Monthly Archives: November 2013

New Solar Projects

This is great news!

The US has 43 nuclear power plants’ worth of solar energy in the pipeline

By Todd Woody @greenwombat November 25, 2013

The boom in solar energy in the US  in recent years? You haven’t seen anything yet. The pipeline of photovoltaic projects has grown 7% over the past 12 months and now stands at 2,400 solar installations that would generate 43,000 megawatts (MW), according to a report released today by market research firm NPD Solarbuzz. If all these projects are built, their peak electricity output would be equivalent to that of 43 big nuclear power plants, and enough to keep the lights on in six million American homes.

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Only 8.5% of the pipeline is currently being installed, with most of it still in the planning stages. Some projects will inevitably get canceled or fail to raise financing.

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Source: NPD Solarbuzz

But there’s reason to believe that a good chunk of these solar power plants and rooftop installations will get built over the next two years. That’s because a crucial US tax break for renewable energy projects is set to fall from 30% to 10% at the end of 2016. So there will be a rush to get projects online. In 2012, for instance, wind developers installed a record 13,131 MW as a key tax credit was set to expire, accounting for 42% of all new US electricity capacity that year.  (The US Congress subsequently renewed the tax break for another year.)

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One sign that solar developers like First Solar and SunPower are gearing up to meet the 2016 deadline is that the balance of projects is shifting to smaller installations that can quickly obtain permits and get built fast. While eight of the 10 largest photovoltaic power plants came online in 2012—those in the 100 MW to 250 MW range—over the past 12 months the number of solar projects under 30 MW has jumped by 33%, according to the report.

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Source: NPD Solarbuzz

All those projects will make the US the third largest solar market, behind China and Japan. The building boom could have another beneficial effect: The race to score subsidies could help make them unnecessary. The pell-mell growth of photovoltaic power should push prices down, to make solar electricity increasingly competitive with fossil fuels.

The author concludes that increasing installation will have a cascading impact on prices.  That is, as more solar projects are installed, prices will continue to fall.  I wonder if the increase in capacity might also cause downward pressure on oil and coal and natural gas prices?   In the mid-2000s the US got ~200-225 GW from coal (per Wikipedia), and that was around 45% of total electrical production.  So if this total is 43 GW, I would think that there might be a significant impact on US demand for coal, oil, and/or natural gas.  Which would create more competitive pressure on solar.  But still, all in all, a good thing.

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Fiscal Drag measurement

When I saw this post from Econbrowser, it made me wonder about how economists define and calculate fiscal drag:

Fiscal Drag in 2013

From Torsten Slok at Deutsche Bank:

[F]iscal drag in 2013 is 2.4%, ie if GDP growth in 2013 ends up being 1.7% then if we had not had the fiscal drag then GDP growth would instead have been 4.1% (=1.7% + 2.4%). ..

…Translated into nonfarm payrolls this means that instead of having nonfarm payrolls at 186k – the average monthly number so far for this year – then nonfarm payrolls would have been more than 400k…

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Posted by Menzie Chinn at November 27, 2013 09:00 AM

So I looked to see if I could find how Mr. Slok did it.  No luck (I really didn’t look very hard).

Then I looked for fiscal drag in general and found this post from September.  Interestingly, Rex Nutting (how come all these fiscal drag guys have such cool names??) has kind of a two part analysis of the effect of government spending on GDP, and what is fiscal drag.  One definition appears to be the net GDP contribution from government.  The second part is a comparison of the government increase compared to previous recoveries.

Today’s fiscal drag is therefore defined as the amount that government spending has not increased since the recovery started.  If that is the case, then I think it’s really a misleading kind of statistic.  Imagine that!

FRED Graph

This graph shows both total government spending and federal spending through and since the recession.  To me, this is showing exactly what Keynesians are supposed to support – spend more during recession then slow down when not a recession.  Am I missing something?  In fact, I think you are supposed to try to save when not in recession, which we are clearly not doing.

This graph shows that at the start of the recession, we started deficit spending in a big way, and although it has started to subside somewhat, maybe, it still continues at a level way beyond prior to the recession.

FRED Graph

So, what part of this is fiscal drag?  It seems like we have stabilized spending at a higher level.  Certainly not compared to GDP, that is, GDP keeps increasing, so the overall spending as a % of GDP is falling.  Same with the deficit – it is definitely going down as a % of GDP.

But who is to say that this is bad?  Or wrong policy?  Why is it called “fiscal drag”?  Why not “government savings”?

It just seems like a misleading name for something that is basically an opinion, not a fact.  And then reported with a number attached, as if it is a fact.  It should really say, “if we did it like before, we would have 2.4% higher GDP.”  Or “I wish government would spend more, because then GDP would increase more.  2.4% more.”  As if that is the only factor.

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Inflammation and Heart Disease

This post from Dr. Dwight Lundell is about the relationship between heart disease, cholesterol, and inflammation, and how statin drugs effect all three.

Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped.

Inflammation is not complicated — it is quite simply your body’s natural defence to a foreign invader such as a bacteria, toxin or virus. The cycle of inflammation is perfect in how it protects your body from these bacterial and viral invaders. However, if we chronically expose the body to injury by toxins or foods the human body was never designed to process,a condition occurs called chronic inflammation. Chronic inflammation is just as harmful as acute inflammation is beneficial.

What thoughtful person would willfully expose himself repeatedly to foods or other substances that are known to cause injury to the body?  Well,smokers perhaps, but at least they made that choice willfully.

The rest of us have simply followed the recommended mainstream dietthat is low in fat and high in polyunsaturated fats and carbohydrates, not knowing we were causing repeated injury to our blood vessels. Thisrepeated injury creates chronic inflammation leading to heart diseasestroke, diabetes and obesity.

Let me repeat that: The injury and inflammation in our blood vessels is caused by the low fat diet recommended for years by mainstream medicine.

What are the biggest culprits of chronic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, flourand all the products made from them) and the excess consumption of omega-6 vegetable oils like soybean, corn and sunflower that are found in many processed foods.

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Extra sugar molecules attach to a variety of proteins that in turn injure the blood vessel wall. This repeated injury to the blood vessel wall sets off inflammation. When you spike your blood sugar level several times a day, every day, it is exactly like taking sandpaper to the inside of your delicate blood vessels.

While you may not be able to see it, rest assured it is there. I saw it in over 5,000 surgical patients spanning 25 years who all shared one common denominator — inflammation in their arteries.

There is but one answer to quieting inflammation, and that is returning to foods closer to their natural state. To build muscle, eat more protein. Choose carbohydrates that are very complex such as colorful fruits and vegetables. Cut down on or eliminate inflammation- causing omega-6 fats like corn and soybean oil and the processed foods that are made from them.

One tablespoon of corn oil contains 7,280 mg of omega-6; soybean contains 6,940 mg. Instead, use olive oil or butter from grass-fed beef.

Animal fats contain less than 20% omega-6 and are much less likely to cause inflammation than the supposedly healthy oils labelled polyunsaturated. Forget the “science” that has been drummed into your head for decades. The science that saturated fat alone causes heart disease is non-existent. The science that saturated fat raises blood cholesterol is also very weak. Since we now know that cholesterol is not the cause of heart disease, the concern about saturated fat is even more absurd today.

Who is Dr. Lundell?  Quackwatch has this blistering bio, which describes medical board disciplinary actions escalating to revocation of his license.  Honestly, reading that, it makes me think maybe he wasn’t so good at following their rules, but having been a heart surgeon for 25 years before any censure is evident, maybe that’s about the time he started making these anti-establishment noises.  I’m not convinced either way by any of this, but with the other information regarding inflammation and insulin resistance out there, Dr. Lundell’s ideas makes a lot of sense to me.

Dr. Dean Ornish also is a proponent of diet as a cure for heart disease.  This research article describes how recommended treatments are going to result in statin prescriptions of $30B per year in the US alone.  That’s a pretty strong incentive for a large group of people to get behind the drugs, even if they do not and cannot work as well as diet.  Dr. Ornish does not put forward the theory that inflammation is behind the problem like Dr. Lundell, but the bottom line is almost exactly the same:  Quit eating sugar and processed foods.

Dean Ornish has critics as well.  He is included in this congressional testimony by Dr. Timothy Gorski in 2001.  This testimony basically badmouths anyone who is not associated with the big money involved in health care.   However, the work of Dr. Ornish has been successful enough, and documented well enough, that insurance companies cover his treatment.

The part that is really obvious to me is that eating the way these guys propose is really not so outlandish.  It’s not like they are saying, eat only bacon! (and by the way that diet was enormously successful).   They are saying, eat fruits and vegetables.  Don’t eat processed foods (meaning, food that is derived by chemically altering its molecular structure).  Cook at home.  Don’t eat meat that is grown in unnatural ways (that is, eat grass fed beef and meat raised without hormones or antibiotics).  Kind of common sense stuff, really.

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PTSD Cure

So doctors have figured out how to erase bad memories, which completely cures PTSD.  I’m not sure if this is a good thing or a bad thing.  It must be good, because it would really help people who are suffering terribly and now have no recourse.  But it has an awful potential for abuse.  Jason Bourne kind of stuff.  Or even just being abused in a for profit setting, for instance, please help me, my boyfriend broke up with me and I’m traumatized.  And maybe someday they will figure out a way to do the Men in Black thing (that’s not what this article describes at all, to be fair).  But to me, the biggest potential for abuse is in the military.  Right now, there is a strong incentive for the military to minimize PTSD and the situations that cause it.  Certainly, the nature of the military will always result in some exposure to traumatic stress.  However, even knowing nothing about the military, I’m pretty confident that planning can increase or decrease the number of people exposed and the amount of exposure.  And then it becomes a matter of expediency and immediate cost.  How much time, how many people, how long is the recovery, and how does it impact the military mission.

How to Erase Bad Memories

By R. Douglas Fields | November 25, 2013 |
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I’ll never forget it. They strapped electrodes to my wrist, cranked up a black dial on a frightening electronic device encrusted with switches and knobs, and shocked me repeatedly with jolts of electricity. No, this was not torture and the memory is not a traumatic one. I was inside the laboratory of Dr. Daniela Schiller, a psychologist at Mt. Sinai Medical School in New York City, experiencing the same treatment that she and her coworkers used to discover a new way to alter traumatic memories. The latest research from her team provides a method to blot out traumatic memories that are stored in a part of the brain called the amygdala, not just suppress them as current treatments for PTSD do, but to alter the memory itself.

Just as the participants in this study did, I watched a computer screen while my right wrist was wired up to an electrical stimulator to deliver a painful shock. A second set of sensing electrodes, two black Velcro strips with wires attached, were strapped like rings around the pads of two fingertips on my left hand. These sensed the amount of nervous perspiration I produced. Sweaty palms are an involuntary reaction to threat; part of the body’s fight-or-flight response that braces the mind and body to defend against an attacker or flee to safety. The heart pounds, stomach churns, muscles twitch with adrenalin-fueled energy, sweat beads up on our forehead and mental focus sharpens to rev up all systems in the body to survive a potentially deadly danger.

These are the bodily sensations of fear, and they are the same reactions in people suffering panic attacks and other anxiety disorders. Fear is a life-saving rapid response, but in some people with anxiety disorders or PTSD, the overwhelming fear becomes debilitating. The problem inside the brain is that panic is triggered inappropriately by stimuli that are unrelated to real threats. Terror can grip them without warning, sometimes crippling their lives. Sleep may become impossible. Others may fear venturing outside or cannot fly in a plane. A military veteran may panic suddenly upon hearing a sound connected in their memory to a past trauma.

New research published this week in the Proceedings of the National Academy of Sciences reports a new discovery of how the brain records and regulates threatening memories. To understand this new finding, it is helpful to know more about threat memories and how PTSD, panic attacks, and other anxiety disorders are treated currently.

Treating anxiety disorders

Current behavioral therapy for treating anxiety disorders utilizes exposure therapy. This is based on animal research in which a painful stimulus becomes associated with another stimulus that is not in itself dangerous. For example, if a rat hears the sound of a bell and then receives a mild electrical shock, it will quickly learn that the bell heralds a nasty jolt of pain to follow. Sound the bell again and the rat freezes in fear even if you do not shock it. This conditioned fear response is how many of us learned as children not to stick hairpins into an electric outlet or play with matches.

Eventually we lost our fear of matchboxes and electric outlets after many subsequent experiences with them that were harmless. This is how exposure therapy works. A soldier who survived a harrowing roadside bombing in Afghanistan might develop extreme anxiety about driving a car. Therapists may treat this disabling fear by having the person drive in a safe environment repeatedly until the terror of the bombing connected in his memory with driving gradually subsides. This can be helpful, but frequently exposure therapy is not effective.

“Some of the bravest people I know are people with PTSD,” Schiller told me as I sat wired up to her experimental apparatus, because unlike individuals who may indeed be fearless, people with PTSD courageously cope with ceaseless terror and persevere in their daily lives.

Rather than suppress the fear, it would be better to break the connection in memory between the bombing incident and the normal experience of riding in a car.

“That memory can change is a natural process that is occurring every day of our lives. We pretty much create a false memory on a daily basis,” Schiller says. So rather than suppress the fear, the scientists set out to change the conditioned fear response recorded inside the brain.

Memory track overdub

Scientists have learned a great deal about how memories are recorded and how emotional memories are suppressed. A paired structure deep inside the brain called the amygdala is an important focus of activity for threat detection, learning, and controlling the body’s emotional and physiological response to danger. The prefrontal cortex, just behind the forehead, can inhibit neural activity in the amygdala and suppress its reaction to a threatening experience. This circuitry from the prefrontal cortex is how exposure therapy suppresses anxiety and fear.

Neuroscientists have also recently learned that when a specific memory is recalled, it becomes vulnerable for a certain window of time to being altered or even eliminated. Recalling a memory is something like pulling a book off the library shelf for review. The book is now subject to alteration or destruction, and it must be placed back in the proper place on the shelf. Disrupt a person’s attention in the middle of browsing, and the book can be easily misfiled. The process of reshelving a memory immediately after it is recalled is called reconsolidation, and research has uncovered the details of how this works down to the specific molecules in synapses that encode information.

Reconsolidation may sound odd, but it does make sense when one considers what memories are for in the first place. Fundamentally, memories allow us to use past experience to direct our behavior appropriately in the future. This means that memories need to be updated, because things change. Your memory of Obama has certainly changed since the first time you heard the name, for example. The memory has become richer, linked with many other experiences, and separated from others that are no longer relevant and forgotten.

“In principle, reconsolidation suggests that in order to change memories one must first retrieve them,” Schiller explains. She deduced that rather than trying to suppress the person’s fearful response to driving, for example, by repeated experiences driving in a safe environment, one might break the terrorizing connection between the traumatic memory of the roadside bombing and the normal experience of being inside an automobile. If the traumatic memory is recalled, it should become especially sensitive to being extinguished. The electrodes on my wrist were how Schiller and her team set out to test the idea.

A blue square flashed on the computer screen. Shortly thereafter a purple square appeared followed by a painful jolt of electricity that made my fingers clench automatically. Ouch! Meanwhile signals from the electrodes testing the perspiration on my fingers traced out a graph on a computer monitor that the scientists were watching. The trace being graphed out in real time shot up the instant I was shocked. Pain triggered my body’s flight-or-flight response.

The next time the purple box appeared on the screen the trace showing my perspiration level spiked again–even before I was shocked. My amygdala had already learned to associate the purple square with the shock. Seeing the purple square tripped my body’s fight-or-flight response just like driving would do for the veteran with PTSD. In contrast, the blue square appearing repeatedly on the screen caused no rise in my perspiration or anxiety. That blue square was safe. Subjects in these experiments will show the same automatic anxiety reaction to the purple square when tested days later.

Now if the scientists began to flash the purple square over and over again without giving the shock, the stress response to the purple square will diminish with time. This is because the prefrontal cortex has learned that bad things don’t always happen every time one sees the purple square, and it sends inhibitory signals to the amygdala to suppress its threat response. Schiller and colleagues, including neurobiologist Joseph LeDoux of New York University, were able to see this happening by having the subjects participate in these experiments while inside an fMRI brain scanner. They saw that the prefrontal cortex was becoming active in addition to the amygdala during extinction, and the functional connections between it and the amygdala were growing stronger. However, when these subjects were tested a day later, the fingertip stress monitor showed that seeing the purple square often triggered the treat and fear reaction again. Exposure therapy helped, but the feared connection between the purple square and an electric shock was still recorded in memory inside the amygdala.

 

A new approach–recall and revise

Next the team tested whether the mechanism of reconsolidation could be exploited to break the connection between the purple square and the electrical shock. To do this, they simply reminded the person of this connection by flashing the purple square on the screen and delivering the shock. Then they followed up immediately with exposure therapy (flashing the square repeatedly without an electric shock). Doing this proved to be far more effective in reducing the stress response to the purple square than if they had used extinction therapy without first reminding the participants of the threat. By monitoring changes in the brain’s activity using an fMRI they could see how this was working inside neural circuits.

Two things could explain why extinction therapy during the reconsolidation period is more effective. It could be that the prefrontal cortex was strongly inhibiting the memory of threat connected to the purple square, or alternatively, the connection between the purple square and the painful shock stored in the amygdala could be diminished. The fMRI showed that the prefrontal lobes did not become activated when the purple square was flashed in people given extinction therapy during the period of memory reconsolidation. In essence the brain (amygdala) had forgotten the connection between the electric shock and the purple square, because the prefrontal cortex was not being activated to inhibit the threat memory. (To be precise, the experiments used various necessary controls that involved three colored squares, one that was used for extinction therapy and one that was used for extinction during the memory reconsolidation period, so that they could compare the efficacy of each approach in each individual.)

To put this new laboratory finding into a real-life scenario, imagine that you are bullied at the school bus stop by neighborhood thugs John and his delinquent brother Greg. Their sister Betty never bothers you, but every time you see John or Greg you become anxious and fearful. If days go by without either brother bothering you, your body’s threat response will gradually subside, but you haven’t forgotten that they are potential threats. An fMRI of your brain would show that your prefrontal cortex was suppressing the threat response in your amygdala from John or Greg attacking you in the past. This is how extinction operates at the level of neural networks.

One morning, John bullies you again when you arrive at the bus stop, but immediately after he reverses his behavior and is friendly toward you. Then days go by without any harassment from either brother. The next time you see John and Greg, what happens? Your body does not react in fear to the sight of John, but when Greg approaches your heart races.

An fMRI would show that there is less neural activity between your prefrontal cortex and amygdala when you see John than when you see Greg. In fact, your body’s defensive response when seeing John is no different from that provoked by seeing Betty. The explanation is that the recent bullying by John forced you to recall the memory of him as a bully, and doing that made the memory subject to being changed. When John began to behave in a friendly manner toward you while the recent bullying incident was being reshelved in your memory, the original conditioned reflex that connected him with a threat was modified by the new experience.

In contrast, your memory of Greg as an aggressor had not been recalled so the conditioned response to him recorded in your amygdala remained intact. Your fear response to seeing Greg in several subsequent friendly encounters was suppressed by the increased activity in your prefrontal cortex inhibiting the fear memory in your amygdala, but your prefrontal cortex did not intervene to suppress the fearful response to seeing John. The research shows that the process of extinction works far better if the traumatic memory is first recalled rather than extinction therapy given at any other time.

This fictional scenario conveys the gist of the new findings; how this might actually play out in real life goes well beyond the controlled findings in the laboratory experiments and several other factors would enter the mix and likely affect the outcome. The important concept is that extinction therapy works better if applied right after recalling the traumatic memory rather than if it is applied at other times, and that there is a critical window of opportunity to modify a memory during the brief period when it is being reconsolidated.

“We hope that the reconsolidation window would prove useful for treating PTSD,” Schiller says. “This would require some modifications in current therapy to specifically target this phase of memory.”

Professor of Neurobiology at the Weizmann Institute in Israel, Yadin Dudai, who was not involved in the study, agrees with Schiller that these new findings are a promising beginning for developing new treatments in the future, but more research is needed.

“In real life, PTSD is very persistent, it involves a very dense web of associations and lingers or even becomes intensified over years and decades,” Dudai explains. “Incidentally, I had a conversation last week with a colleague who experienced trauma in combat 40 years ago. This still haunts him at nights.”

People wishing for better therapies for anxiety disorders should welcome this new research but it is important not to overstate the new scientific understanding in terms of immediate new therapies. “We learn a lot from these studies on how elementary building blocks of memories are retained and updated, but we have to be careful in invoking excessive hope prematurely that results from models, as important as they are, will quickly translate into treatment,” Dudai says.

Nevertheless, new information about how connections from the prefrontal cortex to the amygdala operate in overcoming fears that are conditioned by experience, provides some interesting insights into why some people may be more likely to develop anxiety disorders or PTSD than others. These brain connections may be stronger in some people than in others.

Commenting on this new research, psychologist BJ Casey, Director of the Sackler Institute at Weill Cornell Medical College, (who was not involved in the study), says “These findings are very exciting and have important implications for novel evidence-based treatments of not only PTSD, but other forms of anxiety and stress related disorders such as phobias.” Drawing parallels to her own research on adolescents, she sees some interesting implications, because the prefrontal cortex is not fully developed in adolescents. Thus adolescents may not be able to suppress threat responses in the amygdala as effectively as in adults.

“We have previously shown diminished extinction learning in adolescents due to the maturational changes in the prefrontal cortex,” Casy says. The new findings using extinction therapy during the reconsolidation period could be especially effective in treating adolescent anxiety because it bypasses the need for regulation of emotional responses from the prefrontal cortex.

Despite the important value of this memory research in treating anxiety disorders, some may find the fact that scientists can change memories disconcerting. Dudai agrees, but observes: “Any development of a potential therapeutic tool is accompanied by justified concerns. Even swallowing Tylenol may be harmful.”

Schiller understands the concern too, but agrees with Dudai. “Like any finding in science, this finding can be misused, but it is our social responsibility to find treatments for PTSD, especially when putting soldiers and Special Forces at risk.”

As I watched my brain and body respond automatically to the threatening squares, I was astonished by how robotic at all seemed. There was nothing I could do to control it. I felt some sense of what it must be like for people living with anxiety disorders that overwhelm them suddenly in ways that are entirely beyond their ability to control. As researchers uncover how our brain encodes memory, updates it, and they trace the neurocircuitry that connects emotional fear and threat reactions to specific triggers, we are coming closer to developing better therapies that are based on neuroscience to overcome phobias and anxieties, and break the cycle of reliving horrific post-traumatic terrors.

Reference:

Schiller, D., et al., Extinction during reconsolidation of threat memory diminishes prefrontal cortex involvement. Proc. Natl. Acad. Science, USA, on-line in advance of print, doi/10.1073/pnas.1320322110.

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Total Bond Market

Everybody posts about QE all the time, but this one has some real data about the bond market from both sides.  Good information, thank you Felix Salmon.

The government-dominated bond market

By Felix Salmon
November 22, 2013

JP Morgan’s Nikolaos Panigirtzoglou put a fascinating report out last week, looking at supply and demand in the global bond market in 2014. And although I consider myself something of a bond nerd, I was genuinely astonished by some of the charts he put together, starting with this one:

demand2.png

This chart alone suffices to explain why the markets care so much about the taper: central-bank buying accounts for $1.6 trillion — more than half — of the total demand for bonds in 2013. Meanwhile, private banks are taking the opposite side of the trade: while they were huge buyers of bonds in 2007 and 2008, they’re net sellers in 2013 and 2014, more or less completely negating the buying pressure from pension funds, insurance companies, bond funds, and retail investors. In 2014, it seems, substantially all the net demand for bonds is going to come from the official sector. So it matters a great deal when that demand is diminished.

What’s more, central-bank buying, overwhelmingly from the Fed and the Bank of Japan, accounts for the lion’s share of official-sector buying: sovereign wealth funds and other foreign official institutions will buy just $364 billion of bonds this year, according to JP Morgan’s estimates, down from $678 billion last year. So the heavy lifting is still going to have to be conducted by QE operations, in the face of a taper which JP Morgan estimates at $500 billion over the course of the year. (The assumption is that it starts in January, and is completed by September.) Between the taper and other sources of diminished demand, total bond-buying firepower is likely to be $750 billion smaller in 2014 than it was in 2013. Bad news, for bonds, right?

Not so fast! It turns out that even as demand for bonds is shrinking, the supply of new bonds is shrinking just as fast:

Screen Shot 2013-11-22 at 4.45.23 PM.png

Again, this chart surprised me: I knew that government debt was a very important part of the total bond market, but I wouldn’t have guessed how important it was — or how fast it is shrinking.

Panigirtzoglou puts the two charts together, and you end up with this result:

In total we expect bond supply to decline by $600bn in 2014 to $1.8tr, more than offsetting the $500bn decline in bond demand due to Fed tapering. The balance between supply and demand, i.e. excess supply, looks set to widen from $140bn in 2013 to $280bn in 2014.

That number has pretty large error bars: you could pretty much cover the entire thing just by delaying the taper for three months. So let’s not worry too much about the difference between the two estimates, here. Instead, step back and look at the big picture, which is pretty simple: as a stylized fact, the bond market is dominated on both sides by the official sector. Private participants might sit in the middle as market-makers, or try to borrow money here or there, but overall what you’re looking at, when you look at the bond market, is government issuing debt and governments buying it.

The good news is that this large transfer of money from the official sector’s left hand to its right hand is slowing down, but that’s going to take a while. In any case, there doesn’t seem to be any conceivable way that the private sector could possibly be able to fund the still-substantial government deficits which have been bequeathed to us by the financial crisis. As a result, I suspect that QE is likely going to be around for a while, just as a matter of mathematical necessity. The world’s national deficits can’t get funded any other way.

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Autism

What a great idea, to write this book:

Link here

Book review: Meet one person with autism

William Mandy

15 November 2013

The autism described in The Reason I Jump is quite different from the mostly social disorder that I, as a researcher and clinician, find in textbooks and journal articles.

The new bestselling book, featuring the remarkable testimony of a Japanese boy who has severe autism, is a surprising and engaging memoir that’s full of paradoxes.

Foremost amongst these is the book’s genesis: Even though it suggests a sense of direct, immediate access to the thoughts and ideas of the author, 13-year-old Naoki Higashida, the prose for the book was in fact created by a sequence of processes involving several collaborators.

Higashida finds spoken communication all but impossible, but has learned to express himself by pointing to Japanese hiragana letters printed on a piece of card in order to spell out words. In this manner, he meticulously wrote the book over the course of months with his mother as scribe.

The book then came to the attention of a married couple, who were perhaps uniquely qualified to make it accessible to English speakers: the renowned novelist David Mitchell (author of Cloud Atlas) and his Japanese wife K.A. Yoshida, who have a son with autism. Mitchell and Yoshida translated Higashida’s work for an international audience.

The result is a slim volume whose lucid prose has caused me to reconsider some of the most basic ideas I have about autism.

Over a hundred or so pages of question-and-answer, Higashida displays an originality of thought and poetry of expression that eludes most writers, let alone most 13-year-old boys. For example, when answering “Why do you ignore us when we’re talking to you?” he writes: “A person who’s looking at a mountain far away doesn’t notice the prettiness of a dandelion in front of them. A person who’s looking at a dandelion in front of them doesn’t see the beauty of a mountain far away.”

Further, the level of empathy and emotional insight this teenager displays will surprise many readers, and certainly anyone who has studied autism. The conventional wisdom holds that the disorder, at its heart, is a social disorder, in which the capacity for understanding the thoughts and emotions of others is badly impaired.

Locked in:

Higashida’s account blows this conception out of the water.

He regularly conveys a sense that he understands the reader may have a perspective that is different from his own, and shows extraordinary skill in knowing what that perspective is and in trying to change it. He describes experiencing emotions that rely on social awareness, such as embarrassment and envy; he loves to be with other people; and above all he feels terrible when he thinks he has caused upset or pain for others.

Higashida reveals some of this heartbreaking meta-awareness when describing why he seems to ignore people when they’re talking to him.

Even though I feel guilty toward the person who has spoken to me, I can’t even apologize, so I end up feeling miserable and ashamed that I can’t manage a proper human relationship.

Higashida gives an account of a sort of ‘locked-in’ syndrome, in which he is a person just like anyone else, but has become the victim of a body and mind that he cannot control — “as if my whole body, except for my soul, feels as if it belongs to somebody else and I have zero control over it.”

In this way, his book sometimes evokes an appalling sense of claustrophobia, as if it is a communication painstakingly tapped out in Morse code from within a solitary prison cell. As Mitchell points out in his introduction to the book, Higashida’s social difficulties are not core symptoms of his autism, but rather one of its indirect consequences.

Whatever outward appearances may suggest, this book argues that people with severe autism are not so different from anyone else. Crucially, we are reminded that they are just as sensitive to the reactions of others, and have the same need to be understood and treated with kindness and respect, as the rest of us.

However, at other times, Higashida’s account suggests profound differences between the daily experience of people with and without autism. In particular, he appears to know little distinction between the passing of a day and of a second: “Inside my head there really isn’t much difference between what I was told just now, and what I heard a long, long time ago.”

To my knowledge, scientists have shown no interest in the felt experience of time in autism, and this would seem to be a fundamental feature of the disorder that requires further investigation.

Jumping forward:

But what do we do with these revelations?

The idea that Higashida’s description of his life could suggest a topic for empirical investigation raises the broader question of what we can learn from this book. In its gentle, lyrical way, The Reason I Jump is controversial, because it suggests that the current official consensus about autism is wrong.

As someone who studies autism, and tries to help people with the disorder, I was left wondering how much I should be influenced by this book: Should I continue to trust mainstream opinions, based on clinical wisdom and findings from scientific investigations? Or should I ignore the so-called experts, and be guided instead by this authentic voice of experience?

To grapple with these questions is to ask about how we can know things, and whether some routes to knowledge should be more privileged than others.

Trying to decide whether the book will teach me more than the scientific literature on autism is like asking whether I will learn more about America from reading Moby Dick or from studying reports from the U.S. Census Bureau. Both provide insights. But these insights are qualitatively different, and no universal standard sets one above the other.

In the history of autism research, however, so far there has been too much U.S. Census Bureau, and not enough Moby Dick. The Reason I Jump serves as a reminder that the voices of people with autism must play a greater role in shaping the general understanding of autism, and should be more influential in shaping clinical services and the research agenda.

Naoki Higashida is explicit about why he wrote The Reason I Jump. Speaking on behalf of people with autism he writes, “We are misunderstood, and we’d give anything if only we could be understood properly” and “I hope that, by reading this book, you might become a better friend of someone with autism.”

His book has become a popular sensation, selling out of its first hardcover run and making late-night television. I’m heartened to think of readers all over the world falling under its spell, and discovering in themselves a compassionate curiosity about the worlds of people with autism.

William Mandy is senior lecturer in clinical psychology at University College London.

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Gut microbes and body fat

First seen at Dish.  The eye catching graphics opening this post are one of my pet peeves, of course.  Correlation?  Causation?  Close enough.  Lots of confounding factors here.  Just saying.  But the links in the post are much better, and even acknowledge the correlation/causation issue in relation to these specific graphs, and discuss some of those confounding factors.

This article by Moises Velasquez-Manoff is the best one I have seen yet on our intestinal microbes.  Fascinating.  It’s a long article, but filled with all kinds of facts.  I didn’t verify any of them, and after all, it is from the internet, so who knows if this is all true, but food for thought (haha!).  Here are some highlights, but there is a lot more in the article:

Chronic, low-grade inflammation has long been recognized as a feature of metabolic syndrome, a cluster of dysfunctions that tends to precede full-blown diabetes and that also increases the risk of heart disease, stroke, certain cancers, and even dementia…

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…along with their two-sandwich, two-hash-brown, 910-calorie breakfast, one-third of his volunteers—10 in total—quaffed a glass of fresh OJ. The non-juice drinkers, half of whom drank sugar water, and the other half plain water, had the expected response—inflammation and elevated blood sugar. But the OJ drinkers had neither elevated blood sugar nor inflammation. The juice seemed to shield their metabolism. “It just switched off the whole damn thing,” Dandona says. Other scientists have since confirmed that OJ has a strong anti-inflammatory effect.

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Here’s the traditional understanding of metabolic syndrome: You ate too much refined food sopped in grease. Calories flooded your body. Usually, a hormone called insulin would help your cells absorb these calories for use. But the sheer overabundance of energy in this case overwhelms your cells. They stop responding to insulin. To compensate, your pancreas begins cranking out more insulin. When the pancreas finally collapses from exhaustion, you have diabetes. In addition, you develop resistance to another hormone called leptin, which signals satiety, or fullness. So you tend to overeat. Meanwhile, fat cells, which have become bloated and stressed as they try to store the excess calories, begin emitting a danger signal—low-grade inflammation.

But new research suggest another scenario: Inflammation might not be a symptom, it could be a cause. According to this theory, it is the immune activation caused by lousy food that prompts insulin and leptin resistance. Sugar builds up in your blood. Insulin increases. Your liver and pancreas strain to keep up. All because the loudly blaring danger signal—the inflammation—hampers your cells’ ability to respond to hormonal signals. Maybe the most dramatic evidence in support of this idea comes from experiments where scientists quash inflammation in animals. If you simply increase the number of white blood cells that alleviate inflammation—called regulatory T-cells—in obese mice with metabolic syndrome, the whole syndrome fades away. Deal with the inflammation, it seems, and you halt the dysfunction.

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A DECADE AGO, microbiologists at Washington University in St. Louis noticed that mice raised without any microbes, in plastic bubbles with positive air pressure, could gorge on food without developing metabolic syndrome [15] or growing obese. But when colonized with their native microbes, these mice quickly became insulin resistant and grew fat, all while eating less food than their germ-free counterparts.

The researchers surmised that the microbes helped the rodents harvest energy from food. The mice, which then had more calories than they needed, stored the surplus as fat. But across the Atlantic, Patrice Cani [16] at the Catholic University of Louvain in Brussels, Belgium, suspected that inflammation contributed, and that the inflammation emanated from native microbes.

To prove the principle, he gave mice a low dose of endotoxin [17], that molecule that resides in the outer walls of certain bacteria. The mice’s livers became insulin resistant; the mice became obese and developed diabetes. A high-fat diet alone produced the same result: Endotoxin leaked into circulation; inflammation took hold; the mice grew fat and diabetic. Then came the bombshell. The mere addition of soluble plant fibers [18] called oligosaccharides, found in things like bananas, garlic, and asparagus, prevented the entire cascade—no endotoxin, no inflammation, and no diabetes.

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Oligosaccharides are one form of what’s known as a “prebiotic”: fibers that, because they make it all the way to the colon intact, feed, as it were, the bacteria that live there. One reason we’ve evolved to house microbes at all is because they “digest” these fibers by fermenting them, breaking them down and allowing us to utilize their healthful byproducts, like acetic acid, butyric acid, B vitamins, and vitamin K.

Cani had essentially arrived at the same place as Dandona with his freshly squeezed orange juice

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Then one day in 2008, a morbidly obese man walked into Zhao’s lab in China [19]. The 26-year-old was diabetic, inflamed, had high bad cholesterol, and elevated blood sugar. No one in his immediate family was heavy, but he weighed 385 pounds.

Zhao noticed something odd about the man’s microbes. Thirty-five percent belonged to a single, endotoxin-producing species called Enterobacter cloacae. So he put the man on a version of his own regimen—whole grains supplemented with other prebiotics. As treatment progressed, the Enterobacter cloacae declined, as did circulating endotoxin and markers of inflammation.

After 23 weeks, the man had lost 113 pounds. That bacterial bloom had receded to the point of being undetectable. Counts of anti-inflammatory bacteria—microbes that specialize in fermenting nondigestible fibers—had increased. But could Zhao prove that these microbial changes caused anything? After all, the regimen may have simply contained far fewer calories than the patient’s previous diet.

So Zhao introduced the Enterobacter into mice. They developed endotoxemia, fattened up and became diabetic—but only when eating a high fat diet. Mice colonized with bifidobacteria and fed a high fat diet, meanwhile, remained lean, as did germ-free mice. The enterobacter was evidently unique, an opportunist. Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man.

Zhao, who related his own story to Science [20] last year, has repeated a version of this regimen in at least 90 subjects, achieved similar improvements, and has more than 1,000 patients in ongoing trials.

 

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