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Saturday, 20 July 2013

30 Years of Breast Screening: 1.3 Million Wrongly Treated

30 Years of Breast Screening: 1.3 Million Wrongly Treated About Biography Information 

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30 Years of Breast Screening: 1.3 Million Wrongly Treated

30 Years of Breast Screening: 1.3 Million Wrongly Treated


The breast cancer industry's holy grail (that mammography is the primary weapon in the war against breast cancer) has been disproved. In fact, mammography appears to have CREATED 1.3 million cases of breast cancer in the U.S. population that were not there.

A disturbing new study published in the New England Journal of Medicine is bringing mainstream attention to the possibility that mammography has caused far more harm than good in the millions of women who have employed it over the past 30 years as their primary strategy in the fight against breast cancer.[i]

Titled "Effect of Three Decades of Screening Mammography on Breast-Cancer Incidence," researchers estimated that among women younger than 40 years of age, breast cancer was overdiagnosed, i.e. "tumors were detected on screening that would never have led to clinical symptoms," in 1.3 million U.S. women over the past 30 years. In 2008, alone, "breast cancer was overdiagnosed in more than 70,000 women; this accounted for 31% of all breast cancers diagnosed."


As we revealed in a previous article,[ii] the primary form of mammography-detected breast cancer is ductal carcinoma in situ (DCIS), also known as 'stage zero' or 'non-invasive breast cancer.' Unlike truly invasive cancer, which expands outward like the crab after which it was named (Greek:  Cancer = Crab), ductal carcinoma is in situ, i.e. situated, non-moving – an obvious contradiction in terms.

Also, DCIS presents without symptoms in the majority of women within which it is detected, and if left untreated will (usually) not progress to cause harm to women. Indeed, without x-ray diagnostic technologies, many if not most of the women diagnosed with it would never have known they had it in the first place. The journal Lancet Oncology, in fact, published a cohort study last year finding that even clinically verified "invasive" cancers appear to regress with time if left untreated:

[We] believe many invasive breast cancers detected by repeated mammography screening do not persist to be detected by screening at the end of 6 years, suggesting that the natural course of many of the screen-detected invasive breast cancers is to spontaneously regress.[iii]

The new study authors point out "The introduction of screening mammography in the United States has been associated with a doubling in the number of cases of early-stage breast cancer that are detected each year." And yet, they noted, only 6.5% of these early-stage breast cancer cases were expected to progress to advanced disease. DCIS and related 'abnormal breast findings,' in other words, may represent natural, benign variations in breast morphology. Preemptive treatment strategies, however, are still employed today as the standard of care, with mastectomy rates actually increasing since 2004.[iv]

The adverse health effects associated with overdiagnosis and overtreatment with lumpectomy, radiation, chemotherapy and hormone-suppressive treatments cannot be underestimated, especially when one considers the profound psychological trauma that follows each stage of diagnosis and treatment, and the additional physiological burdens such psychic injuries lead to, including up-regulation of multidrug resistance genes within cancer as a result of the increased adrenaline associated with the 'flight-or-fight' stress response.[v]

Also, it is now coming to light that chemotherapy and radiation actually increase the proportion of the highly malignant cancer stem cells to the relatively non-malignant daughter cells within the tumor colony. Much in the same way that conventional antibiotic agents will drive multidrug resistance within the subpopulation of surviving post-antibiotic bacteria, ensuring recurrence, conventional treatments also drive the surviving stem-cell enriched tumor populations into greater resistance and metastatic potential when it does inevitably recur. Or worse, radiation therapy may actually increase the 'stemness' of breast cancer cells making them 30 times more malignant (capable of forming new tumors).

If it is indeed true that DCIS, other abnormal breast findings, as well as clinically confirmed invasive breast cancer, either remain benign or regress when left untreated, the entire breast cancer industry, which is already deeply mired in cause-marketing conflicts of interest, must radically reform itself, or face massive financial and ethical liabilities vis-à-vis outdated and no longer "evidence-based" practices.

Another serious problem with mammography (and there are dozens of them) not addressed in this latest research finding concerns the unique carcinogenicity of the x-rays the technology employs. We now know that the 30 kVp radiation, colloquially known as "low energy" x-rays, are between 300-400% more carcinogenic than the "higher energy" radiation given off by atomic bomb blasts (200 kVp or higher).[vi]  Present day radiation risk models used to assess the known breast cancer risk associated with mammography against the purported benefits do not take into this profound discrepancy. In fact, these models were developed before DNA was even discovered.

Also, considering that breast cancer susceptibility genes, BRCA1/BRCA2, interfere with the DNA self-repair mechanisms needed to reduce the carcinogenicity associated with radiation exposure within those who carry these genetic variations, the harms associated with mammography may be exponentially higher than the conventional medical community presently understands and communicates to their patients.  Indeed, it is likely that x-ray based mammography screenings have been planting the seeds of future radiation-induced breast cancer within exposed populations.

With top-tier biomedical journals now publishing research diametrically opposed to the policies and recommendations of both governmental, non-governmental and industry-sponsored health organizations, the time is ripe for us to critically evaluate conventional medicine's conventional standard of care and to educate ourselves further to the true causes of cancer, and how to go about preventing and/or removing them.

Thursday, 18 July 2013

Obesity Double Whammy: Sugary Sodas in BPA Cans and Plastic

Obesity Double Whammy: Sugary Sodas in BPA Cans and Plastic Biography

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Obesity Double Whammy: Sugary Sodas in BPA Cans and Plastic

Obesity Double Whammy: Sugary Sodas in BPA Cans and Plastic 

New research from New York State University has confirmed a link exists between Bisphenol A (BPA) and obesity. But there are a few caveats that reveal an even bigger link exposed in other research: The combination of sugary sodas in canned and plastic containers.

The NYSU medical researchers studied 2,838 kids between six and 19 years old, using the National Health and Nutritional Examination Survey between 2003-2008 (NHANES 2003-2008) The scientists compared the intake of the kids' urinary BPA levels with their BMI to determine the relative degree of obesity and general weight status. Out of the population, 1,047 qualified as obese and 590 of the kids were overweight. The researchers also cross-referenced the results with the kids' ages and ethnicity.

Their findings determined that while over 22% of kids with the most urinary BPA levels (highest quartile) were obese, only 10% of kids with the lowest BPA levels (lowest quartile) were obese.

More than twice the obesity rate is more than a strong association. The study's lead researcher Dr. Leonardo Trasande told HealthDay that, "BPA has been associated with adult obesity and heart disease," and the findings "raise further questions about the need to limit BPA exposure in children."


 
But the NYSU study also presented a wrinkle in the data. The association between BPA and obesity was primarily among teenagers of all races, and white children.

This has produced some skepticism regarding whether the relationship with BPA is solid enough, even though the obesity rates were more than twice for those with the most BPA in their urine overall, and other research has also found a definite link between hormone disruption and BPA, along with the potential for weight gain with higher BPA exposure.

For example, another recent study, this one from Shanghai's Jiao-Tong University School of Medicine, found that BPA exposure was related to higher levels of fat mass among women. The study tested 246 premenopausal women over 20 years old who were otherwise healthy.

Most convincing is another study, published this past July from the West Virginia University School of Medicine. This study also found a link between BPA and obesity, but this link was consistent across all genders and races. Interestingly, this study also used the National Health and Nutritional Examination Survey 2003-2008 data to collect the findings.

And the findings were just as stark. Those with the highest levels of BPA in their urine were nearly 70% more likely to be obese.

The difference between the West Virginia University study and the NYSU study? The West Virginia study tracked adult men and women, while the NYSU tracked kids aged six through 19 years old.

As we correlate the data from these two studies, we find that the connection between BPA and obesity is evident amongst all teenagers and all adults. The data is robust and the evidence clear.

This leaves the only yet-to-understand group being younger non-white children.

One of the confounders not discussed or eliminated in the research was breastfeeding. A 2012 study from Australia's Flinders University School of Medicine found that children who were breastfed were significantly less likely to be obese during their childhood than those who did not breastfeed.

Other childhood confounders also exist. Physical activity, diet of the mother and childhood diet are also factors that prove difficult to eliminate.

Sugary Sodas
One of the most important factors to be considered between children and teenagers is the consumption of sugary sodas. Sodas provide the most popular vehicle for BPA consumption – from soda cans to plastic bottles of cola and other drinks.

In a 2011 study by the U.S. Centers of Disease Control, kids between the ages of 12 and 19 – teenagers – were the largest consumers of sugary sodas among all ages. Teenage boys consume an average of 273 kcal of soda per day, and teenage girls consume an average of 171 kcal of sugary drinks a day. This contrasts greatly from kids between six and eleven years old, who only consume an average of 112 kcal (girls) to 141 kcal (boys).

Adults aged 20 to 39 years old also drink less sugary drinks than teenagers, but not by much. They drink between 252 kcal (men) and 138 kcal (women). This is still dramatically higher than children, and almost at par with the teenagers.

This correlation indicates a clear relationship between BPA, sugary drinks and obesity, because after all, most sugary sodas are consumed in BPA containers. And numerous studies have found a link between obesity and the consumption of sugary sodas.

This connection is especially definite for sodas sweetened with high fructose corn syrup (HFCS). For example, in a study from Taipei's National Yang Ming University, kids who drank more HFCS sodas were between three and five times more likely to be obese than those who drank the least amount of HFCS-sweetened sodas.

What we find amongst this combination of research is what we might call a double-whammy: A sugary HFCS soda in a container made with BPA that disrupts hormones and stimulates fat cell growth. This double-whammy is what we are feeding our kids. It is also what our young adults are hooked on - a sugary sweet HFCS caffeine buzz in contaminated containers compounded by overeating and less activity. This combination is quickly turning America into, well, the land of blimps.

REFERENCES
Trasande L, Attina TM, Blustein J. Association Between Urinary Bisphenol A Concentration and Obesity Prevalence in Children and Adolescents JAMA. 2012;308(11):1113-1121.
Zhao HY, Bi YF, Ma LY, Zhao L, Wang TG, Zhang LZ, Tao B, Sun LH, Zhao YJ, Wang WQ, Li XY, Xu MY, Chen JL, Ning G, Liu JM. The effects of bisphenol A (BPA) exposure on fat mass and serum leptin concentrations have no impact on bone mineral densities in non-obese premenopausal women. Clin Biochem. 2012 Sep 9. pii: S0009-9120(12)00505-X.
Scott JA, Ng SY, Cobiac L. The relationship between breastfeeding and weight status in a national sample of Australian children and adolescents. BMC Public Health. 2012 Feb 7;12:107. doi: 10.1186/1471-2458-12-107.
Ogdan CL, Kit BK, Carroll MD, Park S. Consumption of Sugar Drinks in the United States, 2005-2008. NCHS Data Brief. 2011 Aug; 71.
Lin WT, Huang HL, Huang MC, Chan TF, Ciou SY, Lee CY, Chiu YW, Duh TH, Lin PL, Wang TN, Liu TY, Lee CH. Effects on uric acid, body mass index and blood pressure in adolescents of consuming beverages sweetened with high-fructose corn syrup. Int J Obes (Lond). 2012 Aug 14.
Nikpartow N, Danyliw AD, Whiting SJ, Lim HJ, Vatanparast H. Beverage consumption patterns of Canadian adults aged 19 to 65 years. Public Health Nutr.  2012 Aug 29:1-10.
Bray GA. Fructose and Risk of Cardiometabolic Disease. Curr Atheroscler Rep.

Sugar, Inflammation, Angiogenesis & Cancer

Sugar, Inflammation, Angiogenesis & Cancer Biography

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Sugars and the inflammation and acidic environments they create are important constituents of the local environment of tumors. In most types of cancer inflammatory conditions are present before malignancy changes occur. "Smoldering inflammation in tumor microenvironments has many tumor-promoting effects. Inflammation aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents."[4]

The entire subject of inflammation, angiogenesis, sugar and cancer is crucial to understanding the links between cancer and the foods we eat. When we begin to zero in on inflammation and the acid conditions caused by excessive consumption of simple sugars, including fructose and high-fructose corn syrup, we begin to see more clearly how food and cancer are intimately connected.

In July 2012 a leading U.S. cancer lobby group urged the surgeon general to conduct a sweeping study of the impact of sugar-sweetened beverages on consumer health, saying such drinks play a major role in the nation's obesity crisis and require a U.S. action plan. In a letter to U.S. Health Secretary Kathleen Sebelius, the American Cancer Society's advocacy affiliate called for a comprehensive review along the lines of the U.S. top doctor's landmark report on the dangers of smoking in 1964.

The ruckus is about the growing connection between high sugar intake, mineral depletion, dehydration, diabetes, heart disease and cancer. Sugar causes cancer because the tendency of high-carbohydrate consumers tends toward dehydration, which is pro-inflammatory and thus pro-cancer.[5]

Pancreatic cancer cells use the sugar fructose to help tumors grow more quickly.[6] Tumor cells fed both glucose and fructose used the two sugars in two different ways, a team at the University of California Los Angeles found. Their findings, published in the journal Cancer Research, helps explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types. Researchers concluded that anyone wishing to curb their cancer risk should start by reducing the amount of sugar they eat.

This is the first time a link has been shown between fructose and cancer proliferation. "In this study we show that cancers can use fructose just as readily as glucose to fuel their growth," said Dr. Anthony Heaney of UCLA's Jonsson Cancer Center, the study's lead author. "The modern diet contains a lot of refined sugar including fructose and it's a hidden danger implicated in a lot of modern diseases, such as obesity, diabetes and fatty liver." While this study was done on pancreatic cancer, these findings may not be unique to that cancer type, Heaney said. "These findings show that cancer cells can readily metabolize fructose to increase proliferation."

It has been known for decades that cancer cells thrive on glucose. Moreover, foods that cause a sharp rise in blood glucose (i.e. foods with a high-glycemic index ranking) trigger the secretion of insulin and insulin growth factor (IGF-1), two hormones that also promote cancer growth.

Researchers using rats have found that a low-carbohydrate high-protein diet reduces blood glucose, insulin, and glycolysis, slows tumor growth, reduces tumor incidence, and works additively with existing therapies without weight loss or kidney failure.[7] Such a diet, therefore, has the potential of being both a novel cancer prophylactic and treatment.

Otto Warburg

Dr. Otto Warburg's 1924 paper, "On metabolism of tumors," stated, "Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar." If you've ever made wine, you'll know that fermentation requires sugar. The metabolism of cancer is approximately eight times greater than the metabolism of normal cells. Doctors have known for a long time that cancer metabolizes much differently than normal cells. Normal cells need oxygen. Cancer cells disregard oxygen when adequate glucose is present.

Warburg's hypothesis was of course that cancer growth was caused when cancer cells converted glucose into energy without using oxygen. Healthy cells make energy by converting pyruvate and oxygen. The pyruvate is oxidized within a healthy cell's mitochondria, and Warburg theorized that since cancer cells don't oxidize pyruvate, cancer must be considered a mitochondrial dysfunction.

Most, if not all, tumor cells have a high demand on glucose compared to benign cells of the same tissue and conduct glycolysis even in the presence of oxygen (the Warburg effect). In addition, many cancer cells express insulin receptors (IRs) and show hyperactivation of the IGF1R-IR (IGF-1 receptor/ insulin receptor) pathway. Evidence exists that chronically elevated blood glucose, insulin and IGF-1 levels facilitate tumor genesis and worsen the outcome in cancer patients.

Treating diabetic patients, A. Braunstein observed in 1921 that in those who developed cancer, glucose secretion in the urine disappeared. One year later, R. Bierich described the remarkable accumulation of lactate in the micromilieu of tumor tissues and demonstrated lactate to be essential for invasion of melanoma cells into the surrounding tissue. One year after that Warburg began his experiments that eventually ended for him with a Nobel Prize.

Sugar turns the body into a suitable breeding ground for viruses, bacteria, fungi and cancer by devastating the immune system.

Knowing that one's cancer needs sugar, does it make sense to feed it sugar? Does it make sense to have a high-carbohydrate diet?

Of the four million cancer patients being treated in America today, hardly any are offered any scientifically guided nutrition therapy beyond being told to "just eat good foods." Oncologists have no shame about this, insisting that diet has little to do with cancer.

Cancer patients should not be feeding their cancers like they would feed cotton candy to their grandchildren. As long as this cancer cell can get a regular supply of sugar—or glucose—it lives and thrives longer than it should. Now imagine oncologists getting enlightened and they start to advise their patients to starve the cancer instead of bombing it to smithereens with chemotherapy and radiation treatments all the while feeding the cancer with sugar!
Sugar, Inflammation, Angiogenesis & Cancer
  Sugar, Inflammation, Angiogenesis & Cancer
  Sugar, Inflammation, Angiogenesis & Cancer
  Sugar, Inflammation, Angiogenesis & Cancer
  Sugar, Inflammation, Angiogenesis & Cancer
  Sugar, Inflammation, Angiogenesis & Cancer
 Sugar, Inflammation, Angiogenesis & Cancer
Sugar, Inflammation, Angiogenesis & Cancer

Suppress/ Delay/ Slow/ Kill Cancer

Suppress/ Delay/ Slow/ Kill Cancer Biography

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Suppress/ Delay/ Slow/ Kill Cancer
Carbohydrates of one of the three macronutrients—the other two being fats and protein. There are simple carbohydrates and complex carbohydrates. Simple carbohydrates include sugars found naturally in foods such a fruits and fruit juices, sodas, some vegetables, white bread, white rice, pasta, milk and milk products, most snack foods, sweets, etc. But let us not forget the simple sugars added to foods during processing and refining that we may have no awareness of. It's the simple sugars that get most of the credit for causing the insulin response and glycation-associated inflammation that can lead to cancer.

Thus by reducing the amount of simple carbohydrates in the diet, the emergence of cancer can be suppressed or delayed, or the proliferation of already existing tumor cells can be slowed down, stopped and reversed by depriving the cancer cells of the food they need for survival.

Drs. Rainer Klement and Ulrike Kammerer conducted a comprehensive review of the literature involving dietary carbohydrates and their direct and indirect effect on cancer cells, which was published in October 2011 in the journal Nutrition and Metabolism, concluding that cancers are so sensitive to the sugar supply that cutting that supply will suppress cancer.[3] "Increased glucose flux and metabolism promotes several hallmarks of cancer such as excessive proliferation, anti-apoptotic signaling, cell cycle progression and angiogenesis."

Also, eating white sugar (or white anything) causes magnesium mineral deficiencies because the magnesium has been removed in the processing, making sugar a ripe target as a major cause of cancer because deficiencies in magnesium are not only pro-inflammatory but also pro-cancer.

More Ways to Cause Cancer with Sugar

High fructose corn syrup (HFCS) causes cancer in a unique way because much of it is contaminated with mercury due to the complex way it is made. High fructose corn syrup causes selenium deficiencies because the mercury in it binds with selenium, driving selenium levels downward. Selenium is crucial for glutathione production and its deficiency in soils tracks mathematically with cancer rates. Selenium and mercury are also eternal lovers having a strong affinity to bond with each other.

Already touched on briefly, excess sugar spikes insulin levels and insulin's eventual depletion. High insulin and insulin-like growth factor (IGF-1) are needed for the control of blood sugar levels that result from chronic ingestion of high-carbohydrate meals (like the typical American diet, that is full of grains and sugars). Increased insulin levels are pro-inflammatory and pro-cancer and can directly promote tumor cell proliferation via the insulin/ IGF-1 signaling pathway.

When it comes to breast cancer, insulin is no friend. One of the biggest reasons is due to the fact that both normal breast cells and cancer cells have insulin receptors on them. When insulin attaches to its receptor, it has the same effect as when estrogen attaches to its receptor: it causes cells to start dividing. The higher your insulin levels are, the faster your breast cells will divide; the faster they divide, the higher your risk of breast cancer is and the faster any existing cancer cells will grow.

There's also another detriment that high insulin levels can inflict. It makes more estrogen available to attach to the estrogen receptors in breast tissue. Insulin regulates how much of the estrogen in your blood is available to attach to estrogen receptors in your breast tissue. When estrogen travels in the blood, it either travels alone seeking an estrogen receptor, or it travels with a partner, a protein binder, that prevents it from attaching to an estrogen receptor. Insulin regulates the number of protein binders in the blood. So, the higher your insulin levels are, the fewer the number of protein binders there will be and therefore the more free estrogen that will be available to attach to estrogen receptors.

In other words, when your insulin levels are up, free-estrogen levels are up, and both of them speed up cell division. That's why high insulin levels increase your risk of breast cancer so much. Eating sugar increases your risk of breast cancer in another way. It delivers a major blow to your immune system with the force of a prizefighter.

Dr. Horner talks about a study conducted by Harvard Medical School (2004) that found that women who, as teenagers, ate high-glycemic foods that increased their blood glucose levels had a higher incidence of breast cancer later in life. "So, encouraging your teenage daughter to cut back on sugar will help her to lower her risk of breast cancer for the rest of her life," she said.

Cancer & Sugar - Strategy for Selective Starvation of Cancer

Cancer & Sugar - Strategy for Selective Starvation of Cancer Biography

Source(google.com.pk)
According to researchers at the University of California, San Francisco, sugar poses a health risk—contributing to around 35 million deaths globally each year. So high is sugar's toxicity that it should now be considered a potentially toxic substance like alcohol and tobacco. Its link with the onset of diabetes is such that punitive regulations, such as a tax on all foods and drinks that contain "added'' sugar, are now warranted, the researchers concluded. They also recommend banning sales in or near schools, as well as placing age limits on the sale of such products.

Sugar's harmful effects do not stop at diabetes, metabolic syndrome, hyper- and hypoglycemia, GERD and heart disease. Sugar and cancer are locked in a death grip, yet oncologists often fail to do what's necessary to stop their patients from feeding their cancers with sweets.

Whereas many within the mainstream medical community insist on promoting the belief that the link between certain types of food with an increased risk of cancer is "weak" or only "nominally significant." They believe that research "linking foodstuffs to cancer reveals no valid medical patterns." We also find such superficial attitudes promoted in the medical press-all of which lack any kind of medical depth.


 
An increasing number of medical scientists and many alternative practitioners know that the most logical, effective, safe, necessary and inexpensive way to treat cancer is to cut off the supply of food to tumors and cancer cells, starving them with a lack of glucose. The therapeutic strategy for selective starvation of tumors by dietary modification (ketogenic diet) is one of the principle forms of therapy that is necessary for cancer patients to win their war on cancer.

Researchers at Huntsman Cancer Institute in Utah were one of the first to discover that sugar "feeds" tumors. The research published in the journal Proceedings of the National Academy of Sciences said, "It's been known since 1923 that tumor cells use a lot more glucose than normal cells. Our research helps show how this process takes place, and how it might be stopped to control tumor growth," says Don Ayer, Ph.D., a professor in the Department of Oncological Sciences at the University of Utah.

Dr. Thomas Graeber, a professor of molecular and medical pharmacology, has investigated how the metabolism of glucose affects the biochemical signals present in cancer cells. In research published June 26, 2012 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation—that is, depriving cancer cells of glucose—activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species (ROS).[1]

Refined sugars are strongly linked to cancer, not only as a cause of it but also as something that feeds the cancer cells once a person has the disease—Nothing could be more important to consider in the attempt to improve the outcome of cancer treatments. The kinds of sugar so prevalent in today's standard American diet lead to cancer directly by causing inflammation throughout the body but in some places more than others depending on the individual and their constitution. Listen to this video and hear how simple this all really is. Once cancer cells are established in the body, they depend on steady glucose availability in the blood for their energy; they are not able to metabolize significant amounts of fatty acids or ketone bodies,[2]. so they need sugar.

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer & Sugar - Strategy for Selective Starvation of Cancer 

Cancer's Sweet Tooth

Cancer's Sweet Tooth Biography

Source(google.com.pk)
During the last 10 years I have worked with more than 500 cancer patients as director of nutrition for Cancer Treatment Centers of America in Tulsa, Okla. It puzzles me why the simple concept "sugar feeds cancer" can be so dramatically overlooked as part of a comprehensive cancer treatment plan.

Of the 4 million cancer patients being treated in America today, hardly any are offered any scientifically guided nutrition therapy beyond being told to "just eat good foods." Most patients I work with arrive with a complete lack of nutritional advice. I believe many cancer patients would have a major improvement in their outcome if they controlled the supply of cancer's preferred fuel, glucose. By slowing the cancer's growth, patients allow their immune systems and medical debulking therapies -- chemotherapy, radiation and surgery to reduce the bulk of the tumor mass -- to catch up to the disease. Controlling one's blood-glucose levels through diet, supplements, exercise, meditation and prescription drugs when necessary can be one of the most crucial components to a cancer recovery program. The sound bite -- sugar feeds cancer -- is simple. The explanation is a little more complex.

The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first discovered that cancer cells have a fundamentally different energy metabolism compared to healthy cells. The crux of his Nobel thesis was that malignant tumors frequently exhibit an increase in anaerobic glycolysis -- a process whereby glucose is used as a fuel by cancer cells with lactic acid as an anaerobic byproduct -- compared to normal tissues.1 The large amount of lactic acid produced by this fermentation of glucose from cancer cells is then transported to the liver. This conversion of glucose to lactate generates a lower, more acidic pH in cancerous tissues as well as overall physical fatigue from lactic acid buildup.2,3 Thus, larger tumors tend to exhibit a more acidic pH.4

This inefficient pathway for energy metabolism yields only 2 moles of adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of ATP in the complete aerobic oxidation of glucose. By extracting only about 5 percent (2 vs. 38 moles of ATP) of the available energy in the food supply and the body's calorie stores, the cancer is "wasting" energy, and the patient becomes tired and undernourished. This vicious cycle increases body wasting.5 It is one reason why 40 percent of cancer patients die from malnutrition, or cachexia.6

Hence, cancer therapies should encompass regulating blood-glucose levels via diet, supplements, non-oral solutions for cachectic patients who lose their appetite, medication, exercise, gradual weight loss and stress reduction. Professional guidance and patient self-discipline are crucial at this point in the cancer process. The quest is not to eliminate sugars or carbohydrates from the diet but rather to control blood glucose within a narrow range to help starve the cancer and bolster immune function.

The glycemic index is a measure of how a given food affects blood-glucose levels, with each food assigned a numbered rating. The lower the rating, the slower the digestion and absorption process, which provides a healthier, more gradual infusion of sugars into the bloodstream. Conversely, a high rating means blood-glucose levels are increased quickly, which stimulates the pancreas to secrete insulin to drop blood-sugar levels. This rapid fluctuation of blood-sugar levels is unhealthy because of the stress it places on the body (see glycemic index chart, p. 166).


Sugar in the Body and Diet

Sugar is a generic term used to identify simple carbohydrates, which includes monosaccharides such as fructose, glucose and galactose; and disaccharides such as maltose and sucrose (white table sugar). Think of these sugars as different-shaped bricks in a wall. When fructose is the primary monosaccharide brick in the wall, the glycemic index registers as healthier, since this simple sugar is slowly absorbed in the gut, then converted to glucose in the liver. This makes for "time-release foods," which offer a more gradual rise and fall in blood-glucose levels. If glucose is the primary monosaccharide brick in the wall, the glycemic index will be higher and less healthy for the individual. As the brick wall is torn apart in digestion, the glucose is pumped across the intestinal wall directly into the bloodstream, rapidly raising blood-glucose levels. In other words, there is a "window of efficacy" for glucose in the blood: levels too low make one feel lethargic and can create clinical hypoglycemia; levels too high start creating the rippling effect of diabetic health problems.

The 1997 American Diabetes Association blood-glucose standards consider 126 mg glucose/dL blood or greater to be diabetic; 126 mg/dL is impaired glucose tolerance and less than 110 mg/dL is considered normal. Meanwhile, the Paleolithic diet of our ancestors, which consisted of lean meats, vegetables and small amounts of whole grains, nuts, seeds and fruits, is estimated to have generated blood glucose levels between 60 and 90 mg/dL.7 Obviously, today's high-sugar diets are having unhealthy effects as far as blood-sugar is concerned. Excess blood glucose may initiate yeast overgrowth, blood vessel deterioration, heart disease and other health conditions.8

Understanding and using the glycemic index is an important aspect of diet modification for cancer patients. However, there is also evidence that sugars may feed cancer more efficiently than starches (comprised of long chains of simple sugars), making the index slightly misleading. A study of rats fed diets with equal calories from sugars and starches, for example, found the animals on the high-sugar diet developed more cases of breast cancer.9 The glycemic index is a useful tool in guiding the cancer patient toward a healthier diet, but it is not infallible. By using the glycemic index alone, one could be led to thinking a cup of white sugar is healthier than a baked potato. This is because the glycemic index rating of a sugary food may be lower than that of a starchy food. To be safe, I recommend less fruit, more vegetables, and little to no refined sugars in the diet of cancer patients.


What the Literature Says 

A mouse model of human breast cancer demonstrated that tumors are sensitive to blood-glucose levels. Sixty-eight mice were injected with an aggressive strain of breast cancer, then fed diets to induce either high blood-sugar (hyperglycemia), normoglycemia or low blood-sugar (hypoglycemia). There was a dose-dependent response in which the lower the blood glucose, the greater the survival rate. After 70 days, 8 of 24 hyperglycemic mice survived compared to 16 of 24 normoglycemic and 19 of 20 hypoglycemic.10 This suggests that regulating sugar intake is key to slowing breast tumor growth (see chart, p. 164).

In a human study, 10 healthy people were assessed for fasting blood-glucose levels and the phagocytic index of neutrophils, which measures immune-cell ability to envelop and destroy invaders such as cancer. Eating 100 g carbohydrates from glucose, sucrose, honey and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria. Starch did not have this effect.11

A four-year study at the National Institute of Public Health and Environmental Protection in the Netherlands compared 111 biliary tract cancer patients with 480 controls. Cancer risk associated with the intake of sugars, independent of other energy sources, more than doubled for the cancer patients.12 Furthermore, an epidemiological study in 21 modern countries that keep track of morbidity and mortality (Europe, North America, Japan and others) revealed that sugar intake is a strong risk factor that contributes to higher breast cancer rates, particularly in older women.13

Limiting sugar consumption may not be the only line of defense. In fact, an interesting botanical extract from the avocado plant (Persea americana) is showing promise as a new cancer adjunct. When a purified avocado extract called mannoheptulose was added to a number of tumor cell lines tested in vitro by researchers in the Department of Biochemistry at Oxford University in Britain, they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited the growth rate of the cultured tumor cell lines. The same researchers gave lab animals a 1.7 mg/g body weight dose of mannoheptulose for five days; it reduced tumors by 65 to 79 percent.14 Based on these studies, there is good reason to believe that avocado extract could help cancer patients by limiting glucose to the tumor cells.

Since cancer cells derive most of their energy from anaerobic glycolysis, Joseph Gold, M.D., director of the Syracuse (N.Y.) Cancer Research Institute and former U.S. Air Force research physician, surmised that a chemical called hydrazine sulfate, used in rocket fuel, could inhibit the excessive gluconeogenesis (making sugar from amino acids) that occurs in cachectic cancer patients. Gold's work demonstrated hydrazine sulfate's ability to slow and reverse cachexia in advanced cancer patients. A placebo-controlled trial followed 101 cancer patients taking either 6 mg hydrazine sulfate three times/day or placebo. After one month, 83 percent of hydrazine sulfate patients increased their weight, compared to 53 percent on placebo.15 A similar study by the same principal researchers, partly funded by the National Cancer Institute in Bethesda, Md., followed 65 patients. Those who took hydrazine sulfate and were in good physical condition before the study began lived an average of 17 weeks longer.16

In 1990, I called the major cancer hospitals in the country looking for some information on the crucial role of total parenteral nutrition (TPN) in cancer patients. Some 40 percent of cancer patients die from cachexia.5 Yet many starving cancer patients are offered either no nutritional support or the standard TPN solution developed for intensive care units. The solution provides 70 percent of the calories going into the bloodstream in the form of glucose. All too often, I believe, these high-glucose solutions for cachectic cancer patients do not help as much as would TPN solutions with lower levels of glucose and higher levels of amino acids and lipids. These solutions would allow the patient to build strength and would not feed the tumor.17

The medical establishment may be missing the connection between sugar and its role in tumorigenesis. Consider the million-dollar positive emission tomography device, or PET scan, regarded as one of the ultimate cancer-detection tools. PET scans use radioactively labeled glucose to detect sugar-hungry tumor cells. PET scans are used to plot the progress of cancer patients and to assess whether present protocols are effective.18

In Europe, the "sugar feeds cancer" concept is so well accepted that oncologists, or cancer doctors, use the Systemic Cancer Multistep Therapy (SCMT) protocol. Conceived by Manfred von Ardenne in Germany in 1965, SCMT entails injecting patients with glucose to increase blood-glucose concentrations. This lowers pH values in cancer tissues via lactic acid formation. In turn, this intensifies the thermal sensitivity of the malignant tumors and also induces rapid growth of the cancer. Patients are then given whole-body hyperthermia (42 C core temperature) to further stress the cancer cells, followed by chemotherapy or radiation.19 SCMT was tested on 103 patients with metastasized cancer or recurrent primary tumors in a clinical phase-I study at the Von Ardenne Institute of Applied Medical Research in Dresden, Germany. Five-year survival rates in SCMT-treated patients increased by 25 to 50 percent, and the complete rate of tumor regression increased by 30 to 50 percent.20 The protocol induces rapid growth of the cancer, then treats the tumor with toxic therapies for a dramatic improvement in outcome.

The irrefutable role of glucose in the growth and metastasis of cancer cells can enhance many therapies. Some of these include diets designed with the glycemic index in mind to regulate increases in blood glucose, hence selectively starving the cancer cells; low-glucose TPN solutions; avocado extract to inhibit glucose uptake in cancer cells; hydrazine sulfate to inhibit gluconeogenesis in cancer cells; and SCMT.

A female patient in her 50s, with lung cancer, came to our clinic, having been given a death sentence by her Florida oncologist. She was cooperative and understood the connection between nutrition and cancer. She changed her diet considerably, leaving out 90 percent of the sugar she used to eat. She found that wheat bread and oat cereal now had their own wild sweetness, even without added sugar. With appropriately restrained medical therapy -- including high-dose radiation targeted to tumor sites and fractionated chemotherapy, a technique that distributes the normal one large weekly chemo dose into a 60-hour infusion lasting days -- a good attitude and an optimal nutrition program, she beat her terminal lung cancer. I saw her the other day, five years later and still disease-free, probably looking better than the doctor who told her there was no hope.

Cancer's Sweet Tooth

Cancer's Sweet Tooth 

Cancer's Sweet Tooth 

 

Cancer's Sweet Tooth

 

Cancer's Sweet Tooth

Cancer's Sweet Tooth

Cancer's Sweet Tooth


Cancer's Sweet Tooth


 

Cancer's Sweet Tooth

 

Cancer's Sweet Tooth

 

Cancer's Sweet Tooth

Cancer's Sweet Tooth

Cancer's Sweet Tooth