Does body weight tell us much about our health?

When I was in college, I had the luxury of being able to stay incredibly active with collegiate Ultimate Frisbee. And as cliché as it sounds to be an undergrad at Western, playing Ultimate in the rain in Bellingham (which we now know is the wettest place in the lower 48 http://www.seattlepi.com/local/connelly/article/Bellingham-tops-list-of-cities-with-least-sunshine-4954055.php), our team had some ~15 hrs/week of practice, including weekend tournaments all across the region. It was an exhausting sport! Throughout college, I don’t know if I ever thought that I could ‘over eat’. At that time, I basically believed that the more I ate, the better I felt. And even though I look back on this time with a bit of dread, remembering my hands freezing off when the turf field froze over and the snow didn’t melt for months, I think of this time as a luxurious occasion where I literally felt that anything I ate was perfectly okay.

But, as other collegiate athletes have corroborated, going from athlete to non-athlete is awful. You go from eating anything and everything you can possibly get your hands on to, to looking at your gut and thinking, “huh?” For me, the ‘eat everything and anything’ attitude maintained for a couple of years after college. I continued to play Ultimate Frisbee for a year or two, playing for a year with UW while in grad school, then for a club team over the summers, and my body consumed the energy about as fast as I could put it in. But at some point, when I realized I needed to focus on graduate school, when it seemed like I had less time available for the sport, and when I continually fought off injuries, I found myself lacking the energy and excitement to get back into it. I continued to play every once in a while and I got to play for an awesome club team in Germany when I was in Heidelberg (http://www.heidees.de/pages/heidees-news.php), but my competitive training continued to dwindle. Although it was, and sometimes still continues to be, a little painful to stop playing, I feel that I’m learning I need to plan for my health and fitness for the long haul, and training for Frisbee wasn’t going to be sustainable for me. Kudos to those who’ve made it work!

But, when I felt that I fully stepped off the Frisbee field, and I stopped burning thousands of calories a day from training, I did not become less hungry. A normal daily diet for my years of doing sports still seemed…normal. And as predictably as an overfilled glass of water will spill over its edge, I found myself gaining weight, something I never felt was even an option before. What ensued was a continual battle, that I know many, many, people are also fighting, where eating became a thought process. I found myself no longer able to just eat ‘everything and anything’. So, after years of sports, I joined the many who actually have to think about what they eat, so lame!

So, with wanting to think about what I eat, and trying to eat a balanced and ‘healthy’ diet, I find myself asking, what is healthy? To me, health is a vague concept. What does it mean to be healthy? Can one be healthy because they lack disease? Or does it also imply a certain trajectory of disease free survival for the long term? I sometimes just feel healthier if I eat at an organic co-op, does that make me healthier? And why do I feel so unhealthy if I eat, even a relatively low fat, low caloric meal, at a fast-food restaurant? And how on earth can Trader Joe’s, selling to an organic and health conscious market, get away with calling this coconut oil? http://www.amazon.com/Trader-Joes-Organic-Virgin-Coconut/dp/B007UWNBYS. This is a side tangent, but an ‘oil’ implies that it’s liquid at room temperature, this is solid saturated fats, just as bad as any butter or animal fat, but it feels pretty healthy, right?

In my mind, ‘being healthy’ implies a trajectory of long-term survival in the absence of disease. The aspect of ‘feeling healthy’ is when you feel good doing it, and it may include some Trader Joe’s coconut oil, because it’s delicious!

So how can we measure how healthy we are? Of course there a many clinical tests in combination with clinical symptoms that a physician can use to elucidate the presence of a disease. And of course there are clinical measures that are good a predicting disease risk (such as blood pressure, hemoglobin A1C levels, blood lipids, etc…). And of course there are functional measures that can assess general physical fitness and overall wellbeing (i.e. how well one can walk, exercise, etc…). But the simplest measure that can actually be fairly good at predicting risk of disease, and can be measured by anyone in his or her own home, is body weight.

When I last went to the doctor for an annual checkup, after they measured my height, and took my weight, they quickly reported my BMI (body mass index, kg/m²) to be 25.0. As I expected it to be roughly around 25, this wasn’t a surprise to me. But I knew that 25 was the cut-off between what is considered ‘normal weight’ (18.5 – 24.9) and ‘over weight’ (25-30), with obese being 30+. So by just a smidgen, I was considered ‘over weight’. But no one at the clinic seemed to care! With such a daunting clinical condition as ‘over weight’, there has got to be some real evidence to say that I am entering into a category that has an increased risk of mortality, right? Should I be trying to drop that weight to join my ‘normal weight’ counterparts? Can I calculate the number of years I’ll lose by now entering into a trajectory of a health span as an ‘over weight’ person? Well, I don’t quite think that I’m ‘over weight’ in a true sense, although I should definitely try and maintain an active life full of exercise with a diet rich in fruits and vegetables for many reasons, and perhaps my weight will come down a little. But seeing the BMI in action made me want to look more into what evidence we actually have for using the BMI, and try and answer, how bad is being ‘over weight’ or even obese?

Looking into a few recent studies that have conducted large meta-analyses looking into the association between BMI and mortality, it becomes clear that there is some real evidence that being obese (BMI, 30+) increases risk of mortality. In addition, there is real evidence that being underweight (BMI, <18.5) increases risk of mortality. These data appear to show what is considered a J-shaped curve, where, starting at an underweight BMI, as BMI increases mortality drops to an ‘ideal’ level, then mortality risk continues to increase as BMI continues onwards towards the obese range. But what is the ideal BMI? Is there a specific BMI we should all be shooting for? And how normal is the ‘normal’ BMI of 18.5 to 24.9?

In an extremely comprehensive analysis, published by Gonzalez et al. in the NEJM in 2009 http://www.nejm.org/doi/full/10.1056/NEJMoa1000367, the complex relationship between BMI and risk of mortality becomes clear. For this study, the median BMI in 1.46 million white adults of their study population was 26.2. So right away, I’m starting to think that a 'normal' BMI of 18.5 to 24.9, isn’t so ‘normal’. The crux of their data is the non-linear relationship between mortality risk and BMI, as shown below.

Looking at the data, it becomes clear that those in the study population with a BMI of 17.5 seemed to be a part of a category that had a significant increase in mortality risk, upwards of a 2-fold increase in risk to the referent population being those with a BMI between 22.5 and 24.9. The risk of mortality drops as BMI increases, to what appears to be an ‘ideal’ BMI of something around 23-24 in both men and women. When BMI goes above this ‘ideal’, the risk in mortality doesn’t seem to dramatically increase right away. In both men and women, when BMI reached 26, there appeared to be a 6-9% increase in mortality risk in non-smokers. But then it begins to really climb, reaching a 44% increase in mortality risk with those with BMIs of 31, and over 100% increase in risk for those with BMIs above 36 and even greater for those with BMIs above 40.

In almost complete agreement with the Gonzalez study, the Prospective Studies Collaboration, within the British Heart Foundation and Oxford published in Lancet their meta-analysis from 57 studies, looking at BMI and mortality in 900,000 adults http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)60318-4/fulltext. Their main findings of BMI and mortality risk are shown in the figure below.

What they report is that mortality risk is lowest for those with a BMI between 22.5 and 25. Where again, this J-shaped curve appears, where risk of mortality is higher for those with BMIs below 22.5, and increases for those above 25. But really, mortality risk for those with BMIs between 20 and roughly 27.5 appear to be nearly the same, likely small increases in risk for those with 20-22.5 and for those 25-27.5.

So looking at these data, it makes sense why a recent study by Flegal et al. in JAMA in 2013 http://jama.jamanetwork.com/article.aspx?articleid=1555137, found a significant decrease in mortality risk for those with BMIs between 25 and 30 compared to those with BMIs between 18.5 and 24.9. Their table showing hazard ratios (HRs) and BMI is shown below.

This publication got a lot of press, and people seemed to feel that there must be something that’s missing, but when looking at the data before it, these results aren’t too surprising. We know that mortality risk is higher for those with BMIs lower than 22.5, and we know that it begins to climb again for those with BMIs above 25, but not at a very fast rate. So if you combine the people with BMIs between 18.5 and 24.9, you’re going to catch the people with the higher risk of mortality with BMIs below 22.5 and the group with BMIs between 25 and 30, includes those with higher risk between 27.5 and 30, but combined, the overall risk is lower for the 'over weight' group compared to the 'normal weight' group.

So what can we learn from these studies? I think we can safely say that an ‘ideal’ BMI is between 22.5 and 25, and if one is a little lower than that, or a little higher than that, there isn’t really any strong evidence to say that risk of mortality increases. But there does consistently show strong evidence for increased mortality for those with low BMIs and with high BMIs. Overall, I think the ‘normal’ BMI range of 18.5 to 24.9, is a little off, and should probably be more like 22-27, perhaps this will change in the future.

But of course, this analysis is severely limited by the main problem with these studies: BMI is a measure that is adequate at best to predict mortality risk. We all know the examples of the incredibly athletic and muscular person who is not obese, but his/her BMI puts them into a category they don’t want to be in.

The reality is that in these studies, those individuals with high BMIs have a higher risk of mortality due to cardiovascular disease, diabetes, renal disease, cancer, etc., diseases often times due to improper metabolic health. Metabolic health refers to really how our body deals with energy and our diet, such as our blood sugar and insulin sensitivity and our blood lipids and cholesterols. We know that these factors play important causal roles in disease progression and it’s important to get an idea as to how we’re doing on these fronts. What the BMI hopes to assess is metabolic health, and what we really want to know is what is someone’s chance of developing disease due to these improper metabolic controls? And unfortunately, BMI is only a crude and limited measure.

This is why a call for better metrics for metabolic health was made recently in the journal Science http://www.sciencemag.org/content/341/6148/856.full, where the authors discuss how we now know that there are people with normal as well as obese BMIs who are metabolically healthy, just as there are people who have normal as well as obese BMIs who are metabolically unhealthy.

In the figure above, risk of mortality is shown by the elongated triangle at the top, where you can see that risk of mortality is greatest for those who are obese and metabolically unhealthy. But interestingly, someone who is of ‘normal’ BMI but metabolically unhealthy has a higher risk of mortality than someone who is obese but metabolically healthy.

What this highlights is the lack of mortality risk prediction one can get from BMI alone, and of course, any good physician will work with the patient to understand other metabolic factors that are greater predictors of risk, but what can we do at home? When I step on the scale, and reveal my BMI, am I appropriately gauging where I am ‘health’ wise? I don’t think my body weight will tell me everything, but I think if I work to keep my diet and exercise in check, in combination with keeping an eye on such things as cholesterols, blood lipids, blood sugars, and blood pressure, my body weight may help me keep a frame of reference as to how I’m doing, and for now, my BMI of 25 doesn’t sound too bad.

Chad Weldy

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