I Wish I Were Far From the Madding Crowd

April 11, 2010

Some Breast Cancer Cases Caused by a Virus?

It looks like the answer could very well be yes.

The Pink Virus Project

See Dr. Ruddy’s latest post describing her long history in this area.

“Breakthroughs Around the Globe”

Approximately 40% of human breast cancers contain gene sequences that are remarkably similar to a retrovirus known to cause breast cancer in domestic mice. Furthermore, the highest incidence of human breast cancer worldwide occurs in geographic locations where the domestic mouse is native or introduced to the area.

The book, The Pink Virus: Does a Virus Cause Breast Cancer in Women?

Presentation by Dr. Ruddy on The Pink Virus

Summary of Research

http://breastcancerbydrruddy.com/2009/11/01/the-pink-virus-2/

Brief Report on the Pink Virus Breast Cancer Summit

http://www.breasthealthandhealing.com/socialnetworking/messages/20091101.html

Cancer-Causing Virus Linked to Breast Cancer – Includes more info on the Pink Virus Project summit.

Brief bibliography on breast cancer and viruses

Articles cited at bottom of page at http://www.breasthealthandhealing.com/socialnetworking/messages/20091001.html

Updated (and more technical) Bibliography of Research on the Mammary Tumor Virus

http://breastcancerbydrruddy.com/2009/11/15/updated-bibliography-of-research-on-the-mammary-tumor-virus/

Breast Health and Healing’s YouTube Channelhttp://www.youtube.com/user/BreastHealthHealing

A New Virus in a Spontaneous Mammary Tumor of a Rhesus Monkey. Harish C. Chopra and Marcus M. Mason.  Cancer Research 30, 2081-2086, August 1, 1970. http://cancerres.aacrjournals.org/cgi/content/abstract/30/8/2081

Chemical Exposure and Breast Cancer?

The CDC has reported in its Fourth National Report on Human Exposure to Environmental Chemicals that many chemicals are showing up in Americans’ bodies.  (Presence alone does not indicate adverse effects, but as I have blogged about before, exposure during certain windows of development can have long-term effects.)

The Fourth Report includes results for 75 chemicals measured for the first time in the U.S. population.  Among the chemicals: environmental phenols, including bisphenol A and triclosan.  According to the Executive Summary:

  • Bisphenol A (BPA), a component of epoxy resins and polycarbonates, may have potential reproductive toxicity. General population exposure to BPA may occur through ingestion of foods in contact with  BPA-containing materials. CDC scientists found bisphenol A in more than 90% of the urine samples representative of the U.S.population.
  • Polybrominated diphenyl ethers are fire retardants used in certain manufactured products. PBDEs accumulate in the environment and in human fat tissue. One type of polybrominated diphenyl ether,BDE-47, was found in the serum of nearly all of the NHANES participants.

Could women be more vulnerable to a breast cancer virus because of exposure to environmental chemicals (either because the chemicals themselves might contribute, or because they negatively affect the immune system)?  See recent articles at bottom about BPA and phthalates.  See also U.S. News post re what could possibly be one of the more likely sources of BPA exposure—your receipts, not plastic bottles. (Science News itemWarner Babcock Institute for Green Chemistry)

Articles Ahead of Print from Environmental Health Perspectives

Bisphenol A (BPA)

“Placental Transfer of Conjugated Bisphenol A and Subsequent Reactivation in the Rat Fetus.” – Online April 9, 2010.

Nishikawa M, Iwano H, Yanagisawa R, Koike N, Inoue H, Yokota H 2010. Placental Transfer of Conjugated Bisphenol A and Subsequent Reactivation in the Rat Fetus. Environ Health Perspect :-. doi:10.1289/ehp.0901575

Urinary, Circulating and Tissue Biomonitoring Studies Indicate Widespread Exposure to Bisphenol A

Laura N. Vandenberg, Ibrahim Chauhoud, Jerrold J. Heindel, Vasantha Padmanabhan, Francisco J.R. Paumgartten, Gilbert Schoenfelder Online 24 Mar 2010 | doi:10.1289/ehp.0901716

Phthalates

Investigation of Relationships between Urinary Biomarkers of Phytoestrogens, Phthalates, and Phenols and Pubertal Stages in Girls

Mary S. Wolff, Susan L. Teitelbaum, Susan M. Pinney, Gayle Windham, Laura Liao, Frank Biro, Lawrence H. Kushi, Chris Erdmann, Robert A. Hiatt, Michael E. Rybak, Antonia M. Calafat Online 22 Mar 2010 | doi:10.1289/ehp.0901690

Articles notes a weak association between exposure and earlier puberty.  In a press release Dr. Wolff noted that though the association is weak, given the widespread exposure the public health implications are actually quite large.

This was a multi-ethnic longitudinal study of 1151 girls from New York City, greater Cincinnati, and northern California who were 6-8 years old at enrollment (2004-2007).  Measurements were done one year later.

Results: Breast development was present in 30% of girls (ed. note: remember the girls would have been 7-9), and 22% had pubic hair. High-molecular-weight phthalate metabolites were weakly associated with pubic hair development (adjusted PR 0.94 (0.88-1.00), fifth vs first quintile). Small inverse associations were seen for daidzein with breast stage and for triclosan and high-molecular-weight phthalates with pubic hair stage; a positive trend was observed for low-molecular-weight phthalate biomarkers with breast and pubic hair development. Enterolactone attenuated BMI associations with breast development; in the first enterolactone quintile the association of high-BMI with any development was 1.34 (PR, CI 1.23-1.45 versus low-BMI); there was no BMI-association in the fifth, highest quintile of enterolactone.

Conclusions: Weak hormonally active xenobiotic agents investigated in this study had small associations with pubertal development, mainly among those agents detected at highest concentrations.

My point?  There are enough risks for breast cancer from other causes that we do not need to be assaulted by chemicals in our environment.

April 3, 2010

Obesity, HFCS, and fatty liver disease in children (as well as increased heart disease risk)

I personally am very interested in this topic because just over three years ago I had gone in to see my doctor because of abdominal pain.  My triglycerides and LDL were high.  He thought it might be my gallbladder so I went in for an ultrasound, which revealed that I had a fatty liver.

Fatty liver disease has not been considered a children’s disease, so it’s disturbing to read that children and adolescents are developing it, especially since there are usually few symptoms until the disease has progressed to a more advanced stage of steatohepatitis (aka hepatosteatosis) and scarring has already occurred.

According to the American Heart Association, more than 6 million children in the United States are affected.

High Fructose Corn Syrup Linked to Liver Scarring (HealthDay, March 19, 2010)

Reports on a study, “Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease,” which found that increased consumption of HFCS led to increased fibrosis (scarring) in patients suffering from NAFLD.

Fatty Liver Disease May Raise Heart Disease Risk in Overweight, Obese Kids (American Heart Association, April 3, 2010)

A fatty liver disease that is not well-known in overweight and obese children may be a precursor of cardiovascular disease, researchers reported in Circulation: Journal of the American Heart Association.

The overweight children with NAFLD had significant cardiovascular risk including higher levels of fasting glucose, insulin, total cholesterol, low-density lipoprotein (LDL, “bad” cholesterol), triglycerides and higher systolic and diastolic blood pressure than the control group.

NAFLD is the most common cause of liver disease in children and is associated with metabolic syndrome, a clustering of risk factors for the development of cardiovascular disease and type 2 diabetes. NAFLD is characterized by the presence of oily droplets of triglycerides in liver cells. More than 6 million children in the United States are affected.

NAFLD in overweight children is strongly associated with metabolic syndrome. The association is independent of both body mass index and insulin sensitivity.

Fatty liver disease often has no outward symptoms, which contributes to it going undetected. Although some children will have symptoms such as abdominal pain or fatigue, the majority remain symptom-free until the disease is in very advanced stages.

American Heart Association Scientific Statement on Metabolic Syndrome in Children and Adolescents (2009)

Since 2003, substantial new information has emerged in children on the clustering of obesity, insulin resistance, inflammation, and other risk factors and their collective role in conveying heightened risk for cardiovascular disease and type 2 diabetes. A constellation of these interrelated cardiovascular risk factors in adults has come to be known as the metabolic syndrome.

The scientific statement covers the following topics:

Selected References

Steinberger J, Daniels SR. Obesity, insulin resistance, diabetes and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Circulation. 2003; 107: 1448–1453.[Free Full Text]

Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement [published corrections appear in Circulation. 2005;112:e297 and 2005;112:e298]. Circulation. 2005; 112: 2735–2752.[Free Full Text]

Non-alcoholic fatty liver disease (NAFLD)

Once considered an illness of adults over 40, more and more children are being diagnosed with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH).  NAFLD can be a precursor to NASH, which can progress to cirrhosis.

According to Children’s Memorial Hospital in 2005 an estimated 1.6 million children were affected with fatty liver disease

But the American Heart Association now says that 6 million children have NAFLD (see above).

Note: The Children’s Memorial Hospital’s NASH program is a member of the NASH clinical research network.  In 2005, the NASH clinical research network launched a trial for treatment of liver disease in children. The NASH CRN website contains links to related information for patients.  Most of the website, however, is technical and requires an account to access.)

When complications such as cirrhosis cannot be controlled with treatment or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children. Obesity also contributes to diabetes and high blood cholesterol, which can further complicate the health of someone with NASH.  (From the NASH page on the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) website.)

From “Fatty Liver Disease is Common in the US

Source: Spare the exercise, spoil the liver

More information about fatty liver can be found on the American Liver Foundation’s Fatty Liver page and in their Fatty Liver Brochure.

In case you’re wondering what I did after my diagnosis…

At the ultrasound the technician had said, “Your gallbladder is fine, but you have a fatty liver.”  The way she said it made it sound like it was more than just a casual observation, so when I got home I did a quick search on the National Library of Medicine’s website, where I found a lot of information about NAFLD.  (I’m not a teetotaler, but I don’t drink much.)

The progression from NAFLD to NASH to cirrhosis to needing a liver transplant or you die got my attention. Even before I got the formal diagnosis from my doctor I changed my diet (I started eating fish, raisins, and nuts, as well as more fruit, nuts, raisins, whole grains, leafy green vegetables, and fiber (even tried quinoa); and fewer sugar-sweetened drinks) and lots more exercise.  I dropped about twenty pounds in four months and, more importantly, my triglyceride level dropped a lot.

I had relapsed a bit since then, but after viewing Dr. Lustig’s presentation on the effects of fructose (and having done some follow up reading on the topic) I have once again cut back on sugar consumption and have started working out more regularly once more.

If you’re been sort of blasé about fructose you might find yourself changing your mind if you look at the slides on the “Detrimental Effects of Fructose” from a presentation he gave at the National Institute of Environmental Health Sciences (NIEHS) (pp. 15-27, with final slides on p. 27 showing the end result) and look at how fructose metabolized by the liver ultimately results in the creation of lipid droplets (these are what create a “fatty liver”), FFA (free fatty acids) (which help trigger insulin resistance), and triglycerides (TG), resulting in higher blood pressure and inflammation (among other things).

April 2, 2010

Metabolic syndrome and exposure to persistent organic pollutants

Take a spoonful of sugar, add a pinch of chemicals that accumulate in fatty tissue, and voila, metabolic syndrome! So while Dr. Lustig may be on to something, it looks like fructose might not be the only thing to blame for the obesity epidemic.

The reason why persistent organic pollutants (POPs) are a problem is that they can bioaccumulate in fatty tissue.  (If fructose causes metabolic syndrome as Dr. Lustig says, and metabolic syndrome results in increased obesity, which in turn means more fatty tissue, and more fatty tissue can absorb more POPs, we would seem to have started a rather vicious cycle.)

The Editor’s Summary explains why the findings of this study are especially important (emphasis added).

The authors conclude that exposure to POPs through a diet high in fatty fish is capable of inducing insulin resistance and impairing both lipid and glucose metabolism. Furthermore, they found that n-3 polyunsaturated fatty acids failed to counteract the harmful metabolic effects of dietary POP exposure. This finding is important because the presence of n-3-polyunsaturated fatty acids in fish oil has been reported to have a wide range of beneficial effects, including protection against high-fat diet–induced insulin resistance. The authors conclude that there is a need to continue efforts to limit human exposure to dietary POPs even in foods containing protective factors such as polyunsaturated fatty acids.

Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome, Jérôme Ruzzin et al. Environmental Health Perspectives, 118(4) Apr 2010.

Related EHP news item:

Chew on This: Persistent Organic Pollutants May Promote Insulin Resistance Syndrome

Breast cancer and exposure to phthalates, PAHs, and petroleum byproducts

Several recently published studies on links between exposure to chemicals and breast cancer.

Study Links Chemical Exposure to Breast Cancer Risk

(MedPage Today) Women exposed at work at a young age to petroleum byproducts and synthetic fibers such as acrylic and nylon appear to be at the greatest risk of developing breast cancer after menopause.

Source: Labreche F, et al “Postmenopausal breast cancer and occupational exposures” Occup Environ Med 2010; 67: 263-69.

Exposure to Phthalates and Breast Cancer Risk in Northern Mexico

Lizbeth López-Carrillo et al.  Environmental Health Perspectives, 118(4) Apr 2010.

The authors show for the first time that exposure to diethyl phthalate, the parent compound of monoethyl phthalate (MEP), may be associated with increased risk of breast cancer.

Editor’s Summary

Associations between Polycyclic Aromatic Hydrocarbon–Related Exposures and p53 Mutations in Breast Tumors

Irina Mordukhovich et al.  Environmental Health Perspectives, 118(4) Apr 2010.

The findings suggest that PAHs, environmental pollutants formed by incomplete combustion of organic material (for example, smoking, wood burning, vehicle exhaust), may be associated with specific breast tumor p53 mutation subgroups rather than with overall p53 mutations and may also be related to breast cancer through mechanisms other than p53 mutation.

Editor’s Summary

PAHs in stormwater runoff

Another EHP news item on PAHs notes that researchers found that stormwater runoff was the main pathway by which PAHs enter waterways, contributing about half the New York/New Jersey harbor’s PAH load, and atmospheric deposition was an important contributor of smaller PAH compounds.  (Lisa A. Rodenburg, et al. Mass Balances on Selected Polycyclic Aromatic Hydrocarbons in the New York–New Jersey Harbor, doi:10.2134/jeq2009.0264, Journal of Environmental Quality, March-April 2010 39: 642-653.)

March 28, 2010

Risk factors for breast cancer – Missing one of the major ones?

Up to a third of breast cancers could be avoided (Yahoo! News)

http://news.yahoo.com/s/ap/20100325/ap_on_he_me/eu_med_avoiding_breast_cancer

European breast cancer conference in Barcelona. Carlo La Vecchia cited figures from the International Agency for Research on Cancer (website).  I couldn’t find the precise source for the figures, but perhaps they came from “Estimates of cancer incidence and mortality in Europe in 2008” (abstract only).

Conference website – http://www.ecco-org.eu/Conferences-and-Events/EBCC-7/page.aspx/840

Abstracts – http://www.ecco-org.eu/Conferences-and-Events/EBCC-7/Abstracts-online/page.aspx/2177

Or go directly to http://ex2.excerptamedica.com/ciw-10ebcc/

Type in “cancer” in the search field.  You should get 655 abstracts.

The focus of the conference was clearly on diagnosis and treatment with little to no discussion of environmental factors.  Certainly screening, diagnosis, and treatment are critical, but shouldn’t we try to prevent as much as we can?

More from the Yahoo story

Dr. Michelle Holmes of Harvard University, who has studied cancer and lifestyle factors, said people might wrongly think their chances of getting cancer depend more on their genes than their lifestyle.

“The genes have been there for thousands of years, but if cancer rates are changing in a lifetime, that doesn’t have much to do with genes,” she told The Associated Press in a phone interview from Cambridge, Mass.

Could perhaps increasing exposure to substances in the environment change rates in a lifetime?  That doesn’t have much to do with genes either.  Though if you’re being exposed to chemicals that interfered with how your genes were turned on and off before you were born, or are interfering with that now, perhaps it does.

Breast cancer is the most common cancer in women. In Europe, there were about 421,000 new cases and nearly 90,000 deaths in 2008, the latest available figures. The United States last year saw more than 190,000 new cases and 40,000 deaths.

Tara Beaumont, a clinical nurse specialist at Breast Cancer Care, a British charity, noted that three of the major risk factors for breast cancer — gender, age and family history — are clearly beyond anyone’s control.

What about environmental exposure to chemicals?

IARC, on its World Cancer Day page, notes that it has an active program in the identification of carcinogenic risks. The IARC Monographs identify environmental factors—including chemicals, complex mixtures, occupational exposures, physical and biological agents, and lifestyle factors—that can increase the risk of human cancer.

In other words, there are several other environmental factors besides lifestyle that have been identified.  See the articles below for examples of how environmental factors could be contributing to breast cancer.

While the advice to eat less and exercise more is good (in fact, given that no one really has much direct control over environmental exposures that advice is probably even more important), I find it disturbing that the major risk factors cited in news stories seem to be reduced to diet, lifestyle, gender, age, and family history (that is, genetics), leaving environment out of the picture.

Why is that?  Because it’s easier to blame cancer victims than to confront companies and industries that sell us products that release substances that can mess with our health and who continue to release carcinogens and endocrine disruptors into our air and water?  (I’ll refer you again to the TEDX site, “Prenatal Origins of Cancer” for more information on that.)

Another perspective

In a post “do patients need doctor navigators to use the internet?”, David Collins discusses a March 25 New England Journal of Medicine opinion piece titled “Untangling the Web — Patients, Doctors, and the Internet” in which the authors “expressed a lot of concerns about how the internet is putting patients in touch with a lot of questionable information about disease” and about how they thought that changes the doctor-patient relationship in an adverse way.  (While they do raise some good points about the quality of some of the information on the Internet, I tend to agree with Collins.)

The reason I’m citing that here is the following statement from his post:

When I joined cancer public health in the ’70s the medical community almost universally rejected the idea that food and nutrition had anything to do with the prevention of cancer. People who talked about a relation between nutrition and cancer were sneered at and called the “fruits and nuts” crowd. Thirty-five years later as I approached retirement I had to chuckle inwardly many times about the current enthusiasm for the view that diet and nutrition are key to the prevention of much cancer. These days ya gotta eat your greens and grains!

So even the experts can change their minds….

Finally, it seems that environmental factors only really get attention when there are clusters of rare cancers.

Democratic Senators Eye New EPA Role Investigating Local Cancer Clusters

Environmental Policy Alert – March 24, 2010

From InsideEPA.com’s Environmental NewsStand (pay-per-view news)

Note: The site has a one-time offer of three free articles or documents by creating a new account today.

Senate environment committee Chairwoman Barbara Boxer (D-CA) and Sen. Bill Nelson (D-FL) are working on legislation that would give EPA and the Department of Health & Human Services (HHS) a major new role helping local health agencies investigate and address cancer clusters and communicate risks to local residents.

Press release from Sen. Bill Nelson on legislation

Nelson plans to preview testimony he’s been invited to give at next Wednesday’s hearing (my blog post on the March 17 hearing), which aims to find ways to strengthen the federal government’s hand in investigating cancer clusters, like the Acreage.

Recent Acreage blog post on Nelson’s efforts

Right now the federal Environmental Protection Agency ( EPA ) and Department of Health and Human Services ( HHS ) usually don’t get involved absent a request from a state.
“This effort is aimed at finding ways to bring in more federal resources more rapidly to help protect people, especially little children,” said Nelson, who’s also expected on Friday to announce he’s partnering with U.S. Sen. Barbara Boxer on new legislation to do the same.
Sen. Nelson’s testimony at Senate committee hearing on EPA and children’s environmental health
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