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Health news:
June 2010 - Dec 2013

Minimizing breast cancer risk

May 2010

Time to move beyond salt ?

Salt hypothesis vs. reality

Is sodium bad?

April 2010

Salt studies: the latest score

From Dahl to INTERSALT

Salt hypothesis' story

March 2010

Salt war

Do bone drugs work?

Diabetes vs. drugs, 3:0?

February 2010

The MMR vaccine war: Wakefield vs. ?

Wakefield proceedings: an exception?

Who's afraid of a littl' 1998 study?

January 2010

Antibiotic children

Physical activity benefits late-life health

Healthier life for New Year's resolution


December 2009

Autism epidemic worsening: CDC report

Rosuvastatin indication broadened

High-protein diet effects


November 2009

Folic acid cancer risk

Folic acid studies: message in a bottle?

Sweet, short life on a sugary diet


October 2009

Smoking health hazards: no dose-response

C. difficile warning

Asthma risk and waist size in women


September 2009

Antioxidants' melanoma risk: 4-fold or none?

Murky waters of vitamin D status

Is vitamin D deficiency hurting you?


August 2009

Pill-crushing children

New gut test for children and adults

Unhealthy habits - whistling past the graveyard?


July 2009

Asthma solution - between two opposites that don't attract

Light wave therapy - how does it actually work?

Hodgkin's lymphoma in children: better alternatives


June 2009

Hodgkin's, kids, and the abuse of power

Efficacy and safety of the conventional treatment for Hodgkin's:
behind the hype

Long-term mortality and morbidity after conventional treatments for pediatric Hodgkin's


May 2009

Late health effects of the toxicity of the conventional treatment for Hodgkin's

Daniel's true 5-year chances with the conventional treatment for Hodgkin's

Daniel Hauser Hodgkin's case: child protection or medical oppression?

April 2009

Protection from EMF: you're on your own

EMF pollution battle: same old...

EMF health threat and the politics of status quo

March 2009

Electromagnetic danger? No such thing, in our view...

EMF safety standards: are they safe?

Power-frequency field exposure

February 2009

Electricity and health

Electromagnetic spectrum: health connection

Is power pollution making you sick?

January 2009

Pneumococcal vaccine for adults useless?

DHA in brain development study - why not boys?

HRT shrinks brains


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June 2010 - December 2013

I - Breast cancer risk factors

3. Breast cancer risk factors - overview

2 good choices to prevent breast cancer




The biggest risk factor
Risk factors overview
Times change

The whistle
Last decade
Current picture

Digital standard
Breast CT

Predisposing factors
Diet     Other

Earlier diagnosis
Fewer breast cancer deaths

Gamma-ray tests



Breast MRI
AMAS test

False positive
Hormonal: HRT, xenoestrogens, frame size
BMI, bra, screening


Radiation primer
Screen exposure
Radiation risk

Higher all-cause mortality?

• Minimizing breast cancer risk

In the most simplified context, we can say that all it takes for breast cancer - or any other - to start growing and keep growing unopposed is two things:

(1) fatally compromised cell-cycle integrity and

(2) immune system insufficiency.

The former invariably involves malfunction of the cellular DNA which, in turn, requires multiple alterations to it, with the combined effect producing malignant cell. These DNA alterations can be either passed through hereditary line (most or, very seldom, all of them) or, much more often, result of a damage to the DNA by carcinogens.

And such damage can only occur if all protective lines - set by the body's detox system and body's oxidative protection - fail. This can protective inefficiency may and may not be due to the great magnitude of exposure to the carcinogen.

Finally, the damage only counts if repair mechanism, for whatever reason, fails.

So, the typical cancer path is:

multiple exposure to carcinogen
multiple protective systems failure
accumulated DNA damage/repair failure
malignant cell cycle alteration
immune system failure

Considering how incredibly complex all this is - from the protective systems to the cell cycle and immune system  - it is no wonder that the list of known or suspected breast cancer risk factors is a mile long. In order to make it easier to grasp, these factors can be grouped according to their primary role in the disease.

Those that exist before the cancer forms are predisposing breast cancer risk factors.

Those that actually push the cell into cancerous transformation by damaging or inhibiting some of its vital functions, are initiating factors, or carcinogens.

And those that in some way stimulate or make easier growth and proliferation of the existing cancerous cells are breast cancer promoting factors.

The distinction is often vague, since predisposing factors before cancerous transformation often become promoting factors after it. Most of the factors involved with breast cancer formation can have such a dual role.

Following is a lists of major breast cancer risk factors grouped according to this general scheme, with each factor given an expanded window in a table below.



1 - Compromised detox system (including body's oxidative protectioon) due to toxic overload and nutritional deficiencies, chronic stress and/or negative emotions
2 - Compromised oxidative protection
3 - Genetic polymorphism compromising neutralization of carcinogens,  DNA repair and cell cycle control
4 - Compromised immune system increasing likelihood of an
active viral infection
5 - Other
 • Nutritional deficiencies/imbalances
 • Regular alcohol consumption
 • Smoking


- Compromised immune function due to chronic stress, negative emotions and/or chronic internal infections
- Compromised detox system due to toxic overload and nutritional deficiencies, chronic stress and/or negative emotions
- Mitogenic/antiapoptopic hormones
• Ovarian hormones high/unbalanced
• Hormonal medical treatments
• Exposure to environmental estrogens
• Elevated insulin
• Elevated IGF
- Genetic polymorphism compromising cell cycle control
and immune system efficiency
5 - Other
 • Nutritional deficiencies/imbalances
 • Regular alcohol consumption
 • Smoking
 • Low melatonin due to lack of sleep
 • Wearing bra extensively
 • Obesity/weight gain (postmenopausal)
 • Lean body (premenopausal)
 • Insufficient/inadequate checkups



A1 - Compromised detox system
toxic overload toxins from food, air, water, dental implants, medications, internal microorganisms. Overburdened and/or compromised by genetic/nutritional deficiencies detox system can't efficiently metabolize and dispose of toxins; toxic metabolites inflict injury by causing oxidative damage or cross-linking with body molecules, including DNA
nutritional deficiencies detox function is dependant on the wide spectrum of nutrients
chronic stress
psychological trauma
negatively affects entire metabolism, detox and other functions
negative emotions negative self-image, pessimism,  suppression of emotions,
poor organizing
chronic dehydration  sufficient water intake is a must for efficient detox function
A2 - Compromised oxidative protection
oxidative exposure tobacco smoke, chlorine, pesticides, food additives, drugs, air pollutants, heavy metals, ultraviolet light...
nutritional deficiencies oxidative protection depends on many antioxidant nutrients
A3 - Inherent genetic aberrations

BRCA1/2 gene mutation

  tumor-suppressor genes, short for BReast CAncer; mutation increases the risk up to tenfold; estimated 5-10% of all breast cancer cases carry mutated BRCA1 or 2

ATM gene mutation

  also part of tumor-suppressing mechanism, Ataxia-telangiectasia mutated gene is estimated to be  altered (heterozygous carriers) in up to 1% of women; up to 10% of all breast cancer cases are carriers, possibly more

CHEK2 gene mutation

  cell cycle checkpoint regulator gene, acting on signals of DNA damage to prevent cellular division; functionally associated with BRCA1 and TP53; its 1100delC heterozygous polymorphism has estimated <1% incidence and threefold increase in breast cancer risk

TP53 gene mutation

tumor (suppressor) protein p53 gene is mutated in more than half of all cancers, but only in about 20% of breast cancer cases; however, research indicates that TP53 mutations are nearly three times more frequent in BRCA1/2 germline mutation carriers; TP53 is regulated by CHEK2 (which is, in turn, activated by ATM), which activates TP53 to arrest cell cycle for an attempt at DNA repair, and then breaks it down to prevent apoptosis (programmed cell death) if repair succeeds; illustrates genetic interactions and interdependency 

FOK1 gene mutation

vitamin D receptor gene, whose proper function is needed for efficient cellular use of vitamin D, which inhibits cell proliferation, and downregulates both estrogen and progesterone receptors; significantly lower risk increase than for above polymorphisms (indicated ~25% for Ff and ~60% for ff FOK1 polymorphism), but much higher incidence (about 40-50% and 10%, respectively)

PALB2 gene mutation

partner and localizer of BRCA2 protein enables accumulation of BRCA2 protein in the cell nucleus; it is altered in less than 1% of women, doubling the risk of breast cancer

 PTEN gene mutation

  another gene encoding tumor-suppressing protein (phosphatase and tension homolog enzyme), PTEN mutations are very rare, usually associated with Cowden syndrome; carriers have up to 6 times higher breast cancer lifetime risk

A4 - Compromised immune system
chronic stress stimulates production of adrenal hormones, inhibiting immune function, shrinking the thymus gland and weakening antiviral response
chronic internal infections,
intestinal bacterial/fungal overgrowth,
insufficient rest (sleep) time,
high sugar intake,
high blood lipids,
nutritional deficiencies,
smoking, alcohol, overweight,

negative emotions
poor lifestyle choices negatively affect the immune function
A4 - Other predisposing factors
nutritional deficiencies/imbalances compromising detox, antioxidative, and/or cellular function
regular alcohol consumption regular, even quite moderate consumption inked with higher blood estrogen levels; other possible mechanisms include increased solubility of carcinogens, interfering with folate metabolism, elevated oxidative stress and mutagenic effects of its primary metabolite, acetaldehyde
tobacco smoke contains over 4000 chemicals, most of them toxic, and over 50 known carcinogens


B1 - Radiation exposure

medical exposures

radiation exposures before age 20, beginning with fetal exposures and subsequent X-ray and nuclear medicine diagnostic (γ-rays) exposures


cumulative doses in extended periods of time can be significant


imaging of breast's milk ducts by mammography unit; similar exposure as low-level mammography

other adult chest or whole body exposures

other radiology diagnostic procedures, occupational exposures, nuclear fallout, smoking (from Polonium 210), air travel, radon, background radiation

non-ionizing radiation
(power field)

although the evidence is inconclusive, there are clear indications that exposure to non-ionizing radiation can be significant breast cancer risk factor

B2 - Viral infections

sexual intercourse,
physical contact, food (grains), 
pets (?)

human papilloma virus (HPV), mouse mammary tumor virus (MMTV), Epstein-Barr virus (EBV) and bovine leukemia virus (BLV) have been identified at higher to much higher incidence in breast cancer patients; each has the ability to alter cellular DNA, transforming normal cells into malignant

B3 - Chemical carcinogens

industrial chemicals (including food additives, pesticides and herbicides) in construction and household products, food, water and environment

many chemicals have been identified as carcinogenic, mainly in experiments with laboratory animals; little research is done on the role of unknown number of such chemical carcinogens in the initiation and growth of breast cancer, but it is reasonable to assume it to be significant


C1 - Mitogenic/antiapoptopic hormones
ovarian hormones level/balance nominal blood estrogen level is an indicator, although somewhat loose, of the free (bioavailable, active) estrogen, which stimulates cell proliferation; higher estrogen level is likely to result in early menarche and late menopause (also, as a part of the elevated overall hormonal activity, in accelerated growth)
hormonal balance is regulated by a complex co-action of the pituitary gland and hypothalamus, but also affected by other factors, such as exposures to xenoestrogens (environmental estrogens) or chronic stress
exposure to environmental estrogens (xenoestrogens) Phthalates (plasticizers) - chemicals leaking into foods form plastic containers and wraps, tend to accumulate in the body and may disrupt endocrine function
Pesticides - present in many foods and drinking water, may negatively affect body's regulatory functions, including hormonal
Detergents, trichloro-ethylene,
many environmental chemicals can act as estrogen mimics; level of exposure and individual vulnerability vary, but can be significant
Cadmium - toxic contaminant present in food, water and environment (also, in tobacco) that steadily accumulates in the body, acting like estrogen; it can also raise testosterone levels, as additional breast cancer risk factor
Natural food components - some natural food components, for instance, soybean isoflavones genistein and daidzein, can have estrogenic effect; however, Asian populations with high soybean intake have low breast cancer incidence, which suggests that (1) the effect may be more complex, and/or dependant on the overall diet and lifestyle (2) soy isofavones generally act as anti-estrogens, taking estrogen receptors while having much lower estrogenic potency (less than 2%)
Herbal extracts - natural herbal components can also have estrogenic potency; among commonly used herbs with such compounds are angelica, reishi mushroom, licorice, fo-ti and astragalus (they are all considered healthful, hence the above applies here as well)
elevated insulin From high-glycemic diet,
insulin resistance, diabetes;
insulin stimulates cell division and increases the level of free (active) estrogen
elevated IGF insulin-like growth factor, mitogenic, antiapoptotic hormone, enhancing estrogen activity, and vice versa; high levels linked to increased risk of several common cancers, including breast cancer
hormonal medical treatments lHRT - large trials consistently come up with significantly increased risk
Birth control pills - the earlier in life starts the use, and the longer it lasts, the more of the risk factor they become
SERM drugs - Selective Estrogen Receptor Modulator, including those like Tamoxifen, that are used for breast cancer treatment and prevention, evidently are the additional risk factor for some woman
C2 - Compromised immune function
chronic internal infections toot/jaw/root canal infections - appears to have significantly higher incidence in breast cancer patients
intestinal bacterial/fungal overgrowth often accompanied with leaky gut and nutritional deficiencies, burdens and weakens the immune system
chronic stress stimulates production of adrenal hormones, inhibiting immune function, shrinking the thymus gland and weakening protective responses against cancer
insufficient rest (sleep) time, high sugar intake,
high blood lipids, nutritional deficiencies,
smoking, alcohol, overweight,
negative emotions
many poor lifestyle choices alone negatively affect immune function, and their combined negative effect is disproportionally larger
C3 - Compromised detox system
due to toxic overload, toxic intestines (bacterial/fungal overgrowth), leaky gut, nutritional deficiencies, chronic stress and/or
negative emotions, chronic dehydration 
C4 - Genetic aberrations
compromising cell cycle control and immune system efficiency
C5 - Other promoting factors
nutritional deficiencies/imbalances high-glycemic diet - causing elevated blood level of both, insulin (with or without insulin insensitivity) and IGF, which promotes cell proliferation similarly to estrogen
high-sugar diet - in addition to being a high-glycemic food, sugar inhibits the immune system; higher rate of glycolysis (burning glucose for energy within cell) increases concentration of its by-product, lactic acid, making cell more acidic, hence compromising its optimum functioning
low fiber - evidence supports inverse relationship between dietary fiber intake and breast cancer risk
specific mineral/vitamin deficiencies compromising detox, immune, and/or cellular function
regular alcohol consumption regular, even quite moderate consumption inked with higher blood estrogen levels; other possible mechanisms include increased solubility of carcinogens, interfering with folate metabolism, elevated oxidative stress and mutagenic effects of its primary metabolite, acetaldehyde
smoking contains over 4000 chemicals, most of them toxic, and over 50 known carcinogens
low melatonin melatonin is an estrogen antagonist hormone; it also acts as antioxidant, antimitotic and immune-enhancing agent; body produces melatonin mainly during nighttime sleep, in darkness; thus lack of nighttime sleep, or lighted room, inhibit melatonin production, and so does exposure to power (electrical) field
breast compression the risk seems to become the more significant the longer bra is worn over several hours a day, on daily basis
overweight/obesity according to research data, overweight and obesity are risk factors for postmenopausal women;
weight gain (postmenopausal) can enhance estrogen production and lead to estrogen dominance state
lean body (premenopausal) if resulting from diet restriction,
metabolic disturbance or deficiency
insufficient/inadequate checkups latter stages at the time of diagnosis significantly lower chances for recovery
risk of false negatives,
compression risk, radiation risk

The above list of breast cancer risk factors, as overwhelming as it is, is neither complete nor clear with respect to mechanisms leading to carcinogenic transformations. It is barely scratching the surface of the complexity behind the onset and progress of this disease. Many factors are involved, and

their significance and interplay can vary greatly
from one individual to another.

In addition, there are certainly some pieces of the puzzle that we are still unaware of. But what is known so far is both, best reference and best starting point for understanding the disease, and for taking steps to efficiently minimize the risk of becoming a part of the breast cancer statistic.

Obviously, there is much more that can be said about each of these factors. That journey starts with the following page.