Research, Recovery, Quality of Life Care (Palliative); pain

sas-schatzi

Nice YG, A-z about neuropathy. One thing about how you include the bibliography list. It allows the reader to easily check the original research that the study is based on. This can be very helpful for many reasons. Particularily, for accuracy. Or if one is trying to track the origin of a given subject. Saves time when the bib list is right here.

If what I'm about to write is too controversial, let me know and I will delete it and put flowers.

Their was a study that described characteristics of conservatives and liberal. There were many negative descriptions ascribed to conservatives. This was used during the most recent election by media and liberals to ascribe Authortarian characteristics to conservatives.

Lo and Behold several years after the publication of the original article that was subsequently used in over 40 other articles. A researcher from Denmark writing a paper realized the original researcher had flipped his data. Characteristics ascribed to conservatives really applied to liberal. Characteristics ascribed to liberals really applied to conservatives.

The original researcher and all the other researchers had to write errata addendums to their research. The problem with this is the info was out in the internet domain. Spread near and far i.e. worldwide. Many did not pay attention to or did not see that the original research was wrong. It is continuing to be promulgated by segments of the population, even though the information is wrong when it is applied to conservatives

My point is obvious, to anyone doing serious research. One article/ study does NOT tell the whole story. In this particular case, it tells me that the X number of researchers that used the original researchers study as a base, DIDN"T study it well.

It's what I call lazy research. The original researcher maintained, he didn't notice that he flipped his data. He maintained the data was correct, but he mislabeled who the characteristics applied too was wrong. OOPs. That information will be used incorrectly for years and years.

This happens more than you would care to know. But it does support why the steps of the scientific method are so important.

Plus, this part is a real negative. All studies that are published through scientific journals are SUPPOSED to go through peer review. That error by the original researcher should have been caught by one of those reviewers. Very bad that it wasn't.

With the advent of being able to publish on line, the step of peer review can be of questionable quality or absent.

Always approach science with a very critical eye. Just b/c something is written doesn't make it true. Tough to swallow, but true.

yoga_girl

I totally agree, everything we are exposed to in writing may only have the partial truth. Some may be swayed by financial incentives provided by pharmaceutical companies in an attempt to further their research and this could make the written report slanted to favor one drug over another. Thus, what is published may only present a partial reality for any of us. Our take away should always be with open eyes, validate, ask questions, further research and cross check what is published. We are forever learning about and from each other.

yoga_girl

National Cancer Institute

Hormone Therapy for Breast Cancer

Hot flashes, night sweats, and vaginal dryness are common side effects of hormone therapy. Hormone therapy also disrupts the menstrual cycle in premenopausal women.

to read the full research and published papers on this topic select the link.

https://www.cancer.gov/types/breast/breast-hormone-therapy-fact-sheet#q6

What are hormones?

Hormones are substances that function as chemical messengers in the body. They affect the actions of cells and tissues at various locations in the body, often reaching their targets through the bloodstream.

The hormones estrogen and progesterone are produced by the ovaries in premenopausal women and by some other tissues, including fat and skin, in both premenopausal and postmenopausal women and men. Estrogen promotes the development and maintenance of female sex characteristics and the growth of long bones. Progesterone plays a role in the menstrual cycle and pregnancy.

Estrogen and progesterone also promote the growth of some breast cancers, which are called hormone-sensitive (or hormone-dependent) breast cancers. Hormone-sensitive breast cancer cells contain proteins called hormone receptors that become activated when hormones bind to them. The activated receptors cause changes in the expression of specific genes, which can stimulate cell growth.

What is hormone therapy?

Hormone therapy (also called hormonal therapy, hormone treatment, or endocrine therapy) slows or stops the growth of hormone-sensitive tumors by blocking the body's ability to produce hormones or by interfering with effects of hormones on breast cancer cells. Tumors that are hormone insensitive do not have hormone receptors and do not respond to hormone therapy.

To determine whether breast cancer cells contain hormone receptors, doctors test samples of tumor tissue that have been removed by surgery. If the tumor cells contain estrogen receptors, the cancer is called estrogen receptor positive (ER positive), estrogen sensitive, or estrogen responsive. Similarly, if the tumor cells contain progesterone receptors, the cancer is called progesterone receptor positive (PR or PgR positive). Approximately 80% of breast cancers are ER positive (1). Most ER-positive breast cancers are also PR positive. Breast tumors that contain estrogen and/or progesterone receptors are sometimes called hormone receptor positive (HR positive).

Breast cancers that lack estrogen receptors are called estrogen receptor negative (ER negative). These tumors are estrogen insensitive, meaning that they do not use estrogen to grow. Breast tumors that lack progesterone receptors are called progesterone receptor negative (PR or PgR negative). Breast tumors that lack both estrogen and progesterone receptors are sometimes called hormone receptor negative (HR negative).

Hormone therapy for breast cancer should not be confused with menopausal hormone therapy (MHT)—treatment with estrogen alone or in combination with progesterone to help relieve symptoms of menopause. These two types of therapy produce opposite effects: hormone therapy for breast cancer blocks the growth of HR-positive breast cancer, whereas MHT can stimulate the growth of HR-positive breast cancer. For this reason, when a woman taking MHT is diagnosed with HR-positive breast cancer she is usually asked to stop that therapy.

What types of hormone therapy are used for breast cancer?

Several strategies are used to treat hormone-sensitive breast cancer:

Blocking ovarian function: Because the ovaries are the main source of estrogen in premenopausal women, estrogen levels in these women can be reduced by eliminating or suppressing ovarian function. Blocking ovarian function is called ovarian ablation.

Ovarian ablation can be done surgically in an operation to remove the ovaries (called oophorectomy) or by treatment with radiation. This type of ovarian ablation is usually permanent.

Alternatively, ovarian function can be suppressed temporarily by treatment with drugs called gonadotropin-releasing hormone (GnRH) agonists, which are also known as luteinizing hormone-releasing hormone (LH-RH) agonists. These medicines interfere with signals from the pituitary gland that stimulate the ovaries to produce estrogen.

Examples of ovarian suppression drugs that have been approved by the U.S. Food and Drug Administration (FDA) are goserelin (Zoladex®) and leuprolide (Lupron®).

Blocking estrogen production: Drugs called aromatase inhibitors are used to block the activity of an enzyme called aromatase, which the body uses to make estrogen in the ovaries and in other tissues. Aromatase inhibitors are used primarily in postmenopausal women because the ovaries in premenopausal women produce too much aromatase for the inhibitors to block effectively. However, these drugs can be used in premenopausal women if they are given together with a drug that suppresses ovarian function.

Examples of aromatase inhibitors approved by the FDA are anastrozole (Arimidex®) and letrozole (Femara®), both of which temporarily inactivate aromatase, and exemestane (Aromasin®), which permanently inactivates aromatase.

Blocking estrogen's effects: Several types of drugs interfere with estrogen's ability to stimulate the growth of breast cancer cells:

• Selective estrogen receptor modulators (SERMs) bind to estrogen receptors, preventing estrogen from binding. Examples of SERMs approved by the FDA for treatment of breast cancer are tamoxifen (Nolvadex®) and toremifene (Fareston®). Tamoxifen has been used for more than 30 years to treat HR+ hormone receptor–positive breast cancer.
  
  Because SERMs bind to estrogen receptors, they can potentially not only block estrogen activity (i.e., serve as estrogen antagonists) but also mimic estrogen effects (i.e., serve as estrogen agonists). SERMs can behave as estrogen antagonists in some tissues and as estrogen agonists in other tissues. For example, tamoxifen blocks the effects of estrogen in breast tissue but acts like estrogen in the uterus and bone.
• Other antiestrogen drugs, such as fulvestrant (Faslodex®), work in a somewhat different way to block estrogen's effects. Like SERMs, fulvestrant binds to the estrogen receptor and functions as an estrogen antagonist. However, unlike SERMs, fulvestrant has no estrogen agonist effects. It is a pure antiestrogen. In addition, when fulvestrant binds to the estrogen receptor, the receptor is targeted for destruction.

sas-schatzi

YG I love your research.. Could you do a thing related to Triple Negative. I have a friend that has given up on trials. fourth I think.

yoga_girl

Sas

Triple Negative has been added to my research list.

yoga_girl

Triple Negative Breast Cancer – Diet

https://www.sciencedaily.com/releases/2015/07/150714150934.htm

A diet that starves triple-negative breast cancer cells of an essential nutrient primes the cancer cells to be more easily killed by a targeted antibody treatment, UW Carbone Cancer Center scientists report in a recent publication.

The study's senior author, Vincent Cryns, professor of medicine at the University of Wisconsin School of Medicine and Public Health, says the study lays the foundation for a clinical trial to see if a low-methionine diet will help improve outcomes in women with "triple-negative" breast cancer.

Methionine is an essential amino acid that is present in low concentrations in some vegan diets.

Patients with triple-negative breast cancer have limited treatment options because their tumor cells lack the three receptors -- estrogen, progesterone and human epidermal growth factor receptor 2 (HER-2) -- commonly targeted in hormone or chemotherapy.

The journal Clinical Cancer Research chose the paper as a highlighted study in its June 15 edition.

Scientists have known for decades that methionine deficiency can block the growth of many types of cancer, but the underlying mechanisms have puzzled researchers.

"We've shown that removing methionine can have a specific effect on a molecular pathway that regulates cell death to increase the vulnerability of cancer cells to treatments that target this pathway," Cryns says. "What's particularly exciting about our findings is that they suggest that a dietary intervention can increase the effectiveness of a targeted cancer therapy."

Specifically, the researchers showed that when triple-negative breast cancer cells were deprived of methionine -- an essential nutrient abundant in meat, fish, some legumes and nuts, but low in fruits and vegetables -- the stressed cancer cells responded by increasing the amount of a receptor on the cell's surface called TRAIL-R2.

This resulted in the breast cancer cells becoming very sensitive to an antibody that binds to TRAIL-R2 on the surface of the cancer cells and triggers them to die.

"What we didn't anticipate is that the normal, non-cancer cells didn't upregulate the receptor under methionine stress the way the tumor cells did," Cryns says. "This shows that diet can help expose a targetable defect in cancer cells."

Lead author Elena Strekalova, a scientist in the Cryns lab, and the research team fed mice with triple-negative breast tumors a diet lacking methionine and treated them with an antibody that binds to the TRAIL-R2 receptor. Mice, like humans, can tolerate a methionine-free diet for a short period of time. The combination of diet and antibody was more effective at shrinking the breast tumors and preventing metastasis to the lungs than either treatment alone.

The University of Wisconsin team believes that their laboratory studies may pave the way for a clinical trial in breast cancer patients to examine the effectiveness of a low-methionine diet in combination with a TRAIL-R2 monoclonal antibody. When used alone, TRAIL-R2 antibodies have not been effective in patients with metastatic solid tumors.

Cryns hopes that brief exposure to a low methionine diet will boost the effectiveness of TRAIL-R2 antibodies in patients, as it did in mice. "We still have much to learn," Cryns indicates, "but we believe that uncovering the molecular effects of specific nutritional interventions like a low methionine diet will open up new treatment options for cancer."

Story Source:

Materials provided by University of Wisconsin-Madison. Original written by Susan Lampert Smith. Note: Content may be edited for style and length.

Journal Reference:

1.E. Strekalova, D. Malin, D. M. Good, V. L. Cryns. Methionine Deprivation Induces a Targetable Vulnerability in Triple-Negative Breast Cancer Cells by Enhancing TRAIL Receptor-2 Expression. Clinical Cancer Research, 2015; 21 (12): 2780 DOI: 10.1158/1078-0432.CCR-14-2792

yoga_girl

Triple Negative Breast Cancer – Diet

University of Massachusetts Medical School

Methionine deprivation suppresses triple-negative breast cancer metastasis in vitro and in vivo

Authors

Hyein Jeon, Jae Hwan Kim, Eunjung Lee, Young Jin Jang, Joe Eun Son, Jung Yeon Kwon, Tae-Gyu Lim, Sunghoon Kim, Jung Han Yoon Park, Jong-Eun Kim, and Ki Won Lee

Keywords: cancer therapy metastasis, methionine, triple-negative breast cancer

Creative Commons License: This work is licensed under a Creative Commons Attribution 3.0 License.

Rights and Permissions: Citation: Oncotarget. 2016 Oct 11;7(41):67223-67234. doi: 10.18632/oncotarget.11615.

Link to article on publisher's site: http://escholarship.umassmed.edu/oapubs/2923/

8-26-2016

Methionine deprivation suppresses triple-negative breast cancer metastasis in vitro and in vivo

UMMS Affiliation: Program in Molecular Medicine

Date: 8-26-2016

Document Type: Article

Disciplines: Cancer Biology

Abstract

Nutrient deprivation strategies have been proposed as an adjuvant therapy for cancer cells due to their increased metabolic demand. We examined the specific inhibitory effects of amino acid deprivation on the metastatic phenotypes of the human triple-negative breast cancer (TNBC) cell lines MDA-MB-231 and Hs 578T, as well as the orthotopic 4T1 mouse TNBC tumor model. Among the 10 essential amino acids tested, methionine deprivation elicited the strongest inhibitory effects on the migration and invasion of these cancer cells. Methionine deprivation reduced the phosphorylation of focal adhesion kinase, as well as the activity and mRNA expression of matrix metalloproteinases MMP-2 and MMP-9, two major markers of metastasis, while increasing the mRNA expression of tissue inhibitor of metalloproteinase 1 in MDA-MB-231 cells. Furthermore, methionine restriction downregulated the metastasis-related factor urokinase plasminogen activatior and upregulated plasminogen activator inhibitor 1 mRNA expression. Animals on the methionine-deprived diet showed lower lung metastasis rates compared to mice on the control diet. Taken together, these results suggest that methionine restriction could provide a potential nutritional strategy for more effective cancer therapy.

Rights and Permissions

Citation: Oncotarget. 2016 Oct 11;7(41):67223-67234. doi: 10.18632/oncotarget.11615. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Keywords: cancer therapy metastasis, methionine, triple-negative breast cancer

Journal Title: Oncotarget

PubMed ID: 27579534

Repository Citation

Jeon, Hyein; Kim, Jae Hwan; Lee, Eunjung; Jang, Young Jin; Son, Joe Eun; Kwon, Jung Yeon; Lim, Tae-Gyu; Kim, Sunghoon; Park, Jung Han Yoon; Kim, Jong-Eun; and Lee, Ki Won, "Methionine deprivation suppresses triple-negative breast cancer metastasis in vitro and in vivo" (2016). Open Access Articles. 2923.
http://escholarship.umassmed.edu/oapubs/2923

Creative Commons License

This work is licensed under a Creative Commons Attribution 3.0 License.

sas-schatzi

Oh Thank you Yogagirl

sas-schatzi

Another request, can you write it common language as what was recommended? I know pita, but pretty please?

yoga_girl

Will look into the translation of this for you.

yoga_girl

Alternative Cancer Treatment

Chaga mushroom

Common Names: Cinder conk, Birch conk, Clinker polypore

Memorial Sloan Kettering Cancer Center

To read more detail regarding this article, select the link.

https://www.mskcc.org/cancer-care/integrative-medicine/herbs/chaga-mushroom

Search tags: alternative cancer treatment, mushrooms, folk medicine, fatigue, inflammation, mental sharpness, cancer prevention, immune system, liver function

Human studies on the anticancer and immuno-stimulating effects of chaga mushroom are needed.
Chaga mushroom is found in Russia and has been used in folk medicine for various ailments across northern Europe. Laboratory and animal studies show that compounds in chaga can kill cancer cells selectively and stimulate the immune system. It may also have benefits such as reductions in fatigue and inflammation, as well as increased mental sharpness. However, clinical trials are needed to confirm chaga's safety and effectiveness for these uses. In addition, chaga may interact with some drugs and is high in oxalates, which may prevent the absorption of some nutrients and can be toxic in high doses.

To prevent and treat cancer-

Purported Uses:

Laboratory and animal studies show that chaga can inhibit cancer progression. Studies in humans are needed.

• To stimulate the immune system
• Laboratory and animal studies show that chaga can activate some types of immune cells. Studies in humans are needed.
• To reduce inflammation
• Laboratory and animal studies suggest anti-inflammatory effects. A small study in humans also suggested a reduction in markers related to inflammation. Additional clinical trials for this use are needed.
• To protect the liver
• Although protective effects have been reported, these benefits have not yet been studied or confirmed

Do Not Take If:

• You are taking blood-thinning medications (eg, warfarin): Laboratory studies suggest that chaga may cause additional effects.
• You are taking diabetic medications: Laboratory studies suggest that chaga may also lower blood sugar, causing additional effects.

Side Effects:

• No clinical trials have assessed chaga's safety, so there is a lack of information on possible side effects.

Case report

• Kidney damage/disease: In a 72-year-old Japanese woman with liver cancer, caused by taking chaga daily for 6 months.

Special Point

• Chaga is high in oxalates, which may prevent the absorption of some nutrients and can be toxic in high doses.

References:

• Youn MJ, Kim JK, Park SY, et al. Chaga mushroom (Inonotus obliquus) induces G0/G1 arrest and apoptosis in human hepatoma HepG2 cells. World J Gastroenterol. Jan 28 2008;14(4):511-517.
• Hyun KW, Jeong SC, Lee DH, Park JS, Lee JS. Isolation and characterization of a novel platelet aggregation inhibitory peptide from the medicinal mushroom, Inonotus obliquus. Peptides. Jun 2006;27(6):1173-1178.
• Park YM, Won JH, Kim YH, et al. In vivo and in vitro anti-inflammatory and anti-nociceptive effects of the methanol extract of Inonotus obliquus. J Ethnopharmacol. Oct 3 2005;101(1-3):120-128.
• Sun JE, Ao ZH, Lu ZM, et al. Antihyperglycemic and antilipidperoxidative effects of dry matter of culture broth of Inonotus obliquus in submerged culture on normal and alloxan-diabetes mice. J Ethnopharmacol. Jun 19 2008;118(1):7-13.
• Lee SH, Hwang HS, Yun JW. Antitumor activity of water extract of a mushroom, Inonotus obliquus, against HT-29 human colon cancer cells. Phytother Res. Apr 15 2009.
• Zhong XH, Ren K, Lu SJ, Yang SY, Sun DZ. Progress of research on Inonotus obliquus. Chin J Integr Med. Apr 2009;15(2):156-160.
• Youn MJ, Kim JK, Park SY, et al. Potential anticancer properties of the water extract of Inonotus [corrected] obliquus by induction of apoptosis in melanoma B16-F10 cells. J Ethnopharmacol. Jan 21 2009;121(2):221-228.
• Najafzadeh M, Reynolds PD, Baumgartner A, Jerwood D, Anderson D. Chaga mushroom extract inhibits oxidative DNA damage in lymphocytes of patients with inflammatory bowel disease. Biofactors. 2007;31(3-4):191-200.
• Ham SS, Kim SH, Moon SY, et al. Antimutagenic effects of subfractions of Chaga mushroom (Inonotus obliquus) extract. Mutat Res. Jan 10 2009;672(1):55-59.
• Caifa Chen WZ, Gao X, Xiang X, et al. Aqueous Extract of Inonotus obliquus (Fr.) Pilat (Hymenochaetaceae) Significantly Inhibits the Growth of Sarcoma 180 by Inducing Apoptosis. Am J Pharmacol Toxicol. 2007. 2(1):10-17.
• Shashkina MY, Shashkin PN, Sergeev AV. Chemical and Medicobiological Properties of Chaga (Review). Pharmaceutical Chemistry Journal 2006. 40(10):560-568.
• Glamoclija J, Ciric A, Nikolic M, et al. Chemical characterization and biological activity of Chaga (Inonotus obliquus), a medicinal "mushroom". J Ethnopharmacol. Mar 13 2015;162:323-332.
• Ning X, Luo Q, Li C, et al. Inhibitory effects of a polysaccharide extract from the Chaga medicinal mushroom, Inonotus obliquus (higher Basidiomycetes), on the proliferation of human neurogliocytoma cells. Int J Med Mushrooms. 2014;16(1):29-36.
• Pan HH, Yu XT, Li T, et al. Aqueous extract from a Chaga medicinal mushroom, Inonotus obliquus (higher Basidiomycetes), prevents herpes simplex virus entry through inhibition of viral-induced membrane fusion. Int J Med Mushrooms. 2013;15(1):29-38.
• Ying YM, Zhang LY, Zhang X, et al. Terpenoids with alpha-glucosidase inhibitory activity from the submerged culture of Inonotus obliquus. Phytochemistry. Dec 2014;108:171-176.
• Ko SK, Jin M, Pyo MY. Inonotus obliquus extracts suppress antigen-specific IgE production through the modulation of Th1/Th2 cytokines in ovalbumin-sensitized mice. J Ethnopharmacol. Oct 11 2011;137(3):1077-1082.
• Yoon TJ, Lee SJ, Kim EY, et al. Inhibitory effect of chaga mushroom extract on compound 48/80-induced anaphylactic shock and IgE production in mice. Int Immunopharmacol. Apr 2013;15(4):666-670.
• Giridharan VV, Thandavarayan RA, Konishi T. Amelioration of scopolamine induced cognitive dysfunction and oxidative stress by Inonotus obliquus - a medicinal mushroom. Food Funct. Jun 2011;2(6):320-327.
• Mishra SK, Kang JH, Kim DK, et al. Orally administered aqueous extract of Inonotus obliquus ameliorates acute inflammation in dextran sulfate sodium (DSS)-induced colitis in mice. J Ethnopharmacol. Sep 28 2012;143(2):524-532.
• Yue Z, Xiuhong Z, Shuyan Y, et al. Effect of Inonotus Obliquus Polysaccharides on physical fatigue in mice. J Tradit Chin Med. Aug 2015;35(4):468-472.
• Kang JH, Jang JE, Mishra SK, et al. Ergosterol peroxide from Chaga mushroom (Inonotus obliquus) exhibits anti-cancer activity by down-regulation of the beta-catenin pathway in colorectal cancer. J Ethnopharmacol. Sep 15 2015;173:303-312.
• Lee HS, Kim EJ, Kim SH. Ethanol extract of Innotus obliquus (Chaga mushroom) induces G1 cell cycle arrest in HT-29 human colon cancer cells. Nutr Res Pract. Apr 2015;9(2):111-116.
• Zhao LW, Zhong XH, Yang SY, et al. Inotodiol inhabits proliferation and induces apoptosis through modulating expression of cyclinE, p27, bcl-2, and bax in human cervical cancer HeLa cells. Asian Pac J Cancer Prev. 2014;15(7):3195-3199.
• Kikuchi Y, Seta K, Ogawa Y, et al. Chaga mushroom-induced oxalate nephropathy. Clin Nephrol. Jun 2014;81(6):440-444.
• Sun Y, Yin T, Chen XH, et al. In vitro antitumor activity and structure characterization of ethanol extracts from wild and cultivated Chaga medicinal mushroom, Inonotus obliquus (Pers.:Fr.) Pilat (Aphyllophoromycetideae). Int J Med Mushrooms. 2011;13(2):121-130.
• Wang Q, Mu H, Zhang L, et al. Characterization of two water-soluble lignin metabolites with antiproliferative activities from Inonotus obliquus. Int J Biol Macromol. Mar 2015;74:507-514.

yoga_girl

The 7 Essentials – Breast Cancer

To read the full article, select the link.

https://www.cancertutor.com/breast-cancer/#The-7-Essentials

Search tags: food as medicine, toxic exposure, balanced energy, heal emotional wounds, biological dentistry, therapeutic plants, early detection options, diagnosed with BC now what

Dr. Veronique Desaulniers

Most women are overwhelmed, confused, and frustrated when they get a breast cancer diagnosis.

"Maybe they want to do traditional treatments and incorporate some evidence-based natural medicine, or maybe they just want to do natural medicine," she says.

Regardless of whether a woman with breast cancer chooses conventional treatment, evidence-based natural medicine, or a combination of both, there are things you can do to help, according to Dr. V. And this is where her 7 Essentials play a large role in healing.

"If you look at the seven essentials, essential number one is, let food be your medicine. So we advise them about food, and what to eat, what not to eat and monitoring their blood sugar, and changes," she explains. "Foods that are going to make cancer grow and foods that are going to help heal the body, that's just one of the topics." [9]

Essential 1: Let Food Be Your Medicine

Hippocrates, the Greek physician who lived more than 1500 years ago, made the astounding connection with food and how it could heal the body. However, the wisdom of the "founding father of modern medicine" has been ignored by mainstream medical and governmental agencies. Food is the foundation of our health. Food fuels our cells and organs. If we ingest toxic, dead food, then guess what happens to our bodies? Yes, they become toxic, diseased and die prematurely.

Essential 2: Reduce Your Toxic Exposure

According to the University Of Columbia School Of Public health, "95 percent of all cancer is due to diet and the accumulation of toxins." There are many simple steps that you can take in order to reduce your daily exposure to environmental toxins in your home and in your body. Detoxification of the liver and colon play a major role in improving your health.

Essential 3: Balance Your Energy

Everything is energy. In fact, according to a Nobel Prize Laureate, Carlo Rubbia, we are only 1 billionth physical matter…the rest is ALL energy. If the foundation of the body is energy and light, then it makes sense that we keep that energy balanced and free of interference. Your Central Nervous System, your Acupuncture Meridian System and your hormones have a huge impact on the body's energy system. There are also numerous healing arts and practices that balance the body.

Essential 4: Heal Your Emotional Wounds

Have you ever felt stressed out about something and you noticed that your neck muscles or jaw felt really tight? Remember feeling that pit in your stomach or that ache in your solar plexus? That is an example of your "e-motions" or "energy in motion" getting stuck. Scientists have speculated about the emotional connection to dis-ease for years, but now with the study of "psycho-neuro-immunology", we understand how stress impacts our health. In fact, we now have proof that your DNA contracts and relaxes in response to your mood.

Essential 5: Embrace Biological Dentistry

Your teeth are an intricate part of your body…not a separate entity that can be drilled, poked and stuffed with toxic poisons, without having an impact on the rest of your body. Amalgam fillings do NOT belong in your mouth because of the high mercury content. Mercury is one of the most toxic substances on the planet and the effect on the Immune System and overall health have been well documented. Having worked with Bio-energetic Testing devices for over 20 years, I repeatedly saw the relationship between specific diseased organs and the dental meridians. Women with Breast Cancer invariably had a huge filling or root canal in the tooth corresponding to the breast meridian.

Essential 6: Repair Your Body with Therapeutic Plants

As far back as the Egyptian and Persian dynasties, the use of medicinal plants is well recorded in the journals of history. North American natives also used plants extensively to heal various illnesses. Specific plants and herbs contain special compounds that nourish, stimulate, tone, strengthen, detoxify and speed up the healing process. In fact, there are specific plant compounds that actually kill cancer cells without harming the healthy cells of the body.

Essential 7: Adopt Very Early Detection

Thermography: Are you tired of the "big squeeze", aka mammograms? Ever wonder if all that compression and radiation to the breast might be causing some harm to your breast and your body? Digital Infrared Thermal Imaging, also known as Thermography, can detect abnormal breast patterns 5-8 years before tumors are visible on a mammogram. How's that for early detection! Cancer Profiles: There are many blood tests that can detect the development of cancer on a cellular level, before they are detected with conventional tests. Stop cancer before it starts with blood work that detects enzymes and hormones that are produced by cancer cells.

You've been diagnosed with breast cancer, now what?

A diagnosis of breast cancer is not an automatic death sentence, according to Dr. Véronique Desaulniers.

"The first thing you need to realize is that cancer is not a death sentence, number one," says Dr. V. "And it's not an emergency critical situation, unless it's obviously blocking an artery, or involved with your heart, or blocking your gut. I think the key is balance and the key is making an informed decision about what's right for you. It's not a critical emergency situation, so you have time. So don't make any rash decisions and think about it, meditate about it, pray about it and go inward and ask for guidance, and the answers will come.

"And you have to do your due diligence. You do have to get on the Internet, you do have to read books. … Look at things that are evidence-based, and in the end it comes down to what is right for you and your family, your immediate family. Because everybody's gonna have an opinion, but they're not the ones facing the diagnosis.

"You have to feel good about your decision and you have to feel very optimistic and very powerful in your decision. The most potent medicine to me is your belief system. Because if you believe that chemotherapy is going to heal you and you're going to have a great life afterwards, chances are you will, if that's your really, strong belief system. If you really believe that evidence-based natural medicine is the way for you to go, that's going to affect your healing. Because your mind is a powerful thing."

To read the full article, select the link.

yoga_girl

Alternative Cancer Treatments

Frequency Generator Protocols

To read more on this article, select the link.

https://www.cancertutor.com/freqgenerators/

Search tags: frequency generator protocols, cancer cells, cancer research, alternative cancer treatments

Dr. Royal Raymond Rife

http://www.rifevideos.com/

Dr. Rife discovered one of the most groundbreaking medical tools in the last hundred years. He invented the world's best optical microscope and subsequently discovered that the microbes in cancer cells could be totally devitalized by radio frequencies which left patients unharmed. Due to financial and political interests, his discoveries were driven underground. (1)

Today, the Independent Cancer Research Foundation, Inc. (ICRF) is basing their research on true science instead of politics. People who are suffering from cancer and other diseases may participate in their own discovery with in-home research into the effects high radio frequencies. Cancer Tutor will introduce this simple, yet life-changing technology on this web page for those who desire to implement a complete step-by-step protocol for their particular situation.

Dr. Rife's work culminated with The Smithsonian Institution publishing the following quote in their 1944 annual report: "Disease organisms such those of tuberculosis, cancer, sarcoma, typhoid, and others may be observed to succumb when exposed to certain lethal frequencies peculiar to each individual organism, and directed upon them by rays conveying a wide range of waves."

Overview of High RF Frequency Generators

There are two instruments used with the "High RF Frequency Protocol" which are recommended by Cancer Tutor; a frequency generator which is connected to an amplifier.

The more powerful non-contact broadcast system consists of a 20 Mhz sweep/function generator and an oscillator amplifier with a variable carrier frequency. First is the plasma method high RF generator instrument system which consists of three main components: 1) a high RF 20 MHz sweep/function generator, 2) an RF oscillator amplifier which broadcasts multiple frequencies and sidebands via 3) a plasma ray tube antenna. It emits a continuous frequency or wave in the air, much like a small radio tower.

Second is the contact method which creates RF electrical currents by the use of a 1) high RF 20 MHz sweep/function generator and a 2) 15-watt amplifier in which electrodes are plugged in and come in contact with the body.

Microbiologist, Dr. Royal R. Rife used the standard high frequency generating equipment of his day. These two high RF frequency generator systems output the frequencies using the same method used in the original "Rife Machines" of the 1930s, which were designed by Rife. The difference today is that these devices use modern, high-tech circuits.

Both devices are so gentle that the person using one of them barely knows the device is turned on.

Warning: Almost all of the frequency generators on the market today which are called "Rife Machines" output only low audio frequencies. They cannot output the high RF frequencies which Dr. Rife used.

Dr. Rife was a microbiologist who knew that cancer was caused by unique viral microbes which were inside of cancer cells. He called them BX and BY cancer viruses. (2) It is also now known that the Helicobacter Pylori (yes, the same H. Pylori which lives in the stomach) can be another cancer-causing microaerophilic bacterium. (3)

Researchers now know that the original Rife Machines had two frequencies. One frequency was to kill the virus and the other frequency was a carrier frequency to "carry" the first frequency through the cell membrane to the inside of the cancer cells, where the cancer-causing microbes were located. See the What Causes Cancer article for more information about how microbes cause cells to be cancerous.

When Dr. Rife was able to kill the virus and/or bacteria which were inside of a cancer cell, the cancer cell was able to restore its metabolism and become a normal cell (i.e. "revert" into a normal cell). (4)

Let me say that again a different way: It is possible to kill the microbes which are inside of the cancer cells, which allows the cancer cells to restore their metabolism and thus revert into normal cells.

This is the ideal way to attack cancer because there are no dead cancer cells to create debris and there are no dead healthy cells which are killed in the attempt to kill the cancer cells. This method can be used more quickly than tactics that build the immune system or kill cancer cells.

To read more on this article, select the link.

yoga_girl

Alternative Cancer Treatments

Cellect-Budwig Protocol

Mike Vrentas

To read more on this article, select the link.

https://www.cancertutor.com/breast-cancer/#Highly-recommended-treatment-after-Cellect-Budwig

Search tags:Alternative cancer treatments, Cellect-Budwig Protocol

Every breast cancer patient needs to become an expert on hormones, iodine, and cancer. Mike Vrentas — who supports the Cellect-Budwig Protocol for home use, and should support all breast cancer patients who treat their cancer at home — discusses these topics in his lectures.

Recommended primary treatment: Cellect-Budwig Protocol

The Cellect-Budwig Protocol is the highly recommended protocol for breast cancer for two reasons.

1. It is one of the best alternative cancer treatments on earth. It starts working quickly, helps shrink tumors, helps reduce pain, etc.
2. Mike Vrentas is an expert in the protocol he designed. Vrentas is an expert in dealing with advanced breast cancer cases, including large tumors. He also is an expert in dealing with the dental issues facing breast cancer patients and the hormone and iodine issues facing breast cancer cases. Both the protocol and the telephone support make the choice of this protocol a simple one.

This protocol consists of the superb product Cellect, vegetable juicing, laetrile, plenty of sunshine (without sun blockers or suntan lotion) to get Vitamin D, and other protocols.

A key element of this protocol is the High RF Frequency Generator with Plasma Amplifier, which is an electro-medicine device that acts much like a radio tower, meaning it emits a very gentle electrical signal through the air.

This device may help with the dental infections, but it will definitely help with any infection in the breasts. But it is primarily part of the cancer treatment. Thus, it can help both with the cancer treatment — no matter where the cancer is, even if it is in the lymph nodes — and the infection.

It is important to use the liver and lymph protocols (i.e. Auto-Channels) of the High RF Frequency Generator in addition to the cancer protocols.

There are several things which conflict with the Cellect, such as coral calcium (which provides too much alkalinity with the Cellect), or conflict with the Budwig, such as Vitamin C.

There are recommended treatments to be used with the Cellect-Budwig Protocol. For example, Fucoidan kills cancer cells faster than Cellect-Budwig and is synergistic with Cellect-Budwig. The MSM/CS protocol deals with infections which may exist in the bloodstream from the dental infections.

MSM products - search

To read more on the article, select the link.

yoga_girl

What is Peripheral Neuropathy

National Comprehensive Cancer Network

https://www.nccn.org/

https://www.nccn.org/members/network.aspx (clinical research)

Peripheral neuropathy is caused by damage to your peripheral nerves. Peripheral nerves are nerves that are not located in the brain or spinal cord. They are found throughout your body and help you feel things. They also control the function of your organs. The damage is usually to nerves in the hands, feet, arms, and legs.

Cancer treatments are meant to kill cancer cells. A side-effect is that normal cells can also be damaged or killed. When chemotherapy damages peripheral nerves, it is called chemotherapy-induced peripheral neuropathy, or CIPN. Other types of cancer treatments can also cause peripheral neuropathy.

What Cancer Treatments Cause Peripheral Neuropathy?

Drugs for cancer treatment are the most common cause of peripheral neuropathy. But peripheral neuropathy can be also caused by surgery, radiation, the tumor pressing directly on nerves, chemicals released by tumors, and infections.

Peripheral neuropathy can be a side effect of these drugs:

• Platinum drugs, such as cisplatin (Platinol), oxaliplatin (Eloxatin), carboplatin (Paraplatin)
• Taxanes, such as paclitaxel (Taxol, Abraxane), docetaxel (Taxotere)
• Vinca alkaloids, such as vincristine (Oncovin, Vincasar), vinorelbine (Navelbine), and vinblastine (Velban)
• Podophyllotoxins, such as etoposide (Etopophos, VePesid, Toposar, VP-16) and teniposide (Vumon)
• Epothilones, such as ixabepilone (Ixempra)
• Thalidomide (Thalomid) and lenalidomide (Revlimid)
• Bortezomib (Velcade)
• Interferon
• Methotrexate (Rheumatrex, Trexall, Amethopterin, MTX)
• Fluorouracil (5-FU, Adrucil)
• Cytarabine (Cytosar-U)

What are the symptoms of peripheral neuropathy?There are three types of peripheral nerves: sensory, motor, and autonomic. If damage occurs to sensory nerves, you may feel pain, tingling, or numbness. If the damage is mainly to the motor nerves, you may feel weak or off-balance. If the damage is to the autonomic nerves (which control organ function) you may have constipation or dizziness.Symptoms tend to start in the fingers and toes, progressing to hands and feet, then arms and legs. It can become hard to pick things up, hold on to things, walk, and perform tasks like buttoning your shirt.Symptoms can begin any time after your treatment begins. They may start suddenly. Symptoms are usually mild at the beginning and slowly worsen. Symptoms also get better slowly, usually over the course of a few months. Unfortunately, sometimes the damage is permanent and symptoms do not go away.

Common symptoms are:

• Tingling
• Numbness
• Weakness
• Cramping
• Burning
• Pain (may be there all the time or may come and go, like shooting or stabbing pain)
• Not being able to feel things that are touched
• Not being able to sense cold or heat
• Sensitivity to cold or heat or touch
• Feeling off balance
• Dizziness
• Having trouble walking
• ConstipationTell your doctor as soon as possible if you experience any of these symptoms.

Who is at Increased Risk for Peripheral Neuropathy?

Thirty percent to 40 percent of patients treated with chemotherapy develop some degree of peripheral neuropathy. Doctors cannot predict who will develop peripheral neuropathy, but some things make you more likely to develop it:

• Having had chemotherapy, radiation, or surgery before
• Needing a high dose or long course of treatment
• Taking more than 1 drug that can cause neuropathy
• Having a history of alcohol abuse
• Being a diabetic
• Having HIV or AIDS
• Having severe malnutrition
• Having multiple myeloma, lymphoma, or lung or breast cancer
• Having nerve damage from previous injury or illnessH

How is Peripheral Neuropathy Diagnosed?

Tell your doctor if you think that you have peripheral neuropathy. Your doctor may watch you walk and test your reflexes, strength, and ability to feel touch. The doctor may also perform nerve conduction tests, which measure the strength and speed of electrical signals sent by your nerves in response to small shocks.

Can Peripheral Neuropathy be Prevented?

There is no proven way to prevent nerve damage in patients undergoing treatment. It probably helps to give less of the cancer drug. "Stop and go" schedules are also being tested to see if a pre-planned break in treatment prevents neuropathy without reducing the effectiveness of the cancer treatment.Many drugs and supplements are being tested to prevent peripheral neuropathy in patients with cancer. Results have been mixed. More research is needed.

Some prevention treatments being tested are:

• Calcium and magnesium infusion
• Glutathione
• Acetyl-L-carnitine
• Alpha-lipoic acid
• Acetylcysteine
• Glutamine
• Amifostine (Ethyol)
• Xaliproden
• Org 2766
• Carbamazepine
• Vitamin E
• Vitamins B1 and B12

Check with your doctor before taking any supplements. They can make your cancer treatments work less well and might cause problematic side effects, especially if taken at the wrong dose.

If you develop neuropathy symptoms during treatment, your treatment might be stopped. Your treatment can be restarted after you feel better or if the tumor starts to grow again. This treatment break can prevent the nerve damage from getting worse. Without it, your symptoms might worsen and become permanent.

How is Peripheral Neuropathy Treated?

There are no treatments for peripheral neuropathy that fix the nerve damage. Instead, treatment is given to relieve and manage symptoms. And unfortunately, many of the treatments are not proven to help and have side effects of their own. Many patients do find relief, however, with combinations of drugs, dietary supplements, and other types of therapy.

Some of the same drugs and supplements being studied for prevention are also used for treatment. Your doctor may prescribe drugs to help manage the symptoms of peripheral neuropathy, such as:

• An antidepressant (ex, duloxetine, venlafaxine, amitriptyline) for tingling and numbness
• An anticonvulsant (ex, phenytoin, carbamazepine) for pain
• A muscle-relaxant (ex, baclofen)
• An analgesic (ex, ketamine)
• A steroid for short-term use
• Lidocaine patches
• Capsaicin cream (made from chili pepper extract)
• Opioids or narcotics for severe pain

A gentle laxative for constipationYour doctor may recommend some dietary supplements, such as:

• A combination B vitamin
• Folic acid
• Magnesium
• Glutamine

There are other treatments that may help you manage your symptoms, including:

• Transcutaneous nerve stimulation (TENS, in which nerves are stimulated to release endorphins with a gentle electrical current)
• Occupational and/or physical therapy
• Massage
• Exercise
• Guided imagery, meditation, relaxation, and distraction techniques
• Biofeedback
• Acupuncture

What Else can I Do?

When you cannot feel your hands and feet, you are at risk for injuries. Also, injuries can go unnoticed and become infected. You must be careful to protect yourself.

Here are some things you can do:

• Wear good footwear to protect your feet from injury
• Wear gloves when using your hands to protect them from injury
• Inspect your skin for injuries at least once each day
• Be extra careful when handling sharp objects or hot liquids
• Be extra careful on stairs; use the handrail
• Use non-skid surfaces in the bath and other slippery spots
• Set your hot water heater to 120°F or lower to prevent burns
• Use a cane or other device if you have trouble with balance
• Ask for help

In addition, avoid alcohol because it can make symptoms worse. Keep the temperature in your home at a comfortable level because extreme hot or cold can make symptoms worse.

Finally, be sure to get the emotional support you need. You may find a support group near you at www.neuropathy.org. You can also ask your doctor for a referral to a mental health professional.

Questions for Your Doctor

• Can the cancer treatments you are suggesting cause neuropathy?
• What symptoms should I look for?
• Are there different, safer treatments or treatment schedules we can use?
• Would these different treatments or schedules affect my chances for a cure?
• Are there any clinical trials in which I can participate for prevention of neuropathy?
• What can I do to manage my symptoms?
• Are there any clinical trials in which I can participate for treatment of neuropathy?
• What local resources can help me deal with my symptoms?

yoga_girl

Nutrition and cancer: A review of the evidence for an anti-cancer diet

Several diets reviewed in this research: American Omnivorous Diet, Nurses' Health Study, Health Professionals Follow-up Study, Hallelujah Diet, Gerson Therapy, Shanghai Breast Cancer Study (China), Physicians' Health Study, Women's healthy Eating and Living (WHEL) Study

https://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-3-19

To review the full research, all charts and outcome, select the link. Sections of this research have been extracted for breast cancer, other cancers are listed in the full research article.

Nutrition Journal20043:19

https://doi.org/10.1186/1475-2891-3-19

© Donaldson; licensee BioMed Central Ltd. 2004

Received: 28 September 2004; Accepted: 20 October 2004; Published: 20 October 2004

Contact us: BioMed Central Ltd; Editorial email: Jonah.Sescar@springernature.com; Support email: info@biomedcentral.com

Abstract

It has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone.

Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk.

Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures.

When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

Review

Background

The field of investigation of the role of nutrition in the cancer process is very broad. It is becoming clearer as research continues that nutrition plays a major role in cancer. It has been estimated by the American Institute for Cancer Research and the World Cancer Research Fund that 30–40 percent of all cancers can be prevented by appropriate diets, physical activity, and maintenance of appropriate body weight [1]. It is likely to be higher than this for some individual cancers.

Most of the research on nutrition and cancer has been reductionist; that is, a particular food or a nutrient has been studied in relation to its impact on tumor formation/regression or some other end point of cancer at a particular site in the body. These studies are very helpful in seeing the details of the mechanisms of disease. However, they do not help give an overall picture of how to prevent cancer on a dietary level. Even less, they tell little of how to eat when a person already has a cancer and would like to eat a diet that is favorable to their recovery.

This review will focus on those dietary factors which has been shown to be contribute to increased risk of cancer and then on those additional protective dietary factors which reduce cancer risk. Finally, some whole-diet studies will be mentioned which give a more complete picture of how these individual factors work together to reduce cancer risk.

Over Consumption of Energy (Calories)

Eating too much food is one of the main risk factors for cancer. This can be shown two ways: (1) by the additional risks of malignancies caused by obesity, and (2) by the protective effect of eating less food.

Obesity has reached epidemic proportions in the United States. Sixty-four percent of the adult population is overweight or obese [2]. About 1 in 50 are now severely obese (BMI > 40 kg/m2) [3]. Mokdad et al [4] found that poor diet and physical inactivity was the second leading cause of death (400,000 per year in the USA), and would likely overtake tobacco as the leading cause of death.

It was estimated in a recent study, from a prospective cancer prevention cohort, that overweight and obesity accounted for 14 percent of all cancer deaths in men and 20 percent of those in women [5]. Significant positive associations were found between obesity and higher death rates for the following cancers: esophagus, colon and rectum, liver, gallbladder, pancreas, kidney, stomach (in men), prostate, breast, uterus, cervix, and ovary [5]. The authors estimated that over 90,000 cancer deaths per year could be avoided if the adult population all maintained a normal weight (BMI < 25.0) [5]. Clearly, obesity is a major risk factor for cancer.

Fruits and Vegetables

One of the most important messages of modern nutrition research is that a diet rich in fruits and vegetables protects against cancer. (The greatest message is that this same diet protects against almost all other diseases, too, including cardiovascular disease and diabetes.) There are many mechanisms by which fruits and vegetables are protective, and an enormous body of research supports the recommendation for people to eat more fruits and vegetables.

Block et al [80] reviewed about 200 studies of cancer and fruit and vegetable intake. A statistically significant protective effect of fruits and vegetables was found in 128 of 156 studies that gave relative risks. For most cancers, people in the lower quartile (1/4 of the population) who ate the least amount of fruits and vegetables had about twice the risk of cancer compared to those who in the upper quartile who ate the most fruits and vegetables. Even in lung cancer, after accounting for smoking, increasing fruits and vegetables reduces lung cancer; an additional 20 to 33 percent reduction in lung cancers is estimated [1].

Steinmetz and Potter reviewed the relationship between fruits, vegetables, and cancer in 206 human epidemiologic studies and 22 animal studies [81]. They found "the evidence for a protective effect of greater vegetable and fruit consumption is consistent for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon." Vegetables, and particularly raw vegetables, were found to be protective; 85% of the studies that queried raw vegetable consumption found a protective effect. Allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes also had a fairly consistent protective effect [81]. Allium vegetables (garlic, onion, leeks, and scallions) are particularly potent and have separately been found to be protective for stomach and colorectal cancers [82, 83] and prostate cancer [84].

There are many substances that are protective in fruits and vegetables, so that the entire effect is not very likely to be due to any single nutrient or phytochemical. Steinmetz and Potter list possible protective elements: dithiolthiones, isothiocyanates, indole-32-carbinol, allium compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene (and other carotenoids), lycopene, selenium, vitamin E, flavonoids, and dietary fiber [81].

A joint report by the World Cancer Research Fund and the American Institute for Cancer Research found convincing evidence that a high fruit and vegetable diet would reduce cancers of the mouth and pharynx, esophagus, lung, stomach, and colon and rectum; evidence of probable risk reduction was found for cancers of the larynx, pancreas, breast, and bladder [1].

Many of the recent reports from prospective population-based studies of diet and cancer have not found the same protective effects of fruits and vegetables that were reported earlier in the epidemiological and case-control studies [reviewed in [85]]. One explanation is that people's memory of what they ate in a case-cohort study may have been tainted by their disease state. Another problem might be that the food frequency questionnaires (FFQ) used to measure food intake might not be accurate enough to detect differences. Such a problem was noted in the EPIC study at the Norfolk, UK site. Using a food diary the researchers found a significant correlation between saturated fat intake and breast cancer, but using a FFQ there was no significant correlation [86]. So, inaccurate measurement of fruit and vegetable intake might be part of the explanation as well.

It must be noted that upper intakes of fruits and vegetables in these studies are usually within the range of what people on an American omnivorous diet normally eat. In the Nurses Health Study the upper quintiles of fruit and vegetable intake were 4.5 and 6.2 servings/day, respectively [87]. Similarly, the upper quintiles of fruit and vegetable intake in the Health Professionals Follow-up Study were 4.3 and 5.4 serving/day for fruits and vegetables, respectively [87]. Intakes of fruits and vegetables on the Hallelujah Diet are much higher, with median reported intakes of six servings of fruits (646 g/day) and eleven servings of vegetables per day (971 g/day) [88] in addition to a green powder from the juice of barley leaves and alfalfa that is equivalent to approximately another 100 g/day of fresh dark greens. So, it is very possible that the range of intakes in the prospective population based studies do not have a wide enough intake on the upper end to detect the true possible impact of a very high intake of fruits and vegetables on cancer risk.

Cruciferous Vegetables

Cruciferous vegetables (broccoli, cauliflower, cabbage, Brussels sprouts) contain sulforophane, which has anti-cancer properties. A case-control study in China found that intake of cruciferous vegetables, measured by urinary secretion of isothiocyanates, was inversely related to the risk of breast cancer; the quartile with the highest intake only had 50% of the risk of the lowest intake group [89]. In the Nurses' Health Study a high intake of cruciferous vegetables (5 or more servings/week vs less than two servings/week) was associated with a 33% lower risk of non-Hodgkin's lymphoma [90]. In the Health Professionals Follow-up Study bladder cancer was only weakly associated with low intake of fruits and vegetables, but high intake (5 or more servings/week vs 1 or less servings/wk) of cruciferous vegetables was associated with a statistically significant 51% decrease in bladder cancer [91]. Also, prostate cancer risk was found to be reduced by cruciferous vegetable consumption in a population-based case-control study carried out in western Washington state. Three or more servings per week, compared to less than one serving of cruciferous vegetables per week resulted in a statistically significant 41% decrease in prostate cancer risk [92]. Similar protective effects of cruciferous vegetables were seen in a multi-ethnic case-control study [93]. A prospective study in Shanghai, China found that men with detectable amounts of isothiocyanates in their urine (metabolic products that come from cruciferous vegetables) had a 35% decreased risk of lung cancer. Among men that had one or two genetic polymorphisms that caused them to eliminate these isothiocyanates slower there was a 64% or 72% decreased risk of lung cancer, respectively [94].

Broccoli sprouts have a very high concentration of sulforophane since this compound originates in the seed and is not made in the plant as it grows [95, 96]. One sprout contains all of the sulforophane that is present in a full-grown broccoli plant. So, if sulforophane is especially cancer-protective, it would seem reasonable to include some broccoli sprouts in an anti-cancer diet.

Selenium

Selenium is a mineral with anti-cancer properties. Many studies in the last several years have shown that selenium is a potent protective nutrient for some forms of cancer. The Arizona Cancer Center posted a selenium fact sheet listing the major functions of selenium in the body [97]. These functions are as follows:

1. Selenium is present in the active site of many enzymes, including thioredoxin reductase, which catalyze oxidation-reduction reactions. These reactions may encourage cancerous cells to under apoptosis.

2. Selenium is a component of the antioxidant enzyme glutathione peroxidase.

3. Selenium improved the immune systems' ability to respond to infections.

4. Selenium causes the formation of natural killer cells.

5. P450 enzymes in the liver may be induced by selenium, leading to detoxification of some carcinogenic molecules.

6. Selenium inhibits prostaglandins that cause inflammation.

7. Selenium enhances male fertility by increased sperm motility.

8. Selenium can decrease the rate of tumor growth.

A serendipitous randomized, double-blind, controlled trial of a 200 μg/day selenium supplement in the southeastern region of the USA (where soil selenium levels are low) found that the primary endpoints of skin cancer were not improved by the selenium supplement, but that other cancer incidence rates were decreased by selenium [98, 99]. There was a significant reduction in total cancer incidence (105 vs 137 cases, P = 0.03), prostate cancer (22 vs 42 cases, P = 0.005), a marginally significant reduction in colorectal cancer incidence (9 vs 19 cases, P = 0.057), and a reduction in cancer mortality, all cancer sites (40 vs 66 deaths, P = 0.008) (selenium versus control group cases reported, respectively) [98]. The selenium supplement was most effective in ex-smokers and for those who began the study with the lowest levels of serum selenium. Several prospective studies have also examined the role of selenium in cancer prevention

Chlorophyll

All green plants also contain chlorophyll, the light-collecting molecule. Chlorophyll and its derivatives are very effective at binding polycyclic aromatic hydrocarbons (carcinogens largely from incomplete combustion of fuels), heterocyclic amines (generated when grilling foods), aflatoxin (a toxin from molds in foods which causes liver cancer), and other hydrophobic molecules. The chlorophyll-carcinogen complex is much harder for the body to absorb, so most of it is swept out with the feces. The chemoprotective effect of chlorophyll and its derivatives has been tested in laboratory cell cultures and animals [107, 108]. There is so much compelling evidence for anti-carcinogenic effects of chlorophyll that a prospective randomized controlled trial is being conducted in Qidong, China to see if chlorophyllin can reduce the amount of liver cancer cases, which arise from aflatoxin exposure in their foods (corn, peanuts, soy sauce, and fermented soy beans). A 55% reduction in aflatoxin-DNA adducts were found in the group that took 100 mg of chlorophyllin three times a day [109]. It was supposed that the chlorophyllin bound up aflatoxins, but there were chlorophyllin derivatives also detected in the sera (which had a green tint to it) of the volunteers who took the supplement, indicating a possible role in the body besides binding carcinogens in the gut [110].

Protective Vitamins

Vitamin B-12

Vitamin B-12 has not been proven to be an anti-cancer agent, but there is some evidence indicating that it could be beneficial. The form of administered vitamin B-12 may be important.

Some experimental cancer studies have been carried out with various forms of vitamin B-12. Methylcobalamin inhibited tumor growth of SC-3 injected into mice [111], and caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow by the presence of growth-inducing androgen [112]. Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing implanted leukemia tumor cells [113]. 5'-deoxyadenosylcobalamin and methylcobalamin, but not cyanocobalamin, were shown to be effective cytotoxic agents [114]. Methylcobalamin also was able to increase survival time and reduce tumor growth in laboratory mice [115].

Laboratory mechanistic evidence for the effects of vitamin B12 were seen in a laboratory study with vitamin B-12 deficient rats. Choi et al [116] found that the colonic DNA of the B-12 deficient rats had a 35% decrease in genomic methylation and a 105% increase in uracil incorporation, both changes that could increase risk of carcinogenesis. In two prospective studies (one in Washington Country, Maryland and the Nurses' Health Study) a relation between lower vitamin B12 status (but not deficiency) and statistically significant higher risk of breast cancer was found [117, 118]. So, there is evidence from laboratory studies, prospective cohort studies, and mechanistic studies showing that vitamin B-12 is an important nutrient for genetic stability, DNA repair, carcinogenesis, and cancer therapy.

Folic Acid

Folic acid is the dark green leafy vegetable vitamin. It has an integral role in DNA methylation and DNA synthesis. Folic acid works in conjunction with vitamin B-6 and vitamin B-12 in the single carbon methyl cycle. If insufficient folic acid is not available uracil is substituted for thymidine in DNA, which leads to DNA strand breakage. About 10% of the US population (and higher percentages among the poor) has low enough intakes of folic acid to make this a common problem [119]. As shown in Tables 3 and 4, many studies have found a significant reduction in colon, rectal, and breast cancer with higher intakes of folic acid and their related nutrients (vitamin B-6 and B-12). Alcohol is an antagonist of folate, so that drinking alcoholic beverages greatly magnifies the cancer risk of a low-folate diet. Genetic polymorphisms (common single DNA base mutations resulting in a different amino acid encoded into a protein) in the methylenetetrahydrofolate reductase and the methionine synthase genes which increase the relative amount of folate available for DNA synthesis and repair also reduces the risk of colon cancer [120, 121, 122, 123]. Cravo et al [124] used 5 mg of folic acid a day (a supraphysiological dose) in a prospective, controlled, cross-over study of 20 patients with colonic adenoma polyps. They found that the folic acid could reverse DNA hypomethylation in 7 of 12 patients who had only one polyp.

Table 4

Prospective Studies of Folate and Breast Cancer.

Reference	Study	# Cases	# Controls	Outcomes	Comment
[214]	Nurses' Health Study	3,483		↓folate intake + alcohol = ↑risk of breast cancer (OR = 0.55, P-trend = 0.001)	Folate intake not associated with overall risk of breast cancer
[215]	Canadian National Breast Screening Study	1,336	5,382	↓folate intake + alcohol = ↑risk of breast cancer (OR = 0.34, P-trend = 0.004)	Folate intake not associated with overall risk of breast cancer
[216]	Prospective study in USA with postmenopausal women	1,586		Among drinkers, ↓folate intake = ↑breast cancer risk (OR = 1.59)	No association in overall cohort
[125]	Shanghai Breast Cancer Study, China	1,321	1,382	↑folate intake = ↓ risk (OR = 0.71, P-trend = 0.05); ↑folate, ↑methionine, ↑B6, ↑B12 = ↓risk (OR = 0.47, P-trend = 0.01)	No alcohol, no supplements, unprocessed, unfortified foods
[217]	Nurses' Health Study II, study of premenopausal women	714		Vitamin A protective (OR = 0.28); Vitamins C, E, and folate not associated with risk.
[118]	Nurses' Health Study	712	712 matched	↑plasma folate = ↓risk (OR = 0.73, P-trend = 0.06). For women who drank alcohol, ↑plasma folate even more protective, OR = 0.11.	↑plasma B6 and plasma B12 were also protective
[218]	Prospective study in USA with postmenopausal women	1,823, 308 with family history (FH)		FH- +Alcohol = ↑risk (OR = 1.40) FH- + Alcohol + ↑folate = normal risk; FH+ ↓folate = ↑risk for drinkers (OR = 2.21) and non-drinkers (OR = 2.39); FH+ +Alcohol + ↑folate = ↑risk (OR = 1.67); FH+ + ↑folate = normal risk	Women with family history of breast cancer can reduce risk by increasing folate intake and not drinking.

FH = Family History

Folate may be more important for rapidly dividing tissue, like the colonic mucosa. Therefore, the cancer risk associated with low folate intake is probably higher for colon cancer than for breast cancer. Most of the breast cancer studies only found a protective effect of folate among women who consumed alcohol (see Table 4). However, among women residents of Shanghai who consumed no alcohol, no vitamin supplements and ate unprocessed, unfortified foods there was a 29% decreased risk of breast cancer among those with the highest intake of folate [125]. So, there may be a true protective effect that is masked in the western populations by so many other risk factors. Two studies showed that the risk of cancer due to family history can be modified by high folate intake, so a prudent anti-cancer diet would be high in dark green leafy vegetables. The mean intake of folic acid on the Hallelujah Diet was 594 μg/day for men and 487 μg/day for women [88].

Vitamin D

Vitamin D is produced primarily from the exposure of the skin to sunshine. Even casual exposure of the face, hands, and arms in the summer generates a large amount of vitamin D. In fact, simulated sunshine, equivalent to standing on a sunny beach until a slight pinkness of the skin was detected, was equivalent to a 20,000 IU oral dose of vitamin D₂ [126]. (Note that the RDA is 400 IU for most adults.) It has been estimated that 1,000 IU per day is the minimal amount needed to maintain adequate levels of vitamin D in the absence of sunshine [126], and that up to 4,000 IU per day can be safely used with additional benefit [127].

The concentration of the active hormonal form of vitamin D is tightly regulated in the blood by the kidneys. This active hormonal form of vitamin D has the potent anti-cancer properties. It has been discovered that various types of normal and cancerous tissues, including prostate cells [128], colon tissue [129], breast, ovarian and cervical tissue [130], pancreatic tissue [131] and a lung cancer cell line [132] all have the ability to convert the major circulating form of vitamin D, 25(OH)D, into the active hormonal form, 1,25(OH)₂D. So, there is a local mechanism in many tissues of the body for converting the form of vitamin D in the body that is elevated by sunshine exposure into a hormone that has anticancer activity.

Indeed, 25(OH)D has been shown to inhibit growth of colonic epithelial cells [133], primary prostatic epithelial cells [134], and pancreatic cells [131]. So, the laboratory work is confirming what had been seen some time ago in ecological studies of populations and sunshine exposure.

The mortality rates for colon, breast, and ovary cancer in the USA show a marked north-south gradient [135]. In ecological studies of populations and sunlight exposure (no individual data) sunlight has been found to have a protective effect for prostate cancer [136], ovarian cancer [137], and breast cancer [138]. Recently Grant found that sunlight was also protective for bladder, endometrial, renal cancer, multiple myeloma, and Non-Hodgkins lymphoma in Europe [139] and bladder, esophageal, kidney, lung, pancreatic, rectal, stomach, and corpus uteri cancer in the USA [140]. Several prospective studies of vitamin D and cancer have also shown a protective effect of vitamin D (see Table 5). It could be that sunshine and vitamin D are protective factors for cancers of many organs that can convert 25(OH)D into 1,25(OH)D₂.

Table 5

Prospective Studies of Vitamin D and Cancer.

Reference	Study	Vit D measure	# Cases	# Controls	Outcomes	Comment
[219]	19-year cohort study of 1,954 men	Diet history			↑vit D + calcium = ↓colorectal cancer (rates for lowest to highest intakes were 38.9, 24,5, 22,5 and 14.3/1000 population	Significant effect even after adjustments for confounding factors; 2.7 fold reduction.
[220]	Washington county, Maryland cohort	Serum 25(OH)D	34	67 matched	↑serum vit D = ↓colon cancer. Relative risk was 0.25 for 3rd quintile and 0.20 for 4th quintile.	4–5 fold reduction
[221]	Physicians' Health Study	Serum 25(OH)D & 1,25(OH)D2	232	414	No relation between vitamin D metabolite levels and prostate cancer
[222]	Nurses' Health Study	Dietary and supplement intake			Colon cancer RR = 0.42 (SS) for total vitamin D, comparing top and bottom quintiles	Calcium not related to colon cancer risks; 2.4 fold reduction
[223]	Finnish clinical cohort	Serum 25(OH)D & 1,25(OH)D2	146	292	↑serum 25(OH)D = ↓risk of rectal cancer, RR by quartile = 1.00, 0.93, 0.77, 0.37, P trend = 0.06.	Serum 25(OH)D 12% lower in cases than in controls (12.2 vs 13.8 ng/l, P = 0.01; 2.7-fold reduction
[224]	NHANES I Follow-up Study	Sunlight and diet	190 women	Cohort matched	Risk reductions for breast cancer for women in regions with high solar radiation (RR 0.35 – 0.75).
[225]	Helsinki Heart Study	Serum 25(OH)D	149	596	↑serum 25(OH)D = ↓prostate cancer. 1.7 fold greater risk for below median level compared to above median level.	Young men (<52 years old) with low 25(OH)D had much higher risk of advanced prostate cancer (OR = 6.3)
[226]	Randomized controlled trial for colon adenoma recurrence	Serum 25(OH)D & 1,25(OH)D2, and supplementary calcium	803 subjects total		Above medium 25(OH)D and supplemental calcium reduced adenoma recurrence (RR = 0.71)	Calcium and vitamin D appeared to work together to reduce colon cancer risk.
[227]	Norway, Finland, Sweden cohort of men	Serum 25(OH)D	622	1,451	≤ 19 nmol/l and ≥ 80 nmol/l of 25(OH)D at higher risk of prostate cancer. (40–60 nmol/l had lowest risk).

Antioxidants

α- and β-Carotene and other Carotenoids

Carotenoids have been studied vigorously to see if these colorful compounds can decrease cancer risk. In ecological studies and early case-control studies it appeared that β-carotene was a cancer-protective agent. Randomized controlled trials of β-carotene found that the isolated nutrient was either neutral [141] or actually increased risk of lung cancer in smokers [142, 143]. Beta-carotene may be a marker for intake of fruits and vegetables, but it does not have a powerful protective effect in isolated pharmacological doses.

However, there is a large body of literature that indicates that dietary carotenoids are cancer preventative (See Table 6). Alpha-carotene has been found to be a stronger protective agent than its well-known isomer β-carotene. Studies tend to agree that overall intake of carotenoids is more protective than a high intake of a single carotenoid. So, a variety of fruits and vegetables is still a better anti-cancer strategy than just using a single vegetable high in a specific carotenoid.

The richest source of α-carotene is carrots and carrot juice, with pumpkins and winter squash as a second most-dense source. There is approximately one μg of α-carotene for every two μg of β-carotene in carrots. The most common sources of β-cryptoxanthin are citrus fruits and red sweet peppers.

Lycopene

Of the various carotenoids lycopene has been found to be very protective, particularly for prostate cancer. The major dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes being more bioavailable than that in raw tomatoes. Several prospective cohort studies have found associations between high intake of lycopene and reduced incidence of prostate cancer, though not all studies have produced consistent results [144, 145]. Some studies suffer from a lack of good correlation between lycopene intake assessed by questionnaire and actual serum levels, and other studies measured intakes among a population that consumed very few tomato products. The studies with positive results will be reviewed here.

In the Health Professionals Follow-up Study there was a 21% decrease in prostate cancer risk, comparing the highest quintile of lycopene intake with the lowest quintile. Combined intake of tomatoes, tomato sauce, tomato juice, and pizza (which accounted for 82% of the lycopene intake) were associated with a 35% lower risk of prostate cancer. Furthermore, lycopene was even more protective for advanced stages of prostate cancer, with a 53% decrease in risk [146]. A more recent follow-up report on this same cohort of men confirmed these original findings that lycopene or frequent tomato intake is associated with about a 30–40% decrease in risk of prostate cancer, especially advanced prostate cancer [147].

In addition to the two reports above a nested case control study from the Health Professional Follow-up Study with 450 cases and controls found an inverse relation between plasma lycopene and prostate cancer risk (OR 0.48) among older subjects (>65 years of age) without a family history of prostate cancer [148]. Among younger men high plasma β-carotene was associated with a statistically significant 64% decrease in prostate cancer risk. So, the results for lycopene have been found for dietary intakes as well as plasma levels.

In a nested case-control study from the Physicians' Health Study cohort, a placebo-controlled study of aspirin and β-carotene, there was a 60% reduction in advanced prostate cancer risk (P-trend = 0.006) for those subjects in the placebo group with the highest plasma lycopene levels, compared to the lowest quintile. The β-carotene also had a protective effect, especially for those men with low lycopene levels [149].

In addition to these observational studies, two clinical trials have been conducted to supplement lycopene for a short period before radical prostatectomy. In one study 30 mg/day of lycopene were given to 15 men in the intervention group while the 11 men were in the control group were instructed to follow the National Cancer Institute's recommendations to consume at least 5 servings of fruits and vegetables daily. Results showed that the lycopene slowed the growth of prostate cancer. Prostate tissue lycopene concentration was 47% higher in the intervention group. Subjects that took the lycopene for 3 weeks had smaller tumors, less involvement of the surgical margins, and less diffuse involvement of the prostate by pre-cancerous high-grade prostatic intraepithelial neoplasia [150]. In another study before radical prostatectomy surgery 32 men were given a tomato sauce-based pasta dish every day, which supplied 30 mg of lycopene per day. After 3 weeks serum and prostate lycopene levels increaed 2-fold and 2.9-fold, respectively. PSA levels decreased 17%, as seen also by Kucuk et al [150]. Oxidative DNA damage was 21% lower in subjects' leukocytes and 28% lower in prostate tissue, compared to non-study controls. The apoptotic index was 3-fold higher in the resected prostate tissue, compared to biopsy tissue [151]. These intervention studies raise the question of what could have been done in this intervention was longer and combined synergistically with other effective intervention methods, such as flax seed, increased selenium and possibly vitamin E, in the context of a diet high in fruits and vegetable?

Vitamin C

Vitamin C, or ascorbic acid, has been studied in relation to health and is the most common supplement taken in the USA. Low blood levels of ascorbic acid are detrimental to health (for a recent article see Fletcher et al [152]) and vitamin C is correlated with overall good health and cancer prevention [153]. Use of vitamin C for cancer therapy was popularized by Linus Pauling. At high concentrations ascorbate is preferentially toxic to cancer cells. There is some evidence that large doses of vitamin C, either in multiple divided oral doses or intravenously, have beneficial effects in cancer therapy [154, 155, 156]. Oral doses, even in multiple divided doses, are not as effective as intravenous administration. Vitamin C at a dose of 1.25 g administered orally produced mean peak plasma concentrations of 135 ± 21 μmol/L compared with 885 ± 201 μmol/L for intravenous administration [154].

While vitamin C is quite possibly an effective substance, the amounts required for these therapeutic effects are obviously beyond dietary intakes. However, intravenous ascorbate may be a very beneficial adjuvant therapy for cancer with no negative side effects when administered properly.

Other Antioxidants

There are many more substances that will have some benefit for cancer therapy. Most of these substances are found in foods, but their effective doses for therapy are much higher than the normal concentration in the food. For example, grape seed extract contains proanthocyanidin, which shows anticarcinogenic properties (reviewed by Cos et al \ [157]. Also, green tea contains a flavanol, epigallocatechin-3-gallate (EGCG), which can inhibit metalloproteinases, among several possible other mechanisms [158]. And there are claims for various other herbal substances and extracts that might be of benefit, which are beyond the scope of this review.

Probiotics

The bacteria that reside in the intestinal tract generally have a symbiotic relationship with their host. Beneficial bacteria produce natural antibiotics to keep pathogenic bugs in check (preventing diarrhea and infections) and produce some B vitamins in the small intestine where they can be utilized. Beneficial bacteria help with food digestion by providing extra enzymes, such as lactase, in the small intestine. Beneficial bacteria help strengthen the immune system right in the gut where much of the interaction between the outside world and the body goes on. Beneficial bacteria can help prevent food allergies. They can help prevent cancer at various stages of development. These good bacteria can improve mineral absorption, maximizing food utilization.

However, the balance of beneficial and potentially pathogenic bacteria in the gut is dependent on the diet. Vegetable fiber encourages the growth of beneficial bacteria. A group of Adventist vegetarians was found to have a higher amount of beneficial bacteria and lower amount of potentially pathogenic bacteria compared to non-vegetarians on a conventional American diet [159]. Differences in bacterial populations were seen between patients who recently had a colon polyp removed, Japanese-Hawaiians, North American Caucasians, native rural Japanese, and rural native Africans. Lactobacillus species and Eubacterium aerofaciens, both producers of lactic acid, were associated with the populations with the lower risk of colon cancer, while Bacteroides and Bifidobacterium species were associated with higher risk of colon cancer [160]

There is a solid theoretical basis for why probiotics should help prevent cancer, especially colon cancer, and even reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the environment. Lower colon pH is associated with lower incidence of colon cancer. Probiotic bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase, nitroreductase, and azoreductase [161].

L. casei was used in two trials of patients with superficial bladder cancer. In the first trial, the probiotic group had a 50% disease free time of 350 days, compared to 195 days for the control group [162]. The second trial also showed that the probiotics worked better than the placebo, except for multiple recurring tumors [163].

Except for the two studies noted above, most of the research of probiotics and cancer has been done in animals. Studies have looked at markers of tumor growth or at animals with chemically induced tumors.

Studies in rats have shown that probiotics can inhibit the formation of aberrant crypt foci, thought to be a pre-cancerous lesion in the colon. Some of the best results were obtained with a probiotic strain consumed with inulin, a type of fructooligosaccharide. Total aberrant crypt foci, chemically induced, were reduced 74% by the treatment of rats with inulin and B. longum, but only 29 and 21% by B. longum and inulin alone, respectively [164]. There was a synergistic effect in using both products together. Similar synergy was seen in rats with azoxymethane-induced colon cancer in another study. Rats fed Raftilose, a mixture of inulin and oligofructose, or Raftilose with Lactobacilli rhamnosus (LGG) and Bifidobacterium lactis (Bb12) had a significantly lower number of tumors compared to the control group [165]. A probiotic mixture, without any prebiotic, given to rats fed azoxymethane reduced colon tumors compared to the control (50% vs 90%), and also reduced the number of tumors per tumor-bearing rat [166].

In lab mice bred to be susceptible to colitis and colon cancer, a probiotic supplement, Lactobacillus salivarium ssp. Salivarius UCC118, reduced fecal coliform levels, the number of potentially pathogenic Clostridium perfringens, and reduced intestinal inflammation. In this small study two mice died of fulminant colitis and 5 mice developed adenocarcinoma in the control group of 10 mice, while there was no colitis and only 1 mouse with adenocarcinoma in the probiotic test group [167].

The research on probiotics and disease is still an emerging field. There is a high degree of variation of health benefits between different strains of bacteria. As new methods for selecting and screening probiotics become available, the field will be able to advance more rapidly.

Oral Enzymes

Many people diagnosed with cancer have digestion or intestinal tract disorders as well. Impaired digestion will greatly hinder a nutritional approach to treating cancer. If the nutrients cannot be released from the food and taken up by the body, then the excellent food provided by the Hallelujah Diet will go to waste. Digestive enzyme supplements are used to ensure proper and adequate digestion of food. Even raw foods, which contain many digestive enzymes to assist in their digestion, will be more thoroughly digested with less of the body's own resources with the use of digestive enzymes. So, the enzymes taken with meals do not have a direct effect upon a tumor, but assist the body in getting all of the nutrition out of the food for healing and restoring the body to normal function. Recently, an in vitro system was used to test the use of supplemental digestive enzymes. The digestive enzymes improved the digestibility and bioaccessibility of proteins and carbohydrates in the lumen of the small intestine, not only under impaired digestive conditions, but also in healthy human digestion [168].

There is evidence that indicates the presence of an enteropancreatic circulation of digestive enzymes [169]. Digestive enzymes appear to be preferentially absorbed into the bloodstream and then reaccumulated by the pancreas for use again. There appears to be a mechanism by which digestive enzymes can reach systemic circulation.

Enzymes, especially proteases, if they reach systemic circulation, can have direct anti-tumor activity. Wald et al [170] reported on the anti-metastatic effect of enzyme supplements. Mice inoculated with the Lewis lung carcinoma were treated with a proteolytic enzyme supplement, given rectally (to avoid digestion). The primary tumor was cut out, so that the metastatic spread of the cancer could be measured. After surgical removal of the primary tumor (day 0), 90% of the control mice died by day 18 due to metastasized tumors. In the first group, which received the rectal enzyme supplement from the time of the tumor-removal surgery, 30% of the mice had died from metastasized cancer by day 25. In the second group, which received the enzymes from 6 days prior to removal of the primary tumor, only 10% of the animals showed the metastatic process by day 15. In the third group, which received the enzyme treatment since the initial inoculation of the Lewis lung carcinoma, no metastatic spread of the tumor was discernible. One hundred day-survival rates for the control, first, second, and third groups were 0, 60%, 90%, and 100%.

In a similar experiment, an enzyme mixture of papain, trypsin, and chymotrypsin, as used in the preparation Wobe-Mugos E, was rectally given to mice that were inoculated with melanoma cells. Survival time was prolonged in the test group (38 days in the enzyme group compared to 24 days in the control mice) and 3 of the 10 enzyme-supplemented mice were cured. Again, a strong anti-metastatic effect of the proteolytic enzymes was seen [171].

Further evidence of the efficacy of oral enzyme supplementation is available from clinical trials in Europe. Two different studies have demonstrated that two different oral proteolytic enzyme supplements were able to reduce high levels of transforming growth factor-β, which may be a factor in some cancers [172, 173]. In the Slovak Republic an oral enzyme supplement was tested in a placebo-controlled trial of multiple myeloma. For stage III multiple myeloma, control group survival was 47 months, compared to 83 months (a 3 year gain) for patients who took the oral enzymes for more than 6 months [174].

Enzyme supplements have also been shown to reduce side effects of cancer therapy. Enzyme supplementation resulted in fewer side effects for women undergoing radiation therapy for carcinomas of the uterine cervix [175], for patients undergoing radiation therapy for head and neck cancers [176], and for colorectal cancer patients undergoing conventional cancer treatments [177]. In a large multi-site study in Germany women undergoing conventional cancer therapy were put into a control group or a group that received an oral enzyme supplement. Disease and therapy related symptoms were all reduced, except tumor pain, by the enzyme supplement. Also, survival was longer with less recurrence and less metastases in the enzyme group [178]. In all of these studies the oral enzyme supplements were well tolerated, with only a small amount of mild to moderate gastrointestinal symptoms.

Even though these few studies don't give a lot of evidence of the effectiveness of oral enzyme supplementation, it is clear that there are some circumstances that will be helped by enzyme supplementation, with very little danger of negative side effects. At the least, enzymes will improve digestion and lessen the digestive burden on the body, leaving more reserves for disease eradication. However, as the research indicates, the effect may be much greater than that, with the potential for direct anti-tumor activity.

Whole Diet Studies

A diet-based cancer therapy, the Gerson Therapy, was used to treat melanoma cancer. The five-year survival rates from their therapy compared very favorably to conventional therapy reported in the medical literature, especially for more advanced stages of melanoma [179] (see Table 7).

Table 7

Gerson Therapy for Melanoma [179].

Stage of melanoma	Gerson	Historical controls
I – II	100% (N = 14)	79% (N = 15,798)
IIIA	82% (N = 17)	39% (N = 103)
IIIA + IIIB	70% (N = 33)	41% (N = 130)
IVA	39% (N = 18)	6% (N = 194)

An Italian cohort of 8,984 women was followed for an average of 9.5 years, with 207 incident cases of breast cancer during that time. Their diets were analyzed by patterns – salad vegetables (raw vegetables and olive oil), western (potatoes, red meat, eggs and butter), canteen (pasta and tomato sauce), and prudent (cooked vegetables, pulses, and fish). Only the salad vegetable diet pattern was associated with a significantly lower risk of breast cancer, about 35% lower. For women of normal weight (BMI <25) the salad vegetable pattern was even more protective, about a 61% decreased risk of breast cancer [180]. The overall dietary pattern does make a very significant difference.

In US-based studies the "prudent" diet has been shown to be protective for colon cancer, while the "western" diet has been shown to be detrimental. The "western" dietary pattern, with its higher intakes of red meat and processed meats, sweets and desserts, French fries, and refined grains, was associated with a 46% increase relative risk of colon cancer in the Nurses' Health Study [45]. Slattery et al [17] found a two-fold increase in relative risk of colon cancer associated with a "western" dietary pattern, and a 35–40% decrease in relative risk associated with the "prudent" pattern, especially among those diagnosed at an earlier age (<67 years old). The "salad vegetable" pattern is still more likely to be protective compared to the prudent dietary pattern, but this pattern did not exist in this study population.

In an analysis of the colon cancer data from the Health Professionals Follow-up Study, Platz et al [56] found that there was a 71% decrease in colon cancer risk when men with none of six established risk factors were compared to men with at least one of these risk factors (obesity, physical inactivity, alcohol consumption, early adulthood cigarette smoking, red meat consumption, and low intake of folic acid from supplements). So, if all men had the same health profile as these healthier 3% of the study population, colon cancer rates would have been only 29% of what they measured.

A plant-based dietary pattern in being currently tested in the Women's healthy Eating and Living (WHEL) Study. About 3,000 women who were treated for an early stage of breast cancer have been randomized into two groups. The dietary goals for the test group of the study are 5 servings of vegetables, 16 oz of vegetable juice, 3 servings of fruit, 30 g of fiber, and <20% of energy from fat. No guidelines were given for animal product intake, and initial results seem to confirm, since there were no changes in body weight, total cholesterol, or LDL cholesterol [181], which would be affected by animal protein intake. However, over the first year of follow-up vegetable intake did increase to seven servings/day, fruit intake increased to 3.9 servings/day, energy from fat decreased from 28% to 23%. Also, plasma carotenoid concentrations increased significantly in the intervention group, but not in the control group. α-Carotene increased 223%, β-carotene increased 87%, lutein increase 29%, and lycopene increased 17% [182], indicating that a substantial dietary change had been made by these women. It will be very interesting to follow the results of this study.

Conclusions

What is the result when all of the above are put together? What if all of these factors reviewed here were taken into account and put into practice? This anticancer diet would have:

adequate, but not excessive calories, 10 or more servings of vegetables a day, including cruciferous and allium vegetables; vegetable juice could meet part of this goal, 4 or more servings of fruits a day, high in fiber, no refined sugar, no refined flour, low in total fat, but containing necessary essential fatty acids, no red meat, a balanced ratio of omega 3 and omega 6 fats and would include DHA, flax seed as a source of phytoestrogens, supplemented with ~200 μg/day selenium, supplemented with 1,000 μg/day methylcobalamin (B-12), very rich in folic acid (from dark green vegetables), adequate sunshine to get vitamin D, or use 1,000 IU/day supplement, very rich in antioxidants and phytochemicals from fruits and vegetables, including α-carotene, β-carotene, β-cryptoxanthin, vitamin C (from f

yoga_girl

Indole-3-carbinol (I-3-C) or DIM (diindolylmethane)

Cruciferous vegetables may help reduce estrogen-related cancers.

Products that offer I-3-C or DIM:

https://www.vitaminshoppe.com/search?search=dim

https://www.bing.com/search?q=i3c+and+DIM&form=IENTHT&mkt=en-us&httpsmsn=1&refig=90e265721eca4b4fedbb84b200680d93&sp=-1&ghc=1&pq=i3c+and+dim&sc=4-11&qs=n&sk=&cvid=90e265721eca4b4fedbb84b200680d93

Indole-3-carbinol (I-3-C) is produced by the breakdown of the glucosinolate glucobrassicin, which can be found at relatively high levels in cruciferous vegetables such as broccoli, cabbage, cauliflower, brussels sprouts, collard greens and kale. It is also available in dietary supplements.^[2] Indole-3-carbinol is the subject of on-going biomedical research into its possible anticarcinogenic,^[3]antioxidant, and anti-atherogenic effects.^[4] Research on indole-3-carbinol has been conducted primarily using laboratory animals and cultured cells.^[5] Limited and inconclusive human studies have been reported. A recent review of the biomedical research literature found that "evidence of an inverse association between cruciferous vegetable intake and breast or prostate cancer in humans is limited and inconsistent" and "larger randomized controlled trials are needed" to determine if supplemental indole-3-carbinol has health benefits.^[6]

I-3-C and cancer

Investigation of mechanisms by which consumption of indole-3-carbinol might influence cancer incidence focuses on its ability to alter estrogen metabolism and other cellular effects. Controlled studies have been performed on such animals as rats, mice, and rainbow trout, introducing various controlled levels of carcinogens, and levels of Indole-3-carbinol into their daily diet. Results showed dose-related decreases in tumor susceptibility due to Indole-3-carbinol (inferred by decreases in aflatoxin-DNA binding). The first direct evidence of pure anti-initiating activity by a natural anticarcinogen (indole-3-carbinol) found in human diet was claimed by Dashwood, et al., in 1989.^[7]

Indole-3-carbinol induces a G1 growth arrest of human reproductive cancer cells.^[8] This is potentially relevant to the prevention and treatment of cancer, as the G1 phase of cell growth occurs early in the cell life cycle, and, for most cells, is the major period of cell cycle during its lifespan. The G1 phase is marked by synthesis of various enzymes that are required in the next ("S") phase, including those needed for DNA replication.

Overuse of indole-3-carbinol supplements in the hope of preventing cancer may be unwise, as the hormone balance should be tested (via simple blood test) before regular consumption. Such caution is advised, due to its effect on estrogen levels (estrogen has a significant impact on brain function).^[9][10]

It promotes liver cancer in trout when it is combined with aflatoxin B1 and demotes metastasis.^[5]

1.Jump up ^ Data at chemblink.com

2.Jump up ^ Sarubin-Fragakis, Allison; Thomson, Cynthia; Association, American Dietetic (2007-01-01). The Health Professional's Guide to Popular Dietary Supplements. American Dietetic Associati. p. 312. ISBN 9780880913638.

3.Jump up ^ Park, N. I.; Kim, J. K.; Park, W. T.; Cho, J. W.; Lim, Y. P.; Park, S. U. (2010). "An efficient protocol for genetic transformation of watercress (Nasturtium officinale) using Agrobacterium rhizogenes". Molecular Biology Reports. 38 (8): 4947–4953. PMID 21161399. doi:10.1007/s11033-010-0638-5.

4.Jump up ^ Chemical Entities of Biological Interest (ChEBI), The European Bioinformatics Institute (EBI). "indole-3-methanol (CHEBI:24814)". www.ebi.ac.uk. Retrieved 2016-03-25.

5.^ Jump up to: ^{a b} Tilton, S. C.; Hendricks, J. D.; Orner, G. A.; Pereira, C. B.; Bailey, G. S.; Williams, D. E. (2007). "Gene expression analysis during tumor enhancement by the dietary phytochemical, 3,3'-diindolylmethane, in rainbow trout". Carcinogenesis. 28 (7): 1589–1598. PMID 17272308. doi:10.1093/carcin/bgm017.

6.Jump up ^ Higdon, J; Delage, B; Williams, D; Dashwood, R (2007). "Cruciferous vegetables and human cancer risk: Epidemiologic evidence and mechanistic basis". Pharmacological Research. 55 (3): 224–36. PMC 2737735 . PMID 17317210. doi:10.1016/j.phrs.2007.01.009.

7.Jump up ^ Dashwood, Rod H.; Arbogast, D.N.; Fong, A.T.; Pereira, C.; Hendricks, J.D.; Bailey, G.S. (1989). "Quantitative inter-relationships between aflatoxin B1 carcinogen dose, indole-3-carbinol anti-carcinogen dose, target organ DNA adduction and final tumor response". Carcinogenesis. 10 (1): 175–81. PMID 2491968. doi:10.1093/carcin/10.1.175.

8.Jump up ^ Hsu, J; Dev, A; Wing, A; Brew, C; Bjeldanes, L; Firestone, G (2006). "Indole-3-carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein". Biochemical Pharmacology. 72 (12): 1714–23. PMID 16970927. doi:10.1016/j.bcp.2006.08.012.

9.Jump up ^ Culmsee, Carsten; Vedder, Helmut; Ravati, Alexander; Junker, Vera; Otto, D??rte; Ahlemeyer, Barbara; Krieg, J??Rgen-Christian; Krieglstein, Josef (1999). "Neuroprotection by Estrogens in a Mouse Model of Focal Cerebral Ischemia and in Cultured Neurons: Evidence for a Receptor-Independent Antioxidative Mechanism". Journal of Cerebral Blood Flow & Metabolism: 1263–1269. doi:10.1097/00004647-199911000-00011.

10. Jump up ^ "Estrogen's Influence on the Brain". Society for Neuroscience.

11. Jump up ^ Auborn, KJ; Qi, M; Yan, XJ; Teichberg, S; Chen, D; Madaio, MP; Chiorazzi, N (2003). "Lifespan is prolonged in autoimmune-prone (NZB/NZW) F1 mice fed a diet supplemented with indole-3-carbinol". The Journal of Nutrition. 133 (11): 3610–3. PMID 14608082.

12. Jump up ^ Yan, Xiao-jie; Qi, Mei; Telusma, Gloria; Yancopoulos, Sophia; Madaio, Michael; Satoh, Minoru; Reeves, Westley H.; Teichberg, Saul; et al. (2009). "Indole-3-carbinol improves survival in lupus-prone mice by inducing tandem B- and T-cell differentiation blockades". Clinical Immunology. 131 (3): 481–94. PMID 19278904. doi:10.1016/j.clim.2009.01.013.

13. Jump up ^ Rosen, Clark A.; Bryson, Paul C. (2004). "Indole-3-Carbinol for recurrent respiratory papillomatosis: Long-term results". Journal of Voice. 18 (2): 248–53. PMID 15193659. doi:10.1016/j.jvoice.2003.05.005.

14. Jump up ^ Rosen, Clark A.; Woodson, Gayle E.; Thompson, Jerome W.; Hengesteg, Arne P.; Bradlow, H.Leon (1998). "Preliminary results of the use of indole-3-carbinol for recurrent respiratory papillomatosis". Otolaryngology – Head and Neck Surgery. 118 (6): 810–5. PMID 9627242. doi:10.1016/S0194-5998(98)70274-8.

_{Castañon A, Tristram A, Mesher D, et al. Effect of diindolylmethane supplementation on low-grade cervical cytological abnormalities: double-blind, randomised, controlled trial. Br J Cancer. 2012 Jan 3;106(1):45-52. doi: 10.1038/bjc.2011.496.}

_{Dalessandri KM, Firestone GL, Fitch MD, Bradlow HL, Bjeldanes LF. Pilot study: effect of 3,3'-diindolylmethane supplements on urinary hormone metabolites in postmenopausal women with a history of early-stage breast cancer. Nutr Cancer. 2004;50(2):161-7.}

_{Nikitina D, Llacuachaqui M, Sepkovic D, et al. The effect of oral 3,3'-diindolylmethane supplementation on the 2:16α-OHE ratio in BRCA1 mutation carriers. Fam Cancer. 2015 Jun;14(2):281-6. doi: 10.1007/s10689-015-9783-2.}

_{Smith S, Sepkovic D, Bradlow HL, Auborn KJ. 3,3'-Diindolylmethane and genistein decrease the adverse effects of estrogen in LNCaP and PC-3 prostate cancer cells. J Nutr. 2008 Dec;138(12):2379-85.}

_{Staub RE, Onisko B, Bjeldanes LF. Fate of 3,3'-diindolylmethane in cultured MCF-7 human breast cancer cells. Chem Res Toxicol. 2006 Mar;19(3):436-42.}

yoga_girl

Radiation induced nausea and vomiting

https://www.sciencedirect.com/science/article/pii/S0014299913007620

Radiotherapy-induced Nausea and Vomiting

https://www.medscape.com/viewarticle/754392

Prophylactic Management of Radiation-Induced Nausea and Vomiting

https://www.hindawi.com/journals/bmri/2015/893013/

Nausea and Vomiting Related to Cancer Treatment (PDQ®)–Patient Version

https://www.cancer.gov/about-cancer/treatment/side-effects/nausea/nausea-pdq

What has worked for many of my friends and co-workers who have cancer (not just breast cancer):

American Health, Probiotic Acidophilus (Liquid); available at most health food stores:

--in the refrigerated section, The Vitamin Shoppe (check local area for brand availability)

--other brands may be available, Whole Foods

--check the local listings in your area of the country for similar product availability

--available on line:

https://www.bing.com/search?q=american+health+probiotic+acidophilus&src=IE-SearchBox&FORM=IESR4S&pc=EUPP_

Drink it straight from the bottle at the onset of nausea, drink it as often as you need to (do not take or mix with any oral product that will interfere with intestinal distress or bowel distress, these will make it worse or cause additional side effects).