of the new agents. All of them, though, were several times more expensive than the old drugs. In one case, the price was 350 times higher.
WHY THE NEW DRUGS DISAPPOINT
Flawed models for drug development. Obsession with tumor shrinkage. Focus on individual cellular mechanisms to the near exclusion of what’s happening in the organism as a whole. All these failures come to a head in the clinical trial–a rigidly controlled, three-phase system for testing new drugs and other medical procedures in humans. The process remains the only way to get from research to drug approval–and yet it is hard to find anyone in the cancer community who isn’t maddeningly frustrated by it.
In February 2003 a blue-ribbon panel of cancer-center directors concluded that clinical trials are “long, arduous,” and burdened with regulation; without major change and better resources, the panel concluded, the “system is likely to remain inefficient, unresponsive, and unduly expensive.”
All that patients know is that the process has little to offer them. Witness the fact that a stunning 97% of adults with cancer don’t bother to participate.
There are two major problems with clinical trials. The first is that their duration and cost mean that drug companies–which sponsor the vast majority of such trials–have an overwhelming incentive to test compounds that are likely to win FDA approval. After all, they are public companies by and large, with shareholders demanding a return on investment. So the companies focus not on breakthrough treatments but on incremental improvements to existing classes of drugs. The process does not encourage risk taking or entrepreneurial approaches to drug discovery. It does not encourage brave new thinking. Not when a drug typically takes 12 to 14 years to develop. And not with $802 million–that’s the oft-cited cost of developing a drug–on the line.
What’s more, the system essentially forces companies to test the most promising new compounds on the sickest patients–where it is easier to see some activity (like shrinking tumors) but almost impossible to cure people. At that point the disease has typically spread too far and the tumors have become too ridden with genetic mutations. Thus drugs that might have worked well in earlier-stage patients often never get the chance to prove it. (As you’ll see, that may be a huge factor in the disappointing response so far of one class of promising new drugs.)
The second problem is even bigger: Clinical trials are focused on the wrong goal–on doing “proper” science rather than saving lives. It is not that they provide bad care–patients in trials are treated especially well. But the trials’ very reason for being is to test a hypothesis: Is treatment X better than treatment Y? And sometimes–too often, sadly–the information generated by this tortuously long process doesn’t much matter. If you’ve spent ten-plus years to discover that a new drug shrinks a tumor by an average of 10% more than the existing standard of care, how many people have you really helped?
Thus, the trick is to intervene earlier in that process–especially at key points when lesions occur (known to doctors as dysplasias, hyperplasias, and other precancerous cell phases). To do that, the medical community has to break away from the notion that people in an early stage of carcinogenesis are “healthy” and therefore shouldn’t be treated. People are not healthy if they’re on a path toward cancer.
If this seems radical and far-fetched, consider: We’ve prevented millions of heart attacks and strokes by using the very same strategy. Sporn likes to point out that heart disease doesn’t start with the heart attack; it starts way earlier with the elevated blood cholesterol and lipids that cause arterial plaque. So we treat those. Stroke doesn’t start with the blood clot in the brain. It starts with hypertension. So we treat it with both lifestyle changes and drugs. “Cardiovascular disease, of course, is nowhere near as complex as cancer is,” he says, “but the principle is the same.” Adds Sporn: “All these people who are obsessed with cures, cures, cures, and the miraculous cure which is still eluding us, they’re being–I hate to use this word, but if you want to look at it pragmatically–they’re being selfish by ignoring what could be done in terms of prevention.”
For the nation finally to turn the tide in this brutal war, the cancer community must embrace a coordinated assault on this disease. Doctors and scientists now have enough knowledge to do what Sydney Farber hoped they might do 33 years ago: to work as an army, not as individuals fighting on their own.
The NCI can begin this transformation right away by drastically changing the way it funds research. It can undo the culture created by the RO1s (the grants that launched a million me-too mouse experiments) by shifting the balance of financing to favor cooperative projects focused on the big picture. The cancer agency already has such funding in place, for endeavors called SPOREs (short for specialized programs of research excellence). These bring together researchers from different disciplines to solve aspects of the cancer puzzle. Even so, funding for individual study awards accounts for a full quarter of the agency’s budget and is more than 12 times the money spent on SPORE grants. The agency needs to stop being an automatic teller machine for basic science and instead use the taxpayers’ money to marshall a broad assault on this elusive killer–from figuring out how to stop metastasis in its tracks to coming up with testing models that better mimic human response.
From 1975 to 2005, death rates from breast cancer fell from 31 to 24 per 100,000 people, due to earlier detection as well as more-effective treatment. Mortality from colorectal cancer fell from 28 to 17 per 100,000 people, due to better chemotherapy and, even more, to screening: when colonoscopy finds precancerous polyps, they can be snipped out before they become malignant.
But progress has been wildly uneven. The death rate from lung cancer rose from 43 to 53 per 100,000 people from 1975 to 2005. The death rate from melanoma rose nearly 30 percent. Liver and bile-duct cancer? The death rate has almost doubled, from 2.8 to 5.3 per 100,000. Pancreatic cancer? Up from 10.7 to 10.8. Perhaps the most sobering statistic has nothing to do with cancer, but with the nation’s leading killer, cardiovascular disease. Thanks to a decline in smoking, better ways to control hypertension and cholesterol and better acute care, its age-adjusted mortality has fallen 70 percent in the same period when the overall mortality rate from cancer has fallen 7.5 percent. No wonder cancer “is commonly viewed as, at best, minimally controlled by modern medicine, especially when compared with other major diseases,” wrote Harold Varmus, former director of NCI and now president of Memorial Sloan-Kettering Cancer Center in New York, in 2006.
In the 1970s and 1980s they discovered human genes that, when mutated, trigger or promote cancer, as well as tumor suppressor genes that, when healthy, do as their name implies but when damaged release the brakes on pathways leading to cancer.
It made for a lot of elegant science and important research papers. But it “all seemed to have little or no impact on the methods used by clinicians to diagnose and treat cancers,” wrote Varmus. Basic-science studies of the mechanisms leading to cancer and efforts to control cancer, he observed, “often seemed to inhabit separate worlds.” Indeed, it is possible (and common) for cancer researchers to achieve extraordinary acclaim and success, measured by grants, awards, professorships and papers in leading journals, without ever helping a single patient gain a single extra day of life. There is no pressure within science to make that happen. It is no coincidence that the ratio of useful therapy per basic discovery is abysmal. For other diseases, about 20 percent of new compounds arising from basic biological discoveries are eventually approved as new drugs by the FDA. For cancer, only 8 percent are.