On Friends Affected by Cancer, and Environment Oncology

Dear Readers,

Yesterday I learned that a woman I know slightly, a journalist, has Stage 4 lung cancer. Debra Sherman is a reporter for Reuters and began a blog, Cancer in Context.  It’s a moving start of what I hope is a long journey.

What struck me is how Debra describes crossing a line, a bit the way I felt when I found out I had breast cancer. She writes:

I have been writing about medical technology and healthcare for more than a decade. I’ve covered the major medical meetings, including the big one on cancer. I’ve written stories about new cancer drugs and treatments…I wrote those stories objectively and never imagined any would ever apply to me.

She’s shifted from what you might call a “straight” reporter to an i-reporter journalist. And although it’s true that Debra may be less objective than some other writers on the subject, she’s already knowledgeable – through her prior work – on many of the relevant terms and issues. Much of what she knows already, vocabulary included, may allow her to make more informed decisions. It’s possible it may enable her to write in a way that helps readers more than ever.

Earth, from space (NASA image, Wiki-commons)

Earth, from space (NASA image, Wiki-commons

I wish her the best with her column, and with her health ahead.

The bigger issue, of which the story reminds me, is that we’re living among too many young and middle-aged people who have cancer. Every day I read or hear of another case among my neighbors, a friend, a blog. Each reminds me of the need for research, better drugs, and greater knowledge of why so many tumor types – including lung cancer in women who haven’t smoked much, and breast cancer in young women – are on the rise.

The ASCO meeting, where believe me I wish I could be but can’t now, offers a bright picture for targeted drugs, genomics, novel immunotherapy and better data access and analyses through a huge new platform called CancerLinQ, All good. Great, really.

In thinking about each new case in my “world” – if I could pick a field for future investigation that might lead to insight on cancer’s causes and, ultimately, reduce the cancer burden 30 and 50 years from now, I might choose the tiny, under-funded area of environmental oncology

That’s a tough field. Most oncologists want to work with patients. Researchers want to publish papers. Cause-and-effect is hard to demonstrate, especially when most of the data is untenable and you’re up against businesses, politics and people who, understandably, don’t recall precisely what they ingested years ago. But to stop cancer from happening so much, that’s where the money is. IMO, nothing more.

All for this week,


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Reading Toms River

When I was a medical resident working at Memorial Sloan Kettering in the late 1980s, some of us joked about the apparently high cancer rate New Jersey. It seemed, though none of us could prove it, that too many of our patients came from the state across the Hudson. Statistics can be tricky, I knew. Sometimes we notice clusters of disease that are just random blips, constellations or flukes.

river landscape, by Frits Thaulow

river landscape, by Frits Thaulow

So when Dan Fagin’s book, Toms River, came out two months ago, I was drawn. The narrative opens with a gripping portrait of a young man whose frame was irrevocably altered by a childhood cancer. It moves on to the history of the small town in central NJ where Ciba, an international chemical company now subsumed by BASF, set up shop in the early 1950s.

The residents hadn’t a clue what was happening to their water. Fagin, an environmental journalist, wades through a half century of dumping, denial, Greenpeace efforts to expose the situation, local citizens’ mixed responses, real estate, some basic and theoretical chemistry, cancer registries and more.

I value this book highly. Toms River could be a lot of places – pretty much anywhere pollution goes unchecked. As the author points out near the end, the problem’s manifest in China now, and elsewhere. It’s a lesson in business ethics, among other things.

The tale intersperses epidemiology and statistics with local politics and individuals’ lives. It reveals just how hard it is to prove cause and effect when it comes to cancer – which, as I’ve said before, is no reason to let industry go unregulated. Because we’ll rarely if ever get definitive, 100%-style evidence that a particular compound causes cancer in humans. Rather, the story points to the need for lowering the threshold for chemicals on the list, and for regulating toxins in manufacturing.

A subtler point, deeper in some ways, is that there are people who don’t want to think about their neighborhood’s water supply or the food they like to eat…”Out of sight and out of mind,” Fagin says in the thick of it. He’s spot-on, there: when a toxic exposure is disconnected from its outcome by decades – and diluted, we tend not to notice or worry.



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Contemplating Breast Cancer, Beyond October 2012

It’s foggy today, October 3, ten years since the last mammogram I had and will ever need. I’ve been remiss in updating the blog. The reasons include family concerns and other projects. Meanwhile, I’ve been thinking about the big picture – what’s most important for progress against breast cancer in the decade ahead.

So here’s what I see, now – in terms of three priority areas: improving treatment, prevention, and education to inform treatment decisions.

Pumpkins, organized by subtype (WikiCommons image)

As an oncologist, I perceive huge strides in understanding BC since the time of my diagnosis. But these advances are largely invisible to patients because they’re in the realm of pathology and classification of different subtypes. What was essentially a 3-type malignancy with a handful of treatment options has expanded under the molecular microscope to a spectrum of 4, 10 or – what’s probably most accurate – hundreds or thousands of patient-particular conditions, depending on the level of precision by which you define a disease. I’m optimistic, because it looks as though, in my lifetime, BC treatment will be tailored to each patient. There’ll be less surgery and better drugs.

The hitch, now, is not so much with science as with funding– funding to analyze each patient’s tumor at the genetic and protein levels, funding to pay for treatments selected by patients (which might include less treatment and/or palliative care in advanced cases), and funding to educate doctors about BC subtypes and medical progress, so they might offer “modern” advice to each patient in ordinary clinics, apart from clinical trials and academic centers. Newer is not always better in medical care. Same goes for more treatment (especially when it comes to higher doses). Still, the lag between advances in BC science and application of distinct, targeted and better treatments is frustrating at best.

Some of my colleagues call for patience – emphasizing that studies need be confirmed, drugs tested in mice, etc. Their point is that we can’t jump from pathology research and new BC classifications to new therapy. But one lesson I take from progress against AIDS is that maybe we shouldn’t be so patient. At least not for young people with poor-prognosis BC subtypes or stage. We could do studies and studies of particular BC treatments, and studies of studies (those would be meta-analyses) and debate 8 or 10 years from now whether a particular drug or combination of drugs worked in clinical trials that selected for patients with an antiquated subtype of the disease. Or we could move toward “n=1” trials, with smart, well-trained physicians assessing each patient by a combination of old-fashioned physical exams and the most modern of molecular studies of the tumors, considering the options, and moving forward with individual, mini-experimental treatment plans.

I vote for the latter. If the drug works in a patient with advanced BC and the patient feels better, why not?

For people with early-stage BC, prescribing or taking new and essentially untested drugs makes less sense at first glance. That’s because standard treatments are “successful” – leading to long-term remissions and possible cures in over 80 percent of those affected. But these relatively good results may have, paradoxically, hampered development of better drugs that could obviate the need for breast-deforming surgeries and radiation in many women. The possible application of BC drug cocktails, in lieu of surgery for early-stage patients, is a huge question for the future, and one for which trials would be necessary. Just getting those projects going – applying BC science to treatment of early-stage cases – would be a step in the right direction.

As for BC prevention, of course that would be infinitely better than detecting or treating the disease. Unfortunately, I think we’re farther away from preventing the disease than we are from having effective and less brutal treatments for most patients. The problem with lifestyle modification – like staying active and not obese – is that it’s far from full-proof: You can be seemingly fit as a fiddle and get a lethal case of BC. Still, there are plenty of other health-related reasons for women to exercise and eat sensibly. As for avoiding carcinogens or, first, just knowing what chemicals contribute to BC formation and growth, the science isn’t there yet.  It’ll be a long haul before anyone can prove that a particular chemical causes this disease. That said, I advocate research in the slow-growing field of environmental oncology and wish there’d be more enthusiasm for regulating our exposure to likely-toxic chemicals.

The third priority is for improving education in math and science, starting at the elementary school level. Doctors need to understand statistics, but many don’t. They need to know about genomics and basic science in medicine. Patients need this kind of knowledge if they want to have a clue, if they want to engage meaningfully in decisions about which antibody to take, or pill, or whether they want to participate in a clinical trial of pills instead of surgery for a Stage II tumor with high levels of Her2, for example. That’d be a tough decision for an oncologist. I only wish that we could reach the point where we could have those kinds of truly informed conversations about clinical treatment of breast cancer, which happen every day.

We’ve got a lot of information in hand, but we need to learn how to apply that to more patients, faster and more openly.

All for a while. I’m open to ideas on this. Happy October!


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10 Newly-Defined Molecular Types of Breast Cancer in Nature, and a Dream

Breast cancer is not one disease. We’ve understood this for decades. Still, and with few exceptions, knowledge of BC genetics – information on tumor-driving DNA mutations within the malignant cells – has been lacking. Most patients today get essentially primitive treatments like surgical hacking, or carving, traditional chemotherapy and radiation. Some doctors consider hormone therapy as targeted, and thereby modern and less toxic. I don’t.

Until there’s a way to prevent BC, we need better ways to treat it. Which is why, upon reading the new paper in Nature on genetic patterns in breast cancer, I stayed up late, genuinely excited. As in thrilled, optimistic..The research defined 10 molecular BC subgroups. The distinct mutations and gene expression patterns confirm and suggest new targets for future, better therapy.

The work is an exquisite application of science in medicine. Nature lists 31 individuals and one multinational research group, METABRIC (Molecular Taxonomy of Breast Cancer International Consortium), as authors. The two correspondents, Drs. Carlos Caldas and Samuel Aparicio, are based at the University of Cambridge, in England, and the University of British Columbia in Vancouver, Canada. Given the vastness of the supporting data, such a roster seems appropriate, needed. The paper, strangely and for all its worth, didn’t get much press –

Just to keep this in perspective – we’re talking about human breast cancer. No mice.

The researchers examined nearly 2000 BC specimens for genetic aberrations, in 2 parts. First, they looked at inherited and acquired mutations in DNA extracted from tumors and, when available, from nearby, normal cells, in 997 cancer specimens – the “discovery set.” They checked to see how the genetic changes (SNPs, CNAs and/or CNVs) correlated with gene expression “landscapes” by probing for nearly 29,000 RNAs. They found that both inherited and acquired mutations can influence BC gene expression. Some effects of “driver” mutations take place on distant chromosomal elements, in what’s called a trans effect; others happen nearby (cis).

Next, they honed in on 45 regions of DNA associated with outlying gene expression. This led the investigators to discover putative cancer-causing mutations (accessible in supplementary Tables 22-24, available here). The list includes genes that someone like me, who’s been out of the research field for 10 years, might recall – PTEN, MYC, CDK3 and -4, and others. They discovered that 3 genes, PPP2R2A, MTAP and MAP2K4 are deleted in some BC cases and may be causative. In particular, they suggest that loss of PPP2R2A may contribute to luminal B breast cancer pathology. They find deletion of MAP2K4 in ER positive tumors, indicative of a possible tumor suppressor function for this gene in BC.

Curtis, et al. in "Nature": April 2012

The investigators looked for genetic “hotspots.” They show these in Manhattan plots, among other cool graphs and hard figures, on abnormal gene copy numbers (CNAs) linked to big changes in gene expression. Of interest to tumor immunologists (and everyone else, surely!), they located two regions in the T-cell receptor genes that might relate to immune responses in BC. They delineated a part of chromosome 5, where deletions in basal-like tumors marked for changes in cell cycle, DNA repair and cell death-related genes. And more –

Cluster Analysis (abstracted), Wikipedia

Heading toward the clinic, almost there…

They performed integrative cluster analyses and defined 10 distinct molecular BC subtypes. The new categories of the disease, memorably labeled “IntClust 1-10,” cross older pathology classifications (open-access: Supplementary Figure 31) and, it turns out, offer prognostic information based on long-term Kaplan-Meier analyses (Figure 5A in the paper: Supplementary Fig 34 and 35). Of note, here, and a bit scary for readers like me, is identification of an ER-positive group, “IntClust 2” with 11q13/14 mutations. This BC genotype appears to carry a much lesser prognosis than most ER-positive cases.

Finally, in what’s tantamount to a 2nd report, the researchers probed a “validation set” of 995 additional BC specimens. In a partially-shortened method, they checked to see if the same 10 molecular subtypes would emerge upon a clustering analysis of paired DNA mutations with expression profiles. What’s more, the prognostic (survival) information held up in the confirmatory evaluation. Based on the mutations and gene expression patterns in each subgroup, there are implications for therapy. Wow!

I won’t review the features of each type here for several reasons. These are preliminary findings, in the sense that it’s a new report, albeit a model of what’s a non-incremental published set of observations and analysis; it’s early for patients – but not for investigators – to act on these findings. (Hopefully, this will not be the case in 2015, or sooner, preferably, for testing some pertinent drugs in at least a subset of the subgroups identified.) Also, some of the methods these authors used came out in the past decade, after I stopped doing research. It would be hard for most doctors to fully appreciate the nuances, strengths and weaknesses of the study.

Most readers can’t know how skeptical I was in the 1990s, when grant reviewers at the NCI seemed to believe that genetic info would be the cure-all for most and possibly all cancers. I don’t think that’s true, nor due most people involved with the Human Genome Project, anymore. The Cancer Genome Atlas and Project should help in this regard, but they’re young projects, larger in scope than this work, and don’t necessarily integrate DNA changes with gene expression as do the investigators in this report. What’s clear, now, is that some cancers do respond, dramatically, to drugs that target specific mutations. Recently-incurable malignancies, like advanced melanoma and GI stromal tumors, can be treated now with pills, often with terrific responses.

Last night I wondered if, in a few years, some breast cancers might be treated without surgery. If we could do a biopsy, check for the molecular subtype, and give patients the right BC tablets. Maybe we’d just give just a tad of chemo, later, to “mop up” any few remaining or residual or resistant cells. The primary chemotherapy might be a cocktail of drugs, by mouth. It might be like treating hepatitis C, or tuberculosis or AIDS. (Not that any of those are so easy.) But there’d be no lost breasts, no reconstruction, no lymphedema. Can you imagine?

Even if just 1 or 2 of these investigators’ subgroups pans out and leads to effective, Gleevec-like drugs for breast cancer, that would be a dream. This can’t happen soon enough.

With innovative trial strategies like I-SPY, it’s possible that for patients with particular molecular subgroups could be directed to trials of small drugs targeting some of the pathways implicated already. The pace of clinical trials has been impossibly slow in this disease. We (and by this I mean pharmaceutical companies, and oncologists who run clinical trials, and maybe some of the BC agencies with funds to spend) should be thinking fast, way ahead of this post –

And given that this is a blog, and not an ordinary medical publication or newspaper, I might say this: thank you, authors, for your work.

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What Causes Breast Cancer? Reviewing the IOM Report on BC and the Environment

Earlier this month the IOM issued a big report on breast cancer and the environment. The thick analysis, commissioned and sponsored by the Susan G. Komen for the Cure®, was authored by an expert panel. Their task – to assess all available information on what causes BC, and make recommendations accordingly – was essentially impossible. Some immediately critiqued the work and, perhaps implicitly, the funding – for its failure to yield sharp or clearly-actionable insights into BC causes.

The document starts, blandly, with some straightforward stuff. The recommendations for lifestyle changes seem paternalistic when not obvious. Where the report gets interesting, and offers value, is in considering a few specific environmental toxins that might be causative in the current breast cancer epidemic. While proving that any one (or several) of the chemicals listed below causes  BC will be difficult, developing a clear, working list of likely compounds that merit research attention is an important step.

Some background:

Each year, over 230,000 women in the U.S. develop a breast tumor. The problem, in terms of preventing breast cancer, is that most established risk factors – like being older, later age at menopause, being young at the time of first menstruation and some genetic traits – aren’t amenable to intervention.

For this project, the IOM committee interpreted the term “environment” broadly – it considered all possible causes of BC that aren’t directly inherited through DNA, including factors that might influence a genetic disposition. They looked at a wide range of exposures: “how a woman grows and develops during her lifetime; what she eats and drinks; the physical, chemical, and microbial agents she encounters; how much physical activity she engages in; medical treatments and interventions she undergoes; and social and cultural practices…”

What they found, with my comments interspersed and conclusions:

The most convincing evidence linked BC to hormone therapy with estrogen and progesterins, ionizing radiation (as might occur in medical procedures like CT scans; the amount of radiation in mammography is too low for concern, the committee emphasizes), excess weight (i.e. being fat, or more-than-fat) in postmenopausal women, and alcohol (addressed here, previously).

Where they found no clear link: smoking (surprise! the evidence is limited, they say), personal use of hair dyes, non-ionizing radiation (like that emitted by microwaves and other electrical devices).

On the up side: Physical activity appears to lessen a woman’s breast cancer risk.

Quite a few factors fell into a gray zone, for which “the evidence is less persuasive but suggests a possible association with increased risk.” These are: exposure to secondhand smoke (this might be a cause, but smoking isn’t? seems unlikely, ES), nighttime shift work (steroids/stress effect? Or just too much junk food).

Finally, they name some chemicals: benzene, ethylene oxide, or 1,3-butadiene (these may be present in some workplaces; one might be exposed from breathing auto exhaust, pumping gas, or inhaling tobacco smoke, they indicate) and bipsphenol A (BPA) – one of the “biologically plausible hazards in the environment.” As they indicate, animal data provide clear evidence for a mechanism by which BPA, which is widely-used in plastic containers and food packaging, might cause breast cancer. “But studies to assess the risk in humans are lacking or inadequate.”

The IOM committee study authors consider the difficulties in testing environmental hazards. Of course, as they point out, it wouldn’t be ethical to deliberately expose women to potentially harmful substances in a clinical trial. For this reason, they advocate more research in animals and in vitro systems. But those kinds of experiments are limited, in their words: “they can provide indications that a chemical or other agent may cause harm, but these models are approximations of human experience.”

So we’re stuck with a lot of inconclusive data, and an obvious moral imperative not to systematically test the effects of possible environmental toxins on women who might develop BC. There’s a table posted, with strategies to reduce risk, but it recommends for the most part obvious things, and an annoyingly-toned paragraph:

These actions include avoiding unnecessary medical radiation throughout life, avoiding use of postmenopausal hormone therapy that combines estrogen and progestin, avoiding smoking, limiting alcohol consumption, increasing physical activity, and, particularly for postmenopausal breast cancer, minimizing weight gain. Some of these actions may have additional health benefits beyond their potential contribution to reducing breast cancer risk. In many cases, women can be aided by the actions of others, including their families and health care providers.

(Why don’t they just say: “be a good girl, get rest, and stay slim?”)

The segment on the future and needed research emphasizes the need for research on early-life exposure to chemicals, pre-menopausal obesity, and other factors that may influence development of BC later on in a woman’s life. This makes sense to me.

The most troubling findings have to do with the chemicals. Carcinogens like benzene are hard to put a finger on, when it comes to causing cancer in a population where cars are abundant and oil leaks often, and occasionally abundantly, into large gulfs of water. The BPA issue is a genuine concern, with little clear data in humans. Until those data are evident (which, if it takes decades to show the effects on youngsters exposed who develop BC in, say, their 40s), will not be for a while – you have to wonder if doctors should recommend more drastic steps to avoid routine exposure to and ingestion of potentially toxic chemicals.

If you’d like to read about this report and some of the concerns about chemicals that might cause BC, I recommend this post by Julia Brody, of the Silent Spring Institute.

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Cervical Cancer Screening Update: on Pap Smears, Liquid-based Cytology and HPV

The latest issue of the Annals of Internal Medicine contains 2 noteworthy papers on cervical cancer screening. The first, a systematic review of studies commissioned by the USPSTF, looked at 3 methods for evaluating abnormalities in women over 30 years:

high-grade cervical cell dysplasia (Dr. E. Uthman, Wikimedia Commons)

1. Conventional cytology (as in a Pap smear; the cervix is scraped and cells splayed onto a microscope slide for examination);

2. Liquid-based cytology (for LBC, the NHS explains: the sample is taken as for a Pap test, but the tip of the collection spatula is inserted into fluid rather than applied to slides. The fluid is sent to the path lab for analysis);

3. Testing for high-risk HPV (human papillomavirus). Currently 3 tests have been approved by the FDA in women with atypical cervical cells or for cervical cancer risk assessment in women over the age of 30: Digene Hybrid Capture 2 (manufactured by Quiagen), Cobas 4800 HPV (Roche) and Cervista HR HPV (Hologic); another Roche Diagnostics assay, Amplicor HPV, awaits approval.

These HPV assays use distinct methods to assess DNA of various HPV strains.

There’s a lot of jargon here, and I have to admit some of this was new to me despite my nearly-due diligence as a patient at the gynecologist’s office and my familiarity as an oncologist with the staging, clinical manifestations and treatment of cervical cancer. Who knew so many decisions were made during a routine pelvic exam about which manner of screening?

The main points I took away from this paper:

1. Liquid-based cytology is similar to conventional Pap smear cytology for detecting high-grade dysplasia (abnormal cells) and cervical cancer.

2. It seems that at some medical centers, and possibly overall, there’s a lower proportion of inadequate cell specimens when practitioners skip the slides and use the liquid method. This means that fewer women need be called back for another procedure.

3. Finding HPV sequences in the cervix yields many false positives, in terms of malignancy.

The researchers conclude that further studies are needed to sort out how HPV testing can improve or supplement cervical cancer screening. The main limitation is that many young women are infected with potentially cancer-causing strains of HPV, but most don’t get cervical cancer. When cervical cancer does develop that’s usually later on, a decade or longer after the relevant viral infection.

The second Annals article, a helpful narrative review, considers the practical implications of the above findings. The authors state that over 40 types of HPV can infect the cervix. They review that progression to cancer occurs along these 4 steps: HPV transmission, acute infection, persistent infection causing precancerous changes and eventually, in a subset of those infected, invasive cervical cancer.

Figure 1 is remarkably clear:

Prevalence of high-risk HPV and incident cases of cervical cancer in the U.S., 2003–2005. Surveillance Epidemiology and End Results (SEER) data for incident cases among females aged 15 to 19 years and 50 to 64 years.

The graph shows that the prevalence of HPV infection is highest among teens and women in their early 20s, and decreases in older women. By contrast, the incidence of cervical cancer rises steadily in women over 30 years and remains elevated among women in their 40s. The authors show, separately, that the rate of cervical cancer in older women is low.

The central point is that high-risk HPV infection and associated inflammation of the cervix are common in young women, but cervical cancer is rare among those under 30 years. The investigators conclude that cervical cancer screening in women younger than 20 years may be harmful. They also state that evidence supports discontinuation of cervical cancer screening in most women who are over 65 years old.

Two asides on this otherwise non-bloggy topic –

It’s great that the Annals provides the full text of these papers open-access, free of charge to the public.

Amazing how well-accepted is the concept of some viruses causing cancer, today. This was a heretical idea 25 years ago in academic medicine; now it’s dogma.

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President Obama Talks About Smoking and Tobacco

Today’s ML comes straight from the Oval Office. President Obama talks about smoking, and how hard it is to stop, and what can be done to reduce the use and long-term health consequences of tobacco.

What I like about this Presidential health advisory:

He credits the ACS, which is sponsoring a smokeout today.

He’s clear about the problem’s scope: “Today 46 million Americans are still hooked, and tobacco remains the leading cause of preventable, early deaths in this country.”

He doesn’t deny his own history. His experience lends credibility to his words; he understands how hard it is to stop smoking once you’ve begun.

He considers a solution: “We also know that the best way to prevent the health problems that come from smoking is to keep young people from starting in the first place.”

He reflects on the power of tobacco companies, which are fighting requirements for candid warning labels on their products.

All in 1 minute and 34 seconds!

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On Alcohol and Breast Cancer, Guilt, Correlations, Fun, Moderation, Doctors’ Habits, Advice and Herbal Tea

Few BC news items irk some women I know more than those linking alcohol consumption to the Disease. Joy-draining results like those reported this week serve up a double-whammy of guilt: first – that you might have developed cancer because you drank a bit, or a lot, or however much defines more than you should have imbibed; and second – now that you’ve had BC, the results dictate, or suggest at least, it’s best not to drink alcohol.

The problem is this: If you’ve had BC and might enjoy a glass of wine, or a margarita or two at a party, or a glass of whiskey, straight, at a bar, or after work with colleagues, or when you’re alone with your cat, for example, you might end up feeling really bad about it – worse than if you had only to worry about the usual stuff like liver disease and brain damage, or if you could simply experience pleasure like others, as they choose.

The newly-published correlative data, in the Nov 2 issue of JAMA, are clear. The findings, an offshoot of the Nurses’ Health Study, involve over 105,000 women monitored from 1980 until 2008. The bottom line is that even low levels of alcohol consumption, the equivalent to 3-6 drinks per week, are associated with a statistically significant but slight increase in breast cancer incidence. And the more a woman drinks, the more likely she is to develop breast cancer.

All things considered, it might be true that alcohol is a breast carcinogen, as Dr. Steven Narod calls it in the editorial accompanying the research study. Still, there’s no proof of cause and effect: Other factors, like consuming lots of food or perhaps some yet-unidentified particularity about living in communities with abundant food and alcohol, are potential co-variables in this story. But what if it is true?

From the editorial:

These findings raise an important clinical question: should postmenopausal women stop drinking to reduce their risk of breast cancer? For some women the increase in risk of breast cancer may be considered substantial enough that cessation would seem prudent. However, there are no data to provide assurance that giving up alcohol will reduce breast cancer risk.

How I see it is this: Everything’s best in moderation, including enjoyment of one’s life. You work, you rest, you have some fun.

This evidence is not like the strong data linking cigarettes to smoking that officials sat on for a few decades under the influence of the tobacco industry. This is a plausible, mild, and at this point well-documented correlation.

I don’t deny the sometimes harmful effects of alcohol; no sane physician or educated person could. But if you have a glass of wine, or even a second, so long as you don’t drive a car or work while affected, I don’t see it as anyone’s business but your own. More generally, I worry about how much judging there is by people who behave imperfectly, and how that can make individuals who are good people in most ways feel like they don’t deserve to be happy or enjoy their lives.

Women, in my experience, are generally more vulnerable to the put-downs of others. And so my concern about the BC-alcohol link is that this will, somehow, be used, or have the effect of, making survivors or thrivers or women who haven’t even had breast cancer feel like they’re doing the wrong thing if they go to a party and have a drink. And then they’ll feel badly about themselves.

Really I’m not sure what more to say on this loaded topic, except that it points to the deeper and broader ethical dilemma of doctors who are not all perfect examples of moderation, expecting and asking other people to change their personal habits when they themselves like to go out and have fun, and drink, at parties, or have wine in the evenings over dinner in the privacy of their homes.

How shall I resolve this post?

Last night I sipped Sleepytime tea, manufactured by Celestial Seasonings, before reading a book. The stuff is said to be 100% natural, with “a soothing blend of chamomile, spearmint and lemongrass.” I tried it first a few weeks ago and, by a placebo effect or through real chemistry, it helps me sleep more soundly.

I’ve absolutely no idea what are the effects of “Sleepytime tea” on breast cancer. It might help, it might hurt, or it might do nothing at all.

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