Hot Dog!

Processed MeatsAre we knowingly jeopardizing our collective lives? Common more to developed countries, colon cancer is the third most frequently diagnosed form of the disease. The risk in the United States is about 7%, but is based on certain factors: family history, colon polyps, and age among them. At the 2009 All-Star Game, the Physicians Committee for Responsible Medicine (PCRM) posted a 48-feet-wide billboard on the highway near Busch Stadium in St. Louis proclaiming the causative nature of the lowly hot dog in colorectal disease. Why? Because processed meats have been convincingly linked to colorectal cancer.

The physicians hoped to persuade the baseball commissioner, Bud Selig, to put a warning label on hot dogs, similar to that on cigarette packs.  In fact, the billboard portrayed a handful of franks posed inside a cigarette pack, which was labeled, “Unlucky Strike.”  Krista Haynes, a dietitian for the PCRM’s Cancer project, stated that, “Baseball stadiums need to be frank about the cancer risk posed by hot dogs and other processed meats,” adding that, “Like cigarettes, hot dogs should come with a warning label that helps baseball fans and other consumers understand the health risks.”

The National Hot Dog and Sausage Council projected that more than 21 million hot dogs would be sold at ball games that year.  Two years earlier, the American Institute for Cancer Research published a report showing that just one 2-ounce serving of processed meat ingested daily increased the risk of colorectal cancer by 21%.

To add salt to the wound—if not to the hot dog—the PCRM filed lawsuits in New Jersey against Nathan’s, Kraft/Oscar Meyer, Sara Lee and other processors for failing to warn consumers that hot dogs increase the risk of colon cancer.

Hot dogs were probably chosen because of their ubiquity.  Colorectal cancer is not the only disease linked to processed meats.  So, too, are pancreatic, breast, and prostate cancers.  In past years, conventional medicine blamed the saturated fat content of processed meats for risk of disease, but it ignored what are probably worse offenders:  toxins in the fats and, more importantly, additives.

Fats accumulate whatever toxins to which they have been exposed over the lifetime of an animal…or person.  Considering that a cow eats tons of grass in its lifetime, it collects and concentrates toxicants that fell in the rainfall, were sprayed on crops ten miles away (or farther), or that showed up in its man-made supplemental feed.  Heavy metals, pesticides, and even PCB’s have been found in meat, and not just from cattle.

The additives in processed meats include substances that are identified as being carcinogenic, especially the nitrites.  The stuff that meat packers put into sausages and hot dogs makes a list much too detailed to be addressed in this epistle, so attention will be put on what is most likely to cause colorectal cancer.  This does not necessarily apply to red meat—meat from four legs—that is unprocessed.

Nitrites and nitrates historically came into use as naturally occurring contaminants in salt.  People found that meats cured with these contaminants tasted better than meats without them.  After they were identified, nitrites and nitrates (synthetic, of course) were added on purpose.  Both can be toxic, and have to be used carefully.  Natural nitrites come from the breakdown of plant material, particularly from root crops and leaves.  Celery provides a natural source, and is deemed safer than the man-made material, which is cheaper.   Besides adding flavor, they act as antioxidants to prevent rancidity, and they stop bacteria from taking residence in your canned ham.  Think botulism.  Nitrates are not as effective as their cousins until they are broken down into nitrites by micro-organisms.  The problems surface when nitrites form nitrosamines in the digestive system and get into the bloodstream to raise havoc with internal organs.  The government tried to ban this ingredient in the 1970’s, but succumbed to the pressures of the meat industry, which cried that there was no alternative.

Proteins naturally break down into amines and they will mate with nitrites under the right conditions to make nitrosamines.  Such exists in the environs of human stomach acid.  The high cooking temperatures of frying can enhance the formation of nitrosamines.  Ascorbic acid, aka vitamin C, controls the production of this compound, and has been added to some processed meats for a few years.  Canadian cancer scientists discovered that adding salt to processed meats at the table further intensifies the carcinogenic nature of the initial product.  In this case, the list of affected organs expands to include the stomach, bladder, kidneys, and blood (leukemia).  (Hu. 2011)  The possibility of stroke and coronary heart disease are other additions.  (Micha. 2010)

Though it seems that simple red meat is blameless, its cooking process makes a difference.  High-temperature cooking and excessive charring, especially in well-done meats from the grill, add to the burden of cancer risk.  (Sinha. 1999)  This means that nitrite-laden hot dogs need to escape the charring that many people find alluring.

Hot dogs and most other sausage-type meats are normally gray, just like fresh kielbasa or Italian sausage.  People associate the color of their food with quality, red in the case of hot dogs. Nitrates are color fixers besides color enhancers.  Since the USDA and other agencies seem more interested in promoting the interests of industry than the health of the public, we are responsible for assuming our own safety strategies.  Taking vitamin C, and maybe even vitamin E, prior to a nitrite meal is a protective strategy that prevents the formation of nitrosamines.  (Tannenbaum. 1989)  (Tannenbaum and Wishnok. 1991)

Physicians Committee for Responsible Medicine.  Aug. 2009
Hot Dogs Strike Out at All-Star Game and in New Jersey

Eur J Cancer Prev. 2011 Mar;20(2):132-9.
Salt, processed meat and the risk of cancer.
Hu J, La Vecchia C, Morrison H, Negri E, Mery L;
Canadian Cancer Registries Epidemiology Research Group.
Collaborators (8)Paulse B, Dewar R, Dryer D, Kreiger N, Whittaker H, Robson D, Fincham S, Le N.

Int J Vitam Nutr Res Suppl. 1989;30:109-13.
Preventive action of vitamin C on nitrosamine formation.
Tannenbaum SR.

Am J Clin Nutr. 1991 Jan;53(1 Suppl):247S-250S.
Inhibition of nitrosamine formation by ascorbic acid.
Tannenbaum SR, Wishnok JS, Leaf CD.
SourceMassachusetts Institute of Technology, Cambridge 02139.

Cancer Prev Res (Phila). 2010 Jul;3(7):852-64. Epub 2010 Jun 8.
Meat processing and colon carcinogenesis: cooked, nitrite-treated, and oxidized high-heme cured meat promotes mucin-depleted foci in rats.
Santarelli RL, Vendeuvre JL, Naud N, Taché S, Guéraud F, Viau M, Genot C, Corpet DE, Pierre FH.
SourceUniversité de Toulouse, ENVT, INRA, UMR Xénobiotiques, France.

Circulation. 2010; 121: 2271-2283
Expand+Epidemiology and Prevention
Red and Processed Meat Consumption and Risk of Incident Coronary Heart Disease, Stroke, and Diabetes Mellitus  A Systematic Review and Meta-Analysis
Renata Micha, RD, PhD; Sarah K. Wallace, BA; Dariush Mozaffarian, MD, DrPH

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Cell Phones and Cancer

cell phones and cancerThey are called international experts. They work for the International Agency for Research on Cancer, part of the World Health Organization (WHO), and are highly respected in their field. Their recent statement about cell phones and their relationship to cancer has drawn a ho-hum reaction from the garrulous public. This august body has reviewed possible connections between the kind of electromagnetic radiation in cell phones and irregularities in body tissues that might cause brain tumors, both cancerous and non-cancerous, and tumors of the auditory nerves and salivary glands.

Oddly, last year’s studies on the same topic found no direct link of cell phone use to tumor formation anywhere in the body. But there are groups that recoil at the hint of the slightest relationship. Studies conducted in Europe, the United States and New Zealand found that brain tumor patients had not used their cell phones any more often than unaffected persons. Most of the studies fail to show a dose-response relationship, such as would be sought in drug trials. What has been shown in Swedish studies is an increased risk for tumors on the side of the head where the cell phone was held, especially with ten or more years of use. Nonetheless, the WHO team grouped cell phones with category 2B carcinogens that include internal combustion exhausts and DDT, as well as postmenopausal estrogen-progesterone therapy, potassium bromate (a bread additive banned in Europe, Canada, the UK and Brazil, but not in the U.S.), and fiberglass, all of these being modified by the term, “possibly carcinogenic to humans.”

Some of the verifiable dangers of cell phone use include crashing into your garage door, misjudging the arc of a left-hand turn, and getting a ticket in a venue that outlaws the use of such a device while driving.  None of these, however, is 100% predictable.  There are too many “ifs” to allow a definitive answer.

When they became widely available in the early 1990’s, cell phones were suddenly de rigueur.  From the outset they emanated radio waves, the frequencies of which fall between microwaves and FM radio waves.  This might make you feel as though you were caught between a rock and a hard place, being forced to make a decision between your jazz station and the TV dinner.

Your cell phone is more a glorified walkie-talkie defined by a geographical grid in which it will work.  Inside the myriad grids are cells that cover smaller areas.  Each cell uses a set of frequencies to provide service in its specific zone.  Because the power of these frequencies is controlled according to distance from the tower, thus limiting range, the same frequencies may be used in neighboring cells.  Modern antennas are wireless, so they may be set up almost anywhere:  church steeples, trees, atop flagpoles and on tall buildings.  They can even be blocked by trees and topography, just like radio waves.  Your cell message may be routed through the air to a landline, and then through the air again to the person you are calling.  Other times the message goes from your phone to the transmission tower, and then to your recipient.

If you happen to be moving while conversing, the signal weakens as you leave your cell.  At that point your call is handed over to an antenna with a stronger signal.  As long as wireless providers get along with each other, your signal may be relayed to a different provider than yours, who then keeps you in touch.  This is called roaming.

Cell phones cannot cause cancer by directly affecting DNA.  These radio frequency waves are not nearly so strong as x-rays or ultra-violet light.  They are non-ionizing, like visible light waves, heat waves, and FM radio waves.  However, what they do is to heat up the body’s tissues, just as the microwave does to your Idaho potato.  Heating from the inside out, a microwave causes molecules to vibrate and to rub against each other—friction.  This creates the heat that cooks your dinner.  In this cooking technique, a medium-rare piece of meat would be cooked on the inside and pink on the outside, exactly the opposite of what happens inside a broiler, oven, or sauté pan.  Purportedly, the same action occurs when you use a cell phone.  You get hot in the head, if only by a fraction of a degree.  It is speculated that this affects only the cornea of the eye (which, because of lack of vascularization, has no blood vessels to keep it cooled down) more than the rest of the head.  Yet, no cataracts or other pathologies have been noticed.

There is no definitive answer to this poser other than an increase in glucose metabolic activity at the site of cell phone-head contact.   The significance of that is unknown.  People with pacemakers have no special warnings to follow, even if the garage door opens when they cough.  Nonetheless, it is advised that they keep their cell phones out of breast pockets, which is the equivalent of staying indoors to avoid being hit by a meteor or Mary Poppins.

If you have concerns about this issue, you might want to limit cell phone usage.  If you’re a teenager reading this, forget it. You won’t listen, anyway.  You could opt to move the antenna away from your head, which means you either have to yell with all your might and listen really, really hard, or use some kind of hands-free device.  Another option is to buy a phone that gives off very low levels of electromagnetic waves.  What about cordless phones in the house, you know, the kind with a base set and a wireless handset that is lost somewhere in the sofa cushions?  Not a problem, since their power is only .17% (that’s 17/100 percent) of a cell phone.  The last alternative is two tin cans and a string, a very long string.  Except for chemistry, physics and mathematics, most sciences are not as exact as we would like them to be, and reports of their research are sometimes confusing, contradictory, or both.  In some circles these sciences are called practices.


International Commission on Non-Ionizing Radiation Protection (April 1998).
Guidelines For Limiting Exposure To Time-Varying Electric, Magnetic, And Electromagnetic Fields (up to 300 GHz) (PDF).
Health Physics 74 (4): 494–505.

Schüz, J; Jacobsen, R; Olsen, JH; Boice, JD; McLaughlin, JK; Johansen, C (December 2006). Cellular Telephone Use and Cancer Risk: Update of a Nationwide Danish Cohort.
Journal of the National Cancer Institute 98 (23): 1707–1713.

Interphone Study Group (2010).
Brain tumour risk in relation to mobile telephone use: Results of the INTERPHONE international case-control study.
International Journal of Epidemiology 39 (3): 675–694.

Volkow, Nora D.; Tomasi, Dardo; Wang, Gene-Jack; Vaska, Paul; Fowler, Joanna S.; Telang, Frank; Alexoff, Dave; Logan, Jean et al. (2011).
Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism.
JAMA 305 (8): 808–13.

Comments on the Danish cohort study on mobile phones (in German).
Bundesamt für Strahlenschutz [Federal Office for Radiation Protection].
2007-02-22. Retrieved 2010-09-23.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Laundry: A Toxic Venture

laundry productsWe like to think of ourselves as clean and fresh-smelling.  But at what price?  Although suspect for several years, the gentle aromas wafting from our laundry appliances are giving us more than we asked for—pollution.  Venting the dryer outside contributes to the air many of the same chemicals emanating from vehicle and industrial exhausts, but better-smelling.  If the dryer is vented indoors into a bucket of water for lack of a suitable alternative, the effect is concentrated to a much smaller environment.  Although dozens of potentially harmful compounds have been identified in laundry fragrances, from soap to dryer sheets, none, by law, needs to be listed on the product label.  We don’t know what we’re getting for our money, but you can bet it’s more than we bargained for.

The emissions from a dryer are not regulated or monitored.  “If they’re coming out of a smokestack or tailpipe, they’re regulated…” says the lead author of a study performed at the University of Washington.  Reporting in the 2011 online edition of Air Quality, Atmosphere and Health, Anne Steinemann, an environmental engineering professor at the university, found more than two dozen volatile organic compounds emitted through laundry vents.  Of these, seven are named as hazardous air pollutants, two of which are known carcinogens described by the EPA.  Acetaldehyde and benzene enjoy zero safe exposure level.  “These products can affect not only personal health, but also public and environmental health.  The chemicals can go into the air, down the drain and into water bodies,” Steinemann added.   To get a clearer picture of the problem, the aldehydes emitted by using a particular, though unnamed, brand of detergent represents three percent of that emitted by automobiles in the study area (King County, WA).  If combined, the top five brands of laundry products would account for six percent of vehicular aldehyde emissions.  (Steinemann. 2011)

Let’s start with the aldehydes and benzenes.  Acetaldehyde occurs naturally in coffee, breads and ripe fruits, and arises from normal plant metabolism.  It’s produced by the oxidation of alcohol, and is blamed for hangovers.  The liver converts ethanol to acetaldehyde through enzymatic activity.  Occurring also in tobacco smoke, acetaldehyde enhances the addictive effect of nicotine.  It is a probable carcinogen in humans.  (U.S. EPA. 1994)

Benzene is an important industrial solvent, once used as an additive to gasoline to increase octane ratings and to eliminate knocking, but still used to manufacture plastics and synthetic rubber, and, occasionally, some drugs.  Its carcinogenic property is well-established.  It can be formed wherever incomplete combustion of a carbon-rich substance occurs, as in forest fires and volcanoes, and in vehicle exhausts.  Its use in the United States is now limited, although it is making a minimal comeback since tetraethyl lead has been eliminated from vehicular fuel.   (Federal Register. 2006)

Although they can make your clothes soft and cuddly, fabric softeners are some of the most toxic substances around.  Because there are limited alternatives to these handy chemicals, few people are willing to give them up, and even fewer are likely to relate health problems with their use.  If you say they’re made from natural ingredients, remember that arsenic is all natural.  The chemicals in softeners in particular are designed to stay on the clothes for a while, and are absorbed through the skin as well as inhaled.  Because the dryer sheets are heated, they emit their chemicals into the vented air, either outside, inside, or both.  The chemicals that create the softening effect are strong smelling and pungent, so need to be masked with fragrances that are chemically just as bad.

What are some other noxious / toxic ingredients in laundry and other household products and their after effects?  Benzyl acetate in softeners causes pancreatic disease.  Camphor and ethanol affect the central nervous system.  Ethyl acetate affects the kidneys and skin.  Limonene is a sensitizer that is not to be inhaled, although we do anyway, but not on purpose.  The list goes on.  More than ninety-five percent are made from petrochemicals, and may present as neurological maladies, allergic reactions, birth defects, and cancer, not to mention sinusitis and asthma.

What to do?  Look for detergents that have no scent.  If they can’t be found in the supermarket, try a health food store or look online.  There are at least two multi-level marketing firms that offer them; one starts with an “S” and the other with an “A.”  To soften clothes, add a quarter cup of baking soda to the wash water.  The same amount of white vinegar can prevent static cling and still soften fabric…and won’t smell like a salad.

Those aromatic thingies you plug into an outlet?  Chuck ‘em.  Got petroleum-based candles that hide the mackerel miasma?  Dump ‘em.  Find out what’s in your underarm deodorant / anti-perspirants, the furniture polish, the toilet bowl cleaner, shampoo, and even toothpaste.  What makes your trousers wrinkle-free and stain-free, or your baby’s clothes fireproof, or the new sofa stain-resistant?  Nobody would have thought that “April Fresh,” “Ocean Mist,” and “Orange Honey” could be so dangerous.  We might be able to answer a few questions if we keep track of who gets sick and the materials to which they are exposed.  Manufacturers are not required to list ingredients in fragrances, so consumers are at the mercy of the establishment.


Anne C. Steinemann, Lisa G. Gallagher, Amy L. Davis and Ian C. MacGregor
Chemical emissions from residential dryer vents during use of fragranced laundry products
Air Quality, Atmosphere & Health   DOI: 10.1007/s11869-011-0156-1Online First™

University of Washington (2008, July 24).
Toxic Chemicals Found In Common Scented Laundry Products, Air Fresheners.

August 1994

“Control of Hazardous Air Pollutants From Mobile Sources”.
U.S. Environmental Protection Agency. 2006-03-29. p. 15853. Retrieved 2008-06-27.

International Agency for Rescarch on Cancer, World Health Organization. (1988).
Alcohol drinking.
Lyon: World Health Organization, International Agency for Research on Cancer. ISBN 92-832-1244-4. p3

Aberle NS 2nd, Burd L, Zhao BH, Ren J.
Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12.
Alcohol Alcohol. 2004 Sep-Oct;39(5):450-4.

Heisterberg MV, Menné T, Andersen KE, Avnstorp C, Kristensen B, Kristensen O, Kaaber K, Laurberg G, Henrik Nielsen N, Sommerlund M, Thormann J, Veien NK, Vissing S, Johansen JD.
Deodorants are the leading cause of allergic contact dermatitis to fragrance ingredients.
Contact Dermatitis. 2011 May;64(5):258-64.

Jacob SE, Castanedo-Tardan MP.
Alternatives for fragrance-allergic children.
Pediatr Ann. 2008 Feb;37(2):102-3.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Herbicides And Birth Defects

Herbicides & Birth DefectsAfter years of acceptance as a safe and effective weed killer, a popular herbicide is facing the guillotine as teratogenic—it causes malformations in an embryo or fetus. Initial investigations (in the 1970’s) into the safety record of the chemical, glyphosate, indicated that its safety to humans was guaranteed.  An organization called Earth Open Source has now indicted the chemical as a serious risk to public health while accusing the herbicide industry of hiding the truth for decades.

“Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH) are used led us to undertake an embryological approach to explore the effects of low doses of glyphosate in development,” said researchers from the University of Buenos Aires, in Argentina (Paganelli 2010).  But even prior to this, sequestered research from 2007 showed that glyphosate induced fetal malformations in lab animals and “adverse reproductive effects in the male offspring of a certain kind of rat.” (Huffington Post 2011)  The basis for such concern is the interruption of retinoic acid signaling in the development of vertebrate embryos, where Pagnelli et al found that embryos of selected amphibians and chickens demonstrated “…a gradual loss of rhombomere domains, reduction of the optic vesicles, and microcephaly.”

First of all, the terms need description.  Rhombomeres are tiny parts of the neural tube that will become the central nervous system.  Optic vesicles are tiny sacs from which will develop the parts of the eye that actually see things.  Microcephaly is abnormal smallness of the head.  Now that we understand that these characteristics may befall an amphibian or a chicken, must we be concerned that the same could happen to a human embryo?  Could it happen to you or to one of your family from long-term exposure to glyphosate or a related substance?

One of the troublesome things about laboratory experiments is the deliberate exposure of lab animals to doses of chemicals at levels that are unlikely to contact a human.  However, it is a springboard for prudent conjecture, for it introduces the potential “what ifs” of the process.  Related animal testing in Brazil showed that exposure to large amounts of glyphosate caused death in half the study population (Dallegrave 2003), accompanied by severe developmental retardation of fetal skeletons.  A sensible question asks why this data has been kept under wraps for nearly a decade.  The sensible answer is that the chemical industry didn’t want this info to go public for fear of boycott and reprisal that would inflict fiduciary pain.  The industry response is to say that the test results remain unclear, but that might just depend on whose spectacles are covered with petroleum jelly.  After all, testing poisons directly on humans is not, well, um, human.

The EPA, a watchdog that some say wears an eye patch, evaluates biocides every fifteen years in a process called registration review.  Lots can happen in that time.  Glyphosate works on weeds and other plants that are not genetically modified to tolerate it.   That tells the consumer that wherever it is used, the food it protects against weed infiltration is probably a GMO, the long-term effects of which are yet unknown.  When the Argentine government pulled that nation out of recession in the 1990’s it relied on GMO soy to help.  Shortly thereafter, residents near those soy farms—where glyphosate was used—experienced adverse health they had not experienced before.  High rates of birth defects and cancer were among them.  But also, there was destruction of non-tolerant crops and livestock from drifting of the overspray.  Argentine officials were implored by a group of environmental lawyers to ban the glyphosate spray, but the ban was never adopted nation-wide, although several provinces restricted spraying near populated areas.

There is speculation that plants immune to glyphosate develop bacterial infections novel to their species, and that these bacteria pose a threat to animal husbandry by initiating miscarriages.  Corn and soy, the two most heavily genetically modified crops, suffer the most bacterial rampage.  There is a possibility that humans could be affected.  Don Huber, a retired plant pathologist from Purdue, told the agriculture department of these concerns early in 2011, but was offered no comment from the government, while being summarily dismissed by the maker of glyphosate in the United States.  Over a hundred glyphosate formulations are on the market, many made in Asia.  The glyphosate industry labels independent studies as bogus, incomplete, and short-sighted.  They do, however, offer their own research as alternatives.

So, what does retinoic acid have to do with this?  Retinoic acid is the metabolite of Vitamin A that controls growth and development.  If stymied, as happens in the presence of glyphosate, reproductive chaos ensues as hypogonadism and infertility.  We should feel comforted knowing that the glyphosate industry has everything under control.

Chem Res Toxicol. 2010 Aug 9. [Epub ahead of print]
Glyphosate-Based Herbicides Produce Teratogenic Effects on Vertebrates by Impairing Retinoic Acid Signaling.
Paganelli A, Gnazzo V, Acosta H, López SL, Carrasco AE.
Laboratorio de Embriologia Molecular, CONICET-UBA, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 3 degrees piso (1121), Ciudad Autonoma de Buenos Aires, Argentina.

Toxicol Lett. 2003 Apr 30;142(1-2):45-52.
The teratogenic potential of the herbicide glyphosate-Roundup in Wistar rats.
Dallegrave E, Mantese FD, Coelho RS, Pereira JD, Dalsenter PR, Langeloh A.
Department of Pharmacology, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul (UFRGS), Rua Sarmento Leite 500 sala 202, 90046-900 Porto Alegre, RS, Brazil. [email protected]

Environ Mol Mutagen. 1998;31(1):55-9.
32P-postlabeling detection of DNA adducts in mice treated with the herbicide Roundup.
Peluso M, Munnia A, Bolognesi C, Parodi S.

Environ Health Perspect. 2005 Jun;113(6):716-20.
Differential effects of glyphosate and roundup on human placental cells and aromatase.
Richard S, Moslemi S, Sipahutar H, Benachour N, Seralini GE.
Laboratoire de Biochimie et Biologie Moleculaire, USC-INCRA, Université de Caen, Caen, France

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Breast Cancer Prevention

hope-for-a-cureThe natural, alternative approach to cancer treatment and prevention can’t make money for an entity because natural substances cannot be patented.  Therefore, little interest in their exploration and development has emerged.  Without funding, classic studies can’t be performed on a large scale.  Yet, there are a few brave souls who delve into the bright possibilities (hope) of promoting natural substances to heal disease, whether they come directly from foods or indirectly via sensible supplementation.   All the while, common elements that traditional and integrative medicine share are the promotion of health by altering one’s lifestyle and using known factors to predict risk of disease.

There are so many components tied to the onset of cancer that it’s hard to tell which have the strongest influence on prevention or promotion.  In 2009, scientists at the California Pacific Medical Center Research Institute examined a few of these factors and concluded that screening for breast cancer has a positive influence on outcomes, while certain lifestyle interventions may enhance the potential to prevent it.  Estimating breast cancer risk is not a cut and dry matter, but breast density and estradiol levels are strongly associated with disease.  (Cummings. 2009)  Exercise, weight reduction, low-fat diet, and reduced alcohol use are matters to consider because all are associated with reduced risk.  Post-menopausal women appear to fare poorly from breast density factors and are urged to consider chemoprevention if found to be at high risk after all parameters are evaluated.  (Ibid.)  Mammography and self-examination reduce breast cancer mortality by a significant amount, especially among women between ages forty and seventy-four.  (Humphrey. 2002)  Tamoxifen and raloxifene, used for chemoprevention, are not without their side effects, ranging from vision changes to chest pain to hot flashes.  What about alternatives?

Prevention of obesity, or losing weight if already a problem, is essential to addressing breast cancer, both as a risk and as an established disease.  The relationship is complicated, but the association is there.  Body mass index, weight, weight gain, and waist-to-hip ratio have all been positively tied to breast cancer risk in post-menopausal women, though the tie-in is not so strong among pre-menopausal women.  (Carmichael. 2006)  Nonetheless, obesity at the time of diagnosis is significant as a poor prognostic factor.  Weight management as preventive cannot be stressed strongly enough.  Poor dietary choices are the main cause of weight gain, either eating the wrong foods or too much of the right ones.  Eating more plant-based protein and lots of fruits and vegetables, being adequately hydrated, eliminating or limiting simple carbohydrates and sugars, avoiding food preservatives and artificial colors where practicable, and enjoying nuts and seeds are strongly recommended practices.  Look at this as an abundance model rather than a deprivation model.

Certain enzymes are entailed in the incidence and progress of cancer, including breast and other soft tissues.  Their names include aromatase, telomerase, and one simply named AKT.  Inhibition of these substances is one of the goals of cancer researchers, some of whom have found that a food component termed indole-3-carbinol (I3C) is such an inhibitor.  Produced by the Brassica family of vegetables—including Brussels sprouts, cabbages, broccoli, etc.—I3C inhibits cell proliferation and induces cell death (apoptosis) in abnormal breast, prostate, and colon tissues.  What’s more, laboratory-enhanced analogues of I3C were found to be more potent at downregulating AKT in particular and other enzymes in general.  (Kim. 2011)  Additional findings indicated that cell cycle arrest of estrogen-responsive breast cancer lines was initiated by cruciferous vegetable constituents.  (Marconett. 2011)  Under acidic conditions, such as exist in the stomach, I3C is potentiated to its most active metabolite, di-indolylmethane (DIM), the main factor responsible for biological effects inside the body and resulting suppression of cancer cell proliferation.  (Aggarwal.  2005)  I3C supplements are available.

When cells are overstressed and their innate anti-oxidant capabilities are taxed, carcinogenesis may occur.  Several phytochemicals, derived from plants that include herbs and spices and not just fruits and vegetables, have demonstrated excellent chemoprotective characteristics.  Besides the crucifers cited, the simple herb cardamom, a member of the ginger family, shows promise as a provider of DIM to be applied to prophylaxis and treatment not only in carcinogenesis, but also in atherosclerosis and HPV infection.  (Acharya. 2010)  Another Brassica component with breast cancer protection properties is benzyl-isothiocyanate, a material that has exhibited anti-proliferation capability in both breast and pulmonary tissue.  (Kim.  2011)

One of the nutrients in sore supply in humans is iodine, a mineral that has been taken for granted since it appeared as a salt additive years ago.  Iodine deficiency affects almost two billion people on earth and is the number one preventable cause of mental handicap.  With the advent of other salts for culinary use, iodine has been relegated to the back burner.  The consumption of iodine-rich foods, as exemplified by those who eat seaweed as part of their traditional cuisine, does not appear to cause toxicity, but instead may reveal itself as an important element in maintaining breast tissue architecture and function.    (Patrick.  2008)  Seaweed as a dietary preference in Japan, for example, may be associated with the very low incidence of malignant and benign breast disease.  Therapeutic administration of iodine in the presence of selenium has shown anti-oxidant as well as anti-proliferative character.  (Cann.  2000)  Mexican investigators have discovered iodine to be useful as adjuvant treatment in breast cancer therapy, contributing to the integrity of normal mammary tissue.  (Aceves.  2005)  Kelp, yogurt, eggs, strawberries, and seafoods are good food sources.  Revisiting iodized salt is a prudent option.

In active disease, cancer cells may exhibit resistance to radiation.  It is this feature that has led researchers to find a way to make these stubborn cells less so.  Vitamin K, as a newly-synthesized form of K2 (VK2), not only restored radiation sensitivity, but also inhibited growth of cancer cells.  But not just in breast cancer lines.  Lung and colon cancers also responded.  The formation of selective reactive oxygen species, affecting only the cancerous but not the healthy cells, seems to be the driving mechanism.  (Amalia.  2010)   Vitamin K3, a synthetic form also called menadione, is not generally used to make supplements due to its toxic nature, but has been used successfully to alter the course of breast cancer treatment.  (Akiyoshi.  2009)

We don’t think of rest as being part of the armamentarium in treating sickness, but a relationship between sleep and interruption of the circadian clock has been found to have a decided impact on cancer genesis.  When jobs and entertainment interfere with the body’s response to night-time chemical manufacture, maybe we shouldn’t be too surprised that metabolic upset occurs.  Back in the 80’s it was proposed that the increasing use of electricity to light the night could account for the global rise in breast cancer risk.  It was theorized that blindness and long sleep duration reduce risk, and shift work increases risk.

This has spawned an interest in exploring the function of circadian genes, thinking that epigenetic alterations might be causative.  Studies indicate that certain urine melatonin compounds, concentrations of luteinizing hormones, follicle stimulating hormone, and estradiol are indicators of breast cancer risk.  Though not definitive, the implications are not to be ignored.  (Stevens.  2009)  (Davis.  2006)  Getting by on four hours of sleep does a body no good.

Nutrient intake unbalances the scale in favor of breast cancer prevention.  Among the nutrients studied are vitamins B2, B3, B6, B12, folate, and the amino acid methionine.  A study of Chinese women conducted by Vanderbilt University indicates that high folate intake may reduce breast cancer risk and that the association depends on estrogen and progesterone receptor status, particularly as related to pre-menopausal women. (Shrubsole.  2011)   Earlier probes likewise found folate to be preventive in light of hormone conditions, but even more so when combined with vitamin B12.  (Wu.  1999)
(Larsson.  2008)  (Lajous.  2006)  A synergy was discovered when the beneficial effect of folate was accentuated by dietary intake of methionine, vitamin B12, and B6.  (Shrubsole.  2001)  Folinic acid is a form of folate that has vitamin function equivalent to folic acid, but requires no enzymatic conversion.  Folinic acid encourages normal DNA replication and RNA transcription, and has the unique ability to reinforce drug treatment for active disease.

Xanthophylls are pigments that accompany chlorophyll in green plants, and are often identified with lutein.  Being yellow, their color is masked by chlorophyll in mature leaves.  Their job is to absorb certain wavelengths of light not gathered by chlorophyll, then to transfer that energy to the chlorophyll by ramping up electrons.  They are similar to, but not exactly like, carotenes.   Foods that contain xanthophylls have demonstrated protection against the onset of breast and lung cancers, although their claim to fame is protecting vision against both cataracts and age-related macular degeneration.  Research in this arena is somewhat limited, but recommendations for intake align with current dietary guidelines.  (Judy.  2004)  All leafy greens are sources.

Undergoing serious examination as preventive of breast cancer is curcumin, the active ingredient of turmeric.  Cancer cells treated with this polyphenol fail to proliferate and invade at normal rate by virtue of protein disruption (Zong.  2011).  Curcumin’s cytotoxicity as an anti-oxidant is dose-dependent, but its presence in the breast cancer war can’t be overlooked.  (Quiroga.  2010)

It’s been estimated that 30%-40% of all cancers can be prevented by lifestyle and dietary measures alone.  The protective elements in a cancer prevention diet may reduce likelihood of disease by more than 60%, and would favor recovery from disease as well.  (Donaldson.  2004)


Aceves C, Anguiano B, Delgado G.
Is iodine a gatekeeper of the integrity of the mammary gland?
J Mammary Gland Biol Neoplasia. 2005 Apr;10(2):189-96.

Acharya A, Das I, Singh S, Saha T
Chemopreventive properties of indole-3-carbinol, diindolylmethane and other constituents of cardamom against carcinogenesis.
Recent Pat Food Nutr Agric. 2010 Jun;2(2):166-77.

Aggarwal BB, Ichikawa H.
Molecular targets and anticancer potential of indole-3-carbinol and its derivatives.
Cell Cycle. 2005 Sep;4(9):1201-15.

Akiyoshi T, Matzno S, Sakai M, Okamura N, Matsuyama K.
The potential of vitamin K3 as an anticancer agent against breast cancer that acts via the mitochondria-related apoptotic pathway.
Cancer Chemother Pharmacol. 2009 Dec;65(1):143-50.

Amalia H, Sasaki R, Suzuki Y, Demizu Y, Bito T, Nishimura H, Okamoto Y, Yoshida K, Miyawaki D, Kawabe T, Mizushina Y, Sugimura K.
Vitamin K2-derived compounds induce growth inhibition in radioresistant cancer cells.
Kobe J Med Sci. 2010 Sep 28;56(2):E38-49.

Cann SA, van Netten JP, van Netten C.
Hypothesis: iodine, selenium and the development of breast cancer.
Cancer Causes Control. 2000 Feb;11(2):121-7.

Carmichael AR.
Obesity and prognosis of breast cancer.
Obes Rev. 2006 Nov;7(4):333-40.

Cummings SR, Tice JA, Bauer S, Browner WS, Cuzick J, Ziv E, Vogel V, Shepherd J, Vachon C, Smith-
Bindman R, Kerlikowske K.
Prevention of breast cancer in postmenopausal women: approaches to estimating and reducing risk.
J Natl Cancer Inst. 2009 Mar 18;101(6):384-98.

Davis S, Mirick DK.
Circadian disruption, shift work and the risk of cancer: a summary of the evidence and studies in Seattle.
Cancer Causes Control. 2006 May;17(4):539-45.

Michael S Donaldson
Nutrition and cancer: A review of the evidence for an anti-cancer diet
Nutrition Journal 2004, 3:19

Francini G, Petrioli R, Aquino A, Gonnelli S.
Advanced breast cancer treatment with folinic acid, 5-fluorouracil, and mitomycin C.
Cancer Chemother Pharmacol. 1993;32(5):359-64.

Humphrey LL, Helfand M, Chan BK, Woolf SH.
Breast cancer screening: a summary of the evidence for the U.S. Preventive Services Task Force.
Ann Intern Med. 2002 Sep 3;137(5 Part 1):347-60.

Kim EJ, Hong JE, Eom SJ, Lee JY, Park JH.
Oral administration of benzyl-isothiocyanate inhibits solid tumor growth and lung metastasis of 4T1 murine mammary carcinoma cells in BALB/c mice.
Breast Cancer Res Treat. 2011 Nov;130(1):61-71.

Judy D. Ribaya-Mercado, ScD and Jeffrey B. Blumberg, PhD, FACN
Lutein and Zeaxanthin and Their Potential Roles in Disease Prevention
J Am Coll Nutr December 2004 vol. 23 no. suppl 6 567S-587S

Kim DJ, Reddy K, Kim MO, Li Y, Nadas J, Cho YY, Kim JE, Shim J, Song NR, Carper A, Lubet RA, Bode AM, Dong Z.
(3-Chloroacetyl)-indole, a novel allosteric AKT inhibitor suppresses colon cancer growth in vitro and in vivo
Cancer Prev Res (Phila). 2011 Sep 1.

Lajous M, Lazcano-Ponce E, Hernandez-Avila M, Willett W, Romieu I.
Folate, vitamin B(6), and vitamin B(12) intake and the risk of breast cancer among Mexican women.
Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):443-8.

Lajous M, Romieu I, Sabia S, Boutron-Ruault MC, Clavel-Chapelon F.
Folate, vitamin B12 and postmenopausal breast cancer in a prospective study of French women.
Cancer Causes Control. 2006 Nov;17(9):1209-13.

Larsson SC, Bergkvist L, Wolk A.
Folate intake and risk of breast cancer by estrogen and progesterone receptor status in a Swedish cohort.
Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3444-9.

Marconett CN, Sundar SN, Tseng M, Tin AS, Tran KQ, Mahuron KM, Bjeldanes LF, Firestone GL.
Indole-3-carbinol downregulation of telomerase gene expression requires the inhibition of estrogen receptor-alpha and Sp1 transcription factor interactions within the hTERT promoter and mediates the G1 cell cycle arrest of human breast cancer cells.
Carcinogenesis. 2011 Sep;32(9):1315-23

Patrick L.
Iodine: deficiency and therapeutic considerations.
Altern Med Rev. 2008 Jun;13(2):116-27.

Quiroga A, Quiroga PL, Martínez E, Soria EA, Valentich MA.
Anti-breast cancer activity of curcumin on the human oxidation-resistant cells ZR-75-1 with gamma-glutamyltranspeptidase inhibition.
J Exp Ther Oncol. 2010;8(3):261-6.

Shrubsole MJ, Jin F, Dai Q, Shu XO, Potter JD, Hebert JR, Gao YT, Zheng W.
Dietary folate intake and breast cancer risk: results from the Shanghai Breast Cancer Study.
Cancer Res. 2001 Oct 1;61(19):7136-41.

Shrubsole MJ, Shu XO, Li HL, Cai H, Yang G, Gao YT, Gao J, Zheng W.
Dietary B vitamin and methionine intakes and breast cancer risk among Chinese women.
Am J Epidemiol. 2011 May 15;173(10):1171-82.

Stadel BV.
Dietary iodine and risk of breast, endometrial, and ovarian cancer.
Lancet. 1976 Apr 24;1(7965):890-1.

Stevens RG.
Working against our endogenous circadian clock: Breast cancer and electric lighting in the modern world.
Mutat Res. 2009 Nov-Dec;680(1-2):106-8.

Wu K, Helzlsouer KJ, Comstock GW, Hoffman SC, Nadeau MR, Selhub J.
A prospective study on folate, B12, and pyridoxal 5′-phosphate (B6) and breast cancer.
Cancer Epidemiol Biomarkers Prev. 1999 Mar;8(3):209-17.

A. Zaniboni, F. Meriggi, G. Arcangeli, P. Marpicati, E. Montini, E. Simoncini and
G. Marini
L-folinic acid and 5-fluorouracil in the treatment of advanced breast cancer: A phase II study
Ann Oncol (1993) 4 (suppl 2): S41-S43.

Zong H, Wang F, Fan QX, Wang LX.
Curcumin inhibits metastatic progression of breast cancer cell through suppression of urokinase-type plasminogen activator by NF-kappa B signaling pathways.
Mol Biol Rep. 2011 Sep 24. [Epub ahead of print]

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Beta-Glucans, The Healer

oatmeal-and-white-backgroundThere are quite a few products on the market that promise to heal wounds quickly. The one made from a combination of bacitracin, neomycin and polymyxin is so popular that it’s been copied as a generic. But it isn’t all-natural. For those interested in a natural alternative, there’s a new kid on the block, called beta-glucans, found in baker’s yeast and a few other common sources, and destined to be on the shelves as a gel in 2012. Heralded as a “super medicine,” beta-glucans are currently used in veterinary medicine, dietary supplements, and cosmetics. And Norwegian scientists say it has even more potential.

The Research Council of Norway announced the results of a study headed by Rolf Einar Engstad, of Biotec Pharmacon, that proclaimed, “Since the mid-1980’s we have known that these substances (beta-glucans) fight infection and have a bearing on the body’s ability to kill cancerous cells, but never knew why.”  At the start of the project, the researchers were uncertain of the efficacy of the delivery method, but in infected laboratory animals, “…determined that animals receiving beta-glucans orally acquired protection that was at least as good as rats that received an injection into their bloodstream.”  Effectiveness of topical application in the healing of wounds was welcome news.  Incisions, bed sores, diabetic ulcers, and other skin insults can be treated with topical beta-glucans.  A matter that has since been addressed is short shelf life, something that can happen to any organic material, such as organic produce.  To add to beta-glucans’ acclaim is its capacity to enhance the innate immune system, that immunity with which we are born and which is first mobilized if the body is invaded by a pathogen.  (The Research Council of Norway.  2011)

As a supplement, beta-glucans has been around for a while.  These sugars are found in the cell walls of bacteria, fungi, yeasts, algae, lichens, and plants, such as oats and barley.  Orally, they have been used for treating cholesterol, diabetes, cancer and HIV/AIDS, and for bolstering the immune systems of those suffering from chronic fatigue syndrome and emotional or physical stress.  It may be given IV post-surgery to prevent infections.  Topically, it’s been used for dermatitis, eczema, wrinkles, bedsores, radiation burns, and other skin conditions.  The enhancement of macrophage function aids in healing wounds, although the exact mechanism of this improved healing is uncertain. (Portera. 1997)  Besides that, increases in collagen manufacture have been noticed, resulting in improved tensile strength of the new wound covering.  (Browder. 1988)  The activity in this arena includes the stimulation of growth factors and the release of cytokines, regulatory proteins that mediate the immune response.  (Wei. 2002)  This results in stimulation of fibroblast (giving rise to connective tissue) collagen biosynthesis.

Yeast-based beta-glucans is being taken more and more seriously as an immune health ingredient.  Because it can stand a wide range of body pH, yeast-based product could supplant—or at least enhance—probiotics as a first line of defense against invasion by bacteria and viruses.  (Watson, 2011)

Beyond healing wounds, beta-glucans may prevent the absorption of cholesterol from the stomach and intestine when it is taken orally.  The beta-glucan found in oats led oatmeal makers to petition the FDA to allow such a claim on their labels.  The FDA agreed, as long as the amount is 10% of the product.  (Federal Register. 2002)

By injection, beta-glucans stimulate the immune system by increasing chemicals that prevent infections.  Used in immunotherapy, as in treating certain invasive diseases, beta-glucans incites cytotoxicity (cell toxicity) in neoplastic (abnormal new growth) tissue while leaving healthy tissue alone.  (Vetvicka. 1996)

As with any promising developments in alternative approaches to wellness, funding for additional studies becomes a roadblock.  The promise of beta-glucans, which, because it appears in food cannot be patented as a drug (yet), paints a rosy picture for treating cuts and scrapes, and perhaps for the prevention of contagious diseases and chronic illnesses.


Siw Ellen Jakobsen and Else Lie
Baker’s yeast aids healing
The Research Council of Norway. Published: 07.09.2011

Portera CA, Love EJ, Memore L, Zhang L, Müller A, Browder W, Williams DL.
Effect of macrophage stimulation on collagen biosynthesis in the healing wound.
Am Surg. 1997 Feb;63(2):125-31.

Browder W, Williams D, Lucore P, Pretus H, Jones E, McNamee R
Effect of enhanced macrophage function on early wound healing.
Surgery. 1988 Aug;104(2):224-30.

Wei D, Zhang L, Williams DL, Browder IW.
Glucan stimulates human dermal fibroblast collagen biosynthesis through a nuclear factor-1 dependent mechanism.
Wound Repair Regen. 2002 May-Jun;10(3):161-8.

Elaine Watson
Biothera on a roll as yeast beta-glucan moves into the mainstream  12 September, 2011

Food and Drug Administration, HHS
Food labeling: health claims; soluble dietary fiber from certain foods and coronary heart disease. Interim final rule.
Fed Regist. 2002 Oct 2;67(191):61773-83.

Vetvicka V, Thornton BP, Ross GD.
Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells.
J Clin Invest. 1996 Jul 1;98(1):50-61.

Charlotte Sissener Engstad, Rolf Einar Engstad, Jan-Ole Olsen and Bjarne Osterud
The effect of soluble beta-1,3-glucan and lipopolysaccharide on cytokine production and coagulation activation in whole blood.
Int Immunopharmacol 2(11):1585-97 (2002) t

Suzuki I, Hashimoto K, Ohno N, Tanaka H, Yadomae T.
Immunomodulation by orally administered beta-glucan in mice.
Int J Immunopharmacol. 1989;11(7):761-9.

Delatte SJ, Evans J, Hebra A, Adamson W, Othersen HB, Tagge EP.
Effectiveness of beta-glucan collagen for treatment of partial-thickness burns in children.
J Pediatr Surg. 2001 Jan;36(1):113-8.

Borchers AT, Stern JS, Hackman RM, Keen CL, Gershwin ME.
Mushrooms, tumors, and immunity.
Proc Soc Exp Biol Med. 1999 Sep;221(4):281-93.

Akramiene D, Kondrotas A, Didziapetriene J, Kevelaitis E.
Effects of beta-glucans on the immune system.
Medicina (Kaunas). 2007;43(8):597-606.

Ross GD, Vetvicka V, Yan J, Xia Y, Vetvicková J.
Therapeutic intervention with complement and beta-glucan in cancer.
Immunopharmacology. 1999 May;42(1-3):61-74.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Plastic Bottle Education

bottlesPlastic bottles were uncommon until the late 1940’s. They remained expensive until the invention of high density polyethylene in the 1960’s. Popularity then zoomed among both the manufacturers and consumers because plastics were light in weight and cheaper to make.

The controversy about plastic safety is eternal, not only because of health issues, but also because of environmental concerns. Here’s what we need to know. Note that it’s not a good idea to refill any plastic bottle, especially with chlorine-laden tap water.

recycle-1 PETpolyethylene terephthalate—is really a misnomer because it does not contain polyethylene. It really doesn’t contain phthalates, either. It’s used in soft drink, water, and salad dressing bottles, and in peanut butter, pickle, and jelly jars. Only about 30% of the planet’s PET is used for bottles; most is used to make synthetic fibers. The antimony used as a catalytic agent in PET’s manufacture can leach into the contents if exposed to extremely high heat or to the microwave. Rating: GOOD—not known to leach chemicals suspected of carcinogenesis or hormone disruption.

recycle-2 HDPEhigh density polyethylene—is used in milk, water, and juice bottles, in yogurt and margarine containers, and in grocery and trash bags; occasionally in toiletries and water pipes. Rating: GOOD—not known to leach harmful chemicals into the contents.

recycle-3 PVCpolyvinyl chloride—is found in plastic cling films (from the deli, for example), occasionally in juice bottles, in water and sewer pipes, and if unplasticized, in vinyl siding. Traces of the plasticizers, most often phthalates, leach into the foods. Rating: BAD—plasticizers (phthalates) can disrupt normal hormone function and possibly cause cancer.

recycle-4 LDPElow-density polyethylene—is used to make frozen food bags (the low-density is bendable), squeeze bottles for honey and mustard, cling films, and flexible lids. Rating: O. K.—it doesn’t leach anything, but is difficult to recycle.

recycle-5 PPpolypropylene—may be found in reusable microwave containers, in kitchenware, yogurt and margarine tubs, some ketchup bottles, and Legos. Because it’s resistant to fatigue, it’s used to make hinges on flip-top lids. Rating: O. K.—its manufacture is somewhat hazardous, but it doesn’t leach any cancer-causing or hormone-disrupting chemicals.

recycle-6 PSpolystyrene—is commonly found in egg cartons, packing peanuts, disposable cups, plates and trays, and some cutlery. It’s one of the most widely used plastics. Foam insulation is made from PS. Rating: BAD—because it is made from suspected carcinogenic substances and may be neurotoxic, despite its approval for food use. Never put any acidic beverage into a Styrofoam cup. Wine may dissolve it, and fats may absorb it. That means using no cream in coffee.

recycle-7 Other—means polycarbonate, ABS, or BPA, none of which should be used for food contact. It has been used to make baby bottles, water bottles, eating utensils, and linings for metal cans. It may also appear inside juice boxes. It was invented in the 1930’s in the search for synthetic estrogens. It is a hormone disrupter that simulates the physiological activity of estrogen. It will leach into the contents. Rating: BAD—because it also affects neurological function, weight management, infant development and behavior, dopaminergic systems, thyroid hormone receptors, prostate function, and DNA methylation.

That PET has the term terephthalate is misleading. Terephthalate is not the same thing as phthalate. The former comes from terephthalic acid, chemical formula C6H4(COOH)2. The latter comes from phthalic acid, formula C6H4(CO2H)2. The chemical difference is easily seen.

The American Chemistry Council asserts that phthalates are not used to make beverage bottles or any other type of plastic food-contact product. Phthalates, or rather orthophthalates, are used to make PVC flexible, as found in shower curtains and vinyl flooring.
(Enneking, 2006)

A concern about PET is the leaching of antimony, a catalyst in PET manufacture, into the contents of the bottle. Any residue can be removed by washing. Some remains in the material, being released if heated.


Andra SS, Makris KC, Shine JP, Lu C.
Co-leaching of brominated compounds and antimony from bottled water.
Environ Int. 2012 Jan;38(1):45-53.

Bach C, Dauchy X, Chagnon MC, Etienne S.
Chemical compounds and toxicological assessments of drinking water stored in polyethylene terephthalate (PET) bottles: A source of controversy reviewed.
Water Res. 2012 Mar 1;46(3):571-83.

David Biello
Plastic (Not) Fantastic: Food Containers Leach a Potentially Harmful Chemical
Is bisphenol A, a major ingredient in many plastics, healthy for children and other living things?

Scientific American; February 19, 2008

Eilam-Stock T, Serrano P, Frankfurt M, Luine V.
Bisphenol-A impairs memory and reduces dendritic spine density in adult male rats.
Behav Neurosci. 2011 Oct 17.

Patricia A. Enneking
Phthalates Not in Plastic Food Packaging
Environ Health Perspect. 2006 February; 114(2): A89–A90.

Hansen C, Tsirigotaki A, Bak SA, Pergantis SA, Stürup S, Gammelgaard B, Hansen HR.
Elevated antimony concentrations in commercial juices.
J Environ Monit. 2010 Apr;12(4):822-4.

Kate Kelland
Scientists link plastics chemical to health risks
Exposure to a chemical found in plastic containers is linked to heart disease, scientists said on Wednesday, confirming earlier findings and adding to pressure to ban its use in bottles and food packaging.
(Reuters) – Wed Jan 13, 2010

Kolšek K, Mavri J, Sollner Dolenc M.
Reactivity of bisphenol A-3,4-quinone with DNA. A quantum chemical study.
Toxicol In Vitro. 2012 Feb;26(1):102-6. Epub 2011 Nov 20.

Quantitative Analysis of Styrene Dimer and Trimers Migrated from Disposable Lunch Boxes.
Journal of the Food Hygienic Society of Japan. VOL.41;NO.3;PAGE.200-205(2000)

Schmid P, Kohler M, Meierhofer R, Luzi S, Wegelin M.
Does the reuse of PET bottles during solar water disinfection pose a health risk due to the migration of plasticisers and other chemicals into the water?
Water Res. 2008 Dec;42(20):5054-60.

Shotyk W, Krachler M, Chen B.
Contamination of Canadian and European bottled waters with antimony from PET containers.
J Environ Monit. 2006 Feb;8(2):288-92.

Vasami R
Polyethylene Terephthalate and Endocrine Disruptors.
Environ Health Perspect. 2010; 118:A196-A197.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Good News About Coffee

cup-of-coffee-on-saucerThe inveterate coffee drinkers among us will appreciate the good news about one of our favorite beverages. After all the flak we took about the vices of coffee, now’s the chance to respond. After water and tea, coffee is the next most popular drink on the planet, having a starring role in the history of several cultures. It came from the Muslim world, travelled to Italy and then to the rest of Europe, finally landing in the New World. At one time, it was limited only to religious observances.

The coffee bean is contained inside a “cherry” that grows on a small evergreen bush.  The Arabica strain is the more highly regarded of the two chief varieties, but the robusta strain is more resistant to the diseases peculiar to this plant, though less flavorful and more bitter. Arabica prefers the coolness of the mountainside; robusta will grow at lower elevations and in warmer climates. Since the best tasting coffee really is mountain grown, the sales talk of a particular brand is true. But Mrs. Olsen never told us that other brands also use mountain grown beans. She merely capitalized on a little-known fact.

One effect of coffee consumption is moderately elevated blood pressure, which is not surprising because caffeine is a stimulant. Italian studies done in the early 1990’s found that 200 milligrams of caffeine, about two cups’ worth, could raise systolic blood pressure by 10% and diastolic by 5% for up to two hours after consumption. The mechanism points to vasoconstriction (which has its own benefits), but researchers found no variation in heart rate or cardiac contractility (Casiglia, 1991), leading to an assumption that this temporary state is not a major concern, especially in light of later studies that reported no association between long-term coffee consumption and increase of cardiovascular complications (Mesas, 2011) or risk of hypertension (Geleijnse, 2008) (Klag, 2002).

Vitamin B6, known as pyridoxine, is a nutrient occasionally used to tame morning sickness in pregnancy and the throes of PMS. It’s also been used to address homocysteine imbalance, carpal tunnel syndrome, immunity deficiencies, and various behavioral/psychiatric issues. However, careless dosing of vitamin B6 can cause medical concerns that outweigh the benefits of producing the monoamine neurotransmitters, serotonin and dopamine. Large doses of B6 over a period of time can cause nerve fiber damage, particularly auditory neuropathy. You’d never think that coffee can prevent and treat this malady, but it does (Hong, 2008). One active coffee component is called trigonelline (Hong, 2009), an alkaloid also found in pumpkin that is able to modulate blood glucose (van Dijk, 2009) (Yoshinari, 2009). Because auditory neuropathy may be attenuated by trigonelline, why can’t the peripheral neuropathy of diabetes or physical trauma likewise be eased? It’s worth a look (Zhou, 2012).

Late-life dementia and Alzheimer’s disease (AD) are concerns shared by an aging population across the globe. Finnish studies followed a number of middle-agers for more than twenty years, documenting their coffee (and tea) consumption along the way.  Focusing more on caffeine than on coffee’s lesser-known constituents, researchers found that, over the long haul, those who drank three to five cups of coffee a day at midlife had a lower risk of dementia and AD in old age (Eskelinen, 2009, 2010).  American studies later found that long-term coffee consumption protects against cognitive impairment by reducing the formation of amyloid beta, the protein that forms the plaques associated with AD. Here it was inferred that caffeine is part of a synergy that affords the desired effect, with many coffee constituents not yet identified (Cao, 2011).

Because early research had indicated that coffee may be protective against conditions other than neurological, scientists took the trigonelline link a little further. It’s accepted that people with diabetes are at risk for cognitive dysfunction. Initially, it was proposed that coffee was merely to be explored as a tool in the management of diabetes and related sequelae (Biessels, 2010). It was realized, however, that caffeine can decrease the risk of type 2 diabetes and consequent cognitive decline (Salazar-Martinez, 2004) (Tuomilehto, 2004).

In general, coffee increases plasma antioxidant capacity, possibly because of the contribution, bioavailability and activity of its particular group of polyphenols, including chlorogenic acid, one component linked to a reduction of type 2 diabetes risk by virtue of delaying intestinal glucose absorption and the inhibition of gluconeogenesis (Ong, 2010) (Tunnicliffe, 2011). Other medical conditions are purported to be influenced by coffee’s mechanisms, including gastrointestinal diseases (Inoue, 1998), gallstones (Leitzmann, 1999), and Parkinson’s disease (Checkoway, 2002) (Blanchette, 2000).

If coffee has a down side, it’s that it can interact with some drugs, most notably quinolone antibiotics, such as ciprofloxacin and its kin, which increase caffeine concentrations by inhibiting its clearance (Harder, 1989). Coffee’s popularity cannot be ignored. Just look at all the coffee options that run the gamut from hot to cold, from sweet to sweeter, and from low-cal to mega-cal. Since the 1989 expiration of a global agreement to stabilize supply, availability has fluctuated—and so has the price. You can’t even get the cup for a dime any more.


Biessels GJ.
Caffeine, diabetes, cognition, and dementia.
J Alzheimers Dis. 2010;20 Suppl 1:S143-50.

Campdelacreu J.
Parkinson disease and Alzheimer disease: environmental risk factors.
[Article in English, Spanish]

Neurologia. 2012 Jun 13. [Epub ahead of print]

Cao C, Wang L, Lin X, Mamcarz M, Zhang C, Bai G, Nong J, Sussman S, Arendash G.
Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer’s mice.
J Alzheimers Dis. 2011;25(2):323-35.

Casiglia E, Bongiovì S, Paleari CD, Petucco S, Boni M, Colangeli G, Penzo M, Pessina AC.
Haemodynamic effects of coffee and caffeine in normal volunteers: a placebo-controlled clinical study.
J Intern Med. 1991 Jun;229(6):501-4.

Checkoway H, Powers K, Smith-Weller T, Franklin GM, Longstreth WT Jr, Swanson PD.
Parkinson’s disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake.
Am J Epidemiol. 2002 Apr 15;155(8):732-8.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M.
Midlife coffee and tea drinking and the risk of late-life dementia: a population-based CAIDE study.
J Alzheimers Dis. 2009;16(1):85-91.

Eskelinen MH, Kivipelto M.
Caffeine as a protective factor in dementia and Alzheimer’s disease.
J Alzheimers Dis. 2010;20 Suppl 1:S167-74.

Floegel A, Pischon T, Bergmann MM, Teucher B, Kaaks R, Boeing H
Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Germany study.
Am J Clin Nutr. 2012 Apr;95(4):901-8.

Yoichi Fukushima, Takashi Ohie, Yasuhiko Yonekawa, Kohei Yonemoto, Hiroki Aizawa, Yoko Mori, Makoto Watanabe, Masato Takeuchi, Maiko Hasegawa, Chie Taguchi and Kazuo Kondo
Coffee and Green Tea As a Large Source of Antioxidant Polyphenols in the Japanese Population
Journal of Agricultural and Food Chemistry 2009 57 (4), 1253-1259

Gelber RP, Petrovitch H, Masaki KH, Ross GW, White LR.
Coffee intake in midlife and risk of dementia and its neuropathologic correlates.
J Alzheimers Dis. 2011;23(4):607-15.

Geleijnse JM.
Habitual coffee consumption and blood pressure: an epidemiological perspective.
Vasc Health Risk Manag. 2008;4(5):963-70.

Harder S, Fuhr U, Staib AH, Wolff T.
Ciprofloxacin-caffeine: a drug interaction established using in vivo and in vitro investigations.
Am J Med. 1989 Nov 30;87(5A):89S-91S.

Head KA.
Peripheral neuropathy: pathogenic mechanisms and alternative therapies.
Altern Med Rev. 2006 Dec;11(4):294-329.

Hermansen K, Krogholm KS, Bech BH, Dragsted LO, Hyldstrup L, Jørgensen K, Larsen ML, Tjønneland AM.
Coffee can protect against disease
Ugeskr Laeger. 2012 Sep 24;174(39):2293-2297.

Hong BN, Yi TH, Park R, Kim SY, Kang TH.
Coffee improves auditory neuropathy in diabetic mice.
Neurosci Lett. 2008 Aug 29;441(3):302-6. Epub 2008 Jun 22.

Hong BN, Yi TH, Kim SY, Kang TH.
High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.
Biol Pharm Bull. 2009 Apr;32(4):597-603.

Huxley R, Lee CM, Barzi F, Timmermeister L, Czernichow S, Perkovic V, Grobbee DE, Batty D, Woodward M.
Coffee, decaffeinated coffee, and tea consumption in relation to incident type 2 diabetes mellitus: a systematic review with meta-analysis.
Arch Intern Med. 2009 Dec 14;169(22):2053-63.

Inoue M, Tajima K, Hirose K, Hamajima N, Takezaki T, Kuroishi T, Tominaga S.
Tea and coffee consumption and the risk of digestive tract cancers: data from a comparative case-referent study in Japan.
Cancer Causes Control. 1998 Mar;9(2):209-16.

Kaiser permanante Division of Research
Coffee Drinking and Caffeine Associated with Reduced Risk of Hospitalization for Heart Rhythm Disturbances

Klag MJ, Wang NY, Meoni LA, Brancati FL, Cooper LA, Liang KY, Young JH, Ford DE.
Coffee intake and risk of hypertension: the Johns Hopkins precursors study.
Arch Intern Med. 2002 Mar 25;162(6):657-62.

Leitzmann MF, Willett WC, Rimm EB, Stampfer MJ, Spiegelman D, Colditz GA, Giovannucci E.
A prospective study of coffee consumption and the risk of symptomatic gallstone disease in men.
JAMA. 1999 Jun 9;281(22):2106-12.

Mesas AE, Leon-Muñoz LM, Rodriguez-Artalejo F, Lopez-Garcia E.
The effect of coffee on blood pressure and cardiovascular disease in hypertensive individuals: a systematic review and meta-analysis.
Am J Clin Nutr. 2011 Oct;94(4):1113-26. Epub 2011 Aug 31.

Oba S, Nagata C, Nakamura K, Fujii K, Kawachi T, Takatsuka N, Shimizu H.
Consumption of coffee, green tea, oolong tea, black tea, chocolate snacks and the caffeine content in relation to risk of diabetes in Japanese men and women.
Br J Nutr. 2010 Feb;103(3):453-9. Epub 2009 Oct 12.

Ong KW, Hsu A, Tan BK.
Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes.
PLoS One. 2012;7(3):e32718. Epub 2012 Mar 7.

Richelle M, Tavazzi I, Offord E.
Comparison of the antioxidant activity of commonly consumed polyphenolic beverages (coffee, cocoa, and tea) prepared per cup serving.
J Agric Food Chem. 2001 Jul;49(7):3438-42.

Ross GW, Abbott RD, Petrovitch H, Morens DM, Grandinetti A, Tung KH, Tanner CM, Masaki KH, Blanchette PL, Curb JD, Popper JS, White LR.
Association of coffee and caffeine intake with the risk of Parkinson disease.
JAMA. 2000 May 24-31;283(20):2674-9.

Salazar-Martinez E, Willett WC, Ascherio A, Manson JE, Leitzmann MF, Stampfer MJ, Hu FB.
Coffee consumption and risk for type 2 diabetes mellitus.
Ann Intern Med. 2004 Jan 6;140(1):1-8.

Tunnicliffe JM, Eller LK, Reimer RA, Hittel DS, Shearer J.
Chlorogenic acid differentially affects postprandial glucose and glucose-dependent insulinotropic polypeptide response in rats.
Appl Physiol Nutr Metab. 2011 Oct;36(5):650-9. Epub 2011 Oct 6.

Tuomilehto J, Hu G, Bidel S, Lindström J, Jousilahti P.
Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women.
JAMA. 2004 Mar 10;291(10):1213-9.

van Dijk AE, Olthof MR, Meeuse JC, Seebus E, Heine RJ, van Dam RM.
Acute effects of decaffeinated coffee and the major coffee components chlorogenic acid and trigonelline on glucose tolerance.
Diabetes Care. 2009 Jun;32(6):1023-5. Epub 2009 Mar 26.

Yoshinari O, Sato H, Igarashi K.
Anti-diabetic effects of pumpkin and its components, trigonelline and nicotinic acid, on Goto-Kakizaki rats.
Biosci Biotechnol Biochem. 2009 May;73(5):1033-41. Epub 2009 May 7.

Zhou J, Chan L, Zhou S.
Trigonelline: a plant alkaloid with therapeutic potential for diabetes and central nervous system disease.
Curr Med Chem. 2012 Jul 1;19(21):3523-31.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Cancer And Sugar: How Sweet It Isn’t

sugar-cubes-smTalk about linking sugar to cancer can be confusing. The “facts” are often presented in a misleading manner that can cause anxiety in those who have the disease. Yet, learning about the science behind the connection can help us make educated decisions about nutrition choices for better health. Sugar, or rather glucose, feeds every cell in the body. We need it to produce energy. Even if we eliminate sugar from our diets, our bodies will still make glucose from other sources, including proteins and fats. It’s a little more complicated than meets the eye. Eating lots of sugar forces the body to make more insulin, one of whose properties is to tell cells to grow. For healthy cells, this is good because all cells grow, divide, die and get replaced by new ones. However, cancer cells can be told to grow, too, when the body makes too much insulin (Goodwin, 2002) (Duggan, 2013). So, yes, there can be too much of a good thing. Knowing from the start that sugar in itself is not evil, we can proceed to the science.

A recent study at the University Rey Carlos in Madrid found a mechanism that links obesity and diabetes with cancer, based on gene activity that promotes the manufacture of insulin. Once sugar reaches the intestine a hormone called GIP is secreted. This enhances insulin release by the pancreas. GIP is controlled by a protein known as β-catenin, a suspected oncogene whose activity depends on sugar levels. Oncogenes are those that transform normal cells into cancerous ones, and mutations of the β-catenin gene are implicated in the incidence of colon and ovarian cancers, among others. Normal sugar levels do not induce accumulation of this protein in the nucleus, but diabetes and its characteristic elevated blood glucose levels does, and is associated with increased cancer risk (Chocarro-Calvo, 2012). The suspicion of a sugar-cancer link was investigated in Korea more than half a decade earlier, when physicians closed a ten-year study in which was recorded health parameters from the biennial physical exams of people receiving national health insurance. Adjusting for smoking and alcohol use, investigators found that those with the highest glucose levels had higher death rates from all cancers combined (Jee, 2005). Associations of sugar to cancer were strongest in pancreatic cancer for both genders. This was followed by esophagus, liver and colon cancers for men and by liver and cervix cancers for women. The bottom line is that cancer risk is elevated with increased fasting serum glucose (Ibid.).

For the last twenty years, diabetes rates have grown. Almost twenty-six million Americans are so diagnosed, but another seven million remain undiagnosed. The disease has been around since the Egyptians, whose ancient writings mention frequent urination as a disturbing problem. Not to be left out of the medical world, the Greeks coined the word diabetes two hundred years before Christ, and Indian physicians noted that diabetic urine would attract ants. In Type II diabetes, insulin resistance is the underlying pathology, accounting for most diagnoses.

The grading of obesity according to body mass index (BMI) aligns with disease specificity. The BMI of healthy people is 18.5-24.9. Between 25.0 and 29.9, a person is overweight. Grade I obesity runs from 30.0-34.0; Grade II from 35.0-39.9; and Grade III above 40.0. The sixty-six inch person who weighs four hundred pounds is off the charts. You can compute your BMI by multiplying your weight by 703, dividing by your height in inches, and then dividing by your height in inches once more.  A recent issue of the Journal of the AMA announced that obesity Grades II and III are associated with significantly higher all-cause mortality, and that simple overweight is associated with significantly lower all-cause death (Flegal, 2013). Imagine what a person with a BMI of 64.6 has to anticipate!

Of the cancer-awareness organizations, breast cancer support groups receive much attention, and rightly so because of this cancer’s ubiquity and horrid nature. It was realized years ago that a relationship between breast cancer and sugar intake exists, where insulin carries the onus of induction. Elevated sugar intake causes a rise in insulin. If the body’s regulatory mechanism is overtaxed, insulin levels get out of hand. Those with diabetes are especially susceptible (Seely, 1983). Just being overweight, in the absence of diabetes, is also a risk factor for breast disease (Lof, 2009). Men are not excused from soft tissue disease just by virtue of their gender. Dietary sugars, notably sucrose (table sugar), may present an ill-defined risk in males, but a risk nonetheless for pancreas, prostate, testis and even lung cancers (Burley, 1998) (DeStefani, 1998).

The glycemic index (GI) is a measure of the effects of carbohydrates on blood glucose levels. Foods that break down quickly and release glucose rapidly have a high GI; those that break down slowly and release glucose gradually have a lower GI. Glucose is used as the reference point. In light of this, scrutiny has been given to an association of high-GI foods to colon cancer. Although no definitive conclusions were reached, there is enough evidence to suggest avoiding foods that are more energy-dense (read sugars and simple carbs) than nutrient-dense to prevent colon and other gastric disease (Galeone, 2012) (Tuyns, 1992) (Moerman, 1993).

Cancer cells thrive on sugar (Dell’Antone, 2012) (Sandulache, 2011), and glucose transport is misregulated in active disease.  Tumor cells have shown increased levels of glucose uptake, as seen in diagnostic images that use radio-labeled glucose analogs as identifiers (Adekola, 2012) (Jóźwiak, 2012). To compound the disorder, sugar increases angiogenesis, which is the growth of new blood vessels. That’s the last thing we want for a tumor—a feeding tube. Yes, angiogenesis is required for growth and development of an organism and for the healing of wounds, but it needs to stop there. Anti-angiogenic protocols are being studied as novel therapies (Merchan, 2010) (Brown, 1998) (Airley, 2007).

All sugars and carbohydrates need not be avoided. The healthy carbohydrates include vegetables, fruits, whole grains and legumes. There is debate about the value of grains in the diet, but we have to admit they are sources of fiber, phytochemicals, vitamins and minerals, and compounds yet to be identified. To keep insulin levels at bay, be sure to eat protein, fat and fiber. These work even in the presence of simpler carbs and sugars. Compared to the whole fruit with its fiber, fruit juices don’t make the cut. Limit desserts to a few times a week, dump sodas and other concentrated sugars, and focus on whole foods.


Adekola K, Rosen ST, Shanmugam M.
Glucose transporters in cancer metabolism.
Curr Opin Oncol. 2012 Nov;24(6):650-4.

Airley RE, Mobasheri A.
Hypoxic regulation of glucose transport, anaerobic metabolism and angiogenesis in cancer: novel pathways and targets for anticancer therapeutics.
Chemotherapy. 2007;53(4):233-56.

Baron JA, Weiderpass E, Newcomb PA, Stampfer M, Titus-Ernstoff L, Egan KM, Greenberg ER.
Metabolic disorders and breast cancer risk (United States).
Cancer Causes Control. 2001 Dec;12(10):875-80.

Brown NS, Bicknell R.
Thymidine phosphorylase, 2-deoxy-D-ribose and angiogenesis.
Biochem J. 1998 Aug 15;334 ( Pt 1):1-8.

Burley VJ.
Sugar consumption and human cancer in sites other than the digestive tract.
Eur J Cancer Prev. 1998 Aug;7(4):253-77.

Chocarro-Calvo A, García-Martínez JM, Ardila-González S, De la Vieja A, García-Jiménez C.
Glucose-Induced β-Catenin Acetylation Enhances Wnt Signaling in Cancer.
Mol Cell. 2012 Dec 26. pii: S1097-2765(12)00979-3.

Kathleen A. Cooney, MD; Stephen B. Gruber, MD, PhD, MPH
Hyperglycemia, Obesity, and Cancer Risks on the Horizon
JAMA. 2005;293(2):235-236.

Dell’ Antone P.
Energy metabolism in cancer cells: how to explain the Warburg and Crabtree effects?
Med Hypotheses. 2012 Sep;79(3):388-92.

De Stefani E, Deneo-Pellegrini H, Mendilaharsu M, Ronco A, Carzoglio JC.
Dietary sugar and lung cancer: a case-control study in Uruguay.
Nutr Cancer. 1998;31(2):132-7.

Duggan C, Wang CY, Neuhouser ML, Xiao L, Smith AW, Reding KW, Baumgartner RN, Baumgartner KB, Bernstein L, Ballard-Barbash R, McTiernan A.
Associations of insulin-like growth factor and insulin-like growth factor binding protein-3 with mortality in women with breast cancer.
Int J Cancer. 2013 Mar 1;132(5):1191-200.

Katherine M. Flegal, PhD; Brian K. Kit, MD; Heather Orpana, PhD; Barry I. Graubard, PhD
Association of All-Cause Mortality With Overweight and Obesity Using Standard Body Mass Index CategoriesA Systematic Review and Meta-analysis
JAMA. 2013;309(1):71-82.

Galeone C, Pelucchi C, La Vecchia C.
Added sugar, glycemic index and load in colon cancer risk.
Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):368-73.

Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Madarnas Y, Hartwick W, Hoffman B, Hood N.
Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study.
J Clin Oncol. 2002 Jan 1;20(1):42-51.

Sun Ha Jee, PhD, MHS; Heechoul Ohrr, MD, PhD; Jae Woong Sull, PhD, MHS; Ji Eun Yun, MPH; Min Ji, MPH; Jonathan M. Samet, MD, MS
Fasting Serum Glucose Level and Cancer Risk in Korean Men and Women
JAMA. 2005;293(2):194-202.

Jóźwiak P, Lipińska A.
The role of glucose transporter 1 (GLUT1) in the diagnosis and therapy of tumors
Postepy Hig Med Dosw (Online). 2012 Jan 4;66:165-74.

La Vecchia C.
Mediterranean diet and cancer.
Public Health Nutr. 2004 Oct;7(7):965-8.

Lof M, Weiderpass E
Impact of diet on breast cancer risk.
Curr Opin Obstet Gynecol. 2009 Feb;21(1):80-5.

Merchan JR, Kovács K, Railsback JW, Kurtoglu M, Jing Y, Piña Y, Gao N, Murray TG, Lehrman MA, Lampidis TJ.
Antiangiogenic activity of 2-deoxy-D-glucose.
PLoS One. 2010 Oct 27;5(10):e13699.

Moerman CJ, Bueno de Mesquita HB, Runia S.
Dietary sugar intake in the aetiology of biliary tract cancer.
Int J Epidemiol. 1993 Apr;22(2):207-14.

Sakanaka C, Sun TQ, Williams LT.
New steps in the Wnt/beta-catenin signal transduction pathway.
Recent Prog Horm Res. 2000;55:225-36.

Sandulache VC, Ow TJ, Pickering CR, Frederick MJ, Zhou G, Fokt I, Davis-Malesevich M, Priebe W, Myers JN.
Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.
Cancer. 2011 Jul 1;117(13):2926-38.

Schernhammer ES, Hu FB, Giovannucci E, Michaud DS, Colditz GA, Stampfer MJ, Fuchs CS.
Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts.
Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2098-105.

Seely S, Horrobin DF.
Diet and breast cancer: the possible connection with sugar consumption.
Med Hypotheses. 1983 Jul;11(3):319-27.

Tuyns AJ, Kaaks R, Haelterman M, Riboli E.
Diet and gastric cancer. A case-control study in Belgium.
Int J Cancer. 1992 Apr 22;51(1):1-6.

Wang X, Goode EL, Fredericksen ZS, Vierkant RA, Pankratz VS, Liu-Mares W, Rider DN, Vachon CM, Cerhan JR, Olson JE, Couch FJ.
Association of genetic variation in genes implicated in the beta-catenin destruction complex with risk of breast cancer.

Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):2101-8.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.