11 Oct

A report from the 8th Congress on Polyphenols & Health

 

I recently had the opportunity to attend the 8th International Congress on Polyphenols and Health in Quebec City, Canada.  This year more than 300 researchers met here to share their work on the health benefits of polyphenols in the fruits, vegetables, and beverages we eat.  Some were interested in improving cognitive processes – memory, learning, balance, and focus – while others sought to prevent or treat cardiovascular disease, diabetes, or obesity.  All had an appreciation that our diets are powerful influences on our overall health.  There was particular interest in the polyphenols in the so-called “superfoods”: blueberries, cranberries, pomegranates, grapes and wine, turmeric, coffee, and dark chocolate.

Here are a few key observations:

First, as was the case at the 2017 Dynamic Brain conference in Los Angeles, the microbiome is big news indeed.  In Quebec City, keynote speakers emphasized that gut microbes can determine the health benefits of foods.  In these cases, they transform the polyphenols you eat into slightly different compounds – many of them more powerful than those in the food itself.  The bad news is that many neglected gut communities don’t do their jobs very well.  Instead, guts that are ‘out of tune’ have leaky linings that let bad bacteria, in whole or in pieces, into the body where they trigger inflammation.  This was a clear message heard in Los Angeles too.  At the ICPH2017 conference, researchers are treating these complex gut communities like ecosystems.  They are using high-level mathematical models to understand how thousands of different bacterial species come together to form a healthy (or unhealthy) environment.  They are also trying to figure out how these microbes transform the thousands of molecules in our food into thousands of other molecules in our intestines and our colon – a complex and very messy proposition!

Second, let’s all just all agree to eat some berries every day.  Blueberries.  Cranberries.  Blackcurrant berries.  Grapes.  Study after study showed modest improvements in insulin sensitivity, endothelial function, inflammation, memory, executive decision-making, focus, and mood.  A cup or two a day of polyphenol-rich berries show benefits for children, teenagers, adults, and the elderly.  After six months.  Three months.  Sometimes after only 8 hours!  In addition, some studies seem to show that the benefit is greatest in those with the greatest needs, i.e. those with the worst health problems.  Berries are, by themselves, no cure.  But, as best I can surmise from dozens of individual studies, one could expect ~10% improvements in many measures of healthy and performance.  Surely, this is an oversimplification – the details certainly matter – but let’s all worry about the details after a nice cup of blueberries.

It is surprising to realize that, for the most part, researchers don’t really know how dietary polyphenols work to improve our health.  Why are they healthy?  Well, in Quebec City investigators highlighted changes in sugar metabolism, inflammation, blood flow, and a whole range of cellular “switches” that control large numbers of our genes.  These could all be important clues to how polyphenols work.  After all, it is possible that each polyphenol works differently, at different sites inside cells.  But it is also possible that they all pretty much work the same way, at a few yet-to-be discovered intersections of metabolism, where they can have broad impacts on our cellular traffic patterns.  The jury is out, at least until the 9th International Congress on Polyphenols and Health in 2019.

Lastly, it is worth noting the polyphenol content of our foods is not static.  Many of our modern agricultural practices and many aspects of our changing climate tend to decrease the levels of beneficial polyphenols in food.  So while our appreciation of dietary polyphenols is increasing, their concentrations in our foods – and their potential health benefits –  could be decreasing.

28 Jul

Twenty-first century climate change and SAV in the Chesapeake Bay

What does the future hold for the Chesapeake Bay?  We attempted to address part of this question in our new article.

Introduction: The Chesapeake Bay was once renowned for expansive meadows of submerged aquatic vegetation (SAV). However, only 10% of the original meadows survive.  Future restoration efforts will be complicated by accelerating climate change, including physiological stressors such as a predicted mean temperature increase of 2–6°C and a 50–160% increase in CO2 concentrations.

Outcomes: As the Chesapeake Bay begins to exhibit characteristics of a subtropical estuary, summer heat waves will become more frequent and severe. Warming alone would eventually eliminate eelgrass (Zostera marina) from the region. It will favor native heat-tolerant species such as widgeon grass (Ruppia maritima) while facilitating colonization by non-native seagrasses (e.g., Halodule spp.). Intensifying human activity will also fuel coastal zone acidification and the resulting high CO2/low pH conditions may benefit SAV via a “CO2 fertilization effect.”

Discussion: Acidification is known to offset the effects of thermal stress and may have similar effects in estuaries, assuming water clarity is sufficient to support CO2-stimulated photosynthesis and plants are not overgrown by epiphytes. However, coastal zone acidification is variable, driven mostly by local biological processes that may or may not always counterbalance the effects of regional warming. This precarious equipoise between two forces – thermal stress and acidification – will be critically important because it may ultimately determine the fate of cool-water plants such as Zostera marina in the Chesapeake Bay.

Conclusion: The combined impacts of warming, coastal zone acidification, water clarity, and overgrowth of competing algae will determine the fate of SAV communities in rapidly changing temperate estuaries.

 

13 Jun

New Approaches to Fighting Alzheimer’s

The following article was inspired by the Institute for Function Medicine’s 2017 Annual Conference “The Dynamic Brain”.  The aim is to help family, friends, and caregivers of those with cognitive decline – who are just starting out – to understand the process and to provide links to useful resources for treatment and prevention. 

Fighting Alzheimer’s with the kitchen sink

Thomas M. Arnold, Department of Biology, Dickinson College, Carlisle, PA 17007

June 12, 2017
If you are in the fight against Alzheimer’s disease – as a caregiver, health care professional, or one of the 45 million Americans who will develop the disease in their lifetimes – here’s something you must know: your brain is not a computer.  Unlike your mobile device or laptop, it won’t become obsolete.  Healthy brains upgrade themselves continuously.  They adapt, grow, learn, and repair themselves.  This process, is called “neuroplasticity” and it may be our best hope for treating neurodegenerative disorders.

Some hope is sorely needed.  An estimated 15% of U.S. citizens will develop Alzheimer’s, which is set to become our nation’s third leading cause of death.  The staggering cost of Alzheimer’s care is already straining our healthcare systems.  It is estimated that by 2050, when more than 13 million Americans will be affected, the price of Alzheimer’s disease will bankrupt the Medicare system.  One by one, promising new therapies have failed to cure or slow the disease.  As a result, those with cognitive decline hesitate to seek medical help, knowing that their physician is unlikely to offer up any effective treatment. Clearly, we need new approaches.

These new approaches were the topic of the 2017 Dynamic Brain conference in Los Angeles, hosted by the Institute for Functional Medicine.  Here experts described surprising successes in treating Alzheimer’s disease by taking a more holistic, multifaceted approach.  Some of these researchers had become so frustrated by the lack of progress on a miracle pill they opted to try, well, everything.  All at once.  They combined the best of traditional medicine, nutritional science, exercise science, and brain training into comprehensive programs.  One such program, termed reCODE, was created and tested by Dr. Dale Bredesen, a researcher at the Buck Institute for Aging and UCLA.  The results were promising.  In small studies most patients on the program stopped getting worse, then got better and, amazingly, returned to work.  Elsewhere, other researchers were trying other “everything and the kitchen sink” programs.  Their goal: get the brain healthy, however you can, so that they can repair themselves through the power of neuroplasticity.

It helps, of course, that we know more about the brain than ever before.  We know that a healthy brain is fast and flexible, and can mend itself.  We also know that when infected, injured, or denied necessary hormones and growth factors the brain assumes a protective stance: neuroplasticity ceases and the brain deploys defensive countermeasures.

Normally, the brain is protected by the blood-brain barrier but sometimes, when this lining is unhealthy, the brain is more easily breached by pathogens and toxins.  Then neurons must defend themselves.  As it turns out, they have a clever security system.  Each neuron is coated with surface proteins that, when cut into fragments and released, surround and trap pathogens in the brain.  This molecular sticky trap is part of the innate immune response that is required for our survival.

One of these sticky surface protein fragments is amyloid beta – the molecule that forms the plaques and tangles that are the hallmark of Alzheimer’s disease.  These masses may accumulate slowly in the brain as we age or they may form with surprising quickness in response to pathogen attack.  Inside the plaques and tangles researchers find the proof – invading viruses and microbes safely entombed in amyloid.  Luckily, at least some of these plaques and tangles are cleared away in healthy brains.

However, some things interfere with this self-cleaning.  Genetics are important.  Some of us have brains that are just less enthusiastic housekeepers, and more vulnerable to cognitive decline.  But even brains that are normally squeaky-clean can become overrun by amyloid when they are infected, stressed, or exposed to environmental toxins.  So the root cause of Alzheimer’s disease is usually some combination of insults to the brain – anything that causes amyloid beta peptides to pile up.

Unfortunately, there is more trouble ahead for brains accumulating plaques and tangles: a state of persistent inflammation.  This part of the brain’s defense system is controlled primarily by a gene switch called CD33.  Activation of this gene is associated with higher amyloid beta loads and a worsening of cognitive decline.  In addition, CD33 activates brain inflammation and gets the attention of migrating cells called microglia.  These cells normally nurture and care for neurons, but when reprogrammed by CD33 they go rogue, attacking the brain’s neurons and consuming them.  Amazingly, it is possible to observe this in real time thanks to Dr. Rudy Tanzi, Professor of Neurology at Harvard University and Director of the Genetics and Aging Research Unit at Massachusetts General Hospital.  His team cultures neurons in a dish so that they form simple networks, exposes them to “angry” microglial cells, , and watches one type of brain cell consume the other!  Over time this state of affairs causes the brain to become slower, noisier, and disorganized.  Regions of the brain, especially the hippocampus, shrink.  And decades later, after the brain can no longer find ways to compensate, the cognitive symptoms of Alzheimer’s emerge.

What is it then, exactly, that puts us on this road to Alzheimer’s?  Age is the obvious risk factor.  Family history plays a role, especially the inheritance of genetic risk factors, such as the APOE4 gene.  This version of the APOE gene significantly increases the risk of Alzheimer’s by raising background levels of inflammation and slowing the clearance of amyloid beta[1].  Gender matters for Alzheimer’s too.  For reasons not completely understood, women are more likely to suffer from the disease (and to suffer indirectly as caregivers).  The other known and suspected causes of Alzheimer’s are at least partly within our control: exposure to viruses, bacteria, and other pathogens; our pre-packaged fast-food diets; excess sugars and diabetes; obesity and a sedentary lifestyle; head injury, stress, and emotional trauma; air pollution; heavy metal pollution; toxins from mold; pesticides and herbicides; and industrial chemicals and solvents.  All can cause inflammation in the brain and trigger the innate immune response.  Lucky for us, it usually takes a combination of these factors, over time, to start us down the road to Alzheimer’s.

With so many possible triggers working in combination you might expect that not every case of Alzheimer’s is exactly the same.  Indeed, Bredesen suggests that there are some identifiable types.  Some arise mostly from infection, others from deficiencies in hormones, vitamins, and growth factors.  Alzheimer’s associated with diabetes is a bit different.  And cognitive decline caused by exposure to metals or toxic mold prevents special challenges.  All result in inflammation and the build-up of plaques and tangles in the brain, but each requires a slightly different treatment program.

As a result, the reCODE programs are personalized for each patient.  A battery of tests pinpoint the potential problems, which are then addressed one-by-one to promote brain health.  Inflammation is reduced, toxins are eliminated, and sugar levels are normalized.  Levels of nutrients, hormones, and other factors are optimized.  Patients are urged to get eight or more hours of sleep, fast overnight for at least twelve hours, reduce stress, and do some online brain training.  (If you don’t have a device suitable for brain training, you might try Scrabble or the 1980’s-era game Simon. You get the idea.)  And patients should be ready to move.  One of the program’s key goals is to get your brain to produce lots of brain-derived neurotropic growth factor (BDNF), which promotes brain growth and maintenance, including the clearing of amyloid beta.  As it turns out, exercise is the best way to increase BDNF levels.  And the higher the calorie burn, the better the result.  Another way to increase brain BDNF, is to consume green coffee fruit.  Yes, there was a fruit around that wonderful bean – and something in it seems to raise BDNF quite dramatically.  To limit inflammation and stimulate neuroplasticity, patients on these programs take fish oils, curcumin, and vitamins and they consume certain mushrooms.  Most of these aren’t too exotic and are available on the shelves of your local health store, but don’t go try this yourself without good medical advice.  You want to be safe!  Besides, the brands, dosages, and schedules matter, and may depend upon your initial test results.

For those starting out, two aspects of these “kitchen sink” programs deserve special mention.

First, for optimal brain health one must adopt a low-carb, anti-inflammatory diet.  Patients shun processed foods, reduce or eliminate grains and dairy, and limit excess sugar.  Most experts agree it is also important to avoid artificial sweeteners; so say farewell to diet sodas.  Those following the programs nom on fresh organic vegetables and leafy greens, pigments foods rich in polyphenols, and healthy organic meats.  Dr. David Perlmutter, a strong advocate for adopting a healthy diet to fight Alzheimer’s, has published a series of best-selling books on this subject.  Perlmutter is a neurologist and Fellow of the American College of Nutrition.  His books are worth a read, and here’s why.  Your digestive system is alive, teaming with cultures of gut bacteria.  And you really want to keep them happy.  As Permutter advises “You are eating for three trillion” gut bacteria and they have a real impact on your brain.

The story of the gut-brain axis goes something like this.  Your gut microbiome is an ecosystem with a community of helpful and not-so-helpful bacteria.  Yours is unique and has been shaped since birth by where you live and what you eat.  (You also a similar microbial ecosystem in your mouth.  Good oral hygiene helps them, and you, stay healthy.)

Hopefully, you’ve cultivated a healthy gut microbiome through diet and exercise.  Cardiovascular fitness improves the diversity and health of your microbiome about as much as a healthy diet.  If you haven’t, the ecosystem may malfunction, damaging the lining of the gut, allowing bacteria and their products to leak into the blood.  Eventually, they reach the brain and, once again, the brain must defend itself – with inflammation of the accumulation of plaques and tangles.  This explains why studies show a link between the health of the gut microbiome and the size of specific regions of the brain.  There are other ways the gut can impact the brain.  The two organs are connected by a large nerve bundle, and the fibers innervate the entire digestive system.  In fact, there are more nerve cells around your gut than there are in your brain.  These nerves can be a conduit for exchanging information, but some toxic molecules and perhaps even viruses can use this as a direct route to the brain as well.  It is now pretty clear.  To prevent cognitive decline we should cultivate a healthy gut microbiome.

Unfortunately, the modern world is full of threats to a healthy microbiome.  Antibiotics are devastating.  They were designed to kill microbes.  And the microbiome can be harmed by certain water treatments and stress, and chemicals commonly applied to fields of GMO crops.  For most of us, however, the main threat to a healthy gut microbiome is a poor, inflammatory diet.  So you might want to pick up one of Dr. Perlmutter’s books. Your gut bacteria would be grateful.  And if they need new microbial friends, consider a probiotic.

The other part of these programs that is worth special mention is what you can do to help your mitochondria.  Those powerhouses of the cell supply energy, and your brain and gut need a lot.  Early in the evolution of life mitochondria were free-living bacteria but now they are our supportive endosymbionts, along for the ride.  When healthy they act as organic batteries and energy convertors.  You really want to help them flourish.  Because when they are injured they discharge damaging oxygen radicals, and then they self-destruct.  Worse, when they go they tend to take the host cells – including neurons – down with them in a process called apoptosis (“programmed cell death”).  What can endanger your mitochondria?  Environmental toxins are the primary culprit.  These include chemicals designed to kill pests on our crops, weeds on farms, and infections in our bodies.  There’s plenty of evidence that some of the most popular antibiotics and herbicides are essentially mitochondrial toxins.

At this point it may come as no great surprise that toxins from our environment are the primary driver of disease in industrialized world.  And that living in a chemical soup, as Bredesen explained, is bound to be bad for our brains.  So it’s worth becoming informed and eliminating environmental toxins from our diets and homes whenever we can.  While we are at it, we might want to be more careful about spreading them around in the first place; it’s awfully hard to have good personal health in an unhealthy world.

So that, in a nutshell, is the current state-of-knowledge for preventing and treating Alzheimer’s disease.  If these programs seem like combinations of modern medicine and the stuff-we-knew-we-should-have-been-doing all along, that’s about right.  Many aspects of these programs are good for your overall health and may help prevent a range of other diseases, from heart disease to cancer to depression.  Other aspects of the treatment programs require a knowledgeable and dedicated healthcare team, something well beyond the scope of most family physicians.  It can be a challenge to find a well-informed team leader, but it is critical.  It is also helpful if the team includes a “coach” (or family member).  After all, sticking with these programs could be a challenge even for those not suffering from cognitive decline.

If all this feels a bit overwhelming and seems like a lot of change to make late in life, remember this: the goal is simply to make enough positive changes to re-establish a healthy balance between inflammation and neurogenesis.  Your neuroplastic brain will do the rest.

[1] You may be wondering why evolution would allow a gene like APOE4, which increases the risk of cognitive declines and cardiovascular disease, to become so common.  As it turns out the APOE4 gene does confer some advantages.  By putting the body in a low-level inflammatory state APOE4 version of this gene confers superior protections against parasites.  This would have been a real advantage for early humans – who ate raw meat, drank from streams, and walked through a messy world on tender soles.  It was a good trade-off then.  In the era of microwaves, Reeboks, and bottled water, well, not so much.

Resources and acknowledgements:

Audio and video recording of the lectures from the 2017 IFM Dynamic Brain conference are available for purchase through their website.  Or go to YouTube; a few older lectures are there for free.

For those with the APOE4 gene, who are at a greater risk of developing the disease (or anyone interested in prevent in general) the APOE4info website and forum (https://www.apoe4.info/wp/) is an interactive source of useful information and support.  You can find out your APOE status using online genetic sequencing services, if you want to.  Some people want to know, and it motivates them to adopt some preventative measures.  Just remember, being APOE4 does not automatically mean you will develop Alzheimer’s disease.  Also, be aware that knowing your APOE status will tell you something about the status of your parents and children.  They may or may not want their APOE4 status revealed to family, friends, or their employer.  They might not want to know themselves.  Discussing your APOE status could reveal theirs, at least in part.

Dr. David Perlmutter maintains a website of up-to-date information and has published four NY Times best-selling books, including “Grain Brain” and “Brain Maker”.  His lectures at the IFM conference were inspiring.  I laughed more than I thought I would at a conference dedicated to cognitive decline.

Dr. Dale Bredesen has the website of a prolific academic researcher (which he is).  His peer-reviewed scientific articles are listed there.  His reCODE treatment program seems to work for many patients.  You can read about it here: http://www.aging-us.com/article/100690.  And here: http://www.aging-us.com/article/100981.  You can see his interview with Maria Shriver (June 2017) here: http://mariashriver.com/blog/2016/09/alzheimers-prevention-dale-bredesen-maria-shriver/.  He also has a new book “The End of Alzheimer’s” coming out in August 2017.  You can pre-order it on Amazon now.

Dr. Bredesen works with MPI Cognition, an organization that puts people in touch with physicians trained to use reCODE program.  As you may have found, many physicians aren’t up-to-date on these new programs.  So this organization might be helpful. https://www.drbredesen.com/

Dr. Rudolph Tanzi has published 500 scientific scientific papers and several best-selling books, including “Decoding Darkness: The Search the Genetic Causes of Alzheimer’s Disease”, “Super Brain: Unleashing the Explosive Power of Your Mind to Maximize Health, Happiness, and Spiritual Well-Being” and “Super Genes: Unlock the Astonishing Power of Your DNA for Optimum Health and Well-Being” (with Deepak Chopra). His team developed “Alzheimer’s in a dish” as a research tool and created Spark Memories Radio. http://sparkmemoriesradio.com/

Michael Merzenich, PhD, has authored over 150 scientific articles and a book “How the New Science of Brain Plasticity Can Change Your Life”.  He is the co-founder and chief scientific officer of Posit Science and developed the BRAIN HQ training programs that are a part of most treatment programs.  (He is also the reason I can no longer just automatically tell me kids to “get off your phones!”).

I would also acknowledge the influence of Dr. Joe Pizzorno, who spoke about environmental toxins in a way that made it all too clear that we did much of this to ourselves, and Dr. Terry Wahls, who uses a similar program she designed – and large doses of inspiration and humor – to treat patients with multiple sclerosis.

Thanks to Carla Maranto-Arnold, Julie Gregory, and Kris Willing Moore who made helpful suggestions to improve early drafts.

 

15 Dec

Introduction to our laboratory

arnoldtI’m a member of the Biology department and the program in Biochemistry & Molecular Biology at Dickinson College.  I’m also affiliated with the Environmental Studies Department and have held a variety of positions at other institutions, including at the University of Queensland, the Smithsonian Institution, and the College of Charleston as well as the Maryland Department of Natural Resources and the U.S. Fish and Wildlife Service.  I am a broadly-trained plant biochemist who studies the natural products of plants and marine organisms.  Many of these serve as anti-microbials, herbivore deterrents, or chemical cues.  Some are potential new medicines or dietary supplements.  My research starts by understanding how plants respond to stress by re-configuring primary and secondary metabolic pathways in a way that alters the production of these substances.  Then, we seek to understand the role of these substances in nature and as potential drugs.  I am particularly interested in plant polyphenols that may inhibit protein misfolding in Alzheimer’s Disease, and related disorders.

08 Nov

Ocean acidification weakens seagrass defenses

Sea GrassPhotograph © David Liittschwager / National Geographic Stock.

Chesapeake Bay, USA / Island of Vulcano, Italy.  The world’s oceans absorb carbon dioxide (CO2) and slow the pace of climate change.  At the same time the absorbed CO2 lowers the pH of ocean waters, changing seawater chemistry in the process called ocean acidification.  This can have devastating impacts on corals and shellfish, disrupting the process of calcification essential for the construction of coral reefs and the cultivation of oysters and clams in aquaculture.  However, the added CO2 could boost the photosynthesis and growth of coastal seagrasses, according to recent studies suggesting that seagrasses will be “winners” in future acidified seas (1).  This is a critical question for those hoping to manage or restore coastal waterways because seagrass meadows reduce coastal erosion and serve as nursery grounds for fish and shellfish, but have been in steep decline world-wide.

The results of a recent study published in the journal PLoS ONE challenge the assumption that seagrasses would necessarily be “winners” in a future high CO2/ low pH world (2).   The team, led by Dr. Tom Arnold from Dickinson College, examined the effects of ocean acidification on seagrasses, particularly their ability to produce a range of protective chemicals called phenolics.

“Like most plants,” explained Arnold, “seagrasses produce phenolic substances that can act as structural and chemical defenses,inhibiting the growth of disease organisms and deterring fish and other grazers from consuming the leaves.”  Indeed ecologists have long understood that plant phenolics can have numerous roles in plants.  Slight changes to their chemical structure give them useful properties as antimicrobials, antioxidants, sunscreens for harmful UV radiation, bitter-tasting deterrents, digestion reducers, and flower pigments, as well as making them the building blocks for forming wood.  “On land, more CO2 often means more phenolic substances in plants,” Arnold explained “and this too could be beneficial if it helps protect them from insects or disease”.

To test this a team of researchers, including Dr. Whitman Miller from the Smithsonian Environmental Research Center and three undergraduate students from Dickinson College1, simulated ocean acidification using an instrument called a F.O.C.E., which stands for Free Ocean Carbon Enrichment.  The instrument generates high CO2 / low pH seawater and releases it into experimental areas of seagrass meadows.  By dialing in the correct settings on the F.O.C.E. they mimicked conditions predicted to occur within the next 100 years in several meadows of aquatic plants, including widgeon grass Ruppia maritima and redhead grass Potamogeton perfoliatus, in the Chesapeake Bay.  In each of their experiments they found that high CO2 conditions led to a dramatic loss of the phenolic protective substances in these plants.  “We were quite surprised.” said Arnold “This was different than what has been observed on land.”

According to the authors, the surprising observation may be caused by something else that plagues many coastal waterways – nutrient pollution.  On land, plants often struggle to acquire nutrients such as nitrogen and phosphorous for growth and, thus, excess CO2 is diverted to the production of phenolics.  This might protect plants from grazers at a time when they would find it most difficult to regrow lost tissues (3).  However, coastal plants may respond differently because they are often bathed in nutrient-rich waters, the result of nutrient pollution (called “eutrophication”).  In this scenario excess CO2 can be combined with nutrients to fuel rapid plant growth instead of phenolic synthesis (4).

To confirm the discovery, Arnold traveled to the Island of Vulcano in the Mediterranean Sea, where CO2 is emitted not only from volcanic craters on land but also from underwater volcanic seeps, creating a natural laboratory for the study of ocean acidification.  Here a short swim towards the underwater seep provides a glimpse of the future.  As CO2 levels increase closer to the seeps the ecosystem changes visibly – seagrasses and some seaweeds thrive, while creatures such as sea urchins and molluscs disappear (5).  On Vulcano Arnold joined forces with Dr. Jason Hall-Spencer from the University of Plymouth and Dr. Marco Milazzo from the Dipartimento di Scienze della Terra e del Mare at the University of Palermo.  Together they compared populations of the seagrass Cymodocea nodosa growing near the seeps.  They analyzed populations growing at control sites, where the average pH was 8.1 and concentrations of CO2 were 422 ppm – well within the “normal” range for ocean waters.  Closer to the seeps, however, the average pH was as low as 7.3 and CO2 levels were nearly ten times higher.  They once again found the surprising decrease in concentrations of the phenolic protective substances near the vents, confirming the work done thousands of miles away in the Chesapeake Bay.

“What this means for seagrasses and the creatures that depend upon them isn’t clear yet”, says Arnold.  “It is something we are working to understand.”

Recently, he traveled to the world’s second largest sand island, North Stradebroke Island in Australia, to study unusual underground springs flow through mangrove forests to acidify coastal areas.  There the team is working to determine if high CO2 causes seagrasses growing there to become more vulnerable to grazing by local rabbitfishes2.  Other groups are studying CO2 impacts on seagrass pathogens, such as the slime-mold like microbe that triggers outbreaks of the infamous wasting disease, which is believed to have contributed to a world-wide die-off of eelgrass in the 1930s.  “We wonder, will seagrasses really be ‘winners’ in future acidified seas?  If ocean acidification stimulates the growth of seagrasses but at the same time reduces their natural defense mechanisms, what does this mean for grazers such as fishes, turtles and dugongs and microbes that cause disease?” he explains.  “We just don’t know.  We really need this information before we can predict how seagrasses, and therefore coastal communities, will respond.”

14 Jun

Coastal acidification is like beer….

b1_Page_14One of our goals is to communicate the difference between “ocean acidification”, a relatively steady drop in ocean pH caused by carbon dioxide absorption form the atmosphere, and “coastal acidification” which is the result of powerful biological processes in nearshore habitats and is extremely variable.  One way we think about this is to highlight the difference between making a carbonated beverage by direct injection of carbon dioxide (ocean acidification) and brewing a beer, creating carbonation via yeast fermentation of sugars (coastal acidification).  Both are important and troubling consequences of human activities. Both are increasing.  Both can be harmful to marine and estuarine organisms.  But they arise mostly from different processes, and we must manage them accordingly.  Hence, this slide from a recent presentation on climate change in the Chesapeake Bay.

14 Jun

Congratulations! Senior B&MB major awarded program honors.

b1_Page_66Congratulations to Andrew McGowan ’16 who earned B&MB honors for his work on climate change impacts on antimicrobial metabolites in seagrasses.  Andrew’s work showed how natural changes in pH and carbon dioxide levels within seagrass meadows can alter plant biochemistry, suggesting how these plants will respond to increasing coastal acidification.  Andrew also won several senior prizes along the way!  Many thanks to his committee members and advisors.

22 Jul

Tracking acidification in the coastal zone

IMG_0413AIRBORNE CO2 MONITORING IS ONLINE!

One of our goals is to understand an important aspect of climate change called “coastal acidification” and to demonstrate that this process is a bit different than “ocean acidification” occurring in the open oceans.

The process of “ocean acidification” occurs when excess carbon dioxide from the atmosphere enters the oceans to lower the pH and dramatically alter the carbonate chemistry.  This has been termed the “other CO2 problem” and, together with a recent two degree increase in ocean temperatures, is threatening ocean life.  For example, acidification prevents some shellfish from constructing calcium carbonate shells, and is devastating the west coast shellfish industry.  Calcification is also disrupted in many species of coral.  We’ve shown that it alters the metabolism of marine plants and fish grazing rates.  Acidification even hinders the ability of fish to smell and hear, and therefore to find prey, hide from predators, and communicate.  This is the natural consequence of having too much CO2 in the atmosphere.  Carbon dioxide levels are now over 400 ppm, up from 260 ppm at the dawn of the industrial revolution.  The oceans have taken up ~ 1/3 of this excess carbon, slowing climate change, but at a price.  The price is the acidification of the open oceans.

Here’s a description from one of our recent works: “Since the industrial revolution atmospheric carbon dioxide levels have increased from 280 to 400 ppm (parts per million), the highest levels occurring on our planet in 800,000 years (Doney et al. 2009; Sabine et al. 2004). Approximately one-third of the CO2 emitted from human activities has been absorbed by the oceans, slowing the rate of global climate change. However, this generates carbonic acid (H2CO3), resulting in an increase in the total H+ concentration (i.e., increasing seawater acidity and lower pH) and conversion of carbonate ions (CO32-) to bicarbonate ions (HCO3) in seawater. The establishment of high CO2/low pH conditions in blue waters is termed ‘ocean acidification’ (OA).  In the open oceans this process is relatively well understood. In the past 150 years, the oceans have become net CO2 sinks and the average ocean pH has dropped from 8.21 to 8.10 (Royal Society 2005). By the end of the century it is expected to fall another 0.3 to 0.4 units (Doney et al. 2009; Orr et al. 2005). This shift in ocean chemistry represents a 150% increase in hydrogen ions and a 50% decrease in levels of carbonate ions (CO32-) (Doney et al. 2009; Orr et al. 2005). OA lowers the availability of CO32-, and therefore the seawater saturation states with respect to several carbonate minerals (Ω), so that the formation and deposition of new CaCO3 minerals is reduced, and the dissolution of existing minerals is enhanced. This disrupts the growth of many calcifying organisms, including important species of shellfish, plankton, and corals, which struggle to form CaCO3 shells, skeletons, and tests.”

Here’s a good description of the problem, from the Pacific Marine Ecology Lab: http://www.pmel.noaa.gov/co2/story/Ocean+Acidification

And from National Geographic: http://ocean.nationalgeographic.com/ocean/critical-issues-ocean-acidification/

Acidification is also occurring along our coastlines, but the process is somewhat different.  We call it “coastal acidification”.  Here the excess carbon comes mostly from the land as run-off, via rivers, bays, and marshes.  Much of this results from land use practices related to agriculture, nutrient over-enrichment, development, deforestation, etc.  The amount of carbon input is much higher, and much more variable.  For example, the daily fluctuations in carbonate chemistry near coastal marshes can be a thousand times greater than the fluctuations recorded in the open ocean over a period of many years!

Here’s how we described in recently: “Within the Chesapeake Bay, and other estuaries, the process is more complex. The sources of carbon are different: for example, estuarine waters do not generally absorb CO2 from the atmosphere but rather as dissolved organic carbon (DOC) from the land. Powerful biological processes, e.g. respiration and decomposition (i.e., heterotrophy), convert DOC to inorganic carbon.  High levels of CO2 can also be generated from DOC by microbial respiration in anoxic bottom waters as a consequence of eutrophication (Wallace et al 2014; Melzner et al 2013). Other processes can be influential as well. For instance, in some areas acid sulfate soils or nitrogen deposition may contribute to acidification. In other areas, ocean mixing or coastal upwelling may deliver high CO2/low pH waters from the open ocean.  The Chesapeake, like most estuaries, is surrounded by terrestrial and intertidal environments which export massive amounts of organic carbon to the oceans via the “land–ocean continuum” (Cia, 2010). Historically, this terrestrial organic carbon flowed to the oceans where heterotrophy converted it CO2, which was in turn emitted to the atmosphere. However, due to human activities, this has changed in several ways: (1) the mass flow of organic carbon along this land–ocean continuum has increased dramatically and (2) the oceans act as carbon sinks, absorbing excess anthropogenic carbon from the atmosphere. In short, today’s estuaries import terrestrial organic carbon, convert it to inorganic carbon, release a fraction to the atmosphere as CO2, store some, and export the rest as organic carbon to the oceans.”

Both processes are driven by excess carbon.  But to study them, we must employ different strategies.  To work on open ocean systems one must be very precise and patient, to work in coastal systems one must become comfortable with constant variation in large data sets, and design experiments appropriately.

It can be a challenge to obtain the measurements needed to accurately characterize a coastal community – a tidal marsh or seagrass meadow, for example.  Modern technologies are helping us to monitor these systems at multiple locations at rates as high as one observation per second.

In the past we’ve been using an in situ real-time pCO2 monitor, developed by Dr. Whitman Miller (from the Smithsonian Environmental Research Center), to measure carbon dioxide concentrations in estuarine waters.

IMG_0439We have recently expanded our capabilities to monitor atmospheric carbon concentrations in the coastal zone using airborne sensor packages.  This means that, together with our collaborators, we can now monitor carbon above and below the waterline simultaneously, in real-time in coastal waterways, marshes creeks, and in the air above them – all without getting wet!

To see how it works check out this video: IMG_0415

By coordinating many sensor packages, and taking frequent water samples for later analyses, we can track carbon into and out of coastal ecosystems.  By analyzing plant tissues and conducting tracer experiments with stable (non-radioactive) isotopes we can follow the flow of carbon through plants and into metabolic pools of carbohydrates, proteins, and phenolic substances – above and below ground.  We can even track the carbon among trophic levels as plants are consumed by herbivores, and so forth.

Questions we hope to answer:

How to salt marshes process carbon?  How do they take it in and release it?  What are the local conditions that estuarine organisms experience near marshes?

Can seagrass meadows take up and safely store large amounts of excess carbon – acting as a helpful “carbon sponge” to help slow climate change?

Does the carbonate system change in predictable ways within seagrass beds?  And what are the consequences for organisms, such as bay scallops, that live there?

We thank Dickinson College’s Research and Development Committee for funding, and the folks at Valarm for technical assistance.

22 Aug

New publication on seagrass responses to high CO2 / low pH conditions

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Fish collecting is always better at night (but beware sharks!)

Fish collecting is always better at night (but beware sharks!)

We recently published an article in the journal PLoS ONE entitled “Impacts of Groundwater Discharge at Myora Springs (North Stradbroke Island, Australia) on the Phenolic Metabolism of Eelgrass, Zostera muelleri, and Grazing by the Juvenile Rabbitfish, Siganus fuscescens”.  This article describes the impact of natural “acid springs” on eelgrass meadows near North Stradbroke Island, Queensland, Australia.  The data support the findings we published from the Chesapeake Bay (USA) and Sicilian CO2 vent sites (Italy): high CO2/low pH conditions dramatically reduce soluble phenolic levels in seagrasses, often with an increase in the levels of insoluble lignin.  Dickinson students, including co-authors Grace Freundlich,Taylor Weilnau, and Arielle Verdi participated in this research.  Marine scientist and director of global education programs, Ian Tibbets, was our University of Queensland collaborator.  Support was provided by grants from the Smithsonian Institution and NASA.  Seventeen other Dickinson students, enrolled in the College’s Global Scholars pilot program, contributed in other ways.  We’re grateful for Dickinson’s continued support of innovative undergraduate research programs.

05 May

Congratulations to our graduating students!

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Under the Australian Sun!

Congratulations to our three graduating lab members on completing their programs of study and submitting their undergraduate research, Impacts of groundwater discharge at Myora Springs (North Stradbroke Island, Australia) on the phenolic metabolism of eelgrass, Zostera capricorni, and grazing by the juvenile rabbitfish, Siganus fuscescens, for publication this spring!

This work built on the work of the 2012 Global Scholars team.  Check out their site on under “Pages”.

Under the Australian Sun

24 Apr

Ocean Acidification Report: West Coast Seagrass Studies

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This summarizes some interesting, ongoing work on seagrasses and coastal carbon that is similar to what our group is doing in the Mid-Atlantic.

Eric Swenson, Editor
Brad Warren, Publisher

Research exploring how seagrasses in Washington, Oregon, and California bays and estuaries affect carbonate chemistry are due to start this spring and summer. The principal investigators are George Waldbusser of Oregon State University, who will focus on Netarts Bay; Jennifer Ruesink of the University of Washington, working in collaboration with the Washington Department of Natural Resources at several sites; and Tessa Hill, University of California, Davis, studying Bodega and Tomales Bays. Sea Grant is funding the California and Oregon research.

The three will be using different instrumentation, techniques, and measuring systems in a variety of venues, looking to identify habitats and conditions with the greatest potential for local reduction of carbon dioxide dissolved in water. Collectively, they will shed light on how fast seagrasses can draw down carbon dioxide through their photosynthesis, whether this carbon is sequestered longer term, and therefore the potential for primary producers to improve water conditions for sensitive shell-forming organisms.

Ruesink notes that some seagrass habitats may be net emitters of CO2 by trapping organic material that decomposes, releasing the gas. Similarly Waldbusser will be comparing native eel grass and Japanese eel grass habitats as he tries to understand the “carbon budget” of Netarts Bay. The scientists will make their findings known to policymakers, stakeholders, and the public in late 2015 to enable comparisons at broad geographic scales from a variety of estuaries.

Read more here.

14 Feb

A beach bum’s guide to ocean acidification

A beach bum’s guide to ocean acidificationBaltimore native Jim Meyer is a stand up comedian and freelance writer who wrote this piece about ocean acidification.  While it’s probably not going to get him invited to testify before congress he is reaching people that we usually don’t, which is critically important.  And he does mention Jimmy Buffett.  So, thanks Jim and thanks to Lee Karrh for sending this my way.  This is our post of the day:……Over the last 200 years, human pollution has caused the oceans’ pH to drop 100 times faster than it did in the previous 650,000 years. To give you an idea what the oceans are going through, try to imagine taking in the entire six seasons of The Wire in 32.4 seconds. You’d have 11 strokes. And that’s just the tip of the iceberg (a cliché that will baffle your grandkids).  Read more: http://grist.org/basics/bad-acid-trip-a-beach-bums-guide-to-ocean-acidification/

 

12 Feb

The Real “Hot Tub Time Machine”

castleBlog readers will already know about the hydrothermal vents along the Italian coastline, some of which vent pure carbon dioxide into the sea at normal temperatures.  In conjunction with our coworkers we’ve examined these vents as potential ‘living laboratories’ which give us a glimpse of marine life in future high carbon dioxide / low pH oceans.  This photgraph, by Jimmy Harris (see link below), shows the Castello Aragonese near Naples, Italy.  Yes, the Italian translates to the ‘Aragonate Castle’.  It’s carved into the calcium carbonate rock of the island.  Want to see more?  Well our colleague, Jason Hall Spencer, has some great YouTube videos of the site, above and below the waterline.  Well, we thought the title of a recent blog post article, “Hot Tub Time Machine” by Elizabeth Kolbert, was clever.  Here’s the link: Off the coast of Italy, CO2-spewing vents are giving scientists a glimpse at the acidic oceans of our future. The results are frightening.by Elizabeth Kolbert  @ElizKolbert • February 11, 2014  This article is adapted from the author’s new book, The Sixth Extinction: An Unnatural History, on sale today.  http://www.onearth.org/articles/2014/02/elizabeth-kolberts-scary-swim-in-the-acidic-oceans-of-tomorrow.  We haven’t read the book yet.  Have you?  If so, what did you think?

18 Sep

Virtual poster presentation for OAPI meeting (2013)

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C nodosa low pHGreetings to those attending the Ocean Acidification Principle Investigators Meeting in Washington D.C. This is our virtual ‘poster’ presentation, posted here instead of in print in an effort to be more sustainable.

CLICK HERE TO DOWNLOAD OAPI as pdf for reading and teaching.

You are welcome to view our poster now for viewing on your mobile device or download it for viewing later, at your convenience.

Sincerely,

Thomas Arnold (Dickinson College)
Whitman Miller (SERC)
Jason Hall-Spencer (U Plymouth)
Marco Milazzo (U Palermo)

22 Aug

Plant resource allocation: from Goethe and Darwin to today.

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Our new 2013 review of plant defense responses and resource re-allocation published in Frontiers in Plant Science and online HERE.  Read about the uncommon wisdom of early poets and natural historians, who had a pretty good idea of how plants should allocation precious resources to maximize their fitness.  For example The budget of nature is fixed; but she is free to dispose of particular sums by an appropriation that may please her. In order to spend on one side, she is forced to economize on the other side”  (in Darwin 1872)