Should doctors care about environmental health while treating patients?

For the majority of my graduate and postgraduate training, I have studied the pulmonary and cardiovascular effects of air pollution. Through this time, I can recognize that my mindset and understanding of the importance of air pollution in public health continues to shift. In many ways, I would like to think that as I spend more time in this field, I gain greater distance from the minute details, allowing me to put the complex research into a cohesive story that gives me freedom to see this type of public health problem with perspective. As I have written in my previous post, it is challenging to distinguish between environmental exposures that are truly hazardous from those that are mostly hype, and I am still grappling with placing certain highly talked about environmental exposures in one category or another, but air pollution is not confusing for me. In my perspective, fine particulate air pollution (aerosolized particles with a diameter less than 2.5 um, PM_2.5) is truly hazardous, and it has serious public health implications on a population level. I am not alone on this either, in the most recent Global Burdens of Disease report published in Lancet, ambient fine particulate air pollution was found to be the #9 cause of disease worldwide, reaching as high as the #4 cause of disease in East Asia. Even worse, household air pollution, resulting from the practice of combusting solid fuels indoor for cooking, is believed to be the #4 cause of disease worldwide, reaching as high as the #1 cause of disease in South Asia. Household air pollution doesn’t make the list in North America, Western Europe, or Australia, as this cooking practice is generally rare in these areas. Even worse still, tobacco smoking and second hand smoke, is the #2 cause of disease worldwide. Although tobacco smoking isn’t quite the same as ambient or household air pollution, there are many similarities.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)61766-8/abstract

My belief in the importance of air pollution in public health continues to shift due to my own research, where I am becoming exceedingly convinced that in utero and early life exposure to air pollution will have life long effects on susceptibility to cardiovascular disease. As we publish on this, I will write about this more, and my hope is that these observations will be translated to epidemiological studies to investigate if these effects are observed in human populations. In any event, the actual effect of air pollution on disease may very likely be much greater than what we currently know.

But, looking at the top 10 on this list, it is almost amazing to realize that nearly all of these seem to be modifiable factors. Let’s look at the top 10:

1) high blood pressure

2) tobacco smoke

3) alcohol use

4) household air pollution

5) diet low in fruits

6) high BMI

7) high fasting glucose

8) childhood underweight

9) ambient particulate matter

10) physical inactivity

Now, I recognize that there are always going to be many outside factors that influence these risks, and not all of them are easily modified. In the U.S., socioeconomic status, education level, access to fruits and vegetables, access to safe places to exercise, etc., all of these will influence factors such as diet, alcohol use, and physical activity, which will have major impacts on health. But when I look at this list, I ask myself, how does the physician address each one of these?

When looking at the #1 cause of disease, high blood pressure, I know that the physician will treat this in many ways. The physician may utilize behavior modification strategies to try and change diet and activity, encouraging weight loss and lower sodium intake, but also the physician will likely use one of several good pharmacological options to try and drop BP. Looking at tobacco smoke, nearly every physician will counsel their patient on tobacco smoke, they may even be required to counsel their patient on this depending on where they practice. Perhaps the doctor will pull out the 5A’s and 5R’s of tobacco cessation (Ask, Advise, Assess, Assist, and Arrange, Relevance, Risk, Rewards, Roadblocks, Repetition (http://www.primaris.org/sites/default/files/resources/Smoking%20Cessation/sc_algorithm.pdf), and there seems to be evidence that it works (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628990/). The same trend goes with alcohol consumption, diet low in fruits, high BMI, high fasting glucose, and physical inactivity, the clinician has a plan for each one of these… except for air pollution.

Two years ago, a very reputable cardiologist and environmental health researcher from the US EPA and University of North Carolina came to the UW to give several talks and to meet with our group investigating traffic related air pollution and cardiovascular disease. With his visit, he gave the early morning Cardiology Grand Rounds talk at UW, where he met the weary eyes of the residents, fellows, and attendings, looking for CME credit before they start their day in their clinics or hospital units. He gave what was in my opinion, a fascinating talk that highlighted the truly exciting work coming out of the US EPA on air pollution and cardiovascular disease. Looking around the room, I mostly saw physicians sleeping, but a few people seemed to be engaged. After his talk, I was standing around, talking with some colleagues, when one of the highly influential cardiology attendings at UW proceeded to explain to us PhD dimwits, “there is simply no place for air pollution in the cardiology clinics!” At first, I was taken aback by what I thought was a short sighted view of the role of air pollution in population level cardiovascular mortality, but with letting his comments sit for a while, I asked myself, “Is he right? Is there no place for air pollution to be discussed in the clinic?”

Not too long after this encounter, I was invited by a group of physicians in Whatcom County to give my own CME Grand Rounds seminar at St. Joseph Medical Center in Bellingham, WA, on the health effects of fine particulate air pollution. When preparing for this seminar, I was asked to produce a document that would explain what the clinicians would gain from attending my seminar, and specifically, how it would influence their practice of medicine. In trying to answer this question, I had to do a little exploring.

The reality is that air pollution is a major contributor to disease, but the answer to reduce the adverse effects of this type of exposure is simple yet complex: eliminate exposure. Although the concept is simple, unfortunately, reducing exposure isn’t easy. This is why strong air quality policies are critical in playing this role. So what can the physician do? Well, the EPA has some very simple guidelines for clinicians, 1) teach your patients about the air quality index, find it at http://airnow.gov/, and teach them to use it, and 2) if air quality gets bad, make certain recommendations such as, reduce prolonged heavy exertion when air pollution is moderate, to completely avoid physical activity outside when air pollution is truly bad, here are the recommendations http://www.airnow.gov/index.cfm?action=pubs.aqguidepart.

When answering the question of how my seminar will add to doctors' clinical practices, I reluctantly put the EPA guidelines down, but there’s more to it than that, and I wasn’t satisfied with these simple guidelines being the only way clinicians would use air pollution in their clinics.

I find these recommendations to be sound, solid recommendations. They are pretty simple, potentially easy to follow, but will following these guidelines really make a big difference? In a region such as the PNW, bad air pollution events only happen once or twice a year, and perhaps there would be some modest benefit to advise patients who are living with current heart or lung diseases to avoid physical activity outside during this time, but the overall benefit is likely to be quite small. So, other than simple recommendations for those with chronic lung and heart diseases, can the physician play a role in trying to bring air pollution down on the list of causes of disease?

After trying to understand the role for the clinician in environmental health, I have come to believe that the physician has an extremely important role to play in reducing risk of disease from environmental exposures, although my reasoning may be somewhat convoluted, stick with me. As I mentioned above, in nearly every environmental exposure, the way to reduce an adverse effect of exposure on disease risk is to eliminate exposure. Certain environmental exposures can be modified by the individual (take smoking for example, or exposure to consumer products, or heavy metals in fish), but more often than not, environmental exposures occur without permission, where someone passively inhales the fine particulate that emerged from a diesel engine, and subsequently suffers from increased risk of disease. With looking at air pollution, exposure can be looked at as the product of concentration and time (C x T), the physician can advise patients to avoid outdoors and prolonged exercise in bad air pollution events (decreasing T), but if C doesn’t change, it’s going to be tough to truly drop exposure over the long run. This is why I am an avid proponent of a strong regulatory body such as the US EPA, setting regulatory standards that protect those who would suffer the health impacts from the hands of development without any of the financial profit. But what can the physician do in setting regulatory standards?

The reality is that when a patient has questions about health and the environment, they ask their doctor. There is an excellent 2003 review article in Pediatrics, titled “Environmental Risk Communication for the Clinician”, for those who are clinical doctors, I recommend it. When I read this, there were 3 important concepts that stuck with me, 1) clinicians are the #1 trusted and credible source of information on environmental health risks, 2) questions about environmental health rank among the top in questions patients have for their clinicians, yet clinicians have a hard time answering them, and 3) overall, most people go to their doctors. Meaning that when people have questions about environmental health risks, they’re more than likely to ask their doctor.

http://pediatrics.aappublications.org/content/112/Supplement_1/211.full.pdf

So what does this mean for regulatory policy? How will the information the doctor knows about environmental health influence any US EPA standard and reduce exposures? The answer is that our regulatory policies change when the public demands change. As much as we would like to believe that our regulatory standards are set with a perfect communication between environmental health researchers and EPA policy makers (who are obligated by law to set standards without the influence of politics or economics), the public has historically played a critical role to influence policy by demanding change.

Below is an image of the air pollutants sulfur and nitrogen oxides in the Eastern Half of the U.S., comparing the differences in concentration between 1989 and 2004 (From Casarett and Doull’s Toxicology). What is obvious is that air pollution has dramatically improved since reaching its worst in the 60s, 70s, and 80s. The reason it has improved is due to the Clean Air Act and subsequent additions to the law, increasing its regulatory strength. Prior to the CAA, the public was fed up with the poor air quality, and vigorously advocated for change. Even today, nearly everyone I have met who lived in Southern California in those decades remember how bad it was and have their own personalized stories of eyes and lungs burning. The public’s advocacy is what led to this major policy, reducing exposures of air pollution for millions of Americans and improving the health of the public.

http://books.google.com/books/about/Casarett_Doull_s_Toxicology_The_Basic_Sc.html?id=4yi7-j48uhIC, Casarett and Doull’s Toxicology, page 1123

Today, our health hazards from environmental exposures are less obvious. With particulate air pollution, people may not even notice when air quality is truly bad, yet the human health risks are still there. My belief is that physicians, whether they like it or not, have a role to play in educating the public when it comes to environmental exposures. When the public is educated about real and potential health risks from environmental exposures, public advocacy demanding regulatory changes will follow. Although I recognize that with 15 min clinic visits, bringing up environmental health isn’t necessarily at the top of the list (and it shouldn’t be), I do believe that physicians need to have a strong understanding of these risks to better counsel patients when they have questions, or when exposures do become a serious clinical concern.

I would be very interested to hear from any clinicians about their experiences with counseling patients on environmental exposures, is it something that ever comes up in your clinics? Do you have any advice on how to answer these questions?

Thinking back to the influential attending who didn't t believe air pollution had a role in the cardiology clinic; in my view, air pollution is a major cause of cardiovascular disease, and if the goal in medicine is to improve health and ease suffering, air pollution and other environmental factors will be a part of the equation until the exposures are zero, until then, I believe it will always have a place in the clinic.

Chad Weldy

How do you distinguish between hazard and hype in environmental health?

There are times that I find myself extremely envious of toxicologists in the 1950-1980s. Mercury, lead, cigarette smoke, PCBs, etc., all of these were the important toxicants of the era, chemicals and toxic exposures that have such clear adverse health impacts. Of course this is because I am idealizing what it must have been like to be studying toxicology back then, but I am imagining a conversation at a medical department that would go something like this, “Hey, I don't think that developmental exposure to mercury is going to have any effect.” “Oh really? Let me show you.” Then a series of very simple experiments are conducted with amazingly clear results and an extremely high impact publication is produced that continues to be cited for decades. Next week, “Oh, I don’t think cigarette smoke has any bad effects.” “Oh really? Let me show you.” And repeat.

Today, in my view, the most important research question in the field of toxicology is, what are the effects of low-level toxicant exposures? Particularly when the exposure is nearly ubiquitous. (See a recent study that suggests fetal BPA exposure to be nearly ‘universal’ http://pubs.acs.org/doi/abs/10.1021/es402764d)

If we look at the field of toxicology as having two halves to it, the first half being everything that has been studied up until now, and the second half being what will come from now until the field is dead, the first half of toxicology, in my view, was about defining the toxicities of chemical exposures at high doses. Although things such as arsenic, lead, and mercury have been known to be toxic going back to ancient times, the actual investigations into the biological mechanisms and pathological outcomes have not been defined until the 20^th century, where modern biological research techniques we able to be employed. Today, toxicologists often times don’t have the luxury to study the effects of clearly toxic chemicals at high doses; we need to address the concerns that pertain to our public, the chemicals that we are exposed to, at the doses that we are exposed to.

The reality is that due to the toxicologists, the research, and the public outcry and environmental policy that followed this period of investigation, human exposure to many of the major hazardous compounds has largely decreased. But, new chemicals have been introduced, while old toxicants continue to elude complete avoidance.

This brings us to the major question of the future of toxicology, how do you deal with low-level exposures? What are the effects? And, how do you know what exposure is truly hazardous, versus simply hype?

Nearly every day, when I scan the news, I will come across an article about environmental exposures, health, and toxicology. People care about this stuff, but it’s difficult to truly communicate what is something to be concerned about. In trying to understand truly hazardous versus hype, there is rarely a more difficult case than low pesticide exposure and the organic vs traditional food debate.

In a paper published just recently in PLoS One, a graduate student in the UW Dept. of Environmental and Occupational Health Sciences (Cynthia Curl) looked at organic produce consumption and socioeconomic status in a large cohort, (Congrats to Cynthia! this is a great publication).

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0069778

What she found, in many ways, was exactly what you would expect. You are more likely to be eating organic produce if you are: a woman, younger, from a more economically strong an liberal city, have a higher income, more educated, employed, and have closer access to supermarkets.

Although these results are what most people would likely hypothesize, and this data supports this fantastically, I was most struck by the percentages of those saying that they eat organic produce. In total, 40% of their population say they ‘sometimes, often or always consume organic produce’, reaching as high as 61% for those between the ages of 45-54 (the youngest age group).

This strikes me as a large number, and what it says to me is that roughly half of the population (I bet if those between the ages 18-45 were included, they would have an even higher rate) makes the conscious choice to purchase organic produce. So why would half the public make this choice?

Although this question may sound simple, there are many reasons why someone would choose to buy organic produce vs non-organic produce, and people buy organic produce for different reasons. Regardless of the reason someone would buy organic produce, any walk through the supermarket produce section will reveal that organic produce is typically more expensive than traditional produce. Whatever the reason someone chooses to buy organic, he/she did some sort of cost benefit analysis and came to the conclusion that organic produce is worth the added cost. You guys may remember when there was a flurry of excitement and anger when a group from Stanford published a report saying that organic produce was no ‘healthier’ than normal produce.

http://www.nytimes.com/2012/09/04/science/earth/study-questions-advantages-of-organic-meat-and-produce.html?_r=0

Here’s the actual study: http://annals.org/article.aspx?articleID=1355685

The study was a systematic review, in which they extracted data from every single publication on the topic thus far, to combine the data in a more complete statistical analysis. These types of studies are considered an excellent way to look at everything that has been done on a topic so far, which helps to eliminate a ‘single study bias’, where conclusions may be erroneously made following a single study. The review looked at organic vs traditional foods in terms of nutritional value (i.e. vitamins, minerals, etc.) as well as presence of toxic chemicals (arsenic, lead, mercury, as well as pesticide residues). They also reviewed the few studies to date looking at organic vs traditional food consumption and risk of clinical disease. Their conclusions were simple, 1) there is no nutritional difference between organic and traditionally grown foods, 2) there are slightly increased pesticide residues in traditional food produces, and 3) the studies looking at clinical health outcome thus far do not show any adverse health effects. Overall, they report that organic foods are not ‘healthier’.

On my Facebook feed, which I admit has way more toxicologists and public health people than likely the normal Facebook feed, people were freaking out. The general sentiments were, “obviously we don’t eat organic for more nutrients” and “they don’t know what the potential health risks of low level pesticide exposures are”.

But what’s interesting, as the authors’ note in this publication, is that it is a widespread belief that organic produce has more nutritional value. And although the extremely low level pesticide residue on certain traditionally grown produce may have some extremely low level effect, the current investigations into this have proved null. The reality is that we do not have the strong evidence to say that eating organic foods vs traditionally grown foods will result in a better clinical outcome. Now, I’m not saying that eating organic is not worth it, the lesser environmental impacts and sustainable farming practices that are encouraged in organic farming is reason enough, but there is simply not strong enough evidence to say that eating traditionally grown foods is bad for you. What we do have is evidence that eating a large amount of fruits and vegetables daily will dramatically reduce one’s risk of disease, for reasons still unclear (as someone who loves to study antioxidants, we can’t just say this is due to antioxidants). And what we should be encouraging more than anything is to eat fruits and vegetables daily, regardless of organic or not.

The organic vs traditional food argument is the perfect example of the challenge between separating the reality vs the hype in environmental health and toxicology. Most pesticides are extremely toxic to humans. They are a challenging class of toxicants because they are designed to be toxic, and they typically target the exact same biological mechanisms that are shared between insects and humans. But, again here comes the issue of low level exposures, what about these trace residues or produce?

In toxicology, we love to quote Paracelsus, the 15^th century physician who is famously attributed to the phrase, “the dose makes the poison”. In this quote, he reasoned that it is the dose that distinguishes what makes a remedy from a poison. This is a cute saying, and it makes an easy slide when lecturing on the basics of toxicology, but I feel that we often times forget this in toxicology. In my view, the dose truly does make the poison, and in saying so, a pesticide at a high dose, has about as much in common with the same pesticide at a low dose as any other toxic chemical, which is to say it doesn’t have much in common at all. When people discuss the potential health implications of low level pesticide exposures, they tend to discuss mechanisms that have nothing in similarity to the biological mechanism of action that is seen in a high dose pesticide exposure, in my view, this makes it essentially a different poison. Because the known toxic mechanism of high level exposures is not at play in these low level exposures, any potential toxicity would be considered very different from the high dose toxicity, and it’s very possible that these low level exposures do not have a real effect. Currently, this is the view of the FDA, and I have a hard time coming to any other conclusion with the data published so far.

So what should we think about organic vs traditional foods? How do we deal with a low level exposure of something that we know is toxic at high doses? I don’t know if I have a clear answer, but I wanted to make two points that are quite opposed to each other. This is why I am still confused about how to address these concerns.

1) We need to stop focusing on markers, and start focusing on real clinical outcomes.

Often times we overly convince ourselves that we know why certain things are beneficial and why certain things are not. For example, as I mentioned above, we know that eating a large amount of fruits and vegetables will dramatically reduce our risk of a myriad of diseases. But if you ask someone, why are fruits and vegetables are good for us? You will likely get an answer like, “oh the antioxidants!” And as a result, food products will advertise their antioxidant content, creating labels like “Vitamin Water”, claiming to be beneficial because of the antioxidant content. But the reality is that the antioxidant supplement trials have been a complete, and I mean complete, disaster. Millions and millions of NIH dollars later, we can say that taking antioxidant supplements should be avoided. Taking high dose antioxidants increases the risk of cancers in most populations and we cannot see any benefit in terms of most clinical outcomes. What we know is that eating a diet rich in fruits and vegetables, which contain high amounts of antioxidants, will result in longer lifespan and reduced risk of disease; not, eating high amount of antioxidants will result in longer lifespan and reduced risk of disease. As discussed in the Book Oxygen, Nick Lane argues that many of the toxins in fruits in vegetables, naturally produced to prevent bugs from eating them, may actually be mildly toxic to us as well, stimulating an adaptive response that may prove to be protective in the long run. What this says is that we still don’t know for sure why fruits and vegetables are good for us, so focusing on a marker, say looking at antioxidant content, will not allow us to know the full story. Applying this to pesticide residues on fruits and vegetables, without data to support this, we cannot say that traditional foods are less healthy for us due to trace pesticide residues, we can’t say this without actual clinical outcomes.

Here's the link to Oxygen, which is essentially a 300 page complex review article on redox biology, but I highly recommend it for those interested.

http://www.amazon.com/Oxygen-Molecule-World-Popular-Science/dp/0198607830

2) Does it even matter if we know something is actually good or not? Or is our ‘gut’ feeling about something being ‘good’ or ‘bad’ actually better?

If we take the traditional vs organic food argument, many people have come to the conclusion that organic is ‘better’, and it really doesn’t matter what the actual clinical or analytical data says. People buy organic for many different reasons, and it may just feel better to buy organic, is there anything wrong with that? Although I may not be convinced that organic foods are actually a way for us to improve health or reduce our risk of disease, I do believe that the practice of organic farming has its heart in the right place. Perhaps our world would be better with an entirely organic food production system, so if people believe that there will be health benefits to buy organic, regardless of if it is true or not, this may have a benefit to our community. This same argument would apply to the current debate on GMO labeling, although I do not believe there is any health risk to eating GMO foods, perhaps the sustainability and better food practices that come with non GMO foods are worth it to discourage the practice. Although understanding how the public feels about a particular concern in the absence of any supporting data is a tricky situation, I’m starting to believe that when the heart is in the right place, believing in a benefit that may not be there, while simultaneously supporting an industry that has good practices, may turn out to have alternative benefits in the long run.

The point at which this becomes a problem is when someone avoids needed medication because of an unsubstantiated belief in an alternative treatment, I may write more about this in the future.

Overall, our ability to distinguish between the truly hazardous and seriously hyped risks of environmental exposures is a challenge that has important implications. The media reports on these topics don’t help in distinguishing the two, and somehow we expect the general public to have a full understanding of the risks and benefits of certain practices, even when there is no consensus between experts in the field. We need to do better at coming to conclusions ourselves before we can expect the public to understand these risks, and when we do, we need to vigorously engage with the public to help disseminate important public health information.

Chad Weldy

Alcohol consumption before pregnancy and breast cancer, a challenging concern

When I have lectured about toxicology in high school or college classrooms, I have always found it valuable to present examples of ‘toxicants’ or ‘environmental exposures’ that are relevant to the students. Often times I have found that if I come into a classroom and ask the students what they think about when I say, “environmental exposures”, they respond, “Wind! Sun!” etc., and I use this first step as a platform to try and discuss how our ‘environment’ can include the air we breathe, the food we eat, medications we take, and any chemical that we may be exposed to. Looking for examples, I like to ask students about their impressions on the toxicities of certain examples, such as coffee or Tylenol. When I have given the toxicology lectures for the freshman Environmental Health class at the University of Washington, bringing up alcohol is always a topic that immediately gains the attention of the students.

Heavy alcohol consumption has clear toxicologic implications. Acute alcohol poisoning can result in overwhelming nervous system depression leading to respiratory failure, while chronic heavy alcohol consumption is largely dangerous due to repeated liver injury and progression into liver cirrhosis, where liver failure occurs as healthy hepatocytes are replaced with extensive fibrosis. Now we can all agree that heavy alcohol consumption is dangerous and should be avoided, but, as with many questions in toxicology, the question of lower level exposures, or moderate drinking, requires further investigation.

As I was browsing the Health section of the New York Times, I came across this headline:

http://well.blogs.nytimes.com/2013/09/06/drinking-when-young-increases-breast-cancer-risk/

This brief article brought attention to a recent article published in the Journal of the National Cancer Institute, from the Washington University in St. Louis, MO.

http://jnci.oxfordjournals.org/content/early/2013/08/24/jnci.djt213.full.pdf+html

In this study, the authors analyze the data collected from the Nurses’ Health Study II (NHSII) cohort, where roughly 115,000 female registered nurses completed questionnaires biennially from 1989 to 2003 answering numerous questions about their lifestyle and health status, including alcohol consumption at different points in their lives. From these surveys, they addressed the relationship between alcohol consumption prior to first pregnancy and the risk of developing overt breast cancer or benign breast disease. Although alcohol has been suggested to be associated to women’s risk of developing breast cancer for some time, this study was unique in that it addressed alcohol consumption rates for women between the ages of 15 and 40, asking the question of whether or not alcohol consumption between menarche and first pregnancy influences risk of developing breast cancer later in life. Their observations were that women’s alcohol consumption in this time period was positively associated with incidence of breast cancer, where an alcohol consumption rate of 10 g/day (roughly a glass of wine a day) between menarche and first pregnancy was associated with an 11% increase in risk of breast cancer, with continued alcohol consumption after first pregnancy to have less of an effect. This data would suggest that if this trend were linear, a 20 g/day alcohol consumption rate (2 glasses of wine a day) would give over a 20% increase in risk of breast cancer.

These are concerning observations. It is particularly concerning to me that they observed the risk of developing breast cancer increases when the time between menarche and first pregnancy is greater. As the age of menarche in women is continuing to decrease (potentially being driven from environmental factors including, endocrine disruptors) and the age of first pregnancy is continuing to increase (economic and social pressures), this length of time is becoming greater, further influencing population level risk of developing breast cancer.

The authors’ conclude that eliminating or reducing alcohol consumption may be an effective mechanism to reduce cancer risk.

Now, although this is likely to be true, unfortunately breast cancer is not the only disease women are at risk to suffer from. Cardiovascular disease continues to remain the greatest cause of disease in the Western world, and there is strong evidence that moderate alcohol consumption reduces risk of cardiovascular disease and stroke.

In a 2009 article in JAMA, moderate alcohol consumption (described at 5-14 drinks per week, or roughly 7 – 20 g/day) was independently associated with a reduced risk of heart failure in men.

http://jama.jamanetwork.com/article.aspx?articleid=184310

In what is probably the stronger association, moderate alcohol consumption provides a significant reduction in stroke, providing a benefit or no adverse risk in women with alcohol consumption up to 40 g/day (roughly 4 glasses of wine/day), with greater than 40 g/day increasing risk of stroke. Similar benefits were also observe in men.

http://jama.jamanetwork.com/article.aspx?articleid=195880

In addition, consumption of alcohol was found to be associated with a reduced risk of dementia in older adults. In this prospective study, consumption of 1-6 drinks/week was associated with a reduced incident demetia risk in both men and women. Upon stratification of the sexes, women who consumed 7-13 drinks/week appeared to have an even lower risk of dementia, where the calculated odds ratio for all cause dementia in women was 0.23 (95%CI 0.09-0.61), suggesting a potential reduction in risk of developing dementia by 77%.

http://jama.jamanetwork.com/article.aspx?articleid=196197

These data provide insight into the potential for moderate alcohol consumption to reduce risk of cardiovascular disease, stroke, and dementia, but we must remind ourselves that these studies were focused on older adults, and perhaps earlier alcohol consumption has a different effect. Overall, these data are challenging to put together in a cohesive story, it may very well be that alcohol consumption in women between menarche and first pregnancy alters hormonal function in a manner that confers an increased risk of developing breast cancer, a risk that could generally be looked at as an increase in 10% risk for every drink one has on average per day, but there is also strong evidence that this same type of moderate alcohol consumption reduces risk of other diseases, and the question would still remain of what is the overall risk of mortality, and what should the alcohol consumption rate be recommended for younger women? Currently, the American Stroke Association guideline is that men have 1-2 glass of wine per day, while women should have 1 glass of wine per day (they typically recommend red wine, due to the potential benefits of antioxidants and polyphenols, but the epidemiological data rarely finds any difference in beneficial effects when the type of alcohol is controlled for), but should these guidelines be modified for younger women before their first pregnancy?

In a recent study published in the Journal of Clinical Oncology, alcohol consumption before and after breast cancer survival found that moderate alcohol consumption resulted in slightly better overall survival than non-drinkers, potentially suggesting that the benefits of moderate alcohol consumption slightly outweigh the negative effects of increased risk of breast cancer.

http://jco.ascopubs.org/content/early/2013/04/08/JCO.2012.46.5765.abstract

Overall, this is an extremely challenging issue that I believe has strong implications for public health, do any of you have suggestions on this?

Would you recommend a young woman to avoid alcohol completely? Should we take into account those with genetic predisposition to developing breast cancer?

Chad