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Health news:
 
June 2010 - Dec 2013

Minimizing breast cancer risk

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

NEWS ARCHIVE
2009
2008
2007

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June 2010 - December 2013

I - Breast cancer risk factors

4. Times change: The roots of breast cancer epidemic

2 good choices to prevent breast cancer

I - BREAST CANCER
 RISK FACTORS
  

II - SCREENING X-RAY MAMMOGRAPHY

III - ALTERNATIVE TESTS

The biggest risk factor
Risk factors overview
Times change

END OF A MYTH
The whistle
Contra-argument
Last decade
Current picture

 OTHER  X-RAY TESTS
Digital standard
Tomosynthesis
Breast CT

Predisposing factors
Diet     Other

BENEFIT
Earlier diagnosis
Fewer breast cancer deaths

Gamma-ray tests
BSGI/MBI 
PEM

INITIATING  FACTORS
Radiation
Chemicals
Viruses

RISK  &  HARM

OTHER  TESTS
Breast MRI
Ultrasound
Thermography
AMAS test

INACCURACY RISKS False negative
False positive
Overdiagnosis
PROMOTING  FACTORS
Hormonal
Non-hormonal

RADIATION

Radiation primer
Screen exposure
Radiation risk
PHYSICAL EXAM
Clinical
Self-exam

Higher all-cause mortality?

• Minimizing breast cancer risk

Breast cancer, as any other cancer form, stems from malfunction of the controlling cellular molecule, the DNA. This malfunction can be result of direct injury, or some specific form of interference with its function (i.e. gene expression), or both.

Not every cell injury, alteration or interference with the DNA cellular function will result in a cancerous (neoplastic) transformation of the cell. Usually, it requires several disturbances of the cell's regulatory mechanisms - both internal and external - with their specific effects combining to create a basis for the transformation.

One such disturbance may be caused by unrepaired DNA injury, another by an external factor modifying genetic expression, for instance hormonal regulation, or other factors in the mechanism of cellular growth and proliferation, like virus (tumor) proteins, and yet another by inherited negative DNA alteration. In order for these disturbances to push the cell toward neoplastic (malignant) transformation, their combined effect needs to be causing overexpression of genes stimulatory of proliferation (oncogenes) on one, and/or underexpression of genes inhibiting proliferation (anti-oncogenes, or tumor-suppressors), on the other side.

But this is only Stage One of cancer development. In the Stage Two, cancerous transformation faces cell's own regulatory mechanisms. Every cell has self-regulatory and repair mechanisms that should step in and prevent such transformation. But it doesn't always work out that way.

Among the cell's second-line defensive mechanisms is apoptosis, or programmed cell death. Every normal cell has its lifetime determined by the length of telomeres - a part of the DNA chromosomal structure necessary for division, whose length shrinks with each division, limiting number of replications of the cellular DNA. The purpose of it is to prevent cellular degeneration by accumulated DNA and other errors. Many a cell in the initial stages of cancerous transformation is terminated by apoptosis, effectively stopping possible cancerous growth. But not all of them; and if some factor, or factors, inhibits this complex mechanism, it opens up the door for malignant growth.

Finally, if neither cell's self-regulatory/repair mechanisms nor apoptosis stand in the way of cancerous transformation, the transforming cell may learn how to synthesize its telomere, becoming "immortal" - a full-fledged cancer cell, on its way to uncontrolled growth and invasion of other body tissues.

At this point, at the Stage Three of cancer development, the body still can prevent cancerous growth, by detecting abnormal cells and destroying them by the action of the immune system.

 The fact that there is a cancer, specifically, breast cancer growing,

 signals compromised body function on multiple levels:

from cells' internal protective, regulatory and repair mechanisms, to the possible and probable complicity by the external regulatory mechanisms, and to the immune system malfunction.

Of course, the degree of exposure to carcinogens is very important, too. There is no organism strong and healthy enough that won't succumb to a sufficiently high dose/length of exposure to a carcinogen. On the other hand, a body predisposed to breast cancer may fall pray to exposures well within safe level for the average individual.

In all, there is probably no more than a few dozens of genes within cell's DNA whose altered function can result in unrestrained proliferation. However, relatively few breast cancers - less than one in ten - result directly from germline (inherited) alterations. And, while not all genetic mutations are harmful (most of them do not have significant effect, and some can be even beneficial), any change in the genetic code is potentially risky, and the DNA integrity is best to be protected as much as possible.

Vast majority of breast cancer cases starts due to malfunction caused by multiple accumulated changes in the DNA - damage, alteration or functional disruption (e.g. change in gene expression) - that takes place during the lifetime. What is often neglected, especially by the official medicine and pharmacology, is this

true breast cancer cause - the factors inflicting
genetic damage or alteration.

So, what is it that spurs this rising epidemic of breast cancers? Are our genes becoming more vulnerable, or is it more carcinogens around, or both? Recalling the undisputed link between breast cancer incidence rates and the level of Westernization/urbanization in low-incidence countries, gives a hint worth following. What specific changes in the way of life and living environment can be identified as those fueling the breast cancer epidemic?

The contrast between the modern and past ways of life is the greatest if we go back all the way to today's hunter-gatherer societies, closely resembling the conditions modeling genes of our Paleolithic ancestors through many thousands of years. 

The first thing to note is that our genetic code has not changed in any significant way. There is no systemic change in the DNA making us significantly more vulnerable to breast cancer. Where the changes are likely to be significant is gene expression which, as we know from epigenetic research, responds to many environmental inputs. Convincing case can be made that

these changes in gene expression had an overly negative effect on our past natural resistance to breast cancer.

Combined with much higher exposures to carcinogens, it seems to be explaining good part of the breast cancer surge with modernization.

The big picture can be drawn by somewhat modified illustration from Women's Reproductive Cancers in Evolutionary Context (Boyd Eaton et al, 1994).

As the graph implies, the genome-based susceptibility to breast cancer remained generally unchanged, while the segment of population affected by the disease grew from relatively few individuals at the highest risk in older societies, to much greater numbers in modern societies, affecting individuals at a significantly lower genetic risk.

Originally, the illustration is for degenerative diseases in general, but it can be just as well used for breast cancer alone. "Modern societies" refers primarily to Westernized societies, as well as urban population subgroups, while "Older" refers primarily to hunter-gatherer societies, but also more contemporary ones that have preserved significant levels of their old lifestyle customs relevant to breast cancer risks.

What customs are those? Boyd Eaton et al. focused on women's reproductive experience, diet and physical activity. As their estimates show, the magnitude of change related to these factors in modern-time vs. old-time lifestyles is not only enormous, but also consistent in increasing breast cancer risk. 
 

 WOMEN'S REPRODUCTIVE EXPERIENCE

 

Hunter-gatherer

modern
American

Age at menarche

16.1

12.5

Age at 1st birth

19.5

24

Menarche to 1st birth (years)

3.4

11.5

Duration of lactation per birth

2.9 years

3 months

Average number of live births at age 50

5.9

1.8

Age at menopause

47

50.5

Total number of ovulations

160

450[1]

 DIET and PHYSICAL ACTIVITY

Dietary fat intake (% calories)

20

36

Triceps skinfold (mm)

9.6

17

Dietary fiber intake (g/day)

100

15

Maximal O2 consumption (ml/kg/min)[2]

51.8

42.5

 ESTIMATED RELATIVE BREAST CANCER RISK TO AGE 60 [3]

Hunter-gatherer

modern
American

1[4]

114[5]

[1] For women not using oral contraceptives
[2] Based on VO2 max, a measure of aerobic (endurance) fitness, for young man; women's data are "unavailable but believed to be comparable"
[3] Based on women's reproductive experience factors alone
[4] An estimated 9% of hunter-gatherers reach age 60, or beyond
[5] For educated American woman

Roughly three times longer period between menarche and 1st live birth, ten times shorter lactation period per child and 30 times shorter by age 50, as well as somewhat postponed menopause in American women translate into significantly higher lifetime estrogen exposure, and 114 times higher breast cancer risk on that basis alone (the estimate is for educated American women, with 1st childbirth at 2.5 years older age than the average, with other factors as shown in the table).

The estimated risks for epithelial ovarian and endometrial cancers in the study were 24 and 240, respectively (for American women not using oral contraceptives; 6.9 and 75, respectively, for 10-year contraceptive use).

These figures are necessarily (i.e. considering very limited data available for past and present hunter-gatherer societies) very approximate, merely indicating that the magnitude of risk increase is probably very large. Also, the estimate does not account for other diet-related factors related, nor for exposure to carcinogens, which further - and rather significantly - increase the risk.

Significantly higher fat intake of today's American women indicates the increase in caloric intake (which is probably similar for carbohydrates, mainly due to higher sugars intake). Their nearly doubled triceps skinfold reflects significantly increased rate of obesity, direct result of higher caloric intake and lower level of physical activity.

One of the consequences of processed foods diet is drastically lower intake of dietary fiber. It is only one of many negative aspects of the modified food consumption, which changed from nutrient-rich, pure natural foods to calorie-rich, nutritionally depleted, chemically and biologically contaminated processed foods.

Obviously, the 20% caloric intake of healthy, unprocessed fats by a hunter-gatherer woman is in more than one way healthier than 36% caloric intake of often toxic, processed fats by the modern American women, and substantially more so than what the intake figures alone indicate.

The common denominator for all developed non-westernized countries and, more conditionally, rural vs. urban populations, is that their lifestyles have deviated less from this low-risk model of hunters-gatherers, to which our genes are certainly better adapted than to the conditions of the modern Western life.

And, what makes it all worse, is that our exposure to carcinogens - agents capable of initiating cancerous transformations within the cell - is now much higher than before. Following page focuses on factors making women more vulnerable to carcinogens that can initiate breast cancer.

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