Health & Medicine – Page 5

Fish with Melanoma – Our Enduring Environmental Legacy

We’ve all heard the horror stories. Melanoma is one of the most dangerous kinds of skin cancer, killing around 50,000 people worldwide every year. If caught early enough, it can be cured, but once it invades past the skin, it’s deadly. On the advice of doctors, we try to protect ourselves, donning floppy hats and coat upon coat of SPF 50 sunblock. We pick over our bodies in the mirror regularly, looking for dark, irregularly-shaped spots. The recent rise in the incidence of skin cancer, though, is our own fault. It is the result of our environmental hubris, a combination of a chemically-depleted ozone layer and our pathological obsession with a tanned physical appearance. Now, we’re becoming increasingly aware that our choices don’t just impact our own species. The rest of life has to deal with our poor decisions, and studies are just now determining the wide-ranging consequences of our actions.

Histology of healthy skin (left) and melanoma-

diseased skin (right) from coral trout

Unable to slather on sunscreen, the creatures on our planet are much more limited in their ability to deal with the sun’s radiation. Some, like the red seabream, are able to tan much like we do, increasing the melanin content in their skin to defend against damaging rays. But most animals are not so lucky, and are ill-equipped to deal with drastic changes in UV radiation. Yet drastic changes in UV radiation are exactly what occurred in the late 20th century, when chemicals we used as refrigerants and in aerosol sprays quickly depleted one of the most UV-protecting molecules, ozone, from our atmosphere. From 1972 to 1992, places like Australia saw a 20% increase in UV radiation levels, and colder areas like Antarctica saw ozone decreases of 50 percent or more, creating large ozone holes which allow more than double the normal level of UV radiation to pass through.

In the late 1970s, scientists began to realize that certain chemicals we were producing, called chlorofluorocarbons, or CFCs, were making their way into the stratosphere. These chemicals release chlorine atoms which, when combined with cold temperatures, begin a destructive chain reaction that turns UV-blocking ozone into oxygen. By 1987, there was so little protective ozone in the stratosphere over Antarctica that global lawmakers decided CFCs were too dangerous to go unchecked. They established the Montreal Protocol, which set strict limits on the use of CFCs. In the 25 years since, the ozone layer has rebounded some, but it is still 50 to 70 years away from returning to pre-1980s levels. Now, the ozone layer is under a new threat: climate change. Scientists predict that rising carbon dioxide levels will lead to more ozone holes, as carbon dioxide and other greenhouse gasses trap heat at the surface, chilling the stratosphere, and allowing atmospheric chlorine atoms to wreak havoc.

We are only now beginning to fully document the consequences of ozone depletion. In people, the loss of ozone at the end of the 20th century was directly connected to a 16 to 60 percent increase in the incidence of skin cancer. But while we carefully documented the effects on our own species, little research has looked for health effects on other animals. Now, Australian scientists have found an entire population of fish plagued with the deadliest form of skin cancer: melanoma.

The team of researchers from Newcastle University began looking for skin cancer in the commercially and culturally important species of coral trout off Australia in 2010 when a different team of scientists studying sharks first noticed lesions. Because these other scientists from The Australian Institute of Marine Sciences were catching trout to study predator-prey dynamics, Michael Sweet and his colleagues were able to screen over a hundred coral trout (Plectropomus leopardus) for melanoma between August 2010 and February 2012. They examined lesions histologically, to determine the exact type and severity of the cancer. Lastly, they tested lesions for bacteria and viruses, to rule out a microbial cause.

A healthy coral trout (top) as compared to

trout with melanoma

A whopping 15% of the fish surveyed had melanoma. “Studying disease in wild fish populations is very time-consuming and costly so it’s hard to say how long the disease has been around,” explains lead author Michael Sweet. “What we do know is that it is now widespread in the coral trout population. We found evidence of cancer in the common coral trout, the bar-cheeked coral trout, and the blue spotted coral trout.”

While 15% sounds high, Sweet and his colleagues believe it’s only a minimum estimate. “Once the cancer spreads further you would expect the fish to become quite sick, becoming less active and possibly feeding less, hence less likely to be caught. This suggests the actual percentage affected by the cancer is likely to be higher than observed in this study.”

This isn’t the first melanoma to be found in fish, as individual cases have been identified in a wide variety of species, from catfish to nurse sharks. Never before, however, has melanoma been found population-wide. “To the best of our knowledge, cancer of any sort has never been shown in a wild marine fish population before, making this a first for science,” said Sweet

While it is a first, Sweet and his colleagues don’t think coral trout are unique. “We would not be surprised to find [melanoma] in other species as well,” he said, “including some of the smaller reef species.” So far, skin cancer in fish has likely been overlooked due to the high cost of evaluating fish for disease as well as the low likelihood of sick and weakened fish landing in fishermen’s or scientists’ hands.

Extensive laboratory analyses ruled out microbial agents as the driver of the disease, and since the fish were caught far from shore in a marine protected area, it’s unlikely that pollution factored in, either. The samples were also directly compared to UV-induced melanomas in laboratory fish, which are used as a model for human disease; the ones in coral trout looked identical to the lab-created cancers. “This combination of evidence leads us to suspect UV as the casual agent.”

If UV is the cause, then it’s really our fault. “The occurrence of this disease in today’s day and age and not before can be linked to the changes we are experiencing in our climate and the ozone hole,” explained Sweet. “It is highly likely there will be higher prevalence around areas which have these ‘ozone holes’.” While the Montreal Protocol has helped reverse some of the worst damage, Sweet is careful to note that we’re not out of the woods yet. “An increase in smaller ozone holes (other than the two large ones of the Arctic and the Antarctic) is thought to be occurring, and this has been related by other researchers to be due to climate change.”

The overall effect of skin cancer in fish populations could be devastating. In laboratory fish, melanoma cuts the lifespan of Xiphophorus species from four years to only six months, and makes them more susceptible to small changes in their environment like fluctuations in temperature. “It is unclear whether future changes in the ocean environment or climate will similarly exacerbate the effect of melanomas in wild P. leopardus populations,” write the authors, “but clearly further research is urgently needed to understand the distribution, prevalence, ecological and fisheries significance of this syndrome.”

Since lawmakers are hesitant to restrict greenhouse gasses and other pollutants, we’re stuck with whatever happens, for now – especially, as Sweet notes, when it comes to disease. “Without addressing the underlying issues, sadly, there is likely no feasible or practical cure for skin cancer in wild fish populations.” If melanoma is found in other species, too, the consequences will only magnify.

With little natural protection against UV rays, fish and most other species are at our mercy when it comes to radiation-induced disease. Skin cancer only adds to a growing list of pathological consequences to our poor ecological choices – a list which includes devastating diseases like chytridiomycosis and avian malaria. Until we change the way we treat the world around us, that list will continue to grow, while the abundance and vitality of our planet’s biodiversity shrinks.

Citation: “Evidence of melanoma in wild marine fish populations.” M J Sweet, N Kirkham, M Bendall, L Currey, J C Bythell, M Heupel. PLOS ONE. August 2012. DOI: 10.1371/journal.pone.0041989.g005

Histological sections from the paper; photos of coral trout by Michelle Heupel

Toxoplasma’s Dark Side: The Link Between Parasite and Suicide

We human beings are very attached to our brains. We’re proud of them – of their size and their complexity. We think our brains set us apart, make us special. We scare our children with tales of monsters that eat them, and obsessively study how they work, even when these efforts are often fruitless. So, of course, we are downright offended that a simple, single-celled organism can manipulate our favorite organ, influencing the way we think and act.

Toxoplasma gondii is arguably the most interesting parasite on the planet. In the guts of cats, this single-celled protozoan lives and breeds, producing egg-like cells which pass with the cats bowel movements. These find their way into other animals that come in contact with cat crap. Once in this new host, the parasite changes and migrates, eventually settling as cysts in various tissues including the host’s brain, where the real fun begins. Toxoplasma can only continue its life cycle and end up a happy adult in a cat’s gut if it can find its way into a cat’s gut, and the fastest way to a cat’s gut, of course, is to be eaten by a cat. Incredibly, the parasite has evolved to help ensure that this occurs. For example, Toxoplasma infection alters rat behavior with surgical precision, making them lose their fear of (and even become sexually aroused by!) the smell of cats by hijacking neurochemical pathways in the rat’s brain.

Of course, rats aren’t the only animals that Toxoplasma ends up in. Around 1/3 of people on Earth carry these parasites in their heads. Since Toxoplasma has no trouble affecting rats, whose brains are similar in many ways to our own, scientists wonder how much the parasite affects the big, complex brains we love so much. For over a decade, researchers have investigated how this single-celled creature affects the way we think, finding that indeed, Toxoplasma alters our behavior and may even play a role in cultural differences beween nations.

The idea that this tiny protozoan parasite can influence our minds is old news. Some of the greatest science writers of our time have waxed poetic about how it sneaks its way into our brains and affects our personalities. Overall, though, the side effects of infection are thought to be minor and relatively harmless. Recently, however, evidence has been mounting that suggests the psychological consequences of infection are much darker than we once thought.

In 2003, E. Fuller Torrey of the Stanley Medical Research Institute in Bethesda, Maryland his colleagues noted a link between Toxoplasma and schizophrenia – specifically, that women with high levels of the parasite were more likely to give birth to schizophrenics-to-be. The hypothesis given for this phenomenon is that while for most people who are infected, Toxoplasma has minor effects, for some, the changes are much more pronounced. The idea has gained traction – a later paper found, for example, that anti-psychotics worked just as well as parasite-killing drugs in restoring normal behaviors in infected rats, affirming the similarities between psychological disorders and Toxoplasma infection.

Continuing to work with mental patients, scientists later discovered a link between suicide and parasite infection. But, of course, this link was in people who already have mental illness. Similarly, a study found that countries with high Toxoplasma infection rates also had high suicide rates – but the connection between the two was weak, and there was no direct evidence that the women who committed suicide were infected.

What scientists really wanted to understand is whether Toxoplasma affects people with no prior disposition to psychological problems. They were in luck: in Denmark, serum antibody levels for Toxoplasma gondii were taken from the children of over 45,000 women as a part of a neonatal screening study to better understand how the parasite is transmitted from mother to child. Since children do not form their own antibodies until three months after birth, the antibody levels reflect the mother’s immune response. Thus the scientists were both able to passively screen women not only for infection status, but degree of infection, as high levels of antibodies are indicative of worse infections. They were then able to use the Danish Cause of Death Register, the Danish National Hospital Register and the Danish Psychiatric Central Research Register to investigate the correlation between infection and self-directed violence, including suicide.

The results were clear. Women with Toxoplasma infections were 54% more likely to attempt suicide – and twice as likely to succeed. In particular, these women were more likely to attempt violent suicides (using a knife or gun, for example, instead of overdosing on pills). But even more disturbing: suicide attempt risk was positively correlated with the level of infection. Those with the highest levels of antibodies were 91% more likely to attempt suicide than uninfected women. The connection between parasite and suicide held even for women who had no history of mental illness: among them, infected women were 56% more likely to commit self-directed violence.

While these results might seem frightening, they make sense when you think about how Toxoplasma is known to affect our personalities. In 2006, researchers linked Toxoplasma infection to neuroticism in both men and women. Neuroticism – as defined by psychology – is the “an enduring tendency to experience negative emotional states,” including depression, guilt and insecurity. The link between neuroticism and suicide is well established, thus if the parasite does make people more neurotic, it’s not surprising that it influences rates of self-violence.

How does a parasite affect how we think? The authors suggest that our immune system may actually be to blame. When we are infected with a parasite like Toxoplasma gondii, our immune system goes on the offensive, producing a group of molecules called cytokines that activate various immune cell types. The trouble is, recent research has connected high levels of cytokines to depression and violent suicide attempts. The exact mechanism by which cytokines cause depression and other mental illnesses is poorly understood, but we do know they are able to pass the blood-brain barrier and alter neurotransmitters like serotonin and dopamine in the brain.

But the authors caution that even with the evidence, correlation is not causation. “Is the suicide attempt a direct effect of the parasite on the function of the brain or an exaggerated immune response induced by the parasite affecting the brain? We do not know,” said Teodor T. Postolache, the senior author and an associate professor of psychiatry and director of the Mood and Anxiety Program at the University of Maryland School of Medicine, in a press release. “We can’t say with certainty that T. gondii caused the women to try to kill themselves.”

“In fact, we have not excluded reverse causality as there might be risk factors for suicidal behavior that also make people more susceptible to infection with T. gondii,” Postolache explained. But given the strong link between the two, there is real potential for therapeutic intervention. “If we can identify a causal relationship, we may be able to predict those at increased risk for attempting suicide and find ways to intervene and offer treatment.” The next step will be for scientists to affirm if and how these parasites cause negative thoughts. Not only could such research help target at-risk individuals, it may help scientists understand the dark neurological pathways that lead to depression and suicide that the sinister protozoan has tapped into. But even more disconcerting is that scientists predict that Toxoplasma prevalence is on the rise, both due to how we live and climate change. The increase and spread of this parasitic puppeteer cannot be good for the mental health of generations to come.

Citation: Pedersen, M.G., Mortensen, P.B., Norgaard-Pedersen, B. & Postolache, T.T. Toxoplasma gondii Infection and Self-directed Violence in Mothers, Archives of General Psychiatry, DOI: 10.1001/archgenpsychiatry.2012.668

Photos: Toxoplasma gondii parasites in rat ascitic fluid from the CDC’s Public Health Image Library; Brain MRI Scan in Patient with Toxoplasma Encephalitis from the University of Washington’s HIV Web Study

Mythbusting 101: bulking up with bull shark testosterone

This week, the startling image of a 1,000 pound bull shark has been circulating the internets. But what really caught my eye was the quote from the lead researcher. He told news outlets that bull sharks “have the most testosterone of any animal on the planet, so that should tell you a little something.” Tsk tsk. No matter what those websites tell you, it’s simply not true.

This isn’t the first time I have heard this whole bull sharks and testosterone bit. Indeed, all over the internet, you see claims that bull sharks are so aggressive because of their insane testosterone levels. But it was the character Bruce Kibbutz in Grand Theft Auto IV that really got people talking about bull shark testosterone. During the game, the roid-raging fitness freak explains how he juices on testosterone taken from Chilean bull sharks. Suddenly, extreme body builders and skeptics wanted to know if you could really bulk up on bull shark blood.

The rumor, as I’d heard it in college, is that the fierce attitudes of these large and aggressive sharks is due to unfathomably high circulating levels of testosterone. Specifically, these menacing monsters supposedly have higher serum testosterone levels than any species on the planet, land or sea, and that even a female bull shark has higher levels than a testosterone-raged male elephant in musth. I know I’m as much to blame as anyone, as I’ve repeated that line myself. But when I was asked about it, I realized that I didn’t know if it’s true. How do the circulating testosterone levels compare between bull sharks and other species? Could you procure enough testosterone by catching and eating bull sharks to beef up your body?

Let’s start with that elephant. In the red corner, standing up to 11.5 feet tall and weighing in at up to 20,000 lbs, we have the African Bush Elephant (Loxodonta africana). What’s the testosterone level in this whomping beast? During much of the year, not much. Male elephants, on average, have less than 2 ng/ml ciculating in their plasma. But wait! Big boy wants to get his groove on, and he is getting ready for a season of fighting and fornicating. So what’s the male elephant in musth’s testosterone level? As high as 64.4 ng/ml! About a 60 fold increase in average circulating testosterone¹. Ai! That’s a lot of anger-pumping hormone.

How about his opponent, the every day female bull shark (Carcharhinus leucas)? In the blue corner, weighing in at around 505 lbs and stretching almost 12 feet long, is our large and in charge girl. She’s bigger than her man, no doubt, but she still has to keep her femininity about her. After all, as a girl, if her testosterone levels are too high, she might have reproductive issues. Surely her circulating levels are lower than the male elephant’s?

According to the only, extremely obscure published reference with testosterone levels in a female bull shark, actually, yes, they are². Her circulating testosterone level is right around 0.1 ng/ml, a whole lot lower than that angry elephant. Sorry to burst bubbles, but she ain’t gonna give anyone roid rage. Her man, though… My oh my. One of the two male adult bull sharks in that study had a circulating testosterone level of 358 ng/ml. Yeah, that’s one roided out shark. Problem is, the other male bull shark in that study only had 2.7 ng/ml of testosterone in his serum – which is probably less than you male readers out there have pumping in your blood right now. So not all male bull sharks are running around roided out of their minds. To be fair, these were just single sharks, caught once and tested once. Without a more complete study of the average hormone levels in bull sharks, by size, season, etc, we can’t really say that bull sharks have abnormally high or low testosterone levels.

Of course, there is a more complete study. Not a super detailed one, but a study none the less. Rasmussen & Murru³ studied androgen levels in a number of captive sharks over time. They found testosterone levels of 10 ng/ml to 20 ng/ml in two captive bull sharks when they measured every June for three years, just after the sharks’ normal breeding season. Not too impressive, boys – not too impressive, but of course, that is in captivity, and it’s unknown how captivity may affect their hormone levels.

In wild bull sharks caught right before the breeding season, the serum levels were much higher: 185 ng/ml on average – which was 4 to 10 times higher than the levels they found in two other shark species, and is pretty impressive compared to the elephant. But, it turns out, it’s not that hard to find high testosterone levels in fish. Other sharks have high levels, too – like the bonnethead, Sphyrna tiburo, whose highest levels have been recorded at 303 ng/ml⁴. And in that species, even the girls have higher levels than our elephant – a whopping 74 ng/ml at max⁵. Believe me, I’d rather go hunting bonnethead than bull sharks any day. Other fish, too, have been found to have high testosterone. Male rainbow trout have levels around the same as those of the bonnetheads⁶, and heck, they sound a whole lot tastier to me than the other options. Just sayin’. Sorry folks, but according to the best, albeit limited scientific information we have, the idea that bull sharks are super juiced-up compared to other animals just isn’t true.

Yet in the news and even on the Discovery Channel’s infamous Shark Week, the highest-testosterone-in-the-world bull shark is the norm. How did the data end up so skewed towards this single result? As I see it, it is the scientific community that is to blame for the impression that bull sharks are testosterone-pumped. Every other paper I read about shark hormones since the two with bull sharks cites them, specifically mentioning 358 ng/ml and that bull sharks have much higher levels than other sharks.

Now that I read the papers, I see it’s not the media’s fault. It’s the original authors that claim that bull sharks have higher testosterone than other sharks, even without presenting evidence to back it up. It started with how Rasmussen & Gruber were quick to point out how high that 358 ng/ml value is, saying it’s “among the highest recorded in vertebrate serum,” but didn’t talk at all about why the other mature male bull shark (by their own identification) was more than one hundred fold lower. But it’s really Rasmussen & Murru (hmm… that first name sounds familiar), in their discussion, who seem to overinflate their own data. They state that “a species differences in absolute concentrations appears to exist because concentrations of testosterone in both wild and captive bull sharks were about two times higher than those in mature sandbar and lemon sharks” (emphasis mine). Yet their included figure showing the yearly serum concentrations for the two captive bull sharks studied clearly shows the levels between 5 ng/ml and 20 ng/ml, while the levels for the two captive sandbar sharks sampled at the same and different times of year range from 0 ng/ml to over 40 ng/ml! Two to four times higher in bull sharks? Where? When?!

But enough griping about inaccurate inflation of results. Let’s say, for a hypothetical moment, that there is a time of year, size, or whatever where you could go out with a shark hook and some dead fish and guarantee getting a big boy bull shark with upwards of 300 ng/ml in his system. It’s time to address the other part of the myth: Should serious users think about going fishing?

You’ll have one big fish to fry if you’re trying to get a nice dose of testosterone by ingesting sea creatures. First off, I hope you’re feeling vampiric. You want the blood, not the tissues. We don’t know anything about how much testosterone is in bull shark tissues, and besides, that super high amount was in the blood… so, yeah. Cheers. Second off, unless you’re planning on shooting up shark blood, you’re not getting the dose you think. Orally ingested testosterone is rapidly absorbed by the gut, but it’s also converted to inactive metabolites, leaving you with only 1/6^th the dose you took remaining in active form. That’s why pills and injections aren’t actually of straight testosterone, they’re of slightly modified chemicals that the body doesn’t metabolize as easily. It also means that to get the same dose from shark as you would from a prescription (or black market) pill, you have to drink six times what you think you have to.

So let’s say you want to replace that 40 mg pill you bought with bull shark blood. Even if you catch that one shark that had 350 ng/ml in his serum, that means you’ll have to drink down three cups of shark plasma to equal one pill. A shark tends to be about 12.3% blood by weight according to previous studies⁷ – that’s 6.8% blood cells and 5.5% serum, which has a specific gravity (weight per volume) of around 1.03. So say you caught an average bull shark, weighing only 350 lbs instead of the max of 500. He’ll have around 44 cups of blood in him, which is only 44% plasma, so you’ll need to drink 6.8 cups of blood per pill. So at 2-5 pills a day, that shark will only last you one to three days. Hey – I guess it’s legal. Though somehow, I don’t think athletes are going to get away with the old “I was just drinking shark blood” excuse just because of that.

Of course, all of that assumes that the majority of bull sharks are swimming around with high testosterone levels, which as the data reveals, simply isn’t likely. What’s worse, though, is that by perpetuating the idea of roided-out sharks, we’re giving credence to the idea that bull sharks are mindless killing machines with a taste for blood. While bull sharks are certainly dangerous animals, they are far from the angry maneaters they’re portrayed to be. Given that you’re still more likely to die from being struck by lightning that by a shark attack, and that there are probably hundreds of thousands of bull sharks in the Atlantic Ocean alone… I’d say the bull sharks are being pretty restrained.

Citations: 1. JAINUDEEN, M., KATONGOLE, C., & SHORT, R. (1972). PLASMA TESTOSTERONE LEVELS IN RELATION TO MUSTH AND SEXUAL ACTIVITY IN THE MALE ASIATIC ELEPHANT, ELEPHAS MAXIMUS Reproduction, 29 (1), 99-103 DOI: 10.1530/jrf.0.0290099

2. Harold L. Pratt, Jr., Samuel H. Gruber, & Toru Taniuchi (editors) (1990). Elasmobranchs as Living Resources: Advances in the Biology, Ecology, Systematics, and the Status of the Fisheries NOAA Technical Report NMFS 90, 143-155

3. Rasmussen, L., & Murru, F. (1992). Long-term studies of Serum Concentrations of reproductively related Steriod Hormones in individual captive Carcharhinids Marine and Freshwater Research, 43 (1) DOI: 10.1071/MF9920273

4. Manire, C. (1997). Serum Concentrations of Steroid Hormones in the Mature Male Bonnethead Shark,Sphyrna tiburo General and Comparative Endocrinology, 107 (3), 414-420 DOI: 10.1006/gcen.1997.6937

5. Manire, C. (1995). Serum Steroid Hormones and the Reproductive Cycle of the Female Bonnethead Shark, Sphyrna tiburo General and Comparative Endocrinology, 97 (3), 366-376 DOI: 10.1006/gcen.1995.1036

6. Scott, A. P., & Baynes, S. M. (1982). Plasma levels of sex steroids in relation to ovulation and spermiation in rainbow trout (Salmo gairdneri) Proc. Int. Symp. Reprod. Physiol. Fish, 103-106

7. Thorson, T. (1962). Partitioning of Body Fluids in the Lake Nicaragua Shark and Three Marine Sharks Science, 138 (3541), 688-690 DOI: 10.1126/science.138.3541.688

Note: this post is updated from a version posted on Science Blogs in 2010

Conservation is important – for the sake of our health

Growing up, I was one of those lucky kids who wasn’t allergic to anything. I felt like I was invincible – while my friends were pestered by pollen or peanuts, I was able to eat and play with reckless abandon. Childhoods like mine, however, are becoming more and more scarce. A recent study found that in 2008, peanut allergies in kids were three and a half times higher than a decade before, with similar trends occurring in a number of food allergies. Similarly, the prevalence of hay fever in developed countries has increased about 100 percent in each of the last three decades. It’s not just allergies – other chronic inflammatory diseases, from arthritis to asthma, continue to rise in our populations. A new paper in the Proceedings of the National Academy of Sciences suggests that perhaps the problem isn’t what we’re putting into our environment, but what we’re removing from it: that the loss of biodiversity is negatively impacting our health.

One of the most popular hypotheses to explain the rise in inflammatory conditions is known as the Hygiene Hypothesis, which says that our increasingly sterile lifestyle is to blame for our allergic reactions. We now live in a world of antibacterial soaps, instant hand sanitizer, vaccines, and antibiotics, all of which have taken over the job of protecting our children from dirt and germs. Left with nothing to do, kid’s immune systems get a little stir crazy, and start attacking even minor invaders like pollen with increased zeal. But Ilkka Hanski and his colleagues from the University of Helsinki in Finland suggest the Hygiene Hypothesis extends beyond how clean we keep our house. They put forward a Biodiversity Hypothesis, which suggests that less contact with the nature and biodiversity is adversely affecting the microbes on and in our bodies, leading to increased susceptibility to immune disorders.

To test this hypothesis, the research team investigated the relationship between biodiversity, allergen susceptibility, and skin microbial communities in a little over 100 randomly chosen teenagers in Finland. The kids grew up in a variety of settings, from tightly-packed villages to rural farmlands. For each participant, they measured how sensitive their skin was to allergens and what kind of microbes were living on there. Based on their skin’s immune reaction, they classified the students as allergen-sensitive (a condition known as atopy) or not. The researchers also roughly calculated the level of environmental biodiversity where the participants lived by looking at the amount of plant cover of their yards and the major land use types within 3 km of their homes, allowing comparisons between it and the participant’s allergy sensitivity and skin microorganisms.

The team found a strong, significant correlation between the diversity of a particular class of skin bacteria, called gammaproteobacteria, and allergen sensitivity. Though they only represented 3% of the skin bacterial community, gammaproteobacteria were the only class that showed a significant decrease in diversity in the atopic individuals. So, to get a closer look at this phenomenon, directly comparing the presence of different gammaproteobacteria with levels of an anti-inflamatory marker, IL-10, in the subjects’ blood. The presence of one gammaproteobacterial genus, Acinetobacter, was strongly linked to higher levels of IL-10 in healthy individuals but not in the allergen-sensitive ones. As the authors explain, this suggests that these microbes may help teach the immune system to ignore pesky allergens.

“The positive association between the abundance of the gammaproteobacterial genus Acinetobacter and IL-10 expression… in healthy individuals, but not in atopic individuals, is consistent with IL-10’s central role in maintaining immunologic tolerance to harmless substances.” Thus, the authors say, “the lack of association between Acinetobacter and IL-10 expression in atopic individuals in the present study might re?ect a breakdown of the regulatory mechanisms.”

How, exactly, Actinetobacter and other gammaproteobacteria influence our immune system has yet to be determined. What the authors did show is that environment a person grows up in has a strong effect on the presence and diversity of this group of bacteria. Since gammaproteobacteria are are commonly found in soil and on plants (including ?owering plants and their pollen), it may not seem that surprising to the researchers that the environmental diversity around a subject was strongly correlated to increased diversity of their skin gammaproteobacteria. But what is astounding is that this relationship held even when the researchers stepped back and looked at the overall connection between allergen sensitivity and the surrounding environment; the more natural biodiversity where the kid grew up, the less likely he or she was to be sensitive to allergens.

“The present results demonstrate that biodiversity can be surprisingly strongly associated with atopy.”

This suggests that the urban-dwelling nature of developed countries may be to blame for their increasing problem with inflammatory diseases. If so, conservation of natural spaces, including parks and other green initiatives, may be key to protecting the health of future generations. “Interactions with natural environmental features not only may increase general human well being in urban areas, but also may enrich the commensal microbiota and enhance its interaction with the immune system, with far-reaching consequences for public health.”

Since allergies cost us almost $14.5 billion annually including medical expenses, missed school and work, and over the counter drugs, there may be a strong monetary incentive to conserve our natural areas – if only for the sake of our health. That’s not even considering the other economic incentives for conservation, including water filtration and storm protection, which have been estimated at over $4.4 trillion dollars per year.

What all these studies tell us is that the cost of conservation is strongly outweighed by its benefits. Period.

Reference: Hanski, I., von Hertzen, L., Fyhrquist, N., Koskinen, K., Torppa, K., Laatikainen, T., Karisola, P., Auvinen, P., Paulin, L., Makela, M.J. & Environmental biodiversity, human microbiota, and allergy are interrelated, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1205624109

Image of soil and hands © Soil-Net.Com under a Creative Commons License

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Reversing a heart attack: scientists reprogram scar tissue into working muscle

Cardiovascular disease is the world’s leading cause of death. Approximately every 25 seconds, an American has a heart attack. One of the vessels to the heart gets blocked, cutting off blood flow to part of the heart. Then, the starving tissue begins to die, causing pain in the chest and difficulty breathing and, eventually, death. Every minute, someone in America dies from one of these coronary events. Those that survive the attack are still at risk for future problems as dead heart muscle leads to scar tissue that weakens the heart and increases the chance of heart failure. Until now, there was little that could be done for them, other than to encourage healthy lifestyle practices.

Just this week, Gladstone researchers announced a major breakthrough in heart disease research: they successfully reprogrammed scar tissue in live mice back into functional heart muscle.

Screen Shot 2012-04-18 at 1.22.20 PM — A mouse heart a month after a heart attack - scar tissue appears white

The researchers were able to use a virus-based system to deliver three key genes that guide embryonic heart development—Gata4, Mef2c and Tbx5 (GMT)—to areas of mouse hearts that were damaged in a heart attack. Within a month, cells that normally became scar tissue were beating away again as if they were not knocking on death’s door just 30 days before. By the three month mark, treated mice showed marked improvements in cardiac functioning.

“The damage from a heart attack is typically permanent because heart-muscle cells—deprived of oxygen during the attack—die and scar tissue forms,” said Dr. Deepak Srivastava, director of cardiovascular and stem cell research at Gladstone. “But our experiments in mice are a proof of concept that we can reprogram non-beating cells directly into fully functional, beating heart cells—offering an innovative and less invasive way to restore heart function after a heart attack.”

“This research may result in a much-needed alternative to heart transplants—for which donors are extremely limited,” said lead author Dr. Li Qian, a post doc at the California Institute for Regenerative Medicine. But the best part is that this method would use the person’s own cells, removing the need for stem cells or donor hearts. “Because we are reprogramming cells directly in the heart, we eliminate the need to surgically implant cells that were created in a petri dish.”

“We hope that our research will lay the foundation for initiating cardiac repair soon after a heart attack—perhaps even when the patient arrives in the emergency room,” said Srivastava. The ability to regenerate adult heart tissue from its own cells is a promising approach to treating cardiac disease because it may face fewer obstacles to clinical approval than other approaches. However, there is much to be done before this breakthrough becomes a treatment. “Our next goal is to replicate these experiments and test their safety in larger mammals, such as pigs, before considering clinical trials in humans.”

Previous work has been able to do this kind of cellular reprogramming in cultured cells, but clinically it is much more efficient if a treatment can work directly on live hearts. In 2010, coronary heart disease was projected to cost the United States $108.9 billion, including the cost of health care services, medications, and lost productivity. If research such as this can lead to improved functioning after a heart attack, it could save millions in health care costs, not to mention potentially save lives by preventing heart failure down the line. While this research’s implications for heart disease treatment is clear, this kind of in vivo reprogramming may be also useful in a variety of other diseases where tissue damage is a major cause of symptoms, including Alzheimer’s and Parkinson’s disease.

A normal and reprogrammed heart cell beating eight weeks after a heart attackReference: Qian, L. et al. 2012. In vivo reprogramming of murine cardiac fibroblasts into induced cardiomyocytesNature DOI:10.1038/nature11044

Sexually deprived Drosophila become bar flies

“He caresses every bottle like it’s the first one he’s had, saying it ain’t love, but it ain’t bad.”

– Ani DiFranco

Rejection stinks. It literally hurts. But worse, it has an immediate and negative impact on our brains, producing withdrawal symptoms as if we’re quitting a serious addiction cold turkey. It’s no wonder, then, that we are tempted to turn to drugs to make ourselves feel better. But we’re not the only species that drowns our sorrows when we’re lonely – as a new study in Science reveals, rejected Drosophila do, too. Scientists have found not only will these sexually frustrated flies choose to consume more alcohol than their happily mated peers, sex and alcohol consumption activate the same neurological pathway in their brains.

Drosophila melanogaster males sure know how to woo a lady. When placed in the same container as a potential mate, a male fly will play her a delicate love song by vibrating one wing, caress her rear end, and gently nuzzle her most private of parts with his proboiscis to convince her that he is one heck of a lover. But even the most romantic fly can’t convince an already mated female Drosophila to give up the goods, so scientists were able to use the girls’ steely resolve to see how rejection affects fly drinking behavior.

“Alcohol is one of the most widely used and abused drugs in the world,” explains lead author Galit Shohat-Ophir. “The fruit fly Drosophila melanogaster is an ideal model organism to study how the social environment modulates behavior.” Previous studies have found that Drosophila melanogaster exhibit complex addiction-like behaviors. So in the controlled setting of Ulrike Heberlein’s lab at the University of California San Francisco, researchers paired male fruit flies with three types of females: 1) unmated females, which were willing and happy to mate; 2) mated females, which actively rejected the men; and 3) decapitated females, which didn’t actively reject the guys but, well, weren’t exactly willing partners either. After the flies were satisfied or frustrated, they were offered regular food and food spiked with ethanol, and the researchers measured which type they preferred to see if there was any connection between sex and drinking.

The flies that were rejected drank significantly more than their satisfied peers, but so did the ones paired with incapacitated girls, suggesting that it wasn’t the social aspect of rejection but sexual deprivation that drives male flies to increase their ethanol consumption (see the video at the end!). This alcoholic behavior was very directly related to the guy fly ever getting laid, for even after days of blue balls, if he was allowed to spend some time with a willing woman, he no longer preferred the spiked food.

What the scientists really wanted to understand, though, was why. What drives a frustrated fly to the flask? So to look at the underlying mechanism of this phenomenon, the scientists examined the flies’ brains. A body of scientific literature has connected one particular neurotransmitter, neuropeptide F (NPF), to ethanol-related behaviors in Drosophila, so it was a logical place to start. A very similar neurotransmitter in our brains, called neuropeptide Y (NPY), is linked to alcoholism.

Screen Shot 2012-03-13 at 12.03.14 AM — Increased expression of NPF in mated male brains, as shown through immunochemistry.

The team found that sexual frustration caused an immediate decrease in the expression of NPF, while sex increased expression. Furthermore, when they used genetics to artificially knock down NPF levels in the satisfied flies, they drank as much as their not-so-satisfied friends. Similarly, when the researchers artificially increased NPF levels, flies stayed sober. This is the first time NPF levels have connected sexual activity to drinking. Clearly, NPF levels controlled the flies’ desire to drink, so the team further explored how NPF works in the fly’s brain.

Many animals, including ourselves, possess a neurological reward system which reinforces good behavior. Through this system, we ascribe pleasure or positive feelings to things we do that are necessary for species survival, including sex, eating, and social interaction. Drugs tap into this system, stimulating pleasure which can lead to addiction. Previous studies have shown that flies find intoxication rewarding, so the researchers hypothesized that NPF may play a role in the reward system.

Preference tests showed that artificially increasing NPF levels in the absence of sex or ethanol was rewarding to the flies, confirming the scientists’ hypothesis. This was further supported by the discovery that constantly activating NPF abolished the flies’ tendency to consider ethanol rewarding.

“NPF is a currency of reward” explains Shohat-Ophir. High NPF levels signal good behavior in Drosophila brains, thus reinforcing any activities which led to that state. This is a truly novel discovery, for while NPF and the mammal version, NPY, have been linked to alcohol consumption, no animal model has ever placed NPF/NPY in the reward system.

Understanding the role of NPF in reward-seeking behaviors may lead to better treatments for addicts. “In mammals, including humans, NPY may have a similar role [as NPF],” says Shohat-Ophir. “If so, one could argue that activating the NPY system in the proper brain regions might reverse the detrimental effects of traumatic and stressful experiences, which often lead to drug abuse.” Already, NPY and drugs that affect the function of its receptors are in clinical trials for anxiety, PTSD, mood disorders and obesity. This study suggests that perhaps they should be tested as treatment for alcoholism, too, as well as other reward-based addictions.

Research: Shohat-Ophir, G, KR Kaun & R Azanchi (2012). Sexual Deprivation Increases Ethanol Intake in Drosophila. Science 335: 1351-1355.

Flies turn to drinking after sexual refusal

This sequence of three videos shows a male fly courting and successfully mating with a female fly, another male fly being rejected by a female, and a male choosing to consume an alcohol-infused solution over a non-alcohol solution. Video © Science/AAAS

Images:

Fruit fly from Wikimedia Commons, posted by Thomas Wydra, edited in Photoshop.

Immunochemistry reproduced from Shohat-Ophir, G, KR Kaun & R Azanchi. Science 335: 1351-1355 (2012).

Who said cells aren’t romantic?

Happy Valentine’s Day!

From: Heinz Kutzner (2001). For Valentine’s Day: Epithelial Sheath Neuroma Cancer, 91 (4)

The Benefits of Thanks

Today is Thanksgiving – a day to relax, take a step back, and honestly express gratitude.

Gratitude. By definition, it is the state of being grateful or thankful. It is universally seen as a positive human attribute. You can hear how highly gratitude is thought of over and over again in sayings from all over the world:

A thankful heart is not only the greatest virtue, but the parent of all the other virtues. -Roman saying

The truly rich are those who enjoy what they have. – Yiddish proverb

If you’re not thankful then you’re a wizard. – African Proverb

Perhaps the merits of gratitude have been parised for centuries in so many cultures for good reason. Studies have shown that expressing gratitude is connected to a wide variety of positive outcomes.

Gratitude may help us deal with stress, for example. Over the past decade, evidence has been mounting to show that gratitude mitigates the negative consequences of traumatic events. Studies have found that soldiers who score higher on dispositional gratitude are less likely to develop post-traumatic stress disorder (PTSD). Similarly, another study found an inverse correlation between gratitude and PTSD symptom levels in college women who experienced trauma.

Of course, the benefits of gratitude extend far beyond serious traumatic events. Simply expressing gratitude has positive effects on our daily lives. In one study, Kent State researchers had students write one letter every two weeks with the simple ground rules that it had to be positively expressive, require some insight and reflection, be nontrivial and contain a high level of appreciation or gratitude. After each letter, students completed a survey to gauge their moods, satisfaction with life and feelings of gratitude and happiness – all of which increased after each letter – the more they wrote, the happier they were.

Similar results have been found in a number of other studies. Middle school students that counted their blessings expressed enhanced self-reported gratitude, optimism, life satisfaction, and decreased negative feelings. In adults, the keeping of gratitude journals led to overall happier thoughts. Not only were the journal keepers in a better mood, they also were more likely to to report having helped someone with a personal problem or offered emotional support to another, suggesting that the positive affects of gratitude expand outward.

Given the benefits of expressing thanks, I decided to do so myself. Yesterday, I sat on my couch with a pad of paper and my favorite purple sharpie pen and wrote out all the little things in my life that I am thankful for. It turned out to be quite a long list – about 8 pages long, actually. So rather than bore you with the whole thing, I’ve included a few of my favorite highlights:

I am thankful for all of the people in my life who have made me smile. If you have ever been my friend, then you have surely made me smile a lot, so I am extra grateful for you.
I am thankful for my family, who helped me become the woman I am today.
I am thankful for Bora, for the term ‘BlogFather’ is more fitting than he knows, and for the rest of my eccentric but lovable blogging family.
I am thankful for cheese. Yes, cheese. Cheese, bacon, sushi, curry, pasta and Dippin’ Dots. My six basic food groups.
I’m thankful to the natural world for providing beautiful, intricate and complex puzzles that I, as a scientist, am lucky enough to study.
I am thankful for my liver, for without its championship team of Alcohol Dehydrogenase and Aldehyde Dehydrogenase, I never could have become the marine scientist I am today. (#drunksci)
I am thankful for the people and things that inspire me to do what I love.
I am thankful for my wonderful roommate, who always knows whether a situation requires a bottle of wine, a hug, or a patient ear.
I am thankful to her cat, Yoshi, for finally forgiving me for making him do the cat dance.
I am thankful to the people who remind me that the greatest thing you can do for yourself is to love someone else fully.
I am thankful for little surprises.
And last but not least, thank you, for it is you, my readers, that make blogging worthwhile.

Enjoy your day of thanks, and don’t forget to express to the people you love just how thankful you are to have them. Happy Thanksgiving!

Image c/o holidays.kaboose.com

Mythbusting 101: Sharks will cure cancer

Sharks are incredible animals. They’re some of the world’s most well known creatures, popular enough to get entire weeks of television dedicated to them. They hold a special place in our hearts and minds. Whether you fear them or love them, or a bit of both, they’ve dominated our oceans for hundreds of millions of years, and still manage to evoke powerful emotions from us.

But, as amazing as they are, they are not going to cure cancer.

First off, there will never be a “cure for cancer”. Not now, not in 50 years, no matter how much we know about how cancers form and spread. And no, it won’t be because there is some big conspiracy, where doctors and pharmaceutical companies are keeping some miracle drug from hitting the market.

You see, there can’t be a cure for cancer, because cancer isn’t a single disease. Cancer is a category of diseases, like rock is a category of music. While rock music is characterized by being song-based, usually with a 4/4 beat and a verse-chorus form, cancer is characterized by cell growth gone terribly wrong, allowing a group of cells to grow uncontrollably. You wouldn’t say that Korn and Elvis sound the same, would you? Well not all cancers are the same, either. Some cancers are slow growing, some are fast. Some are always fatal, others go away on their own.

The thing is, there is no universal trait to all cancers that can be attacked with one treatment, except for the fact that they are cells that grow out of control. Thus a universal cure for cancer would have to be something that prevented and reversed cell growth, which will never, ever be safe to take over an extended period of time. You need cells to grow and replicate in your body – just not when and where they shouldn’t be.

The treatment for a given cancer is heavily dependent on where it is and what it’s doing. There may eventually be a million cures – a cure for Acute Lymphoblastic Leukemia, a cure for Basal Cell Carcinoma, a cure for Craniopharyngioma, and so on and so forth from A to Z – but there will never, ever be a cure for cancer.

But I digress.

The notion that sharks may hold they key to curing cancer rests on the idea that sharks don’t get cancer. Out of all they myths in the world, there are few that have been more ecologically damaging and pervasive despite unequivocal scientific evidence to the contrary. This simply untrue statement has led to the slaughter of millions of sharks via the industry for shark cartilage pills, which are sold to desperate cancer patients under the false pretense that they can help reduce or cure their illness.

The myth started way back in the 1970s when Henry Brem and Judah Folkman from the Johns Hopkins School of Medicine first noted that cartilage prevented the growth of new blood vessels into tissues. This creation of a blood supply, called angiogenesis, is one of the key characteristics of malignant tumors, as the rapidly dividing cells need lots of nutrients to continue growing. It’s not shocking, then, that angiogenesis is a common target for those seeking potential cancer therapies.

Brem and Folkman began studying cartilage to search for anti-angiogenic compounds. They reasoned that since all cartilage lacks blood vessels, it must contain some signaling molecules or enzymes that prevent capillaries from forming. They found that inserting cartilage from baby rabbits alongside tumors in experimental animals completely prevented the tumors from growing¹. Further research showed calf cartilage, too, had anti-angiogenic properties². A young researcher by the name of Robert Langer decided to repeat the initial rabbit cartilage experiments, except this time using shark cartilage. Since sharks’ skeletons are entirely composed of cartilage, Langer reasoned that they would be a far more accessible source for potential therapeutics. And indeed, shark cartilage, like calf and rabbit cartilage, inhibited blood vessels from growing toward tumors ³.

Around the same time, a scientist by the name of Carl Luer at Mote Marine Laboratories in Sarasota, FL was looking into sharks and cancer, too. He’d noticed that sharks seem to have relatively low rates of disease, especially cancer, and wanted to test their susceptibility experimentally. So he exposed nurse sharks to high levels of aflatoxin B₁, a known carcinogen, and found no evidence that they developed tumors⁴.

That’s when Dr. I William Lane stepped in. He’d heard about the studies done by Langer and Luer, and become immediately entrenched in the idea that oral shark cartilage could be a treatment for cancer. In 1992 he published the book Sharks Don’t Get Cancer: How Shark Cartilage Could Save Your Life. The book was a best-seller, popular enough to draw in the media from 60 Minutes who did a special on Lane and his new cancer cure. The segment featured Lane and Cuban physicians and patients who had participated in a non-randomized and shoddily done ‘clinical trial’ in Mexico which heralded spectacular results. He then co-authored a second book, Sharks Still Don’t Get Cancer, in 1996.

Of course, Lane started up his own shark fishing and cartilage pill making business called LaneLabs (which still made and sold cartilage pills until recently). But Lane was not alone – many companies began selling shark cartilage pills and powders as alternative therapies or nutritional supplements. The world market for shark cartilage products was estimated to have exceeded $30 million in 1995, prompting more and more harvesting of sharks for their cartilage.

The results have been devastating. North American populations of sharks have decreased by up to 80% in the past decade, as cartilage companies harvest up to 200,000 sharks every month in US waters to create their products. One American-owned shark cartilage plant in Costa Rica is estimated to destroy 2.8 million sharks per year⁵. Sharks are slow growing species, and simply cannot reproduce fast enough to survive such sustained, intense fishing pressure. Unless fishing is dramatically decreased worldwide, a number of species of sharks will go extinct before we even notice.

It’s bad enough that all this ecological devastation is for a pill that doesn’t even work. Shark cartilage does not cure or treat cancer in any way, even in mouse models⁶. These are also the results of at least three randomized, FDA-approved clinical trials – one in 1998⁷, another in 2005⁸, and a final one presented in 2007 (published in 2010)⁹. Ingestion of shark cartilage powders or extracts had absolutely no positive effects on cancers that varied in type and severity. To paraphrase Dr. Andrew Vickers, shark cartilage as a cancer cure isn’t untested or unproven, it’s disproven¹⁰. Indeed, the Federal Trade Commission stepped in by 2000, fining Lane $1 million as well as banning him from claiming that his supplements, or any shark cartilage derivatives, could prevent, treat or cure cancer.

But what’s worse is that this entire fraudulent enterprise that steals the money of those desperate for any kind of hope is based on a myth. No matter what a money-grubbing man with a PhD in Agricultural Biochemistry and Nutrition tries to tell you, sharks do get cancer.

Shark Tumors — L: Kidney Tumor, R: Cartilage Tumor

In 2004, Dr Gary Ostrander and his colleagues from the University of Hawaii published a survey of the Registry for Tumors in Lower Animals¹¹. Already in collection, they found 42 tumors in Chondrichthyes species (the class of cartilaginous fish that includes sharks, skates and rays). These included at least 12 malignant tumors and tumors throughout the body. Two sharks had multiple tumors, suggesting they were genetically susceptible or exposed to extremely high levels of carcinogens. There were even tumors found in shark cartilage! Ostrander hoped that this information would finally put to rest the myth that sharks are somehow magically cancer-free.

But it hasn’t. I still see all kinds of shark cartilage pills for sale at the local GNC. But furthermore, the myth that sharks are cancer-free is still believed by many intelligent people. I read a tweet from The National Aquarium a while ago that said “It must be something in the water. Sharks are the only known species to never suffer from cancer.” The National Aquarium has over 9,000 twitter followers, and this inaccurate tweet was passed on by a number of them, including The Smithsonian Marine Station in Fort Pierce, FL. How can such a large non-profit, dedicated to “extending the knowledge and resources gained through daily operations toward the betterment of the natural environment” perpetuate such an erroneous and ecologically damaging myth?

Then there’s the BBC, whose division called BBC Earth decided to run a “trick or treat” campaign for Halloween last year featuring truths or falsehoods about different animals. Among them?

When I called them out on their egregious error, they didn’t even admit they were wrong. Instead they simply said that “the science behind their immune systems is still an area of fascination which we know little about, and thankfully people are still studying.”

Maybe I haven’t been clear. Maybe we don’t know everything about shark immune systems, but there is one thing that we do know with 100% certainty.

SHARKS DO GET CANCER.

We can’t even really say they get cancer less often than other species. It’s true that the number of sharks that we have observed with cancer is low. However, only a couple studies have even attempted to look at disease rates in shark species. Furthermore, these studies are hampered by the fact that sharks tend to be wide-ranging, open ocean fish. They live in some of the least contaminated areas on earth. This means that, odds are, they have low levels of exposure to the chemicals that cause cancer in so many land and near-shore species. Furthermore, the odds that a really sick shark would make it into a researcher’s hands to study are slim. A shark whose function is compromised by tumors would likely end up the meal of other, hungry sharks long before they’d end up on a hook cast by scientists. So even the idea that sharks have low rates of cancer or disease is hard to scientifically support.

Perhaps the most disappointing part is that the shark immune system is incredibly fascinating and worth study whether or not it can squash out cancer. Sharks are the earliest evolutionary lineage to have developed an adaptive immune system complete with immunoglobin, T-cell receptors, MHCs and RAG proteins¹², and they do it without bone marrow, the source of almost all of our immune system cells. Instead, they have two completely unique immune organs, the Leydig’s and Epigonal organs, that are barely understood. Studying the shark immune system is essential to understanding the evolution of adaptive immunity that is present in all higher vertebrates. And if, indeed, they are resistant to cancer, then that makes the study of their immune system all that much more important.

Sharks at fish market in Japan, by Alex Hofford — Carcasses of sharks fished for their fins

Instead, we mindlessly kill millions of them a year to make Asian delicacies and ineffective cancer treatments, and we perpetuate the myth that sharks don’t get cancer. Be assured that whenever I see someone say that sharks don’t get cancer, I will call them out, especially if they should know better. It’s time that this myth is busted once and for all.

Images: A 5′ tiger shark at Coconut Island, photo © Christie Wilcox; LaneLabs Shark Cartilage Powder; Tumor examples from Ostrander et al. 2004. Left: a shark kidney tumor, right: a tumor in shark cartilage; Sharks at a factory finning plant in Japan, photo © Alex Hofford

References

Brem H, & Folkman J. (1975). Inhibition of tumor angiogenesis mediated by cartilage. J Exp Med (141), 427-439 DOI: 10.1084/jem.141.2.427

Langer R, & et al (1976). Isolations of a cartilage factor that inhibits tumor neovascularization. Science (193), 70-72 DOI: 10.1126/science.935859

Lee A, & Langer R. (1983). Shark cartilage contains inhibitors of tumor angiogenesis. Science (221), 1185-1187 DOI: 10.1126/science.6193581

Luer CA, & Luer WH (1982). Acute and chronic exposure of nurse sharks to aflatoxin B1 Federal Proceedings, 41

Camhi M. Costa Rica’s Shark Fishery and Cartilage Industry. http://www.flmnh.ufl.edu/fish/Organizations/SSG/sharknews/sn8/shark8news9.htm (1996).

Horsman MR, Alsner J, & Overgaard J (1998). The effect of shark cartilage extracts on the growth and metastatic spread of the SCCVII carcinoma. Acta oncologica (Stockholm, Sweden), 37 (5), 441-5 PMID: 9831372

Miller DR, Anderson GT, Stark JJ, Granick JL, & Richardson D (1998). Phase I/II trial of the safety and efficacy of shark cartilage in the treatment of advanced cancer. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 16 (11), 3649-55 PMID: 9817287

Loprinzi CL, Levitt R, Barton DL, Sloan JA, Atherton PJ, Smith DJ, Dakhil SR, Moore DF Jr, Krook JE, Rowland KM Jr, Mazurczak MA, Berg AR, Kim GP, & North Central Cancer Treatment Group (2005). Evaluation of shark cartilage in patients with advanced cancer: a North Central Cancer Treatment Group trial. Cancer, 104 (1), 176-82 PMID: 15912493

Lu C, Lee JJ, Komaki R, Herbst RS, Feng L, Evans WK, Choy H, Desjardins P, Esparaz BT, Truong MT, Saxman S, Kelaghan J, Bleyer A, & Fisch MJ (2010). Chemoradiotherapy with or without AE-941 in stage III non-small cell lung cancer: a randomized phase III trial. Journal of the National Cancer Institute, 102 (12), 859-65 PMID: 20505152

Vickers, A (2004). Alternative cancer cures: “unproven” or “disproven”? CA: A Cancer Journal For Clinicians, 54, 110-118 DOI: 10.3322/canjclin.54.2.110

Ostrander GK, Cheng KC, Wolf JC, & Wolfe MJ (2004). Shark cartilage, cancer and the growing threat of pseudoscience. Cancer research, 64 (23), 8485-91 PMID: 15574750

Flajnik MF, & Rumfelt LL (2000). The immune system of cartilaginous fish. Curr Top Microbiol Immunol (249), 249-270

In the immortal words of Tom Petty: “I won’t back down”

In the responses to my article on organic myths, I have been called an industrial shill, liar, and an organic hater. People have questioned my motives, saying I am a bioengineer or paid by Monsanto^*. They have called for my head, or at the very least, the retraction of my article.

In most of them, my arguments were inflated, twisted, or flat-out re-written. I don’t think GMOs “are the only way to feed the world.” I don’t think organics are “trying to take over.” So, screw the myths. This time around, I’m just going to focus on the facts.

Fact #1: Organic farming uses pesticides – and yes, organic pesticides are bad for you, too.

My main point in the first myth I brought up was simply to say that organic farms do use pesticides, contrary to what many people think. Since none of the people attacking my article can disagree with this fact (since it’s 100% true), they have instead warped my argument, saying I claim that organic farms are “seething hotbeds of toxic pesticide use” or that I believe all “naturally occurring pesticides pose the same risk as same as [sic] synthetic ones” when “the truth is, they’re [sic] don’t.”

I didn’t say either of those things. I did say that you can’t automatically assume a natural pesticide is safer, which was my point with rotenone. But Jason Mark claims it’s unfair to use rotenone as an example as it’s now banned in the US ~~– fair enough~~ (turns out the National Organic Program re-approved it in 2010 despite mounting evidence of its links to Parkinson’s. So my point stands). He then goes on to say that he chooses organic because he wants “to eat food that I know doesn’t involve the use of chemicals that harm ecosystems and have been linked to human health impacts.” Similarly, a response to my post on the Rodale Institute’s website says that the consumer can confidently state that they “buy organics because they don’t use the kinds of pesticides that create public and environmental health hazards, harm pollinators and other indicator species, make farmers and farmworkers sick, and/or persist for years in the environment accumulating up the food chain.”

Oh, really?

Let’s look at the details, shall we? The claim is that organic pesticides and fungicides are better to use because they’re less dangerous for us – and though he accuses me of ‘cherry-picking’, Jason only briefly talks about the health side effects of copper sulfate and conveniently doesn’t talk about the dangers of the most widely used organic fungicide: pyrethrum, though he delves deeply into the dangers of synthetics.

So let’s pit the most used organics against the most used conventional ones for a moment. In the USA, the top synthetic pesticide used is chlorpyrifos while the top fungicide is chlorothalonil. Yes, they are nasty chemicals, which in high doses are known to cause some serious health effects. But what about the organic alternatives? One way to compare is to look at their acute toxicity, often represented by an LD50 value. LD50, “lethal dose for 50%,” represents the dose at which 50% of a population will die from exposure.

In rats, the LD50 for copper sulfate is 30 milligrams per kilogram of body weight – which is a lot¹. But copper sulfate has also been shown to have chronic effects at lower doses of exposure. In animals, chronic exposure has led to anemia, stunted growth, and degenerative diseases^1,2,3. Furthermore, copper sulfate has been shown to disrupt reproduction and development, including inhibition of sperm development, loss of fertility, and lasting effects from in-utero exposure^3,4. Copper sulfate is also mutagenic and carcinogenic⁴. And because copper is a trace element, it is strongly bioaccumulated, meaning consistent low doses can lead to toxic levels^3,5. In people, increased exposure has been linked to liver disease and anemia^3,6.

What about chlorpyrifos? The LD50 is 95 to 270 mg/kg – 2.5 to 10 times less toxic than copper sulfate¹. As for its chronic effects, dogs fed chlorpyrifos at high doses daily did show increased liver weight and cholinesterase inhibition, meaning potential for neurological toxicity. But the effects went away immediately when feeding was stopped, and no long-term health effects were seen in either the dog or a similar rat study^7,8. Furthermore, no evidence of mutagenicity was found in any of four tests reviewed by EPA⁹. It’s also not considered carcinogenic – rats and mice fed high doses for two years showed no increases in tumor growth⁹.

As with copper sulfate, those who work with pesticides for a living have experienced acute toxic exposure to chlorpyrifos. Studies have also linked fetal and chronic exposure to neurological complications and cancer risk, but these studies are hard to interpret, as they rely on a biomarker which may overestimate exposure by 10 to 20 fold¹⁰. Unlike copper sulfate, chlorpyrifos does not build up or persist in body tissues, and thus is not considered have significant bioaccumulation potential¹¹. In humans, chlorpyrifos and its principal metabolites are eliminated rapidly following a single dose, within a day or so¹².

What about those fungicides? The LD50 for pyrethrum in rats ranges from 200 mg/kg to around 2,000 mg/kg. Those that get a lethal dose suffer from tremors, convulsions, paralysis and respiratory failure before they finally die¹. The LD50 for chlorothalonil? Well, it’s more than 10,000 mg/kg. That was the highest dose tested, but the rats still didn’t reach the 50% death rate target¹. Rats fed a range of doses of chlorothalonil by the EPA over time showed no effects on physical appearance, behavior, or survival¹³. Yes, in some other high-dose feeding studies, chlorothalonil showed the potential to act as a mutagen or carcinogen¹⁴. But so has pyrethrum, with exposure leading to increases in tumors in the lungs, skin, liver, and thyroid of mice and rats¹⁵.

Ecologically, pyrethrum is extremely toxic to aquatic life and slightly toxic to bird species¹⁶. Chlorothalonil is toxic to fish as well, but it is non-toxic to birds¹⁷. Perhaps the kicker is that pyrethrum has been shown to be highly toxic to bees and wasps, which are keystone species necessary for the pollination of crops and other plants¹⁸. Chlorothalonil, on the other hand, isn’t.

Tell me, do you feel like the organic alternatives are totally safe? Sorry, but organic pesticides do make farmers sick. They do bioaccumulate. They do harm non-target species.

Oh, and I forgot to mention: organic alternatives are applied in higher concentrations and more frequently because they’re less effective at controlling the species they’re meant to kill.

While it’s true that some organic farms may not use any pesticides, those organic foodstuffs in your supermarket are almost guaranteed to have used them, and liberally. As Tom Laskawy notes, “copper and sulfur in particular are often overused, especially among fruit growers.” As with conventional fruits and vegetables, most of what you’re getting at the supermarket is factory farmed. And as Michael Pollan and Samuel Fromartz, among others, have pointed out: factory farming is factory farming, even if it’s organic.

My point is, a pesticide is a pesticide. If it kills things, it does so for a reason, and you probably don’t want to go around eating it. Do I want to chow down on food coated with chlorpyrifos and chlorothalonil? Well, no, of course not. That’s why we screen for synthetic pesticide residues. However, we don’t screen for organic pesticide residues. Given what you just read, wouldn’t you want to know how much of those chemicals are ending up on your plate?

Of course, to be fair, the other most widely used organic pesticide is Bt toxin – which is, by just about any tests so far, non-toxic to people. That’s exactly why it was chosen for use in GMOs: because you can eat it all you want and it has no ill effects. But I’ll get into that more later.

Fact #2: Science has yet to support claims that organic foods are healthier.

In my second myth, I said that “science simply cannot find any evidence that organic foods are in any way healthier than non-organic ones – and scientists have been comparing the two for over 50 years.” I was attacked for this statement, with citations of studies that show increased nutritional quality in organic strawberries, tomatoes and milk. It’s true – you can find single, unrepeated studies which have found some nutritional improvements. But that’s not how science works. When scientists weigh in on a topic, they can’t just rely on single studies that support their view. Instead, they have to consider all the studies on a topic, and examine the results of each. That is exactly what a meta-analysis does.

I actually cited not one but two separate papers which summarize the studies to date on nutritional quality, one of which was a meta-analysis^19,20. In both, the results were clear: any nutritional benefits are slim, variable, and not universal. In other words, overall, the science hasn’t supported any claims of unilateral nutritional benefits.

If you really want a more in depth look, check out Erin Prosser’s detailed explanation of the research. She concludes that the science is mixed at best, and even if organic foods are nutritionally superior, “it won’t be by much, meaning it may make no substantial difference in terms of your health.”

Fact #3…

Ok, my third myth got attacked on two fronts that are so separate, I feel the need to address them independently. So, instead of Fact #3, I have 3a and 3b.

Fact #3a: Certified organic farms don’t have yields that equal conventional ones.

Organic farming – and by organic farming, I mean farming that is officially organic through some certification process – has lower yields than conventional. At least, that’s what a 21-year study published by Science in 2002 found – that organic farming methods produced 80% what conventional farming methods did²¹. A 2008 review of the literature found organic yields were 50 – 75% of those of conventional farms²². An even more recent meta-analysis puts the value at 82%²³. In fact, only one study to date has said that organic methods get average yields higher than that.

This is the paper by Badgley and colleagues which many claim shows organic farms produce just as well as conventional ones²⁴. But that’s not what the paper says. The paper models whether or not organic farming can feed the world based on different yield percentages. The lowest yield they test for organic farming: 91%.

Where did the 91% figure come from? The authors averaged the yields from 293 studies they found looking at organic production. But the paper flat-out states that it considers a wide variety of agricultural systems in this analysis. The authors explicitly state that by organic, they are not “referring to any particular certi?cation criteria” and that they “include non-certi?ed organic examples.” They don’t just include a few – of their 293 ‘organic’ comparisons, 100 are not certified organic, including ones which likely used synthetic pesticides and GMOs²⁵. The paper’s methods, math and modeling have been critiqued strongly by two separate sources ^25,26.

Even still, I never, and still don’t, make any claim that sustainable agriculture can’t have the same yields as conventional farming. It definitely can. But you have to broaden the definition of “sustainable”, as Badgley et al. did, to include non-organic methods.

For example, a recent study found that alternative management strategies outperformed both conventional and organic methods. These strategies, like no-till methods, demonstrated greater production efficiencies than either conventional or organic, and even had greater average yields²⁷.

Do yields matter? Yes, they do. While we can argue left and right about whether hunger and famine now are a matter of production or politics, when the planet reaches 9 billion people or so in 2050, production will matter. That’s not to say that lower-yielding methods can’t be used in areas of abundance, or where people can afford it. But to feed nine billion mouths, we are going to have to be careful and efficient in our use of land if we are to produce enough food without destroying what little habitat is left for the world’s other species.

Fact #3b: GMOs aren’t evil, and yes, they might even do some good for the world.

By far the most passionate responses to my post centered around the issue of GMOs. I would argue that the rumors about my stance on GMOs have been greatly exaggerated. After all, I never claimed that “organic agriculture can be redeemed if only its definition can be broadened to include GMOs,” or that “genetic modification is all benefit and no risk.”

Do I think GMOs have the potential to up crop yields, increase nutritional value, and generally improve farming practices while reducing synthetic chemical use? Yes, yes I do. I’m not alone on this – the science supports me.

GM crops have been in fields and on the market for decades now, and studies are starting to weigh in on their benefits. A recent review of results of farmer surveys found that of 168 comparisons between GM adopters and non-adopters, 124 show positive results for the GM adopters, 32 indicate no difference and only 13 show negative yields – and that these increases were highest in developing countries²⁸.

Most of the yield increases have come from the use of Bt crops. I specifically called out organic proponents on the hypocrisy of using Bt toxin liberally but not being willing to consider a GM Bt variety. As Jason Mark says, this means I claim that “there’s no distinction between spraying Bt and placing it directly into the plant” – but that’s not true at all. Of course there’s a difference. The GMO is the better solution. Studies have shown that spraying insecticides have a much stronger, negative effect on biodiversity than the use of transgenic crops²⁹, which is particularly important when you consider that Bt crops have reduced pesticide use by 30% or more³⁰. Furthermore, the pesticide use reduction wasn’t just in GM Bt fields – planting Bt varieties benefited non-GM growers, allowing them to reduce pesticide use and produce more crops³¹.

Bt crops not only increase yields and decrease pesticide use – they increase biodiversity. Three separate meta-analyses have confirmed that Bt crops benefit non-target species including bees and other insects^29,32,33.

Have GM crops failed their debut? No, they haven’t. “There is now considerable evidence that transgenic crops are delivering significant economic benefits,” writes Clive James in a review of transgenic crops published in Current Science. His final sentence unequivocally states that “improved crop varieties are, and will continue to be the most cost effective, environmentally safe and sustainable way to ensure global food security in the future.” A 2010 review study found that “results from 12 countries indicate, with few exceptions, that GM crops have benefited farmers.” Similarly, a review examining 155 peer-reviewed articles determined that “by increasing yields, decreasing insecticide use, increasing the use of more environmentally friendly herbicides and facilitating the adoption of conservation tillage, GM crops have already contributed to increasing agricultural sustainability.”

That’s not to say all GM crops are stunning examples of the potential benefits of GMOs. Herbicide resistant crops are perfect examples of how GM technology can be used poorly. I don’t like Roundup Ready corn any more than my critics. How anyone could have thought that making a crop resistant to an herbicide (thus ensuring that we use MORE of this herbicide) was a good idea is beyond me. But I’ve been told not to judge organic pesticides by rotenone, so how is it fair to judge the future potential of all genetic engineering by Roundup Ready crops?

While Tom Laskawy says that in listing the potential benefits of GMOs, I have transgressed from “science to science fiction” and that most of the GM varieties I mentioned “don’t even exist in the lab”, every one of them is being or has been produced (hence the links) – including virus-resistant sweet potatoes, high-calcium carrots, high-antioxidant tomatoes, vaccine-producing fruits and vegetables, and allergen-free foods. He’s right that they don’t exist commercially, but how can they when all GMOs are universally demonized?

The real problem is that although GMO technology can be used to produce large social and ecological benefits, most GM crops developed to date have been designed to benefit Big Ag. This trend will only continue if the public keeps its negative attitude towards GMOs. I don’t like Monsanto any more than you do – so why let them control how GM technology is used? If there was more public pressure and desire for socially and ecologically beneficial GMOs, more scientists could get involved and use the technology better.

That’s what happened when the Rockefeller Foundation funded researchers at the Swiss Federal Institute of Technology’s Institute for Plant Sciences. The result was Golden Rice – a vitamin-A rich variety that the foundation had hoped to freely give to third world countries to help fight malnutrition³⁴. The Swiss were working on a iron-rich variety, too, until widespread protesting of GMOs in Europe pressured the foundation into not renewing the institute’s funding.

Do I think all GMOs are perfect? Of course not. But should they be considered among the many different farming practices which may contribute to better farming in the future? Absolutely.

Fact #4: Farming practices of all types should be considered and weighed for their merits independent of labels.

The dichotomy between organic and conventional is misleading at best, and dangerous at worst. There is so much variation in each category that they are almost meaningless, except when it comes to our wallets.

I’m not pro factory farming. Nor am I pro organic. As Benton et al. write in their review of conventional, organic and alternative farming methods:

“rather than creating a misleading contrast by dividing farming systems into either organic/extensive and conventional/intensive there needs to be greater recognition that future farming has the potential to maintain yield whilst becoming “greener” by further optimizing inputs and practices to reduce environmental impacts”

Andy Revkin said it far better than me in his recent commentary on the destruction of GM wheat in Australia:

“It’s clear to me that genetics, intensified agriculture, organic farming, crop mixing, improved farmer training, precision fertilization and watering, improved food preservation and eating less wastefully and thoughtlessly will all play a role in coming decades — each in its place”

The central point of my mythbusting article, and of this one, is that the future of agriculture needs to examine all potential methods and determine if they are right for a given area. Landscapes are different – growing crops in Africa isn’t the same as growing crops in the Midwest, and if we universally apply the same methods globally, we are destined to fail both in terms of efficiency and sustainability. It is only through the breakdown of this arbitrary and variable distinction between methodologies and integration of a variety of practices that we will achieve our ultimate goal of a bright future both agriculturally and ecologically.

Links to the critiques of my first article:

Tom Laskawy, Grist: In Defense of Organic
Tom Philpott, Mother Jones: 3 Ways Scientific American Got The Organic Ag Story Wrong
Heather Pilatic, Pesticide Action Network, on Rodale.Com: Why The Organic Haters Are Dead Wrong
Jason Mark, Earth Island Journal, on Scientific American’s Guest Blog: Myths: Busted – Clearing Up the Misunderstandings about Organic Farming

*As for the attacks of my career and character, I can say without any hesitation that exactly 0% of my PhD funding comes from any kind of agribusiness. I study the population genetics and evolution of lionfish – you know, those frilly fish that are horribly invasive in the Atlantic. So no, Monsanto and bioengineering companies aren’t interested in what I do. If anyone really wants to know, my research funding and interests are freely disclosed and readily available on my website. And if anyone would like to contribute to said funding (bioengineering company or otherwise), there’s a nice contact form that you can use to get in touch with me. It’s a rough time to be studying science – I’ll take whatever funding I can get!

NOTE: I accidentally switched the uses of Copper Sulfate (actually an organic fungicide) with Pyrethrum (actually an organic insecticide). Oops! The points still stand, though – if you look at the information I provided, the organics are much more acutely and chronically toxic.

References:

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New York State Department of Health. 1984. Chemical fact sheet: Copper sulfate. Bureau of Toxic Substances Management. Albany, NY.

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