Breast Cancer

PART I

The science of endocrinology has taught us that organs whose growth and function are under hormonal control will become malignant from excessive hormone stimulation. Based on the science of endocrinology, breast cancer is defined as a hormonal imbalance involving the over stimulation of cells by growth and reproductive hormones, and usually develops in women in their middle ages or older. A time at which, both growth hormones and reproductive hormones should be declining.

Since, breast cancer is not inherited nor the result of an infection it is most probable that breast cancer more accurately reflects the total accumulation of hormone stimulating dietary habits over one’s lifetime.

With respect to dietary sources, dairy is unique because it contains substantial amounts of both growth and reproductive hormones.

In 1986 a study of 1,010 breast cancer cases in France reported a positive association between the risk of breast cancer and the daily consumption of whole milk. In 1989 a study in Italy set out to investigate the association between breast cancer and the intake of animal fat. A considerable reduction in the risk of breast cancer was found in women who were consuming total fat intake below 28% of the total calories.

In this article the word dairy was not used in the title, or in the author’s introductory abstract of the article, or in the author’s summary of the article, since a study of dairy was not the purpose of the experiment. However, the author could not keep from commenting that the data results from his study reveals a positive association exist between breast cancer and the consumption of dairy.

In 2002 a study in Uruguay investigated an association with dairy intake and cancer. Out of 311 women studied 111 women had breast cancer. In this study whole milk was associated with a significant increase in the risk of breast cancer, whereas non-fat yogurt was not.

In 2003 a large population study took place in Boston. Premenopausal women were found to have an association between the intake of fat and the risk of breast cancer. The authors consider the risk of breast cancer to be only slightly increased. Nevertheless, among the food items studied it was dairy and red meat that was associated with an increased risk.

During this time, parallel research groups were focusing on what components in dairy might be contributing to the disease. In one study, 1,893 women were treated for invasive breast cancer and followed for 11 years. During this period, 349 women experienced a recurrence and 189 women died from breast cancer. Dairy was associated with higher risk of mortality from breast cancer; and elevated estrogen hormone levels could be a contributing factor.

In 1995 the first epidemiological confirmation of a link between estrogen and breast cancer took place in New York City. This study group set out with the sole purpose of assessing the risk of breast cancer in relation to the blood levels of estrogens in women. All women who developed breast cancer had higher blood levels of estrogen compared to those women who remained cancer free.

In 2006, 418 breast cancer patients are found to have higher levels of estrogens compared to women without cancer. Interestingly, the risk of breast cancer was not dependent of a family’s history of breast cancer, but more dependent on a women’s overall lifetime exposure to estrogens and dietary habits.

Subsequent to these earlier studies, biochemists and geneticists have identified estrogen binding receptor sites on cell membranes from specimens’ of breast cancer tissues. The mere presence of these estrogen receptors can generally be taken as a strong indication that breast cancer must be estrogen dependent. Indeed, DNA damage from estrogen is now considered to be the silent source of breast cancer and estrogen has been defined as a cancerous agent.

Any dietary habits that could decrease intake of estrogens, decrease blood levels of estrogens, or decrease endogenous production of estrogens could reduce the risk of developing breast cancer.

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Since, breast cancer is not inherited nor the result of an infection it is most probable that breast cancer more accurately reflects the total accumulation of hormone stimulating dietary habits over a woman’s lifetime.

PART II

In addition to the estrogens, concerns have also been raised about the growth hormones found in milk. Specifically a family of hormones referred to as the insulin-like growth factors (and the one were interested in is abbreviated as IGF-1) because IGF-1 blood levels are associated with the risk of breast cancer.

One problem stems from the fact that the hormones from milk do survive the pasteurization process, are absorbed in the human intestinal tract, and do remain bioactive in humans. Dietary experiments, with milk intake, has been shown to increase IGF-1 levels in both children and adults by up to 20%.

Furthermore, the growth hormones from milk are identical to the hormones already present in humans since birth. They share an identical genetic amino acid sequence; dairy-based growth hormones will bind to the same receptor sites on human cell membranes as do human hormones.

IGF-1 hormones are found naturally in all humans and is a requirement for the growth and development from the embryonic stage through puberty. After puberty blood levels of IGF-1 will decrease every year at a rate of approximately 2 to 6 ng / ml. Regardless of age, after puberty, blood levels of IGF-1 should be declining each year in all women.

However, like estrogen, the normal age-related expected decline in IGF-1 hormone levels is exacerbated by the long-term consumption of milk. In addition, there is a component of milk protein that, after ingestion, increases the endogenous production of IGF-1 hormones; this component is known as casein. The casein content from milk protein stimulates the human body to increase its own production of IGF-1 hormones independently of the IGF-1 hormones already in milk that will be transferred by ingestion of milk.

Thus, consumption of milk will increase IGF-1 blood levels in humans through two independent pathways.

High blood levels IGF-1 in adulthood shifts the natural order of human life by signaling the body to continue to grow after the body is no longer capable of growth. This over stimulation from the untimely presence of growth hormones disrupts the normal life cycle of a cell.

Supporting information on this subject comes from a patent application filed in 2010 requesting protection for the capability to inhibit elevated IGF-1 concentrations in humans caused by the consumption of milk. The patent identifies ten different organ diseases considered to be associated with the consumption of milk.

The grounds for this patent are based upon the claims that, in the scientific community, consumption of milk is regarded as a violation of a physiological principal in mammalian nutrition development during the eons of mammalian evolution.

As a consequence, the casein in milk has been identified as the basic environmental factor promoting a permanent shift in the insulin/IGF-1 axis to higher levels which are inadequate for humans. Gynecologist should advise women not to consume milk during pregnancy. Oncologist should advise their cancer patient families to refrain from milk and milk protein consumption. Dermatologists and pediatricians should recommend to reduce milk consumption in patients with acne. Pediatricians and general practitioners should consider milk restriction in patients with obesity.

Thus, the milk consumed by the general public will contain enough hormones that are transferred to humans, do remain biologically active, and have a negative impact on human health.

In summary, any dietary habits that could decrease intake of IGF-1, decrease blood levels of IGF-1, or decrease endogenous production of IGF-1 could reduce the risk of developing breast cancer.

High blood levels IGF-1 in adulthood shifts the natural order of human life by signaling the body to continue to grow after the body is no longer capable of growth. This over stimulation from the untimely presence of growth hormones disrupts the normal life cycle of a cell.

PART III

Based on parts I and II, science has proven that dietary choices are principal regulators of human hormones, and their associated diseases.

More specifically, the reproductive hormone estrogen and the growth hormone IGF-1 are both classified as proliferation and anti-apoptotic types of hormones. Proliferation is an abnormally accelerated rate in growth and number of cells. The apoptosis (a-pop-to-sis) process is the natural programmed cell death that all cells must go through in order to eliminate cellular waste from genetic mutations and for the dying cell to completely vanish. For any organ to function properly apoptosis is a requirement.

In its most simplistic context, cancer is the direct result of cells failing to undergo their genetically programmed cell death known as apoptosis.

Out of all of the chemicals in food, defined as essential nutrients, vitamin-A and vitamin-D are classified as anti-proliferative and pro-apoptosis nutrients. The inhibiting effects of both vitamin A and vitamin-D on the growth of cancer cells has been documented and explained in detail.

Within the nucleus, Vitamin A and Vitamin D displaces the estrogen nuclear-receptors from binding to their DNA sites. By down regulating the estrogen nuclear receptors, vitamin-A and vitamin-D function in tandem at the molecular level as growth inhibiting agents, counteracting the uncontrolled growth caused by overstimulation of IGF-1 induced by high estrogen concentrations.

Vitamin-A and vitamin-D inhibits proliferation and induces apoptosis, and are naturally occurring anti-cancer agents found in certain foods.

In its most simplistic context, cancer is the direct result of cells failing to undergo their genetically programmed cell death known as apoptosis.

PART IV

The relationship between vitamin A and vitamin D is best explained from a genetic point of view. In humans there is a family of proteins located within the nucleus of cells termed nuclear-receptors. This family of specialized proteins are capable of forming macromolecular complexes with each other referred to as a dimer. Dimer complexes are the actual molecular structures that will attach to a specific sequence of nucleotides in a DNA gene.

Out of the 48 known nuclear-receptors identified in the human genome, there is one, and only one that will chemically react with vitamin-D, referred to as the vitamin D-receptor. But for the vitamin D-receptor to bind to its DNA strand it must first form a dimer with a second nuclear receptor known as a retinoid-x-receptor.

Since vitamin-D-receptors require binding to the retinoid-x-receptors for genetic transcription and all retinoid compounds are derivatives of vitamin A then vitamin-D must be dependent to some extent on vitamin-A.

With this hypothesis in mind, it is logical to assume, since vitamin D has been shown to regulate bone health then vitamin A might have some effect on bone health as well.

Indeed, at the macro level, high concentrations of vitamin A derivatives (retinoic acid) inhibits the activity of bone cells responsible for the synthesis of bone, known as osteoblast. While at the same time stimulates the formation of bone cells responsible for the release of calcium from bone, known as osteoclast. When the osteoclast activity overtakes the osteoblast activity there will be a decrease in bone formation and an increase in bone loss.

Excessive dietary intake of vitamin A over a prolonged period of time can create an antagonist action on the metabolism of vitamin-D and calcium, that normal blood levels of vitamin D and calcium may not be able to overcome.

In a study known as the “Rancho Bernardo Study” in San Diego California the effects of vitamin A on bone density was investigated in elderly men and women. This was a study in a community-dwelling of individuals over 55 years old consisting of 570 women and 388 men. Measurements of the total hip, neck of the femoral bone, and lumbar spine were recorded in the beginning and after four years. Individuals consuming multivitamins containing vitamin-A had lower bone mineral density at all measured locations, and a greater over-all loss of bone compared to those consuming no vitamins.

Similar results were found in a larger study of registered nurses living within 11 U.S. states, known as the Nurse’s Health Study. This was an 18 year analysis of vitamin A intake and hip-fractures among postmenopausal professional women. In this study women who were consuming vitamin A supplements had a 40% increased risk of hip-fractures compared to the non-supplement group.

It was not the intake of a supplement, per se, that was suspect in the above studies. Vitamin A from a supplement will have no more nor less of a damaging or a beneficial effect than an equal amount of vitamin A from food. It is the total vitamin A intake over a period of years that is important and not its source, as the above studies confirmed.

The problem lies with the observations that individuals are prone to be overly reliant on supplementation without first knowing their dietary vitamin A intake. In addition, the public may be unaware of the toxic effects associated with vitamin A intakes above the RDA over a long-period of time known as hyper-vitaminosis A. Especially if supplements are consumed along with a vitamin A rich diet.

Supplementation with vitamin A should not be discontinued when used for conditions for which benefits have been documented, but this must be determined on an individual basis and only by a physician.

Just like someone would not trust his or her dental care to an auto mechanic nor should one make decisions, on their own, about supplementing with fat soluble vitamins. Fat soluble vitamins, like vitamin A, are prone to build up to toxic concentrations without any symptoms, and will go unnoticed by the untrained eye.

The next area of concern is to determine how much vitamin A should individuals be consuming on a daily basis to lower the risk of becoming deficient or toxic, and what blood levels of vitamin A can be considered a safe target to shoot for.

In one study, a vitamin A intake corresponding to about one large serving of liver diminished the ability of vitamin D to increase intestinal calcium absorption. In this experiment ingestion of 15 mg of retinyl palmitate resulted in a significant decrease of calcium blood levels. In a study of Swedish women the risk of hip-fractures was doubled in women consuming 3000 mcg of vitamin A per day compared women consuming 1000 mcg per day.

In chronic vitamin A toxicity cases the total daily intake of vitamin A was always above the RDA for several years and the patients were completely unaware of any potential dangers.

To put blood levels of vitamin A in a proper perspective, towards the lower end of the range considered to be acceptable blood levels below 40 mcg/dL (micrograms/deciliter) is associated with a mild level of night blindness, based on dark adaptation testing, and is a reliable indicator of a mild subclinical deficiency and a deficient diet.

Towards the upper end of the range considered to be acceptable, blood levels of vitamin A above 75 mcg/dL is associated with an increased risk of hip-fractures in elderly men and women from consuming a diet too rich in vitamin A. Thus, it is reasonable to propose a theoretical optimal blood level for vitamin A midway between 40 to 75 mcg / dL.

The problem we have is that many laboratories consider blood levels of vitamin A between 30 mcg to 95 mcg / dL to be normal.

Thus, intakes of vitamin A above the RDA and blood levels of vitamin A currently considered to be acceptable have the potential to intensify or cause hip-fractures by interfering with calcium and vitamin D metabolism and by doing so, may indirectly contribute to the risk of breast cancer. Thus, controlling blood levels of vitamin A and estimating dietary intake of vitamin A will help in managing vitamin D and assist in determining whether or not; vitamin D supplementation is necessary.

Excessive dietary intake of vitamin A over a prolonged period of time can create an antagonist action on the metabolism of vitamin-D and calcium, that normal blood levels of vitamin D and calcium may not be able to overcome.

PART V

In addition to vitamin A, vitamin-D metabolism is regulated by blood levels of phosphorus and the parathyroid hormones, and both are regulated by dietary intake of phosphorus. In one dietary experiment of healthy men, a high phosphorus intake induced declines’ in blood concentrations of vitamin-D. When dietary phosphorus was restricted for ten days, blood concentrations of vitamin-D increased and within a week stabilized at almost twice the value than when phosphorus intake was normal.

In second small study for 8 days, 7 healthy adult males participated in a phosphorus restriction experiment under strictly controlled normal metabolic conditions. Blood concentrations of phosphorus and vitamin-D were measured hourly over a 24 hour period before and after the experiment. Results showed a dietary phosphorus restriction from 2300 mg / day to 625 mg / day induced an increase in blood levels of vitamin-D by 53%. Thus, before managing vitamin D to reduce the risk of cancer, blood levels of phosphorus and dietary intake of phosphorus must be a priority.

PART VI

When one first thinks of vitamin D what immediately comes to mind is bone. However, attention is no longer focused on just bone, but more importantly on the fact that specialized vitamin D proteins, termed nuclear-receptors (as mentioned above) have been discovered in tissue cells in all major organs including the breast.

It is now accepted that an inverse relationship does in fact exist between vitamin D and breast cancer, and the association between vitamin D and cancer is incontrovertible.

Blood concentrations of vitamin D is currently believed to be the best assessment of the body’s status of vitamin D, unlike vitamin A and phosphorus whose blood concentrations are unrevealing until in advanced stages of liver and kidney disease.

However, dietary recommendations for vitamin D intake has led to some confusion among some nutritionist and dietitians, since the recommendations from three different advisory groups differs considerably. The National Endocrine Society recommends adults should be consuming up to 1600 IU (International Units) of vitamin D per day. The National Osteoporosis Foundation recommends that postmenopausal women should be consuming 800 to 1000 IU /day.

Whereas, the Institute of Medicine, which is the committee responsible for our current RDA, recommends only 600 IU/ day.

In the scientific community there is a general consensus that blood levels of vitamin D should be maintained above 30 ng / ml (nanograms / milliliter) to allow sufficient reserves for use by the organs not containing bones.

In a study of nursing home patients, women consuming 600 IU / day for five months had blood levels of vitamin D peak at 24 ng / ml. Only when given 800 IU / day for 5 months did patient blood levels rise above 30 ng / ml. Women were unable to raise blood concentrations of vitamin D to levels considered to be sufficient until vitamin D intake exceeded the RDA by 200 IU. In the absence of sunlight exposure, vitamin D intake at the RDA amount may not be adequate to avoid a long-term subclinical deficiency in a percent of the population.

The committee responsible for establishing the RDA used as the foundational bases the information taken from studies on only calcium and bones. The committee considered the research used in arguing for higher intakes to be inconclusive, since some studies had failed to show similar results.

Variability in study results does not disprove either study; variability simply reflects differences in model design and choice of parameters. Inconclusive results between different research teams does not justify the lack of making decisions based on the research teams that discovered plausible medical reasons. Since the absence of proof proves nothing, the scientific studies who found possible associations between nutrient levels and disease must trump over those that did not.

The vitamin D recommendations of 600 IU per day is underestimated since it fails to take into account the body’s needs for vitamin D in organs not containing bones, such as the breast, prostate, colon, rectal, lungs, liver, and kidneys. Laboratory experiments have found favorable response with vitamin D intake between 800 to 1100 IU / day and blood levels between 60 to 80 ng / ml.

The Upper Limit for Nutrients

Before closing I must comment on the dietary intake known as the Upper Limit. The Institute of Medicine has established a recommendation for vitamin A for male adults at 900 micrograms per day with an Upper Limit of 3000 micrograms per day.

I find the whole concept and logic for an Upper Limit to be troubling. If you have established a recommendation for a particular nutrient’s intake, which was based on science, then you should recommend using the recommendation you initially recommended instead of an upper limit that allows for the intake of a nutrient in amounts greater than normally found in food.

The use of an Upper Limit sends a message to the general public that it is safe to consume vitamin A in intakes above the RDA when it is not. Unless under medical supervision, there are no well-established therapeutic benefits to consuming intake of vitamin A above the RDA. Toxicity and hip fractures at intake levels between the RDA and the Upper Limits have been documented.

Even moderate amounts of vitamin A just above the RDA, if ingested over a prolonged period of time may interfere with vitamin D’s regulation of calcium and may be reflected in hip fractures.

Intakes of vitamin A currently considered to be safe based on the logic of an Upper Limit has the potential for exacerbating osteoporosis and bone fractures which are already serious public health problems, and if continued on a regularly basis could result in an increased risk of bone disease, liver disease, and breast cancer.

Blood concentrations of vitamin D is currently believed to be the best assessment of the body’s status of vitamin D, unlike vitamin A and phosphorus whose blood concentrations are unrevealing until in advanced stages of liver and kidney disease.

SUMMARY

First, in all of the risk factors that can be modified dietary factors remains the most promising for the prevention of cancer. Because the growth hormones and reproductive hormones signaling pathways are linked, targeting both pathways concurrently by dietary modifications, such as eliminating dairy, could result in a significant reduction in the risk of developing breast cancer.

Thus the nutritional advice to reduce the risk of breast cancer is to first block estrogen from supporting the growth of breast cells by eliminating all dairy. Humans are the only mammals on earth that continues to consume milk after weaning.

Secondly, start recoding and tracking blood levels of estrogens and IGF-1 hormones, and make sure they are declining each year.

The induction of apoptosis by maintaining adequate intake and blood levels of both vitamin A and vitamin D could provide the ultimate avenue for eradicating abnormal clones or premalignant cells that may have occurred under previous inadequate nutrient intakes.

Therefore, nutritional advice, is to first maintain blood levels of phosphorus at the lower end of the range considered to be normal, and restrict dietary intake of phosphorus to the RDA recommendations for age and gender. Secondly, maintain blood levels of vitamin A between 40 to 75 mcg / dL while maintaining dietary intake at the RDA amounts based on age and gender. After controlling dietary intake of both phosphorus and vitamin A maintain blood levels of vitamin D at the upper end of the range by maintaining intake of vitamin D between 800 to 1000 International Units (IU) per day.

Maintaining a certain dietary intake of vitamin D is a little tricky and will require a little time on your part because approximately 90% of the vitamin D circulating throughout your body is synthesized from sunlight exposure.

Before you could make an informed decision on supplementing with vitamin D it would be nice to know what your personalized vitamin D synthesis is in response to sunlight exposure. First have both blood levels of vitamin A and vitamin D tested. Next adjust intake of vitamin A based on the estimated dietary intake from the nutrient data found in the chapter on vitamin A. Then every day for three weeks between 10:00 AM to 3:00 PM take a brief walk for 30 minutes in full sunlight exposure without sun screen. Remember your health depends on this so be serious. After three weeks have both Vitamin A and Vitamin D re-tested and consult with your physician.