What your cholesterol number really says

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By David S. Martin, CNN

August 17, 2011 3:57 p.m. EDT

Editor's note: Dr. Sanjay Gupta explores the signs, tests and lifestyle changes that could make cardiac problems a thing of the past on "The Last Heart Attack" at 8 p.m. ET Sunday on CNN. 

(CNN) -- Learning your cholesterol numbers -- the good, the bad and the total -- is a well-established part of the annual physical exam.

A high cholesterol number results in angst and possible treatment. A low number brings relief. But are we putting too much stock in cholesterol as a sign of our heart attack risk?

"The cholesterol number is essentially worthless," says Dr. Arthur Agatston. The Miami cardiologist and South Beach diet books author says the cholesterol of people who have heart attacks and those who don't are almost identical.

"The overlap is troubling," Dr. Kwame Akosah at the University of Virginia agrees. "As an isolated predictor, it falls short."

As a sign of the weakness in cholesterol numbers alone, one large study found the average LDL cholesterol of people hospitalized for heart disease was 105, which is considered "near optimal."

The study, published in the American Heart Journal in 2009, found almost half of the hospital admissions had LDL cholesterol levels below 100, traditionally considered "low risk."

What causes a heart attack?

Ways to keep your cholesterol healthy

RELATED TOPICS

• Cardiovascular Medicine
• Cholesterol
• Heart Attacks

Another study found that only half of heart attacks occurred in people with high cholesterol (at or above 240), while a fifth of the heart attacks struck people whose cholesterol levels (below 200) deemed them safe based on long-held guidelines.

Agatston says the cholesterol numbers fall short because they measure cholesterol in your blood. They don't tell you the amount of LDL, or bad cholesterol, building up as plaque in the blood vessel walls. Plaque is what causes heart attacks.

As a result, studies show some people who think they're high risk based on cholesterol numbers are not, while others who think they are in the clear are developing dangerous plaques.

Your body needs cholesterol. The waxy substance is in the lining of every cell in your body. You also use cholesterol to make hormones, vitamin D and other substances.

Cholesterol circulates in the blood stream with the help of lipoproteins. The low-density lipoprotein, or LDL, carries cholesterol away from the liver. The high-density lipoprotein, or HDL, scavenges excess cholesterol and brings it back to the liver.

Your body produces cholesterol in the liver. You can also get cholesterol in fatty foods. When the LDL in the blood outstrips the HDL's ability to scavenge it, plaque can accumulate. The buildup of plaque is a lifelong process, beginning in childhood, but everyone is different.

Your genes play a role in whether you are prone to accumulating LDL as plaque. High blood pressure also makes you more prone to plaque buildup. If you are obese or diabetic or a smoker or suffer from a chronic inflammatory condition like lupus, you are also more likely to accumulate plaque than someone with the same LDL cholesterol number.

Akosah says he uses all these factors to determine a patient's "global risk" and tailors the treatment accordingly.

Also, there are different LDL particle sizes. Smaller particles tend to penetrate the vessel wall more easily than larger LDL particles.

Most heart attacks are not caused by the slow narrowing of blood vessels but by a rupture of a blister or bubble of plaque in an artery that is less than 50 percent blocked. Half of all heart attacks come with no warning at all, making diagnostic tests all the more important.

Younger women may be particularly jeopardized by a heavy reliance on cholesterol numbers. One study that looked at heart attacks in women under 65 found none had been deemed "high risk" for a heart attack using the traditional Framingham Risk Score, which looked at age, smoking, blood pressure, total cholesterol and HDL.

A class of drugs called statins lowers LDL cholesterol. Exercise and a low-fat diet rich in fruits, vegetables, whole grains and legumes can also lower LDL and raise HDL. Smokers who quit also improve their cholesterol numbers.

But the numbers themselves may be only the first step in learning your heart health.

"High cholesterol is not a diagnosis. It's a symptom. It's like a fever. The first step is to figure out what's going on," says Dr. James A. Underberg, a professor at New York University School of Medicine who specializes in preventive cardiovascular medicine.

What It Is:Vitamin D is a fat-soluble vitamin. There are two major forms of vitamin D  D₂ (ergocalciferol) and D₃ (cholecalciferol). Both vitamin D₂ and D₃ and appear to be absorbed with equal efficiency and, at moderate doses, are equally able to raise levels of 25-hydroxyvitamin D the hormonally active form of vitamin D and a clinical measure of vitamin D status.  However, at very high doses, D₃, may be more efficient at raising 25-hydroxyvitamin D levels.

Vitamin D₂ (ergocalciferol) is made by the conversion of a sterol found in plants and yeast. Vitamin D₂ is used in some dietary supplements.

Vitamin D₃ is produced naturally in human skin exposed to ultraviolet B light and occurs in some animal products, such as cod liver oil, and, in smaller amounts, in other fatty fish such as herrings, mackerel, sardines, and tuna. Vitamin D₃ is the most common form used in dietary supplements and is the form generally used to fortify foods such as milk (which naturally contains a small amount of vitamin D₃). Vitamin D₃ is made by the conversion of cholesterol compounds, such as 7-dehydroxycholesterol from lanolin found in sheep's wool.

What It Does:

Bone

Vitamin D regulates the amount of calcium and phosphorus in the body, partly by controlling their levels of absorption. Vitamin D treats and prevents rickets in children and osteomalacia (bone softening) in adults. Given to breast-fed infants, vitamin D may help increase bone density.

Taken with calcium, vitamin D can help decrease post-menopausal bone loss and prevent osteoporosis (loss of bone density), as well as improve tooth retention in the elderly. In girls ages 9 to 13, regular supplementation with calcium and vitamin D has been shown to significantly increase bone density and bone strength (measured in arms and legs) compared to placebo (Greene, Osteoporosis Int 2011).Other effects:

A study found that older women (69 years and older) whose vitamin D levels were not between 20 and 29.9 ng/mL had a greater risk of being frail.¹⁸ Frail individuals were those experiencing at least three of the following criteria: weight loss, weakness, exhaustion, slowness, and low physical activity.  The risk of frailty was increased by 47% among those with vitamin D levels below 15 ng/mL, 24% among those with levels below 20 ng/mL, and 32% among those with levels above 29.9 ng/mL.  An average of 4.5 years after these measurements were made, those originally not frail but whose blood levels had been below 20 ng/mL were 21% more likely to have become frail or died. These findings correspond with the 2010 report from the Institute of Medicine (IOM) indicating that 20 ng/mL is a sufficient level for vitamin D and that levels above 30 ng/mL may be associated with certain risks.¹⁷

Research has found that men with low levels of vitamin D in the blood (15 ng/mL and lower) were at increased risk for heart attack compared to those with sufficient levels (30 ng/mL and higher) even after adjusting for other risk factors and physical activity. This may contribute to the higher rate of cardiovascular mortality among black Americans compared to white Americans, as blacks tend to have lower vitamin D levels.¹ More recently, an analysis of two large studies showed that men who consumed 600 IU or more per day of vitamin D from foods and supplements were 16% less likely to have cardiovascular disease and stroke over a period of approximately 20 years compared to men consuming less than 100 IU per day. The same association was not seen among women; the reason for this is unclear but one possible explanation given is that women may need higher intake of vitamin D because they tend to have a higher percentage of body fat than men and vitamin D is fat soluble. In addition, vitamin D intake during the study period, which ended in 2006, may have been too low to produce meaningful differences.²¹ A large trial giving 2,000 IU per day as a supplement is underway and may yield additional insights (principal investigator is J.E. Manson).
Lower levels are also associated with a higher risk and severity of depression.  A study in Italy, for example, showed that older women with low vitamin D levels (below 20 ng/mL) were twice as likely to develop depressive mood as those with higher levels.  Older men with low levels were 60% more likely to develop depressive mood.⁹ Data from the same study showed that those who were severely vitamin D deficient (below 10 ng/mL) were approximately 60% more likely than those who were vitamin D sufficient (above 30 ng/mL) to experience substantial cognitive decline, although there was no such association attention level.¹³

 

A study from Finland suggested that high vitamin D status provides protection against Parkinson's disease. People with the highest vitamin D levels (above 20 ng/mL) had a 65% lower risk of developing Parkinson disease than those with the lowest vitamin D levels (below 10 ng/mL).  A limitation of the study was that none of the groups had sufficient vitamin D levels (due to limited sun exposure in Finland).¹⁴ It is possible that greater risk reduction would have been observed in people with sufficient vitamin D levels.

 Low levels of vitamin D are also associated with a higher risk in women of developing rheumatoid arthritis. There is conflicting evidence about whether vitamin D helps reduce the overall risk of dying from cancer, although studies have consistently shown that higher vitamin D serum levels were associated with decreased risk of death from gastrointestinal cancers.

Studies suggest that vitamin D may also improve balance and reduce the risk of falls in older adults, for reasons that aren't clear. However, a recent study in women aged 70 and older who were at-risk for bone fracture showed an increase in falls and fractures among those given an extremely high, single, annual dose (500,000 IU) of vitamin D_3.¹⁰  This unexpected finding may have resulted from unusual effects of the extreme dose.¹¹ Much weaker evidence hints that giving vitamin D supplements to infants might decrease the risk of type 1 diabetes later in life, and that if women avoid vitamin D deficiency it might reduce their risk of multiple sclerosis.

A study in post-menopausal women showed 400 IU of vitamin D₃ and 1,000 mg of calcium daily were less likely to gain small to moderate amounts of weight compared to women taking placebo.

 

Researchers in Japan studied the effect of vitamin D₃ supplements (1,200 IU per day from December through March) on the incidence of seasonal influenza A in school children. Influenza A infection occurred in 18.6% of children in a placebo group versus 10.8% of children who received the supplement a 42% reduction in risk among those taking the supplement. The reduction was more prominent among children who had not been taking other vitamin D supplements. Influenza infection was not reduced among a subgroup of asthmatic children but those who became infected were significantly less likely to have an asthmatic attack if they received vitamin D than if they had not. Supplementation did not affect the incidence of influenza B (which is less common than influenza A and is not seasonal).¹⁴

A review of medical studies published from 1950 to 2009 that looked at, among other variables, vitamin D intake and asthma, suggested that vitamin D deficiency may be linked to airway inflammation, decreased lung function and poor asthma control. The researchers conducting the review hypothesized that vitamin D supplementation may lead to improved asthma control, although this cannot be established as many of the studies were not specifically designed to test the effects of vitamin D supplementation on patients with asthma.¹⁵
Higher serum vitamin D levels are associated with a reduced risk of allergy in children and adolescents. A review of data from a nationwide study of over 6,000 individuals showed that allergic sensitization was more common in those with serum vitamin D of less than 15 ng/mL compared to those with 30 ng/mL or greater for 11 out of 17 allergens.  Results were adjusted for potentially confounding factors like time spent on indoor activities. The strongest associations were for allergy to oak (5 times the risk), peanut (2.4 times the risk), and ragweed (1.8 times the risk). There was also increased risk of allergy to dog, cockroach, mite, shrimp, ryegrass, Bermuda grass, birch and thistle. In adults, there was no consistent association between allergy and vitamin D levels.¹⁹

Vitamin D Protects Against Age-Related Vision Loss

Vitamin D Protects Against Age-Related Vision Loss

For Women Under 75, Extra Vitamin D Could Ward Off Macular Degeneration

1 COMMENT

BY COURTNEY HUTCHISON, ABC NEWS MEDICAL UNIT

April 11, 2011

Many women must resort to using reading glasses as they age, but for Dorrette White, 47, the blurriness at the center of her vision was something more. After a routine visit to her eye doctor, this Brooklyn mother of four was told she was in the early stages of age-related macular degeneration (AMD), a leading cause of vision loss and blindness among older Americans that strikes 8 and half million Americans.

Fortunately for White, her condition is unlikely to lead to blindness any time soon, and for now her only "prescription" is a healthy lifestyle complete with lots of vitamin D-rich foods, said her ophthalmologist, Dr. Shantan Reddy. Reddy has prescribed her a healthy dose of vitamin D-rich dairy and leafy greens.When she first heard the news, she worried "that it's like months down the lineyou'll go blind or something like that," White said.

"She's got very early signs…and most of these patients don't progress to more advanced types. But to decrease risk further, I recommend her adding vitamin D rich foods," said Reddy, who is an assistant professor of Ophthalmology at NYU Langone Medical Center.

In Monday's study, women who consumed the most vitamin D cut their risk of developing early AMD by more than half when compared to women with vitamin D-poor diets. Researchers found that risk was lowest when patients consumed 720 international units of Vitamin D per day through foods such as cold water fish, leafy greens, and dairy.

A little over three ounces of blue fin tuna would meet the daily dose, for example.

Vitamin D as Medicine

Reddy said the findings are "wonderful" because currently there are "limited treatment in preventing the progression of macular degeneration and…no established means to prevent its occurrence. With this study we know there are vitamins that you can take through your diet that can decrease the odds of developing [it]."

"We can hit the problem before it even begins," he said.

Though vitamin D can be obtained from foods, supplements, or by exposure to the sun, researchers found that vitamin D levels among patients in the study were most affected by the amount of vitamin D they consumed, not by the amount of outdoor exposure they had.

Considering many Americans are actually deficient in vitamin D, this study may offer one more reason for women to include vitamin D-rich foods in the diet, especially because women with vitamin D levels well above the recommended minimum saw the most benefit, said the lead author on the study, Amy Millen of the University of Buffalo.

White Male Life Expectancy 75.7 years, Black Male 70.9 years

Death rate down, life expectancy up in U.S.

By Nanci Hellmich, USA TODAY

Updated 9h 26m ago

100 | 6

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Children born today can expect to live longer than ever in U.S. history, according to preliminary government data released Wednesday.

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  For white males, life expectancy is 75.7 years; for white females, 80.6.

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For white males, life expectancy is 75.7 years; for white females, 80.6.

Life expectancy at birth increased to 78.2 years in 2009, up from 78 years in 2008.

"What this means is that somebody born in 2009 can expect to live to an average of 78.2 years. This is a new record high for life expectancy," says Kenneth Kochanek, a statistician with the National Center for Health Statistics, which is part of the Centers for Disease Control and Prevention.

Death rates for 10 of the 15 leading causes of death decreased significantly between 2008 and 2009, including for heart disease, cancer and stroke.

"Basically, this is nothing but good news," Kochanek says.

The reasons for the decline will be examined when the final data is released later this year, he says.

Other findings from the National Vital Statistics System, which is data from death certificates from all 50 states and Washington, D.C.:

•For white males, life expectancy is 75.7 years; for white females, 80.6. For black American males, life expectancy is 70.9 years; for females, 77.4 years.

•Infant mortality in the U.S. hit a record low in 2009 at 6.42 infant deaths for every 1,000 live births. This is a 2.6% decline from 6.59 deaths per 1,000 births in 2008.

•Age-adjusted death rate for the U.S. population fell for the 10th year in a row to an all-time low of 741 deaths per 100,000 in 2009. This is down from 758.7 deaths in 2008.

•There were 2,436,682 deaths in the U.S. in 2009, down from 2,473,018 in 2008.

•Death rates declined for heart disease (down 3.7%), cancer (1.1%), chronic lower respiratory diseases (4.1%), stroke (4.2%), accidents (4.1%), Alzheimer's disease (4.1%), diabetes (4.1%), influenza and pneumonia (4.7%), septicemia (1.8%) and homicide (6.8%).

The increase in life expectancy and decline in death rates for major diseases are encouraging, says Ralph Sacco, a neurologist and president of the American Heart Association, and show "that our treatments and prevention programs are working."

But "death is not always the best measure of the burden of disease, since disability and quality of life are also important measures," he says.

"The continuing differences between blacks and whites also highlight the need to more effectively prevent cardiovascular diseases and stroke among African Americans."

Somethings really wrong with our water.

This Study conducted in CT points to Birth Control pills and BPA as just two of many compounds that are effecting humans.

21 FEB 2011: INTERVIEW

Unraveling the Mystery Of
The Bizarre Deformed Frogs

Yale ecologist David Skelly wanted to know why a sizable percentage of frogs in the northeastern United States suffered from deformities. His ongoing research has implicated human activity — but not in the way many researchers had thought.

by carl zimmer

For the last two decades, strange things have been happening to frogs. Some frog populations have high rates of limb deformities, while others have high incidences of what is known as “intersex” — traits associated with both males and females, such as male frogs whose testes contain eggs.

David K. Skelly, professor of ecology at the Yale School of Forestry & Environmental Studies, set out to discover what was causing these deformities, which some researchers were attributing to the use of an agricultural pesticide called atrazine. Skelly launched an experiment in ponds throughout Connecticut, studying frogs in four landscapes: forests, agricultural areas, suburbs, and cities. And what he found was surprising — the highest rates of deformities were not occurring in and around farmlands, but in cities and suburbs.

Yale University

David K. Skelly

In an interview with Yale Environment 360 contributing writer Carl Zimmer, Skelly described what chemicals may be causing these abnormalities in frog populations, and explained why this phenomena may have troubling implications not only for amphibians, but for other vertebrates, including humans. One thing seems clear: The deformities showing up in frogs are almost certainly not caused by a single chemical, but rather by a whole suite of substances — including medicines excreted by humans into the environment — that act in concert to mimic hormones like estrogen or cause other ill effects.

“The fact that these kinds of estrogens out in the environment can have this kind of effect on a vertebrate — many people would say that that alone is a basis for us to be concerned,” says Skelly.

Yale Environment 360: You came to the question of pollution not as a medical researcher but as a wildlife biologist — you studied frogs. Tell us how that happened.

David Skelly: Well, as an ecologist, I start with the animals. When I started on this project I really didn’t know whether I was going to be studying pollution or what. I started off trying to understand where sexual deformities in amphibians came from in the environment. There had been some laboratory work that did in fact use pollutants and figure out whether exposure through pollutants like pesticides might cause these kinds of deformities. But to me, the cart was before the horse because we really didn’t understand the natural history of reproductive deformities in many groups.

e360: When did people first notice that there was something weird going on with these frogs?

Skelly: Really the laboratory work in this case came first. About ten years ago people started doing laboratory experiments with amphibians, and some work on atrazine, a pesticide, was important because it was showing that extremely low concentrations of the pesticide might lead to these kinds of deformities.

e360: And what deformities are you talking about?

Skelly: The deformities in particular are traits that are associated with animals that have characteristics of both males and females. And there are lots of different possibilities. The ones that we’ve been concentrating on and the ones that are most clear are, say, a frog that looks like a male and has testes, but when you look inside the testes there are eggs growing in there. That’s an attribute that you can say suggests intersex, a condition in between male and female.

David Skelly/Yale University

Skelly found deformities in almost all ponds sampled in suburban and urban landscapes.

So then after these lab results came out people started going out into the field and, lo and behold, they found these deformities sometimes to be quite common in natural populations. That was interesting because certainly in the past we’ve known about these deformities for a hundred years. And in fact, a lot of what we know about sexual development in animals, and invertebrates in particular, was worked out in amphibians as a model system. And people have looked for them in natural populations before, but until this recent spate of work starting about ten years ago they hadn’t been found to be common in too many places. What we found more recently is that in a variety of studies people are finding them to be quite common. What worried me about the work that had been done so far is that because the laboratory work had been focusing on agricultural pesticides, people went out and basically looked at gradients of agricultural intensity, or just worked in agricultural landscapes.

e360: So they think because atrazine in the lab can cause intersex deformities, let’s go look at places where these pesticides are used, like on farms?

Skelly: Yeah. On one level that makes a lot of sense. But on another level it can be misleading. You can tend to reach a conclusion that isn’t warranted because if you say I’m just going to go look in agricultural landscapes and I find these deformities there and I’ve done the laboratory work to show that exposure to the pesticide can lead to these deformities, you might just wipe your hands and say we’re done here. But what we didn’t know is what about all these other landscape types? Are deformities showing up in those landscapes as well? And that was really our goal — to ask very broadly, how often is this happening? Where is it happening? What does the landscape of amphibian intersex look like? And what we found was pretty surprising.

e360: Where did you go and what did you do to do the study?

Skelly: The prior work on amphibian intersex had primarily been done in the West and the Midwest. There was a study down in Florida. Nobody had looked at all in the northeastern United States and that’s where I’m based. So we worked in Connecticut, specifically in the Connecticut River Valley, and one of the nice things about Connecticut is that it’s got a pretty

We find intersex frogs in agricultural landscapes, but in suburban and urban landscapes at three times the rate.”

compact size but there is pretty high diversity of land-cover types. So there is an active agricultural landscape in Connecticut, there are certainly a lot of suburbs. There are urban areas and there are still a lot of forests in Connecticut. Connecticut ranks third or fourth in the nation for population density, and it ranks third or fourth in the nation for the proportion forested. We can take advantage of that. So we worked in a set of land cover types: agricultural; undeveloped, which in Connecticut means forested; suburban, people with lawns and houses and schools and that sort of stuff; and urban, mostly around Hartford.

So essentially we took the entire state and categorized areas around small ponds as fitting into one of those categories and then sub-sampled them randomly. And what we found is that we can find intersex frogs in a variety of landscapes. We find them in agricultural landscapes, but we find them in suburban and urban landscapes at three times the rate. So if they’re concentrated anywhere, they’re concentrated in these more densely settled places — places where people live and work. We didn’t find them in wooded landscapes, these undeveloped landscapes.

e360: So whatever is happening has something to do with human activity, since you’re not seeing it in the wooded landscapes.

Skelly: Right. So we feel very confident at this point that whatever is going on seems to be associated with some kind of human activities and we are finding it in agricultural landscapes so it’s not that whatever goes on in agricultural landscapes is inconsistent with it happening... [But] I think the fact that we found that in those kinds of landscapes where corn is being grown, the great majority of the ponds we sampled didn’t have any deformities at all. It suggests to me that whatever is going on in those landscapes compared with the suburban and urban ones, we’re not getting a signal that strongly points towards agricultural pesticides. Not at this point — we’ve got more work to do. But one of the striking things is that almost all the ponds in the suburbs and urban landscapes have deformities in them. So this is something that is practically ubiquitous in those places and yet is showing up in a much more spotty manner in agricultural landscapes.

e360: So if atrazine is not the only factor, what are your suspicions about what else might be going on?

Skelly: Well it’s pretty well known that amphibians, fish, and frankly vertebrates in general can be influenced by hormones that are just out there in the environment. There are actually whole biological systems that depend on that happening naturally. But it’s also clear that we put a lot of hormones into the environment. And in particular we know that estrogen exposure can lead to the kinds of deformities we are seeing. So we would be irresponsible if we didn’t at least explore that avenue. It seems like a pretty reasonable set of hypotheses at this point just to imagine that there’s a bunch of estrogens out there in the environment and perhaps atrazine is one of them.

There are dozens of chemicals that humans create to actually act as estrogen. Birth control pills are a perfect example. The estrodial people take as birth control or as prostate medicine, it goes through our bodies, it may get complexed with something, and then we excrete it and it can become active again in the environment. I mean that’s not hype, that’s

It is widely accepted that the way that toxins work in the environment is often in concert.”

absolutely been shown to happen as a matter of course. So that’s a very potent estrogen. And those molecules are reasonably durable. But there are many other chemicals that were not created to be estrogens and yet can act like estrogens once they’re out there. So one that many people may have heard of is Bisphenol A. That’s the chemical BPA and there was federal legislation to remove it from baby bottles. It’s a plasticizer. So it’s an industrial chemical that’s supposed to help us create something and then as a totally unintentional byproduct it can have this other kind of biological activity.

And it turns out there’s a variety of chemicals with molecules shaped such that they can bind to receptors on our cells, or in cells of frogs that are intended to receive estrogen molecules. And when these receptors bind with these other chemicals they turn that into a signal that says, okay, some estrogen just arrived. And if that happens often enough there are physiological responses in our bodies that in a frog’s testes could lead it to start creating eggs.

So the biology of all that is pretty well worked out. It doesn’t mean there aren’t other possibilities for what might be going on, but we know that these estrogens are out in the environment. We know that a species like frogs can respond to them. What we need to do is see whether the dots connect and whether the exposure happens in these ponds. And then as a follow-up to that, if all that comes together, then another step we need to take is do experiments — not in the laboratory, but out in the natural environment, and see whether we can actually create this kind of a cycle where there’s exposure going on and we can see inside of a natural pond.

So the way that you would nail this down is by experimentally exposing some animals in the field to this kind of cocktail of chemicals that we can first demonstrate are out there in the field, and then see what kind of biological responses we get. That’s the way we can with great certainty figure this out. And it’s important to be pretty certain about it because we’re talking about a variety of chemicals that are in the environment because they’re useful. You know these are people’s medications, they are industrial chemicals, they’re not out there for no reason. And we’re not going to be able to change people’s minds about them unless we have very good evidence suggesting that these effects are happening. And then the question is, what do you do about it?

e360: When you hear that frogs are having these sexual deformities, it sounds creepy. But does it have an actual ecological impact? I mean does the fact that we may be changing the nature of these frogs actually mean something to the wildlife itself?

David Skelly/Yale University

A deformed leopard frog metamorph found near Lake Champlain in Vermont.

Skelly: I think these results are important in two very different ways. Beyond being creepy, the fact that these kinds of estrogens out in the environment can have this kind of effect on a vertebrate — many people would say that that alone is a basis for us to be concerned. Because there are many other species that share some of the same biological pathways that frogs have. And that includes people, where we don’t want the possibility of this going on. So you can get precautionary about it and just say this isn’t about frog population viability. This is about not wanting to have chemicals that have that kind of biological activity out there.

e360: So back when Rachel Carson was writing Silent Spring, she was focusing on DDT and there was a certain clarity there where she could focus on one pollutant. And here we have a situation today where you have to think about atrazine and all these other chemicals that each individually might have an impact on these frogs and on people, or maybe together cumulatively have an impact. It makes the problem more complicated. How do you deal with that?

Skelly: It is complicated. And I think we’re still grappling, maybe struggling is a better word. The EPA [Environmental Protection Agency] and ecotoxicologists in general have been trying to figure out how to deal with mixtures for some time. So it is widely accepted that the way that toxins work in the environment is often in concert. But the paradigm that you described where beginning with Rachel Carson we were thinking about one chemical at a time — people like the clarity that comes from that. It’s clean and if you do this in the lab you get beautiful results. This standard of pure clear repeatable results has kind of gotten in the way of thinking about how bad things happen out in nature.

One thing that I can see on the horizon is that people are thinking about looking at biological pathways. So we’ve been talking about pathways where estrogens get turned into physiological responses. And instead of thinking about one chemical at a time, what are the chemicals out there that could cause that, and shouldn’t we be managing those as a group? Because we’re talking about medications, we’re talking about industrial chemicals, we’re talking about pesticides. 

I think first what we need to do is come up with clear field-based cases where you can show very clearly that it is mixtures causing this and that managing chemicals one at a time isn’t going to work... It’s ironic you mentioned Rachel Carson because she started with a natural history phenomenon and then followed her nose to figure out what was going on, and traced it to a single chemical. It could have easily been traced to a group of chemicals and perhaps the history of environmental regulation would have rolled out differently.

e360: And so we would conceivably be regulating these chemicals in groups? I mean, wouldn’t somebody who makes the birth control pill say, well, we only contribute a tiny amount to this problem so why are you picking on us?

MORE FROM YALE e360

A Warning by Key Researcher
On Risks of BPA in Our Lives

The synthetic chemical, BPA — found in everything from plastic bottles to cash register receipts — is a potent, estrogen-mimicking compound. In an interview, biologist Frederick vom Saal harshly criticizes U.S. corporations and government regulators for covering up — or ignoring — the many health risks of BPA.
READ MORE

Skelly: I think that if we do get into thinking about and regulating mixtures of chemicals based on their action, as opposed to their intended use and their origin, it’s going to be an incredibly hairy regulatory problem. And I don’t pretend to understand how to deal with that except to say that there are a couple of bright hopes in this particular example. The first is that we can deal with a lot of chemicals regardless of their origin and regardless of their intent by changing how we manage waste. Right now a state-of-the-art sewage treatment plant has three stages. And what comes out the back end of that includes a lot of organic molecules, including estrogens, that really don’t get molested by the sewage treatment activities very much. If we could add a fourth stage – charcoal, sand bed, or something like that – that could remove a whole suite of things without thinking about what they are. The other way that we can deal with this is to build it into the front end. To build it into research and development of these chemicals so that we’re trying to think about could you create a plasticizer that works like BPA, but doesn’t act like a steroid? 

POSTED ON 21 FEB 2011 IN BIODIVERSITY SCIENCE & TECHNOLOGY