Sitcom Sensation Vicki Lawrence Shares Health Challenge


Vicki Lawrence, comedienne and Emmy® Award-winning actress reveals her struggle with chronic idiopathic urticarial or ICU.


She joins me with Dr. Beth Corn, Board-certified allergist, Associate Professor and member of AAFA’s National Board of Directors.
Vicki Lawrence is no stranger to being quick on her feet and playing off improv lines on stage.  In fact, she’s a legend.
But when the comedienne and Emmy® Award-winning actress was diagnosed with CIU, she was caught off-guard. 
Vicki, best known as the star of sitcom Mama’s Family…
And as part of the ensemble cast of the The Carol Burnett Show, known for inducing uncontrollable belly laughs.
And, more recently, appearing on Hannah Montana. 
She was diagnosed with CIU four years ago.  It appeared out of the blue and can happen to anyone.
Vicki wants to help motivate others to talk to their doctors about their symptoms as she did.
CIU is characterized by hives that spontaneously occur without an identifiable cause and reoccur for six weeks or more.
Symptoms come and go unpredictably. They include red, itchy hives on the skin which can last months and even years.
In the U.S., it is estimated that approximately 1.5 million people suffer from CIU.
Now, Vicki is partnering with the Asthma and Allergy Foundation of America (AAFA), Novartis Pharmaceuticals Corporation and Genentech to share her experience with CIU to encourage people to have a robust and meaningful dialogue with their medical specialist as part of a new national campaign called CIU & You.
CIU & You is an educational program focused on supporting the specific needs of people who have CIU.
It aims to empower patients to talk to their doctors to discuss treatment options with an allergist or dermatologist.
The program also provides a downloadable symptom tracker and discussion guide for patients to use when talking with doctors.
CIU & You is developed in partnership with the Asthma and Allergy Foundation of America (AAFA), and made possible by Novartis Pharmaceuticals Corporation and Genentech. For additional information, visit
For more information, speak with your doctor to better understand the disease and potential treatments.



 More About Vicki Lawrence
Vicki Lawrence is a comedienne and Emmy® Award-winning actress. She is famous for her role on The Carroll Burnett Show and Mama’s Family, and, more recently, on Hannah Montana. In 2010, Lawrence was diagnosed with CIU. For her official bio, please visit
More About Dr. Corn

Dr. Beth Corn is a Board Certified Allergist practicing in New York City and an Assistant Professor of Medicine with over 20 years of experience in healthcare. She serves on the national board of the Asthma and Allergy Foundation of America (AAFA) and is a Fellow of the American Academy of Allergy, Asthma and Immunology.


You may be surprised to learn something new about Vicki Lawrence and your health by watching the interview here:


And visiting for more information.

headshot  MARIA DORFNER is the founder of Healthy Within Network.  She can be reached at


“When We Tell Stories…People Listen.”

Do Kids Cause Gray Hair? What Does Plucking One Gray Hair Do?

flu61 Time for some gray hair myth busting. Parents often joke stress caused by their children is to blame for gray hair.


But Cleveland Clinic Dermatologist, Dr. Wilma Bergfeld says that’s not true.


Stress actually creates a whole different hair hassle.


CG: Dr. Wilma Bergfeld/Cleveland Clinic

“It does have an impact on hair loss because stress elevates your adrenal gland’s activity and also activates some of the receptors at the hair follicle level, which induce a shed, which is hair falling out by the roots.” :16



“Most people will naturally gray as they age.”


DR. BERGFELD adds hair turns gray when pigment-producing cells die.










CG: Dr. Wilma Bergfeld/Cleveland Clinic 

“When you pluck the hair it generally returns gray. It doesn’t return in multiples though. ” :05








(Broadcast Media: See Pathfire #9923 for SOT and VO)    For more information visit

I have more questions. If you do too send them in comments and we’ll follow-up.


  mariawalking5MARIA DORFNER is the founder of Healthy Within   Network.

10 Cold Weather Safety Tips


As temperatures drop this winter, the American Red Cross offers ten steps people can take to stay safe.

1. Layer up! Wear layers of lightweight clothing to stay warm. Gloves and a hat will help prevent losing your body heat.

2. Don’t forget your furry friends. Bring pets indoors. If they can’t come inside, make sure they have enough shelter to keep them warm and that they can get to unfrozen water.

3. Remember the three feet rule. If you are using a space heater, place it on a level, hard surface and keep anything flammable at least three feet away – things such as paper, clothing, bedding, curtains or rugs.

4. Requires supervision – Turn off space heaters and make sure fireplace embers are out before leaving the room or going to bed.

5. Don’t catch fire! If you are using a fireplace, use a glass or metal fire screen large enough to catch sparks and rolling logs.

6. Protect your pipes. Run water, even at a trickle, to help prevent your pipes from freezing. Open the kitchen and bathroom cabinet doors to allow warmer air to circulate around the plumbing. Be sure to move any harmful cleaners and household chemicals out of the reach of children. Keep the garage doors closed if there are water lines in the garage.

7. Better safe than sorry. Keep the thermostat at the same temperature day and night. Your heating bill may be a little higher, but you could avoid a more costly repair job if your pipes freeze and burst.

8. The kitchen is for cooking. Never use a stove or oven to heat your home.

9. Use generators outside. Never operate a generator inside the home, including in the basement or garage.

10. Knowledge is power. Don’t hook a generator up to the home’s wiring. The safest thing to do is to connect the equipment you want to power directly to the outlets on the generator.

For more information on how to stay safe during the cold weather, visit winter storm safety.

We’ll add make sure to use moisturize with SPF.  Snow reflects the sun and you can still get burned by sun or wind. Cover all exposed skin to prevent frostbite.  Drink lots of water to stay hydrated.  Questions? Write to us in comments below.

About the American Red Cross:
The American Red Cross shelters, feeds and provides emotional support to victims of disasters; supplies about 40 percent of the nation’s blood; teaches skills that save lives; provides international humanitarian aid; and supports military members and their families. The Red Cross is a not-for-profit organization that depends on volunteers and the generosity of the American public to perform its mission. For more information, please visit or visit us on Twitter at @RedCross.
About MedCrunch:
MedCrunch covers what’s hot in health for consumers and is a division of Healthy Within Network (HWN).
Maria Dorfner is the founder of Healthy Within Network.  You can follow her @Maria_Dorfner or @DorfnerMaria
A few of her credits include being asked to create and host a health series for NBC Universal, writing and producing 21st Century Medicine documentary series for the Discovery Health Channel, developing, senior producing and co-hosting medical programming for CNBC (her program was the highest revenue generating one for 3 years airing weekly on CNBC), health and special projects producer for NBC Miami, launching CCNS (the Cleveland Clinic News Service), helped launch MedPage Today, Healthology, CNBC and NewsMD Communications, working as a reporter for the nationally-syndicated series, Top Cops on CBS (first reality show) pilot and series, and director of research and producer for Roger Ailes production company.  She is the author of 3 books including Healthy Within.  Her production company, NewsMD provides media training, marketing, publicity and PR services. Her clients have included a Who’s Who in health brands.

Keep Your Teeth Healthy As You Age!


Fortunately, my family won the genetic lottery when it comes to teeth. My parents both have perfect smiles and good health.


And some say I have a trillion dollar smile.  But what happens to our smiles as we age?


Does everyone’s teeth eventually fall out?


Most people assume losing teeth are a natural part of aging. Not so. It’s not natural.


There are only five  things cause teeth to fall out:

1. Trauma
2. Severe illness (diabetes, cancer, osteomyelitis or autoimmune diseases)
3. Gum disease
4. Lifestyle, what you eat and drink along with your oral hygiene
5. Drugs such as heroin and methamphetamine (also called speed, ice or meth), cocaine, or crack cause severe tooth decay and teeth falling out in a very short amount of time.


Another form of tooth decay comes in a can. Soda is toxic to your teeth.


Other things that harm your teeth include:  acidic foods and drinks (soda is highly acidic), some mouth fresheners, some tooth whiteners and a lack of vitamin C and K.

Foods high in sugar (sweets) and carbs can also cause tooth decay.

See your dentist if your gums bleed or you feel any pain or sensitivity, as that may be an early warning sign of gum disease.  It’s worth it to keep an annual cleaning and checkup appointment.


Teeth begin to age and shift in your mid-20s. In your 30s, you start to lose bone, which makes gums recede.


In your 40s and 50s, top teeth will appear shorter as the lower teeth shift. Chewing, grinding and stress all affect your teeth. Women in perimenopause and menopause will have more stress than usual due to sleep problems as will men with high levels of stress.


A lot of stress goes to people’s jaws, which causes grinding and pressure on back teeth. Tooth grinding is also known as bruxism and can cause chipped, fractured and worn tooth enamel or increased sensitivity –even headaches.


If you have stress in your life, try to alleviate it with getting rest, exercise and fresh air. You can also get fitted for a night guard. This prevent clenching or grinding your teeth in your sleep.  It’s pricey, so you may want to try eliminating any stressors first.


Surprising new information from a recent issue of the Journal of Dental Research indicates seniors who sleep in dentures are at higher risk of developing pneumonia as bacteria from the mouth can be inhaled into the lungs.


The American Dental Association warns bacteria allowed to linger in the mouth can cause tooth decay, gum disease and tooth loss.


If you want to keep your natural teeth forever, it’s important to take care of them now.


There is a higher risk of dental disease leading to other health problems as we age.


Seniors may need to enlist family members and other loved ones to assist with dental hygiene.


The ADA encourages caregivers, whether the seniors are at home or in a nursing home, to supervise or aid in maintaining seniors’ dental health by making sure they brush twice a day, floss once a day, eat a healthy diet and visit the dentist regularly.


Hearing impairment is common among seniors.


For this reason, a caregiver can play an important communications role between a senior and the dentist by helping them prepare questions prior to their dental appointment.


Dentists providing written instructions helps in communicating with seniors too.


The ADA provides dental health tips for seniors and their caregivers


Judith Jones, DDS, from the American Dental Association is the director of the Center for Clinical Research at the University Goldman School of Dental Medicine in Boston. She is also a published researcher and serves on the editorial boards of The Journal of the American Dental Association.


Turns out, the same advice dentists gave you when you were a kid still holds true when you’re a senior.


BRUSH TWICE A DAY (Rinse with water anytime you eat)


FLOSS ONCE A DAY (My favorite are floss toothpicks. Portable and super easy to use)


EAT HEALTHY (Best foods for teeth are apples, cheese, yogurt, foods high in calcium)




Click here for Dr. Judith Jones answers to the following questions:

•What are some specific oral health concerns of older Americans?
•What can caregivers do to help seniors maintain their dental health?
•Why is it important for people with dentures to visit their dentist?
•Are there any dental products that are particularly suited for the needs of older people?

Dr. Jones offers the following Dental Tips for caregivers:

Encourage seniors to:

  • Use an electric toothbrush twice a day with a fluoride toothpaste
  • Use an interdental cleaner to floss teeth once  day
  • Eat a healthy diet
  • Tell dentist if they develop dry mouth, which can lead to tooth decay
  • Clean gums daily and remove dentures at night if they wear them



For More Information including the ADA® Find-a-Dentist™ tool:



BIOLASE, Global Leadership in Lasers (PRNewsFoto/BIOLASE, Inc.)



peggysuefilmquoteThis blog is a division of Healthy Within Network (HWN)

Stay Healthy!

Blog contact:

doggiePhoto: Maria Dorfner

Kidney Disease: More Common Than You Think


Twenty-six million Americans suffer from some sort of kidney disease –more people are unaware they suffer from it. Kidney disease kills 90,000 Americans each year, more than breast and prostate cancer combined.


One in three American adults are currently at risk for developing kidney disease, and many are unaware of it.


One of the lesser known diseases that injures the kidney is called vasculitis.




It can cause a need for a kidney transplant if it goes untreated.


We will learn more about it today in my interview with Dr. Giullian.


Jeffrey A. Giullian, MD/MBA, a nephrologist and partner at South Denver Nephrology Associates, in Denver, Colorado, practices both general and transplant nephrology, including care of patients with chronic kidney disease (CKD), end stage renal disease (ESRD), immunosuppression, hypertension and kidney stones.


In addition to his clinical responsibilities, he has an active research clinic focusing on phase 2 and 3 clinical trials.


He is active in renal research for patients with electrolyte abnormalities, polycystic kidney disease and diabetes.


Currently, Dr. Giullian is the Chairman of Medicine at Castle Rock Adventist Hospital, the Chief of Nephrology at Swedish Hospital, and a member of the Porter Hospital Kidney and Pancreas Transplant team. He is also a Group Medical Director for the APEX group of DaVita Dialysis covering dialysis centers in nine states.


After earning a MD from Vanderbilt School of Medicine in 2001, Dr. Giullian completed an internal medicine residency at Baylor College of Medicine in Houston, TX. He served as Baylor’s Chief Medical Resident from 2004-2005.


After completing his residency, he returned to Vanderbilt University Medical center for his nephrology training. During this time, from 2006-2007, he was Vanderbilt University Medical Center’s Chief Fellow for the division of nephrology.

In addition to his MD degree, Dr. Giullian holds a MBA degree from the University of Colorado at Denver.


Learn about vasculities at red link below.

Click here for Interview with Dr. Giullian:


Health Story? Contact:


Cynthia’s Story: Helping Women Who Live with Chronic Pain


Cynthia Toussiant is a former ballerina and actress (FAME) who has suffered with chronic pain disorder for more than thirty years.


The strong, graceful ballerina’s life changed when a minor ballet injury triggered chronic pain.


The chronic pain left the strong and graceful ballerina mute and in a wheelchair for years.


She visited countless physicians and was continually told it was all in her head.


Her husband, John Garrett, who has been with her for 34 years helped her get to the bottom of it.


Turns out, Cynthia had Complex Regional Pain Syndrome (CRPS) for 32 years. She later developed Fibromyalgia and Chronic Fatigue Syndrome.


I talk to Cynthia and John about it:


According to the Mayo Clinic, Complex Regional Pain Syndrome is an uncommon form of chronic pain that usually affects an arm or a leg. Complex regional pain syndrome typically develops after an injury, surgery, stroke or heart attack, but the pain is out of proportion to the severity of the initial injury.


The cause of complex regional pain syndrome isn’t clearly understood. Treatment for complex regional pain syndrome is most effective when started early. In such cases, improvement and even remission are possible.


Signs and symptoms of complex regional pain syndrome include:
•Continuous burning or throbbing pain, usually in your arm, leg, hand or foot
•Sensitivity to touch or cold
•Swelling of the painful area
•Changes in skin temperature — at times your skin may be sweaty; at other times it may be cold
•Changes in skin color, which can range from white and mottled to red or blue
•Changes in skin texture, which may become tender, thin or shiny in the affected area
•Changes in hair and nail growth
•Joint stiffness, swelling and damage
•Muscle spasms, weakness and loss (atrophy)
•Decreased ability to move the affected body part

Symptoms may change over time and vary from person to person. Most commonly, pain, swelling, redness, noticeable changes in temperature and hypersensitivity (particularly to cold and touch) occur first.

Over time, the affected limb can become cold and pale and undergo skin and nail changes as well as muscle spasms and tightening. Once these changes occur, the condition is often irreversible.

Complex regional pain syndrome occasionally may spread from its source to elsewhere in your body, such as the opposite limb. The pain may be worsened by emotional stress.

In some people, signs and symptoms of complex regional pain syndrome go away on their own. In others, signs and symptoms may persist for months to years. Treatment is likely to be most effective when started early in the course of the illness.


If you experience constant, severe pain that affects a limb and makes touching or moving that limb seem intolerable, see your doctor to determine the cause. It’s important to treat complex regional pain syndrome early.



Once Cynthia and John learned more about it, they rechanneled their efforts to help other women.



Since 1997, she has been a leading advocate for women in pain. Cynthia gave testimony at two California Senate hearings. The first was dedicated to CRPS awareness. The second explored the chronic under treatment of and gender bias toward women in pain. Both of these efforts were the first of their kind in the nation.

Cynthia founded For Grace to raise awareness about CRPS and all women in pain.

In 2006, Toussaint ran for the California State Assembly to bring attention to her CRPS Education Bill that Governor Schwarzenegger vetoed after she got it to his desk in its first year. Her current Step Therapy bill will reform an unethical prescription practice used by the health insurance industry to save money in a way that increases the suffering of California pain patients.


Toussaint was the first CRPS sufferer to be featured in the New York Times, Los Angeles Times and on the Public Broadcasting System and National Public Radio. She is a consultant for The Discovery Channel, ABC News, FOX News, the National Pain Report and PainPathways, the official magazine of the World Institute of Pain. Also, she is a guide and guest contributor for Maria Shriver’s Architects of Change website. Her many speaking engagements include the National Institutes of Health and Capitol Hill.


She is the author of Battle for Grace: A Memoir of Pain, Redemption and Impossible Love. Also, Toussaint is experiencing her first-ever partial CRPS remission largely due to the narrative therapy of writing this book.

Toussaint continues to be a leading advocate for health care reform in California. She was instrumental in changing public opinion which sparked sweeping HMO reform legislation that was signed by Governor Gray Davis in 1999. Her focus has now shifted to creating a single-payer, universal health care plan in California that would provide a model for the rest of the country.

Cynthia’s husband, John serves as Director at For Grace and was instrumental in launching the organization in April 2002 along with his partner Cynthia Toussaint, who has suffered with CRPS (and later other over-lapping auto-immune conditions) for 32 years. Garrett has been partner and caregiver to Toussaint for 34 years. He has done extensive research about the gender disparity toward women in pain, compiling a comprehensive library on that issue along with specific chronic pain conditions.


Garrett has assisted Toussaint in all aspects of media relations and advocacy regarding CRPS awareness and the pain gender divide. His work focuses on speech presentation, grant writing, research, media outreach and the development of branding strategies. Garrett has also advised California’s Department of Managed Health Care and other state agencies regarding pain management practices in the HMO industry.


Commenting on her long-term partnership with Garrett, Toussaint says, “My story as a woman in pain is also a love story because John’s support has been total and unwavering. Without his loving presence in my life, I wouldn’t be here.”

Garrett made numerous writing contributions in Toussaint’s memoir, Battle for Grace: A Memoir of Pain, Redemption and Impossible Love. He candidly shares the virtues and challenges of the caregiving experience.



Elizabeth Taylor Quote on Living with Pain

Women with Chronic Pain, please visit:

           

Hip-Hop Legend Rev Run & wife Justine on Adult Diabetes

It’s Diabetes Awareness Month.  More than 1 in 3 Americans is at risk for diabetes, and it doubles for African-Americans.

It’s one of the reasons one of the most iconic figures in music is passionate about raising awareness about risk factors for adult diabetes.

Another reason is his father has it, which also places him at risk. His manager’s father also had it. Since 5,000 new people are diagnosed each day, he wants to make sure everyone gets screened.

Rev Run is not only a legend in Hip-Hop, front man for RUN DMC, selling tens of millions of records worldwide, but he is widely credited for ushering rap music into the mainstream culture. He also starred in MTV’s “Run House,” co-authored several books and is a sought after DJ and speaker.

His latest venture is teaming with The Novo Nordisk Ask Screen Know Campaign to help people know if they are at risk and to share tips on making healthy changes at home.

He created a website called to raise awareness and help others take precautions just as he is doing. I asked him how he gets people to get screened.

“I tell people do it for the ones you love…I look in my children’s eyes and realize I can be neglecting my health and hurt everybody in my family.” -Rev Run

Joining him is wife, Justine Simmons.  Justine is an accomplished author, jewelry designer on HSN, co-author of a best-selling book with her husband, philanthropist and loving wife and mom.

Justine also works with the Simmons family charity organization helping children with art resources.  She joins Rev Run in urging people to take a Risk Assessment Test.

She discusses how they keep their family healthy since they are at high risk for adult diabetes.

[On Men Being Afraid to Get Tested] “You hear about these men passing (away) and it could have been prevented.” -Justine Simmons

Learn More. Get Screened.

Rev Run & Justine Simmons


CLICK HERE FOR INTERVIEW:  Hip-Hop Legend Rev Run & his wife Justine on Adult Diabetes


Risk Factors for Adult Diabetes include:diabetes51

1.  Age 45 or older

2.  Race/Ethnicity

3.  Diabetes in Family

4.  Lack of Physical Activity

5.  Being Overweight

6.  High Blood Pressure


Increased Thirst

Increased Need To Urinate

Blurry Vision

Recurring Skin, Gum, or Bladder Infections

Dry, Itchy Skin

Unexpected Weight Loss

Slow-Healing Cuts or Bruises

Tingling Feet or Hands

Loss of Feeling in Extremities 




As Rev Run and Justine say, “Do it for the ones you love.”


headshot  Maria Dorfner is a health journalist and founder/CEO of NewsMD and Healthy Within Network (HWN). Her stories have appeared on NBC, CBS, ABC, CNN, Fox, CNBC and Discovery Health.  Her new book, “Healthy Within” is available at

Partial list of her awards include an Outstanding Achievement Award from March of Dimes, Media Recognition Award from American Heart Association for a series she created for CNBC called “Heart Smart,” a Medical Reporting Scholarship from American Medical Association, a Freddie Award for Excellence in Medical Reporting, an Outstanding Leadership Abilities Award and Commitment to the Advancement of Women in Media from Pace University, Women in Corporate America and National Association of Female Executives, Angel of a Sponsor Award from Make-A-Wish Foundation. She’s part of the CNBC Originals team that launched the cable network and also co-founded Cleveland Clinic News Service and more. She is listed in Marquis Who’s Who in American Women. She began her career as an intern at NBC in New York City during her sophomore year of college at Pace University. NBC awarded her a scholarship to attend graduate school at Columbia University at night during her tenure.

This is her blog

Health story you’d like to share? Contact



Learn More. Get Screened:

Healthy Within: A Story About Loss and Gain by Maria Dorfner


The following is an excerpt from my book.  It is available at:


A true story about how I connect the dots looking backwards to discover the true meaning of being healthy within in the world– by being healthy without. Oftentimes, it’s through unexpected loss that we experience our greatest gain.  May you read this book and learn to value things you can never lose in life.

Realize how past and present thoughts, relationships, pop culture, news, daily habits and stress impact your overall well-being. Discover your power to change thoughts at any moment. Acquire healthy coping mechanisms during dark times to shine light to reveal your true values and higher purpose.

Know you are beautiful and loved right now with all your flaws. Journey through pain to transform it into self-awareness, acceptance & art.  There should never be any loss in life –only transformation. You are not alone. Explore being Healthy Within.

PREFACE:   Early Influences


The year is 1984. I schlep a must-have accessory for the 80’s aspiring female executive, a soft, brown Italian leather briefcase that protects my bibles of business inspiration; The Woman’s Dress for Success by John T. Molly, In Search of Excellence by Thomas J. Peters and Robert H. Waterman, Jr. and The One Minute Manager by Kenneth Blanchard and Spencer Johnson. I am an Italian-American, wide-green eyed and wider-smiled, petite, slender brunette from Brooklyn, New York.


I am a middle child with two siblings. Parents aren’t supposed to label their children, but mine continually call me “the smart one” and the one with “a big heart.” The first from being an encyclopedia nerd, and the latter from dragging in stray or injured pets to nurse back to health, and friends who are hungry or need to escape an abusive household. Our door is always open to the less fortunate.

Brooklyn is a small community, where neighbors are one big happy, albeit dysfunctional family. My interest into the human psyche, communications and health ignite early as I witness the ravages of addiction, and try to understand or save these colorful cast of characters I love.

The constant flurry of activity in our home and that of relatives and friends prepares me for feeling perfectly at home the first time I enter a chaotic newsroom. I am used to remaining calm and centered amidst crisis, breaking news and dozens of people speaking at once.


My mother, a homemaker and part-time seamstress from Italy courageously arrives in Brooklyn by plane alone, at the age of sixteen. My father, who she has only met once in Italy, arrives in Brooklyn by boat before her. His sister has already married my mom’s older brother, so they are introduced through family. They write love letters to each other for months, which I later find hidden in a kitchen cabinet, when I climb our washing machine to reach a box of cookies. At the curious age of ten, I immediately recognize my parent’s hand writing, and feel giddy at seeing the word “amore” repeatedly. Each day after school, I look forward to secretly reading more of the Italian letters before mom gets home from work at 3 p.m. I am overjoyed to discover their love for each other.


After six-months of dating, they marry after both families give their blessings. Family approval is mandatory prior to marriage. My father takes whatever work is available when he arrives in America, but the entrepreneur in him is frustrated at each job, so he quits a string of them. Finally, after working in construction in New York City, he saves enough to open an Italian restaurant, where he finally thrives.

We reside in a comfortable three-bedroom brick home, as he continues to work a bazillion hours before retirement. He has six siblings. While attending grade school, I am sent home with a letter telling my mother that I must learn to speak English. I know no other language than Italian, but just like my parents, I learn. I grow up within a mile radius of twenty-four cousins, who I adore. We are still close to this day, honoring my grandparents wish for all of us to “love each other”. They ingrain in us an unbreakable lifetime family bond of unconditional love, laughter, joyful traditions, commitment, values and hard work.


In 1984, my parents sacrifice it all to send me to college. The economy rebounds and the United States enters one of the longest periods of sustained economic growth since WW II. My grandparents tell me stories about needing to dig a ditch in their backyard to protect themselves during bomb raids. There is no TV on their farm in Italy, only a fireplace, where they seek warmth and share stories with their eight children. I am told I have it good today because times were tough back then. I watch grandma cook, clean and scrub clothing by hand on a washboard in her bathtub –all with a smile.


In my world, consumer spending is up in response to federal tax cuts. I am given an opportunity my parents never had –to attend college in the greatest city in the world. I work part-time every spare minute at Barnes and Noble Bookstore on Fifth Avenue and Saks Fifth Avenue, earning $8.00 an hour at each job. My earnings since high school, afford me employee discounts on loads of books, and satin blouses with bows, and wide-legged, loose slacks with matching blazers infused with oversized shoulder pads sewn in.


They create the illusion of having broader shoulders, like Walter Payton, the most prolific running back in the history of the NFL, nearly indestructible and infinitely powerful.


It helps me proclaim myself as an equal in the male-dominated workforce of network news.


My nickname during college is Jackie O.


My inspiration for my career choice is from an early love of writing, which garners five stars, as early as grade school at Saint Ephrem, a private Catholic school. I also win awards for creativity in designing graduation brochures, decorating classrooms and painting local store windows during holidays.


I have a natural curiosity about health and news. We do not have a fireplace in our home. Instead, we gather around a brown, Magnavox TV, known as “the cold fire” with an antenna on top, which needs to repeatedly be adjusted to avoid fuzzy programming. Sometimes, I stand there and hold it during an entire show. This is the norm back then.


One Saturday at 9 1970, six-year-old me is inspired watching the first single, independent career woman cast in a leading role on TV. It’s The Mary Tyler Moore Show, an American sitcom created by James L. Brooks and Allan Burns, airing on CBS. I watch in awe as Mary applies for a secretarial position on the “Six O’clock News” at the fictional TV station, WJM in Minneapolis. She is told the job is filled. So, she is offered an associate producer position. I’m thrilled. The opening sequence ends with Mary tossing her hat in the air to the theme song, “Love Is All Around.” She looks confident, independent and happy. Then, a cat meows as the MTM logo appears, which tells me a woman can be all that and own her own company too. Fourteen years later, I channel Mary Richard’s enthusiasm to smash the glass ceiling in broadcast news.

Love Is All Around Me.

Or so I think.


In the ‘80’s sad songs about love dominate the airwaves. One song was even called, Sad Songs Say So Much by Elton John. Pat Benatar shouts, Love Is a Battlefield. The number one hit song is Tina Turner’s, What’s Love Got To Do With It? These songs play like a broken record on the radio infusing my mind with the message that love leads to a broken heart. So instead of making love a priority, as my parents and grandparents did, I place my efforts into building a career.

I will be different. I will be a career girl just like Mary Richards, even though on my first day at NBC, an anchorman, who is my perceived equal says, “Here kid…Xerox this.”

Clearly, he doesn’t see my Frisbee-size shoulder pads. Yep, I am powerful.


I carry a can of hairspray to tame my power, bouffant, Jackie O. brunette hairstyle. I am grateful to all the women before me who worked so hard to pave the way to push through the revolving door at 30 Rockefeller Plaza in my Columbo inspired trench coat and overstuffed briefcase.


It’s the year of “supply side” economics. Ronald Reagan is President of the United States. George Bush is Vice President. Unemployment is at 9.6%. I use my artistic skills to sketch designs of more power suits, which my mom enthusiastically sews for me with linen material on her Sear’s machine.

It enables me to dress like Royalty, even though I’m only an unpaid Intern at NBC in New York City.  Anchorwoman at NBC ask where I get my clothing. When I tell them, they offer to pay my Mom any price to make their suits. Mom turns down the offer, saying she prefers working with her friends, who speak Italian at a factory in Brooklyn.


Meantime, in the rest of the world, Japan agrees to impose a voluntary quota on its car exports to the U.S. I read IOCOCCA, the autobiography of Lee Iacocca and MAYOR by Ed Koch. Nancy Reagan reinforces my motto in her 1985, “Just Say No” campaign to educate young Americans about dangers of drug use. Back then, top fashion models like Elle Macpherson run on the beach drinking pink diet TAB during commercials. The message is anyone who drinks diet colas and fits into slim designer jeans like Brooke Shields is healthy, even if they order a diet TAB with what we call “murder burgers’ from White Castle.


Four years later, Oprah goes on a liquid diet for months to fit into her skinny jeans. The world cheers. The movie, FAME moves dancing into gyms. The aerobics craze begins. I own a headband and mimic moves to the song, “She’s a Maniac…maniac on the floor.” Yep, I am fit and healthy.  Or so I think.


Since I already think drinking TAB makes me healthy, it’s time to be WEALTHY. I already feel rich growing up because I always have nice clothing. I have brand new white shoes for church on Sundays, new earth shoes for school, and one pair of sneakers for after school. Mom delights in sewing lots of identical outfits for my sister and me in pastel colors. Jeans are a no-no. I’m told bad kids wear them. Imagine my shock when I first see my cousins Giulia and Angelina wearing (gasp!) Gloria Vanderbilt jeans, while I stand there in plaid pastel pants. Well, at least I’m not a hippie. I am a clean-cut, well-dressed kid with tons of food in the refrigerator and clean linens in a warm, cozy bedroom with all white girly furniture.


I also have a jump rope, polo stick, hoola-hoop and bicycle to keep me active. Today, Mom says I influence her with healthy habits, but back then she influences me. I recall her saying I would not be able to think in school if I did not eat a healthy breakfast. Two boiled or poached eggs were always ready for me. She packs a tuna or turkey sandwich with an apple for lunch, and makes pasta for dinner. If she isn’t around, I know a dish covered with tinfoil waits in the refrigerator for me. I can heat it up myself. I am taught to cook and clean as soon as I can stand on a chair and reach the kitchen sink to wash dishes. I am aware some neighbors are richer because they have a dishwasher. In summers, they also go to something called, “the cabana.”


All I know is the cabana has an in-ground pool. I go to the nearby park with free sprinklers or look out the back window until my neighbor with an above ground pool invites me in. They can only see my sad face pining out the window. What they don’t see is I already have my swimsuit on when they ask me to join them. I still feel rich.


It isn’t until I see the first television show featuring the lives of the wealthy that I feel dirt poor. Suddenly, “…champagne wishes and caviar dreams” enters my mind. Once again, my thoughts are infused and influenced by external influences. I enter the workforce in a new era of celebrity worship. Robin Leach’s “Lifestyles of the Rich and Famous” brings the extravagant lifestyles of moguls, athletes and entertainers right into our humble living room. I am mesmerized by the lavish homes, fancy cars and opulence. To top that off, I am exposed to the sagas of Dallas oil magnate, J.R. Ewing and his family, and Dynasty, another wealthy Denver family in the oil business. I begin dressing like Krystle Carrington with Billy Joel’s, Uptown Girl playing in my impressionable young mind. Suddenly, New York City represents everything Brooklyn is not.

My parents tell me if I attend Pace University, they can afford the 6K tuition a year, so I don’t have to get a loan. I accept, even though at the time, Pace is an accounting school, and I hate accounting. I will make the best of this privilege. Fortunately, most accountants hate journalism, which enables me to stand out, and be placed in Sigma Tau Delta, the National English Honor Society.  Uptown girl begins living in her Uptown world.


I also agree to continue to work part-time in Barnes and Noble bookstore as a sales associate (fancy title for working a cash register) to pay for my textbooks. I transfer to the one across the street from Pace University in freshman year. I also continue to work at Saks Fifth Avenue as a “sales associate” in New York City on days off, only so I can be closer to where I really want to work, NBC, the National Broadcasting Company.


NBC is located at 30 Rockefeller Plaza, which peaks my interest. Every time I want something my Dad yells, “No…we are not the Rockefeller’s!” Clearly, these Rockefeller people are not average. The average median price of a house in 1984 is 75K. The average rent is $375/month. The average new car cost 9K. A gallon of gas is $1.09 and a movie ticket is $2.75. The median average income is 22K. I want to be ABOVE average, like the people I see on Lifestyles of the Rich and Famous, Dallas and Dynasty. So, the first time I see a building with the Rockefeller name on it, I am determined to work there. It must be where “…champagne wishes and caviar dreams” come true.


During my lunch hour, I run to 30 Rock to get in line to take the NBC tour. During each tour, a Page asks, “Who wants to be Johnny Carson?” I eagerly raise my hand and get to play Johnny on a mock “Tonight Show” set. When I’m not practicing to be Johnny Carson, I read every book on success while at the bookstore. I am in heaven, having access to the greatest minds of all time. I add Stephen Covey’s, The 7 Habits of Highly Effective People to my collection. Success and wealth are at the top of my priority list, more important than personal relationships. When I have free time, I spend it taking ski lessons, getting certified in scuba-diving, learning to sail, water-ski, learning other cultures, write produce, edit, report, sketch and take voice lessons to get rid of my Brooklyn accent. I fear it all.


Fortunately, I read something by Eleanor Roosevelt that stays with me. She says, “You gain strength, courage, and confidence by every experience in which you really stop to look fear in the face. You must do the thing which you think you cannot do.”

These are all things I think I can’t do, so I do them. Steve Jobs said, “You can’t connect the dots looking forward; you can only connect them looking backwards. So you have to trust that the dots will somehow connect in your future.”



Looking backwards, I see my 3 primary values are externally influenced, materialistic, shallow and ego-driven:











The above list is the polar reverse of being HEALTHY WITHIN.  I’m also spiritual. God first.


It would take the loss of every “thing” in my life to gain this wisdom. I reverse all these superficial thoughts and priorities, and return to the intangible values my family instilled in me from the start. I learn self-awareness brings health in mind, body and spirit and self-love, which leads to genuine love and peace in all your relationships. Then, all the rest falls into place. Out of my loss, I gain a spiritual awakening into what it truly means to be healthy and wealthy. I had to journey from darkness into this light. It’s the only time I toss my hat into the air like Mary Richards, to the tune of Love Is All Around.


“Just when the caterpillar thought the world was over, it became a butterfly.” – Proverb


“The Beauty You See In Others Is Within You.”


Fast forward. 2007. I think the world is over. During this time, I hear the most powerful words ever said to me. They are, “The beauty you see in others is within you.” They are emphatically stated by an elderly woman, who says them to me, as she grips my arms in a crowded store, before vanishing into thin air. She is a stranger. I tremble from the experience. Never, in all my life, have I previously been so conscious of God’s presence.

Who was she?


HEALTHY WITHIN: A STORY ABOUT LOSS AND GAIN is a story about how I redefine the true meaning of health and beauty in the world following a personal tragedy and spiritual encounter. I gain so much wisdom from the experience that I feel compelled to share it with the world.  Society and Media constantly sends us subliminal messages that success is out there –how we look, dress, what we own. It has zero to do with that.

The world will continually have stress.  I can assure you that if you are healthy in mind, body and spirit you can survive anything. I’ve always been blessed with amazing health. Actually, blessed makes it sounds like it was handed to me –when the truth is it’s my daily habits (which people made fun of) since I was a child that lead to it.

Too many people in the world do not have healthy coping mechanisms for stress. In my book, I speak about how after Sept. 11 when the world was devastated –media spent major air time repeatedly re-traumatizing them through horrific images. The entire world needed HEALING then and media could have helped. When people were glued to their television sets all they did was add to existing fear and anxiety. If you look at what is at the core of illness and disease it’s stress that releases cortisone in the human body.

My traumatic event was a sudden, unexpected divorce. I don’t get into details of what happened because that’s not what’s important. What’s important is this major loss wiped away everything I had worked so hard for and built all my life.  As a journalist, I listened to countless stories of loss through natural disasters, drunk drivers, disease or any other number of tragedies. I saw how it destroyed people and ultimately made them physically sick or bitter.  I had a choice. I could fight for. years and make myself sick or I could walk away from it all and keep my health. I did the latter. Fourteen years of my life, but it was all just stuff. I placed health first, and continue to educate people on how it truly is your greatest wealth.

Chapters include recognizing major stressors in life that cause illness, healthy coping mechanisms for them and powerful advice on how to fix existing problems in oneself and in the world. It takes you along on my lifelong journey to redefining health from the inside out.  If little “health nerd” me didn’t know the true meaning of health, then I can only imagine what is going through young minds today. These same influences are there.  Time to stop and pay attention.  I believe every person in the world needs to read this book.  It can change the world, making it a healthier place –one person at a time, from the inside out.




“Just had the honor and privilege of pre-reading (proofing) this amazing new book by Maria Dorfner ! It right sides up everything wrong with our current world; offering simple easy things you can do to start living Healthy Within. Compelling, timely insight everyone needs to read now! Highly recommend this wonderful book nominated for the Pulitzer Prize! Awesome work Maria! Carpe Diem. A timely masterful work desperately needed for NOW…for everyone, a must read and share with the world! I Highly recommend it!” -Lisa Ditalia



headshot    Maria Dorfner is the founder of Healthy Within Network and NewsMD Communications, LLC.   She can be reached at

Nutrition & Breast Cancer


Good nutrition may reduce the incidence of breast cancer and the risk of breast cancer progression or recurrence. There are many studies in progress to help further understand how diet and cancer are related. We do know, however, that improved nutrition reduces risk of chronic diseases, such as diabetes, obesity, hypertension and heart disease, and also enhances overall quality of life. It is estimated that one third of cancer deaths in the U.S. can be attributed to diet in adulthood [1].

Here are comprehensive guidelines from Natalie Ledesma, MS, RD, CSO and Ida and Joseph Friend Cancer Resource Center, UCSF Helen Diller Family Comprehensive Cancer Center and the University of California, San Francisco.


Guidelines for a Healthy Diet

o Plenty of fruits and vegetables

o High fiber – whole grains and beans/legumes

• Low fat diet with emphasis on healthy fats

• Limit processed and refined grains/flours/sugars

• Drink plenty of fluids

• Be physically active to help achieve and maintain a healthy weight


Plant based diet

A lifelong commitment to a plant based diet may lower a woman’s risk of developing breast cancer

and may also reduce the risk of recurrent breast cancer. A plant based diet consists primarily of fruits,

vegetables, whole grains, beans/legumes, and other plant protein sources.

* All words noted with an asterisk ( * ) are defined in the glossary

SHINE ON:  Foods for Healthy, Glowing Skin

Fill your plate with approximately

50% vegetables, 25% protein,

and 25% whole grain.



Contain vitamins, minerals, fiber, and various cancer-fighting phytonutrients* (for example: carotenoids, lycopene, indoles, isoflavones, flavonols).

• Vibrant, intense COLOR is one indicator of phytonutrient* content.

• There is extensive and consistent evidence that diets high in fruits and vegetables are associated

with decreased risks of many cancers, and while results for breast cancer risk are not yet conclusive,

they are promising [2-12].

• In a study of about 3000 postmenopausal women, a protective effect for vegetables was observed [2].

SHINE ON:  Foods for Healthy, Glowing Skin

o Women who consumed 25 or more servings of vegetables weekly had a 37% lower risk of

breast cancer compared with women who consumed fewer than 9 vegetable servings weekly.


• An epidemiological study reported a significant protective effect of vegetables against breast cancer

when case-control* and cohort* studies were considered together [4].

• A meta-analysis* – looking at the data from 17 studies [13] revealed that high vs. low vegetable

consumption was associated with a 25% reduction in breast cancer risk, but these findings were not

confirmed by collected data from 8 studies [14].

• A recent case-control* study reported women who consumed more than 3.8 servings of fruits and

vegetables daily had a lower risk of breast cancer when compared with women who consumed

fewer than 2.3 daily servings [15].

• Japanese women following a prudent dietary pattern (high in fruits and vegetables, low in fat) had a

27% decreased risk of breast cancer [5].

• A Korean case-control study* reported that a high intake of certain fruits and vegetables resulted in

a significantly lower risk of breast cancer in premenopausal (tomatoes) and postmenopausal women

(grapes and green peppers) [6].

• While no effect was observed for vegetables, increasing total fruit intake significantly lowered the risk

of breast cancer when comparing those in the highest to lowest tertile [16].


o This effect was greater for those with estrogen-receptor positive (ER+) tumors.

• Eating a salad vegetable dietary pattern (high consumption of raw vegetables and olive oil) exerted a

significant protective effect against HER-2-positive cancers [10].

• A study assessing plasma or blood carotenoids as a marker for fruit and vegetable intake reported

that individuals in the top 1/4 had a 43% lower risk of breast cancer recurrence when compared to

those in the lowest 1/4 [17].

• However, no association was observed between fruit and vegetable consumption and breast cancer

recurrence when women consumed five servings daily vs. eight servings daily [18].

• Breast cancer survivors significantly reduced mortality by following a diet low in fat, high in

vegetables, high in fiber, and high in fruit [19].

• The combination of consuming five or more daily servings of vegetables and fruits, and accumulating

540+ metabolic equivalent tasks-min/wk (equivalent to walking 30 minutes 6 d/wk) decreased

mortality by nearly 50% [11].

o The effect was stronger in women who had hormone receptor-positive cancers.

• Vegetable intake has been inversely associated with serum insulin-like growth factor-I (IGF-I) levels [20].



• Beta-carotene is one of the 600 carotenoids that can be partially converted into vitamin A in the body.

• Carotenoids have a protective role for certain sites of cancer, including breast cancer [7, 21-24].

• Carotenoid intake was significantly associated with reduced mortality in breast cancer survivors [19].

• In various studies, serum beta-carotene levels were lower among breast cancer patients compared

to women without cancer [21,25-29].


o One of these studies reported the risk of breast cancer to be 221% greater for women in the

lowest quartile of serum beta-carotene compared to women in the highest quartile [29].

• A case-control* study reported that increased plasma levels of beta-carotene, retinol, and total

antioxidant* status were associated with about a 50% reduced risk of breast cancer [28].

• In vitro research indicates that carotenoids may inhibit the production of breast cancer cells [30-31].

o Beta-carotene may inhibit ER+ and estrogen-receptor negative (ER-) breast tumor development


• Beta-carotene may hinder the development of breast cancer cells by inducing apoptosis*, or

programmed cell death [32].

• Research indicates that dietary sources of beta-carotene are likely much more protective than

supplemental sources against the risk of cancer [33-35].

o Women who consumed higher amounts of dietary beta-carotene, lycopene, and betacryptoxanthin

were associated with a lower risk of breast cancer among Chinese women [23].

o Dietary alpha-carotene, beta-carotene, and lycopene were inversely associated with risk of

ER+PR+ breast cancer [24].

o Dietary beta-carotene intake was inversely associated with IGF-I levels in a large case-control

study [20].


Cruciferous Vegetables

• Some evidence suggests that the cruciferous vegetables, in particular, are associated with a

reduced risk of breast cancer [36-40].

• A Swedish study of postmenopausal women reported one to two daily servings of cruciferous

vegetables to reduce the risk of breast cancer, possibly by as much as 20-40% [37].

• Women who ate more turnips and Chinese Cabbage, in particular, significantly reduced the risk of

postmenopausal breast cancer [40].

• Consumption of cruciferous vegetables, particularly broccoli, was inversely, though not statistically

significant, associated with breast cancer risk in women [36].

• The U.S. component of the Polish Women’s Health Study found that women who consumed raw- or

short-cooked cabbage and sauerkraut 3 or more times weekly had a significantly reduced risk of

breast cancer [39].

o Cabbage that was cooked for a long time had no effect on breast cancer risk.

o Researchers suggested that glucosinolates, compounds in cabbage, may affect both the

initiation phase of carcinogenesis*, cell mutation*, and inhibit apoptosis*.

• Cruciferous vegetables appear to shift estrogen metabolism in a favorable manner; increasing

2-hydroxyestrone:16-a-hydroxyestrone [41-42]. Fowke and colleagues [42] concluded that

consuming more cruciferous vegetables across the population may very well have an impact on the

incidence of breast cancer.

• Several studies suggest that compounds found in these foods, isothiocyanates (sulforaphane), have

inhibitory effects on breast cancer cells in both cell studies and animal studies [38, 43, 44].

o One mechanism appears to be through potent inhibition of phase I and induction of phase II

detoxifying enzymes, such as glutathione-s-peroxidase [36,40,43].

o Furthermore, these compounds exhibited reduced cell proliferation and inhibited

cyclooxygenase-2 (COX-2) expression in breast cancer cells [45].

o Inhibited cell growth and induced apoptosis has also been observed [46].

• Indole-3-carbinol (I3C) is a compound found in cruciferous vegetables that has anticancer

properties and anti-proliferative effects on breast cancer cells [47].

o I3C may inhibit the growth of blood vessels that the tumor needs to grow (anti-angiogenesis)


• I3C and diindolylmethane (DIM) induce apoptosis*, or cell death, in breast cancer cells [41,49] for

both ER+ and ER- tumor cells [50].

• Furthermore, I3C and tamoxifen have been shown to act separately and/or cooperatively to inhibit

the growth of ER+ breast cancer cells [51].

• Dietary I3C may have effects that bolster immune function [52].

• Calcium-D-glucarate has been shown to inhibit beta-glucuronidase, an enzyme involved in phase

II liver detoxification. Elevated beta-glucuronidase activity is associated with an increased risk for

various cancers, particularly hormone-dependent cancers such as breast cancer [53].

Nutrient Dietary Sources Recommendation


Carrots, sweet potatoes, winter squash, cantaloupe, and mango.

Include these fruits and vegetables daily.


Cruciferous vegetables

Arugula, broccoli, Brussels sprouts,

cabbage, cauliflower, collard greens,

horseradish, kale, kohlrabi, mustard

greens, radishes, rutabaga, turnips

and turnip greens, and watercress

Include these vegetables daily.


Organic Produce

• Organic fruits and vegetables have fewer pesticides, lower levels of total pesticides, and less overall

pesticide toxicity than fruits and vegetables grown with chemicals. Although more research is

needed, recent evidence indicates a significant increase in antioxidants* in organic and sustainably

grown foods versus conventionally grown foods [54-58].

o Organic vegetables contained a greater concentration of phytonutrients* (phenolic acids) when

compared to conventionally grown vegetables [57,58].

• Consuming organic foods appears to increase salicylic acid, which may contribute to a lower risk of

cancer [57].

• Pesticides such as organochlorine compounds (OCC), known as environmental pollutants, have

been implicated in the etiology of estrogen-related disorders due to their potential estrogenic and

anti-estrogenic properties [59].

• Results of some studies [59-61], but not all [62] suggest that environmental exposure to

organochlorine pesticide residues or PCBs may contribute to multifactorial pathogenesis of breast



o In a study of women living on Long Island, New York, breast cancer risk was associated with

lifetime residential pesticide use [63].

o Organochlorine pesticide residues, including DDTs and HCHs, may increase women’s risk of

breast cancer, particularly in premenopausal women in China [60].

o Exposure to beta-HCH, an organochlorine pesticide residue, both accelerated the appearance

and incidence of breast cancer tumors when compared to control mice [61].

• The level of exposure may be integral in determining the effects of these OCC.

o One study found that when breast adipose tissue reached levels higher than 2600 ppb, women

with postmenopausal ERalpha-positive breast cancer exhibited high proliferation [64].

• Choosing organic produce will help you reduce your levels of pesticide exposure and will most likely

increase your phytonutrient* consumption.

o Although washing and peeling your non-organic fruits or vegetables may help to reduce

pesticide residues, it will not eliminate them.


• Listed below are produce with the most and least pesticide contamination, both in terms of number

of pesticides used and the level of pesticide concentration on an average sampling. Thus, for the

fruits and vegetables shown on the most contaminated list, it is wise to buy organic. Alternatively, if

organic choices are not available, you may want to consider substituting with produce that tends to

contain the least amount of pesticides.


Produce most contaminated by pesticides: Produce least contaminated by pesticides:

Peaches Onions

Apples Avocado

Bell peppers Sweet corn

Celery Pineapples

Nectarines Mango

Strawberries Sweet peas

Cherries Asparagus

Lettuce Kiwi

Grapes–imported Bananas

Pears Cabbage

Spinach Broccoli

Potatoes Eggplant

**Adapted from Environmental Working Group – A Shopper’s Guide to Pesticides in Produce


It is most important, however, to eat fruits and vegetables – organic or conventional. If the

availability or cost of organic produce is a barrier, you may wish to avoid those fruits and vegetables

that have the highest pesticide residue content.

Pomegranate (Punica granatum; Punicaceae)

• Various parts of the pomegranate fruit (for example: seed oil, juice, fermented juice and peel extract)

have expressed the suppressive effects on human breast cancer cells in laboratory research [65].

• Pomegranate seed oil and fermented juice block the cancer cells’ oxygen supply, slow cell growth,

and promote cell death [66].

• Fermented pomegranate juice polyphenols* appear to have twice the anti-proliferative effect as

fresh pomegranate juice polyphenols* [67].

• Furthermore, one study suggests that pomegranate seed oil may have the greatest preventive

activity (87% reduction in lesions) compared to fermented pomegranate juice (42% reduction) [68].


• A diet rich in natural fiber obtained from fruits, vegetables, legumes (for example: lentils, split peas,

black beans, pinto beans), and whole-grains may reduce cancer risk and/or reduce risk of cancer


• Fiber binds to toxic compounds and carcinogens, which are then later eliminated from the body [69].

• Various mechanisms have been proposed for the protective effects of dietary fiber against cancer.

These include:

o Increased fecal bulk and decreased intestinal transit time, which allow less opportunity for fecal

mutagens to interact with the intestinal epithelium [70].

o Binding to bile acids, which are thought to promote cell proliferation [71].

o Fermentation in the gut, producing short-chain fatty acids (SCFA). SCFA improve the gut

environment and may provide immune protection beyond the gut [70,71].

o Additionally, whole grains are rich in antioxidants*, including trace minerals and phenolic

compounds, which have been linked to disease prevention [71].

• Furthermore, a high fiber diet works to reduce hormone levels that may be involved in the

progression of breast cancer [70,72-75].

o A high-fiber, low-fat diet intervention found that fiber reduced serum estradiol* (estrogen breaks

down into estradiol* in the body) concentration in women diagnosed with breast cancer, the

majority of whom did not exhibit weight loss. Thus, increased fiber intake was independently

related to the reduction in serum estradiol* concentration [74].

o This decrease in estrogen levels in the blood thereby may potentially reduce the risk of

hormone-related cancers, such as breast cancer.

o Reduced levels of serum estrone* and estradiol* were observed in premenopausal women with

a greater intake of dietary fiber [73].

o Similarly, a high intake of dietary fiber was significantly associated with low serum levels of

estradiol in postmenopausal breast cancer survivors [75].

o Dietary fiber intake increases the amount of estrogen excreted in the stool [76].

• A high fiber diet is also associated with less obesity [72].

• Total dietary fiber intake, particularly from cereals and fruit, was found to significantly reduce the

risk of breast cancer in pre-menopausal, but not post-menopausal women [77].

• A recent cohort* study reported that high fiber intakes were associated with a 42% lower risk of

postmenopausal breast cancer, when comparing women in the highest quintile of fiber intake

compared to the lowest quintile [78].

An earlier prospective cohort* study, however, reported no protective effect of fiber against breast

cancer when comparing women who consumed fewer than 26 grams dietary fiber compared to

those who consumed even less [79]. This finding is not surprising given that the total grams of fiber

consumption was less than 30 grams.

o Similarly, another study that reported no significant findings compared women consuming less

than 25 grams fiber daily [80].

• Overall, case-control* studies have reported the greater the fiber intake, the lower the incidence of

breast cancer [8,81-84]. Data from prospective studies is mixed, reporting protective effects [78,85]

or no effect observed [79,80].

• Women who ate beans and lentils at least twice a week had a 24% lower risk of developing breast

cancer than women who ate them less than once a month [86].


High-Fiber Sources


Food Serving Size Fiber Grams/ Serving

Apple 1 medium 3.7

Banana 1 medium 2.8

Blackberries 1/2 cup 1.9

Blueberries 1 cup 1.3

Cantaloupe 1/2 cup 6.0

Figs (dried) 1/4 cup 6.0

Grapefruit 1 medium 3.4

Grapes 1 cup 1.6

Guava 1 medium 4.9

Kiwi 1 medium 2.6

Orange 1 medium 3.1

Pear 1 medium 4.0

Persimmon 1 medium 6.0

Prunes 1/4 cup 3.1



Food Serving Size Fiber Grams/ Serving

Amaranth 1/4 cup dry 7.4

Barley 1/2 cup cooked 3.0

Beans, black 1/2 cup cooked 8.3

Beans, red kidney 1/2 cup cooked 8.2

Beans, garbanzo 1/2 cup cooked 5.0

Bran cereals 3/4 cup Check labels (5.0-22.0)

Brown rice 1/2 cup cooked 1.4

Bulgur 1/2 cup cooked 4.0

Cream of wheat 1/2 cup cooked 0.5

Oatmeal 1/2 cup cooked 2.0

Peanuts 1/4 cup 2.9

Quinoa 1/4 cup dry 2.5

White rice 1/2 cup cooked 0.3



Food Serving Size Fiber Grams/ Serving

Artichokes 1 medium 6.9

Beets 1/2 cup cooked 1.7

Broccoli 1/2 cup cooked 2.3

Brussel sprouts 1/2 cup cooked 2.0

Carrots 1/2 cup cooked 2.6

Kale 1/2 cup cooked 1.3

Lima beans 1/2 cup cooked 4.5

Peas, green 1/2 cup cooked 4.4

Spinach 1/2 cup cooked 2.2

Squash, winter-type 1/2 cup cooked 3.4

Sweet potatoes (yams) 1/2 cup cooked 2.7



• High sugar foods are usually highly processed and refined, low in nutrient value, and also low in

dietary fiber. In addition, these foods appear to increase serum insulin* and serum IGF-I levels [87],

which appear to stimulate cancer cell growth.

o Overexpression, or high amounts, of IGF increases mammary tumors in mice [88].

o IGF’s may work by stimulating cell cycle progression & prevent cells from premature death [89-92].

o IGF-I may promote tumor growth via upregulation of ovarian steroid secretion [92,93].

o Research indicates a synergistic effect between IGF-I and estrogen [94] as well as IGF-I and

insulin* resistance [95] in breast cancer.

• A prospective cohort* study observed a significant 310% increased risk of breast cancer in

premenopausal women who had the highest quartile of IGF-I compared to women with the lowest

quartile [88].

o A weaker association was found with fasting insulin* levels where premenopausal women in the

two highest quartiles had a 70% greater risk for breast cancer.

o In premenopausal women, women in the highest quartile of serum glucose had a 280%

increased risk of breast cancer compared with women in the lowest quartile.

o In postmenopausal women, the associations of glucose, insulin*, and IGF-I were associated

with breast cancer risk in heavier subjects (BMI>26 1).

o Overall, these findings indicate that chronic change of glucose/ sugar metabolism is related to

breast cancer development.

• Other studies support a stronger link between IGF-I and breast cancer in premenopausal women


• Additionally, a case-control* study in China found that IGF-I significantly increased the risk of breast

cancer [95].

• Nonetheless, a recent meta-analysis* review of 18 studies reported no overall statistically significant

association between circulating IGF-I levels and risk of breast cancer although the levels were

greater in breast cancer patients than controls [90].

o However, IGF-I levels did appear to increase breast cancer risk in premenopausal women by

almost 40%.

• Similarly, a large prospective trial reported IGF-I significantly increased risk of breast cancer

in premenopausal women under the age of 50; no significant relationship was noted for

postmenopausal women [97].

• While not all studies [98] agree, a cohort* study reported that higher insulin* levels significantly

increased risk of breast cancer for both pre- and post-menopausal women [99].


• Recent studies indicate that high insulin* levels, increased concentration of IGF-I, and greater

abdominal fat are associated with increased risk for breast cancer [100].

• It has been suggested that decreasing IGF-I levels may be one factor that contributes to

tamoxifen’s anti-tumor activity in breast cancer therapy [101].

•Research is inconsistent regarding the association of IGF-I and disease-free survival or overall

survival [91].

• One study noted a direct association, though not statistically significant, between non-fasting serum

insulin* levels and 10-year mortality in postmenopausal breast cancer women [102].

• Among other factors, a diet low in fiber may favor the development of insulin* resistance and

hyperinsulinemia [89].

1BMI refers to body mass index, which is calculated by body weight (kg)/height2(m2).

• Hyperinsulinemia may contribute to the development of breast cancer in overweight or obese

women [103].

• Additionally, obesity and fasting hyperinsulinemia have been associated with a poorer prognosis in

women with established breast cancer [104].

• A recent case-control* study reported that carbohydrate intake significantly increased risk of breast

cancer; sucrose (table sugar) imparted the greatest risk [105]. This risk was lessened considerably

with a higher fiber intake.

• Furthermore, an Italian case-control* study found that women who consumed the highest tertile

of desserts and sugars had a 19% increased risk of breast cancer compared with women in the

lowest tertile [106].


• The consumption of sweet foods with a high glycemic index (GI) and glycemic load (GL) have been

implicated as a risk factor for breast cancer due to their effects on insulin and IGF-I [107-110].

o Women who consumed the greatest intake of desserts (including biscuits, brioches, cakes,

puffs and ice-cream) and sugars (including sugar, honey, jam, marmalade and chocolate) had a

19% increased risk of breast cancer compared with women who consumed the least desserts

and sugars [107].

• Adding credence to the idea that blood sugar levels may affect disease progression, women who

consumed a high GI and GL diet had a 57% and 253% increased risk of breast cancer, respectively


o This effect was most pronounced in premenopausal women and those women at a healthy

body weight.

• GI and GL were both associated with an increased risk of breast cancer among postmenopausal

overweight women; this effect was most pronounced for women with ER- breast cancer [109].

• This evidence was further supported by a meta-analysis that reported GI to modestly increase the

risk of breast cancer [110].


INSULIN HIGH TIDE. The observed link between obesity and cancer may be explained by the growthpromoting

activities of insulin and IGF-1. One theory posits that excess weight sets off a biochemical

cascade that increases insulin and, in turn, IGF-1 levels. Both hormones may activate IGF-1 receptors

on cells, which can spur cell growth and inhibit cell death pathways that usually protect against tumor


E. Roell/Source: Nature Reviews Cancer, 2004


Sugars & Insulin* – Bottom Line

• To help control your insulin* level:

o Eat a high-fiber diet with limited refined/processed foods

o Follow a low fat diet rich in omega-3 fatty acids

o Exercise

o Maintain a healthy body weight



Several studies have investigated the relationship of fat and the risk of breast cancer, but the results

remain inconsistent. However, two recent trials showed some promise in the area. The Women’s

Intervention Nutrition Study (WINS) found that a reduced fat intake improves relapse-free survival

by 24% in postmenopausal women with breast cancer compared with women following a standard

diet [111]. The risk of recurrence for women with ER- breast cancer decreased by 42%. Later, the

European Prospective Investigation into Nutrition and Cancer (EPIC) Study reported that eating a

higher fat diet significantly increased the risk of breast cancer; women who had a 35% and 39% fat

diet were at a greater risk than those eating a 31% fat diet [112]. While neither of these diets would

be considered low fat, a significant effect was still observed.


The potential elevated cancer risk may be, in part, due to the fact that a high fat diet stimulates

increased estrogen levels, which is associated with breast cancer growth. A study of adolescent

females found that modest reductions in fat intake during puberty resulted in significantly lower concentrations

of sex hormones (estradiol*, estrone*, progesterone) [113]. Further research is needed to

determine if in fact these lower levels lead to a reduced risk of breast cancer.

Additionally, a low fat, high carbohydrate diet may result in a significant reduction in breast density,

particularly in women going through menopause. Aim for close to 20% of your total calories from

fat, with less than 8% of total calories from saturated fat. Research indicates that the type of fat

may be of paramount importance.

Saturated Fats

• Several studies indicate a positive association between saturated fat intake from meat and

dairy products (animal sources) and cancer [114-117]. The breast cancer research, however, is


• Total saturated fatty acid intake was significantly associated with breast cancer risk in cohort*

studies in postmenopausal women, but not premenopausal women [118].

• Based on a seven-day diary for evaluating saturated fat intake, a high intake of saturated fat was

reported to increase the risk of breast cancer [116].

• A meta-analysis* observed a 19% increased risk of breast cancer with greater intake of saturated

fats [119].

• Other studies, however, have not found a significant association between saturated fats and breast

cancer [120-122].

Trans-Fatty Acids

• Preliminary research indicates that these fatty acids may be associated with an increased risk of

cancer [123-126].

• Minimal research exists on the relationship between trans-fatty acids and risk of breast cancer, thus,

more research is needed for conclusive evidence. However, some evidence points to a positive

association between these fats and breast cancer risk [125,127].

• These fats may disrupt hormonal systems that regulate healing, lead to the destruction of defective

membranes, and encourage the development of cancer.

• One study reported a 40% increased risk of breast cancer in postmenopausal women who had

higher tissue levels of trans-fatty acids [128].

• Women who consumed greater amounts of trans-fatty acids significantly increased their risk of

breast cancer [126].

o Women in the highest quintile of trans-fatty acid consumption had a 75% increased risk

compared with women in the lowest quintile.

Omega-9 Fatty Acids (Monounsaturated Fats)

• Most research at this time indicates a neutral relationship [120,126] or a slightly protective effect

[122,129-131] between these fats and risk of breast cancer.

• Several case-control* studies reported that olive oil consumption, rich in omega-9 fats, resulted in a

13-34% reduction in breast cancer risk [132-135].

o One study found that women who consumed ≥8.8 g/day of olive oil had a 73% lower risk of

breast cancer [131].

• Oleic acid, an omega-9 fatty acid found in olive oil, has been observed to synergistically enhance

the efficacy of trastuzumab (Herceptin) [136,137].

• A meta-analysis*, however, that included three cohort* studies reported total monounsaturated fatty

acids and oleic acid, a type of omega-9 fatty acid, to significantly increase breast cancer risk [118].

Essential Fatty Acids (EFA)

Essential fatty acids are necessary for the formation of healthy cell membranes, the proper

development and functioning of the brain and nervous system, and for the production of hormonelike

substances called eicosanoids* (thromboxanes, leukotrienes, prostaglandins). Among other body

functions, these chemicals regulate immune and inflammatory responses.

Eicosanoids* formed from the omega-6 fatty acids have the potential to increase blood pressure,

inflammation, platelet aggregation, allergic reactions and cell proliferation. Those formed from the

omega-3 fatty acids have opposing affects. Current research suggests that the levels of essential

fatty acids and the balance between them may play a critical role in the prevention and treatment of


Omega-3 Fatty Acids

• Research is growing supporting a protective relationship between omega-3 fatty acids [alpha

linolenic acid (ALA), eicosapentanoic acid (EPA), and docosahexanoic acid (DHA)] against the risk of

breast cancer [118,120,135-141].

• Studies show that omega-3 fatty acids inhibit breast cancer tumor growth and metastasis.

Additionally, these fats are immune enhancing.

• Mechanisms proposed for their protective effects include:

o Suppression of eicosanoid synthesis from arachidonic acid (omega-6 fatty acid), which

impedes immune function [139,142].

o Inhibit cell growth and differentiation via effects on gene expression and signal transduction

pathways [139,142].

o Alter estrogen metabolism, which reduces estrogen-stimulated cell growth [139,142].

o Effects on insulin* sensitivity and membrane fluidity [142].

• A prospective study reported that women who consumed 44 g or more of dietary marine sources of

omega-3 fatty acids reduced their risk of breast cancer by 26% when compared with women who

consumed 25 g or less [120].

• Women with the greatest EPA, DHA, and total omega-3 fatty acids in their red blood cell

membranes from fish had a 73%, 94%, and 89% lower risk of breast cancer, respectively [140].

• An inverse relationship was found between omega-3 fatty acids in breast tissue and the risk of

breast cancer [137].

o When comparing women in the highest tertile of ALA and DHA to the lowest tertile, cancer risk

was reduced by 61% and 69%, respectively.

• Preliminary research indicates that DHA may synergistically enhance taxane cytotoxicity [143]. More

research is needed, but these findings would indicate that DHA during taxane administration may

improve the effects of chemotherapy for breast cancer patients.

• Fish and plant-based foods, however, contain different types of omega-3 fatty acids.

o Fish contains EPA and DHA, two specific fatty acids that have shown promising results in the

research literature [135,140,144].

o Fish consumption in general has been associated with a protective effect against breast cancer


o The plant-based omega-3 fatty acid sources, such as flaxseed and others listed in the table

below, contain ALA. In an ideal environment, ALA is converted to EPA and DHA, however, this

process is inefficient [69,142,146]. On the positive side, the conversion process is enhanced by

following a diet that is low in saturated fats and low in omega-6 fatty acids [142,147].

Omega-6 Fatty Acids

• Recent studies indicate that a high intake of omega-6 fatty acids (linoleic acid, which can

be converted to arachidonic acid) promote breast tumor development and metastasis


• A meta-analysis* of 3 cohort* studies found palmitic acid, a type of omega-6 fatty acid, to be

significantly associated with an increased risk of breast cancer [118].

• Additionally, researchers reported that arachidonic acid, an omega-6 fatty acid almost exclusively

from meat, significantly increased oxidative damage as measured by urinary biomarkers [150].

• It is known that cyclooxygenase is the rate-limiting enzyme that catalyzes the conversion of

arachidonic acid to prostaglandins. Furthermore, COX-2 is known to be overexpressed in various

human cancers. In this breast cancer study, COX-2 overexpression was significantly correlated with

larger tumor size and advanced clinical stage, which indicates a poorer prognosis [149].

• A very interesting finding was reported in a prospective study that found no overall association

between omega-6 fatty acids and risk of breast cancer [120]. However, omega-6 fat consumption

increased risk by 87% in women who consumed 25 g or less of marine omega-3 fatty acids. This

effect was even greater for advanced breast cancer.

o Thus, the balance between omega-6 and omega-3 fatty acids may be of paramount

importance. This was further supported by other studies [137,138,151,152].

Fat – Bottom Line

• Less fat is better.

• Limit animal fats.

• Avoid hydrogenated fats.

• Extra-virgin olive oil, canola oil, macadamia nut oil or almond oil is preferred for salads

and cooking.

• Increase omega-3 fatty acids.

Fatty Acid Dietary Sources Recommendation

Saturated fatty acids Meats, poultry skin, baked goods,

and whole milk dairy products,

including butter, cheese, and ice


Reduce or eliminate meat and

whole milk dairy products.

Trans fatty acids Margarine, fried foods, commercial

peanut butter, salad dressings and

various processed foods including

breads, crackers, cereals, and


Avoid trans or hydrogenated


Products may be labeled “trans

fat free” if they contain less

than 0.5 mg per serving.

Omega-9 fatty acids Extra-virgin olive oil, almond oil,

canola oil, macadamia nut oil,

almonds, and avocados

Include these healthy fats daily.

Limit consumption of nuts to no

more than ¼ cup with meal

or snack to limit total fat and



Omega-3 fatty acids:



Cold-water fish (for example:

salmon, sardines, black cod, trout,

herring), breastmilk, and DHAenriched


Flaxseeds, chia seeds, walnuts,

hempseeds, and pumpkin seeds

Include these healthy fats

daily through diet and/or


It may be wise to consume

cold water fish or fish oil

supplements at least twice

weekly to obtain an adequate

amount of EPA and DHA.

If you choose to use a

supplement, opt for one that

is highest in EPA and DHA


Omega-6 fatty acids:

Arachidonic acid

Linoleic acid

Meats, butter, egg yolks, whole milk,

and whole milk dairy products

Common vegetable oils, such as

corn oil, safflower oil, sunflower

oil, and cottonseed oil, and

processed foods made with these


Reduce or eliminate meat and

whole milk dairy products.

Limit consumption of linoleic

acid-rich oils.

Substitute an omega-9 fatty

acid-rich oil for your current

cooking oil or fat.


• In a study of over 35,000 women, meat consumption significantly increased the risk of breast

cancer in both premenopausal and postmenopausal women [153].

o Women eating 1.75 ounces of processed meat daily increased the risk of breast cancer by

64% in postmenopausal women compared to women who did not eat meat.

• Consumption of red and fried meat quadrupled the risk of breast cancer in a case-control study in

Brazil [12].

• Meat consumption increased the risk of breast cancer risk by 56% for each additional 100 g (3.5

oz) daily of meat consumption in a French case-control study [135].

• Regular consumption of fatty red meat and pork fat increased the risk of breast cancer by 348%

and 632%, respectively in a small Brazilian study [154].

• A large case-control* study found that women who consumed very well-done meat for hamburger,

bacon, and steak had a 54%, 64%, and 221% increased risk for breast cancer, respectively [155].

o Frequent consumers of these well-done meats had a 462% greater risk of breast cancer.


Food Category Summary Recommendation

Fruits and vegetables One serving =

½ cup fruit or vegetable

1 cup raw leafy greens

¼ cup dried fruit or vegetable

6 oz fruit or vegetable juice

Eat 1 cup or more vegetables with

lunch and dinner.

At least 5, preferably 8-10 total

servings daily [156]

5 or more vegetable servings

3 fruit servings

Fiber Choose breads with 3 or more

grams of fiber per slice.

First ingredient on the label should

be whole or sprouted grain flour,

not white flour, unbleached white

flour, or enriched wheat flour.

Whole grains include, among

others, oats, barley, brown rice,

quinoa, amaranth, bulgur, millet,

buckwheat, spelt, wild rice, and


30-45 grams daily

This goal can be achieved

by meeting your fruit and

vegetable goal plus one

serving of legumes or at least

two servings of whole grains.

Refined carbohydrates and


Dietary sources include products

made with refined flours (for

example: white bread, white rice,

white pasta) or refined grains,

alcohol, sodas, drinks containing

added sugars, and desserts, such

as candy, cookies, cakes, and


Limit or avoid consumption.

Meat Dietary sources include beef, pork,

and lamb.

Reduce or eliminate meat


Avoid processed, grilled or fried


GENOTOXINS: Heterocyclic Amines (HCAs) & Polycyclic Aromatic Hydrocarbons (PAHs)

• Natural components in meat, such as amino acids, creatine*, and polysaccharide precursors,

are converted to HCAs during high-temperature cooking. HCAs are known to cause cancer in

laboratory animals [157,158].

• While human research is forthcoming, the majority of studies [155,157-162] although not all

[163,164] have observed a significant association between HCAs and breast cancer.

• Carcinogenic activity of HCA’s is affected by various dietary factors [165]:

o Factors that enhance carcinogenesis* when combined with HCAs include:

• High-fat diet

• Caffeine


o Factors that inhibit carcinogenesis* when combined with HCAs include:


• Conjugated linoleic acid (CLA)

• Isoflavones

• Diallyl Sulfides (found in the allium family, such as garlic, onions, leaks, and shallots)

• Green tea catechins*

• Indole-3 carbinol

• Probiotics

• Gamma-tocopherol

• The most important variables contributing to the formation of HCAs are:

o Cooking temperature (greater than 300°F)

o Cooking time (greater than 2 minutes)

o Cooking method (frying, oven grilling/broiling, barbecuing)

• Charring of food (charcoal-broiled or smoked foods) contribute to PAHs [166].

• Meat can potentially be made “safer” to eat by being cooked in a way that does not lead to HCA


o Choose lean, well-trimmed meats to grill.

o Using marinades significantly reduces the amount of HCAs.

o Brief microwave preheating substantially reduces HCA content of cooked meat.

o Small portions require less time on the grill.

• Additionally, the type of protein cooked can also affect the concentration of HCAs. It has been

reported, for example, that chicken has more than 100 times the number of HCAs than salmon [165].

London broiled steak had more than 600 times the amount of HCAs when compared to salmon.

• Grill vegetables or meat alternatives that do not lead to the formation of HCAs or PAHs.


• Regular consumption of alcohol may increase the risk for breast cancer [167-176].

o A recent review study reported that data from many well-designed studies consistently shows

a small rise in breast cancer risk with increasing consumption of alcohol [172].

• A recent study found that as little as a half a glass of wine a day raised a woman’s risk of

developing breast cancer by 6% (increased risk by 18% in postmenopausal women) [167].

o Furthermore, 1-2 drinks a day increased risk by 21% and 2 or more drinks a day increased risk

by 37%.

o The heightened risk was more pronounced for women with ER+ and progesterone-receptor

positive (PR+) tumor types.

•Women who drank two or more alcoholic drinks daily in the five years prior to diagnosis had an


82% increased risk of breast cancer compared to non drinkers [173].

•A pooled analysis of six prospective studies suggests that the risk of breast cancer increases

linearly by 9% with each 10 g /day (~ 1 drink) alcohol [177]. The risk increased to 41% when

comparing women who consumed 30-60 g/day (~2-5 drinks) to nondrinkers.

•A large meta-analysis* revealed that one drink daily increased breast cancer risk by 11% [178]. A

later meta-analysis* found similar findings [179].

•Since then, another meta-analysis* reported that breast cancer risk increased by 32% and 46% in

women who consumed 35-44 g alcohol (~3-4 drinks) daily and 45 g or more (~4.5 drinks or more)

daily, respectively [170].

o For each additional 10 g of alcohol (~1 drink) daily, risk increased by 7%.

•Other studies [168] claim that one glass of alcohol daily does not increase risk, but consuming 2-5

drinks daily increases the risk of breast cancer by 40% compared to non-drinkers [168].

o Greatest risk was among heavy drinkers who were also postmenopausal and had a history of

benign breast disease or who used hormone replacement therapy (HRT) [168].

•Similarly, a French study found that drinking 10-12 g wine (~ 1-1.5 drinks) daily lowered the risk of

breast cancer, but when intake increased above 12 g daily, the risk of breast cancer increased [180].

•Among ER+ postmenopausal women, those who consumed approximately 3 drinks or more daily

had a 76% increased risk of breast cancer when compared with women who did not consume

alcohol [181].

o The association between alcohol and ER- tumors was less clearly associated.

o Additionally, there was no clear association between alcohol and premenopausal risk of breast


•A recent cohort* study of postmenopausal women reported that alcohol consumption was

associated with an increased risk of breast cancer in ER+, but not ER- tumors [182].

•On a similar note, a recent meta-analysis reported that an increase in 10 g (~1 drink) alcohol daily

increased the risk of breast cancer, especially for women with ER+ breast cancers –ER+ (12%

risk), all ER- (7% risk), ER+PR+ (11% risk) ER+PR- (15% risk), ER-PR- (no effect) [174].

•Petri and colleagues [171] observed a stronger relationship between alcohol and breast cancer in

postmenopausal women compared to premenopausal women.

o Premenopausal women drinking more than 27 drinks per week had a 3.5% higher risk than

women who had one drink per week.

o Postmenopausal women drinking six or more alcoholic beverages per week had a 2.4% higher

risk than women who had one drink per week.

•On the contrary, women who drank about 1.5 drinks per week had a 40% greater likelihood of

developing breast cancer compared to non drinkers and this was most pronounced in women who

were premenopausal at diagnosis [175].

•Alcohol consumption (1 drink/day) during a woman’s fifties increased risk for postmenopausal

breast cancer by 12% in a large cohort* study, but statistical significance was not reached for

women in their twenties, thirties, or forties [169].

•These differing findings between pre- and postmenopausal women are likely related to the effect of

alcohol on estrogen levels. Alcohol appears to increase endogenous* estrogen levels [183-187].

•Folate, a B vitamin, may be of even greater significance with alcohol consumption. It has been

observed that women with low folate and high alcohol consumption had a 43% greater risk of


breast cancer when compared with nondrinkers with adequate folate intake [188].

Alcohol –Bottom Line

•It is best to limit or avoid alcohol.


The functions of water in the body include the following:

o Carries nutrients and waste products.

o Participates in chemical reactions.

o Acts as a lubricant and cushion around joints.

o Acts as a shock absorber in the eyes and spinal cord.

o Aids in the body’ temperature regulation.

o Maintains blood volume.

•Increased fluid intake is needed for a high fiber diet.

•Drink plenty of water daily to help meet fluid needs.


•The risk of breast cancer is much higher in industrial countries than in developing countries where

women are characterized by lower energy intake and higher energy expenditure.

•Modest caloric restriction has been shown to inhibit tumor growth in animal models decrease

oxidative DNA damage [189].

•Modest caloric restriction has been shown to decrease oxidative DNA damage.

•The mechanism involved may be related to the decrease in IGF-I observed when caloric intake is

restricted [190,191].

•Furthermore, evidence suggests that a high calorie diet may increase IGF-I levels [192].


•Epidemiologic evidence suggests a positive association between body mass and postmenopausal

breast cancer [193-196].

o Increasing BMI was associated with a 40% increased incidence and mortality of breast cancer

in postmenopausal women [197].

o Women with a BMI of ≥5 had a 58% increased risk of breast cancer [5].

o Obese postmenopausal women had 3.26-fold increased risk for breast cancer compared to

healthy weight women [198].

o In women with breast cancer, height and BMI were associated with postmenopausal breast

cancer [199].


•This effect was most pronounced in women with ER+ tumors.

o Obese postmenopausal women had a 50% increased risk for breast cancer [196].

•A recent case-control* study of 2000 women found that women who gain weight, particularly after

age 50, significantly increase their risk of breast cancer [200]. Conversely, women (young and

middle-aged) who lose weight may decrease the risk of breast cancer.

o This study suggests excess body fat increases estrogen levels, which may in turn increase the

risk for breast cancer.

o An earlier study reported similar findings with total weight gain serving as a strong predictor of

breast cancer risk, specifically among former and never HRT users [193].

•Increasing BMI was associated with a 40% increased incidence and mortality of breast cancer in

postmenopausal women [197].

•Results from a systematic review showed that, when adjusted for BMI, a larger waist size increased

risk of breast cancer among premenopausal women [202]. This study supports the idea that central

obesity is of greater concern than general obesity in regards to breast cancer risk.

o However, for postmenopausal women, a large trial found that, while general obesity was a

significant predictor of breast cancer risk, central obesity did not appear to be associated with

increased risk [203].

•Total body weight, BMI, and hip circumference were significantly associated with breast cancer risk

among HRT nonusers; obese women (BMI > 30) had a 31% greater risk compared to women with

BMI < 25 [203].

•Overweight or obesity is associated with poorer prognosis in the majority of the studies that have

examined body mass and breast cancer [204-210].

•Various studies report increased BMI or body weight to be a significant risk factor for recurrent

disease, survival, or both [204-210].

o May be related to increased estrogen [196,211,212] and elevated insulin* and IGF, which can

stimulate cell proliferation [101,204].

o Obese postmenopausal women (BMI >30) had 35% higher concentrations of estrone* and

130% higher concentrations of estradiol* compared with lighter-weight women (BMI < 22.0)

[211]. Additionally, free estradiol* and free testosterone were two to three times greater in

overweight and obese women compared with lighter-weight women.

o Recent findings indicated that oxidative damage, measured by urinary biomarkers, was

significantly greater in women with a higher BMI [150].

o Obesity among premenopausal women, however, may not be associated with increased risk

of breast cancer. Nonetheless, obesity during menstruating years is associated with obesity

throughout life and therefore to an eventual increased risk of breast cancer [132]. However,

other research suggests a stronger relationship between body weight and breast cancer in

premenopausal women [208,210].

o A cohort* study of 1300 women reported that breast cancer recurrence and death increased

with body weight in both premenopausal and postmenopausal women [158].

•Body weight prior to breast cancer diagnosis significantly increased risk of recurrence and death in

nonsmokers [208].

o Additionally, nonsmokers who gained weight after diagnosis had an elevated risk of breast cancer

death during follow-up (median, 9 years), compared with women who maintained their weight.


•Women with a BMI of ≥5 had a 58% increased risk of breast cancer [5].

•Research suggests a potential link between obesity, diabetes mellitus and breast cancer [214].

•Eating foods high in vitamin C, such as fruits and vegetables, may provide a protective effect from

breast cancer for overweight women (BMI>25) [215].


•Low levels of physical exercise appear to be associated with the risk of breast cancer [172,195,216-218].

•Lifetime total physical activity has been associated with a decreased risk of breast cancer


o Some studies indicate that physical activity has a more significant effect in reducing risk of

breast cancer in postmenopausal women [222].

o Exercise between the years of 14-20 appears to be the most beneficial in reducing risk of

breast cancer [219].

•A case-control* study reported significantly reduced breast cancer risk among women who

maintained, on average, 17.6 (MET)-hr of activity/week2 from menarche onward [195]. This

decreased risk with physical activity was limited to women without a family history of breast cancer

when adjusted for BMI.

•A cohort* study reported that postmenopausal women who were most physically active (> 42.0

MET-h/week)3 at baseline had a 29% lower incidence of breast cancer than active women with the

least activity (> 0-7.0 MET-h/week) 4 [218]. This difference was greatest for women who did not use

HRT at enrollment.

•Women who engaged in regular strenuous physical activity at age 35 had a 14% reduced risk of

breast cancer compared with less active women [217]. A similar trend was observed for regular

strenuous activity at age 18 and at age 50. These findings were consistent with women who did

and did not use HRT.

•Furthermore, a prospective observational study reported that physical activity after a breast cancer

diagnosis may reduce the risk of death from this disease [216]. The greatest benefit occurred in

women who performed the equivalent of walking 3 to 5 hours per week at an average pace. The

benefit of physical activity was particularly apparent among women with hormone-responsive


•As noted earlier, the combination of consuming five or more daily servings of vegetables and fruits,

and accumulating 540+ metabolic equivalent tasks-min/wk (equivalent to walking 30 minutes

6 d/wk) decreased mortality by nearly 50% [11].

o The effect was stronger in women who had ER+ cancers.

•Increased physical activity following breast cancer diagnosis significantly decreased the risk of

dying from breast cancer and improved overall survival when compared with women who exercised

<2.8 MET-h/wk [224].

•Survival may be enhanced by physical activity in those women who exercised the year prior to

diagnosis, especially women who were overweight or obese [225].

•Exercise was associated with improved quality of life among survivors [226,227].


•Physical activity can help ease cancer-related fatigue during and following cancer treatment


•Physical activity may reduce the risk of breast cancer through an influence on ovarian function and

a decrease in progesterone and estrogen concentrations via reduced body fat [217]. Furthermore,

exercise may increase sex hormone-binding globulin* (SHBG) levels and thereby reduce estradiol*.

•An increase in lean body mass (often achieved through physical activity) was associated with

a favorable change in 2-hydroxyestrone: 16-α-hydroxyestrone, a proposed biomarker of breast

cancer risk [230].

•Additionally, exercise reduces serum insulin levels [231], serum IGF-I levels [217,232], and improves

insulin* sensitivity [217].

•Greater physical activity in obese women was associated with significantly less mammographic

density, possibly suggesting another mechanism for the protective effect of physical activity [233].

•Healthy weight control is encouraged with an emphasis on exercise to preserve or increase lean

muscle mass.

2 This is equivalent to a 150lb individual burning 1257 kcals/week through physical activity.

3 This is equivalent to a 150lb individual burning about 3000 kcals/week through physical activity.

4 This is equivalent to a 150lb individual burning 500 kcals/week or less through physical activity.

Additional Nutritional and Lifestyle Factors for Breast Cancer Survivors

ANTIOXIDANTS* –Found in abundance in fruits and vegetables!

•Prevent oxidative damage in body cells.

o Research indicates a link between oxidant damage and breast carcinogenesis*.

•Examples of antioxidant* nutrients and non-nutrients include vitamins A, C, and E, selenium,

lycopene, and beta-carotene.

•Note that patients may be advised to NOT consume high-dose antioxidant* supplements during

chemotherapy or radiation therapy. Antioxidant* consumption via food sources and a basic

multivitamin supplement are very safe.


•Antioxidant* that scavenges free radicals and suppresses damage due to oxidation. Also is

essential for the immune system.

•Promising evidence indicates that selenium may decrease the risk of breast cancer [234-239].

o Inhibits cell proliferation and induces apoptosis* [238,239].

•Selenium may interfere and alter estrogen receptors decreasing mammary tumor incidence [236].

• Research shows that selenium reduces the incidence of malignant cells in animal models [237], and

enhances the effects of chemotherapeutic drugs, such as [235] taxol and adriamycin [235,239].

• Toenail selenium concentrations tended to be lower in postmenopausal breast cancer patients when

compared with healthy non-cancer patients, but the differences did not reach statistical significance [240].

o Interestingly, this study also found that plasma triiodothyronine (T3) (a thyroid hormone)

concentration was positively associated with toenail selenium in breast cancer patients and

controls. T3 concentration was significantly lower in breast cancer patients compared to

healthy non-cancer patients.

• A recent study suggested the combination of selenium and iodine, typical of a Japanese diet, act

synergistically in decreasing breast cancer risk [241]. It is known that iodine plays an important role in

thyroid function. Thus, selenium status may affect both thyroid hormone status and iodine availability.

• Selenium is a precursor to the glutathione* (GSH) antioxidant* system. GSH is the principal

protective mechanism of the cell and is a crucial factor in the development of the immune response

by the immune cells [242].

o Studies suggest the ratio of selenium to glutathione* is at lower levels in breast cancer patients

[234]. Research indicates that dietary selenium supplements correct abnormal glutathione*


Turmeric (Curcumin)

• Curcumin, the yellow pigment and active component of turmeric and many curries, is a potent

antioxidant*, that exhibits chemopreventive and growth inhibitory activity in several tumor cell lines


• Evidence suggests that curcumin may suppress tumor initiation, promotion and metastasis [245,247].

o This may occur through enhanced apoptosis* [243,245].

• Additionally, curcumin promotes detoxification in the liver and possesses anti-inflammatory activity,

possibly by inhibiting COX-2 activity [248,249].

Vitamin C

• Most research [250-255], although not all [7,19,256,257], has shown no protective relationship

between vitamin C and the risk of breast cancer.

o Vitamin C induces apoptotic effects on breast cancer cells [257].

• Low plasma levels of vitamin C have been associated with a greater risk of breast cancer [258].

• Dietary vitamin C has been significantly associated with reduced mortality in breast cancer

survivors [19].

• Furthermore, risk of recurrence and mortality was reduced in women who consumed vitamin C

supplements for more than three years [259].

Vitamin E

• Vitamin E acts as a cellular antioxidant* and an anti-proliferating agent. It consists of both

tocopherols and tocotrienols.


o Some research indicates that tocotrienols are the components of vitamin E responsible for

growth inhibition in human breast cancer cells [260].

• Research is inconsistent on the protective effects of vitamin E and breast cancer. Data from most

prospective studies have not revealed a protective relationship between vitamin E and risk of breast

cancer [250].

• Supplemental vitamin E does not consistently appear to offer protection against breast cancer [150]

although taking vitamin E for more than three years has been associated with a modest protective

effect [259]. Additionally, these researchers reported a decreased risk of recurrence and mortality

associated with long-term use of vitamin E supplements.

• However, low plasma levels of vitamin E have been associated with a greater risk of breast cancer [258].

• It was demonstrated recently that dietary vitamin E, unlike supplemental sources of vitamin E,

significantly reduced oxidative damage as measured by urinary biomarkers [150].

• Note that findings suggest that vitamin E supplements may interfere with the therapeutic effects of

tamoxifen [261].


• Resveratrol is a polyphenol found primarily in red grape skins with known antioxidant and antiinflammatory

properties, and is emerging as a potent chemopreventive and anticancer drug [262].

• Resveratrol has exhibited potential anticarcinogenic activities in several studies.

o Reduced tumor growth, decreased angiogenesis, and induced apoptosis in mice [263].

o Less tumors and longer tumor latency in a rat study [264].

o May inhibit IGF-I mediated cell migration in breast cancer cells [265].

o Induces apoptosis in breast cancer cells [262,263].

o Decreased levels of vascular endothelial growth factor (VEGF) in breast cancer cells [263].

o Inhibited cell growth and regulates IGF-II in breast cancer cells [266].

• Recent evidence indicates that resveratrol and glucans have significant synergistic effects on

immune function [267].

Nutrient/Phytonutrient Summary Recommendation

Selenium Dietary sources include Brazil nuts,

seafood, enriched brewer’s yeast,

and grains.

Selenium content depends

somewhat on the amount of

selenium in the soil in which the

products are grown.

200 mcg selenium daily through

diet and/or supplements

Two Brazil nuts provide 200

mcg selenium.

Turmeric (curcumin) A deep orange-yellow spice

commonly used in curries and

Indian cuisine.

Eat liberally.


Vitamin C Dietary sources include various fruits

and vegetables, including papaya,

citrus fruits, kiwi, cantaloupe,

mango, strawberries, bell peppers,

broccoli, and tomatoes.

Include these fruits and

vegetables daily.

Vitamin E Dietary sources include vegetable

oils, wheat germ, sweet potatoes,

nuts, seeds, and avocados.

Eat vitamin E-rich foods


More research is needed to

assess whether or not

supplements would be


Resveratrol Dietary sources include grapes,

grape products, peanuts, soy,

mulberries, and cranberries.

Eat resveratrol-rich foods


More research is needed

to assess whether or not

supplements would be



• Flax may also work to block tumor growth, inhibit angiogenesis*, and enhance the immune system [268].

• Consumption of 5 or 10 g flax for 7 weeks significantly decreased blood levels of estrone* and

estradiol* [269].

• Flax has been shown to enhance the effects of tamoxifen [270].

• Flaxseed is the greatest source of mammalian lignans* [271,272], phytoestrogens found in flax,

which appear to bind with estrogen and lower circulating levels of estrogen. This action may act as

one of the protective mechanisms of flax for breast cancer.

o Lignans* facilitate the removal of estrogens via increased retention within the gut, which are

later eliminated in the feces [273,274].

• Furthermore, lignans* positively influence estrogen metabolism by improving the ratio of 2:16a

hydroxyestrone [273,274].

• A recent study indicates that flaxseed (25 g daily) and its metabolites, such as lignans*, reduced

tumor growth in patients with breast cancer [271].

• Additionally, a recent pilot study observed lower breast density with a greater intake of dietary

lignans* [275]. Dense breasts are a risk factor for breast cancer.

• Flax has been shown in vitro and in human trials to decrease tumor proliferation of breast cancer

cells [271].

• An animal study reported that flaxseed inhibited established human breast cancer growth and

reduced incidence of metastasis by 45% [272].

• Tumor growth was reduced by 26% and 38%, respectively, when mice consumed a 5% flaxseed

diet and 10% flaxseed diet compared with those who ate no flaxseed [270].

o This effect may be partially due to its downregulation of IGF-I [270,272,276], decreased cell

proliferation [270], and increased apoptosis [270].



• Tea contains phytonutrients* known as polyphenols* (flavonoids) that provide antioxidant* and

anticancer properties [277].

o May block the formation of cancer-causing nitrosamines* [278].

o Prevents DNA damage [279].

o May inhibit tumor growth and induce apoptosis* [280-282].

o Increase immune response [281].

o Epigallocatechin gallate (EGCG) alters gene expresssion to lower the risk of breast cancer


• There is a significant amount of in vitro and in vivo evidence suggesting tea polyphenols* have

chemopreventive agents against various cancers [280,284,285]. More human data is needed.

o Green tea and its catechin* components inhibit breast cancer growth and angiogenesis* in both

in vitro and in vivo studies.

o Studies suggest green tea extract has been successful inhibiting cell proliferation and breast

cancer [277].

• Many studies indicate a lower risk of breast cancer with green tea consumption, but more research

is needed for conclusive evidence [286-289].

• EGCG has been shown in human studies to inhibit human breast cancer cell proliferation, reduce

tumor invasion and metastasis and prevent recurrence of breast cancer in early stage cases (stage I

& II) [290-292].

• A meta-analysis* reported that drinking green tea decreased the risk of breast cancer by 22% when

comparing women with the highest vs lowest intake [286].

• A case-control study* found that green tea consumption was associated with a significant reduction

in risk of breast cancer [289].

o Risk by 13% for women consuming 1-249 g of dried green tea leaves annually.

o Risk by 32% for women consuming 250-499 g of dried green tea leaves annually.

o Risk by 41% for women consuming 500-749 g of dried green tea leaves annually.

o Risk by 39% for women consuming ≥750 g of dried green tea leaves annually.

o Moreover, protection was greater with a longer duration of drinking green tea, a greater number

of cups consumed and the more new batches prepared daily.

• However, combined studies of 35000 Japanese women found that green tea did not affect risk of

breast cancer [293].

• Research suggests that while green tea did significantly decrease tumor mass, when green tea was

combined with soy phytonutrients*, the tumor mass decreased even further [294]. Further evidence

indicates a possible synergistic relationship between soy and green tea consumption [288].

• Similarly, a synergistic effect of green tea and Ganoderma lucidum extracts on the suppression of

growth and invasiveness of metastatic breast cancers was observed [295].

• Additionally, green tea increased the inhibitory effect of tamoxifen on the proliferation of ER + breast

cancer cells [296].

• Furthermore, some evidence suggests that the association of tea catechins* and breast cancer may

depend on specific genotypes [284].



• Associated with reduced rates of heart disease [297-299], protection against osteoporosis

[300,301], and certain types of cancer, including breast cancer [302,303].

• While there has been contention regarding soy and breast cancer, research findings are

predominantly neutral [304], if not protective [6,305,306].

o The majority of short-term soy intervention studies conducted in premenopausal women show

a reduction in endogenous* estrogen levels in association with soy intake, and thus, possibly

protecting from breast cancer.

o The conflicting data on the effects of soy isoflavones and breast tumor growth are based on in

vitro (test tube) studies.

• Recent human research has been more promising.

o A statistically significant inverse association between plasma genistein and breast cancer was

reported among Japanese women [305].

o A recent meta-analysis of well-controlled studies that included high-soy-consuming Asians

reported a significant trend of decreasing risk with increasing soy food intake. Risk was lowest

among those who consumed ≥20 mg isoflavones daily [306].

o High soybean intake in Korean women resulted in a significantly lower risk of breast cancer in

postmenopausal women [6].

• It’s becoming more apparent that the timing of soy exposure is critical. Consumption of soy foods

or an exposure to a soy isoflavone genistein during childhood and adolescence in women, and

before puberty onset in animals, appears to reduce the risk of breast cancer later in life [307].

• The type of soy consumed may provide some insight to the inconsistent findings. It has been

demonstrated that soy processing increases tumor growth in mice for postmenopausal ER+ breast

cancer [308].

o The difference in tumor growth observed may be related to isoflavone metabolism and

bioavailability, but more research is needed [309].

o Nonetheless, these studies suggest that WHOLE SOY FOODS appear to not have a

negative effect on postmenopausal ER+ breast cancer.

o A recent cohort* study of breast cancer patients found that soy foods had no negative impact

on breast cancer survival [310,311].

• An Asian-American study on soy found that women, pre- and postmenopausal, who consumed

tofu, had a 15% reduced risk of breast cancer with each additional serving per week [302].

• Moreover, a recent trial reported that women in the highest tertile intake of tofu had a 51% decrease

risk of premenopausal breast cancer when compared with women in the lowest tertile [303]. No

statistical significant association was observed between soy intake and breast cancer risk among

postmenopausal women.

• Soy consumption has been suggested to exert potential cancer-preventive effects in

premenopausal women, such as increased menstrual cycle length and SHBG* levels and reduced

estrogen levels.

o 40 mg/day soy isoflavones increased menstrual cycle length in Western women [312].

o Research also suggests that soy isoflavones may significantly improve the

2-hydroxyestrone:16-a-hydroxyestrone ratio [313].


o Additionally, soy intake increases time spent in the follicular cycles, when proliferation is at its

lowest [312].

• Furthermore, vegan protein sources, such as soy, appear to decrease circulating IGF-I activity,

which may impede cancer induction [298,314,315].

• Recent literature assessing the effects of soy and tamoxifen have yielded neutral [316] or beneficial

findings [317].

o In a study of Asian American breast cancer survivors on tamoxifen, soy intake had no effect on

levels of tamoxifen or its metabolites [316].

o The combination of tamoxifen and genistein inhibited the growth of ER+/HER2- human breast

cancer cells in a synergistic manner in vitro [317].

Source Amount of Soy

Protein (gm)

Amount of Soy

Isoflavones (mg)

Miso (1 tbsp) 2 7-10*

Soybeans, edamame (1/2 cup) 11 35*

Soymilk (8 fl oz) 10 23*

Soy nuts (1/4 cup) 19 40-50*

Tempeh (1/2 cup) 19.5 36*

Tofu (4 oz) 13 39*

* Isoflavone content varies by brand

Vitamin D

• Epidemiological studies suggest an inverse relationship between sun exposure, serum levels of

25(OH)-vitamin D, and vitamin D intake and the risk of developing and/or surviving cancer [318].

o Possible mechanisms that may explain the protective effects of vitamin D may be its role as

a nuclear transcription factor that regulates cell growth, differentiation, apoptosis and a wide

range of cellular mechanisms central to the development of cancer.

o Furthermore, breast density, a factor that may increase the risk of breast cancer, was inversely

associated with vitamin D intake [319].

• The women in the Nurses’ Health Study observed a 30% reduction in risk of breast cancer

comparing the highest with lowest quintiles of 25(OH)-vitamin D levels. [320].

•Post-menopausal breast cancer risk was significantly inversely associated with serum 25(OH)-

vitamin D levels [321].

o Risk decreased as women’s levels increased from 30 nM (12 ng/ml) to ≥75 nM (30 ng/ml).

•It is now believed that the recommended vitamin D dose should be between 800 and 2,000 IU per


o Research indicates that vitamin D3 (cholecaciferol) is better absorbed than vitamin D2

(ergocalciferol) [322].


Due to the likelihood of a biochemical deficiency without clinical symptoms or signs, a serum

25(OH)-vitamin D level is recommended.

o Optimal serum 25-hydroxy vitamin D levels have not been established though research

suggests 36-40 ng/ml may be ideal [323]. Some believe the normal level of vitamin D should be

50-60 ng/ml.

o While supplementation may be recommended, more appropriate dosing of vitamin D

supplementation can be made once a serum 25(OH)-vitamin D level has been established.

Food or Beverage Summary Recommendation

Flaxseed Good source of omega-3 fatty

acids and fiber, contains protein,

calcium, potassium, B vitamins,

iron, and boron.

Opt for ground flax seeds rather

than whole flax seeds, flax seed

oil, flax supplements to increase


Flax seeds may be ground in a

coffee grinder, blender, or food


2 Tbsp ground flaxseed daily

Flax can have a laxativelike

effect, thus, it is wise

to gradually increase


Sprinkle into various foods

and beverages, including

hot cereals, tomato sauces,

fruit smoothies, brown rice or

other grains.

Store flax in the refrigerator or


Green tea Green tea contains does contain

caffeine though much less than

coffee or black tea.

If opting for decaffeinated green

tea, opt for those naturally

decaffeinated with water as typical

caffeine extraction results in a

significant loss of phytonutrients.

1-4 cups daily

Soy Contains various nutrients, including

protein, fiber, calcium, and B


Rich in antioxidants*, known as

isoflavones, namely genistein and


Among others, dietary sources

include soybeans, edamame, tofu,

soymilk, tempeh, miso, and soy


Unless soy has been a part

of your diet for years,

postmenopausal individuals

with ER+ breast cancer

may be advised to limit soy

consumption to 1-3 daily


Soy supplements or

isoflavone extracts are not


Vitamin D A fat-soluble vitamin that we generate

through skin synthesis of sunlight

(ultraviolet rays).

Dietary sources include cold-water

fish, eggs, and fortified products,

such as milk, soy milk, and cereals.

400-2000 IU daily

Maintain serum 25 (OH)-vitamin

D >35 ng/mL.



• Melatonin is a hormone produced by the pineal gland. Its primary function involves the regulation of

the body’s circadian rhythm, endocrine secretions, and sleep patterns.

• Some research indicates that individuals with low levels of melatonin are at greater risk for breast


• The risk of breast cancer was reduced by 33% in postmenopausal women who slept 9+ hours

compared to those who slept ≤6 hours daily [324].

o Melatonin levels were 42% higher in those who slept 9+ hours vs ≤6 hours daily.

o Previous studies have reported an increased risk of breast cancer in night-shift workers who

are exposed to light at night [325-327].

• It may be that the length of time working night shifts makes a difference as

evidenced by this study where women who reported more than 20 years of rotating

night shift work faced an increased risk of breast cancer compared with women who

did not report any rotating night shift work [326].

o In vitro and animal research has supported the protective effect of melatonin against breast

cancer [328].

o A recent study found that women with higher urinary melatonin levels had a 30-41% reduced

risk of breast cancer [329].

• Melatonin may act by:

o Inhibiting cell proliferation [330,331].

o Inducing apoptosis* [332].

o Enhancing the immune system [330,333].

• May improve survival in cancer patients by protecting the immune system from

damage caused by chemotherapy [332].

o Reducing IGF-I [334,335].

o Decreasing the number and activity of estrogen receptors, thus reducing ways that the cancer

cell connects to estrogen [336].

• Various studies indicate that melatonin may inhibit breast cancer by interfering with estrogen

pathways, thus acting in an anti-estrogenic manner [331,333,337,338].

o Melatonin decreases the formation of estrogen from androgens by inhibiting aromatase activity


• Furthermore, the combination of melatonin and retinoids* [339] as well as the combination of melatonin

and vitamin D3 [340] appear to work synergistically to inhibit the growth of breast cancer cells.

• Melatonin does have blood thinning properties, thus it is recommended to not use supplemental

melatonin 7-10 days prior to surgery.


• Especially important for those with weakened or impaired immune systems and while on



• The following recommendations have been adapted from guidelines provided by the American

Cancer Society.

o Wash foods thoroughly before eating.

o Keep all aspects of food preparation meticulously clean.

o Use special care in handling raw meats, poultry, and eggs.

• Thoroughly clean all utensils, countertops, cutting boards, and sponges that

contacted raw meat.

• Thaw meats and fish in the refrigerator.

o Transfer large volumes of leftovers, such as soup, rice, or casseroles, to shallow containers and

place in refrigerator. This process ensures proper cooling.

o Do not eat perishable foods that have been left out of the refrigerator for more than two hours.

o Store foods at low temperatures (less than 40oF) to minimize bacterial growth.

o When eating in restaurants, avoid foods that may have bacterial contamination, including sushi,

salad bars, buffets, unpasteurized beverages or food products, and raw or undercooked meat,

poultry, fish, and eggs.


• Eat 8 to 10 colorful fruit and vegetable servings daily

o Two to three pieces of fruit

o One cup or more of vegetables with lunch and dinner

o 8 fl oz vegetable juice

• Consume 30 to 45 grams of fiber daily

o You will likely meet your fiber goal if you eat 8 to 10 servings of fruits and vegetables plus one

serving of beans/legumes or at least two servings of whole grains daily.

• Avoid processed and refined grains/flours/sugars

o Keep WHITE off your plate: bread, pasta, rice, cream sauces, cakes, and more.

• Limit meats and whole milk dairy products

• Include healthy fats like cold-water fish, flaxseed, walnuts, soybeans, olive oil, avocados

• Eat 2 Tbsp ground flax daily

• Limit alcohol consumption

• Drink 1 to 4 cups of green tea daily

• Maintain serum 25 (OH)-vitamin D levels above 35 ng/mL

• Drink plenty of fluids, water or non-caffeinated beverages, daily to help meet fluid needs

• Engage in daily physical activity to help achieve and maintain a healthy weight


Bone Health

• Pre- and postmenopausal survivors of breast cancer are at great risk for development of


o Thus, screening and preventive strategies for osteoporosis are imperative.

• Even small amounts of increased bone mass provide great risk reduction for fractures.

• Generally, humans reach peak bone mass around 30 years. After the age of 30, the goal is to

maintain or prevent loss of bone mass.

o On average, humans lose 0.3 – 0.5% bone mass yearly after 30 years.

• First signs of osteoporosis are seen in spine, hip, and wrist.

o Symptoms include back pain or tenderness, loss of height, and slight curving of upper back.

• Risks for osteoporosis include: female, Asian or white ethnicity, age, menopause, amenorrhea, low

testosterone levels in men, sedentary lifestyle, family history, diet low in calcium, diet low in vitamin

D, excessive alcohol and tobacco use, excessive caffeine use, diet high in sodium, diet excessive in

protein or very low in protein, certain medications (diuretics, steroids, thyroid meds), celiac disease

• Many nutrients have bone-building effects, including calcium, vitamin D, phosphorus, magnesium,

vitamin K, potassium, and boron (see table below).

• Exercise increases bone mass before menopause and slows bone loss after menopause.

o Include weight-bearing exercise, such as walking, jogging, skiing, stair climbing, aerobics, and


o Resistance training exercises are useful to strengthen muscles and bones.

• Recent research indicates diets high in fruits and vegetables have a positive effect on bone health.

o Good source of minerals (potassium, magnesium) that may have direct effects on bone cells.

o Counteract acid environment.

o Lower urinary calcium loss.

o Enhanced calcium bioavailability of most vegetables.

• Soy protein and/or soy isoflavones have been proposed to delay bone loss.

o May help to prevent urinary calcium loss.

o Soy contains phytosterols that mimic the actions of estrogen.

o May help to prevent rapid bone loss of menopause years.

o Studies report that soy may BMD.

• Calcium supplements

o Take 500 mg or less per meal to maximize absorption.

o Calcium citrate, lactate, or gluconate are recommended if you have iron deficiency.

• These do not decrease iron absorption like calcium carbonate.

o Calcium carbonate is least expensive, but may increase gas and bloating in some individuals.


• What about antacids with calcium?

o Trace minerals like zinc or iron may be less well-dissolved and absorbed with a lower stomach


o If you’re only taking enough antacid for the purpose of calcium needs, should not present a

major problem, but not ideal.

o May interact with thyroid medication.

• DEXA (dual-energy X-ray absorptiometry) instruments allow rapid, painless, noninvasive, and highly

reproducible measurements of bone density to be made [341].

o These measurements are used to diagnose osteoporosis, low bone density, and risk of fracture

and to determine rates of bone loss or the effectiveness of treatment over time [342,343].

Bone Health – Bottom Line

• Balanced diet – high in fruits and vegetables

• Calcium

o Aim for 3 rich sources daily.

o Include a supplement if necessary.

• Vitamin D

o Meet needs from sun, multivitamin, or other supplement.

o Consider serum vitamin D test.

• Exercise

o Weight-bearing exercise for at least 30 minutes on most days.

• Good posture

• Request to have a full body DEXA scan.


Bone Building Nutrients

Nutrient* Dietary Sources Function Recommendation

Calcium Dairy products, canned

fish with soft bones,

beans, leafy greens

(especially collard

greens, bok choy, and

kale), tofu, almonds,

fortified products, such

as soy milk, cereal, and

orange juice

calcium absorption

and bioavailability from

foods, especially plant


Vitamin D is essential for

calcium absorption.

1000-1200 mg


Vitamin K Dark leafy greens, liver,

tomatoes, soybeans,

and garbanzo beans

Also produced by

intestinal bacteria

Associated with bone

turnover and urinary

calcium excretion.

90 mcg daily

Phosphorus Meat, poultry, fish, eggs,

milk, products, legumes,

and nuts

Combines with calcium to

strengthen bones.

700 mg daily

Magnesium Whole grains, nuts, seeds,

spinach, and most fruits

and vegetables

Important in calcium and

potassium uptake.

320 mg daily

Potassium Bananas, strawberries,

tomatoes, prunes,

potatoes, spinach, and


Associated with

urinary calcium and

phosphorus excretion.

4700 mg daily

Boron Apples, avocados, beans,

milk, peanuts, peanut

butter, pecans, raisins,

prunes, and potatoes

Improves calcium


effects of vitamin D and

magnesium deficiency.

2 mg daily

Zinc Seafood, meats, tofu,

whole grains, blackeyed

peas, wheat bran

and germ

Important in calcium

uptake and immune


8-15 mg daily

* Vitamin D is listed in the previous table


Hot Flashes

• Hot flashes are a major cause of morbidity among postmenopausal women, including many

survivors of breast cancer.

• Approximately 75% of postmenopausal women who had breast cancer report experiencing hot

flashes [344].

o More than 90% of young survivors also experience hot flashes, which can be more severe and

long lasting, with iatrogenic ovarian ablation or antiestrogen therapy.

• Various non-hormonal therapies have been studied for improving hot flashes, including soy, black

cohosh, red clover, and vitamin E – none have shown much significant clinical value.

• Supplemental vitamin E at 400 IU/day [345] and 800 IU/day [346] has shown some limited efficacy

in improving hot flashes.

• Systematic reviews of randomized controlled trials have observed contradictory results, and

meta-analyses* demonstrate no statistically significant reduction of vasomotor symptoms for

phytoestrogens [347].

o Individual trials report significant reductions in vasomotor symptoms for red clover and soy


o The placebo effect in many of these studies was quite strong [348].

o Studies assessing black cohosh and red clover have had inconsistent results, with some trials

showing benefit and some no difference compared with placebo [349].

o In one study, women receiving black cohosh reported a mean decrease in hot flash score of

20% compared with a 27% decrease for patients on placebo [350].

• Mean hot flash frequency was reduced 17% on black cohosh and 26% on placebo.

o A previous study reported reduced hot flashes with soy isoflavones by 9 to 40% in some trials,

but most trials observed no effect when compared with placebo [349].

• Black cohosh extract had no effect on serum estrogenic markers [351].

• The use of black cohosh appears to be safe in breast cancer patients [352].

• Psychoeducational interventions, including relaxation, seem to alleviate hot flashes in menopausal

women and breast cancer survivors; however, the methodological quality of published research has

been considered to be fair or poor [353].


“Let food be your medicine and medicine be your food.”

– Hippocrates

For additional information or resources, please visit the Ida and Joseph Friend Cancer Resource

Center at 1600 Divisadero St. on the first floor, or call at (415) 885-3693. The information in this

publication is designed for educational purposes only and is not intended to replace the advice of

your physician or health care provider, as each patient’s circumstances are individual. We encourage

you to discuss with your physician any questions and concerns that you may have.


Three Day Menu Plan: 3 Meals + Snack

This menu is based on 1600 calories, calories can be adjusted by altering portion sizes. The menu

has been designed to merely serve as a guide in making healthy food choices. Experiment with

substitutions as desired.

Day 1 Day 2 Day 3

Oatmeal, cooked (1 cup)

Soy milk (1 cup)

Flaxseed, ground (2 tbsp)

Blueberries (1/2 cup)

Green tea (2 cups)

Bagel, whole grain (1 med)

Hummus (2 tbsp)

Tomato (6 slices)

Lemon pepper

Cantaloupe (1 cup)

Green tea (2 cups)

Tofu scramble

Tofu (4 oz)

Onions (1/4 cup)

Peppers (1/2 cup)

Mushrooms (1/2 cup)

Toast, whole grain (1 slice)

Jam (1 tbsp)

Turkey sandwich

Whole grain bread (2 slices)

Turkey (2 oz)

Lettuce (1/2 cup)

Tomato (4 slices)

Red peppers (1/4 cup)

Onions (2 tbsp)

Mustard (1 tsp)

Carrots (1/2 cup)

Snap peas (1/2 cup)

Vegetable Bean Soup (2 cups)

Corn tortilla (1 med)

Green salad (2 cups)

Oil/vinegar dressing (1 tbsp)


Spinach (3 cups)

Broccoli (1/2 cup)

Carrots (1/2 cup)

Tomato (1/2 cup)

Garbanzo beans (1 cup)

Barley, cooked (1/2 cup)

Avocado (4 slices)

Olive oil (1/2 tbsp)

Vinegar, balsamic (1 1/2 tbsp)

Roll, whole grain (1 med)

Orange (1 med)

Vegetable juice (12 oz)

Granola bar (1 each)

Fruit smoothie

Banana (1 med)

Berries (1 cup)

Flaxseed, ground (2 tbsp)

Yogurt, plain nonfat (1/2 cup)

Soy milk (1 cup)

Green tea (2 cups)

Popcorn, air-popped (3 cups)

Fish (3 oz)

Pasta, whole grain (1 1/2 cups)

Tomato sauce (1 cup)

Mushrooms (1/2 cup)

Olive oil (1/2 tbsp)

Broccoli (1 cup)

Mixed fruit (1 cup)

Chicken & vegetable stir-fry

Chicken breast (4 oz)

Mixed vegetables (2 cups)

Walnuts (2 tbsp) OR

Olive oil (1/2 tbsp)

Brown rice, cooked (1 cup)

Salmon (4 oz)

Quinoa, cooked (1 cup)

Asparagus (1 cup)

Fruit salad (1 cup)



Baked Tofu


• 1 pound tofu, firm, drained

• 3-4 tbsp marinade or sauce (personal favorite: Veri Veri Teriyaki by Soy Vay)

Chop drained firm tofu into 1” cubes. Place tofu cubes in glass dish for baking. Pour marinade or

sauce over tofu, stir well. Place tofu in oven at 350 F for 1 hour. Stir every 15-20 minutes.

Makes four 4-ounce servings.

Nutrition Information (per 4 oz serving):

Calories: 96 Dietary fiber: <1 gm

Protein: 8 gm Sodium: 318 mg

Fat: 5 gm Calcium: 155 mg

Saturated fat: <1 gm Iron: 1.4 mg

Recipe developed by Natalie Ledesma, MS, RD, CSO

Washington Insider Salad


• 1 can (15 oz) kidney beans, drained

• 1 can (15 oz) black eyed peas, drained

• 1 1/2 cups cooked barley

• 6 tbsp cilantro, chopped finely

• 1 can (11 oz) corn

• 1 1/2 cups tomatoes, diced

• 3 tbsp balsamic vinegar

• 2 tbsp olive oil

Prepare vegetables. Mix all ingredients together, and serve on a bed of dark green leafy lettuce. Add

salt and pepper to taste.

Makes 8 servings (1 cup each).

Nutrition Information (per serving):

Calories: 215

Protein: 10 gm

Fat: 4 gm

Dietary fiber: 9 gm

Recipe developed by Sous Chef Chris at the Occidental Grill, Washington D.C.

Spinach Spread


• 1 package (10.5 ounces) silken tofu

• 1 tbsp lemon juice


• 1/4 tsp garlic powder

• 3/4 tsp onion powder

• 1/2 tsp dried tarragon

• 1/4 tsp salt

• 1 box (10 ounce) frozen chopped spinach, thawed

• 1 cup coarsely shredded carrots

• 1/4 cup chopped green onion

Puree the tofu and lemon juice in blender until smooth. Whirl in the garlic and onion powders,

tarragon, and salt just to blend. Scrape into a mixing bowl. Squeeze the spinach as dry as possible.

Stir it into the tofu, along with the carrots and green onion. Mix well. Serve with crackers, pita

triangles, or vegetables.

Makes 8 servings (1/4 cup each).

Nutrition information (per serving):

Calories: 39 Sodium: 82 mg

Fat: 1 gm Calcium: 51 mg

Saturated fat: 0 gm Carbohydrate: 5 gm

Protein: 4 gm Dietary Fiber: 2 gm

Recipe from the U.S. Soyfoods Directory, 1998.

Tofuntastico – Tofu Sauce


• 1 package (12.3 ounce) silken tofu

• 1/2 cup water

• 3/4 cup fresh basil, chopped

• 4 tbsp nutritional yeast

• 3 tbsp Bragg’s liquid aminos (or tamari or soy sauce)

•1 tbsp lemon juice

•1 tsp garlic, minced

•3/4 tsp black pepper

•Alternative: Use lime/cilantro rather than lemon/basil

Blend all ingredients together in a blender or food processor. Serve over pasta, vegetables, baked

potato, or other.

Makes 6 servings (1/2 cup each).

Nutrition Information (per serving):

Calories: 47 Carbohydrate: 4 gm

Protein: 7 gm Dietary fiber: 2 gm

Fat: <1 gm

Recipe developed by Natalie Ledesma, MS, RD, CSO


Alaska Salmon Bake with Walnut Crunch Coating


• 1 pound salmon fillets, thawed if necessary

• 2 tbsp Dijon-style mustard

• 1-2 tbsp olive oil

• 4 tsp honey

• 1/4 cup bread crumbs

• 1/4 cup walnuts, finely chopped

• 2 tsp parsley, chopped

• Salt and pepper to taste

• Lemon wedges

Mix together mustard, olive oil, and honey in a small bowl; set aside. Mix together bread crumbs,

walnuts, and parsley in a small bowl; set aside. Season each salmon fillet with salt and pepper. Place

on a lightly greased baking sheet or broiling pan. Brush each fillet with mustard-honey mixture. Pat

top of each fillet with bread crumb mixture. Bake at 450 F for 10 minutes per inch of thickness or until

salmon just flakes when tested with a fork. Serve with lemon wedges.

Makes 4 servings (4 oz each).

Nutrition Information (per serving):

Calories: 228

Protein: 20 gm

Fat: 12 gm

Omega-3 fatty acids: 1.7 gm

Adapted from Alaska Seafood Marketing Institute.

Banana Bread


• 3/4 cup ground flax seed

• 1 cup mashed banana

• 1/4 cup apple juice concentrate

• 1/2 cup brown sugar

• 1/4 cup applesauce

• Egg replacer for 2 eggs or 2 eggs (Ener-G Egg Replacer is made from potato starch & tapioca

flour; works wonderfully in baked goods.)

• 1 1/2 cup whole wheat pastry flour

• 1 tsp baking soda

• 1/2 tsp salt

• Additional optional ingredients may include 1/2 cup walnuts, raisins, or chocolate chips.

Mix all ingredients together. Pour in a coated 8”x4” pan. Bake at 350 F for about 40-45 minutes.

Makes 10 servings.

Nutrition Information (per serving):


Calories: 168 Carbohydrate: 29 gm

Protein: 5 gm Dietary fiber: 5 gm

Fat: 4 gm Omega-3 fatty acids: 1.4 gm

Recipe developed by Natalie Ledesma, MS, RD, CSO

Dilled Salmon Salad with Peas


• 1 can (15 oz) salmon, drained

• 1 package (16 oz) frozen peas, thawed

• 1/4 cup lemon juice

• 1/4 cup fresh dill (or 1-2 tbsp dried dill)

• 2 tbsp Dijon-style mustard

• 2 shallots, sliced thinly (about 1/2 cup)

• 1 bunch radishes (about 11 medium), thinly sliced

• 6 cups red leaf lettuce

• Salt and pepper to taste

Drain salmon, place in a mixing bowl, and break into pieces. Prepare the lemon juice, shallots,

radishes, and lettuce. Add to the salmon the peas, lemon juice, dill, mustard, shallots, and radishes.

Mix together gently. Add salt and pepper to taste. Serve salmon mixture over lettuce.

Makes 6 servings (2 cups each).

Nutrition Information (per serving):

Calories: 160

Protein: 17 gm

Fat: 4 gm

Dietary fiber: 5 gm

Adapted from the Women’s Healthy Eating & Living Study (WHEL) at the University of California,

San Diego. Developed by Vicky Newman, MS, RD, WHEL nutrition coordinator.

Neat Loaf


• 2 cups cooked brown rice

• 1 cup walnuts, finely chopped

• 1 onion, finely chopped

• 1/2 medium bell pepper, finely chopped

• 2 medium carrots, shredded or finely chopped

• 1 cup wheat germ

• 1 cup quick-cooking rolled oats

• 1/2 tsp each: thyme, marjoram, sage


• 2 tbsp soy sauce

• 2 tbsp stone ground or Dijon mustard

• Barbecue sauce or ketchup

Preheat the oven to 350 F. Combine all the ingredients except the barbecue sauce or ketchup. Mix for

2 minutes with a large spoon. This will help bind it together. Pat into an oil-sprayed 5×9” load pan and

top with barbecue sauce or ketchup. Bake for 60 minutes. Let stand 10 minutes before serving.

Makes 8-10 servings.

Nutrition Information (per serving):

Calories: 204 Sodium: 248 mg

Protein: 9 gm Cholesterol: 0 mg

Fat: 9 gm

Carbohydrate: 19 gm

Recipe from The Peaceful Palate written by Jennifer Raymond (1996).

Chinese Cabbage and Radish Salad


• 4 cups Chinese cabbage, quartered and then thinly sliced

• 1/4 cup radishes

• 1/4 cup red onion, thinly sliced

• 2 tbsp white miso

• 2 tbsp brown rice vinegar

• 1 tsp maple syrup

• 1 tsp dill, dried

• 2 tbsp sunflower seeds, toasted

With a fork, mix the miso, vinegar, maple syrup, and dill. Mix the vegetables and press with a plate until

submerged in liquid for about 1 hour. Fluff the vegetables to serve and garnish with sunflower seeds.

Makes 4 servings.

Nutrition Information (per serving):

Calories: 64 Carbohydrate: 9 gm

Protein: 2 gm Cholesterol: 0 mg

Fat: 2 gm Sodium: 275 mg

Source anonymous.

Quinoa/Sweet Potato Patties


• 1 1/2 cups sweet potato, peeled and chopped

• 1 cup quinoa

• 2 tbsp parsley, fresh

• 1/2 tsp sea salt


• 2 tsp extra-virgin olive oil

Steam or bake sweet potatoes until done. Drain and mash potatoes. Wash the quinoa well and drain.

Dry toast the quinoa in a skillet until slightly browned. Meanwhile, bring a pot of water to a boil. Add

the toasted quinoa to the boiling water and cook, with lid off, for ~15 minutes. Drain well. Mix the

mashed potatoes and quinoa. Add the parsley and salt. Form 8 patties and place in a lightly oiled pan

over medium-high heat. Cook for about 5 minutes on each side and serve warm.

Makes 8 servings.

Nutrition Information (per serving):

Calories: 125 Sodium: 165 mg

Protein: 4 gm Cholesterol: 0 mg

Fat: 2 gm

Carbohydrate: 22 gm

Recipe adapted from the Vegetarian Resource Group (1997).

Nutrition Resources


How to Prevent & Treat Cancer with Natural Medicine – written by Michael Murray (2002)

The Color Code – written by James Joseph, Daniel Nadeau, & Anne Underwood (2002)

Ultra Metabolism – written by Mark Hyman (2006)


Cancer Lifeline Cookbook – written by Kimberly Mathai & Ginny Smith (2004)

Fat-Free and Easy: Great Meals in Minutes – written by Jennifer Raymond (vegetarian cookbook) (1997)

Lickety-Split Meals – written by Zonya Foco (1998)

One Bite at a Time – written by Rebecca Katz, Marsha Tomassi, & Mat Edelson (2004)

The Peaceful Palate – written by Jennifer Raymond (vegetarian cookbook) (1996)

12 Best Foods Cookbook: Over 200 Recipes Featuring the 12 Healthiest Foods – written by Dana

Jacobi (2005)


Cooking Light Fax: (205) 445-6600

Environmental Nutrition (800) 829-5384

Nutrition Action Health Letter Fax: (202) 265-4954


American Cancer Society (415) 394-7100

American Institute for Cancer Research (800) 843-8114


Caring4Cancer – Provides up-to-date & comprehensive information on the connection between

nutrition & cancer –

Center for Informed Food Choices – Offer cooking classes in the Bay Area that emphasize plantbased


Consumer Lab – Evaluates quality of over-the-counter supplements

Diana Dyer, MS, RD – Breast cancer survivor & dietitian

Ida & Joseph Friend Cancer Resource Center – UCSF Mt.Zion

(415) 885-3693

National Cancer Institute (800) 4-CANCER (800-422-6237)

Oncolink – Provides information regarding clinical trials, newsgroups, psychosocial support, & more.

San Francisco Vegetarian Society – Monthly restaurant outings & pot-luck dinners; call 415-273-5481.


The Vegetarian Resource Group – Provides vegetarian nutrition information & vegetarian recipes




Angiogenesis – The formation of new blood vessels.

Antioxidant – A substance that inhibits oxidation or inhibits reactions promoted by oxygen or peroxides.

Apoptosis – Programmed cell death.

Carcinogenesis – Beginning of cancer development.

Case-Control Studies – An epidemiological study in which a group of, say, cancer patients (cases)

is compared to a similar but cancer-free population (controls) to help establish whether the past or

recent history of a specific exposure such as smoking, alcohol consumption and dietary intake, etc.

are causally related the risk of disease.

Catechin – One of the tannic acids; phytonutrient, specifically, one of the flavonoids found in green tea.

Creatine – An amino acid that is formed in the muscle tissue of vertebrates; supplies energy for

muscle contraction.

Cohort Studies – Follow-up study of a (usually large) group of people, initially disease-free.

Differences in disease incidence within the cohort are calculated in relation to different levels of

exposure to specific factors, such as smoking, alcohol consumption, diet and exercise, that were

measured at the start of the study and, sometimes, at later times during the study.

Eicosanoids – Biologically active compounds that regulate blood pressure, blood clotting, and other

body functions. They include prostaglandins, thromboxanes, and leukotrienes.

Endogenous – Originating from within, as within the body.

Estradiol – A naturally occurring powerful estrogen secreted by the mammalian ovary.

Estrone – A naturally occurring weak estrogen secreted by the mammalian ovary.

Glutathione – A polypeptide produced primarily in the liver; involved in DNA synthesis and repair,

protein and prostaglandin synthesis, amino acid transport, metabolism of toxins and carcinogens,

immune system function, prevention of oxidative cell damage, and enzyme activation.

Insulin – Insulin is a hormone produced by the pancreas in the body that regulates the metabolism of

carbohydrates and fats, especially the conversion of glucose to glycogen, which lowers the body’s

blood sugar level.

Lignans – Phytoestrogens that have a similar chemical structure to estradiol and tamoxifen; appear

to offer protection against breast cancer.

Meta-analysis – The process of using statistical methods to combine the results of different studies.

Mutation – Abnormal cell development.

Nitrosamines – Derivatives of nitrites that may be formed in the stomach when nitrites combine with

amines; carcinogenic in animals.

Phytonutrients – Plant compounds that appear to have health-protecting properties.

Polyphenols – Phytonutrients that act as an antioxidant; compounds that protects the cells and body

chemicals against damage caused by free radicals, reactive atoms that contribute to tissue damage

in the body.

Retinoids – Chemically related compounds with biological activity similar to that of retinol; related to

vitamin A.

Sex hormone-binding globulin (SHBG) – A protein in the blood that acts as a carrier for androgens

and estradiol; inhibits the estradiol-induced proliferation of breast cancer cells.



1. Byers T, Nestle M, McTiernan A, Doyle C, Currie-Williams A, Gansler T, et al. American Cancer Society 2001 Nutrition and

Physical Activity Guidelines Advisory Committee. American Cancer Society guidelines on nutrition and physical activity

for cancer prevention: Reducing the risk of cancer with healthy food choices and physical activity. CA: Ca J Clin. 2002;


2. Gaudet MM, Britton JA, Kabat GC, Steck-Scott S, Eng SM, Teitelbaum SL, et al. Fruits, vegetables, and micronutrients

in relation to breast cancer modified by menopause and hormone receptor status. Cancer Epidemiol Biomarkers Prev.


3. World Cancer Research Fund. Food, nutrition, physical activity, and the prevention of cancer: a global perspective.

Washington, DC: American Institute for Cancer Research, 2007.

4. Riboli E, Norat T. Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk. Am J Clin Nutr.

2003;78(3 Suppl):559S-569S.

5. Hirose K, Matsuo K, Iwata H, Tajima K. Dietary patterns and the risk of breast cancer in Japanese women. Cancer Sci.


6. Do MH, Lee SS, Kim JY, Jung PJ, Lee MH. Fruits, vegetables, soy foods and breast cancer in pre- and postmenopausal

Korean women: a case-control study. Int J Vitam Nutr Res. 2007;77(2):130-141.

7. Zhang S, Hunter DJ, Forman MR, Rosner BA, Speizer FE, Colditz GA, et al. Dietary carotenoids and vitamins A, C, and E and

risk of breast cancer. J Natl Cancer Inst. 1999;91(6):547-556.

8. Freudenheim JL, Marshall JR, Vena JE, Laughlin, R, Brasure JR, Swanson MK, et al. Premenopausal breast cancer risk and

intake of vegetables, fruits, and related nutrients. J Natl Cancer Inst. 1996;88(6):340-348.

9. La Vecchia C, Altieri A, Tavani A. Vegetables, fruit, antioxidants and cancer: a review of Italian studies. Eur J Nutr.


10. Sant M, Allemani C, Sieri S, Krogh V, Menard S, Tagliabue E, et al. Salad vegetables dietary pattern protects against HER-2-

positive breast cancer: a prospective Italian study. Int J Cancer. 2007;121(4):911-914.

11. Pierce JP, Stefanick ML, Flatt SW, Natarajan L, Sternfeld B, Madlensky L, et al. Greater survival after breast cancer in

physically active women with high vegetable-fruit intake regardless of obesity. J Clin Oncol. 2007;25(17):2345-2351.

12. de Lima FE, do Rosário Dias de Oliveira Latorre M, de Carvalho Costa MJ, Fisberg RM. Diet and cancer in Northeast

Brazil: evaluation of eating habits and food group consumption in relation to breast cancer. Cad Saude Publica.


13. Gandini S, Merzenich H, Robertson C, Boyle P. Meta-analysis of studies on breast cancer risk and diet: the role of fruit and

vegetable consumption and the intake of associated micronutrients. Eur. J. Cancer 2000;36:636-646.

14. Smith-Warner SA, Spiegelman D, Yaun SS, Adami HO, Beeson WL, van den Brandt PA, et al. Intake of fruits and vegetables

and risk of breast cancer: a pooled analysis of cohort studies. JAMA 2001;285:769-776.

15. Shannon J, Ray R, Wu C, Nelson Z, Gao DL, Li W, et al. Food and botanical groupings and risk of breast cancer: a casecontrol

study in shanghai, china. Cancer Epidemiol Biomarkers Prev. 2005;14(1):81-90.

16. Lissowska J, Gaudet MM, Brinton LA, Peplonska B, Sherman M, Szeszenia-Dabrowska N, et al. Intake of fruits, and

vegetables in relation to breast cancer risk by hormone receptor status. Breast Cancer Res Treat. 2008;107(1):113-117.

17. Rock CL, Flatt SW, Natarajan L, Thomson CA, Bardwell WA, Newman VA, et al. Plasma carotenoids and recurrence-free

survival in women with a history of breast cancer. J Clin Oncol. 2005;23:6631-6638.

18. Pierce JP, Natarajan L, Caan BJ, Parker BA, Greenberg ER, Flatt SW, et al. Influence of a diet very high in vegetables, fruit,

and fiber and low in fat on prognosis following treatment for breast cancer: the Women’s Healthy Eating and Living (WHEL)

randomized trial. JAMA. 2007;298(3):289-298.

19. McEligot AJ, Largent J, Ziogas A, Peel D, Anton-Culver H. Dietary fat, fiber, vegetable, and micronutrients are associated

with overall survival in postmenopausal women diagnosed with breast cancer. Nutr Cancer. 2006;55(2):132-140.

20. Norat T, Dossus L, Rinaldi S, Overvad K, Grøbaek H, Tjøneland A, et al. Diet, serum insulin-like growth factor-I and IGFbinding

protein-3 in European women. Eur J Clin Nutr. 2007;61(1):91-98.

21. Ito Y, Gajalakshmi KC, Sasaki R, Suzuki K, Shanta V. A study on serum carotenoid levels in breast cancer patients of Indian

women in Chennai (Madras), India. J Epidemiol. 1999;9(5):306-314.

22. Tibaduiza EC, Fleet JC, Russell RM, Krinsky NI. Excentric cleavage products of beta-carotene inhibit estrogen receptor

positive and negative breast tumor cell growth in vitro and inhibit activator protein-1-mediated transcriptional activation. J

Nutr. 2002;132(6):1368-1375.


23. Huang JP, Zhang M, Holman CD, Xie X. Dietary carotenoids and risk of breast cancer in Chinese women. Asia Pac J Clin

Nutr. 2007;16 Suppl 1:437-442.

24. Cui Y, Shikany JM, Liu S, Shagufta Y, Rohan TE. Selected antioxidants and risk of hormone receptor-defined invasive

breast cancers among postmenopausal women in the Women’s Health Initiative Observational Study. Am J Clin Nutr.


25. Nkondjock A, Ghardirian P. Intake of specific carotenoids and essential fatty acids and breast cancer risk in Montreal,

Canada. Am J Clin Nutr. 2004;79(5):857-864.

26. Kim MK, Park TG, Gong G, Ahn SH. Breast cancer, serum antioxidant vitamins, and p53 protein overexpression. Nutr

Cancer 2002;43(2):159-166.

27. Sato R, Helzlsouer KJ, Alberg AJ, Hoffman SC, Norkus EP, Comstock GW. Prospective study of carotenoids, tocopherols,

and retinoid concentrations and the risk of breast cancer. Cancer Epidemiol Biomarkers Prev. 2002;11(5):451-457.

28. Ching S, Ingram D, Hahnel R, Beilby J, Rossi E. Serum levels of micronutrients, antioxidants and total antioxidant status

predict risk of breast cancer in a case control study. J Nutr. 2002;132(2):303-306.

29. Toniolo P, Van Kappel AL, Akhemedkhanov A, Ferrari P, Kato I, Shore RE, et al. Serum carotenoids and breast cancer. Am J

Epidemiol. 2001;153(12):1142-1147.

30. Li Z, Wang Y, Mo B. [The effects of carotenoids on the proliferation of human breast cancer cell and gene expression of

bcl-2][Article in Chinese] Zhonghua Yu Fang Yi Xue Za Zhi 2002;36(4):254-257.

31. Prakash P, Russell RM, Krinsky NI. In vitro inhibition of proliferation of estrogen-dependent and estrogen-independent

human breast cancer cells treated with carotenoids or retinoids. J Nutr. 2001;131(5):1574-1580.

32. Li Z, Hu CY, Mo BQ, Xu JD, Zhao Y. Effect of beta-carotene on gene expression of breast cancer cells] [Article in Chinese]

Ai Zheng 2003;22(4):380-384.

33. Negri E, La Vecchia C, Franceschi S, D’Avanzo B, Talamini R, Parpinel M, et al. Intake of selected micronutrients and the

risk of breast cancer. Int J Cancer 1996;65(2):140-144.

34. Schuurman AG, Goldbohm RA, Brants HA, van den Brandt PA. A prospective cohort study on intake of retinol, vitamins C

and E, and carotenoids and prostate cancer risk (Netherlands). Cancer Causes Control 2002;13(6):573-582.

35. Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, et al. Lack of effect of long-term supplementation with

beta carotene on the incidence of malignant neoplasms and cardiovascular disease. New Engl J Med. 1996;334(18):1145-1149.

36. Ambrosone CB, McCann SE, Freudenheim JL, Marshall JR, Zhang Y, Shields PG. Breast cancer risk in premenopausal

women is inversely associated with consumption of broccoli, a source of isothiocyanates, but is not modified by GST

genotype. J Nutr. 2004;134(5):1134-1138.

37. Terry P, Wolk A, Persson I, Magnusson C. Brassica vegetables and breast cancer risk. JAMA. 2001;285(23):2975-2977.

38. Brandi G, Schiavano GF, Zaffaroni N, De Marco C, Paiardini M, Cervasi B, et al. Mechanisms of action and antiproliferative

properties of Brassica oleracea juice in human breast cancer cell lines. J Nutr. 2005;135(6):1503-1509.

39. [No authors noted] Change in Diet at Any Age May Help Protect Against Breast Cancer (Abstract #3697. American

Association for Cancer Research’s 4th annual Frontiers in Cancer Prevention Research meeting. Nov 2005.

40. Lee SA, Fowke JH, Lu W, Ye C, Zheng Y, Cai Q, et al. Cruciferous vegetables, the GSTP1 Ile105Val genetic polymorphism,

and breast cancer risk. Am J Clin Nutr. 2008;87(3):753-760.

41. Bradlow HL, Sepkovic DW, Telang NT, Osborne MP. Multifunctional aspects of the action of indole-3-carbinol as an

antitumor agent. Ann N Y Acad Sci. 1999;889:204-213.

42. Fowke JH, Longcope C, Hebert JR. Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal

women. Cancer Epidemiol Biomarkers Prev. 2000;9(8):773-779.

43. Jackson SJ, Singletary KW. Sulforaphane: a naturally occurring mammary carcinoma mitotic inhibitor, which disrupts tubulin

polymerization. Carcinogenesis. 2004;25(2):219-227.

44. Tseng E, Scott-Ramsay EA, Morris ME. Dietary Organic Isothiocyanates Are Cytotoxic in Human Breast Cancer MCF-7 and

Mammary Epithelial MCF-12A Cell Lines. Exp Biol Med (Maywood). 2004;229(8):835-842.

45. Jo EH, Kim SH, Ahn NS, Park JS, Hwang JW, Lee YS, et al. Efficacy of sulforaphane is mediated by p38 MAP kinase

and caspase-7 activations in ER-positive and COX-2-expressed human breast cancer cells. Eur J Cancer Prev.


46. Pledgie-Tracy A, Sobolewski MD, Davidson NE. Sulforaphane induces cell type-specific apoptosis in human breast cancer

cell lines. Mol Cancer Ther. 2007;6(3):1013-1021.

47. Chatterji U, Riby JE, Taniguchi T, Bjeldanes EL, Bjeldanes LF, Firestone GL. Indole-3-carbinol stimulates transcription of the

interferon gamma receptor 1 gene and augments interferon responsiveness in human breast cancer cells. Carcinogenesis



48. Wu HT, Lin SH, Chen YH. Inhibition of Cell Proliferation and in Vitro Markers of Angiogenesis by Indole-3-carbinol, a Major

Indole Metabolite Present in Cruciferous Vegetables. J Agric Food Chem. 2005;53(13):5164-5169.

49. Ge X, Fares FA, Yannai S. Induction of apoptosis in MCF-7 cells by indol-3-carbinol is independent of p53 and bax.

Anticancer Res. 1999;19(4B):3199-3203.

50. Telang NT, Katdare M, Bradlow HL, Osborne MP, Fishman J. Inhibition of proliferation and modulation of estradiol

metabolism: novel mechanisms for breast cancer prevention by the phytochemical indole-3-carbinol. Proc Soc Exp Biol

Med. 1997;216(2):246-252.

51. Cover CM, Hsieh SJ, Cram EJ, Hong C, Riby JE, Bjeldanes LF, et al. Indole-3-carbinol and tamoxifen cooperate to arrest the

cell cycle of MCF-7 human breast cancer cells. Cancer Res. 1999;59(6):1244-1251.

52. Brignall MS. Prevention and treatment of cancer with indole-3-carbinol. Altern Med Rev. 2001;6(6):580-589.

53. [No authors listed] Calcium-D-glucarate. Altern Med Rev. 2002;7(4):336-339.

54. Lombardi-Boccia G, Lucarini M, Lanzi S, Aguzzi A, Cappelloni M. Nutrients and antioxidant molecules in yellow

plums (Prunus domestica L.) from conventional and organic productions: a comparative study. J Agric Food Chem.


55. Grinder-Pedersen L, Rasmussen SE, Bugel S, Jorgensen LV, Dragsted LO, et al. Effect of diets based on foods from

conventional versus organic production on intake and excretion of flavonoids and markers of antioxidative defense in

humans. J Agric Food Chem. 2003;51(19):5671-5676.

56. Asami DK, Hong YJ, Barrett DM, Mitchell AE. Comparison of the total phenolic and ascorbic acid content of freeze-dried

and air-dried marionberry, strawberry, and corn grown using conventional, organic, and sustainable agricultural practices. J

Agric Food Chem. 2003;51(5):1237-1241.

57. Baxter GJ, Graham AB, Lawrence JR, Wiles D, Paterson JR. Salicylic acid in soups prepared from organically and nonorganically

grown vegetables. Eur J Nutr. 2001;40(6):289-292.

58. Ferreres F, Valentao P, Llorach R, Pinheiro C, Cardoso L, Pereira JA, et al. Phenolic compounds in external leaves of

tronchuda cabbage (Brassica oleracea L. var. costata DC). J Agric Food Chem. 2005;53(8):2901-2907.

60. Li JY, Li H, Tao P, Lei FM. [Serum organochlorines pesticides level of non-occupational exposure women and risk of breast

cancer:a case-control study]. [Article in Chinese] Wei Sheng Yan Jiu. 2006;35(4):391-394.

61. Wong PS, Matsumura F. Promotion of breast cancer by beta-hexachlorocyclohexane in MCF10AT1 cells and MMTV-neu

mice. BMC Cancer. 2007;7:130.

62. Khanjani N, Hoving JL, Forbes AB, Sim MR. Systematic review and meta-analysis of cyclodiene insecticides and breast

cancer. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2007;25(1):23-52.

63. Teitelbaum SL, Gammon MD, Britton JA, Neugut AI, Levin B, Stellman SD. Reported residential pesticide use and breast

cancer risk on Long Island, New York. Am J Epidemiol. 2007;165(6):643-651.

64. Muñoz-de-Toro M, Durando M, Beldoménico PM, Beldoménico HR, Kass L, García SR, et al. Estrogenic microenvironment

generated by organochlorine residues in adipose mammary tissue modulates biomarker expression in ERalpha-positive

breast carcinomas. Breast Cancer Res. 2006;8(4):R47.

65. van Elswijk DA, Schobel UP, Lansky EP, Irth H, van der Greef J. Rapid dereplication of estrogenic compounds in

pomegranate (Punica granatum) using on-line biochemical detection coupled to mass spectrometry. Phytochemistry


66. Toi M, Bando H, Ramachandran C, Melnick SJ, Imai A, Fife RS, et al. Preliminary studies on the anti-angiogenic potential of

pomegranate fractions in vitro and in vivo. Angiogenesis 2003;6(2):121-128.

67. Kim ND, Mehta R, Yu W, Neeman I, Livney T, Amichay A, et al. Chemopreventive and adjuvant therapeutic potential of

pomegranate (Punica granatum) for human breast cancer. Breast Cancer Res Treat. 2002;71(3):203-217.

68. Mehta R, Lansky EP. Breast cancer chemopreventive properties of pomegranate (Punica granatum) fruit extracts in a mouse

mammary organ culture. Eur J Cancer Prev. 2004;13(4):345-348.

69. Harris PJ, Roberton AM, Watson ME, Triggs CM, Ferguson LR. The effects of soluble-fiber polysaccharides on the

adsorption of a hydrophobic carcinogen to an insoluble dietary fiber. Nutr Cancer 1993;19(1):43-54.

70. Slavin JL. Mechanisms for the impact of whole grain foods on cancer risk. J Am Coll Nutr. 2000;19(3 Suppl):300S-307S.

71. Slavin J. Why whole grains are protective: biological mechanisms. Proc Nutr Soc. 2003;62(1):129-134.

72. Stoll BA. Can supplementary dietary fibre suppress breast cancer growth? Br J Cancer 1996;73(5):557-559.

73. Bagga D, Ashley JM, Geffrey SP, Wang HJ, Barnard RJ, Korenman S, et al. Effects of a very low fat, high fiber diet on serum

hormones and menstrual function. Implications for breast cancer prevention. Cancer 1995;76(12):2491-2946.


74. Rock CL, Flatt SW, Thomson CA, Stefanick ML, Newman VA, Jones LA, et al. Effects of a high-fiber, low-fat diet intervention

on serum concentrations of reproductive steroid hormones in women with a history of breast cancer. J Clin Oncol.


75. Wayne SJ, Neuhouser ML, Ulrich CM, Koprowski C, Baumgartner KB, Baumgartner RN, et al. Dietary fiber is associated

with serum sex hormones and insulin-related peptides in postmenopausal breast cancer survivors. Breast Cancer Res

Treat. 2007 Dec 5. [Epub ahead of print]

76. Goldin BR, Adlercreutz H, Gorbach SL, Warram JH, Dwyer JT, Swenson L, et al. Estrogen excretion patterns and plasma

levels in vegetarian and omnivorous women. N Engl J Med. 1982;307:1542-1547.

77. Cade JE, Burley VJ, Greenwood DC; UK Women’s Cohort Study Steering Group. Dietary fibre and risk of breast cancer in

the UK Women’s Cohort Study. Int J Epidemiol. 2007;36(2):431-438.

78. Mattisson I, Wirfalt E, Johansson U, Gullberg B, Olsson H, Berglund G. Intakes of plant foods, fibre and fat and risk of

breast cancer–a prospective study in the MalmÃDiet and Cancer cohort. Br J Cancer 2004;90(1):122-127.

79. Terry P, Jain M, Miller AB, Howe GR, Rohan TE. No association among total dietary fiber, fiber fractions, and risk of breast

cancer. Cancer Epidemiol Biomarkers Prev. 2002;11(11):1507-1508.

80. Cho E, Spiegelman D, Hunter DJ, Chen WY, Colditz GA, Willett WC. Premenopausal dietary carbohydrate, glycemic index,

glycemic load, and fiber in relation to risk of breast cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(11 Pt 1):1153-1158.

81. Howe GR, Hirohata T, Hislop TG, Iscovich JM, Yuan JM, Katsouyanni K, et al. Dietary factors and risk of breast cancer:

combined analysis of 12 case-control studies. J Natl Cancer Inst. 1990;82:561-569.

82. De Stefani E, Correa P, Ronco A, Mendilaharsu M, Guidobono M, Deneo-Pellegrini H. Dietary fiber and risk of breast

cancer: a case-control study in Uruguay. Nutr Cancer 1997;28:14-19.

83. La Vecchia C, Ferraroni M, Franceschi S, Mezzetti M, Decarli A, Negri E. Fibers and breast cancer risk. Nutr Cancer


84. Challier B, Perarnau JM, Viel JF. Garlic, onion and cereal fibre as protective factors for breast cancer: a French case-control

study. Eur J Epidemiol. 1998;14: 737-747.

85. Rohan TE, Howe GR, Friedenreich CM, Jain M, Miller AB. Dietary fiber, vitamins A, C, and E, and risk of breast cancer: a

cohort study. Cancer Causes Control 1993;4:29-37.

86. Adebamowo CA, Cho E, Sampson L, Katan MB, Spiegelman D, Willett WC, et al. Dietary flavonols and flavonol-rich foods

intake and the risk of breast cancer. Int J Cancer 2005;114(4):628-633.

87. Muti P, Quattrin T, Grant BJ, Krogh V, Micheli A, Schunemann HJ, et al. Fasting glucose is a risk factor for breast cancer: a

prospective study. Cancer Epidemiol Biomarkers Prev. 2002;11(11):1361-1368.

88. Hadsell DL, Bonnette SG. IGF and insulin action in the mammary gland: lessons from transgenic and knockout models. J

Mammary Gland Biol Neoplasia 2000;5(1):19-30.

89. McCance KL, Jones RE. Estrogen and insulin crosstalk: breast cancer risk implications. Nurse Pract. 2003;28(5):12-23.

90. Shi R, Yu H, McLarty J, Glass J. IGF-I and breast cancer: a meta-analysis. Int J Cancer 2004;111(3):418-423.

91. Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst.

2000; 92:1472-1489.

92. Muti P. The role of endogenous hormones in the etiology and prevention of breast cancer: the epidemiological evidence.

Ann N Y Acad Sci. 2004;1028:273-282.

93. Osborne CK, Clemmons DR, Arteaga CL. Regulation of breast cancer growth by insulin-like growth factors. J Steroid

Biochem Mol Biol. 1990;37(6):805-809.

94. Lee AV, Jackson JG, Gooch JL, Hilsenbeck SG, Coronado-Heinsohn E, Osborne CK, et al. Enhancement of insulin-like

growth factor signaling in human breast cancer: estrogen regulation of insulin receptor substrate-1 expression in vitro and in

vivo. Mol Endocrinol. 1999;13:787-796.

95. Malin A, Dai Q, Yu H, Shu XO, Jin F, Gao YT. Evaluation of the synergistic effect of insulin resistance and insulin-like growth

factors on the risk of breast carcinoma. Cancer 2004;100(4):694-700.

96. Hankinson SE, Willett WC, Colditz GA, Hunter DJ, Michaud DS, Deroo B, et al. Circulating concentrations of insulin-like

growth factor-I and risk of breast cancer. Lancet 1998;351(9113):1393-1396.

97. Schernhammer ES, Holly JM, Pollak MN, Hankinson SE. Circulating levels of insulin-like growth factors, their binding

proteins, and breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2005;14(3):699-704.

98. Eliassen AH, Tworoger SS, Mantzoros CS, Pollak MN, Hankinson SE. Circulating insulin and c-peptide levels and risk of

breast cancer among predominately premenopausal women. Cancer Epidemiol Biomarkers Prev. 2007;16(1):161-164.


99. Lawlor DA, Smith GD, Ebrahim S. Hyperinsulinaemia and increased risk of breast cancer: findings from the British Women’s

Heart and Health Study. Cancer Causes Control 2004;15(3):267-275.

100. Stoll BA. Biological mechanisms in breast cancer invasiveness: relevance to preventive interventions. Eur J Cancer Prev.


101. Pollak M, Constantino J, Polychronakos C, Blauer SA, Guyda H, Redmond C, et al. Effect of tamoxifen on serum insulinlike

growth factor I levels in stage I breast cancer patients. J Natl Cancer Inst. 1990;82(21):1693-1697.

102. Borugian MJ, Sheps SB, Kim-Sing C, Van Patten C, Potter JD, Dunn B, et al. Insulin, macronutrient intake, and physical

activity: are potential indicators of insulin resistance associated with mortality from breast cancer? Cancer Epidemiol

Biomarkers Prev. 2004;13(7):1163-1172.

103. Gonullu G, Ersoy C, Ersoy A, Evrensel T, Basturk B, Kurt E, et al. Relation between insulin resistance and serum concentrations

of IL-6 and TNF-alpha in overweight or obese women with early stage breast cancer. Cytokine 2005;31(4):264-269.

104. Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Madarnas Y, et al. Fasting insulin and outcome in early-stage

breast cancer: results of a prospective cohort study. J Clin Oncol. 2002;20:42-51.

105. Romieu I, Lazcano-Ponce E, Sanchec-Zamorano LM, Wallett W, Hernandez-Avila M. Carbohydrates and the risk of breast

cancer among Mexican women. Cancer Epidemiol Biomarkers Prev. 2004;13(8):1283-1289.

106. Tavani A, Giordano L, Gallus S, Talamini R, Franceschi S, Giacosa A, et al. Consumption of sweet foods and breast cancer

risk in Italy. Ann Oncol. 2005 Oct 25. [Epub ahead of print]

107. Tavani A, Giordano L, Gallus S, Talamini R, Franceschi S, Giacosa A, et al. Consumption of sweet foods and breast cancer

risk in Italy. Ann Oncol. 2006;17(2):341-345.

108. Sieri S, Pala V, Brighenti F, Pellegrini N, Muti P, Micheli A, et al. Dietary glycemic index, glycemic load, and the risk of

breast cancer in an Italian prospective cohort study. Am J Clin Nutr. 2007;86(4):1160-1166.

109. Lajous M, Boutron-Ruault MC, Fabre A, Clavel-Chapelon F, Romieu I. Carbohydrate intake, glycemic index, glycemic load,

and risk of postmenopausal breast cancer in a prospective study of French women. Am J Clin Nutr. 2008;87(5):1384-1391.

110. Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, et al. Glycemic index, glycemic load, and chronic

disease risk–a meta-analysis of observational studies. Am J Clin Nutr. 2008;87(3):627-637.

111. Chlebowski RT, Blackburn GL, Thomson CA, Nixon DW, Shapiro A, Hoy MK, et al. Dietary fat reduction and breast cancer

outcome: interim efficacy results from the Women’s Intervention Nutrition Study. J Natl Cancer Inst. 2006;98(24):1767-1776.

112. Schulz M, Hoffmann K, Weikert C, Nöhlings U, Schulze MB, Boeing H. Identification of a dietary pattern characterized by

high-fat food choices associated with increased risk of breast cancer: the European Prospective Investigation into Cancer

and Nutrition (EPIC)-Potsdam Study. Br J Nutr. 2008 Apr 1:1-5. [Epub ahead of print]

113. Dorgan JF, Hunsberger SA, McMahon RP, Kwiterovich PO Jr, Lauer RM, Van Horn L, et al. Diet and sex hormones in girls:

findings from a randomized controlled clinical trial. J Natl Cancer Inst. 2003;95(2):132-141.

114. Nothlings U, Wilkens LR, Murphy SP, Hankin JH, Henderson BE, Kolonel LN. Meat and fat intake as risk factors for

pancreatic cancer: the multiethnic cohort study. J Natl Cancer Inst. 2005;97(19):1458-1465.

115. Qiu JL, Chen K, Zheng JN, Wang JY, Zhang LJ, Sui LM. Nutritional factors and gastric cancer in Zhoushan Islands, China.

World J Gastroenterol. 2005;11(28):4311-4316.

116. Gonzalez CA, Navarro C, Martinez C, Quiros JR, Dorronsoro M, Barricarte A, et al. [The European prospective investigation

about cancer and nutrition (EPIC)] [Article in Spanish] Rev Esp Salud Publica 2004;78(2):167-176.

117. Alothaimeen A, Ezzat A, Mohamed G, Muammar T, Al-Madouj A. Dietary fat and breast cancer in Saudi Arabia: a casecontrol

study. East Mediterr Health J. 2004;10(6):879-886.

118. Saadatian-Elahi M, Norat T, Goudable J, Riboli E. Biomarkers of dietary fatty acid intake and the risk of breast cancer: a

meta-analysis. Int J Cancer 2004;111(4):584-591.

119. Boyd NF, Stone J, Vogt KN, Connelly BS, Martin LJ, Minkin S. Dietary fat and breast cancer risk revisited: a meta-analysis

of the published literature. Br J Cancer 2003;89(9):1672-1685.

120. Gago-Dominguez M, Yuan JM, Sun CL, Lee HP, Yu MC. Opposing effects of dietary n-3 and n-6 fatty acids on mammary

carcinogenesis: The Singapore Chinese Health Study. Br J Cancer 2003;89(9):1686-1692.

121. Holmes MD, Hunter DJ, Colditz GA, Stampher MJ, Hankinson SE, Speizer FE, et al. Association of dietary intake of fat and

fatty acids with risk of breast cancer. JAMA 1999;281(10):914-920.

122. Wolk A, Bergstrom R, Hunter D, Willett W, Ljung H, Holmberg L, et al. A prospective study of association of

monounsaturated fat and other types of fat with risk of breast cancer. Arch Intern Med. 1998;158(1):41-45.

123. Bakker N, Van’t Veer P, Zock PL. Adipose fatty acids and cancers of the breast, prostate and colon: an ecological study.

EURAMIC Study Group. Int J Cancer 1997;72(4):587-591.


124. Slattery ML, Benson J, Ma KN, Schaffer D, Potter JD. Trans-fatty acids and colon cancer. Nutr Cancer 2001;39(2):170-175.

125. Voorrips LE, Brants HA, Kardinaal AF, Kiddink GJ, van den Brandt PA, Goldbohm RA. Intake of conjugated linoleic acid,

fat, and other fatty acids in relation to postmenopausal breast cancer: the Netherlands Cohort Study on Diet and Cancer.

Am J Clin Nutr. 2002;76(4):873-882.

126. Chajès V, Thiébaut AC, Rotival M, Gauthier E, Maillard V, Boutron-Ruault MC, et al. Association between serum transmonounsaturated

fatty acids and breast cancer risk in the E3N-EPIC Study. Am J Epidemiol. 2008;167(11):1312-1320.

127. Rissanen H, Knekt P, Jarvinen R, Salminen I, Hakulinen T. Serum fatty acids and breast cancer incidence. Nutr Cancer


128. Kohlmeier L, Simonsen N, van’t Veer P, Strain JJ, Martin-Moreno JM, Margolin B, et al. Adipose tissue trans fatty acids

and breast cancer in the European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast

Cancer. Cancer Epidemiol Biomarkers Prev. 1997;6(9):705-710.

129. Bartsch H, Nair J, Owen RW. Dietary polyunsaturated fatty acids and cancers of the breast and colorectum: emerging

evidence for their role as risk modifiers. Carcinogenesis 1999;20(12):2209-2218.

130. Solanas M, Hurtado A, Costa I, Moral R, Menendez JA, Colomer R, et al. Effects of a high olive oil diet on the clinical

behavior and histopathological features of rat DMBA-induced mammary tumors compared with a high corn oil diet. Int J

Oncol. 2002;21(4):745-753.

131. Garcí-Segovia P, Sáchez-Villegas A, Doreste J, Santana F, Serra-Majem L. Olive oil consumption and risk of breast

cancer in the Canary Islands: a population-based case-control study. Public Health Nutr. 2006;9(1A):163-167.

132. Martin-Moreno JM, Willett, WC, Gorgojo L, Banegas JR, Rodriguez-Artalejo F, Fernandez-Rodriguez JC, et al. Dietary fat,

olive oil intake and breast cancer risk. Int J Cancer 1994;58(6):774-780.

133. la Vecchia C, Negri E, Franceschi S, Decarli A, Giacosa A, Lipworth L. Olive oil, other dietary fats, and the risk of breast

cancer (Italy). Cancer Causes Control 1995;6(6):545-550.

134. Trichopoulou A, Katsouyanni K, Stuver S, Tzala L, Gnardellis C, Rimm E, et al. Consumption of olive oil and specific food

groups in relation to breast cancer risk in Greece. J Natl Cancer Inst. 1995;87(2):110-116.

135. Wakai K, Tamakoshi K, Date C, Fukui M, Suzuki S, Lin Y, et al. Dietary intakes of fat and fatty acids and risk of breast

cancer: a prospective study in Japan. Cancer Sci. 2005;96(9):590-599.

136. Caygill CP, Charlett A, Hill MJ. Fat, fish, fish oil and cancer. Br J Cancer 1996;74(1):159-164.

137. Maillard V, Bougnoux P, Ferrari P, Jourdan ML, Pinault M, Lavillonniere F, et al. N-3 and N-6 fatty acids in breast adipose

tissue and relative risk of breast cancer in a case-control study in Tours, France. Int J Cancer 2002;98(1):78-83.

138. Bagga D, Anders KH, Wang HJ, Glaspy JA. Long-chain n-3-to-n-6 polyunsaturated fatty acid ratios in breast adipose

tissue from women with and without breast cancer. Nutr Cancer 2002;42(2):180-185.

139. Hardman WE. (n-3) fatty acids and cancer therapy. J Nutr. 2004;134(12 Suppl):3427S-3430S.

140. Kuriki K, Hirose K, Wakai K, Matsuo K, Ito H, Suzuki T, Hiraki A, Saito T, Iwata H, Tatematsu M, Tajima K. Breast cancer

risk and erythrocyte compositions of n-3 highly unsaturated fatty acids in Japanese. Int J Cancer. 2007;121(2):377-385.

141. Shannon J, King IB, Moshofsky R, Lampe JW, Gao DL, Ray RM, Thomas DB. Erythrocyte fatty acids and breast cancer

risk: a case-control study in Shanghai, China. Am J Clin Nutr. 2007;85(4):1090-1097.

142. Larsson SC, Kumlin M, Ingelman-Sundberg M, Wolk A. Dietary long-chain n-3 fatty acids for the prevention of cancer: a

review of potential mechanisms. Am J Clin Nutr. 2004;79(6):935-945.

143. Menendez JA, Lupu R, Colomer R. Exogenous supplementation with omega-3 polyunsaturated fatty acid

docosahexaenoic acid (DHA; 22:6n-3) synergistically enhances taxane cytotoxicity and downregulates Her-2/neu

(c-erbB-2) oncogene expression in human breast cancer cells. Eur J Cancer Prev. 2005;14(3):263-270.

144. Rose DP, Connolly JM. Effects of fatty acids and eicosanoid synthesis inhibitors on the growth of two human prostate

cancer cell lines. Prostate 1991;18(3):243-254.

145. Favero A, Parpinel M, Franceschi S. Diet and risk of breast cancer: major findings from an Italian case-control study.

Biomed Pharmacother. 1998;52:109-115.

146. Davis BC, Kris-Etherton PM. Achieving optimal essential fatty acid status in vegetarians: current knowledge and practical

implications. Am J Clin Nutr. 2003;78(3 Suppl):640S-646S.

147. Gerster H. Can adults adequately convert alpha-linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and

docosahexaenoic acid (22:6n-3)? Int J Vitam Nutr Res. 1998;68(3):159-173.

148. Shim JY, An HJ, Lee YH, Kim SK, Lee KP, Lee KS. Overexpression of cyclooxygenase-2 is associated with breast

carcinoma and its poor prognostic factors. Mod Pathol. 2003;16(12):1199-1204.


149. Sonestedt E, Ericson U, Gullberg B, Skog K, Olsson H, Wirfält E. Do both heterocyclic amines and omega-6

polyunsaturated fatty acids contribute to the incidence of breast cancer in postmenopausal women of the Malmö diet and

cancer cohort? Int J Cancer. 2008 Jul 17. [Epub ahead of print]

150. Thomson CA, Guiliano AR, Shaw JW, Rock CL, Ritenbaugh CK, Hakim IA, et al. Diet and biomarkers of oxidative damage

in women previously treated for breast cancer. Nutr Cancer 2005;51(2):146-154.

151. Chajes V, Bougnoux P. Omega-6/omega-3 polyunsaturated fatty acid ratio and cancer. World Rev Nutr Diet 2003;92:133-151

152. Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic

diseases. Exp Biol Med (Maywood). 2008;233(6):674-688.

153. Taylor EF, Burley VJ, Greenwood DC, Cade JE. Meat consumption and risk of breast cancer in the UK Women’s Cohort

Study. Br J Cancer. 2007;96(7):1139-1146.

154. Di Pietro PF, Medeiros NI, Vieira FG, Fausto MA, BellóKlein A. Breast cancer in southern Brazil: association with past

dietary intake. Nutr Hosp. 2007;22(5):565-572.

155. Zheng W, Gustafson DR, Sinha R, Cerhan JR, Moore D, Hong CP, et al. Well-done meat intake and the risk of breast

cancer. J Natl Cancer Inst. 1998;90(22):1724-1729.

156. Pierce JP, Faerber S, Wright FA, Rock CL., Newman V, Flatt SW, et al. A randomized trial of the effect of a plant-based

dietary pattern on additional breast cancer events and survival: the Women’s Healthy Eating and Living (WHEL) Study.

Controlled Clin Trials 2002;23(6):728-756.

157. Vikse R, Reistad R, Steffensen IL, Paulsen JE, Nyholm SH, Alexander J, et al. [Heterocyclic amines in cooked meat] [Article

in Norwegian] Tidsskrift for den Norske Laegeforening 1999;119(1):45-49.

158. Felton JS, Knize MG, Salmon CP, Malfatti MA, Kulp KS. Human exposure to heterocyclic amine food mutagens/

carcinogens: relevance to breast cancer. Environ Mol Mutagen. 2002;39(2-3):112-118.

159. Ferguson LR. Meat consumption, cancer risk and population groups within New Zealand. Mutation Res.


160. De Stefani E, Ronco A, Mendilaharsu M, Guidobono M, Deneo-Pellegrini H. Meat intake, heterocyclic amines, and risk of

breast cancer: a case-control study in Uruguay. Cancer Epidemiol Biomarkers Prev. 1997;6(8):573-581.

163. Delfino RJ, Sinha R, Smith C, West J, White E, Lin HJ, et al. Breast cancer, heterocyclic aromatic amines from meat and

N-acetyltransferase 2 genotype. Carcinogenesis 2000;21(4):607-615

164. Ambrosone CB, Freudenheim JL, Sinha R, Graham S, Marshall JR, Vena JE, et al. Breast cancer risk, meat consumption

and N-acetyltransferase (NAT2) genetic polymorphisms. Int J Cancer 1998;75(6):825-830.

165. Sugimura T, Wakabayashi K, Nakagama H, Nagao M. Heterocyclic amines: Mutagens/carcinogens produced during

cooking of meat and fish. Cancer Sci. 2004;95(4):290-299.

166. Wilkinson GR. The effects of diet, aging and disease-states on presystemic elimination and oral drug bioavailability in

humans. Adv Drug Delivery Rev. 1997;27(2-3):129-159.

167. Chen WY, Willett WC, Rosner B, Colditz GA. Moderate alcohol consumption and breast cancer risk. 2005 ASCO Annual

Meeting, Abstract #515.

168. Horn-Ross PL, Canchola AJ, West DW, Stewart SL, Bernstein L, Deapen D, et al. Patterns of alcohol consumption and

breast cancer risk in the California Teachers Study cohort. Cancer Epidemiol Biomarkers Prev. 2004;13(3):405-411.

169. Tjonneland A, Christensen J, Thomsen BL, Olsen A, Stripp C, Overvad K, et al. Lifetime alcohol consumption and

postmenopausal breast cancer rate in Denmark: a prospective cohort study. J Nutr. 2004;134(1):173-178.

170. Hamajima N, Hirose K, Tajima K, Rohan T, Calle EE, Heath CW, et al. Alcohol, tobacco and breast cancer–collaborative

reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067

women without the disease. Br J Cancer 2002;87(11):1234-1245.

171. Petri AL, Tjonneland A, Gamborg M, Johansen D, Hoidrup S, Sorensen TI, et al. Alcohol intake, type of beverage, and risk

of breast cancer in pre- and postmenopausal women. Alcohol Clin Exp Res. 2004;28(7):1084-1090.

172. Key TJ, Schatzkin A, Willett WC, Allen NE, Spencer EA, Travis RC. Diet, nutrition and the prevention of cancer. Public

Health Nutr. 2004;7(1A):187-200.

173. Berstad P, Ma H, Bernstein L, Ursin G. Alcohol intake and breast cancer risk among young women. Breast Cancer Res

Treat. 2008;108(1):113-120.

174. Suzuki R, Orsini N, Mignone L, Saji S, Wolk A. Alcohol intake and risk of breast cancer defined by estrogen and

progesterone receptor status–a meta-analysis of epidemiological studies. Int J Cancer. 2008;122(8):1832-1841.

175. Visvanathan K, Crum RM, Strickland PT, You X, Ruczinski I, Berndt SI, et al. Alcohol dehydrogenase genetic

polymorphisms, low-to-moderate alcohol consumption, and risk of breast cancer. Alcohol Clin Exp Res.



176. Zhang SM, Lee IM, Manson JE, Cook NR, Willett WC, Buring JE. Alcohol consumption and breast cancer risk in the

Women’s Health Study. Am J Epidemiol. 2007;165(6):667-676.

177. Smith-Warner SA, Spiegelman D, Yaun SS, van den Brandt PA, Folsom AR, Goldbohm RA, et al. Alcohol and breast cancer

in women: a pooled analysis of cohort studies. JAMA. 1998;279(7):535-540.

178. Longnecker MP. Alcoholic beverage consumption in relation to risk of breast cancer: meta-analysis and review. Cancer

Causes Control 1994;5(1):73-82.

179. Ellison RC, Zhang Y, McLennan CE, Rothman KJ. Exploring the relation of alcohol consumption to risk of breast cancer.

Am J Epidemiol. 2001;154(8):740-747.

180. Bessaoud F, Daurè JP. Patterns of Alcohol (Especially Wine) Consumption and Breast Cancer Risk: A Case-Control Study

among a Population in Southern France. Ann Epidemiol. 2008 Apr 25. [Epub ahead of print]

181. Enger SM, Ross RK, Paganini-Hill A, Longnecker MP, Bernstein L. Alcohol consumption and breast cancer oestrogen and

progesterone receptor status. Br J Cancer 1999;79(7-8):1308-1314.

182. Suzuki R, Ye W, Rylander-Rudqvist T, Saji S, Colditz GA, Wolk A. Alcohol and postmenopausal breast cancer risk defined

by estrogen and progesterone receptor status: a prospective cohort study. J Natl Cancer Inst. 2005;97(21):1601-1608.

183. Onland-Moret NC, Peeters PH, van der Schouw YT, Grobbee DE, van Gils CH. Alcohol and endogenous sex steroid levels

in postmenopausal women: a cross-sectional study. J Clin Endocrinol Metab. 2005;90(3):1414-1419.

184. Holmes MD. Does diet affect breast cancer risk? Breast Cancer Res. 2004;6(4):170-178.

185. Dorgan JF, Baer DJ, Albert PS, Judd JT, Brown ED, Corle DK. Serum hormones and the alcohol-breast cancer association

in postmenopausal women. J Natl Cancer Inst. 2001;93(9):710-715.

186. Maskarinec G, Morimoto Y, Takata Y, Murphy SP, Stanczyk FZ. Alcohol and dietary fibre intakes affect circulating sex

hormones among premenopausal women. Public Health Nutr. 2006;9(7):875-881.

187. Rinaldi S, Peeters PH, Bezemer ID, Dossus L, Biessy C, Sacerdote C, et al. Relationship of alcohol intake and sex steroid

concentrations in blood in pre- and post-menopausal women: the European Prospective Investigation into Cancer and

Nutrition. Cancer Causes Control. 2006;17(8):1033-1043.

188. Sellers TA, Vierkant RA, Cerhan JR, Gapstur SM, Vachon CM, Olson JE, et al. Interaction of dietary folate intake, alcohol,

and risk of hormone receptor-defined breast cancer in a prospective study of postmenopausal women. Cancer Epidemiol

Biomarkers Prev. 2002;11(10 Pt 1):1104-1107.

189. Kritchevsky D. Caloric restriction and experimental mammary carcinogenesis. Breast Cancer Res Treat. 1997;46(2-3):161-167.

190. Meyer F, Bairati I, Fradet Y, Moore L. Dietary energy and nutrients in relation to preclinical prostate cancer. Nutr Cancer


191. Sonntag WE, Lynch CD, Cefalu WT, Ingram RL, Bennett, SA, Thornton PL, et al. Pleiotropic effects of growth hormone and

insulin-like growth factor (IGF)-1 on biological aging: inferences from moderate caloric-restricted animals. The Journal of

Gerontology. Series A, Biol Sci Med Sci. 1999;54(12):B521-B538.

192. Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst.


193. Feigelson HS, Jonas CR, Teras LR, Thun MJ, Calle EE. Weight gain, body mass index, hormone replacement therapy, and

postmenopausal breast cancer in a large prospective study. Cancer Epidemiol Biomarkers Prev. 2004;13(2):220-224.

194. Sweeney C, Blair CK, Anderson KE, Lazovich D, Folsom AR. Risk factors for breast cancer in elderly women. Am J

Epidemiol. 2004;160(9):868-875.

195. Carpenter CL, Ross RK, Paganini-Hill A, Bernstein L. Effect of family history, obesity and exercise on breast cancer risk

among postmenopausal women. Int J Cancer 2003;106(1):96-102.

196. Key TJ, Verkasalo PK, Banks E. Epidemiology of breast cancer. Lancet Oncol. 2001;2:133-140.

197. Reeves GK, Pirie K, Beral V, Green J, Spencer E, Bull D; Million Women Study Collaboration. Cancer incidence and

mortality in relation to body mass index in the Million Women Study: cohort study. BMJ. 2007;335(7630):1134.

198. Yumuk PF, Dane F, Yumuk VD, Yazici D, Ege B, Bekiroglu N, et al. Impact of body mass index on cancer development. J

BUON. 2008;13(1):55-59.

199. Iwasaki M, Otani T, Inoue M, Sasazuki S, Tsugane S; for the Japan Public Health Center-Based Prospective Study Group.

Body size and risk for breast cancer in relation to estrogen and progesterone receptor status in Japan. Ann Epidemiol.


200. Eng SM, Gammon MD, Terry MB, Kushi LF, Teitelbaum SL, Britton JA, et al. Body size changes in relation to

postmenopausal breast cancer among women on Long Island, New York. Am J Epidemiol. 2005;162(3):229-237.


201. Han D, Nie J, Bonner MR, McCann SE, Muti P, Trevisan M, et al. Lifetime adult weight gain, central adiposity, and the risk

of pre- and postmenopausal breast cancer in the Western New York exposures and breast cancer study. Int J Cancer.


202. Harvie M, Hooper L, Howell AH. Central obesity and breast cancer risk: a systematic review. Obes Rev. 2003;4(3):157-173.

203. Lahmann PH, Hoffmann K, Allen N, van Gils CH, Khaw KT, Tehard B, Berrino F, et al. Body size and breast cancer risk:

findings from the European Prospective Investigation into Cancer And Nutrition (EPIC). Int J Cancer 2004;111(5):762-771.

204. McTiernan A. Obesity and cancer: the risks, science, and potential management strategies. Oncology (Williston Park).


205. Dignam JJ, Wieand K, Johnson KA, Raich P, Anderson SJ, Somkin C. Effects of obesity and race on prognosis in lymph

node-negative, estrogen receptor-negative breast cancer. Breast Cancer Res Treat. 2005;1-10.

206. Whiteman MK, Hillis SD, Curtis KM, McDonald JA, Wingo PA, Marchbanks PA. Body mass and mortality after breast

cancer diagnosis. Cancer Epidemiol Biomarkers Prev. 2005;14(8):2009-2014.

207. Berclaz G, Li S, Price KN, Coates AS, Castiglione-Gertsch M, Rudenstam CM, et al. Body mass index as a prognostic feature

in operable breast cancer: the International Breast Cancer Study Group experience. Annal Oncol. 2004;15(6):875-884.

208. Kroenke CH, Chen, WY, Rosner B, Holmes MD. Weight, weight gain, and survival after breast cancer diagnosis. J Clin

Oncol. 2005;23(7):1370-1378.

209. Ryu SY, Kim CB, Nam CM, Park JK, Kim KS, Park J, et al. Is body mass index the prognostic factor in breast cancer?: a

meta-analysis. J Korean Med Sci. 2001;16(5):610-614.

210. Loi S, Milne RL, Friedlander ML, McCredie MR, Giles GG, Hopper JL, et al. Obesity and outcomes in premenopausal and

postmenopausal breast cancer. Cancer Epidemiol Biomarkers Prev. 2005;14(7):1686-1691.

211. McTiernan A, Rajan KB, Tworoger SS, Irwin M, Bernstein L, Baumgartner R, et al. Adiposity and Sex Hormones in

Postmenopausal Breast Cancer Survivors. J Clin Oncol. 2003;21(10):1961-1966.

212. Baglietto L, English DR, Hopper JL, Macinnis RJ, Morris HA, Tilley WD, et al. Circulating steroid hormone concentrations in

postmenopausal women in relation to body size and composition. Breast Cancer Res Treat. 2008 May 29. [Epub ahead of


213. Abrahamson PE, Gammon MD, Lund MJ, Flagg EW, Porter PL, Stevens J, et al. General and abdominal obesity and

survival among young women with breast cancer. Cancer Epidemiol Biomarkers Prev. 2006;15(10):1871-1877.

214. Resta F, Triggiani V, Sabba C, Licchelli B, Ghiyasaldin S, Liso A, et al. The impact of body mass index and type 2 diabetes

on breast cancer: current therapeutic measures of prevention. Curr Drug Targets Immune Endocr Metabol Disord.


215. Michels KB, Holmberg L, Bergkvist L, Ljung H, Bruce A, Wolk A. Dietary antioxidant vitamins, retinol, and breast cancer

incidence in a cohort of Swedish women. Int J Cancer 2001;91(4):563-567.

216. Holmes MD, Chen WY, Feskanich D, Kroenke CH, Colditz GA. Physical activity and survival after breast cancer diagnosis.

JAMA 2005;293(20):2479-2486.

217. McTiernan A, Kooperberg C, White E, Wilcox S, Coates R, Adams-Campbell LL, et al. Recreational physical activity and the

risk of breast cancer in postmenopausal women: the Women’s Health Initiative Cohort Study. JAMA 2003;290:1331-1336.

218. Patel AV, Callel EE, Bernstein L, Wu AH, Thun MJ. Recreational physical activity and risk of postmenopausal breast cancer

in a large cohort of US women. Cancer Causes Control 2003;14(6):519-529.

219. Kruk J. Lifetime physical activity and the risk of breast cancer: a case-control study. Cancer Detect Prev. 2007;31(1):18-28.

220. Adams SA, Matthews CE, Hebert JR, Moore CG, Cunningham JE, Shu XO, et al. Association of physical activity with

hormone receptor status: the Shanghai Breast Cancer Study. Cancer Epidemiol Biomarkers Prev. 2006;15(6):1170-1178.

221. Lahmann PH, Friedenreich C, Schuit AJ, Salvini S, Allen NE, Key TJ, et al. Physical activity and breast cancer risk: the

European Prospective Investigation into Cancer and Nutrition. Cancer Epidemiol Biomarkers Prev. 2007;16(1):36-42.

222. Monninkhof EM, Elias SG, Vlems FA, van der Tweel I, Schuit AJ, Voskuil DW, et al.; TFPAC. Physical activity and breast

cancer: a systematic review. Epidemiology. 2007;18(1):137-157.

223. Friedenreich CM, Cust AE. Physical Activity and Breast Cancer Risk: Impact of Timing, Type and Dose of Activity and

Population Sub-group Effects. Br J Sports Med. 2008 May 16. [Epub ahead of print]

224. Holick CN, Newcomb PA, Trentham-Dietz A, Titus-Ernstoff L, Bersch AJ, Stampfer MJ, et al. Physical activity and survival

after diagnosis of invasive breast cancer. Cancer Epidemiol Biomarkers Prev. 2008;17(2):379-386.

225. Abrahamson PE, Gammon MD, Lund MJ, Britton JA, Marshall SW, Flagg EW, et al. Recreational physical activity and

survival among young women with breast cancer. Cancer. 2006;107(8):1777-1785.

226. Valenti M, Porzio G, Aielli F, Verna L, Cannita K, Manno R, Masedu F, Marchetti P, Ficorella C. Physical exercise and quality

of life in breast cancer survivors. Int J Med Sci. 2008;5(1):24-28.


227. Milne HM, Gordon S, Guilfoyle A, Wallman KE, Courneya KS. Association between physical activity and quality of life

among Western Australian breast cancer survivors. Psychooncology. 2007;16(12):1059-1068.

228. Cramp F, Daniel J. Exercise for the management of cancer-related fatigue in adults. Cochrane Database Syst Rev.


229. Labourey JL. Physical activity in the management of cancer-related fatigue induced by oncological treatments. [Article in

English, French] Ann Readapt Med Phys. 2007;50(6):450-454, 445-449.

230. Campbell KL, Westerlind KC, Harber VJ, Bell GJ, Mackey JR, Courneya KS. Effects of aerobic exercise training on

estrogen metabolism in premenopausal women: a randomized controlled trial. Cancer Epidemiol Biomarkers Prev.


231. Ligibel JA, Campbell N, Partridge A, Chen WY, Salinardi T, Chen H, et al. Impact of a mixed strength and endurance

exercise intervention on insulin levels in breast cancer survivors. J Clin Oncol. 2008;26(6):907-912.

232. Fair AM, Dai Q, Shu XO, Matthews CE, Yu H, Jin F, et al. Energy balance, insulin resistance biomarkers, and breast cancer

risk. Cancer Detect Prev. 2007;31(3):214-219.

233. Irwin ML, Aiello EJ, McTiernan A, Bernstein L, Gilliland FD, Baumgartner RN, et al. Physical activity, body mass index, and

mammographic density in postmenopausal breast cancer survivors. J Clin Oncol. 2007;25(9):1061-1066.

234. Chidambaram N, Baradarajan A. Influence of selenium on glutathione and some associated enzymes in rats with

mammary tumor induced by 7,12-dimethylbenz(a)anthracene. Mol Cell Biochem. 1996;156(2):101-107.

235. Vadgama JV, Wu Y, Shen D, Hsia S, Block J. Effect of selenium in combination with Adriamycin or Taxol on several

different cancer cells. Anticancer Res. 2000;20(3A):1391-1414.

236. Lee SO, Nadiminty N, Wu XX, Lou W, Dong Y, Ip C, et al. Selenium disrupts estrogen signaling by altering estrogen

receptor expression and ligand binding in human breast cancer cells. Cancer Res. 2005;65(8):3487-3492.

237. Liu JZ, Gilbert K, Parker HM, Haschek, WM, Milner JA. Inhibition of 7,12-dimethylbenz(a)anthracene-induced mammary

tumors and DNA adducts by dietary selenite. Cancer Res. 1991;51(17):4613-4617.

238. El-Bayoumy K, Sinha R. Mechanisms of mammary cancer chemoprevention by organoselenium compounds. Mutat Res.


239. Li S, Zhou Y, Dong Y, Ip C. Doxorubicin and selenium cooperatively induce fas signaling in the absence of Fas/Fas ligand

interaction. Anticancer Res. 2007;27(5A):3075-3082.

240. Strain JJ, Bokje E, van’t Veer P, Coulter J, Stewart C, Logan H, et al. Thyroid hormones and selenium status in breast

cancer. Nutr Cancer 1997;27(1):48-52.

241. Cann SA, van Netten JP, van Netten C. Hypothesis: iodine, selenium and the development of breast cancer. Cancer

Causes Control 2000;11(2):121-127.

242. Bounous G, Molson JH. The antioxidant system. Anticancer Res. 2003;23(2B):1411-1415.

243. Choudhuri T, Pal S, Das T, Sa G. Curcumin selectively induces apoptosis in deregulated cyclin D1-expressed cells at G2

phase of cell cycle in a p53-dependent manner. J Biol Chem. 2005;280(20):20059-20068.

244. Mehta K, Pantazis P, McQueen T, Aggarwal BB. Antiproliferative effect of curcumin (diferuloylmethane) against human

breast tumor cell lines. Anticancer Drugs 1997;8(5):470-481.

245. Aggarwal BB, Shishodia S, Takada Y, Banerjee S, Newman RA, Bueso-Ramos CE, et al. Curcumin suppresses the

paclitaxel-induced nuclear factor-kappaB pathway in breast cancer cells and inhibits lung metastasis of human breast

cancer in nude mice. Clin Cancer Res. 2005;11(20):7490-7498.

246. Shao ZM, Shen ZZ, Liu CH, Sartippour MR, Go VL, Heber D, et al. Curcumin exerts multiple suppressive effects on human

breast carcinoma cells. Int J Cancer 2002;98(2):234-240.

247. Huang MT, Lou YR, Xie JG, Ma W, Lu YP., Yen P, et al. Effect of dietary curcumin and dibenzoylmethane on formation of

7,12-dimethylbenz[a]anthracene-induced mammary tumors and lymphomas/leukemias in Sencar mice. Carcinogenesis


248. Wallace JM. Nutritional and botanical modulation of the inflammatory cascade–eicosanoids, cyclooxygenases, and

lipoxygenases–as an adjunct in cancer therapy. Integr Cancer Ther. 2002;1(1):7-37.

249. Ramsewak RS, DeWitt DL, Nair MG. Cytotoxicity, antioxidant and anti-inflammatory activities of curcumins I-III from

Curcuma longa. Phytomedicine 2000;7(4):303-308.

250. Zhang SM. Role of vitamins in the risk, prevention, and treatment of breast cancer. Curr Opin Obstet Gynecol. 2004;16(1):19-25.

251. Bohlke K, Spiegelman D, Trichopoulou A, Katsouvanni K, Trichopoulos D. Vitamins A, C and E and the risk of breast

cancer: results from a case-control study in Greece. Br J Cancer 1999;79(1):23-29.

252. Nissen SB, Tjonneland A, Stripp C, Olsen A, Christensen J, Overvad K, et al. Intake of vitamins A, C, and E from diet and

supplements and breast cancer in postmenopausal women. Cancer Causes Control 2003;14(8):695-704.


253. Verhoeven DT, Assen N, Goldbohm RA, Dorant E, van’t Veer P, Sturmans F, et al. Vitamins C and E, retinol, beta-carotene

and dietary fibre in relation to breast cancer risk: a prospective cohort study. Br J Cancer. 1997;75(1):149-155.

254. Kushi LH, Fee RM, Sellers TA, Zheng W, Folsom AR. Intake of vitamins A, C, and E and postmenopausal breast cancer.

The Iowa Women’s Health Study. Am J Epidemiol. 1996;144(2):165-174.

255. Negri E, La Vecchia C, Franceschi S, D’Avanzo B, Talamni R, Parpinel M, et al. Intake of selected micronutrients and the

risk of breast cancer. Int J Cancer. 1996;65(2):140-144.

256. Levi F, Pasche C, Lucchini F, La Vecchia C. Dietary intake of selected micronutrients and breast-cancer risk. Int J Cancer


257. Hong SW, Jin DH, Hahm ES, Yim SH, Lim JS, Kim KI, et al. Ascorbate (vitamin C) induces cell death through the

apoptosis-inducing factor in human breast cancer cells. Oncol Rep. 2007;18(4):811-815.

258. Singh P, Kapil U, Shukla NK, Deo S, Dwivedi SN. Association between breast cancer and vitamin C, vitamin E and

selenium levels: results of a case-control study in India. Asian Pac J Cancer Prev. 2005;6(2):177-180.

259. Fleischauer AT, Simonsen N, Arab L. Antioxidant supplements and risk of breast cancer recurrence and breast cancerrelated

mortality among postmenopausal women. Nutr Cancer 2003;46(1):15-22.

260. Nesaretnam K, Ambra R, Selvaduray KR, Radhakrishan A, Canali R, Virgili F. Tocotrienol-rich fraction from palm oil and

gene expression in human breast cancer cells. Ann NY Acad Sci. 2004;1031:143-157.

261. Peralta EA, Brewer AT, Louis S, Dunnington GL. Vitamin E Increases Biomarkers of Estrogen Stimulation When Taken With

Tamoxifen. J Surg Res. 2008 Apr 22. [Epub ahead of print]

262. Alkhalaf M, El-Mowafy A, Renno W, Rachid O, Ali A, Al-Attyiah R. Resveratrol-induced apoptosis in human breast cancer

cells is mediated primarily through the caspase-3-dependent pathway. Arch Med Res. 2008;39(2):162-168.

263. Garvin S, Ollinger K, Dabrosin C. Resveratrol induces apoptosis and inhibits angiogenesis in human breast cancer

xenografts in vivo. Cancer Lett. 2006;231(1):113-122.

264. Whitsett T, Carpenter M, Lamartiniere CA. Resveratrol, but not EGCG, in the diet suppresses DMBA-induced mammary

cancer in rats. J Carcinog. 2006;5:15.

265. Tang FY, Su YC, Chen NC, Hsieh HS, Chen KS. Resveratrol inhibits migration and invasion of human breast-cancer cells.

Mol Nutr Food Res. 2008;52(6):683-691.

266. Vyas S, Asmerom Y, De Leó DD. Resveratrol regulates insulin-like growth factor-II in breast cancer cells. Endocrinology.


267. Vetvicka V, Volny T, Saraswat-Ohri S, Vashishta A, Vancikova Z, Vetvickova J. Glucan and resveratrol complex–possible

synergistic effects on immune system. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2007;151(1):41-46.

268. Dabrosin C, Chen J, Wang L, Thompson LU. Flaxseed inhibits metastasis and decreases extracellular vascular endothelial

growth factor in human breast cancer xenografts. Cancer Letters 2002;185(1):31-37.

269. Hutchins AM, Martini MC, Olson BA, Thomas W, Slavin JL. Flaxseed consumption influences endogenous hormone

concentrations in postmenopausal women. Nutr Cancer 2001;39(1):58-65.

270. Chen J, Power KA, Mann J, Cheng A, Thompson LU. Flaxseed alone or in combination with tamoxifen inhibits MCF-7

breast tumor growth in ovariectomized athymic mice with high circulating levels of estrogen. Exp Biol Med (Maywood).


271. Thompson LU, Chen JM, Li T, Strasser-Weippl K, Goss PE. Dietary flaxseed alters tumor biological markers in

postmenopausal breast cancer. Clin Cancer Res. 2005;11(10):3828-3835.

272. Chen J, Stavro PM, Thompson LU. Dietary flaxseed inhibits human breast cancer growth and metastasis and downregulates

expression of insulin-like growth factor and epidermal growth factor receptor. Nutr Cancer 2002;43(2):187-192.

273. Haggans CJ, Hutchins AM, Olson BA, Thomas W, Martini MC, Slavin JL. Effect of flaxseed consumption on urinary

estrogen metabolites in postmenopausal women. Nutr Cancer 1999;33(2):188-195.

274. Haggans CJ, Travelli EJ, Thomas W, Martini MC, Slavin JL. The effect of flaxseed and wheat bran consumption on urinary

estrogen metabolites in premenopausal women. Cancer Epidemiol. Biomarkers Prev. 2000;9(7):719-725.

275. Nagel G, Mack U, von Fournier D, Linseisen J. Dietary phytoestrogen intake and mammographic density — results of a

pilot study. Eur J Med Res. 2005;10(9):389-394.

276. McCarty MF. A low-fat, whole-food vegan diet, as well as other strategies that down-regulate IGF-I activity, may slow the

human aging process. Med. Hypotheses 2003;60(6):784-792.

277. Sartippour MR, Heber D, Henning S, Elashoff D, Elashoff R, Rubio R, et al. cDNA microarray analysis of endothelial cells in

response to green tea reveals a suppressive phenotype. Int J Oncol. 2004;25(1):193-202.

278. Takabayashi F, Tahara S, Kaneko T, Harada N. Effect of green tea catechins on oxidative DNA damage of hamster pancreas

and liver induced by N-Nitrosobis(2-oxopropyl)amine and/or oxidized soybean oil. Biofactors 2004;21(1-4):335-337.


279. Glei M, Pool-Zobel BL. The main catechin of green tea, (-)-epigallocatechin-3-gallate (EGCG), reduces bleomycin-induced

DNA damage in human leucocytes. Toxicol In Vitro. 2005 Sep 24.

280. Mittal A, Pate MS, Wylie RC, Tollefsbol TO, Katiyar SK. EGCG down-regulates telomerase in human breast carcinoma

MCF-7 cells, leading to suppression of cell viability and induction of apoptosis. Int J Oncol. 2004;24(3):703-710

281. Crespy V, Williamson G. A review of the health effects of green tea catechins in in vivo animal models. J Nutr. 2004;134(12


282. Thangapazham RL, Passi N, Maheshwari RK. Green tea polyphenol and epigallocatechin gallate induce apoptosis and

inhibit invasion in human breast cancer cells. Cancer Biol Ther. 2007;6(12):1938-1943.

283. Guo S, Yang S, Taylor C, Sonenshein GE. Green tea polyphenol epigallocatechin-3 gallate (EGCG) affects gene expression

of breast cancer cells transformed by the carcinogen 7,12-dimethylbenz[a]anthracene. J Nutr. 2005;135(12 Suppl):2978S-


284. Wu AH, Tseng CC, Van Den Berg D, Yu MC. Tea intake, COMT genotype, and breast cancer in Asian-American women.

Cancer Res. 2003;63(21):7526-7529.

285. Baliga MS, Meleth S, Katiyar SK. Growth inhibitory and antimetastatic effect of green tea polyphenols on metastasisspecific

mouse mammary carcinoma 4T1 cells in vitro and in vivo systems. Clin Cancer Res. 2005;11(5):1918-1927.

286. Sun CL, Yuan JM, Koh WP, Yu MC. Green tea, black tea and breast cancer risk: a meta-analysis of epidemiological

studies. Carcinogenesis 2006;27(7):1310-1315

287. Seely D, Mills EJ, Wu P, Verma S, Guyatt GH. The effects of green tea consumption on incidence of breast cancer and

recurrence of breast cancer: a systematic review and meta-analysis. Integr Cancer Ther. 2005;4(2):144-155.

288. Wu AH, Yu Mc, Tseng CC, Hankin J, Pike MC. Green tea and risk of breast cancer in Asian Americans. Int J Cancer


289. Zhang M, Holman CD, Huang JP, Xie X. Green tea and the prevention of breast cancer: a case-control study in Southeast

China. Carcinogenesis. 2007;28(5):1074-1078.

290. Inoue M, Tajima K, Mizutani M, Iwata H, Iwase T, Miura S, et al. Regular consumption of green tea and the risk of breast

cancer recurrence: follow-up study from the Hospital-based Epidemiologic Research Program at Aichi Cancer Center

(HERPACC), Japan. Cancer Lett. 2001;167(2):175-182.

291. Fujiki H, Suganuma M, Okabe S, Sueoka E, Suga K, Imai K, et al. Mechanistic findings of green tea as cancer preventive

for humans. Proc Soc Exp Biol Med. 1999;220(4):225-228.

292. Nakachi K, Suemasu K, Suga K, Takeo T, Imai K, Higashi Y. Influence of drinking green tea on breast cancer malignancy

among Japanese patients. Jpn J Cancer Res. 1998;89(3):254-261.

293. Suzuki Y, Tsubono Y, Nakaya N, Suzuki Y, Koizumi Y, Tsuji I. Green tea and the risk of breast cancer: pooled analysis of

two prospective studies in Japan. Br J Cancer 2004;90(7):1361-1363.

294. Zhou JR, Yu L, Mai Z, Blackburn GL. Combined inhibition of estrogen-dependent human breast carcinoma by soy and tea

bioactive components in mice. Int J Cancer 2004;108(1):8-14.

295. Thyagarajan A, Zhu J, Sliva D. Combined effect of green tea and Ganoderma lucidum on invasive behavior of breast

cancer cells. Int J Oncol. 2007;30(4):963-969.

296. Sartippour MR, Pietras R, Marquez-Garban DC, Chen HW, Heber D, Henning SM, et al. The combination of green tea and

tamoxifen is effective against breast cancer. Carcinogenesis. 2006;27(12):2424-2433.

297. Jenkins DJ, Kendall CW, D’Costa MA, Jackson CJ, Vidgen E, Singer W, et al. Soy consumption and phytoestrogens: effect

on serum prostate specific antigen when blood lipids and oxidized low-density lipoprotein are reduced in hyperlipidemic

men. J Urol. 2003;169(2):507-511.

298. McCarty MF. Vegan proteins may reduce risk of cancer, obesity, and cardiovascular disease by promoting increased

glucagon activity. Med Hypotheses 1999;53(6):459-485.

299. Arliss RM, Biermann CA. Do soy isoflavones lower cholesterol, inhibit atherosclerosis, and play a role in cancer

prevention? Holistic Nurs Pract. 2002;16(5):40-48.

300. Setchell KD, Lydeking-Olsen E. Dietary phytoestrogens and their effect on bone: evidence from in vitro and in vivo, human

observational, and dietary intervention studies. Am J Clin Nutr. 2003;78(3 Suppl):593S-609S.

301. Ho SC, Woo J, Lam S, Chen Y, Sham A, Lau J, et al. Soy protein consumption and bone mass in early postmenopausal

Chinese women. Osteo Intl. 2003;14(10):835-842.

302. Wu AH, Ziegler, Horn-Ross PL, Nomura AM, West DW, Kolonel LN, et al. Tofu and risk of breast cancer in Asian-

Americans. Cancer Epidemiol Biomarkers Prev. 1996;5(11):901-906.

303. Hirose K, Imaeda N, Tokudome Y, Goto C, Wakai K, Matsuo K, et al. Soybean products and reduction of breast cancer

risk: a case-control study in Japan. Br J Cancer 2005;93(1):15-22.


304. Travis RC, Allen NE, Appleby PN, Spencer EA, Roddam AW, Key TJ. A prospective study of vegetarianism and isoflavone

intake in relation to breast cancer risk in British women. Int J Cancer. 2008;122(3):705-710.

305. Iwasaki M, Inoue M, Otani T, Sasazuki S, Kurahashi N, Miura T, et al.; Japan Public Health Center-based prospective study

group. Plasma isoflavone level and subsequent risk of breast cancer among Japanese women: a nested case-control

study from the Japan Public Health Center-based prospective study group. J Clin Oncol. 2008;26(10):1677-1683.

306. Wu AH, Yu MC, Tseng CC, Pike MC. Epidemiology of soy exposures and breast cancer risk. Br J Cancer. 2008;98(1):9-14.

307. Warri A, Saarinen NM, Makela S, Hilakivi-Clarke L. The role of early life genistein exposures in modifying breast cancer

risk. Br J Cancer. 2008;98(9):1485-1493.

308. Allred CD, Twaddle NC, Allred KF, Goeppinger TS, Doerge DR, Helferich WG. Soy processing influences growth of

estrogen-dependent breast cancer tumors. Carcinogenesis 2004;25:1649-1657.

309. Allred CD, Twaddle NC, Allred KF, Goeppinger TS, Churchwell MI, Ju YH, et al. Soy processing affects metabolism and

disposition of dietary isoflavones in ovariectomized BALB/c mice. J Agric Food Chem. 2005;53(22):8542-8550.

310. Boyapati SM, Shu XO, Ruan ZX, Dai Q, Cai Q, Gao YT, et al. Soyfood intake and breast cancer survival: a followup of the

Shanghai Breast Cancer Study. Breast Cancer Res Treat. 2005;92(1):11-17.

311. Nishio K, Niwa Y, Toyoshima H, Tamakoshi K, Kondo T, Yatsuya H, et al. Consumption of soy foods and the risk of breast

cancer: findings from the Japan Collaborative Cohort (JACC) Study. Cancer Causes Control. 2007;18(8):801-808.

312. Kumar NB, Cantor A, Allen K, Riccardi D, Cox CE. The specific role of isoflavones on estrogen metabolism in

premenopausal women. Cancer 2002;94(4):1166-1174.

313. Xu X, Duncan AM, Merz BE, Kurzer MS. Effects of soy isoflavones on estrogen and phytoestrogen metabolism in

premenopausal women. Cancer Epidemiol Biomarkers Prev. 1998;7(12):1101-1108.

314. Sanderson M, Shu XO, Yu H, Dai Q, Malin AS, Gao YT, et al. Insulin-like growth factor-I, soy protein intake, and breast

cancer risk. Nutr Cancer 2004;50(1):8-15.

315. Takata Y, Maskarinec G, Rinaldi S, Kaaks R, Nagata C. Serum insulin-like growth factor-I levels among women in Hawaii

and Japan with different levels of tofu intake. Nutr Cancer. 2006;56(2):136-142.

316. Wu AH, Pike MC, Williams LD, Spicer D, Tseng CC, Churchwell MI, et al. Tamoxifen, soy, and lifestyle factors in Asian

American women with breast cancer. J Clin Oncol. 2007;25(21):3024-3030.

317. Mai Z, Blackburn GL, Zhou JR. Genistein sensitizes inhibitory effect of tamoxifen on the growth of estrogen receptorpositive

and HER2-overexpressing human breast cancer cells. Mol Carcinog. 2007;46(7):534-542.

318. Ingraham BA, Bragdon B, Nohe A. Molecular basis of the potential of vitamin D to prevent cancer. Curr Med Res Opin.


319. Tseng M, Byrne C, Evers KA, Daly MB. Dietary intake and breast density in high-risk women: a cross-sectional study.

Breast Cancer Res. 2007;9(5):R72.

320. Giovannucci E. Vitamin D and Cancer Incidence in the Harvard Cohorts. Ann Epidemiol. 2008 Feb 19. [Epub ahead of print]

321. Abbas S, Linseisen J, Slanger T, Kropp S, Mutschelknauss EJ, Flesch-Janys D, et al. Serum 25-hydroxyvitamin D and risk

of post-menopausal breast cancer–results of a large case-control study. Carcinogenesis. 2008;29(1):93-99.

322. Heaney RP. Vitamin D in Health and Disease. Clin J Am Soc Nephrol. 2008 Jun 4. [Epub ahead of print]

323. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations

of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18-28.

324. Wu AH, Wang R, Koh WP, Stanczyk FC, Lee HP, Yu MC. Sleep duration, melatonin and breast cancer among Chinese

women in Singapore. Carcinogenesis. 2008;29(6):1244-1248.

325. Schernhammer ES, Hankinson SE. Light at night: a novel risk factor for cancer in shift workers? Clin Occup Environ Med.


326. Schernhammer ES, Kroenke CH, Laden F, Hankinson SE. Night work and risk of breast cancer. Epidemiology.


327. Franzese E, Nigri G. [Night work as a possible risk factor for breast cancer in nurses. Correlation between the onset of

tumors and alterations in blood melatonin levels] [Article in Italian] Prof Inferm. 2007;60(2):89-93.

328. Leman ES, Sisken BF, Zimmer S, Anderson KW. Studies of the interactions between melatonin and 2 Hz, 0.3 mT PEMF on

the proliferation and invasion of human breast cancer cells. Bioelectromagnetics 2001;22:178-184.

329. Schernhammer ES, Hankinson SE. Urinary melatonin levels and breast cancer risk. J Natl Cancer Inst. 2005;97(14):1084-1087.

330. Jones MP, Melan MA, Witt-Enderby PA. Melatonin decreases cell proliferation and transformation in a melatonin receptordependent

manner. Cancer Lett. 2000;151:133-143.


331. Srinivasan V, Spence DW, Pandi-Perumal SR, Trakht I, Esquifino AI, Cardinali DP, et al. Melatonin, environmental light, and

breast cancer. Breast Cancer Res Treat. 2008;108(3):339-350.

332. Lissoni P, Barni S, Mandala M, et al. Decreased toxicity and increased efficacy of cancer chemotherapy using the pineal

hormone melatonin in metastatic solid tumor patients with poor clinical status. Eur J Cancer 1999;35:1688-1692.

333. Sanchez-Barcelo EJ, Cos S, Mediavilla D, Martinez-Campa C, Gonzalez A, Alonso-Gonzalez C. Melatonin-estrogen

interactions in breast cancer. J Pineal Res. 2005;38(4):217-222.

334. Lissoni P, Barni S, Meregalli S, Fossati V, Cazzaniga M, Esposti D, et al. Modulation of cancer endocrine therapy by

melatonin: a phase II study of tamoxifen plus melatonin in metastatic breast cancer patients progressing under tamoxifen

alone. Br J Cancer 1995;71:854-856.

335. Lissoni P, Paolorossi F, Tancini G, Ardizzoia A, Barni S, Brivio F, et al. A phase II study of tamoxifen plus melatonin in

metastatic solid tumour patients. Br J Cancer 1996;74:1466-1468.

336. Hill SM, Collins A, Kiefer TL. The modulation of oestrogen receptor-alpha activity by melatonin in MCF-7 human breast

cancer cells. Eur J Cancer 2000;36(Suppl 4):117-118.

337. Cos S, Martinez-Campa C, Mediavilla MD, Sanchez-Barcelo EJ. Melatonin modulates aromatase activity in MCF-7 human

breast cancer cells. J Pineal Res. 2005;38(2):136-142.

338. del Rio B, Garcia Pedrero JM, Martinez-Campa C, Zuazua P, Lazo PS, Ramos S. Melatonin, an endogenous-specific

inhibitor of estrogen receptor alpha via calmodulin. J Biol Chem. 2004;279(37):38294-38302.

339. Czeczuga-Semeniuk E, Wolczynski S, Anchim T, Dzieciol J, Dabrowska M, Pietruczuk M. Effect of melatonin and all-trans

retinoic acid on the proliferation and induction of the apoptotic pathway in the culture of human breast cancer cell line

MCF-7. Pol J Pathol. 2002;53(2):59-65.

340. Bizzarri M, Cucina A, Valente MG, Tagliaferri F, Borrelli V, Stipa F, et al. Melatonin and vitamin D3 increase TGF-beta1

release and induce growth inhibition in breast cancer cell cultures. J Surg Res. 2003;110(2):332-337.

341. Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride. Standing

Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board. 1997. National Academy


342. National Osteoporosis Foundation. 2001.

343. Heaney RP. Bone biology in health and disease. In Modern Nutrition in Health and Disease, 9th ed. Shils ME et al., eds.

1999. Williams & Wilkins.

344. Chang YC, Parker J, Dooley WC. Hot flash therapies in breast cancer survivors. Support Cancer Ther. 2006;4(1):38-48.

345. Ziaei S, Kazemnejad A, Zareai M. The effect of vitamin E on hot flashes in menopausal women. Gynecol Obstet Invest.


346. Barton DL, Loprinzi CL, Quella SK, Sloan JA, Veeder MH, Egner JR, et al. Prospective evaluation of vitamin E for hot

flashes in breast cancer survivors. J Clin Oncol. 1998;16(2):495-500.

347. Tempfer CB, Bentz EK, Leodolter S, Tscherne G, Reuss F, Cross HS, et al. Phytoestrogens in clinical practice: a review of

the literature. Fertil Steril. 2007;87(6):1243-1249.

348. Lethaby AE, Brown J, Marjoribanks J, Kronenberg F, Roberts H, Eden J. Phytoestrogens for vasomotor menopausal

symptoms. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD001395.

349. Carroll DG. Nonhormonal therapies for hot flashes in menopause. Am Fam Physician. 2006;73(3):457-464.

350. Pockaj BA, Gallagher JG, Loprinzi CL, Stella PJ, Barton DL, Sloan JA, et al. Phase III double-blind, randomized, placebocontrolled

crossover trial of black cohosh in the management of hot flashes: NCCTG Trial N01CC1. J Clin Oncol.


351. Ruhlen RL, Haubner J, Tracy JK, Zhu W, Ehya H, Lamberson WR, et al. Black cohosh does not exert an estrogenic effect on

the breast. Nutr Cancer. 2007;59(2):269-

352. Walji R, Boon H, Guns E, Oneschuk D, Younus J. Black cohosh (Cimicifuga racemosa [L.] Nutt.): safety and efficacy for cancer

patients. Support Care Cancer. 2007 Aug;15(8):913-21.

353. Tremblay A, Sheeran L, Aranda SK. Psychoeducational interventions to alleviate hot flashes: a systematic review. Menopause.



 Thank you


10 Healthy Start-up Tips from Pirates by Maria Dorfner



Ahoy!  I found a few metaphors for life in the Pirates of the Caribbean films, a la buried treasure:





WILL TURNER:  This is either madness…or brilliance.

JACK SPARROW:   It’s remarkable how often those traits coincide.




JACK SPARROW:  People aren’t cargo mate!




SWANN:  Even a good decision if made for the wrong reasons can be a wrong decision.





JACK SPARROW:  What a ship is…the black pearl really is…is FREEDOM.





WILL TURNER:  A craftsman is always proud to hear his work is appreciated.





GIBBS:  Not quite according to plan.

JACK SPARROW:  Complications arose, ensued, were overcome.





JACK SPARROW:  You look bloody awful, what are you doing here?

 NORRINGTON:  You hired me.  I can’t help it if your standards are lax.





WILL TURNER:  No cause is lost if there is but one fool left to fight for it.





JACK SPARROW:  We have a need to travel upriver.

GIBBS:  By “need,” do you mean a trifling need?  Fleeting?  As in, say a passing fancy?

JACK SPARROW:  NO, a resolute and unyielding need!!





JACK SPARROW:  Close your eyes and pretend it’s all a bad dream.  That’s how I get by.






JACK SPARROW:  You’ve seen it all, done it all.  Survived.  That’s the trick, isn’t it?  To survive?

CAPTAIN TEAGUE:  It’s not just about living forever, Jackie.  The trick is still living with yourself forever.







JACK SPARROW:  You can’t upright a ship if it’s not already capsized.










Hope these quotes help you navigate your vessel through any unexpected treacherous waters!   Stay healthy.  🙂



[Quote Sources: Pirates of the Caribbean:  Dead Man’s Chest (2006), Pirates of the Caribbean: At World’s End (2007), Pirates of the Caribbean: The Curse of the Black Pearl (2003); photos: Pirates of the Caribbean films; Jake and the Never Land Pirates (Disney TV cartoon 2011)]




Today, this blog rec’d a 200 posts Award on its one-year anniversary…41,486 views, 32.10 views per visitor, 200+ likes.