Exercise, part 2: Moderation in all things?

In part 1 of this series I made the following points:

1.         Barring extenuating circumstances, older folks can sustain muscle strength and muscle mass well into “old age.”

2.         Protein synthesis appears to be sustained throughout life, perhaps to the same extent as found in young people;

3.         This is counter to the prevailing paradigm, which holds that muscle wasting is an inevitable consequence of aging.

4.          Resistance exercise is rarely recommended for old folks; generally they are urged to “go walk in the mall for 30 minutes” as if that is all they are capable of.

5.         Muscle wasting in older adults may occur primarily because of their sedentary lifestyle.

Pretty exciting stuff, no?

But there is emerging evidence that “too much” exercise, at least exercise that gets the heart rate up to a “high” level for extended periods, may not be good for you—whether you are young OR old.  Further, data indicates that there are “optimal” levels of exercise.  Scientists have not, however, zeroed in on how often and how hard we should exercise to achieve maximum health benefits.

In a medical-screening study published in 2011*, researchers surveyed 416,175 Taiwanese individuals about their level of exercise upon enrollment in the study and then repeated this survey each year for the next 8 years.  Based on their answers to the survey questions, each subject was placed into one of five exercise categories:  “inactive,” “low volume,” “medium volume,” “high volume,” and “very high volume.”  During the course of the study, the researchers recorded deaths as well as the incidence of cancer, diabetes, cardiovascular disease, heart attack, and stroke .

Simply put, here is what they found:  As the participants’ level of activity increased, the rate of overall mortality decreased, as well as rates of death from cancer, diabetes, and cardiovascular disease.  All statistically significant.  The same results were found for every tested category, whether male or female, young or old.  Surprisingly, the results held true even for individuals with chronic kidney disease, metabolic syndrome, hypercholesterolemia, obesity, diabetes, or high blood pressure.   The conclusion is that exercise, even in very moderate amounts, helps EVERYONE at any age, regardless of the state of their health.

In fact, exercising for only 92 minutes PER WEEK decreased all-cause mortality and resulted in an increased life expectancy of 3 years.  Amazingly, all-cause mortality was further reduced by each additional15 minutes of exercise beyond a minimal 15 minutes per day.

BUT the benefit maxed out at 90 minutes of exercise per day.  So the authors concluded that exercising beyond this amount has no additional benefit as far as mortality is concerned.   And for those in the “vigorous” group, the maximum benefit was achieved after about 45 minutes.

Similar results were found in a 15-year study of 52,000 people, 14,000 of whom runners.  Overall, the runners had a 19% lower rate of mortality than non-runners, but the benefit was NOT seen in those who ran the fastest or the farthest.  For example, those who ran at 7 mph had the least mortality (17% reduction compared with non-runners), but those who ran faster than 8 mph had the same mortality as those who ran 1-5 mph (~10% reduction).   Similarly, those who ran the greatest distances (over 25 miles per week) had mortality reductions of 5-10%, while those who ran 0.1-19.9 miles per week had reductions of about 25%.

So this study indicates that there is an “optimal” level of running for fitness—and too much may be, well, too much.

Finally, the really big news in this area is the recent evidence that athletes who do EXTREME amounts of running may be damaging their cardiovascular systems.  The issue at hand is reminiscent of the legend of Pheidippides, the famous Greek runner who ran 150 miles in 48  hours to deliver the message “Victory is ours!” after the Battle of Marathon in 490 BC—and then dropped dead.  Read on.

Dr. James O’Keefe, professor of medicine at the University of Missouri-Kansas City, has published several articles concerning the effects of extreme running on heart health.  His publications have been pretty radical, prompting lots of discussion in exercise physiology circles.  In fact, they have sent a tremor through the exercise world.

Here are some examples:

1.         A 2012 study reports that sudden cardiac death in marathoners who run the full 26.2 miles is 1/100,000.  I could not find statistics for the expected rate of sudden cardiac death among non-marathoners.  However, between the year 2000 and 2010, 11 million people ran in full and half marathons.  59 experienced cardiac arrest (0.54/100,000).  For half marathons (13.1 miles)), the rate of sudden cardiac death was 0.27/100,000, and for full marathons the rate was 1/100,000.   Although these numbers are really low, they do suggest that something is going on.

2.         In a 2010 study, 60 male patients with cardiovascular disease were divided into two groups.  One group exercised for 30 minutes, and the other for 60 minutes.  The researchers took blood pressure measurements and performed an EKG (electrocardiogram) on each of the participants.  They found that the two groups did not differ with regard to blood pressure (rather counter to the idea that exercise decreases blood pressure).  More importantly, they also found that the 30-minute group had MORE favorable EKG results than the 60-minute group.

3.         A 2010 study looked at a particular chemical that is generally considered to be associated with cardiac damage—troponin.  (Troponins are molecules that help with muscle contraction, and when they leak out of muscle fibers, it may be an indication of muscle damage.  So, finding cardiac troponins in blood plasma may be diagnostic of several types of heart damage, including heart attacks.)  The authors reviewed 18 studies involving various types of exercise:  walking (18 to 30 miles), running (full and half marathons), cycling (124 miles), and one iron man triathlon (swim 2.2 miles, cycle 112 miles, run 26.2 miles).  Although 0% to 100% of the participants in a given event showed elevated cardiac troponin, the shorter the duration of the event, the HIGHER the troponin levels.  This suggests that shorter events, which are more intense and require greater cardiac output, result in the production of more troponin—and possibly more heart damage.

The hearts of athletes are different from those of normal people.  Overall an athlete’s heart is larger—which makes sense, since a larger heart can do more work.  The concern is that the hearts of some athletes involved in endurance events may show signs of “strain,” such as scarring (fibrosis), diastolic dysfunction, large-artery wall stiffening, and coronary artery calcification (plaque build up).  And in particular, the right ventricle may have decreased functionality.

Here are some more studies comparing the cardiovascular systems of endurance athletes to those of “normal” people:

1.         A 2008 study looked at forty athletes who participated in marathons (7), triathlons (11), ultra-triathlons (13), or alpine cycling events (9).  90% were males, their average age was 37, they had an average of 10 years in training, and they exercised an average of 16 hours per week.   Each athlete was examined before a race, immediately after a race, and one week later.  What the researchers found is that the function of an athlete’s right ventricle immediately following a race was reduced in comparison to its function before the race, and after one week it was almost back to baseline.  However, 5 of the 40 athletes showed areas of tissue damage in the septum  (tissue separating left and right ventricles), and those athletes also had hearts that pumped less blood.   The authors concluded that (a) intense endurance exercise caused dysfunction of the right ventricle (but not the left), (b) eventual recovery was nearly total, and (c) reduced right ventricle function was most evident in some of the most “practiced” athletes.

2.)         A 2009 study looked at 102 runners, age 50 or older, who had completed at least five full marathons in the last three years and had no history of heart disease.  It  showed that 12% of them had heart tissue damage; this compared to 4% of a “normal” population.

3.)         A 2010 study looked at 49 marathon runners who were, on average, 38 years old.   It showed that these athletes had significantly higher blood pressure than a group of “normal” people did. 

I could go on and on, but it seems that a consistent story is emerging:  very intense aerobic exercise such as running, cycling, and rowing over a long period of time may lead to damaged heart and arterial tissues. 

These studies also suggest that, at least in some individuals, there is an optimal level of exercise and exceeding it may be harmful, or at least provide no benefit.  This may be genetic, and it may be true in only a “small” percentage of the population.  So unfortunately there are no rules here—and few recommendations, except that some is good and too much may be bad.

It may behoove us, as we age, to have our cardiovascular system checked out more thoroughly than is possible with a family doctor’s stethoscope.  As we enter our “golden” years, and especially if we are beating ourselves up with lots of exercise, perhaps it is worth having an echocardiogram every 5-10 years, just as a status check.

Finally, I’d like to point out that the “intensity” of exercise is measured by one’s heart rate, regardless of the type of exercise.  (After all, the heart does not know if it is beating fast because we are running or lifting weights.  I personally find my highest heart rates occur when wall climbing, and weight lifting gets my rate as high as if I were running.)  There is growing interest in highly-intense exercise of short duration—this is the regime advocated by the increasingly popular “Crossfit” program,  which is designed to maximize heart rate through running, weight lifting, and various body-weight exercises.  In light of recent studies, is it possible that there are negative consequences to a lifetime of causing our hearts to beat wildly, even if only for 10 minutes at a time?  No one knows.

Useful References:

*http://vivafit.eu/pdf/Pang_Wen_minimum_amount_PA_reduced_mortality_Lancet_2011.pdf

http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=32617aef-b494-41b8-b2bc-3d49357a8976&cKey=984e0396-f663-4068-bbf3-1dc4023c17e1&mKey={FCDB1C1C-280A-4DF1-95F8-2DAA9AB6A8BE}

http://www.msma.org/docs/communications/momed/Excessive_Endurance_Exercise_and_Heart_Disease_MOMED_JulyAug2012.pdf

http://www.nejm.org/doi/full/10.1056/NEJMoa1106468?viewType=Print

http://jama.jamanetwork.com/article.aspx?articleid=185622

http://www.ncbi.nlm.nih.gov/pubmed/21357374           

http://eurheartj.oxfordjournals.org/content/early/2011/12/05/eurheartj.ehr397.full

http://radiology.rsna.org/content/251/1/50.full.pdf

http://www.ncbi.nlm.nih.gov/pubmed/20489686

http://ajh.oxfordjournals.org/content/23/9/974.long

Vigorous Exercise: Not only for the young

We all know that muscular weakness and wasting will eventually catch up with us because a decline in physical vigor is an inevitable part of the aging process.  After all, we have seen our parents and grandparents slowly deteriorate, and many studies show a correlation between aging, muscular weakness, and loss of lean muscle mass.  Might as well just accept it . . . right?

But what if the frailty that we see in senior citizens is mainly due to a sedentary lifestyle, and the loss of muscular strength and endurance is the result of disuse?  What if the progression from vitality to frailty is just a self-fulfilling prophecy?

Surprisingly, it has been shown that sitting on our fannies is a significant factor in the aging syndrome—perhaps the major factor.  Some pretty remarkable studies indicate that lean muscle mass and strength, as well as muscular and cardiovascular endurance, may be maintained well into advanced age. 

But before we get into the juicy details, first some vocabulary and basic concepts.

Physical fitness can be assessed different ways, but the two we are most familiar with are cardiovascular function and musculature.

Cardiovascular Function.  The most widely used measure of cardiovascular fitness is “V0₂ max,” the maximum amount of oxygen that is available for the performance of  a task.  V0₂ max is generally measured by having the subject run on a treadmill while wearing a mask that delivers oxygen and tracks consumption.  For those of you who don’t have a treadmill and an oxygen mask readily available, you can estimate your V0₂ max as follows:  divide your maximum heart rate by your resting heart rate and multiply by 15.  The result is an estimate of your V0₂ max. 

The average untrained male has a V0₂ max of 35-40 ml/kg/min, meaning that he consumes 35 to 40 milliliters of oxygen per kilogram of weight each minute.  Elite male runners can consume 85 ml/kg/min.   Remarkably, thoroughbred horses have a V0₂ max of around 180 ml/kg/min, and sled dogs that run the Iditarod have a V0₂ max of 240 ml/kg/min.  At the other end of the spectrum, a human must have a V0₂ of 15-20 ml/kg/min to live independently, and a decline of 0.4-0.5 ml/kg/min per year, or 5-10% per decade, is normal after age 50.

Musculature.  Muscular fitness is measured not only by muscle size and fat concentrations, but also by strength, power, and endurance.  Strength is an easy concept—how much you can lift or push—and it is measured in pounds or the equivalent.  Power is more complicated though; expressed in watts, it tells you how much weight you can move in a given amount of time.  And endurance, of course, refers to how long you can make a particular muscle perform.

So now, what is the effect of exercise on aging adults?  One of the best ways to answer this question is by studying “masters athletes,” defined as individuals who are over 40 and train for fitness and sports competitions.

A 2011 study* looked at 20 men and 20 women who were (a) over 40 years old, (b) trained for competitions MORE than 4-5 times per week, and (c) did not have an injury that limited their ability to compete.  They were divided into four age groups with 5 men and 5 women in each group: 40-49 years, 50-59 years, 60-69 years, and over 70 years.  Using the cross-sectional images of each subject’s upper leg provided by MRI (magnetic resonance imaging) scans, researchers calculated the amount of fat and muscle in the thigh as well as the extent to which the fat had penetrated the muscle.

And what did they find?  Here are the shockers:

Total mid-thigh mass (muscle and fat):   no difference between age groups.

Lean mass (muscle without fat):   no difference between age groups.

Size of quadriceps (the big muscle on the top of your thigh):  no difference between age groups except in those over 70, who had a 20% decrease compared to the other groups.

Physical torque (the amount of force that can be generated by pushing your leg against resistance):  no difference between the 40-49 and the 50-59 age groups and no difference between the 60-69 and the over-70 age groups, but the 40-59 group exerted more force than the over-60 group.

In summary, no muscular decline was observed until age 60, and after 60 it did not deteriorate further except for a 20% decrease in quadriceps size in those over 70.

A 2008 paper that looked at previous studies comparing elite male athletes with untrained “normal” men concluded that elite athletes can achieve remarkable performance into their 90’s.  For example, knee strength in 90-year-old weightlifters was higher than that of 40-year-old normal males.  The VO₂ max of 70-year-old elite runners was equal to that of untrained 25-year-olds.  The power generated by 75-year-old weightlifters was equal to that of ordinary 25-year-olds.

Now, my purpose in going through these statistics is NOT to suggest that we can all look like Arnold Schwarzenegger as we slide into our golden years.  Unfortunately, there are very real events that occur as we age—and the list is depressingly long! 

What is known, again by looking at the performance of elite athletes, is that all of the above measures—strength, power, V0₂ max—decrease with age.  A weight-trained 90-year-old is never going to be able to compete with a weight-trained 20-year-old.  In fact, in all these studies the trained youngsters outperformed the trained oldsters by great margins in all age categories.  Peak endurance running, for example, is maintained until approximately 35 years old, with modest decreases thereafter until 50-60 and larger drop-offs after that.  This decline in athletic performance is well known in all sports.

My intent is to make the point that recent studies reveal that people of all ages show remarkable improvement with training, and therefore some aspects of the aging stereotype are simply WRONG.  What is going on at the biochemical level is not yet fully known, but it appears that the capacity for protein synthesis may remain essentially unchanged as we age.   Think about THAT!

So what is the evidence?  Looking at masters athletes is useful in many ways—but maybe there is something different about them other than their capacity for continuous training.  What we really need to know is how “normal” people respond to training.

But first, a little vocabulary that is used in the exercise world.  “Resistance training” essentially means lifting weights by any mechanism—a mechanical apparatus (think Nautilus machines) or free weights (barbells, for example) or “body weight” (such as pull-ups or push-ups).  Resistance training with free weights or machines is often structured around percentages of  the “one rep maximum” (1RM), which is the maximum weight that can be lifted or pushed one time for a given exercise.  A “low” workout could incorporate groups of repetitions (reps) at 60% 1RM, so your exercise on a given day might consist of three sets of 10 reps at your 60% 1RM.   Obviously the possible variations on this theme are endless.

A 2010 meta-analysis of 47 studies covered 1079 subjects ranging in age from 50-92 (average age 67) who were subjected to resistance training.   Depending on the parameters of each individual study, the subjects worked out 1-3 times per week (average 2.7) at 40%-85% of their 1RM.  The number of exercises ranged from 5 to 16 (average 8.3). The number of sets per exercise ranged from 1 to 6, (average 2.5) and the number of repetitions per set ranged from 2 to 20 (average 10).  The length of the rest periods between sets varied from 60 seconds  to 360 seconds.  The types of exercises performed were leg presses, chest presses, knee extensions, and “lat” (latissimus dorsi) pull-downs.  The studies varied in length from 6 to 52 weeks. 

It is clear that some of these studies involved workouts that were pretty intense by any standard.  And remember, these were folks who were, on average, 67 years old!

So what were the results?

Statistically significant improvements were found across the board.  Strength increased by 29% for the leg press, 24% for the chest press, 33% for the knee extension, and 25% for the lat pull-down.   And get this:  as the intensity of the training increased, so did the rate of improvement (an average 5.3% increase in strength from one level of intensity to the next).

These are huge improvements, especially when you consider that the test subjects were assumed to be declining in strength because of “aging.”  The good news is that when their muscles were strained and their tissues torn (which always happens with resistance training), their bodies recovered and were even better afterwards.  It means protein synthesis was going on.  And surprisingly, the level of improvement was the same for both men and women in all age groups (although some studies have found that youngsters gain strength more rapidly than oldsters).

Clearly these results suggest whole new types of exercise programs for the elderly, not only modifying exercise intensity but also varying the exercise program over time—what’s called “periodization.”  An exercise program that incorporates “periodization” would involve, for example, two weeks of high-intensity training followed by a week at low intensity, followed by high intensity, etc.  Periodization has been well-studied in young athletes, but among the aged not at all.  Why?  Because, I guess, they weren’t expected to respond.  Because they are OLD, you know? 

The general importance of exercise, even very moderate exercise, is well known—case closed on that.  What these studies show is that for all ages, the more you exercise the better.  And the harder it is, the more you gain.  The old saying “no pain no gain” apparently applies no matter what your age (up to a certain point that is, which I’ll discuss in another blog).

Finally, I’d like to share another study supporting the benefits of exercise—not only cardiovascular fitness but muscular fitness as well.  The two are different, but certainly related.

From 1980 to 1989, 10,265 men entered the study and were categorized by age, weight, minimal ability to work out on a treadmill (as a measure of cardiovascular fitness), and ability to perform leg and chest presses (as a measure of muscular fitness).  By the end of the study in 2003, 8,762 subjects remained, ranging in age from 20 to 80.   Some of them had died or suffered heart attacks, strokes, cancer, or diabetes, but the average man was followed for 19 years.

The researchers divided the men into three groups (low, middle, and high) according to their muscular strength at the time they entered the study.  Basically they found that the stronger the group, the less mortality there was from any cause, including cancer and cardiovascular disease.  This was true even after controlling for varying initial levels of cardiovascular health (although greater cardiovascular health was correlated with higher muscular strength).  

This study’s focus on muscular strength makes it different from many others because the majority have focused on the health benefits of cardiovascular exercise (running, walking, etc.).   It is not known how muscular strength protects against disease, but some researchers believe that it may be due to the type of muscle fibers one has.

Given the fact that aging baby boomers constitute 26% percent of the United States population, these kinds of studies are very important.  The results are changing the paradigms of aging as well as the vocabulary, as evidenced by the fact that terms like “successful aging,” “active aging,” “positive aging,” and “active living” are increasingly in use.

And those of us who are no longer young need to actively counter stereotypes of aging and the cultural expectations about “what we can do.”

The Pepsi Generation may be getting old, but we are still a force to be reckoned with!

Useful References:

https://physsportsmed.org/sites/default/files/rpsm.2011.09.1933_secure.pdf

http://kines.umich.edu/sites/webservices.itcs.umich.edu.drupal.kinesprod/files/resource_files/CJSMAgingEliteMaleAthletes.pdf

http://www.sciencedirect.com/science/article/pii/S1568163710000279

http://www.bmj.com/content/337/bmj.a439

---

PATENTING HUMAN GENES: The Myriad Case

The U.S. Supreme Court has made a number of important decisions in the last few months, two of which are relevant to topics on this blog:  (1) Bowman v. Monsanto; and (2) Association for Molecular Pathology v. Myriad Genetics.

I wrote about the Bowman v. Monsanto case last February, and I won’t repeat myself here—except to say that the Supreme Court ruled that farmers can’t save patented seeds and reproduce them by using them to grow a new generation of plants.  In my opinion, that case was almost a no-brainer, in that prohibiting others from copying your patented inventions or copyrighted works is central to intellectual property law, and the Court HAD to rule in favor of Monsanto.

The second case is more far reaching in its consequences.

The Supreme Court made two basic rulings in Myriad:  you can’t patent human DNA sequences as they occur in humans (“native DNA”), but you CAN patent human DNA that has been changed artificially.

The Myriad case was directed to two genes involved in causing breast cancer:  BRCA1 and BRCA2.  There were three patents in question:  U. S. Patent 5,747,282, U.S. Patent 5,693,473 and U. S. Patent 5,837,492.  It is historically interesting to note that these patents were filed way back in the early 1990’s—at a time when the human genome  had not yet been sequenced and published, which didn’t happen until the early 2000’s.  So the Myriad patents were revolutionary at the time—but by today’s standards, not so much.  In fact, the Myriad genes could not be patented today.  In order to be patentable, an invention has to be “novel”, and the publication of the human genome made the native DNA sequences of all human genes “not novel.”

Since Myriad’s patent applications on the BRCA genes were filed before publication of the human genome, Myriad couldn’t be denied a patent on those grounds.  But the Supreme Court’s ruling was not based on “novelty,” but rather on the assertion that a native DNA sequence is a “product of nature.”  And U.S. patent law says that that a product of nature is not eligible for patenting, the logic being that it is not a human invention—nature made it. 

The problem is that actually discovering at least SOME products of nature requires a heck of a lot of inventiveness.  It is not entirely clear to me where a “product of nature” that has been identified and laboriously extracted from nature differs from an “article of manufacture”, which is one of the categories of things that CAN be patented.  And, in fact, many naturally-occurring products have been patented in the past—aspirin, insulin, vitamin B12, and adrenalin, to name just a few.  Actually isolating these compounds required inventive activity and a recognition that they would be useful.  And back 1990’s when Myriad’s patents were issued, the U.S. Patent and Trademark Office obviously thought that isolated DNA sequences were patentable subject matter.  In fact, their identification and isolation required a high degree of inventiveness.

In their native state, the BRCA1 and BRCA2 genes are wrapped up with various proteins—scaffolding proteins such as histones that help maintain a 3-dimensonal structure.  Additionally, each gene has methyl groups spread around particular nucleotides, particularly the cytosines, to help regulate gene expression.  But the Myriad BRCA patents in question only cover the gene sequences (each consisting of about 80,000 base pairs), but NOT the methyl groups or the histones.

So the patented BRCA1 and BRCA2 genes don’t look anything like the BRCA1 and BRCA2 genes found on a human chromosome.  It’s kind of like the difference between a baseball bat and the limb of the ash tree from which it was made.  Certainly the baseball bat existed within the tree limb—but getting it out took skill and inventiveness, wouldn’t you agree?  (Unfortunately I can’t take credit for that great metaphor.  Wish I had thought of it though.) 

The bottom line is that the Supreme Court says “native gene sequences” are not patentable, and that’s that.  Also, a narrow reading of the Court’s opinion indicates that its decision is restricted to human gene sequences.

But even so, and this is an important point, it is possible that the Myriad decision could put the entire field of “natural product” patents in jeopardy.  Take, for example, natural products that have medicinal uses.  The same logic used by the Supreme Court to invalidate Myriad’s  patents also could be used to preclude patenting of a plant-derived cure for AIDS, for example.  I just don’t see the difference.  And if pharmaceutical companies can’t get patent protection on plant-based drugs, they might just quit doing the costly research that leads to the discovery of those drugs in the first place.

Want some cool examples of natural products that have been patented, and may not be in the future?  Here are a few:

(1) Sirolimus, a chemical isolated from a bacteria found on Easter Island (how cool is that?), is both an antifungal and antibiotic, as well as an immunosuppressant that is used to prevent organ rejection in kidney transplants.  Sold by the trade name Rapamune.  U.S. Patent 3,929,992.

(2) Aplidine was first isolated from sea squirts (even cooler!) is a novel antitumor agent that has received orphan drug status for the treatment of multiple myeloma, a blood cell cancer.  U.S. Patent 5,834,586.

(3)  Exenatide is a chemical compound first found in the saliva of Gila monsters (way cool!) that is used for the treatment of diabetes.  U.S. Patent 5,424,286.

I could go on and on with such examples, but you get the idea.

As mentioned at the beginning of this blog, the Supreme Court ruled in Myriad that human DNA could be patented if it had been artificially changed from its native state.  Well, this almost had to be the case.  If something is artificially changed, it becomes an article of manufacture, and articles of manufacture ARE patentable.  No controversy there.

So what are the consequences of the Myriad decision?

Thousands of gene-related patents have been issued in the last 30 years, and even more “natural product” patents have been issued in the last 100 years.  Since the biotechnology industry is very dependent on products of nature, some areas of biotechnology, such as stem cell research, for example, could be in jeopardy.  After all, deriving a stem cell line from a skin cell or umbilical blood is about as “natural” as you can get.  Since patent protection can be a big part of what makes new ventures profitable, certainly investors will be, or should be, more cautious than they have been in the past about putting money into these types of products. 

Another potential unintended consequence of the Court’s decision is that inventors may decide to keep their discoveries secret rather than publish them.  The patent system is really a trade-off in which the government says, “In exchange for disclosing your invention to the public in a patent application, we will give you the right (a patent) to keep others from making, using, or selling that invention for a limited period of time.”  But if the government doesn’t keep its side of the bargain by issuing a patent, can inventors really afford to let everybody else in on their secrets?

Then again, the stock price of Myriad is trading at nearly all-time highs.  The market seems to have taken the Supreme Court’s decision in stride, and we may very well find that it was mainly a political decision, and thus without significant consequence.

But I doubt it. 

Climate Change (Part 4)

In this post, the last of a four-part series on climate change, I’ll start with the conclusions reached so far:

1.            There is overwhelming data indicating that the planet is in a warming trend—at least up until the last 10 years or so.

2.            Warming trends are historically correlated with increasing levels of CO₂, with emphasis on “correlated with” (not “caused by”).

3.            Mathematical models of future global temperatures are now predicting less warming than previously thought.

4.            Natural “forcings” of climate are significant.

5.            How the various natural forcings will interact with increased CO₂ and other greenhouse gases is, of course, unknown.

6.            C0₂, which acts like a natural fertilizer, stimulates plant growth significantly in some species.

7.            Plant species differ in response to elevated C0₂, with some being stimulated more than others.

8.            Elevated C0₂ increases water-use efficiency in some species.

9.            Elevated C0₂ stimulates growth in some ocean plants (e.g., phytoplankton), while other species, such as corals, may be destroyed or depleted.

10.            Ocean acidification may dissolve shells, corals, and other structures built of calcium carbonate, though some phytoplankton can apparently overcome any dissolving of their calcium carbonate structures by increased photosynthesis.

11.            Overall, ecosystems will respond to climate change by modifications ranging from slight to great, but they certainly will adapt.

In the course of researching ocean acidification, I learned of a recent report** on ocean warming.  It is proving to be very controversial, and may be wrong, but then again, it may be right.  And it does present some anomalies—like most everything else in science.  Here is the critical graph from the paper:

The lefthand side of the graph is a measure of heat, so what we have is a historical view of ocean temperatures from 1960 through 2008.

What the scientists found is that since the late 1970’s, the ocean has been getting warmer as far down as 700 meters, with the warming trend punctuated by periodic cooling caused by volcanic eruptions and a significant heat spike in the late 1980s caused by an El Nino event.  The authors conclude that the reason there hasn’t been any appreciable warming of the atmosphere during the last 10 years is because heat has been absorbed out of the atmosphere into the ocean.  In other words, the ocean is where the “missing heat” has gone.

When you look closely at the data, you can see that the region below 300 meters has warmed MORE than the upper 300 meters.  And this is the source of some criticism, since other scientists can’t figure out how the heat “skipped” detection in the upper ocean while showing up in the lower.   As a result, questions have been raised about the temperature-detection methods used by the researchers, as well as the manner in which the missing heat was calculated.

I certainly can’t evaluate the scientific integrity of this study, but it does seem strange that the upper layers didn’t warm first.  I wouldn’t be surprised if this data becomes a central part of the global warming debate.

A related issue regarding the ocean is, of course, rising sea levels.  Now this is a pretty easy concept as far as global warming is concerned:  ice melts, water flows into the sea, and the sea rises.  And as water heats up, it expands and the sea rises.

But actually measuring the sea level seems daunting, as anyone who has been to the beach can appreciate.  Tides, waves—these all need to be “smoothed out” or averaged.  However, sea height has been measured since 1700 in places like Amsterdam, where it is a daily concern due to the fact that 20% of the Netherlands—along with 50% of its population—is below sea level, and half of its land is less than 3 feet above sea level (most of the area below sea level is manmade after centuries of peat extraction). 

Sea heights were, and still are, measured by “tide gauges.”  Early calculations were made by measuring the height of the water relative to a specific point, such as a marking on a cliff.  Modern tide gauges (about 1750 of them around the world) do essentially the same thing using electronic sensors and small computers.   And incredibly, satellite measurements—using satellite altimetry—are so accurate that changes in sea level of only a few millimeters can be detected.

In any event, from 1870 to 2004, global sea levels rose by 195 mm or 7.7 inches, with an average rise of 1.4 millimeters per year.  And sea level rise seems to be noncontroversial, making it yet another proxy that provides evidence of global warming.  And given the melting of glaciers and the ice sheets of Greenland and Antarctica, sea levels should continue to rise—although, surprisingly, the rate of sea level rise has not accelerated along with increasing temperatures.  Perhaps inaccuracies in measurement would account for this.

So the planet is warming.  Ecosystems will change.  Cropping systems may also change, but they will adapt.  Forests will change.  Ocean fisheries may change.  New regions may become habitable.  Others may become less desirable.  Sea levels are rising.  Coastal communities will probably be affected.  Populations may be dislocated—and new phrases such as “environmental refugees”, “environmental migrants” and “climate refugees” have entered our vocabulary.

Because it is believed by most people that manmade greenhouse gases are responsible for the rise in temperatures, many proposals have been made to slow down the release of these gases into the atmosphere.  Complex international agreements have been developed allowing countries to trade “carbon credits,” while other proposals such as the Kyoto Protocol have tried to get commitments from countries to limit greenhouse gas production.  Other proposals have been made to slow down global warming, including methods to “absorb” gases or reflect sunlight from the planet.

But these proposals for limiting greenhouse gases are far beyond my expertise to review, summarize, or even comment on.  All I can really say is that limiting greenhouse gas production or increasing its absorption/sequestration will probably have a minimal impact on the temperature of the planet.  In fact, since the recent global recession has had no apparent impact on atmospheric C0₂, I’d say we have actually done an experiment of sorts—and found it to be ineffective.  It seems very unlikely that Homo sapiens will voluntarily agree to limit greenhouse gases if the cost equals or exceeds that of the recent recession.  I suspect that we will simply learn to adapt to a warming planet.

Assuming that the climate does not reverse itself and start getting cooler, that is.

Reference:

**http://onlinelibrary.wiley.com/doi/10.1002/grl.50382/abstract

CLIMATE CHANGE (part 3)

In what I THOUGHT would be the last of blogs on climate change, I’ll again start with the conclusions reached so far:

            (1) there is overwhelming evidence that the planet has been in a warming trend—at least up until the last 10 years or so;

            (2) warming trends are historically correlated with increasing levels of CO₂;

                  (3) mathematical models of future global temperatures are now predicting much less warming than previously thought;

            (4) historically, climate change has been cyclic, with small cycles within larger cycles;

            (5) how the various natural “forcings” of climate change (such as the Milankovitch cycle) will interact with increased CO₂ and other greenhouse gases is, of course, unknown.

There are three greenhouse gases of interest to us here (or at least to me!):  water vapor, methane, and C0₂.  As mentioned previously, greenhouse gases are gases that trap heat and thus warm the atmosphere.  The earth we know and love has a temperature that is “just right” because of greenhouse gases.  It is estimated that if our atmosphere did not contain greenhouse gases, the surface of the planet would be, on average, about 2F rather than the comfortable 57F it is now.

When water vapor, carbon dioxide, and methane are ranked in terms of their relative contribution to the greenhouse effect, water vapor and clouds account for 36-72%, carbon dioxide 9-26%, and methane 4-9%.  Further, there is a feedback loop in which atmospheric water vapor increases as the planet warms and temperatures increase as water vapor increases, until some equilibrium is reached.

Now, methane and C0₂ do not have the same global warming potential because there is less methane than C0₂ in the atmosphere.  But this is counterbalanced somewhat by the fact that methane hangs around in the atmosphere for about 12 times longer than C0₂.  The residence time of a C0₂ molecule is about 3-4 years, but a methane molecule lasts about 36-48 years.

C0₂ is the most famous (or infamous) of the greenhouse gases, and I’ll spend the rest of this blog on it.  We’ve seen earlier that it fluctuates along with global temperatures, going back at least 400,000 years.  And, unless you have been living under a rock, you know that C0₂ has received most of the attention in terms of climate change because, at least in theory, humans can slow down or even reverse the warming of the planet by reducing their C0₂ output.

At the present moment, there seems to be something of a disconnect between the increasing C0₂ levels we are seeing and the “flat” global warming we’ve had for the last 10 years. This doesn’t mean that C0₂ is not influencing warming;  rather it just indicates that there is something else going on that may be “blunting” the effects of C0₂.  Does this mean the models are wrong?  Or is there something else that is causing the planet to cool?

The Fourth Assessment Report of the United Nations Intergovernmental Panel of Climate Change states that the increased warming we’ve seen since the mid 1900’s is at least 50% due to increased C0₂ levels.

And there are numerous potential effects of increasing C0₂ levels that go well beyond warming.  These include increasing plant growth; decreasing plant growth (?!); changing species mixtures; changing ecosystems, both natural and artificial (agriculture); and ocean acidification.

As mentioned above, C0₂ hangs around in the atmosphere for a relatively short period of time.  What happens to it?  It either gets absorbed by plants via photosynthesis or it gets taken up by the oceans.

The C0₂ cycle is very interesting, highly complex, and is essential to an understanding of the role of C0₂ on the planet.  There are about 800 billion tons of C0₂ in the atmosphere.  Of that 800 billion tons, about 215 billion tons are taken up by the planet each year, either by plant growth (123 billion tons) or absorption into the ocean (92 billion tons).  219 billion tons are released back into the atmosphere—60 billion tons are released by plants (through respiration), 90 billion tons are released back into the atmosphere by the ocean, and 60 billion tons are released by microbial decomposition.  And finally, humans release 9 billion tons of C0₂ into the atmosphere by burning fuel, making cement, and stirring up the soil.  So, if you do the math, this means that there are about 4 billion tons left over, and this accounts for the increasing levels of C0₂ in the atmosphere—now about 400 parts per million (ppm) compared to the estimated 280 ppm of the pre-industrial world.

Now I got the information in the last paragraph from Wikipedia.  Which presumably represents a collective opinion of scientists around the world.  But, these numbers really do beg credulity—for example, there is no scientific estimation that does not include a range of estimates that spans, for example, a 95% probability.  After all, the 9 billion tons of C0₂ produced by humans is only 1.1% of the 800 gigatonnes in the atmosphere.  That is a pretty small number to estimate correctly.  I mean, you’d think the ocean’s absorption would be estimated at 92 billion tons plus or minus at least this number. 

Further, I looked at a European study published in 2011 that compared the C0₂ production of countries around the world, and THOSE scientists said that the amount of C0₂ released by humans each year is 34 billion tons.  So what’s to be believed?

Nevertheless, C0₂ IS going up according to measuring stations around the world, and they are pretty concordant.  So I don’t think the fact that C0₂ is increasing is a matter of scientific controversy.  Additional evidence that C0₂ levels are being accurately measured is that levels of C0₂ track growing seasons.  In other words, atmospheric C0₂ levels increase during the winter months when the northern hemisphere is cold (because of decreased photosynthesis) and decrease during the summer months (because of increased photosynthesis).

However, there is one curious anomaly:  although global emissions of C0₂ dropped about 1-2% during the recent worldwide recession, there was no concomitant drop in atmospheric C0₂ levels as measured by reporting stations.  What’s the deal with that?  Perhaps a 1-2% reduction of emissions is not enough to impact atmospheric C0₂ on a global scale.  If that is true, it has a lot of ramifications vis-à-vis the use of economic mitigation for C0₂ reduction.

To change topics, it is interesting to speculate on what effect increased C0₂ will have on the planet other than warming.  We have already alluded to two of them—plant growth/ecosystem change and ocean acidification.

C0₂ is an atmospheric “fertilizer” for plant growth—it has been used for decades in commercial greenhouse operations.  Consequently, it is natural to posit that increased C0₂ will in turn increase the yield of crop plants, forests, and pastures.  Which can’t be a bad thing, right?

So, what does the data show? There have been literally hundreds of studies published on the effect of elevated C0₂ (EC) on different species of plants under varying conditions.  And the results have been, well, varying.  In general, the answer is, yes, elevated C0₂ increases crop yields and as well as woody plant growth, which occurs primarily through stimulation of photosynthesis.  Studies show that increasing current C0₂ levels by 400 ppm to 550 ppm will increase crop yields by 10-20% for C₃ plants (like wheat, rice, soybeans) and 0-10% for C₄ plants (such as corn).  Under these conditions, the above-ground biomass of trees increases from 0% -30%, with younger trees being most affected and little to no change in mature forests.

However, the results of these controlled studies will probably not be seen in nature because there are many other factors that could limit plant growth such as insect pests, lack of nutrients, and insufficient water, all of which may be augmented by increased temperatures.  For example, at 450 ppm C0_2, the yield of rain-fed wheat increased along with increased C0₂ until the temperatures increased by 0.8^oC, but decreased when temperatures increased by 1.5^oC or more.  And additional water was required to offset the increased warming.  Recent results with soybeans show similar results—increasing temperatures may negate the fertilizing effects of elevated C0₂.  However, results with tropical rice varieties show consistently higher yields with increased C0₂ and temperature. 

Only one such experiment with desert plants has been reported, and that was this year (2013).  It showed that elevated C0₂ had no effect on either above- or below-ground biomass over a 10-year period in the Mojave Desert (southern California). The authors concluded that this was probably due to low rainfall.

Further, EC may have very unexpected results, such as, for example, “undoing” the dwarfing genes of dwarf rice.  That’s right, it was shown that EC caused high-yielding dwarf rice to grow taller and fall over, thus losing the benefit of the dwarfing genes. 

For reasons in addition to the fact that I like northern Wisconsin and its forests, I’d like to talk about a 2011 report on a long-term (12-year) elevated C0₂ study of forest trees in Wisconsin—because I think there are some important lessons here.  Experimental plots of poplar, sugar maple, and birch were established with different varieties, using varieties of each species that are known to respond differently to elevated C0₂.  It was found during the LAST three years of the study that total above-ground biomass production increased 40% in 2006, 14% in 2007, and 25% in 2008.  The growth rate of some varieties of each species increased, and the growth rate of other varieties was unchanged.  This is important because  (1) it is counter to other studies finding that older trees showed no response to EC, and (2) it indicates that there is genetic variability with respect to EC response.

The latter point is very important, I believe, because the extent of genetic variability with respect to elevated C0₂ is really unknown at this point in time.  However, if we assume that genetic variability for EC is a general phenomenon (which I bet is the case because it holds for every other trait that has been examined), this means that further crop improvement in an EC world is possible.  That is, I’d be optimistic that although present day crops of wheat and soybeans, for example, may have dampened effects from EC combined with increased temperatures, varieties with favorable responses to EC and elevated temperature probably can and will be developed.

This also suggests that natural ecosystems will adapt. They will change for sure—some species will adapt and some will not. Maybe northern hardwoods will move further north into Canada.  Maybe grasslands will move to where forests now reside.  Or maybe the opposite. Certainly species compositions will alter in existing forests.  And, overall, the earth may in fact have increased productivity due to EC.  Plant breeders will just develop new varieties under different conditions in the future.

And finally, elevated C0₂ generally increases a plant’s ability to use water.  That is, EC improves the efficiency of plants to make more plant tissue. This is because when there is more C0₂ in the air, the plants can close down little pores in their leaves (called stomata) that let C0₂ in and water out—and still get all the C0₂ they need, while losing less water through transpiration.  This improvement can be quite large—increased water-use efficiencies of 30% have been observed.

Overall, this does not strike me as being a catastrophic result of elevated C0_2.

Another issue is that of “ocean acidification.”  Estimates indicate that the surface of the ocean has already become more acid.  Acidity, as measured by an index called “pH,” has gone from a value of 8.25 in 1751 to 8.14 at present.  This might not seem like much, but pH scales go from 0 to 14, where “7” is neutral.  Any value lower than 7 is “acid”, and anything above 7 is “basic.”  So at present, the ocean is basic, but it is becoming more acid.

The theory is that due to the increase in greenhouse gases in the atmosphere, lots of C0₂ (an estimated 30-40% of the C0₂ released by human activity) is being absorbed by the ocean.  And when C0₂ is dissolved in water, it makes carbonic acid (H₂C0₃).

The most obvious effect of a more acidic ocean is that the increased acid dissolves calcium carbonate (CaC0₃).  This is important because shells, coral, and the exterior structures of many sea animals are made up of CaC0₃.  A good example of an animal whose life history could be interrupted is the Coccolithophore, a tiny algae or phytoplankton covered in a thin layer of CaC0₃.   This could have catastrophic consequences for other life forms because phytoplankton are the ocean’s analogy to land plants: they are the lowest level of the food chain and serve as food for many animals that either eat them directly or eat the animals that eat them.  Entire food chains could be impacted by anything that diminishes phytoplankton populations.

So it is obvious that losing CaC0₃ in the ocean is a dangerous consequence of acidification.  A less obvious result is that as the ocean becomes more acidic, CaC0₃ itself degrades into C0₂, making for even more C0₂. 

But wait.  Oops!  It turns out that the above theory does not hold up with regard to all experimental results or field observations.  At least in some coccolithophore species.

A 2008 study showed that increasing C0₂ levels in water INCREASED calcification of at least one coccolithophore species.  Further, studies of calcification during a period 55 million years ago when C0₂ levels may have been more than 1000 ppm and temperatures were elevated 11^oF over a period of 20,000 years (the “Paleocene-Eocene Thermal Maximum”) showed NO changes in calcified nanofossils with regard to abundance or species compositions.  Nor has there been a decrease in coccolithophore species from 1800 to modern times—in fact there has been a slight increase in coccolith total mass.  So apparently C0₂ fertilization increases photosynthesis enough to allow phytoplankton to regenerate their shells rapidly enough to replace any dissolved calcium, and even increase growth.

My point here is NOT to make the case that ocean acidification does not matter.  It does, and there are many studies showing its negative effects on many organisms. My point is that different species react to their environments differently, as with the elevated C0₂ studies in land plants cited above.

I also want to make the point that elevated C0₂ and elevated temperature will not result in planetary collapse.  It may and probably will lead to changes in species and ecosystems, but nature seems to be robust in its ability to evolve, thanks to genetic diversity.  A future world may not look like the one we have now—perhaps no ice sheets, no glaciers, a rise in sea levels, increased desertification in some places, as well as displaced or relocated human populations.  And, of course, not all species may survive, at least in their present distributions—the iconic polar bear may give way to its grizzly cousin.

And new ecosystems may expand—a recent report found that tundra on Ellesmere Island “came back to life” upon retreat of the glacier that had covered it with ice for 400 years.

Don’t forget that mammals started their ascendancy during the “Paleocene-Eocene Thermal Maximum” time period—and be glad for that!

There is more to be said about global warming.  There is the issue of a rising sea level—and of course the various proposals that have been advanced to halt or reverse global warming.

More next time.

Useful references:

*http://edgar.jrc.ec.europa.eu/CO2REPORT2012.pdf

http://www.mpg.de/6650626/carbon-dioxide-crop-yields

http://onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.2004.01224.x/full

http://www.sciencedirect.com/science/article/pii/S0378429012003462

http://www.pnas.org/content/104/50/19686.long

http://www.fsl.orst.edu/~bond/fs561/references/poorter-navas-2003.pdf

http://ns.umich.edu/new/releases/8614

http://onlinelibrary.wiley.com/doi/10.1111/j.1461-0248.2011.01692.x/full

http://www.sciencemag.org/content/320/5874/336.full.pdf

http://onlinelibrary.wiley.com/doi/10.1111/gcb.12177/full