Surrounding Ourselves with Carcinogens: When in Rome

Caveman Doctor watches very little television (ever since the National Geographic living room fiasco on ’95).  However, he was recently watching Rome, which along with John Adams and Parks and Recreation, is possibly the greatest show ever created.  They actually ran out of money and crammed several seasons into Season 2, providing Caveman Doctor with non-stop action.  A few days later, he was sitting around the bonfire talking to some of his doctor friends about the show.  They were all commenting on how amazing it was that the women in Ancient Rome put lead on their face and that Romans drank wine out of lead glasses.  This got Caveman Doctor thinking.  What kind of unhealthy and dangerous chemicals do we lather ourselves with on a daily basis and what’s lining our wine glasses?


Plastics, Toxins, Chemicals, Carcinogens and Cancer: Why Losing the Fat May Be More Important than You Ever Imagined

One probably doesn’t need the definition of adipose or adipose tissue to know that it is fat that we all struggle to lose. We also likely do not need an in-depth discussion on the reasons why having too much fat is so bad. However, many are unaware of the connections with cancer. Fat tissue produces many inflammatory hormones that can lead to cancer. Fat tissue also causes the production and increase of estrogen circulating throughout the body.

Many breast tumors express estrogen receptors with which high levels of circulating estrogens can bind to these receptors and are correlated with an increased risk of breast cancer recurrence after treatment1 by upregulating cancer proliferation. These hormones also stimulate tumor growth and progression.2 Fat tissue is also capable of turning androgens to estrogen, further adding to the problem.3 Finally, excess adipose tissue results in decreased levels of sex hormone-binding globulin (SHBG),4 which binds and inhibits estrogen. As a result, excess fat increases cancer risk on both sides as it increases estrogen and decreases hormones that inactivate estrogen. Not a great combination if you are trying to avoid cancer.

The icing on the cake (a common product of a low-fat, standard American diet diet) , is the fact that estrogen up-regulates leptin expression and leads to increases in insulin and it’s cancer-causing partner, insulin-like growth factors (IFG-1). Both of these pesky hormones bind to the insulin receptor ramping up cancer growth and are increased from high carbohydrate diets (resulting in increased cancer and worse outcomes).5-7 Lastly, let’s not forget about all the inflammatory markers that are increased from having excess fat tissue on the body, especially around the abdomen. Fat cells secrete inflammatory mediators that stress the body excessively, including tumor necrosis factor alpha (TNFα), interleukin 6 (IL-6), and retinol-binding protein-4 (RBP4), all which promote cancer development.8

All-in-all, it is becoming abundantly clear that more body fat is leading to more cancer and worse outcomes with treatment.9 Adding this up, the fight against fat is indeed imperative in the fight against cancer.

However, what if reducing adipose tissue provided another substantial benefit against cancer that is rarely discussed?

Toxins in Our Environment, Stored in Our Fat

Toxins, pesticides, cancer-causing chemicals and other potential substances that stand in the way of good health are often neglected in our society. Conversely, those that don’t neglect them, with their aluminum water jugs and reusable cloth bags, often get an eye roll from the rest of society

Dr. Patricia Hunt, from the Washington State University, is a reproductive biologist. She may have been one of these people that would get an eye roll when talking about environmental toxins; however, the eye rolling may have stopped.

As a reproductive biologist, she studies meiosis, which is a form of cell division that produces sperm and egg cells, which are necessary for reproduction. She studies the errors that can occur during this basic process of life. To accomplish this, she has performed many experiments on mice. One such study didn’t turn out as planned.

Dr. Hunt was researching reproductive errors that were tied to hormone levels (much like breast cancer and estrogen discussed above). However, during the experiment, she found 40% of defects in the eggs of her pregnant control mouse population. Importantly, this was in the control, i.e. the cohort of mice that were not receiving any intervention. After months of searching for a cause, the answer for these reproductive errors came from an unsuspected place. She kept her mice housed in plastic cages and drinking out of plastic water bottles. Interestingly, these are the same bottles I drank out of during my outdoor basketball games in the hot sun leaching plastic into the water that I used to replenish my fluid loss. However, one night a janitor cleaned the cages with a corrosive substance that caused the chemicals in the plastic to leach out. In fact, the Bisphenol A (BPA) within plastic, which is a synthetic estrogen, was the main culprit. Much like estrogen’s ability to bind to cancer cells, stimulating growth and malignancy, the BPA from plastic was able to increase the hormonal levels within these mice, causing birth defects. Maybe that water bottle sitting in the sun all day wasn’t the best source of replenishment during my teenage years, when hormones are vital to development…

BPA is an unavoidable presence in many aspects of our life, including its usage as an additive for flame-retardants, brake fluids, paper, resins used in place of metal and glass, CDs, and DVDs, to name a few.10

How Can We Avoid Harmful Chemicals like BPA?

In the end of this article, many of the harmful daily chemicals will be listed along with a description of some of the risks. However, one main fact often overlooked is that we are likely unable to avoid many of these chemicals. They are ubiquitous to our environment. At this point, a good defense becomes a good offense.

For instance, Agent Orange, the chemical used during the Vietnam War, has been found in the adipose tissue of people who have no history of exposure.11 More importantly, exposure is actually measured by sampling the adipose (fat) tissue of those with whom exposure is suspected!12 These chemicals are all around us, in our products, environment, and even food. Scary, yes, but also enlightening.

The fact that those who are “unexposed” test positive for the toxins and chemicals in their adipose tissue brings us to the main reality – we can’t avoid these chemicals as they are already littered throughout environment. The next logical step is to attempt to reduce them by minimizing the storage capacity of such chemicals. In other words, a best defense is minimizing our amount of fat.

The big issue here is that these toxins are lipophilic, i.e. fat (lipid)-loving (philic). This means that when they enter your body, they are able to latch onto your fatty tissue for the long haul. Just as conjugated linoleic acid, which helps fight cancer, grabs onto your fat and settles there to fight disease, these toxins do the same only causing potential destruction. While it is impossible to reduce all adipose tissue, especially for women, and many aspects of our anatomy rely on lipids, reducing it may provide a method of decreasing our continued internal exposure to these chemicals. These chemicals are also passed to our offspring in breast milk, another fatty product.13

Perhaps a better definition is:

Plastics: All Around Us and All Just as Dangerous?

Plastic contains many chemicals, some shown to be harmful, some not.  While risks are often thought to be dose-dependent, finding an exact dose is nearly impossible as such studies in humans would be highly unethical. The harmful ingredients in plastics do not end with BPA, as plastics also contain phthalates, polybrominated diphenyl ethers (PBDE) and tetrabromobisphenol A (TBBPA). Due to Dr. Hunt, BPA receives most of the notoriety these days and has recently been banned from baby bottles.

However, other chemicals may be just as harmful, but the crosshairs have not been placed on them yet.  Phthalates block androgen function,14 and much like BPA, disrupt normal hormonal levels. BPA is also an endocrine disruptor (i.e. it disrupts the normal function of our thyroid and endocrine system) and mimics the action of estrogen, the bane of all evil, on our system.15 While we already know that increasing estrogen can result in an increased risk of malignancies, like breast cancer, disrupting our thyroid function can lead to obesity and metabolic dysfunction. In fact, a recent study has revealed that children exposed to high amounts of plastics (and phthalates) have five times the risk of being obese,16 and animal studies have shown the same results.17 The authors concluded that this is likely related to androgen and thyroid disruption. While this is only a correlation and perhaps other factors account for obesity in these children, other studies echo the detrimental health effects of plastic on children. Plastic in the walls of homes has also been shown to be associated with respiratory tract symptoms, asthma, and pneumonia in children.18

Phthalates have also been shown to cause testicular dysgenesis syndrome in animal studies14, which is clearly not healthy or normal. Plastic workers in Finland experience significantly increased risks of spontaneous abortion, along with workers in rayon factories.19 However, the ALARA principle holds here (as low as reasonably achievable). It is even used to hold blood products in the hospital, though studies show the chemicals in plastic leach out into the donor blood, potentially causing lung, liver, and fetal damage, among other problems.20

And if we think we are avoiding BPA, we’re not. It is present in the urine of up to 95% of the population.21

Endocrine Disruptors:

“An exogenous agent that interferes with the synthesis, secretion, transport, binding, action, or elimination of natural hormones in the body that are responsible for the maintenance of homeostasis, reproduction, development and/or behavior.22

Our endocrine system involves a fine interplay of chemical messengers and hormones between our brain (hypothalamus and pituitary) and body (thyroid, adrenal gland, and many other parts). BPA, and more specifically flame retardants containing BPA, have the distinct ability to bind to the thyroid hormone receptor and antagonize its function by blocking the binding of T3.23 Merely limiting these to small doses may not be enough, as endocrine disruption has been shown at even small amounts.24

Xenoestrogens: BPA and Beyond

Six billion pounds of Bisphenol A (BPA) are produced per year, giving this substance a significant presence within our environment. It is seen littered throughout parks and fills most trashcans in the form of water bottles and other plastic products. It lines cans, paper, cardboard, and other common materials, and it has been shown to be able to leach from aluminum cans, which are often lined with BPA. It has even been proven to wander from packaging and into baby formula.25

It has been shown to mimic estrogen in animal experiments and even stimulates prolactin secretion, which is the hormone that causes breast milk secretion. One interesting study took high doses of BPA and showed that it caused dose-dependent cellular proliferation (or growth) within the uterus and vagina, mimicking the effects of estrogen. However, the study’s data also showed that much lower doses released from continuous release capsules, closer to what we may encounter in our daily lives, resulted in hypertrophy and hyperplasia of the uterus, nearly identical to the actions of the hormone estradiol.26 These effects may be similar to diethylstilbestrol (DES), the pharmacological substance that was given to pregnant mothers several decades ago, which resulted in serious issues in their offspring.

BPA binds to and activates estrogen receptors27, even in very small doses.28 Estrogen is a major risk factor for the development and growth of breast cancer2,  and prostate cancer29, as estrogen receptors are often located on these  cancer cells. This is in essence why women who do not have children, early periods, or late menopause are at increased risk of breast and endometrial cancer, as they experience longer periods of estrogen release within the body. Fat tissue also secretes estrogen, which is also likely why it is associated with an increased occurrence of breast cancer and poorer outcomes with treatment.30

In cell cultures, BPA has been shown to stimulate growth and proliferation of estrogen-responsive breast cancer cells.31 Not only is BPA estrogenic, but it is antiandrogenic as it blocks androgens like testosterone as well. In fact, in rats, it inhibited the production of steroids within the testicles and resulted in decreased testosterone. Also, levels of BPA in pregnant mothers have been associated with recurrent miscarriages.32 Dose dependence may be irrelevant, as there is evidence that BPA and other xenoestogens in small doses could sensitize the organs in children to be more sensitive to these toxins in the future.

Finally, AKT, PI3K, and mTOR, the same pathways that we decrease through fasting, ketosis, and autophagy are stimulated by BPA33 and low levels of xenoestrogens.34 Activation of these pathways can also lead to the induction and promotion of cancer.

Organopesticides: Killing Insects but Not Harming Humans and the Environment?

This study first looked at polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), both which at first glance satisfy my rule that if a substance has more than 12 syllables then it must be bad for you. Reading where they come from: hazardous waste incinerators, solid waste from paper processing, metal reclamation, petroleum refining, wood preservation, and the production of chlorinated chemicals, my rule was once again reaffirmed. Human exposure occurs with these compounds via inhalation, ingestion, and skin contact.

Another similar chemical is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which clearly satisfies the 12 syllable rule as well. It is the toxic chemical in Agent Orange.35  After a plant explosion, residents in Italy were exposed to some of the highest levels of TCDD on record. Scientists flew in to run their experiments, because up until this point, they only showed significant increases in cancer and endocrine disruption in animal studies.36 This population initially experienced a significant increase in breast cancer, but over the long-term experienced a significant increase in all cancers from exposure to TCDD.37

Another major harmful chemical in our environment is polychlorinated biphenyls (PCBs). With 14 syllables, they are members of the group of semivolatile organic compounds, which by name, leaves no surprises that they are toxic to humans as well. Testing for these chemicals has been performed in humans alongside p,p-DDT (dichlordiphenylethylene), or DDT, which most of you are familiar with as the pesticide that was apparently a major threat to the bald eagle, and its ban is quoted as a major reason the eagle population has surged back from near-extinction.38 While the discovery of DDT resulted in a Nobel Prize for Paul Hermann Muller and helped to minimize malaria and dengue fever, dramatically reducing mortality in the South Pacific at first, he likely did not see this chemical resulting in the potential environmental damage and health issues, including prenatal death39 and a five-fold increased risk of breast cancer.40 Yes, these are epidemiologic studies, but the findings are remarkable nonetheless. To add insult to injury, many of the insects in the area where DDT was used developed resistance, and rates of transmission even increased. As a result, they were left with the same insect problems, but now humans and the environment were exposed to a potentially vicious toxin.

One study revealed that there was double the amount of PCDDs, PCDFs, and TCDD present in adults over the age of 45 versus that in children under the age of 14.41 These results likely show that as we age, our fat tissue accumulates more and more toxins due to exposure. A similar study showed PCBs present in amounts 188-706% higher in adults 45 years or older versus children under 14.42 The production of estrogen, the chemical that has been implicated in the causes and reduced outcome of breast cancer has been found to be elevated from organochlorine-based pesticides.43 The issue of hormone disruption is a reoccurring theme with toxin and chemical exposure.

Organopesticides are even found in salmon, a food de jour of the modern caveman.44 In fact one study showed that you can quantify how much fish someone is consuming by measuring plasma concentrations of PCDDs and PCBs in Finnish populations.45

While there have been many animal and epidemiologic studies discussing the known and potential health detriments of these chemicals, the smoking gun in humans remains unloaded. However, extrapolating from epidemiologic and animal studies, arguing against the health issues of such chemicals is a tough battle.

Phthalates and Parabens:

Phthalates are found in PVC and plastics, clay, waxes, paints, glue, toys. Added to allow plastic objects can smoothly rub along each other. They are easily released into the environment as they break down.

Beauty comes before health in the case of parabens. They are found in many cosmetics and are used as a preservative. They kill bacteria and fungi and are found in makeup, moisturizers, shampoo, deodorant, shaving gel, spray tan, and even toothpaste. They are estrogenic as well, and as such, have been found to be associated with breast cancer. An even more worrisome factor is that they are capable of penetrating the skin.

Parabens were found in the tumor specimens of 20 breast cancer patients.46 Did they cause the cancer? We have no clue, but this is an interesting finding because it shows that the skin absorbed the parabens, they traveled through the blood or lymphatic system, and ended up in breast cancer cells. No smoking gun, but more cause for concern. In their review of the data, the authors made a good point that they are not sure if the parabens caused the cancer or not, but they are found at the cancer site, so why not avoid them.47

Parabens have recently been shown to induce independent growth of breast cancer cells in a lab setting, even in very small concentrations.48 In mastectomy tumor specimens, paraben concentrations were compared across the breast, and they were found in significantly higher concentrations in the axilla (armpit area), where cancer occurs most often (the upper/outer quadrant).49

The final ironic nail in the coffin is recent research that has shown that parabens, which are used in sunblock, have been shown to increase skin damage in the presence of sunlight by causing free radical damage!50,51

In Conclusion

Caveman Doctor wants to lessen his exposure to Agent Orange, estrogen mimetics, and other harmful chemicals, but unfortunately, it is not up to him, as his environment is full of these substances. As a result, he strives to avoid them externally as much as possible and avoid them internally by reducing the areas where they could build up – his adipose tissue. For over two million years the adage hasn’t changed: The best offense is a good defense.


1. Rock CL, Flatt SW, Laughlin GA, et al: Reproductive Steroid Hormones and Recurrence-Free Survival in Women with a History of Breast Cancer. Cancer Epidemiology Biomarkers & Prevention 17:614-620, 2008,
2. Clemons M, Goss P: Estrogen and the Risk of Breast Cancer. New England Journal of Medicine 344:276-285, 2001,
3. Siiteri P: Adipose tissue as a source of hormones. The American Journal of Clinical Nutrition 45:277-282, 1987,
4. Cauley JA, Gutai JP, Kuller LH, et al: The epidemiology of serum sex hormones in postmenopausal women. American journal of epidemiology 129:1120-31, 1989,
5. Nam SY, Lee EJ, Kim KR, et al: Effect of obesity on total and free insulin-like growth factor (IGF)-1, and their relationship to IGF-binding protein (BP)-1, IGFBP-2, IGFBP-3, insulin, and growth hormone. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 21:355-9, 1997,
6. Kahn SE, Hull RL, Utzschneider KM: Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 444:840-6, 2006,
7. Champ CE, Volek JS, Siglin J, et al: Weight Gain, Metabolic Syndrome, and Breast Cancer Recurrence: Are Dietary Recommendations Supported by the Data? International Journal of Breast Cancer 2012:9, 2012,
8. Rivas MA, Carnevale RP, Proietti CJ, et al: TNF alpha acting on TNFR1 promotes breast cancer growth via p42/P44 MAPK, JNK, Akt and NF-kappa B-dependent pathways. Experimental cell research 314:509-29, 2008,
9. Calle EE, Rodriguez C, Walker-Thurmond K, et al: Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med 348:1625-38, 2003,
10. Fernandez MF, Arrebola JP, Taoufiki J, et al: Bisphenol-A and chlorinated derivatives in adipose tissue of women. Reproductive Toxicology 24:259-264, 2007,
11. Andrews Jr JS, Garrett Jr WA, Patterson Jr DG, et al: 2,3,7,8-tetrachlorodibenzo-p-dioxin levels in adipose tissue of persons with no known exposure and in exposed persons. Chemosphere 18:499-506, 1989,
12. Patterson Dg JHRENLL, et al.: 2,3,7,8-tetrachlorodibenzo-p-dioxin levels in adipose tissue of exposed and control persons in missouri: An interim report. JAMA: The Journal of the American Medical Association 256:2683-2686, 1986,
13. González MJ, Jiménez B, Hernández LM, et al: Levels of PCDDs and PCDFs in Human Milk from Populations in Madrid and Paris. Bulletin of Environmental Contamination and Toxicology 56:197-204, 1996,
14. Talsness CE, Andrade AJM, Kuriyama SN, et al: Components of plastic: experimental studies in animals and relevance for human health. Philosophical Transactions of the Royal Society B: Biological Sciences 364:2079-2096, 2009,
15. Maffini MV, Rubin BS, Sonnenschein C, et al: Endocrine disruptors and reproductive health: The case of bisphenol-A. Molecular and Cellular Endocrinology 254–255:179-186, 2006,
16. Society E: Phthalate, environmental chemical is linked to higher rates of childhood obesity., in ScienceDaily (ed), 26 Jun. 2012.
17. Newbold RR, Padilla-Banks E, Jefferson WN, et al: Effects of endocrine disruptors on obesity. International journal of andrology 31:201-8, 2008,
18. Jaakkola JJ, Verkasalo PK, Jaakkola N: Plastic wall materials in the home and respiratory health in young children. American journal of public health 90:797-9, 2000,
19. Hemminki K, Franssila E, Vainio H: Spontaneous abortions among female chemical workers in Finland. International Archives of Occupational and Environmental Health 45:123-126, 1980,
20. Rubin RJ, Ness PM: What price progress?: An update on vinyl plastic blood bags. Transfusion 29:358-361, 1989,
21. Calafat AM, Kuklenyik Z, Reidy JA, et al: Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Environmental health perspectives 113:391-5, 2005,
22. Kavlock RJ, Daston GP, DeRosa C, et al: Research needs for the risk assessment of health and environmental effects of endocrine disruptors: a report of the U.S. EPA-sponsored workshop. Environmental health perspectives 104 Suppl 4:715-40, 1996,
23. Vandenberg LN, Maffini MV, Sonnenschein C, et al: Bisphenol-A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption. Endocrine Reviews 30:75-95, 2009,
24. Welshons WV, Thayer KA, Judy BM, et al: Large effects from small exposures. I. Mechanisms for endocrine-disrupting chemicals with estrogenic activity. Environmental health perspectives 111:994-1006, 2003,
25. Vandenberg LN, Hauser R, Marcus M, et al: Human exposure to bisphenol A (BPA). Reproductive Toxicology 24:139-77, 2007,
26. Steinmetz R, Mitchner NA, Grant A, et al: The Xenoestrogen Bisphenol A Induces Growth, Differentiation, and c-fos Gene Expression in the Female Reproductive Tract. Endocrinology 139:2741-2747, 1998,
27. Gould JC, Leonard LS, Maness SC, et al: Bisphenol A interacts with the estrogen receptor α in a distinct manner from estradiol. Molecular and Cellular Endocrinology 142:203-214, 1998,
28. Welshons WV, Nagel SC, vom Saal FS: Large Effects from Small Exposures. III. Endocrine Mechanisms Mediating Effects of Bisphenol A at Levels of Human Exposure. Endocrinology 147:s56-s69, 2006,
29. Bonkhoff H, Fixemer T, Hunsicker I, et al: Estrogen receptor expression in prostate cancer and premalignant prostatic lesions. The American journal of pathology 155:641-7, 1999,
30. Brown KA, Simpson ER: Obesity and breast cancer: progress to understanding the relationship. Cancer research 70:4-7, 2010,
31. Rivas A, Lacroix M, Olea-Serrano F, et al: Estrogenic effect of a series of bisphenol analogues on gene and protein expression in MCF-7 breast cancer cells. The Journal of steroid biochemistry and molecular biology 82:45-53, 2002,
32. Sugiura-Ogasawara M, Ozaki Y, Sonta S, et al: Exposure to bisphenol A is associated with recurrent miscarriage. Human reproduction 20:2325-9, 2005,
33. Masuno H, Iwanami J, Kidani T, et al: Bisphenol A Accelerates Terminal Differentiation of 3T3-L1 Cells into Adipocytes through the Phosphatidylinositol 3-Kinase Pathway. Toxicological Sciences 84:319-327, 2005,
34. Goodson WH, 3rd, Luciani MG, Sayeed SA, et al: Activation of the mTOR pathway by low levels of xenoestrogens in breast epithelial cells from high-risk women. Carcinogenesis 32:1724-33, 2011,
35. Kang HK, Watanabe KK, Breen J, et al: Dioxins and dibenzofurans in adipose tissue of US Vietnam veterans and controls. American journal of public health 81:344-9, 1991,
36. Birnbaum LS: The mechanism of dioxin toxicity: relationship to risk assessment. Environmental health perspectives 102 Suppl 9:157-67, 1994,
37. Warner M, Mocarelli P, Samuels S, et al: Dioxin Exposure and Cancer Risk in the Seveso Women’s Health Study. Environ Health Perspect 119, 2011,
38. Stokstad E: Can the Bald Eagle Still Soar After It Is Delisted? Science 316:1689-1690, 2007,
39. Rogan WJ, Chen A: Health risks and benefits of bis(4-chlorophenyl)-1,1,1-trichloroethane (DDT). The Lancet 366:763-773
40. Cohn BA, Wolff MS, Cirillo PM, et al: DDT and breast cancer in young women: new data on the significance of age at exposure. Environmental health perspectives 115:1406-14, 2007,
41. Orban JE, Stanley JS, Schwemberger JG, et al: Dioxins and dibenzofurans in adipose tissue of the general US population and selected subpopulations. American journal of public health 84:439-45, 1994,
42. Lordo RA, Dinh KT, Schwemberger JG: Semivolatile organic compounds in adipose tissue: estimated averages for the US population and selected subpopulations. American journal of public health 86:1253-9, 1996,
43. Bradlow HL, Davis D, Sepkovic DW, et al: Role of the estrogen receptor in the action of organochlorine pesticides on estrogen metabolism in human breast cancer cell lines. Science of The Total Environment 208:9-14, 1997,
44. Huang X, Hites RA, Foran JA, et al: Consumption advisories for salmon based on risk of cancer and noncancer health effects. Environmental Research 101:263-274, 2006,
45. Kiviranta H, Vartiainen T, Tuomisto J: Polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in fishermen in Finland. Environmental health perspectives 110:355-61, 2002,
46. Darbre PD, Aljarrah A, Miller WR, et al: Concentrations of parabens in human breast tumours. Journal of applied toxicology : JAT 24:5-13, 2004,
47. Harvey PW, Everett DJ: Significance of the detection of esters of p-hydroxybenzoic acid (parabens) in human breast tumours. Journal of Applied Toxicology 24:1-4, 2004,
48. Khanna S, Darbre PD: Parabens enable suspension growth of MCF-10A immortalized, non-transformed human breast epithelial cells. Journal of Applied Toxicology:n/a-n/a, 2012,
49. Barr L, Metaxas G, Harbach CAJ, et al: Measurement of paraben concentrations in human breast tissue at serial locations across the breast from axilla to sternum. Journal of Applied Toxicology 32:219-232, 2012,
50. Okamoto Y, Hayashi T, Matsunami S, et al: Combined activation of methyl paraben by light irradiation and esterase metabolism toward oxidative DNA damage. Chemical research in toxicology 21:1594-9, 2008,
51. Handa O, Kokura S, Adachi S, et al: Methylparaben potentiates UV-induced damage of skin keratinocytes. Toxicology 227:62-72, 2006,

© 2015 CDR Health and Nutrition LLC. All Rights Reserved.


  1. Katalin

    Very interesting and informative post. Thank you!

    1. cavemandoctor (Post author)

      Thanks! Glad you enjoyed it.

  2. Caitlin Weeks

    Thanks for your hard work! Great article!

  3. Scott Moore

    This is an astoundingly useful article. I appreciate the time and effort you took to gather and synthesize all of this information. Thank you very much.

    1. cavemandoctor (Post author)

      Thanks Scott! Glad you liked it!

  4. Sheryl

    Thank you for this informative article. Great argument, as adipose tissue is a contributor, but there are other mediators and contributors to cancer. For instance, I had melanoma skin cancer at age 33 when I was btw 10% -12% body fat. At the time, I was a competitive natural bodybuilder and also diagnosed with osteopenia, high cholesterol, B 12 deficiency, hypothyroid, and depression. I was prescribed meds for the appropriate protocols.

    Since that was 10 years ago, I’ve connected some of the dots and had my doc test me for Hashimoto’s to which I was not surprised came up positive.

    Body fat is a contributor. Inflammation from the SAD, vaccinations, BPAs and other environmental toxins, along with stress can kill our amazing bodies. I am glad I caught the skin cancer and got mad, because now I am protecting myself and my family with free range organic locally raised meats, vegetables, and a warm loving home environment with no TV or processed foods.

    1. cavemandoctor (Post author)

      You hit the nail on the head.

      Take care,

  5. G. Suarez

    Great article! Very informative. Some things seem to make sense even though there is no scientific “proof” as of yet. Man made chemicals are being utilized at an alarming rate. The testing for them is always focused on that one chemical in small amounts. What most are neglecting are the cumulative effects of the interactions of a multitude of chemicals over a lifetime. We are bombarded with multiple products containing these chemicals. Their interactions are worrisome!

  6. Suzie_B

    Since toxins accumulate in adipose tissue, they would be released when one loses weight. Assume you have been obese for decades and then lose 100 lbs. Does this somehow increase or enhance your metabolic exposure to these toxins which could in the end make you sick with something like cancer? Thanks.

  7. Sarabi

    You mention that paraben concentration and tumor occurence are higher near the armpit area. You also mention antiperspirants contain paraben, and that this substance can be absorbed through the skin. Curious correlation.

  8. Pingback: The Bitter Benefits of Anticancer Vegetables - Part 2

Leave a Comment

Your email address will not be published. Required fields are marked *