Bill Gates recently purchased the rights to a series of lectures by renowned physicist and teacher Richard Feynman. Feynman was a nobel winner for and essentially the father of the field of quantum electrodynamics, and also did a lot of work on superfluidity of liquid helium. The breadth of his contributions has to mark him as one of the top physicists of all time, possibly top-five, certainly top-ten.
Feynman proves the adage that it is not science that is staid and boring, but rather scientists are staid and boring. Anyone who has written journal publications will know what I'm talking about here.
Project Tuva: The Messanger Series
You will need to download and install (Firefox users: manual installation) a Microsoft plug-in to view them but they are really a great resource. In short, they are a perfect way for someone who has only a cursory understanding of science and wants to know more, yet doesn't know where to start. For experts, they are still useful to get your mind out of the minor details that dominate scientific discourse today and thinking about the big picture once again.
My favourite lecture by far is #6 on the dual wave-particle nature of fundamental particles like photons and electrons. This lecture is very close to one of my thesis topics, on the double slit experiment. Interestingly, around thirty minutes in Feynman becomes partially incorrect as he talks about the coherent and incoherent modes as in reality, there is only partial coherence.
Har har har... (you have to be a physicist).
For very small angle scattering, i.e. ΔE/Eo is very small, the interference is less but still present. To put numbers on these, we're talking about ΔE=1-20 eV energy loss compared to Eo=300,000 eV in the denominator, or angles less than 0.004 °.
26 August 2009
22 July 2009
Vacation
I'm going to Richmond, VA for a conference followed by vacation in Ottawa, ON until the 7th of August. I might crank out a post in the in-term, although I wouldn't bet on it.
Toodles.
Toodles.
29 June 2009
Ontario Cancels New Nuclear Power Plant Plans
Via Karen Howlett at The Globe and Mail, we learn that Ontario has suspended its plans to build some new nuclear power plants. The leading bid was from AECL. There have been rumblings that Atomic Energy Canada Ltd., which is a crown corporation, may be privatized by the federal government. This sort of leaking about the corporation's future probably isn't helping them land any sales. I suspect part of these funds will (have to) be restored to refurbish the existing reactors since they are going to need it to continue operating in the future. Ontario is about 50 % nuke powered; the only other nuclear plant in Canada is located in New Brunswick.
My long-standing belief is that civilization will need to build another generation of nuclear power plants to supply base-load electrical power. I've also long felt that nuclear power is more expensive, notwithstanding subsidies, than renewable sources like solar or wind will become. Initially the renewables will have to be backed by hydro where available, and natural gas everywhere else. This will eventually result in a big arbitrage opportunity for anyone who can buy cheap wind or solar power and resell it in the future, i.e. electricity storage, and make money on the margin. However, very few large thermal power plants are getting built anymore in North America or Europe, whether they be nuclear or coal powered. The experience of nations like Finland with new nuclear is not comforting.
Not replacing base-load power on schedule will accelerate the take-over of solar, wind, and natural gas but probably also result in some expensive power bills as supply and demand breaks into this natural monopoly. Using natural gas for base-load isn't the wisest use for what should be our future long-distance transport fuel, IMO.
My long-standing belief is that civilization will need to build another generation of nuclear power plants to supply base-load electrical power. I've also long felt that nuclear power is more expensive, notwithstanding subsidies, than renewable sources like solar or wind will become. Initially the renewables will have to be backed by hydro where available, and natural gas everywhere else. This will eventually result in a big arbitrage opportunity for anyone who can buy cheap wind or solar power and resell it in the future, i.e. electricity storage, and make money on the margin. However, very few large thermal power plants are getting built anymore in North America or Europe, whether they be nuclear or coal powered. The experience of nations like Finland with new nuclear is not comforting.
Not replacing base-load power on schedule will accelerate the take-over of solar, wind, and natural gas but probably also result in some expensive power bills as supply and demand breaks into this natural monopoly. Using natural gas for base-load isn't the wisest use for what should be our future long-distance transport fuel, IMO.
14 May 2009
White, Organic LEDs Achieving New Efficiency Levels
From the journal Nature, Reineke et al. (2009) report that they have successfully developed an organic, 'white'-light LED with superior efficiency to that of fluorescent tubes. They achieved efficiencies around 90 lumens/Watt, compared to fluroscent tubes at 70 lumens/Watt. In fact, if one is willing to accept less intense lighting, they were pushing 120 lumens/Watt.
Organic LEDs are more efficient when made in thinner layers, but this limits the total amount of light they can produce per unit area. So while you could technically paper the entire ceiling with them, as a manufacturer you wouldn't want to because the substrate costs money and so does shipping.
This report is really fascinating in terms of all the optical design elements they are incorporating to prevent wastage of electrons and photons. Or, at least, it is to me. Basically in order to get a material to emit light you have to have a bunch of energetic electrons. You have them decay/lose energy. One possible way to lose energy is in the form of a photon (i.e. light), but you could also shed energy as heat or just spread it out to other electrons (particularly if there are defects in the material). Or you could successfully emit the photon but it will just get trapped and absorbed by the LED before it gets into the air. For organic LEDs, photons being reabsorbed is the biggest problem.
The question-mark with organic LEDs remains lifetime, particularly for the blue wavelength versions. The ones discussed in this article only last a couple of hours. This was still the case when I first learned about them five years ago. Basically, they don't react well to oxygen.
Organic LEDs are not necessarily any better than conventional, semiconductor LEDs. They are being pursued because they are potentially very cheap and have the novelty of flexibility.
Night Lighting
The strategy behind efficiency in lighting is not simply in producing the most photons per Watt of applied power, but matching the emission spectrum to that of the human eye. The unit for this is the lumen, which is the perceived brightness.
Figure 1: Sensitivity of the human eye as a function of wavelength.
The objectives for day-vision, known as phototopic, and night-vision, known as scotopic, are not quite the same. Night-vision is actually more efficient, and it peaks at a wavelength of 507 nm, which is squarely in the green part of the colour spectrum. For reference, 450 nm is the centre of the blue spectrum and 630 nm would be red.
Of interest here is the use of yellow Sodium-vapour street lamps. Low-pressure sodium lamps are highly efficient in turning electricity into light, on the order of 50-80 %. However, the human eye is not very good at detecting the yellow light (589 nm) when using the rods in the eye for night-vision. As can be seen from Figure 1, night-vision is actually piss-poor at using yellow light so when driving or walking under street-lamps, you are actually using your day vision.
Table 1: Eye efficiency as a function of wavelength.
Compared to yellow sodium street lamps, a green LED could be potentially 3-times less efficient and still beat it in lumens per Watt. Of course, this isn't sufficient for driving. Depth perception requires phototopic vision, since the cones are concentrated at the centre of vision whereas night-vision is predominately peripheral. For walking paths and other applications, green LED lighting could potentially beat the pants off of sodium lamps. The ideal case would probably be a 507 nm LED with a phosphor that emits light at a longer, redder wavelength. Then both scotopic and photopic vision could be covered. Or you could just build an array that emits two wavelengths of light. In this case, the need for a blue wavelength is not quite so necessary.
Organic LEDs are more efficient when made in thinner layers, but this limits the total amount of light they can produce per unit area. So while you could technically paper the entire ceiling with them, as a manufacturer you wouldn't want to because the substrate costs money and so does shipping.
This report is really fascinating in terms of all the optical design elements they are incorporating to prevent wastage of electrons and photons. Or, at least, it is to me. Basically in order to get a material to emit light you have to have a bunch of energetic electrons. You have them decay/lose energy. One possible way to lose energy is in the form of a photon (i.e. light), but you could also shed energy as heat or just spread it out to other electrons (particularly if there are defects in the material). Or you could successfully emit the photon but it will just get trapped and absorbed by the LED before it gets into the air. For organic LEDs, photons being reabsorbed is the biggest problem.
The question-mark with organic LEDs remains lifetime, particularly for the blue wavelength versions. The ones discussed in this article only last a couple of hours. This was still the case when I first learned about them five years ago. Basically, they don't react well to oxygen.
Organic LEDs are not necessarily any better than conventional, semiconductor LEDs. They are being pursued because they are potentially very cheap and have the novelty of flexibility.
Night Lighting
The strategy behind efficiency in lighting is not simply in producing the most photons per Watt of applied power, but matching the emission spectrum to that of the human eye. The unit for this is the lumen, which is the perceived brightness.
Figure 1: Sensitivity of the human eye as a function of wavelength.Of interest here is the use of yellow Sodium-vapour street lamps. Low-pressure sodium lamps are highly efficient in turning electricity into light, on the order of 50-80 %. However, the human eye is not very good at detecting the yellow light (589 nm) when using the rods in the eye for night-vision. As can be seen from Figure 1, night-vision is actually piss-poor at using yellow light so when driving or walking under street-lamps, you are actually using your day vision.
Table 1: Eye efficiency as a function of wavelength.
| Wavelength (nm) | Photopic Efficiency (lum/W) | Scotopic Efficiency (lum/W) |
| 470 (blue) | 62 | 1150 |
| 507 (green) | 303 | 1700 |
| 555 (green) | 683 | 683 |
| 589 (yellow) | 517 | 111 |
Compared to yellow sodium street lamps, a green LED could be potentially 3-times less efficient and still beat it in lumens per Watt. Of course, this isn't sufficient for driving. Depth perception requires phototopic vision, since the cones are concentrated at the centre of vision whereas night-vision is predominately peripheral. For walking paths and other applications, green LED lighting could potentially beat the pants off of sodium lamps. The ideal case would probably be a 507 nm LED with a phosphor that emits light at a longer, redder wavelength. Then both scotopic and photopic vision could be covered. Or you could just build an array that emits two wavelengths of light. In this case, the need for a blue wavelength is not quite so necessary.
07 May 2009
Vibram Five-Fingers KSO Review
So I purchased a shiny (err.. matte black) new pair of Vibram Five-finger KSOs (Keep Stuff Out) last Wednesday. I tried on the Sprint as well, which pinched my right Achilles tendon.
Note that if your feet lie in the overlap region of men's and women's shoes you can fit the shoes in 1/4" rather than 1/2" intervals, with the women's being effectively 1.5 sizes smaller than a men's. I think that fit-wise, you should gage it by pulling back on the grab-loop on the back tense. Aim for 1/2" seperation between your heel and that of the slipper.
Compared to the Sprint, the KSO has a mesh upper which is supposed to keep debris from getting in and underneath the feet. The only debris I got in mine was stuff that was already stuck to my foot when I put them on. The suspension of the KSO is sort of a pulley system that attaches at the heel, comes forward and turn to pass over the top of the foot, where it attaches with velcro. The KSO (and Flow) appears to be built on a slightly wider rand than the Sprint or Classics.
The soles are remarkably sticky. There is a waffle pattern cut into the ball and heel that probably increases the friction, particularly on pavement or other flat surfaces. Running in them is not quite the same as barefoot but the degree of protection is very good. You feel everything you're running on, and sometimes things hurt a bit but only for a second and there's no lasting pain. Like barefoot, you have to watch where you place your feet, but you have considerably more insurance whenever you make a mistake, so you can run briskly. Running on a gravel track wasn't possible for me, but trails and grass were both very enjoyable experiences. I think the most dangerous thing to avoid running on would be thorns, which could conceivably slip through the toe pads and into the side of your toes.
These things appear to be very popular, and I can immediately see why. I bought my slippers on Wednesday, the saleswoman said that they got their shipment in on Monday and had already sold 1/3rd of their stock. They are sort of on the level of things like Gore-tex, Marmot's DriClime base layers, or kernmantle rope in terms of game-changing the technology and utility of outdoor gear.
Initially there was some shelf in the big-toe of my right slipper that was irritating the nail. However, with time to work in the slipper (and some work with a nail clipper) I don't notice this anymore. Pro-tip: cut your toe nails before you go to fit these. I've found the best way to set the toes is to sit with your feet flat on the floor and then raise your heels while planting your toes.
The shoes are a little sweaty, although I think this may be a feature rather than a bug: when wet the Five-fingers suction onto your foot better.
With regards to the other models, the Classic, at least to my eyes, looked to be the ultimate camp shoe for backpacking and mountaineering. Want to get your feet out of those plastic boats? Do a technical scramble? Ford a stream? The Classic model is only slightly lighter than the Sprint or KSO, however. All Five-finger models are considerably lighter than my Chaco sandles, for example, and very compact. I also think the Flow model would make a good watershoe for kayaking.
Note that if your feet lie in the overlap region of men's and women's shoes you can fit the shoes in 1/4" rather than 1/2" intervals, with the women's being effectively 1.5 sizes smaller than a men's. I think that fit-wise, you should gage it by pulling back on the grab-loop on the back tense. Aim for 1/2" seperation between your heel and that of the slipper.
Compared to the Sprint, the KSO has a mesh upper which is supposed to keep debris from getting in and underneath the feet. The only debris I got in mine was stuff that was already stuck to my foot when I put them on. The suspension of the KSO is sort of a pulley system that attaches at the heel, comes forward and turn to pass over the top of the foot, where it attaches with velcro. The KSO (and Flow) appears to be built on a slightly wider rand than the Sprint or Classics.
The soles are remarkably sticky. There is a waffle pattern cut into the ball and heel that probably increases the friction, particularly on pavement or other flat surfaces. Running in them is not quite the same as barefoot but the degree of protection is very good. You feel everything you're running on, and sometimes things hurt a bit but only for a second and there's no lasting pain. Like barefoot, you have to watch where you place your feet, but you have considerably more insurance whenever you make a mistake, so you can run briskly. Running on a gravel track wasn't possible for me, but trails and grass were both very enjoyable experiences. I think the most dangerous thing to avoid running on would be thorns, which could conceivably slip through the toe pads and into the side of your toes.
These things appear to be very popular, and I can immediately see why. I bought my slippers on Wednesday, the saleswoman said that they got their shipment in on Monday and had already sold 1/3rd of their stock. They are sort of on the level of things like Gore-tex, Marmot's DriClime base layers, or kernmantle rope in terms of game-changing the technology and utility of outdoor gear.
Initially there was some shelf in the big-toe of my right slipper that was irritating the nail. However, with time to work in the slipper (and some work with a nail clipper) I don't notice this anymore. Pro-tip: cut your toe nails before you go to fit these. I've found the best way to set the toes is to sit with your feet flat on the floor and then raise your heels while planting your toes.
The shoes are a little sweaty, although I think this may be a feature rather than a bug: when wet the Five-fingers suction onto your foot better.
With regards to the other models, the Classic, at least to my eyes, looked to be the ultimate camp shoe for backpacking and mountaineering. Want to get your feet out of those plastic boats? Do a technical scramble? Ford a stream? The Classic model is only slightly lighter than the Sprint or KSO, however. All Five-finger models are considerably lighter than my Chaco sandles, for example, and very compact. I also think the Flow model would make a good watershoe for kayaking.
05 May 2009
Reading Assignment
I've been digging around, looking for something to interesting to write about on an energy topic without a lot of luck. Unfortunately I think alternative energy development will slow faster than the rest of the economy. If anyone has any suggestions, please voice them.
In lieu of that, I offer some reading material:
Monsters, Inc.
An article in the New Yorker about how overgrown the finance industry as become, and why it should shrink to better fit the size of the rest of the economy. It's nice to see this meme appear in more 'respectable' corners of the world.
You Walk Wrong
An article from NY Mag on how shoes screw up the natural human walking mechanics.
Civilization's Cost: The Decline and Fall of Human Health
(requires subscription)
An short update on the status of research into the health status of paleolithic humans. Not only have humans shrunk physically since the introduction of grains to the diet some 10,000 years ago, Americans are now also shorter than in the 1950s. What the article doesn't mention is that brain volume is now much smaller than it was in the paleolithic-era too. The cynic in me wonders if brain volume has also shrunk since the 1950s.
Diet and health. What can you believe: or does bacon kill you?
Are nitrates/nitrites in meat hazardous (as opposed to nitrates/nitrites in vegetables)? David Colquhoun takes a look at the science and finds it wanting. In particular, check out the dose response curves. Any actual correlation is probably due to healthy patient bias. People who are concerned about their health don't eat bacon because they think its unhealthy, not because it necessarily is. Personally, I think that the quality of processed meats varies wildly from vendor to vendor. I buy bacon from Hutterites; it doesn't have an ingredient label.
Comparative Anatomy and Physiology Brought Up to Date
The site Beyond Vegetarianism seems to exist primarily to beat up on all fruit diets. Now there's a hard target! Nonetheless, they have some excellent articles on the likely dietary habits of paleolithic man. The article I linked goes through an extended discussion of what humans probably evolved to eat, given what we know about the anatomy of modern humans and our ancestors.
In lieu of that, I offer some reading material:
Monsters, Inc.
An article in the New Yorker about how overgrown the finance industry as become, and why it should shrink to better fit the size of the rest of the economy. It's nice to see this meme appear in more 'respectable' corners of the world.
You Walk Wrong
An article from NY Mag on how shoes screw up the natural human walking mechanics.
Civilization's Cost: The Decline and Fall of Human Health
(requires subscription)
An short update on the status of research into the health status of paleolithic humans. Not only have humans shrunk physically since the introduction of grains to the diet some 10,000 years ago, Americans are now also shorter than in the 1950s. What the article doesn't mention is that brain volume is now much smaller than it was in the paleolithic-era too. The cynic in me wonders if brain volume has also shrunk since the 1950s.
Diet and health. What can you believe: or does bacon kill you?
Are nitrates/nitrites in meat hazardous (as opposed to nitrates/nitrites in vegetables)? David Colquhoun takes a look at the science and finds it wanting. In particular, check out the dose response curves. Any actual correlation is probably due to healthy patient bias. People who are concerned about their health don't eat bacon because they think its unhealthy, not because it necessarily is. Personally, I think that the quality of processed meats varies wildly from vendor to vendor. I buy bacon from Hutterites; it doesn't have an ingredient label.
Comparative Anatomy and Physiology Brought Up to Date
The site Beyond Vegetarianism seems to exist primarily to beat up on all fruit diets. Now there's a hard target! Nonetheless, they have some excellent articles on the likely dietary habits of paleolithic man. The article I linked goes through an extended discussion of what humans probably evolved to eat, given what we know about the anatomy of modern humans and our ancestors.
03 May 2009
Barefoot
I went sprinting barefoot for the first time ever today. I'm sure I've run fast as a kid on the beach, but I've never done so on a field, to my recollection. It was an impressively... natural movement. There was no pain at all in my feet, although afterward I noticed I abraded some of my calluses a bit. I did step on a clear plastic bottle cap at one point (that went into the garbage) but it didn't really hurt since I just skipped with the opposite foot.
I think I was just as fast as with shoes and I had far better control at top-speed. Normally when I reach top-speed I am wind-milling my feet as fast as possible and I feel distinctly like I am not in control until I stop running and free-wheel down to a stop. I tried to articulate my feet; I'm not sure how successful I was but like I said earlier, the movement was very natural. In retrospect, it seems obvious that bare foot running should feel extremely comfortable, as long as you don't puncture your foot. Of course, one of the advantages of sprints is you can easily scout your route for anything you really don't want to step on.
I've had flat feet for a long time, and used orthopedics in my shoes to correct my gait to avoid shin splints and other muscle and knee problems from running and walking. I'm very tempted to try and toughen up my feet enough that I can try some moderate distance running, say a couple of kilometers, barefoot and see if I develop shin splints.
I've been looking around for Vibram Five Fingers awhile now but no one local in Edmonton seems to carry them. One of my friends said she had spotted them at Mountain Equipment Co-op, but alas, they were not there today when I checked. They are present on the website, but they don't seem like the type of shoes one orders via mail order without fitting. C'est la vie.
I think I was just as fast as with shoes and I had far better control at top-speed. Normally when I reach top-speed I am wind-milling my feet as fast as possible and I feel distinctly like I am not in control until I stop running and free-wheel down to a stop. I tried to articulate my feet; I'm not sure how successful I was but like I said earlier, the movement was very natural. In retrospect, it seems obvious that bare foot running should feel extremely comfortable, as long as you don't puncture your foot. Of course, one of the advantages of sprints is you can easily scout your route for anything you really don't want to step on.
I've had flat feet for a long time, and used orthopedics in my shoes to correct my gait to avoid shin splints and other muscle and knee problems from running and walking. I'm very tempted to try and toughen up my feet enough that I can try some moderate distance running, say a couple of kilometers, barefoot and see if I develop shin splints.
I've been looking around for Vibram Five Fingers awhile now but no one local in Edmonton seems to carry them. One of my friends said she had spotted them at Mountain Equipment Co-op, but alas, they were not there today when I checked. They are present on the website, but they don't seem like the type of shoes one orders via mail order without fitting. C'est la vie.
17 April 2009
Synthesis of Fat in the Liver
One of my hobby horses is the idea that you have to go through the glycogen stores in your liver before your body switches into fat burning mode and that this is one of the reasons cardio-style exercise is so ineffective for fat loss on a conventional low-fat diet. The opposite state, where the liver is completely full of glycogen, is also an interesting case. In this situation the liver starts manufacturing fatty acids from glucose. This is called de novo lipogenesis in the biology vocabulary. If you break this down from Latin to English, it is "generation of new fat."
There are three main stores of fat in the body: subcutaneous (under the skin), interstitial (in-between muscle fibres), and visceral (in and around the vital organs in the belly). Of the three types, visceral fat is dangerous to health while the others are relatively benign (Porter et al., 2009).
Visceral fat, typically measured by waist-to-hip circumference ratio, or more advanced imaging techniques, is a much better predictor of future diabetes or heart disease risk than the body mass index (Westphal, 2008). For example, diabetics who are relatively thin (i.e. have a low BMI) very often have what's called central obesity (Ruderman et al., 1998) or more colloquially, are "skinny fat." Fat tissue, as it happens is efficient at producing a wide variety of hormones such as adiponectin, leptin (e.g. Angulo et al., 2004), and resistin. For want of a better explanation, packing a lot of hormone-producing fat around the vital organs is bad juju.
I pose a couple of questions for the reader to ponder:
Why is visceral (belly) fat so contrary to good health? and,
What is it in our modern diet that is driving such an excess of visceral fat?
A distinct condition whereby fat deposits around the liver cause it to dysfunction is non-alcoholic fatty liver disease (see the New England Journal of Medicine review by Angulo (2002). As the name suggests, it is characterized by the appearance of fatty deposits in the liver tissue itself. Think fois gras. In addition to the formation of fat deposits, some of the more advanced forms of chronic liver disease feature the formation of fibrosis, which is the formation of scar tissue in the liver in response to repeated, chronic injury.
Funnily enough, this condition is tightly correlated with metabolic syndrome which is in turn associated with diabetes and many other debilitating conditions. Loria et al., 2005 (free) state that:
The problem with fatty liver disease really appears to be the combination of insulin resistance (from ingesting too much glucose) and high circulating triglyceride levels. From the review by Petta et al., 2009, "In fact IR [RM: insulin resistance] is the key factor in the promotion of liver fat accumulation not only by inducing an increase of liver FFA [RM: free-fatty acid] influx, but also, via hyperinsulinemia, by stimulating the activity of enzymes implicated in de novo hepatic lipogenesis."
Incidentally non-alcoholic fatty liver disease was almost certainly what Morgan Spurlock was doing to himself with his soda-laden diet in the movie Super Size Me. I noticed when watching that movie that some of his doctors (2 of 3, IIRC) didn't know that the condition existed. Non-alcoholic fatty liver disease reached incidence levels of 20-25 % in an Italian population study (Bedogni et al., 2005).
Ok, so abdominal/visceral fat causes some combination of metabolic syndrome and/or fatty liver disease. So what causes people to preferentially deposit fat around their mid-section rather than elsewhere? In researching non-alcoholic fatty liver disease, I came across the following paragraph by Postic and Girard (2008, free access), which I think is instructive:
If you will permit me an aside, most all of our actual information about diet and nutrition comes not from the 'top-down' approach of observation or intervention trials but from the 'bottom-up' approach of trying to establish the mechanics of human physiology. I like to call the 'bottom-up' approach the 'physicsification' of biology. Most properly the 'bottom-up' approach in biology can be described as the combination of biophysics, biochemistry, and genetics (bio-computer science).
In physics, one establishes base laws that govern a system, known as first principles, and then one gradually expands on the complexity until theory adequately matches experiment. Technically any other science can be described in terms of physics, but often we are stymied by excessive computational requirements or too many unknown, confounding factors. However, gradually scientists are slowly unraveling the secrets of biology.
The main advantage of having first principles is that it allows you to construct hypotheses that are likely true, and then test them. There are a lot of famous and successful predictions in physics. Observational nutritional science, not so much. For example, Einstein's general relativity predicted that light would bend (or 'lens') around strong gravitational objects like black holes; it does.
Now, back to the topic as to what drives visceral fat accumulation...
One potential source for abdominal fat is fats produced in the liver itself, most commonly by the conversion of carbohydrates to fat. Typically the total contribution of liver-synthesized triglycerides (de novo lipogenesis) to the total number of triglycerides in the blood stream (i.e. VLDL) is relatively small, on the order of 10 % (Marques-Lopes et al., 2001). This is too small a proportion to seriously be considered as a cause of obesity.
However, if you recall from the paragraph I quoted above, the liver only really starts to kick out a lot of lipids when you exceed its capacity for storing glycogen. A study by McDevitt et al. (2001, free access) specifically looked into the case of overfeeding versus not and what effect it had on fat synthesis in the liver. They found that with overfeeding by 50 % over basal metabolic rates, de novo lipogenesis increased 2-3 fold. Overfeeding on sugar (glucose-fructose) was uniformly worse than overfeeding on glucose, but only slightly.
A study of rats fed a diet of 60 % fructose versus conventional rat chow (Ackerman et al., 2005). After five weeks, the fructose-fed rats had 15 % higher blood pressure, 198 % higher blood triglycerides, and 90 % higher blood cholesterol levels. A similar study in overweight women found similar results: when fed 25 % of calories in the form of fructose for ten weeks resulted in a 140 % increase in circulating triglyceride levels (Stanhope and Havel, 2008). These rates of sugar consumption are consistent with soda pop intake for a significant hunk of the American populace.
One question is, why does fructose (and alcohol) intake result in visceral fat, and not the more benign sub-cutaneous or intra-muscular fat? I have one possible explanation that I like to term the 'circulatory fat deposition model.' When you ingest a toxin like fructose or alcohol, the body automatically increases circulation to the vital organs (and in particular the liver) so that it can be filtered out of the blood stream. Since any ingested substance will naturally diffuse to even concentration throughout the blood, this is the only way to preferentially increase the flux of toxin to the liver.
Fructose is well known to contribute greatly to post-meal triglyceride levels (Chong et al., 2007). The liver takes fructose and produces palmatic acid (i.e. a stable saturated fat) from it. It then releases that fat into the blood stream. Since the filtering of fructose isn't instant, the circulation in the body core is still heightened. As a result, the visceral fat tissues see a higher rate of triglyceride flux than the more benign skin or muscle fat (Note: flux in a scientific sense typically means mass or volume per second — put those Star Trek thoughts out of your mind). The visceral fat, which sees the most fabricated triglycerides floating on by, also happens to absorb the most. Hence fructose tends to promote visceral fat. On the other hand, if you ingest excess calories in the form of fat, it's not any more likely to deposit around the liver than it is your thighs, so it's not nearly so dangerous.
One sees a similar effect with amateur body-builders who ingest calorie-heavy shakes and energy drinks after or during exercise where their muscles are generating a lot of lactic acid. The body increases blood flow to those muscles to remove the lactic acid, but the fat deposits inside the muscle also see a much higher flux of fat and fat-building substrate as a result. This results in a characteristic thick and pasty muscle texture without a lot of functional power. Think of well-marbled beef steak.
If this hypothesis is true then combining dietary fat with any chemical that requires extensive liver processing (e.g. caffeine, artificial sweeteners) would also tend to result in visceral fat deposition. Oh look, a prediction. I did say something about those.
This information on de novo lipogenesis, and what we know of the fat-sparing properties of insulin, provides some support to the notion that carbohydrates and fats should not be mixed in meals. It's only when you eat an excess of glucose, or any fructose, that one can transform a pure carbohydrate meal into body fat. On the other hand, if you eat fats and carbohydrates in combination, the insulin response will prevent your body from burning the fat directly. Note that if you have a dysfunctional carbohydrate metabolism (i.e. metabolic syndrome) this precept probably does not apply. Of course this advice is only useful if you are capable of restricting your caloric intake on a pure carbohydrate diet.
Fats are satiating whereas carbohydrates most definitely are not. The hormonal reason for this is related to the fact that they each use a different mechanism for regulation. With insulin, as it ramps down, it promotes the production of ghrelin, one of the primary 'appetite' hormones. Fat metabolism doesn't appear to have a similar analogue, and as a result hunger on a high-fat diet lacks the ravenous component of the insulin roller coaster.
When you think about, there's plenty of reason to believe that carbohydrates promote over-eating. By in large, most of the plant carbohydrate sources our paleolithic ancestors would have access to all mature around the same time, late summer and fall. This is a time period when it is particularly advantageous for primitive man to pack on some fat to sustain him over the winter. On the other hand, for Joe 6-Pack with his year-round supermarket access, this doesn't work out so well.
The conclusions we can draw from this body of research are that one can safely ingest glucose regularly with the aim of not saturating the liver's glycogen storage capacity. The maximum reasonable glucose intake level will vary significantly from person to person depending on general activity level and overall health based on how insulin resistant they are. Where one gets into trouble is when you overfill your liver by eating too many calories, with a significant fraction of glucose calories, or significant fructose intake (likely in the form of sugar or corn syrup). This is likely to lead insulin resistance and liver dysfunction.
There are three main stores of fat in the body: subcutaneous (under the skin), interstitial (in-between muscle fibres), and visceral (in and around the vital organs in the belly). Of the three types, visceral fat is dangerous to health while the others are relatively benign (Porter et al., 2009).
Visceral fat, typically measured by waist-to-hip circumference ratio, or more advanced imaging techniques, is a much better predictor of future diabetes or heart disease risk than the body mass index (Westphal, 2008). For example, diabetics who are relatively thin (i.e. have a low BMI) very often have what's called central obesity (Ruderman et al., 1998) or more colloquially, are "skinny fat." Fat tissue, as it happens is efficient at producing a wide variety of hormones such as adiponectin, leptin (e.g. Angulo et al., 2004), and resistin. For want of a better explanation, packing a lot of hormone-producing fat around the vital organs is bad juju.
I pose a couple of questions for the reader to ponder:
Why is visceral (belly) fat so contrary to good health? and,
What is it in our modern diet that is driving such an excess of visceral fat?
A distinct condition whereby fat deposits around the liver cause it to dysfunction is non-alcoholic fatty liver disease (see the New England Journal of Medicine review by Angulo (2002). As the name suggests, it is characterized by the appearance of fatty deposits in the liver tissue itself. Think fois gras. In addition to the formation of fat deposits, some of the more advanced forms of chronic liver disease feature the formation of fibrosis, which is the formation of scar tissue in the liver in response to repeated, chronic injury.
Funnily enough, this condition is tightly correlated with metabolic syndrome which is in turn associated with diabetes and many other debilitating conditions. Loria et al., 2005 (free) state that:
Given that metabolic syndrome and non-alcoholic fatty liver disease affect the same insulin-resistant patients, not unexpectedly, there are amazing similarities between metabolic syndrome and non-alcoholic fatty liver disease in terms of prevalence, pathogenesis, clinical features and outcome.Loria does state that fatty liver disease does not cause metabolic syndrome, or vice versa. Since metabolic syndrome is a catch-all description of many symptoms, I think it would be fair to describe fatty liver disease as one potential component of metabolic syndrome.
The problem with fatty liver disease really appears to be the combination of insulin resistance (from ingesting too much glucose) and high circulating triglyceride levels. From the review by Petta et al., 2009, "In fact IR [RM: insulin resistance] is the key factor in the promotion of liver fat accumulation not only by inducing an increase of liver FFA [RM: free-fatty acid] influx, but also, via hyperinsulinemia, by stimulating the activity of enzymes implicated in de novo hepatic lipogenesis."
Incidentally non-alcoholic fatty liver disease was almost certainly what Morgan Spurlock was doing to himself with his soda-laden diet in the movie Super Size Me. I noticed when watching that movie that some of his doctors (2 of 3, IIRC) didn't know that the condition existed. Non-alcoholic fatty liver disease reached incidence levels of 20-25 % in an Italian population study (Bedogni et al., 2005).
Ok, so abdominal/visceral fat causes some combination of metabolic syndrome and/or fatty liver disease. So what causes people to preferentially deposit fat around their mid-section rather than elsewhere? In researching non-alcoholic fatty liver disease, I came across the following paragraph by Postic and Girard (2008, free access), which I think is instructive:
Insulin is essential for the maintenance of carbohydrate and lipid homeostasis. Insulin is secreted by pancreatic β cells in response to increased circulating levels of glucose after a meal. A large fraction of glucose absorbed from the small intestine is immediately taken up by hepatocytes [RM: liver cells], which convert it into glycogen. However, when the liver is saturated with glycogen (roughly 5% of liver mass), any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which will be esterified into TG [RM: triglycerides] to be exported to adipose tissue as very low-density lipoproteins (VLDLs). Insulin inhibits lipolysis [RM: fat burning] in adipose tissue by inhibiting hormone-sensitive lipase (HSL), the enzyme regulating FFA [free-fatty acid] release from adipose tissue (10). Therefore, from a whole-body perspective, insulin has a “fat-sparing” effect by driving most cells to preferentially oxidize carbohydrates instead of fatty acids for energy. Insulin also regulates glucose homeostasis at many sites, reducing hepatic glucose production (HGP) (via decreased glucose biosynthesis [gluconeogenesis] and glycogen breakdown [glycogenolysis]) and increasing the rate of glucose uptake, primarily into skeletal muscle and adipose tissue.A very interesting review that hypothesized on a link between diabetes and fructose said the following (Johnson et al., 2009):
For example, very high doses of fructose (250 g/d x 7 d) cause insulin resistance in 1 wk (147), whereas slightly lower doses (216 g/d for 4 wk) only induce insulin resistance at sites where fructokinase is highly expressed (liver and adipocyte) (148), and even lower doses (100 g/d x 4 wk) result in no insulin resistance at all (149).If you read through any significant amount of human biology on diet it's impossible to avoid the fact that the hormone system (and insulin and growth hormone in particular) is paramount in determining whether the body is in a state of fat gain or fat loss. It's only at the nutritional level that the facts become obscured by experimenting with too many variables at once.
If you will permit me an aside, most all of our actual information about diet and nutrition comes not from the 'top-down' approach of observation or intervention trials but from the 'bottom-up' approach of trying to establish the mechanics of human physiology. I like to call the 'bottom-up' approach the 'physicsification' of biology. Most properly the 'bottom-up' approach in biology can be described as the combination of biophysics, biochemistry, and genetics (bio-computer science).
In physics, one establishes base laws that govern a system, known as first principles, and then one gradually expands on the complexity until theory adequately matches experiment. Technically any other science can be described in terms of physics, but often we are stymied by excessive computational requirements or too many unknown, confounding factors. However, gradually scientists are slowly unraveling the secrets of biology.
The main advantage of having first principles is that it allows you to construct hypotheses that are likely true, and then test them. There are a lot of famous and successful predictions in physics. Observational nutritional science, not so much. For example, Einstein's general relativity predicted that light would bend (or 'lens') around strong gravitational objects like black holes; it does.
Now, back to the topic as to what drives visceral fat accumulation...
One potential source for abdominal fat is fats produced in the liver itself, most commonly by the conversion of carbohydrates to fat. Typically the total contribution of liver-synthesized triglycerides (de novo lipogenesis) to the total number of triglycerides in the blood stream (i.e. VLDL) is relatively small, on the order of 10 % (Marques-Lopes et al., 2001). This is too small a proportion to seriously be considered as a cause of obesity.
However, if you recall from the paragraph I quoted above, the liver only really starts to kick out a lot of lipids when you exceed its capacity for storing glycogen. A study by McDevitt et al. (2001, free access) specifically looked into the case of overfeeding versus not and what effect it had on fat synthesis in the liver. They found that with overfeeding by 50 % over basal metabolic rates, de novo lipogenesis increased 2-3 fold. Overfeeding on sugar (glucose-fructose) was uniformly worse than overfeeding on glucose, but only slightly.
A study of rats fed a diet of 60 % fructose versus conventional rat chow (Ackerman et al., 2005). After five weeks, the fructose-fed rats had 15 % higher blood pressure, 198 % higher blood triglycerides, and 90 % higher blood cholesterol levels. A similar study in overweight women found similar results: when fed 25 % of calories in the form of fructose for ten weeks resulted in a 140 % increase in circulating triglyceride levels (Stanhope and Havel, 2008). These rates of sugar consumption are consistent with soda pop intake for a significant hunk of the American populace.
One question is, why does fructose (and alcohol) intake result in visceral fat, and not the more benign sub-cutaneous or intra-muscular fat? I have one possible explanation that I like to term the 'circulatory fat deposition model.' When you ingest a toxin like fructose or alcohol, the body automatically increases circulation to the vital organs (and in particular the liver) so that it can be filtered out of the blood stream. Since any ingested substance will naturally diffuse to even concentration throughout the blood, this is the only way to preferentially increase the flux of toxin to the liver.
Fructose is well known to contribute greatly to post-meal triglyceride levels (Chong et al., 2007). The liver takes fructose and produces palmatic acid (i.e. a stable saturated fat) from it. It then releases that fat into the blood stream. Since the filtering of fructose isn't instant, the circulation in the body core is still heightened. As a result, the visceral fat tissues see a higher rate of triglyceride flux than the more benign skin or muscle fat (Note: flux in a scientific sense typically means mass or volume per second — put those Star Trek thoughts out of your mind). The visceral fat, which sees the most fabricated triglycerides floating on by, also happens to absorb the most. Hence fructose tends to promote visceral fat. On the other hand, if you ingest excess calories in the form of fat, it's not any more likely to deposit around the liver than it is your thighs, so it's not nearly so dangerous.
One sees a similar effect with amateur body-builders who ingest calorie-heavy shakes and energy drinks after or during exercise where their muscles are generating a lot of lactic acid. The body increases blood flow to those muscles to remove the lactic acid, but the fat deposits inside the muscle also see a much higher flux of fat and fat-building substrate as a result. This results in a characteristic thick and pasty muscle texture without a lot of functional power. Think of well-marbled beef steak.
If this hypothesis is true then combining dietary fat with any chemical that requires extensive liver processing (e.g. caffeine, artificial sweeteners) would also tend to result in visceral fat deposition. Oh look, a prediction. I did say something about those.
This information on de novo lipogenesis, and what we know of the fat-sparing properties of insulin, provides some support to the notion that carbohydrates and fats should not be mixed in meals. It's only when you eat an excess of glucose, or any fructose, that one can transform a pure carbohydrate meal into body fat. On the other hand, if you eat fats and carbohydrates in combination, the insulin response will prevent your body from burning the fat directly. Note that if you have a dysfunctional carbohydrate metabolism (i.e. metabolic syndrome) this precept probably does not apply. Of course this advice is only useful if you are capable of restricting your caloric intake on a pure carbohydrate diet.
Fats are satiating whereas carbohydrates most definitely are not. The hormonal reason for this is related to the fact that they each use a different mechanism for regulation. With insulin, as it ramps down, it promotes the production of ghrelin, one of the primary 'appetite' hormones. Fat metabolism doesn't appear to have a similar analogue, and as a result hunger on a high-fat diet lacks the ravenous component of the insulin roller coaster.
When you think about, there's plenty of reason to believe that carbohydrates promote over-eating. By in large, most of the plant carbohydrate sources our paleolithic ancestors would have access to all mature around the same time, late summer and fall. This is a time period when it is particularly advantageous for primitive man to pack on some fat to sustain him over the winter. On the other hand, for Joe 6-Pack with his year-round supermarket access, this doesn't work out so well.
The conclusions we can draw from this body of research are that one can safely ingest glucose regularly with the aim of not saturating the liver's glycogen storage capacity. The maximum reasonable glucose intake level will vary significantly from person to person depending on general activity level and overall health based on how insulin resistant they are. Where one gets into trouble is when you overfill your liver by eating too many calories, with a significant fraction of glucose calories, or significant fructose intake (likely in the form of sugar or corn syrup). This is likely to lead insulin resistance and liver dysfunction.
26 March 2009
Feast and Fast: the dichotomy of insulin and growth hormone
At its heart the human body is a machine. A very complicated machine to be sure, unknowable in completion given our current basis of knowledge, but it still obeys certain engineering concepts in the end. One of those concepts is that the operation of a machine is governed by its control system. When it comes to health, the hormonal system is the control system that governs just how well we feel. We stimulate it in various ways and it causes our bodies to react to those stimulus. Trying to pick apart these relationships is, in my opinion, the key to understanding how to obtain good health throughout our lives.
Today I'm going to write predominately about growth hormone and how it metabolizes fat. I got the idea primarily from the writings of Brad Pilon. I have not read his book; I worked from review articles in scientific journals.
Introduction
The human body has two signaling systems:
When it comes to metabolism, the endocrine system is the one in control. There is a portion of the nervous system that controls the gut, the autonomic nervous system, but it acts largely independently of the brain. It controls aspects like opening sphincters, e.g. stomach emptying.
If the nervous system is a digital system, then the endocrine system is very much like an analogue circuit composed of resistors, capacitors, and inductors (in biological analogue circuits these are usually called push-pots). These elements can be formed into circuits that perform various functions (amplification, integration, differentiation, etc.). However, there are many, many elements that compose the endocrine system of the human body. If you were to draw a circuit diagram of the human body it would resemble not so much a Pentium CPU as a Gordian knot with its mass of interconnections.
Conceptually the hormone system is divided into the whole-body hormones (endocrine), local tissue hormones (paracrine), and single cell hormones (autocrine). I am mostly concerned with endocrine system since it is the one that affects multiple types of tissues such as fat, muscle, and vital organs. There are certain hormones related to digestion and metabolism that can be considered the premiere, most vital hormones to control such tasks.
Examples of top-tier hormones involved in the process of eating include:
For people who are trying to lose fat, a reasonable objective is to tweak one or more hormonal levels to upset the existing equilibrium. A kilo here, a kilo there, and pretty soon you're talking about real weight loss. However, like any complex system, you have to feed it the proper inputs for it to function properly: Garbage in = garbage out.
The feast and fast cycle
Insulin is the primary regulator of carbohydrate and protein metabolism. (Human) growth hormone (abbreviated GH) is the primary regulator of fatty acid metabolism. Today, we're going to talk mostly about GH since most people already know a fair amount about insulin. If you don't, you can get started with my review of Gary Taubes' book, "Good Calories, Bad Calories."
So, to review, insulin is the hormone responsible for regulating the metabolism of glucose and most amino acids (exceptions are lysine and leucine) derived from the protein in your diet that are converted to glucose for the purpose of fuel (Gröschl et al., 2003). High levels of insulin also prevent your muscles from absorbing fatty acids in the blood: the body prefers to burn the low-energy density carbohydrates first and hold onto the superior fatty acids for lean times. A person with high levels of insulin in their blood is said to be in the feasted state.
The opposite to the feasted state is the fasted state. The hormone that characterizes the fasted state is growth hormone (review: Møller and Jørgensen, 2009). The general course of progressing from feasted to fasted goes something like this:
Figure 2. from Møller and Jørgensen (2009) on the interrelation of growth hormone, insulin growth factor, and insulin in the fed and fasted cycle.
However, this is not all growth hormone does. As the name suggests, GH, in conjunction with insulin-like growth factor, is involved in the growth of lean body mass: it increases the amount of protein in your muscles and vital organs, it increase the uptake of calcium by bones, etc. Growth hormone alone is insufficient to boost protein synthesis, however. I'll probably save the discussion of IGF-1 for another time (for further reading, start with Gibney, Healy, and Sönksen, 2007). In this context, growth hormone may be poorly named.
In addition to promoting fatty acid metabolism, GH shuts down the uptake of glucose into muscle tissue and stops the conversion of amino acids into glucose (Rabinowitz, Klassen, and Zieler, 1965). The fact that GH shuts down not just carbohydrate metabolism but also protein metabolism is critically important. It means that when one enters the fasted state, your muscle and organs are protected against being consumed to fuel your body (Nørrelund et al., 2006). This clearly illustrates the greatest failing of the high-carbohydrate, calorie-restricted "semi-starvation" diet that Taubes pans: if you maintain high insulin levels but insufficient calories, there's little to protect the protein in your muscles and vital organs from being consumed while your fat tissue goes untouched.
Furthermore, once a person becomes insulin resistant (and most obese individuals are), they become locked in a vicious cycle: insulin levels remain high for a long time after a meal, and stay high until the next meal, so the body never makes the transition from feasted to fasted and hence never burns any body fat. Let me reiterate: once you are obese, you will have a harder time losing body fat than a thinner individual. Unsurprisingly, growth hormone levels in obese people are depressed (Scacchi et al., 1999). The number one priority for losing weight then is improving insulin sensitivity. As an aside, this is a good reason to avoid supplementation with synthetic growth hormone: it may leave you with unnaturally elevated blood sugar for an extended period of time. Essentially growth hormone makes your tissues insulin resistant, but it normally only does so when blood glucose levels are depleted.
Body composition — whether you are lean or fat, i.e. the ratio of fat mass to lean body mass — is basically a function of the ratio of time you spend in the feasted state versus time you spend in the fasted state. Now, on the face of it, this statement is self-evident and rather useless. However, it's also very fundamental. In the natural situation, insulin and human growth hormone levels are reciprocal: GH is low when insulin is high, insulin is low when GH is high. A meta-analysis of GH found that high levels of growth hormone led to an increased basal metabolic rate of 141 [69-213] kcal/day (Liu et al., 2007). This corresponds to roughly a pound of fat per month.
What controls growth hormone levels?
So if growth hormone controls the release of fat from your fat tissues, what controls the release of growth hormone? Growth hormone is typically released in pulses from the pituitary gland. This pulsitile nature of growth hormone is similar to that of insulin in a healthy individual.
Figure 4 from Ho et al., 1988, showing the Fourier transform of GH secretion. Filled boxes are (24-hr) fasted subjects, open boxes are fed controls. Normally the horizontal axis of a Fourier transform is frequency but in this case it is period. This plot shows peaks at 110 min, 206 min, and 24 hr. The 24 hour cycle is likely caused by sleeping, the sources of the other peaks are less clear.
Growth hormone is primarily up-regulated by growth hormone releasing hormone (GHRH) and growth hormone releasing peptide, better known as ghreline. Growth hormone is primarily down-regulated by human growth inhibiting hormone (GHIH), typically known as somatostatin, and high blood glucose levels. I eagerly await the discovery of growth hormone releasing hormone releasing hormone (GHRHRH). Ok, I jest, low-levels of growth hormone and insulin stimulate GHRH.
Notice something interesting: ghrelin is an appetite controlling hormone. When you fast, GH production goes up and up and ghrelin goes down. When fasting, the hardest part is about six hours after your last meal when your insulin levels have dropped down and you have a strong appetite. However, if you get over this 'hump' you will find that your appetite largely goes away as the ghrelin circulating in your blood starts the secretion of GH. You will still get thirsty, but not ravenously hungry. I would generally recommend sleeping through this stage.
So what's the difference between controlling your body's overall insulin/GH levels very controlling your appetite to avoid binge eating? Can we actually separate the appetite hormones, leptin and ghrelin from the metabolism control hormones, insulin and growth hormone? As far as I can tell, appetite and blood sugar levels are basically the same thing. Trying to separate the two as wholly independent variables and then claiming that fat people simply lack self control when it comes to food is very very wrong. The science clearly shows that the two are deeply inter-related.
Figure 4. from Hartmann et al., 1992, showing the negative correlation between GH release and body-mass index in fasted subjects.
Production of growth hormone typically declines as we age. However, research has shown that growth hormone levels are more tightly correlated with visceral fat (belly fat) than age (Vahl et al, 1997). So do we get fat because we get old or do we get old because we get fat? Both answers appear to be correct, each to a degree. No one will live forever, but most of us would like to age gracefully. I'm about a decade younger than I was at this time one year ago.
Real-world means of increasing growth hormone levels
There are three basic ways to increase the amount of GH your body produces:
VO2 max lactate threshold (Pritzlaff et al., 1999). VO2 max Lactate threshold is the level at which the demands of your exercise exceeds your body's ability to breath in oxygen, causing the body to go anaerobic and produce lactic acid. Note that VO2 max lactate threshold is for your whole body, so you need to exercise your whole body or at least the biggest muscles (core, glutes, quads). You can do bicep curls until your arms fall off but since they're small muscles you won't get much of a GH boost from doing so. The best exercise for putting your whole body into the anaerobic threshold is probably sprint intervals.
Figure 1. from Pritzlaff et al., showing GH secretion pulses as a function of lactate threshold (LT) reached.
Of course, (2) and (3) can be combined. A word of warning, if you exercise hard at the end of a fast, be prepared for sore muscles (i.e. delayed onset muscle soreness) the next day.
A low-carbohydrate diet may have the advantage in this situation as the overall insulin pulse should be small and of shorter duration. The reason is fairly obvious: the body's tissues will be less insulin resistant and hence absorb glucose from the blood stream more readily. Hence one should enter the fasted state quicker after a low-carbohydrate diet than not. The more time you spend in the fasted state, the faster you're going to shed body fat.
The $64,000 dollar question is then, what effect does dietary fat have on growth hormone secretion? It appears that dietary fat intake increases the production of somatostatin from the gut, otherwise known as growth-hormone inhibiting hormone, although somatostatin down-regulates many many other hormones (Cappon et al., 1993). Anecdotal evidence from people who regularly fast is that fasting is easier to handle on a low-carbohydrate diet than a low-fat diet. I dug around for awhile on PubMed, but I wasn't able to find any research where subjects were fed diets of pure glucose and pure triglycerides and then their transition from feasted to fasted tested. It would be a good Master's thesis for someone if it really hasn't been done before. I did find tests that tested intravenously applied fatty acids in fasting but since somatostatin is produced by the digestive system their relevance isn't clear. The Hartman study from 1992 seems to be the best starting point for this line of research.
References
in alphabetical order:
Cappon JP, et al. "Acute effects of high fat and high glucose meals on the growth hormone response to exercise." J Clin Endocrinol Metab. 1993 Jun;76(6):1418-22.
Gibney J, Healy ML, Sönksen PH. "The growth hormone/insulin-like growth factor-I axis in exercise and sport." Endocr Rev. 2007 Oct;28(6):603-24.
Gröschl M, et al., "Endocrine responses to the oral ingestion of a physiological dose of essential amino acids in humans.", J Endocrinol. 2003 Nov;179(2):237-44.
Hartman ML, et al., "Augmented growth hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day fast in normal men." J Clin Endocrinol Metab. 1992 Apr;74(4):757-65.
Ho KY, et al. "Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man."J Clin Invest. 1988 Apr;81(4):968-75.
Jensen MD, et al., "Lipolysis during fasting. Decreased suppression by insulin and increased stimulation by epinephrine." J Clin Invest. 1987 Jan;79(1):207-13.
Liu H, et al. "Systematic review: the effects of growth hormone on athletic performance."
Ann Intern Med. 2008 May 20;148(10):747-58.
Pritzlaff CJ, et al. "Impact of acute exercise intensity on pulsatile growth hormone release in men." J Appl Physiol. 1999 Aug;87(2):498-504.
Møller N, Jørgensen JO, "Effects of Growth Hormone on Glucose, Lipid, and Protein Metabolism in Human Subjects." Endocr Rev. 2009 Mar 19.
Nørrelund H, et al., "The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown." Diabetes. 2001 Jan;50(1):96-104.
Jesse Roth, et al., "Hypoglycemia: A Potent Stimulus to Secretion of Growth Hormone." Science 140(3570):987 - 988 (May 1963).
Scacchi M, Pincelli AI, Cavagnini F. "Growth hormone in obesity." Int J Obes Relat Metab Disord. 1999 Mar;23(3):260-71.
Vahl N, et al., "Abdominal adiposity rather than age and sex predicts mass and regularity of GH secretion in healthy adults." Am J Physiol. 1997 Jun;272(6 Pt 1):E1108-16.
David Rabinowitz, Gerald A. Klassen and Kenneth L. Zierler, "Effect of Human Growth Hormone on Muscle and Adipose Tissue Metabolism in the Forearm of Man." J. Clin. Invest. 44(1): 51-61 (1965).
Today I'm going to write predominately about growth hormone and how it metabolizes fat. I got the idea primarily from the writings of Brad Pilon. I have not read his book; I worked from review articles in scientific journals.
Introduction
The human body has two signaling systems:
- The nervous system, which primarily controls fast actions such as motion and thought.
- The endocrine (or hormonal) system, which primarily handles slower processes..
When it comes to metabolism, the endocrine system is the one in control. There is a portion of the nervous system that controls the gut, the autonomic nervous system, but it acts largely independently of the brain. It controls aspects like opening sphincters, e.g. stomach emptying.
If the nervous system is a digital system, then the endocrine system is very much like an analogue circuit composed of resistors, capacitors, and inductors (in biological analogue circuits these are usually called push-pots). These elements can be formed into circuits that perform various functions (amplification, integration, differentiation, etc.). However, there are many, many elements that compose the endocrine system of the human body. If you were to draw a circuit diagram of the human body it would resemble not so much a Pentium CPU as a Gordian knot with its mass of interconnections.
Conceptually the hormone system is divided into the whole-body hormones (endocrine), local tissue hormones (paracrine), and single cell hormones (autocrine). I am mostly concerned with endocrine system since it is the one that affects multiple types of tissues such as fat, muscle, and vital organs. There are certain hormones related to digestion and metabolism that can be considered the premiere, most vital hormones to control such tasks.
Examples of top-tier hormones involved in the process of eating include:
- Macronutrient metabolism hormones (insulin, growth hormone)
- Sex hormones (testosterone, estrogen)
- Appetite hormones (ghrelin, leptin)
- Basal metabolism (thyroid)
- Stress hormones (cortisol, epinephrine) (Jensen et al., 1987)
For people who are trying to lose fat, a reasonable objective is to tweak one or more hormonal levels to upset the existing equilibrium. A kilo here, a kilo there, and pretty soon you're talking about real weight loss. However, like any complex system, you have to feed it the proper inputs for it to function properly: Garbage in = garbage out.
The feast and fast cycle
Insulin is the primary regulator of carbohydrate and protein metabolism. (Human) growth hormone (abbreviated GH) is the primary regulator of fatty acid metabolism. Today, we're going to talk mostly about GH since most people already know a fair amount about insulin. If you don't, you can get started with my review of Gary Taubes' book, "Good Calories, Bad Calories."
So, to review, insulin is the hormone responsible for regulating the metabolism of glucose and most amino acids (exceptions are lysine and leucine) derived from the protein in your diet that are converted to glucose for the purpose of fuel (Gröschl et al., 2003). High levels of insulin also prevent your muscles from absorbing fatty acids in the blood: the body prefers to burn the low-energy density carbohydrates first and hold onto the superior fatty acids for lean times. A person with high levels of insulin in their blood is said to be in the feasted state.
The opposite to the feasted state is the fasted state. The hormone that characterizes the fasted state is growth hormone (review: Møller and Jørgensen, 2009). The general course of progressing from feasted to fasted goes something like this:
- You eat a meal with carbohydrates and protein. Digestion occurs over the course of several hours and insulin levels rise in response to the absorption of these macronutrients.
- Insulin sensitive tissues absorb glucose from the blood-stream. Glucagon, a second-tier hormone, causes the liver to break down the glycogen it stores into glucose, releasing it into the blood. This slows the rate at which insulin drops.
- Insulin continues to drop as the liver's supply of carbohydrate is reduced. Ghrelin (which I'll discuss later) is produced, which promotes appetite and the production of growth hormone. If the increase in appetite caused by ghrelin causes you to eat, you go back to stage 1. Otherwise, you make the transition into the fasted state as GH levels rise and blood sugar levels drop (Roth et al., 1963).
Figure 2. from Møller and Jørgensen (2009) on the interrelation of growth hormone, insulin growth factor, and insulin in the fed and fasted cycle.However, this is not all growth hormone does. As the name suggests, GH, in conjunction with insulin-like growth factor, is involved in the growth of lean body mass: it increases the amount of protein in your muscles and vital organs, it increase the uptake of calcium by bones, etc. Growth hormone alone is insufficient to boost protein synthesis, however. I'll probably save the discussion of IGF-1 for another time (for further reading, start with Gibney, Healy, and Sönksen, 2007). In this context, growth hormone may be poorly named.
In addition to promoting fatty acid metabolism, GH shuts down the uptake of glucose into muscle tissue and stops the conversion of amino acids into glucose (Rabinowitz, Klassen, and Zieler, 1965). The fact that GH shuts down not just carbohydrate metabolism but also protein metabolism is critically important. It means that when one enters the fasted state, your muscle and organs are protected against being consumed to fuel your body (Nørrelund et al., 2006). This clearly illustrates the greatest failing of the high-carbohydrate, calorie-restricted "semi-starvation" diet that Taubes pans: if you maintain high insulin levels but insufficient calories, there's little to protect the protein in your muscles and vital organs from being consumed while your fat tissue goes untouched.
Furthermore, once a person becomes insulin resistant (and most obese individuals are), they become locked in a vicious cycle: insulin levels remain high for a long time after a meal, and stay high until the next meal, so the body never makes the transition from feasted to fasted and hence never burns any body fat. Let me reiterate: once you are obese, you will have a harder time losing body fat than a thinner individual. Unsurprisingly, growth hormone levels in obese people are depressed (Scacchi et al., 1999). The number one priority for losing weight then is improving insulin sensitivity. As an aside, this is a good reason to avoid supplementation with synthetic growth hormone: it may leave you with unnaturally elevated blood sugar for an extended period of time. Essentially growth hormone makes your tissues insulin resistant, but it normally only does so when blood glucose levels are depleted.
Body composition — whether you are lean or fat, i.e. the ratio of fat mass to lean body mass — is basically a function of the ratio of time you spend in the feasted state versus time you spend in the fasted state. Now, on the face of it, this statement is self-evident and rather useless. However, it's also very fundamental. In the natural situation, insulin and human growth hormone levels are reciprocal: GH is low when insulin is high, insulin is low when GH is high. A meta-analysis of GH found that high levels of growth hormone led to an increased basal metabolic rate of 141 [69-213] kcal/day (Liu et al., 2007). This corresponds to roughly a pound of fat per month.
What controls growth hormone levels?
So if growth hormone controls the release of fat from your fat tissues, what controls the release of growth hormone? Growth hormone is typically released in pulses from the pituitary gland. This pulsitile nature of growth hormone is similar to that of insulin in a healthy individual.
Figure 4 from Ho et al., 1988, showing the Fourier transform of GH secretion. Filled boxes are (24-hr) fasted subjects, open boxes are fed controls. Normally the horizontal axis of a Fourier transform is frequency but in this case it is period. This plot shows peaks at 110 min, 206 min, and 24 hr. The 24 hour cycle is likely caused by sleeping, the sources of the other peaks are less clear. Growth hormone is primarily up-regulated by growth hormone releasing hormone (GHRH) and growth hormone releasing peptide, better known as ghreline. Growth hormone is primarily down-regulated by human growth inhibiting hormone (GHIH), typically known as somatostatin, and high blood glucose levels. I eagerly await the discovery of growth hormone releasing hormone releasing hormone (GHRHRH). Ok, I jest, low-levels of growth hormone and insulin stimulate GHRH.
Notice something interesting: ghrelin is an appetite controlling hormone. When you fast, GH production goes up and up and ghrelin goes down. When fasting, the hardest part is about six hours after your last meal when your insulin levels have dropped down and you have a strong appetite. However, if you get over this 'hump' you will find that your appetite largely goes away as the ghrelin circulating in your blood starts the secretion of GH. You will still get thirsty, but not ravenously hungry. I would generally recommend sleeping through this stage.
So what's the difference between controlling your body's overall insulin/GH levels very controlling your appetite to avoid binge eating? Can we actually separate the appetite hormones, leptin and ghrelin from the metabolism control hormones, insulin and growth hormone? As far as I can tell, appetite and blood sugar levels are basically the same thing. Trying to separate the two as wholly independent variables and then claiming that fat people simply lack self control when it comes to food is very very wrong. The science clearly shows that the two are deeply inter-related.
Figure 4. from Hartmann et al., 1992, showing the negative correlation between GH release and body-mass index in fasted subjects.Production of growth hormone typically declines as we age. However, research has shown that growth hormone levels are more tightly correlated with visceral fat (belly fat) than age (Vahl et al, 1997). So do we get fat because we get old or do we get old because we get fat? Both answers appear to be correct, each to a degree. No one will live forever, but most of us would like to age gracefully. I'm about a decade younger than I was at this time one year ago.
Real-world means of increasing growth hormone levels
There are three basic ways to increase the amount of GH your body produces:
- Get adequate sleep. GH production spikes during sleep. Try not to eat before bedtime.
- Fast occasionally, for relatively short durations.
- Conduct intense exercise. Don't eat before or during your exercise.
Figure 1. from Pritzlaff et al., showing GH secretion pulses as a function of lactate threshold (LT) reached.Of course, (2) and (3) can be combined. A word of warning, if you exercise hard at the end of a fast, be prepared for sore muscles (i.e. delayed onset muscle soreness) the next day.
A low-carbohydrate diet may have the advantage in this situation as the overall insulin pulse should be small and of shorter duration. The reason is fairly obvious: the body's tissues will be less insulin resistant and hence absorb glucose from the blood stream more readily. Hence one should enter the fasted state quicker after a low-carbohydrate diet than not. The more time you spend in the fasted state, the faster you're going to shed body fat.
The $64,000 dollar question is then, what effect does dietary fat have on growth hormone secretion? It appears that dietary fat intake increases the production of somatostatin from the gut, otherwise known as growth-hormone inhibiting hormone, although somatostatin down-regulates many many other hormones (Cappon et al., 1993). Anecdotal evidence from people who regularly fast is that fasting is easier to handle on a low-carbohydrate diet than a low-fat diet. I dug around for awhile on PubMed, but I wasn't able to find any research where subjects were fed diets of pure glucose and pure triglycerides and then their transition from feasted to fasted tested. It would be a good Master's thesis for someone if it really hasn't been done before. I did find tests that tested intravenously applied fatty acids in fasting but since somatostatin is produced by the digestive system their relevance isn't clear. The Hartman study from 1992 seems to be the best starting point for this line of research.
References
in alphabetical order:
Cappon JP, et al. "Acute effects of high fat and high glucose meals on the growth hormone response to exercise." J Clin Endocrinol Metab. 1993 Jun;76(6):1418-22.
Gibney J, Healy ML, Sönksen PH. "The growth hormone/insulin-like growth factor-I axis in exercise and sport." Endocr Rev. 2007 Oct;28(6):603-24.
Gröschl M, et al., "Endocrine responses to the oral ingestion of a physiological dose of essential amino acids in humans.", J Endocrinol. 2003 Nov;179(2):237-44.
Hartman ML, et al., "Augmented growth hormone (GH) secretory burst frequency and amplitude mediate enhanced GH secretion during a two-day fast in normal men." J Clin Endocrinol Metab. 1992 Apr;74(4):757-65.
Ho KY, et al. "Fasting enhances growth hormone secretion and amplifies the complex rhythms of growth hormone secretion in man."J Clin Invest. 1988 Apr;81(4):968-75.
Jensen MD, et al., "Lipolysis during fasting. Decreased suppression by insulin and increased stimulation by epinephrine." J Clin Invest. 1987 Jan;79(1):207-13.
Liu H, et al. "Systematic review: the effects of growth hormone on athletic performance."
Ann Intern Med. 2008 May 20;148(10):747-58.
Pritzlaff CJ, et al. "Impact of acute exercise intensity on pulsatile growth hormone release in men." J Appl Physiol. 1999 Aug;87(2):498-504.
Møller N, Jørgensen JO, "Effects of Growth Hormone on Glucose, Lipid, and Protein Metabolism in Human Subjects." Endocr Rev. 2009 Mar 19.
Nørrelund H, et al., "The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown." Diabetes. 2001 Jan;50(1):96-104.
Jesse Roth, et al., "Hypoglycemia: A Potent Stimulus to Secretion of Growth Hormone." Science 140(3570):987 - 988 (May 1963).
Scacchi M, Pincelli AI, Cavagnini F. "Growth hormone in obesity." Int J Obes Relat Metab Disord. 1999 Mar;23(3):260-71.
Vahl N, et al., "Abdominal adiposity rather than age and sex predicts mass and regularity of GH secretion in healthy adults." Am J Physiol. 1997 Jun;272(6 Pt 1):E1108-16.
David Rabinowitz, Gerald A. Klassen and Kenneth L. Zierler, "Effect of Human Growth Hormone on Muscle and Adipose Tissue Metabolism in the Forearm of Man." J. Clin. Invest. 44(1): 51-61 (1965).
19 March 2009
Economic Limits to Energy Reserves
If you have a passing familiarity with energy policy, you probably are aware that the scale of potentially available resources is enormous. For example, the USA is purported to maintain coal reserves sufficient for 250 years of consumption, or 1600-3600 billion metric tons. From wind, the total world resource that is considered to be commercially viable is about 72 TerraWatts. However, that figure only includes the wind resources that exceed some average velocity (probably 7 m/s) so the actual total resource is somewhere around 500 TW. An enormous figure.
The viability of renewable power is largely a function of the price of fossil fuel commodities, the action of government in regulation and subsidy/taxation, and the technology level of the renewable sector. The conception that renewable power will be composed of a mélange of many different sources does not fully illustrate the likely outcome.
The term, commercially viable, then is key. What matters is not how big a resource is in absolute terms, but how that resource is distributed in terms of quality relative to alternative energy resources.
One possible metric for energy resource quality would be the EROEI (Energy Return On Energy Invested) which is especially popular in the Peak Oil community. It is an expression which can be derived in engineering terms so it is quantitative. However, the metric that really matters is the economic one: how many dollars do I have to spend to get my unit of energy? How can I further parametrize an alternative energy resource to evaluate when it will become economical to exploit?
Inertia and vested interests will have an influence over the short-term but eventually the cheaper source of energy will win. It's much more fuzzy than EROEI, since adding money adds many more degrees of freedom (i.e. value of fiat currency, cost of credit, cost of technology, etc.) and anything money related has a big rationalization factor, but it's fundamentally closer to the truth. If the EROEI metric was the determining factor, we'd all be powered by hydroelectric dams (and yes I am aware that after you amortize, hydro power is dirt cheap... smart ass).
The real metric then for energy quality is going to be the rate of return in dollars, not energy. Unfortunately, dollars per unit of energy is going to be a datum with many degrees of freedom behind it, making analysis complicated and prone to change on a month to month basis. Still, we can construct some hand-waving arguments based on best guesstimates to make some general conclusions.
Figure 1: Schematic of renewable energy resource economic distribution. Not to scale, seriously based on established data, etc. but rather a illustration for the eye. There's no reason for these curves to be symmetrical, it just looks better.
Most resources can be described as a sharp peak with heavy tails. For wind, you have some select areas where the terrain funnels katabatic winds coming off of mountain ranges and you find a strong, consistent wind resource. On the other hand, much of the Earth is covered in forests which increase the surface drag and results in a poor quality wind resource. On the geothermal power front, you have a few select areas where vents circulate magma from the Earth's mantle near to the surface and a lot of heat power can be extracted. However, most deep geothermal is going to be pulling heat energy out of the crust which isn't replenished quickly. Most rocks only conduct around 30 mW/m2 so it's easy to exhaust the resource. It's not clear, then, if deep geothermal can easily amortize the capital costs of drilling. Solar is an exception, in that not only does it dwarf all other resources in total potential but it's also very stubby.
If you look at the scale of various renewable and non-renewable power sources it quickly becomes obvious that solar dwarfs them all. There is about 190000 TW of solar power incident on the earth at any one time. Even when you factor in scattering from the atmosphere and clouds, it's still ~ 125x greater than the wind resource. Moreover, solar is also the most uniformly distributed. The best solar resources in the world, such as Arizona and North Africa, only receive about 3x more power than cloudy Northern Germany. This means that any graph of solar resource quality as a function of the total available resource is very squat and shallow. It's the Olympus Mons of power quality-potential curves. So why am I going on and on about solar? Well, it provides an economic floor to all other sources of power. Any portion of a resource that economically falls below the top of the solar curve, won't be significantly exploited, due to the extreme width of the solar curve.
The significance of the above statement is mostly of interest as a tool for formulating public energy policy. Should all alternative energy technologies be pursued with the aid of the public purse? Primary research at the academic level should not be funded on the whim of politicians, but when it comes to issues like production subsidies, the introduction of politics is unavoidable. Thus, I would like to propose a check-list for all those prospective deciders out there (and of course investors in the private funding world):
There are also a number of more auxiliary issues that can have a significant impact on how edit( economical a particular technology can be in a given locale. Some are simply a function of geography, such as how concentrating solar power only works in terrain that sees little cloud cover. ) These parameters make the situation fuzzier than before, but we can at least account for them in some qualitative, if inadequate, sense. An example that I've discussed is the increased speed of deployment and improvement of energy technologies that can be deployed in an incremental fashion.
Inertia of existing technologies is one of the most important parameters. Inertia in terms of an existing energy technology can be summed up as: embedded capital costs. As an example, buying an electric car or a plug-in hybrid costs quite a lot of money. Even buying a depreciated used SUV compared to a new Prius requires a huge number of miles driven to recoup the price premium between the two. The nature of inertia means that as the best of the fossil resources continue to be consumed, there will naturally be some overshoot before the renewables come to the fore.
Arbitrage opportunities should also be a great way of making money in the future. The giant disadvantage of renewable technologies like photovoltaic solar and wind is that they are not dispatchable (and in the case of wind, not reliably predictable). If 100 % of your generating capacity has to be backed with natural gas turbines, that adds a great deal of capital cost to your power generating infrastructure. I.e. it makes wind more expensive than the cost of the turbines alone would imply. However, balancing supply and demand with a reserve of turbines is probably the most expensive path you could take.
If you are an investor and want to start a new thin-film photovoltaic company, you are probably too late to catch the leaders. The depression of global trade and financial services will slow down the existing photovoltaic manufacturers, but you still have to navigate an uncertain minefield of failed technologies and patents. However, there's still plenty of opportunity to find niche applications to match daytime electricity generation to nighttime demand. Plug-in hybrids are generally seen as an excellent means of smoothing out the supply and demand curves, especially because they can justify a higher battery cost since they are purchased primarily for driving and not regulating the electrical grid. There are also other demand shaping potential means of arbitrage out there.
The viability of renewable power is largely a function of the price of fossil fuel commodities, the action of government in regulation and subsidy/taxation, and the technology level of the renewable sector. The conception that renewable power will be composed of a mélange of many different sources does not fully illustrate the likely outcome.
The term, commercially viable, then is key. What matters is not how big a resource is in absolute terms, but how that resource is distributed in terms of quality relative to alternative energy resources.
One possible metric for energy resource quality would be the EROEI (Energy Return On Energy Invested) which is especially popular in the Peak Oil community. It is an expression which can be derived in engineering terms so it is quantitative. However, the metric that really matters is the economic one: how many dollars do I have to spend to get my unit of energy? How can I further parametrize an alternative energy resource to evaluate when it will become economical to exploit?
Inertia and vested interests will have an influence over the short-term but eventually the cheaper source of energy will win. It's much more fuzzy than EROEI, since adding money adds many more degrees of freedom (i.e. value of fiat currency, cost of credit, cost of technology, etc.) and anything money related has a big rationalization factor, but it's fundamentally closer to the truth. If the EROEI metric was the determining factor, we'd all be powered by hydroelectric dams (and yes I am aware that after you amortize, hydro power is dirt cheap... smart ass).
The real metric then for energy quality is going to be the rate of return in dollars, not energy. Unfortunately, dollars per unit of energy is going to be a datum with many degrees of freedom behind it, making analysis complicated and prone to change on a month to month basis. Still, we can construct some hand-waving arguments based on best guesstimates to make some general conclusions.
Figure 1: Schematic of renewable energy resource economic distribution. Not to scale, seriously based on established data, etc. but rather a illustration for the eye. There's no reason for these curves to be symmetrical, it just looks better.Most resources can be described as a sharp peak with heavy tails. For wind, you have some select areas where the terrain funnels katabatic winds coming off of mountain ranges and you find a strong, consistent wind resource. On the other hand, much of the Earth is covered in forests which increase the surface drag and results in a poor quality wind resource. On the geothermal power front, you have a few select areas where vents circulate magma from the Earth's mantle near to the surface and a lot of heat power can be extracted. However, most deep geothermal is going to be pulling heat energy out of the crust which isn't replenished quickly. Most rocks only conduct around 30 mW/m2 so it's easy to exhaust the resource. It's not clear, then, if deep geothermal can easily amortize the capital costs of drilling. Solar is an exception, in that not only does it dwarf all other resources in total potential but it's also very stubby.
If you look at the scale of various renewable and non-renewable power sources it quickly becomes obvious that solar dwarfs them all. There is about 190000 TW of solar power incident on the earth at any one time. Even when you factor in scattering from the atmosphere and clouds, it's still ~ 125x greater than the wind resource. Moreover, solar is also the most uniformly distributed. The best solar resources in the world, such as Arizona and North Africa, only receive about 3x more power than cloudy Northern Germany. This means that any graph of solar resource quality as a function of the total available resource is very squat and shallow. It's the Olympus Mons of power quality-potential curves. So why am I going on and on about solar? Well, it provides an economic floor to all other sources of power. Any portion of a resource that economically falls below the top of the solar curve, won't be significantly exploited, due to the extreme width of the solar curve.
The significance of the above statement is mostly of interest as a tool for formulating public energy policy. Should all alternative energy technologies be pursued with the aid of the public purse? Primary research at the academic level should not be funded on the whim of politicians, but when it comes to issues like production subsidies, the introduction of politics is unavoidable. Thus, I would like to propose a check-list for all those prospective deciders out there (and of course investors in the private funding world):
- How large is the renewable resource that lies significantly above the solar resource and how does that compare to the amount of proposed investment? Note that this will change significantly from region to region. Britain isn't a great solar resource, but it has a much larger wave power resource than most. So for Britain you have a wider effective wave power peak and a lower solar base-line.
- Is there a significant body of academic research (typically 10-20 years) behind the concept or is it pie in the sky? Too many big energy ideas/start-ups try and do research and development without doing the research part. Needless to say, it usually ends in tears. Lithium-ion iron-phosphate batteries didn't pop out out of the ether, and neither did First Solar.
- What sort of (general) technologies developments on on the horizon that may effect the size and shape of the resource's economic curve? This is a really tough question for a politician to answer unfortunately. My advice is to keep it simple: only the really big changes matter on a macro scale.
- Does the technology deliver power at night? Statistically, wind and solar power have an almost identical standard deviation, the difference is solar is predictable. Looking forward, it seems inevitable that electrical power will be cheaper during the day than at night. This may necessitate, for example, plug-ins at work — we already have such things in Edmonton, but for powering the block heater in your car so the oil pan doesn't freeze into a solid pane of grease.
There are also a number of more auxiliary issues that can have a significant impact on how edit( economical a particular technology can be in a given locale. Some are simply a function of geography, such as how concentrating solar power only works in terrain that sees little cloud cover. ) These parameters make the situation fuzzier than before, but we can at least account for them in some qualitative, if inadequate, sense. An example that I've discussed is the increased speed of deployment and improvement of energy technologies that can be deployed in an incremental fashion.
Inertia of existing technologies is one of the most important parameters. Inertia in terms of an existing energy technology can be summed up as: embedded capital costs. As an example, buying an electric car or a plug-in hybrid costs quite a lot of money. Even buying a depreciated used SUV compared to a new Prius requires a huge number of miles driven to recoup the price premium between the two. The nature of inertia means that as the best of the fossil resources continue to be consumed, there will naturally be some overshoot before the renewables come to the fore.
Arbitrage opportunities should also be a great way of making money in the future. The giant disadvantage of renewable technologies like photovoltaic solar and wind is that they are not dispatchable (and in the case of wind, not reliably predictable). If 100 % of your generating capacity has to be backed with natural gas turbines, that adds a great deal of capital cost to your power generating infrastructure. I.e. it makes wind more expensive than the cost of the turbines alone would imply. However, balancing supply and demand with a reserve of turbines is probably the most expensive path you could take.
If you are an investor and want to start a new thin-film photovoltaic company, you are probably too late to catch the leaders. The depression of global trade and financial services will slow down the existing photovoltaic manufacturers, but you still have to navigate an uncertain minefield of failed technologies and patents. However, there's still plenty of opportunity to find niche applications to match daytime electricity generation to nighttime demand. Plug-in hybrids are generally seen as an excellent means of smoothing out the supply and demand curves, especially because they can justify a higher battery cost since they are purchased primarily for driving and not regulating the electrical grid. There are also other demand shaping potential means of arbitrage out there.
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