Clarifying Butter (i.e. Ghee) Guide

Mmm... butter, one of the tastiest of all fats. It also happens to be one of the most nutritious forms of dietary fat, containing the fat soluble vitamins A and D in their animal usable forms. It is also a good source of vitamin K₂, which regulates calcium metabolism; K₂ has become quite rare in our modern diet with its lack of fermented foods. Unfortunately, butter does contain some milk solids, so if you are gluten intolerant you may also be intolerant of the α-casein that makes up some 80 % of cow milk proteins. It also contains a little bit of lactose, which might make someone with lactose intolerance hurl. What to do? Why remove the milk solids of course. This process is called clarification and can easily be done on the stove top. The finished produce is often called Ghee, as it was once a staple of Indian cooking.

An additional advantage to clarifying butter is that it does not brown or burn nearly as easily so cooking with it at high temperatures is safer. Traditionally ghee is often flavoured with cinnamon or cloves. Incidentally cinnamon is a folk-method for treating diabetes; it has an insulin-like effect in addition to being high in chromium.

I typically clarify two pounds of butter at a time. Since the volume of the butter will be reduced by about 1/4 (primarily water and the filtered milk solids) this yields about 750 mL of high quality cooking fat. You'll want the following ingredients and apparatus:

• 2 lbs. butter (cultured butter will taste better)
• optional: wholes cloves and cinnamon stick
  
• sauce pan
• ladle
  
• thermometer, digital w/ alarm
• strainer
• elastic band (like the type broccoli stalks come with)
• terrycloth or cheesecloth

First start by melting the butter in the pan on low. As it melts to cover the bottom of the pan you can turn it up to medium and stick your thermometer into the oil. Set the alarm to 110 °C (230 °F). You don't want to use high heat here, as there's only a limited amount of water in the butter so it's mostly just a matter of time for the oil to heat up.

When water evaporates it takes away an enormous amount of heat, so the temperature of the ghee will stall a bit at or just above 100 °C (212 °F). At this point, the butter will separate into its three constituents: the milk solids, which will settle on the bottom, the golden-coloured oil itself, and a layer of foam on the top.

The foam does not contain casein, but it is unsightly and we want to get rid of it with our strainer. Just skim around the top, and then wash the strainer off with hot water. After 2-3 skims, you should have a cleaner looking product.

After cleaning off the foam you are essentially just boiling away the water content of the butter. Honestly if you know what you're doing and watch the butter carefully you don't need the thermometer. As the oil heats up, the bubbles will get smaller and smaller. When the oil stops bubbling, that means all the water has evaporated and the temperature of the oil will start to rise very quickly. When or if the milk solids at the bottom of the pan start to turn brown, remove the pan from the heat immediately. I generally wait until 125 °C (257 °F) to finish heating.

At this point it's time to transfer the clarified butter into your jar. I use terrycloth instead of cheese cloth for a few reasons. One, it is far cheaper and easier to find. It's even reusable, and it seems to do a better job of filtering the milk solids than cheesecloth. I do wash it beforehand. The elastic is wrapped around the base of the strainer to hold the filter in place.

That's it! Now just cap your jar and clean up. The hot ghee will be transparent and look a fair bit like thick urine. If any milk solids did make it through the filter process, they will settle on the bottom. As it cools to room temperature, it will become more solid and turn a pale yellow colour.

Ghee is shelf-stable although I would store it in a cupboard away from light. It can be refrigerated but it becomes very hard at colder temperatures and impossible to get out of the jar with a spoon.

If you can't afford high-quality grass-fed organic butter (I certainly can't), you may want to consider adding vitamins D₃ and/or K₂ if you can buy them in drop form. Add them to the finished ghee in the jar and stir.

Vegetarians who Eat Meat

I made a comment on my last post about the paleolithic principle on the notion of, "vegetarians who eat meat." I had to laugh when I read this post on TheAtlantic.com by Marion Nestle, "Are Vegetarian Diets Healthy?" A quote that illustrates the funny:

But before getting into all this, there is the pesky problem of definition. What, exactly, is a vegetarian? As it happens, people who call themselves vegetarians eat many kinds of diets. The least restrictive vegetarians do not eat beef but occasionally eat pork or lamb. Next come the groups that eat no red meats, or restrict poultry, dairy, fish, or eggs. The most restrictive are vegans who eat no foods of animal origin at all.

It's as if everyone claims CAFO pork is better for you than grass-fed beef, it must be true...

I've covered this briefly in the past. Vegetarians who eat fish had lower overall incidence levels of cancers than vanilla vegetarians, and both were better than the British Standard Diet eaters. Once again, maybe it isn't meat that's the problem per say, but that people who don't eat it have a better relationship to their food (on average) than people who do (on average). What, exactly, does a vegetarian eat at a fast food restaurant? Do they eat at fast food restaurants? Or do they bring a bag lunch to eat most work days?

Your, "food culture of one," matters. Eat that which doesn't make you sick.

The Paleolithic Principle

I would like to share an overview of how and what I eat, and why. Rather than list individual food items, I will discuss the approach in general terms. I won't really be rigorously supporting many of my statements since that would require an entire book or more worth of writing. I will try to keep this brief and information dense.

I structure my nutritional philosophy around the notion of the Paleolithic Principle. The principle is that the human animal has been around and eating a relatively consistent diet for a couple of million years with Homo Sapiens being around for almost 100k years. It was only really with the introduction of the neolithic age that technology brought new foodstuffs to consume such as dairy, grains, and the other modern cultivars of plants that we eat. The paleolithic principle states that we have not fully adapted to these new types of foods and hence they may be harmful to our health, on a case by case basis.

These new sources of food were introduced roughly 5000 - 7000 years ago, which is perhaps some 300 generations worth of time. Humans, being long-lived, evolve quite slowly. Humans, being highly social sentient apex predators, also don't necessarily experience the same degree of natural selection as other species. The question is then, just how well adapted are we to these neolithic food groups?

We know for a fact that food tolerances have an ethnic bias. We know that the closer one's ancestors hailed from Mesopotamia the less likely they are to be intolerant to wheat gluten. Similarly, Asians are far more likely to be lactose intolerant than Europeans. Thus, clearly, only certain segments of the human population have adjusted to each particular Neolithic foodstuff. These are established facts, and they provide a basis for the paleo principle as a reasonable hypothesis.

If one has an ethnic background that strongly identifies with a particular ethnic diet then you might be best off following it since you're probably selected for it. This doesn't always work well however, especially in the immigrant nations such as the USA and Canada, where there has been a great deal of mixing in ethnic groups. Personally, I'm a mix of Polish-Romanian jew, Italian, French, Norwegian, Scottish, Austrian, and English, with a few other nationalities thrown in for fun. If I were to follow an ethnic diet, which of the ten or so should I pick? Almost all of the neolithic food groups give me some trouble. Perhaps I'm simply lacking in intestinal fortitude.

The largest quantity of pharmaceuticals that one ingests by far is in the form of foodstuffs. Plants especially contain an enormous number chemical compounds, not all of which are broken down before they cross the gut-blood barrier. For whatever reason, the gut-blood barrier and the associated bacterial biofilm has broken down more commonly in modern man.

Of course, even foodstuffs that we have been (slowly) adapting to over 5000 - 7000 years have changed a great deal. For example, the heavy fertilization of dwarf wheat strains has resulted in higher protein yields but that protein predominantly comes in the form of increased gluten content. So when people scratch their heads about the increased incidence of celiac and other gluten related autoimmune disorders, it may just be that the wheat is changing rather than the people, n'est pas? Similarly ever compared a wild strawberry to a super-fertilized all-season Californian monstrosity? We have started supplementing our diet with artificial food additives, such as mono-sodium glutamate (MSG), which only further complicates our understanding of nutrition.

Modern farming practices, cultivars of plants, and breeds of animals sacrifice micro-nutrient content for economy in the form of macro-nutrient content. In some cases, you don't even get more macronutrient, but just more water content for the check-out scale. Thus you have the paradox of a person who is obese yet simultaneously starving thanks to a diet of soda pop and it comes about due to the imbalance in the ratio of micro-nutrients to macro-nutrients in the foods we eat. This is the tyranny of the middles aisles in the supermarket.

Now, the paleolithic principle is sort of like using a sledgehammer to pound in a finishing nail (HT: Chris). It works, it works quite well actually, but it is an excessive means to the task. I don't ascribe to the fairy tale view that everyone was engaged in happy-fun-time back before the introduction of agriculture but there's little doubt that hunter-gatherers were physically far more impressive animals than the more numerous agriculturalists and pastoralists that out-competed them.

It's clear to me that industrialization and technology has had a number of negative consequences to human health which we call the "diseases of civilization." The most obvious of these are heart disease, diabetes and obesity (including metabolic syndrome), but they also include autoimmune disorders (which are far more common than is generally recognized) as well as many neurological disorders. I don't think it has to be this way, but there have been some very wrong-headed paths taken in the field of nutrition over the past fifty-odd years.

From an evolutionary perspective, the more recently a particular foodstuff was introduced, the more likely it is to cause distress. This implies that refined oils and large quantities of fructose, both of which were entirely absent in the 1800s, are two of the more obvious places to eliminate and cut-back in order to restore the good health nature intended us to have.

If I were to sum up a reasonably brief list on what to do and what not to do, this would be it:

1. Control appetite hormones like gherlin by eating regular, satiating meals. By satiating I mean protein, fat, and fibre. Try to avoid snacking.
   
2. Restrict fructose and alcohol consumption to reasonable levels, day-to-day. 20 g/day of both combined would be a very healthful level, 50 g/day is I think an upper bound for people with healthy livers.
3. Eliminate industrial, refined oils, particularly refined polyunsaturates such as soy and canola oil. Go for fresh and high quality fats, in particular clarified butter, extra-virgin coconut oil, extra-virgin olive oil, and the fats from animals fed their native diet. Unstable oils should be stored in the refrigerator or freezer to prevent them from going rancid, e.g. Omega-3 fish oil capsules. Most industrial oils are deodorized to prevent you from smelling when they go bad.
   
4. Eat more than just muscle meat from an animal. Have you eaten liver pate or roasted heart lately? Bone broth?
5. Fast occasionally for approximately 24-hours to give your liver a break and restore insulin sensitivity. Many religious groups noted for their good health (i.e. Seventh-day Adventists, Mormons, and the Greek-Orthodox of Crete and Corfu) regularly fast — is the the shared common trait. Fasting and starving are not the same thing, don't conflate the two.
6. Go on elimination dietary trials of the common food allergies: wheat (including barley and rye), cow dairy, legumes, especially soy and peanuts, tree nuts, eggs, fish, and shellfish. Test assays may be insufficient to recognize many of the idiopathic problems (i.e. autoimmunity, neurological disorders) that these types of food may induce. It took me six months wheat-free to get better.
   
7. Supplement with Vitamin D, on the order of 1000 IU/12 kg of body mass per day. Consider that the recommended doses for infants are 400 IU/day, so if you mass ten-times that of an infant, you need ten-times as much vitamin D; recommended adult doses are a joke. Also consider that you produce about 10,000 IU/ 30 minutes in full-sun. Vitamin D is not a vitamin, it is the precursor material to most of the steroid hormones in your body. When the endocrine (hormone) system has adequate signaling compounds, the whole body works better.

I do not eat much in the way of carbohydrates primarily since wheat and dairy are off-limits to me but even more so was the realization that foodstuffs that are good sources of glucose are also bereft of micro-nutrients. I.e. they are empty calories. You know how some people drink socially? I eat grains socially (with the notable exception of wheat, which I find incredibly destructive to my body). This said I don't believe glucose is inherently a problem and I do carb-load from time to time.

You may have noticed that I haven't talked about exercise at all, and that's because I think it is relatively unimportant. If you apply the 80/20 rule to how well you feel, I think perhaps 80 % of your wellness comes from diet, 15 % from adequate restful sleep, and perhaps 5 % from physical activity. Trying to lose body fat from exercise is a fool's errand and more than likely will result in over-training and the associated chronic injuries. While I personally do get a lot of physical activity, it's all for fun. My current hobby is whitewater kayaking, so any physical training I do is oriented towards improving my performance in that regime rather than building bulging biceps. I don't bother lifting weights in the gym since I find it quite dull. The fact of the matter is I got healthy through diet first and only then started exercising more.

Now, you may have noticed me talk about autoimmunity a lot and that is because I think it plays a key role in the diseases of civilization. Autoimmunity is simply the case in which the immune system, which is responsible for both healing and repealing foreign invaders, starts attacking the tissues of its host body. Autoimmunity has a genetic component, but something needs to trigger it. Examples are viral or bacterial infections, or dietary allergies. Celiac is one type of autoimmune disorder, type 1 diabetes is another.

If the diet is introducing strange, novel foreign bodies into the gut and the gut is compromised, they will penetrate into the circulatory system. The immune system sees these foreign bodies and goes berserk trying to hunt them all down and destroy them. Then, four to six hours later, you eat another meal and the cycle repeats. The solution is to remove the stimulus, i.e. fix the diet.

Any sort of food allergy or intolerance is likely to result in the immune system being depressed. The immune system only has a finite capacity for fighting infection, and if you're making it waste its time chasing gluten peptides or whatever, it is not going to be so strong at fighting off the latest pathogen. Similarly if you are not providing the immune system with enough micro-nutrients to operate at full capacity you will not only get sick more often, but you will also heal more slowly.

If I could sum up my nutritional philosophy in one sentence it would be:

Don't eat things that cause your immune system to run around like it has a hole in its head.

A touch different from Michael Pollan, but I digress.

Wanted: Muse

I'm trying to write a post and an article, but words are just not coming onto the page. Isn't it funny how sometimes you've just "got it" and sometimes you have absolutely nothing?

Breakthough in Flow Batteries?

So there's been a little Google explosion on the subject of flow batteries recently, with a German group claiming a breakthrough. From the press release,

Until now, however, redox flow batteries have had the disadvantage of storing significantly less energy than lithium-ion batteries. The vehicles would only be able to cover about a quarter of the normal distance – around 25 kilometers – which means the driver would have to recharge the batteries four times as often. “We can now increase the mileage four or fivefold, to approximately that of lithium-ion batteries,” Noack enthuses.

Mmm... vague, yes? As anyone who has been following the alternative energy scene for any length of time knows, the bigger the claim and the fewer facts behind it, the more likely it is to be BS. As always, it pays to be skeptical rather than credulous.

If you aren't familiar with the technology of flow batteries, I suggest you buck up to Wikipedia and take a read. The strong point of flow batteries has always been that the power and energy storage characteristics are decoupled: the power is a function of the size of exchange membrane, while the energy storage is determined by the volume of the storage tanks. In this fashion, they are a lot like fuel cells except that they are reversible. However, the energy density (as a function of weight or volume) has never been terribly impressive, lying around that of lead acid batteries.

The engineer who is quoted in the story, Noack, appears to be involved with the design of the exchange membrane and I can't see the mechanical bits resulting in a 4 - 5 fold improvement in energy density. I found a paper he wrote here comparing the various known chemistries applied to a new membrane stack design. There must have been some new chemistry developed, either that or there's smoke and no fire here. The article does mention collaboration with the University of Applied Sciences, Ostphalia [sic], but I can't find anything pertinent on the university's web site.

The previous king of the various redox flow battery chemistries is the Vanadium redox battery. It can, in general, obtain a 75 % round-trip efficiency which is fairly decent, being roughly in-between Li-ion batteries and Nickel-metal hydride batteries. The Achilles heel has always been the chicken and egg problem of the cost of Vanadium. Vanadium is not a particularly rare element, but it isn't mined in large quantities due to lack of demand and hence it is quite expensive. A single utility scale redox battery would consume a significant portion of the world's annual Vanadium production. Thus the conundrum, if no one can afford to buy a Vanadium redox battery, you'll never generate enough demand for Vanadium to open up new mines and drive the price down. The best hope, I always thought, was for one of the Vanadium-contaminated oil deposits of the world to be developed and glut the world Vanadium market.

As far as I know the intellectual property behind the Vanadium redox battery was held by VRB Power Systems but they went bankrupt earlier this year. They seem to have been acquired by a Chinese firm, Prudent Energy. It's probably worthwhile that the dollar numbers for Vanadium redox batteries didn't work out, even way back in 2005 when I last looked at it.

The Chronic Infection Theory of Heart Disease

Introduction

Heart disease, or more specifically atherosclerosis, is a chronic disease whereby cardiac arteries become partially occluded by the growth of plaques. Narrowed arteries are more likely to trap dislodged blood clots, resulting in blood supply being cut off to a portion of the heart, resulting in oxygen depletion of the cardiac muscle tissue and eventually myocardial infarction or heart attack.

Contrary to common wisdom, dietary fat does not deposit on the arterial wall and "clog your arteries;" plaques grow inside the arterial cell wall and consist of a mix of the smooth muscle cells that naturally line the interior lining of the artery and immune-system cells such as macrophages and lymphocytes. Macrophages, or white blood cells, are the large, amoeba-like cells that form the last line of defense for the immune system. This mix of cells are called foam cells. Foam cells tend become bloated by absorbing large amounts of cholesterol from the blood stream and they form a cyst or lesion which compresses the arterial wall, reducing the effective diameter.

By way of background, there are three times of muscle in the body: cardiac, skeletal (meat muscle, like your bicep), and smooth muscle (such as your scalp or vital organs). Smooth muscle is quite a bit different from the other types in that its cytoskeleton has no deterministic, regular structure. Rather, it just consists of a chaotic jumble of actin filaments. Unlike the other two types, smooth muscle is not normally controlled by the electronic action potentials of the nervous system; rather, it is controlled by the much slower chemical hormonal system.

With time, atherosclerotic lesions may harden by absorbing calcium from the blood which makes the artery stiffer and tends to result in high blood pressure. This is not unlike how bone tissue is formed by the mineralization of connective tissue, which in turn suggests some sort of hormone dysfunction is in play. Hardened arteries are considered more hazardous than pliable yet still narrow arteries. The likely reason for this is that a narrowed yet pliable artery can distend under pressure to allow a blood clot through, while a calcified artery cannot.

Thus we have three criteria for heart attacks (with some simplification):

1. The wall of the cardiac artery has to be sufficiently narrowed so that,
2. A dislodged blood clot gets stuck in it, and/or an atherosclerotic lesion ruptures (in the majority of heart attacks anyway), and
3. The arterial wall is too stiff to allow the build-up of pressure caused by the obstruction to allow the clot through, resulting in down-stream oxygen deficiency and eventually cell death.
   

To reduce heart attacks, you can attack any of these three processes. Take the Masai tribesmen of Tanzania: they have a great deal of atherosclerosis thanks to their milk-based diet, but they don't necessarily suffer heart attacks, likely due to their adequate intake of vitamin K₂.

I want to talk about the first requisite, atherosclerosis. The question is of course, what causes immune system bodies to form colonies inside the lining of one's arteries? There are two basic possibilities: auto-immune disorder, where the immune system recognizes legitimate tissue as foreign, or actual foreign bodies, such as chronic bacterial or viral infection of the blood vessel. Or both.

Enter Chlamydia pneumoniae, bacterium

The idea that atherosclerosis might be caused by chronic infection of the lining of blood vessels is not a new one. In 1999, the American Heart Journal devoted a supplementary issue to the topic. It is, essentially, an alternative theory for heart disease as compared to the diet-heart hypothesis, whereby diet modifies serum cholesterol levels which in turn causes heart disease by some unknown mechanism. As it contraindicates the standard lipid model, it is considered controversial. The first potential pathogen candidate was cytomegalovirus (aka herpes) but it turned out to be a bust.

Further research suggested a better candidate. Chlamydia pneumoniae (aka Chlamyophila pneunomiae) is the bacterium most commonly associated with heart disease in the literature. As the name suggests, it is one of the sources of pneumonia and other respiratory infections. It has also been associated with Alzheimer's and asthma. It is a relatively recently discovered pathogen (in that the diet-heart hypothesis was formulated before anyone knew it existed), and its responsibility for respiratory infection was only discovered in 1986 (Grayson etl al., 1986). The association with heart disease was made very quickly (Saikku et al., 1988), since the hunt for a potential atherosclerotic pathogen had been underway since the early 1980s.

Bellard et al. (2003) lay down the case for C. pneumonaie succinctly,

Exposure to Chlamydia pneumoniae is extremely common, and respiratory infections occur repeatedly among most people. Strong associations exist between C. pneumoniae infection and atherosclerosis as demonstrated by: (i) sero-epidemiological studies showing that patients with cardiovascular disease have higher titres of anti-C. pneumoniae antibodies compared with control patients; (ii) detection of the organism within atherosclerotic lesions, but not in adjacent normal tissue by immunohistochemistry, polymerase chain reaction and electron microscopy and by culturing the organism from lesions; and (iii) showing that C. pneumoniae can either initiate lesion development or cause exacerbation of lesions in rabbit and mouse animal models respectively.

This list is not exhaustive, and it does not note probably the most important point: C. pneumoniae can create foam cells in vitro (i.e. in a Petri dish). C. pneunomiae has been shown to infect the constituent cells in foam colonies (i.e. macrophages and smooth muscle) (Fryer et al., 1997), inhibit the mechanism whereby cholesterol (LDL) is relinquished (Kalayoglu, 1999), and oxidize low-density lipoprotein (LDL) via releasing heat shock proteins (Kol et al., 1998). More on this later.

The physical presence of C. pneunomiae in atherosclerotic lesions has, as previously mentioned, been detected by a wide variety of methods. It's also highly prevalent. Of many studies that have found C. pneumoniae in foam colonies, (Muhlestein et al., 1996) is probably the most solid. From a population of 90 patients, they found evidence of C. Pneumoniae in 79 % of atherosclerotic plaques, but only 1 of 24 control biopsies.

A basic question then is how does one particular type of bacteria manage to not only evade the immune system, but distort its response in order to cause great harm to the host? (Belland et al., 2003) explore the mechanism,

Chlamydial growth is biphasic, consisting of two alternating functional and morphological forms (Fig. 1). The elementary body (EB) is the metabolically inert, infectious form of the organism that is capable of transient extracellular survival. EBs bind to as yet undefined host cell receptors, are internalized via a pathogen-specified process and are detectable within a membrane-bound vesicle immediately after entry. This vesicle is capable of interacting with post-Golgi secretory vesicles in ways that allow for the incorporation of host phospholipids [RM: phospholipids are cell membranes, i.e. camouflage] (Hackstadt et al., 1996; 1997). Chlamydiae also block intracellular host cell responses, such as fusion of the pathogen-containing endosome with lysosomes, and thus avoid host cell factors that would be detrimental to intracellular survival. Soon after entry, chlamydiae differentiate from infectious EB to the intracellular replicative form of the organism, referred to as the reticulate body or RB. This differentiation, which is dramatic in terms of altered chlamydial morphology, must reflect an orchestrated sequence of differential gene expression. Transformation of EB to RB results in loss of the disulphide cross-linking of the outer membrane complex, decondensation of the genome and initiation of DNA, RNA and protein synthesis. RB multiplication results in the formation of an intracellular microcolony (termed the inclusion) of chlamydiae.

Ok so that's a wordy quote, but to sum it up in one word it is mimicry. A big area of research in bio-nanotechnology is the development of phospholipid coatings on implanted medical devices to prevent the immune system from recognizing them as foreign and attacking them. This technique is known as, "stealth technology." Here we have an example of an organism that has evolved this technique. <acerbic>But don't you dare eat any eggs, they have cholesterol in them</acerbic>.

It's not clear if C. pneumoniae causes all atherosclerosis but I do believe it causes a majority of such. Another potential source of plaque-forming bacteria is Helicobacter pylori, which among other things, is thought to be responsible for ulcers. Unlike C. pneumoniae, which enters through the lungs, H. pylori typically lives in the gut. A study by Mayr et al. (2000) found an association between H. pylori antibodies and cardiovascular disease, but only in the low status (i.e. poor) individuals in their population. This study was conducted in Austria, so one wonders what might poor Austrians be eating that would cause them to suffer H. pylori infections?

The same paper also found odds ratios for: IgA type antibodies to the C. pneumoniae bacteria, elevated C-reactive protein levels in the blood, and (clinical) chronic respiratory infection. Now, odds ratio is a funny, non-intuitive statistic, but we can directly compare it to odds ratios found in other studies.

Table 1: Odds ratios for various diseases of affluence.

Description	Odds Ratio
Top quartile LDL cholesterol developing coronary artery disease within six years. (El Harchaoui et al., 2007)	1.73
Any one of: IgA antibodies to C. Pneumoniae. Elevated C-reactive protein levels. Clinical chronic respiratory infection.	1.5
Two of above.	4.33
Three of above.	10.28
Smokers developing Lung Cancer, versus non-smokers (Doll & Hill, 1956)	12.8

As you can see, three out of three is quite a strong association, far stronger than the cholesterol testing that is the most common method of screening for heart disease risk in medicine today. It is actually getting close to that of smoking and lung cancer, which is the gold-standard for causation. If you break it down individually, the strongest of the three criteria is chronic respiratory infection (OR of 3.8), followed by C-reactive protein (OR of 2.4). Since C. Pneumoniae antibodies has the poorest odds-ratio, while the chronic conditions are much higher, we can probably surmise that being infected once isn't going to cause atherosclerosis, in the same sense that over-drinking once is not going to cause fatty liver disease. Heart disease is a chronic condition, caused by chronically applied vectors (i.e. diet and environment). For the same reason, antibiotics were found to be ineffective in treating atherosclerosis: they are effective for acute infection, but in the long run they cause as many problems as they solve, since many of the bacteria in our bodies are beneficial and help out-compete teh nasties [sic].

Heat Shock Proteins

Another issue, that I eluded to above, is what exactly is causing inflammation in this case? Medicine has identified oxidized-LDL as a major danger factor, but is this a cause or just a symptom?

One potential candidate is a class of proteins that are produced by cells under stress, collectively known as heat shock proteins. The name is not well chosen, heat shock proteins should be termed temperature stress proteins. They are produced by cells that are under elevated temperatures (or many other forms of environmental stress) and they protect the other functional machinery of the cell from future elevated temperatures. They are considered to be a part of the general inflammation response of the body, although they tend to operate on a small, single-cell (i.e. autocrine) scale.

Foam cell colonies produce one particular type of heat shock protein, HSP60, in large amounts.
This particular heat shock protein is usually associated with mitochondria, the energy factories of cells, but it's also known to interfere with apoptosis, or programmed cell death. Apoptosis is the way in which the body normally disposes of broken or old cells. Elevated levels of HSP60 prevent apoptosis from occurring (Gupta and Knowlton, 2005).

One study on 1003 Chinese men found an odds ratio of 2.3 for atherosclerosis by simply being in the top half of the population for HSP60 levels in the blood (Zhang et al., 2008, full-text link on Pubmed is broken and is available here). Those in the top quartile for HSP60 levels had an odds ratio of 4.87, which higher yet than the range usually seen for c-reactive protein, which is the standard marker for inflammation.

The high odds ratio with c-reactive protein has been seen as one of the supporting features for the slowly evolving, mainstream view that inflammation and not blood lipids are responsible for heart disease. But is inflammation the cause or symptom again, and what causes localized inflammation of the blood cell wall anyway? The fact that arterial foam cells produce heat shock proteins and a bevy of other inflammatory markers in quantity suggests that atherosclerosis causes inflammation, rather than the other way around. Indeed, studies have claimed that the chlamydial heat shock protein 60 (cHsp60) oxidizes LDL particles in a test tube (Kalayoglu et al., 1999). This is big deal, since the actual mechanism whereby LDL oxidizes isn't known. For example, see Steinberg, 1997:

First, patients and animals totally lacking the LDL receptor nevertheless accumulate cholesterol in foam cells much the same way as do patients and animals with normal LDL receptors; second, the two cell types in lesions that give rise to cholesterol-laden foam cells (the monocyte/ macrophage and the smooth muscle cell) do not accumulate cholesterol in vitro even in the presence of very high concentrations of native LDL (3,4). This paradox could be resolved if circulating LDL underwent some form of modification and if the modified form, rather than native LDL itself, then served as the ligand for delivery of cholesterol to developing foam cells.

There are no paradoxes in medicine, just an inadequate understanding of nature. That, and a heaping load of bias. If it is the heat-shock proteins that are causing much of the trouble, then we have some idea as to why foam cells are sustained by the body. The heat shock proteins produced by these bacteria closely mimic the same heat shock protein produced by the arterial wall (Hsp60). Heat shock proteins are one of the basic lego blocks of living cells, and there's not a great deal of variation between those HSPs produced by highly evolved human cells compared to say, yeast. The fact that HSP60 inhibits programmed cell death is another fascinating thread to pull on. Another possibility that occurs to me is that real bacterial infection may be transformed over a long time into an auto-immune disorder, even if the original bacteria have died off. More research is needed to assess just what the half-life of C. pneumoniae is in foam cell colonies.

Known correlations with heart disease

So how are these bacteria getting through the mucous tissues and into the blood stream? The correlation between smoking and heart disease is explained nicely by this hypothesis. Smoking compromises the lungs, leading to C. pneumonia or some other form of infection, which in turn results in atherosclerosis.

One might expect then that other chronic conditions that break down the walls of the mucous membrane/exterior environment barrier could also lead to atherosclerosis: dietary components that cause leaky gut, periodontal disease, and possibly fungal infections. Alternatively, substances that suppress immune system function could be associated with cardiovascular disease.

Other chronic diseases that results in a breakdown of the bloodstream-mucus-environment barrier should also show increased rates of heart disease. The two most obvious choices to me are celiac disease (where wheat gluten destroys the lining of the intestines) and periodontal disease (of the gums in the mouth). For celiac disease, there doesn't seem to have been any research on the topic. Of course, it would be ethically impossible in a clinical setting to find undiagnosed celiac patients and follow them to assess heart disease. Once celiacs are diagnosed, their treatment is straight-forward (i.e. don't eat wheat or casein). However, perio is more difficult to resolve and the results on periodontal disease seem to be consistent, with perio causing a small (relative risk 1.24-1.34) yet consistent and significant increase in heart disease average over many studies (Cronin, 2009).

Similarly, substances or deficiency of certain materials in the diet that suppress or deform the immune system response could have an impact on heart disease. The most obvious would be insufficient vitamin D intake.

Conclusion

When it comes to the diseases of Western civilization/diet, we always must ask the question, what is the mechanism? A top-down approach is simply insufficient because separating correlation and causation in living organisms is so difficult and one is consistently tempted to simplify the details rather than break them down into first principles. Hence the enormous failure of pursuing cholesterol as a cause of heart disease, instead of recognizing it as a symptom. The false path of the cholesterol hypothesis has to rank of one of the greatest scientific blunders of all time and is indirectly responsible for the premature deaths of millions.

On the other hand, the chronic infection theory of heart disease is internally consistent with the data that are available to us. We know that C. pneumoniae is a common form of respiratory infection, and that once in the bloodstream it can infect smooth muscle and macrophage cells both in vivo and in vitro. We know that C. pneumoniae can disrupt the cholesterol metabolism of foam cell colonies in vitro. The chameleon nature of C. pneumoniae illustrates how foam colonies can be be persistent in the face of the immune system and morph an acute infection into a chronic condition. I just don't see any gaping holes in the theory. We still need to explain why C. pneumoniae (and other bacteria like H. pylori) affects some individuals and not others, but the how is reasonably explained and justified.

Author's note: I started writing this post on May 13th, 2009.

Feynman Lectures on the Web

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/E_o 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 E_o=300,000 eV in the denominator, or angles less than 0.004 °.

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.

Observational Study on "Cancer incidence in British vegetarians"

Key et al. reported in the British Journal of Cancer a large observational study that compared cancer incidence between groups based on diet. This article claims to be free access to the public. The corporate media love to report on research like this because they find it simple to tease good headlines out of them. Unfortunately, the closer you look at observational studies, the less sure of anything you end up being.

The study split 61566 Britons into three groups, 'meat-eating' (N = 32403), 'fish-eating vegetarians' (N = 8562), and 'vegetarian' (N=20601). Unfortunately, the study did not split up lacto-ovo vegetarians from vegans, as that may have been interesting due to the removal of another food group in the form of dairy.

The 'meat eating' group could be better described as the 'standard British diet' group. There are substantial differences in the approach to food between vegetarians and the stereotypical general population. This is particularly evident in the degree of industrial, processed food consumed although when I go to organic food markets I still see plenty of crap in the middle aisles.

There were, of course, differences between the three groups that were not dietary:

The mean age at recruitment was lower in the fish eaters and vegetarians than in the meat eaters. Smoking rates were low overall, with only 14.4% of meat eaters, 11.2% of fish eaters and 11.4% of vegetarians reporting that they were smokers at the time of recruitment. The median BMI was 1.5 kg m^-2 lower in vegetarians than in meat eaters, and the median alcohol consumption was 1.0 g per day lower in vegetarians than in meat eaters. Fish eaters had similar mean BMI to the vegetarians and had similar alcohol consumption to the meat eaters. The proportions of men and women who reported a relatively high level of physical activity were higher among fish eaters and vegetarians than among meat eaters. The proportion of women who were nulliparous at recruitment was higher among fish eaters and vegetarians than among meat eaters, and the proportion of women who had ever used oral contraceptives was lower among fish eaters and vegetarians than among meat eaters.

The authors claim to have corrected for these factors in their results for cancer risk factors, and that an uncorrected analysis had similar results to the corrected one (i.e. that the differences did not impact the results).

Table 1: Relative risks of cancer for various forms, RR = 1.0 for the 'Meat Eaters' group.

Selected Major Cancer Types	Fish Eaters’ Relative Risk to Meat Eaters	Vegetarians’ Relative Risk to Meat Eaters
Upper GI tract	0.44 (0.16–1.25)	0.81 (0.45–1.46)
Stomach	0.29 (0.07–1.20)	0.36 (0.16–0.78)
Colorectum	0.77 (0.53–1.13)	1.12 (0.87–1.44)
Lung	0.59 (0.29–1.23)	1.11 (0.75–1.65)
Melanoma	0.90 (0.55–1.47)	0.89 (0.61–1.29)
Female breast	1.05 (0.86–1.28)	0.91 (0.77–1.08)
Prostate	0.57 (0.33–0.99)	0.87 (0.64–1.18)
Lymphatic	0.85 (0.56–1.29)	0.55 (0.39–0.78)
Cervix	2.05 (0.91–4.63)	2.08 (1.05–4.12)
Overall	0.82 (0.73–0.93)	0.88 (0.81–0.96)

The results were statistically significant only for stomach, lymphatic, and cervical cancers, and the overall results were also significant. The uptick in cervical cancer is interesting, but not particularly important given how easily it can be avoided through vaccination. What's interesting is that the fish-eating vegetarians appear to have lower risk factors than the pure vegetarians.

It's a little hard to make the claim that meat per-say is the causative factor when you take vegetarians and feed them fish and their cancer incidence drops. In the discussion, the authors' implication focuses on nitrates and other work has shown that heterocyclic amines produced by charing/burning food (not just meat) can be hazardous. Alternatively it could be something like deep frying food in vegetable oil, since its polyunsaturated content is so easily oxidized in such an environment. Could vegetarians be buying more organic food and ingesting lower levels of pesticides? Etc. To paraphrase Simon Pegg, identifying the causative factor is like trying to hit the bull-eye on a dart-board that is mounted on a F1 car, while blind-folded, and riding a horse.

This is the drawback of observational studies: you can't make any definitive conclusions from it. At best, it can act as a guide, but it's sort of like hiking in the mountains: do you follow that old blaze when the trail forks or do you try and orient yourself? The drops in cancer rates (-18 % for fish-eaters, -12 % for vegetarians) are no smoking gun. The drop in stomach cancer is impressive. By way of comparison, the rate of lung cancer in non-smokers is roughly 3 % (i.e. RR = 0.03) compared to heavy smokers.

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.

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.

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.

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.

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.

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.

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.

Adapted from Figure 1 in (Bataller and Brenner, 2005).

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.

Using a Neti Pot on April 1st

Let's say you've just finished a world-record set of sprint intervals after taking bozolol. Now you live in a city like I do and there's a lot of 'refinery dirt' in your sinuses. How to expel it? With a Neti pot:



Direct link:www.youtube.com/watch?v=aQm7YpxgOnA

The Failure of the American Elite

I would like to direct my readers to an article written by William Deresiewicz in the summer of 2008, "The Disadvantages of an Elite Education." To wet your appetite, I would like to present the conclusion:

The world that produced John Kerry and George Bush is indeed giving us our next generation of leaders. The kid who’s loading up on AP courses junior year or editing three campus publications while double-majoring, the kid whom everyone wants at their college or law school but no one wants in their classroom, the kid who doesn’t have a minute to breathe, let alone think, will soon be running a corporation or an institution or a government. She will have many achievements but little experience, great success but no vision. The disadvantage of an elite education is that it’s given us the elite we have, and the elite we’re going to have.

Deresiewicz does an excellent job of explaining why the Anglo-American elite has failed their countries so badly: they have pursued the establishment of a new class system, eradicating the existence of a meritocracy. It used to be, when you screwed up and lost trillions of dollars and indirectly put millions of people out of work, you resigned in disgrace. Not anymore, now you write whiny letters to the New York Times and rationalize away any of your responsibility. And all your peers insulate you from the negative consequences of your treacle-like mind, because they also have achieved their power and wealth with no evidence of wit or effort. It is a sad situation, because random-guy-on-the-internet-with-a-blog is clearly so much smarter. Admittedly, that is damning with faint praise; chimpanzees would also be an improvement.

I recall someone once said, with regards to NASA, "when failure is not an option, success becomes very expensive."

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:

1. The nervous system, which primarily controls fast actions such as motion and thought.
2. The endocrine (or hormonal) system, which primarily handles slower processes..
   

The characteristic time scale of the nervous system is milliseconds. It operates on the principle of action potentials: electrical impulses driven by the fast pumping of sodium and potassium ions. Hormones do not travel down specialized pathways, instead they use the circulatory system. In the endocrine system, the characteristic time is on the order of minutes or hours as hormones decay within the blood stream. From an evolutionary perspective, the endocrine system is much older, since even bacteria use a variety of signaling peptides to control their operation. The nervous system had to await the development of such advanced animals as the mighty squid.

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)
  

Many of these hormones interrelate with each other, either directly or through the mechanism of secondary, lower-tier hormones, in a very complicated system that is difficult to pick apart. Typically the hormonal system operates on the principle of negative feedback, so if production of one hormone surges, that will in turn generate feedback that will eventually damp it back to normal levels.

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:

1. 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.
2. 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.
3. 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).

Growth hormone is basically the hormone that controls when your adipose (fat) tissues release fatty acids to be metabolized by the rest of your body. No growth hormone, no significant fat loss.

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:

1. Get adequate sleep. GH production spikes during sleep. Try not to eat before bedtime.
   
2. Fast occasionally, for relatively short durations.
   
3. Conduct intense exercise. Don't eat before or during your exercise.
   

'Intense' exercise in this context means you should exceed 75 % of your 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).

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):

1. 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.
2. 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.
   
3. 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.
   
4. 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.

And what of the non-renewable resources? Well those curves are actively being consumed, with the highest quality reserves (i.e. the peaks of the mountains) going first. Of course, with improving technology, their are fossil reserves that are becoming more economic at the same time. It took a fairly enormous investment to get the oil sands of Alberta viable, but here we are now, making oil from asphalt.

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.

Richard Florida on Economic Resets

I recently listened to an interesting talk by U of Toronto's Richard Florida on recessions and where do we go from here? Florida's idea is that recessions act as resets for the economy, allowing the big old companies to die off so that new operations can grow and take their place.
Perhaps a better analogy is 'forest fire'. The US stimulus plan is specifically failing to eliminate the failures. As the Russians would say, don't reinforce failure.

Richard Florida on the Current podcast

The podcast does come across as a bit of a pump job for the greater Toronto area. I generally agree with his thesis, however. Royal Bank logged a C$1.14 billion profit in 1Q2009, and CIBC was similar (C$141 million with a C$708 million write-down). So yes, the Canadian banks are doing very well, relatively speaking. He's totally correct that too much money has been spent on housing and consumer goods. I found it interesting primarily because Florida is suggesting ways forward. There's too much hand wringing going on these days.

Canada's biggest weaknesses in my opinion are a lack of consistent funding for the 4th sector of the economy (R&D) and lack of diversity in some areas (i.e. too much reliance on resource extraction). For example, the Canadian government is inordinately fond of funding infrastructure and equipment purchases for universities rather than providing on-going support for salaries and maintenance. Greater emphasis should be placed on processing raw materials before they exit the country. Why do we export raw logs from time to time?

Trial Lead Balloons

It's been amusing over the past month or so watching the new Treasury Secretary, Tim Geither, float off a new trial balloon every weekend on a new plan to deal with the insolvency of the US financial sector. I personally, don't see any easy way out. The only reasonable solution appears to be nationalization, and I don't pretend it will be easy for those involved in managing it (last September):

Bank of America, CitiGroup, and JP Morgan Chase have all been busy building the Jenga tower higher (see making the pie higher) in the effort to become too ginormous to fail. Clearly they all expect to be bailed out, which is a pretty amoral way to run a business. "Bail us out or your retirement savings get it!" The appropriate response at this stage is to raise their moral hazard one and audit them, find out that, "Surprize, you're broke!" and nationalize the lot of them temporarily. Cashier the executives, amalgamate the trash from all three and quarantine it, then start breaking them into non-antitrust sized chunks and IPO them off in sequence.

So now, after attempting to float many balloons full of lead, we are finally getting there. Citi now wants the government to buy 40 % of its stock, stopping just short of nationalization. Does anyone really believe we'll be done at that point?

The only question I have, is were these leaks that came from the Treasury real ideas or was Geither just buying time and making an appearance of exhausting all the alternatives? Afterall, nationalization isn't part of the American culture. Cultures change; sometimes tumulteously, sometimes without even noticing.

All Medical Science is Wrong within a 95 % Confidence Intervalor: A Review of Taubes' "Good Calories, Bad Calories"

Recently I read a very impressive book by Gary Taubes, previously a reporter for the journal Science. The work in question is, "Good Calories, Bad Calories."' In the book, Taubes collects research to challenge the common knowledge of nutrition: that fat is bad for you, that we should eat polyunsaturated vegetable oils, that we should exercise for sixty minutes a day, etc.

The genesis of Taubes' book is an article he wrote for the NY Times in 2003. Five years later, Good Calories, Bad Calories was published. As background, there is a video of Taubes here where he overviews his thesis (1 hour 11 minutes, not safe for work since there are pictures of naked obese individuals) and adds a few pieces that were not in the book. Even if you have read the book, I recommend listening to the lecture. You can see from the video, Taubes is very solidly built.

In return for knocking down a bunch of accepted "common knowledge" hypotheses , Taubes presents ten new hypotheses (p.454) and I will add a few more than I extracted from reading the book:

Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.

The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.

Sugars—sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because of the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer's diseases, and the other chronic diseases of civilization.

Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

Consuming excess calories does not cause us to grow fatter, any more than it causes a child of grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

Fattening and obesity are caused by an imbalance—a disequilibrium—in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses the balance.

Insulin is the primary regulator of fat storage. When insulin levels are elevated—either chronically of after a meal—we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.

By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.

By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.

1. RM: Man, being the premier predator on the planet, evolved to eat a diet high in fat (and in particular the saturated and mono-unsaturated fat found in animal tissue). In the absence of clinical data, we should endeavor to structure our diet to be similar to that we evolved eating, prior to the introduction of agriculture approximately 10,000 BCE.
   
2. RM: Advanced Glycation End-products (abbreviated AGEs) may be a cause or byproduct of the oxidative stress that causes aging and many of the maladies associated with it.
3. RM: A low-calorie, high-carbohydrate diet will make you lethargic as chronically high insulin levels will try to convert glucose to fat while not leaving sufficient calories for the remainder of your basal metabolism. In comparison, low-carbohydrate, moderate-calorie diet will leave you energetic and lean.
   

One cannot help but wonder how a number of the weak hypotheses that Taubes explores came to become common knowledge in the field of nutrition? Taubes paints a picture of a few egotistical researchers who were able to effect what was essentially scientific fraud, by fitting their bias to the data rather than examining it critically. In Taubes words (p. 451), "it is difficult to use the term "scientist" to describe those individuals who work in these disciples [ed: nutrition, chronic disease, and obesity], and, indeed, I have activity avoided doing so in this book."

More importantly, once they established the common wisdom, they were able to better direct government funding to only support their hypotheses. I came to a somewhat different conclusion to Taubes, in that I see the puritanical aspects of American culture in the formation of these bogus hypotheses. For example, Taubes' quotes Jean Mayer, one of the fieriest preacher that lack of exercise causes obesity, in a 1955 The Atlantic magazine article:

Obesity, it is flatly stated, comes from eating too much and that is all there is to it. Any attempt to search for causes deeper than self-indulgence can only giver support to patients already seeking every possible means to evade their own responsibility.

Like I said, puritanical. This line of thinking can be traced all the way back to people like Sylvester Graham in the 1800s. The idea that cardiac disease might be caused by inflammation and bacterial infection and not by living a sinful life has been remarkably slow to percolate through the American consciousnesses yet it is well understood to be the case now. Obesity is probably not dissimilar.

Prior to my introduction to the world of low-carbohydrate diet, I hadn't paid too much attention to nutritional science. I worked on biophysics, where I formed the opinion that medical science was mostly garbage. This isn't largely the fault of the scientists involved; there's little opportunity for adequate learning though experience of repeated experiments and the systems involved are extraordinarily complex. As a physicist, if I get an correlation coefficient, R² < 0.9997 in an experiment, I would consider that a poor result. A nutritional researcher working with human patients cannot even dream of achieving the degree of control or characterization I can, and their data are overloaded with spurious noise.

Researchers in the soft sciences typically do not have sufficient math skills to understand the statistical methods that are they are using to evaluate their data. I've lost track of how many times I've seen evaluations of the mean and standard deviation for distributions that are clearly not normal (also known as Gaussian). Don't even get me started on p-values. More importantly, very few medical studies attempt to test a single hypothesis. Far too many studies will compare apples to bananas, rather than apples to no apples, or they'll compare apples, oranges, and bananas to no fruit. Making conclusions from such messily designed experiments is rife with the potential for misinterpretation. Drug studies are often an exception.

The Insulin Hypothesis

The central thesis of "Good Calories, Bad Calories" is that chronically elevated insulin levels is likely responsibly for the, "diseases of Civilization," such as diabetes, heart disease, cancer, etc. I put, "diseases of Civilization," in scare quotes because although these diseases are absent from primitive cultures, it is obnoxious to explain to individuals of non-Western ancestry that they do not suffer from these diseases because they are uncivilized (Burkitt and Trowell). Wikipedia calls these Lifestyle diseases, which seems a more apt terminology.

Let me be clear: nothing about Taubes' insulin hypotheses are actually owned by Taubes. The idea that carbohydrates are fattening has been known from well before the discovery insulin. The knowledge that diabetes could be cured by avoiding carbohydrates was also known before the discovery of insulin. Taubes is merely going over old research and bringing it together as a strong argument.

When viewed through the prism of evolutionary science, this makes a lot of sense. Fat stores would have been necessary to maintain the organism when hunting failed and there were insufficient edible plants. Carbohydrate stores, on the other hand, requires a huge amount of water to act as solvent. Each gram of glycogen that you store needs ~2.5 g of water solvent, so at 4 kcal/g carb, you have an effective storage capacity of 4 kcal/3.5 g = 1.15 kcal/g. Fat is 9 kcal/g and it doesn't require a solvent when stored in adipose tissue so that's a 7-fold increase in storage capacity. Fat is a vastly superior way to store energy.

So what was the source of carbohydrates for humans before we developed agriculture? Presumably wild fruit. Fruit matures, more or less, all at once as anyone who has owned an apple tree knows, and rots rather quickly after it has fallen off the tree. Thus, when fruit is available, it is perfectly logical to gorge oneself and use all that easily harvested sugar energy to synthesize fat storage for consumption in lean times. Thus the evolutionary reason for our sweet-tooth is easily explained.

Effectively, we evolved to preferentially burn-off the glycogen in our muscles and liver before we switched to fat. There's ~300 g of carbohydrates stored in the body, which corresponds to ~1500 kcal. Just you try and burn 1500 calories via a cardio-workout. Eating three square meals a day with carbs at every serving implies that you will never burn through your reserves and hence the body will never resort to burning fat.

So, briefly, how does one use these conclusions to achieve a healthy low body fat (and BTW, waist circumference is the #1 metric for heart disease)? Certainly not by the standard, low-calorie, high-carbohydrate diet (semi-starvation diet in Taubes' terms) which has been nothing but a dismal failure from a clinical and practical perspective. There are three basic strategies:

1. Very long and very slow exercise (4+ hrs), typically hiking or cycling in my case. This is a far cry from the type of anaerobic-limit cardio exercise one typically sees recommended, for example, by the American Heart Association. There is a yawning gulf between walking and jogging. I personally approve of anaerobic exercise, such as sprint intervals or plyometrics.
   
2. Consistently eat carbohydrates at a low enough level that the brain (which prefers glucose over ketones) consumes the entirety of carbohydrates that you eat, leaving the body to burn ketones. This is a slow process.
   
3. Periodically fast for an extended period of time so that your basal metabolism burns through your glycogen reserve and then begins to mobilize fat. This is not a calorie reduction method, rather you are simply not eating three times a day (on average), and as such having more extremely calories negative and calorie positive periods.
   

Eventually, everyone will plateau at a certain level of body fat. The number of fat cells in your body is more or less set by age twenty; dieting simply changes how full they are. Eventually, fat cells will revolt and through leptin demand a stronger appetite. So is there any need at all for carbohydrates in the diet?

Grains are the ultimate, "empty calories," in terms of micronutrients. Not only to grains have essentially no micronutrients (they are fortified for a reason), they also have a number of anti-nutrients that impede the uptake of nutrients from vegetables and animal tissue. From a health perspective, there's no need to eat grains or starchy vegetables such as potatoes.

Typically one might recommend 50-80 grams per day simply to supply the brain with glucose, but even this is not strictly necessary as the liver can convert fatty acids to glycogen. Of course, people who are obese are likely suffering from hyperinsulina (insulin resistance/metabolic syndrome) and as such may suffer discomfort upon undertaking an low-carbohydrate diet.

For the record, I dropped 22 lbs. (20 lbs. by August 2008) going from a BMI of 24.7 in May 2008 to 21.4 as of now. I've been as low as 143 lbs. in the past but I was never able to maintain that; typically I got to such a weight by bicycling 12+ hours a week at 30-40 km/h. I'm now sitting at 145 lbs. (edit: now 144 lbs.), in January (ed. February), in Edmonton, with no chronic cardio. This is a totally new scenario for me as I almost always put on 10 lbs. over winter.

When I put on weight it is prominently in the form of visceral and subcutaneous fat; I've never had significant interstitial muscular fat so I've always had relatively hard muscles. I try and aim for a distribution of 60 % fat, 25 % protein, and 15 % carbohydrate in my diet. Since my blood sugar/insulin isn't riding a roller coaster up and down throughout the day, I generally don't get hungry. I am much better at concentrating throughout the course of the day, irrelevant of when I last ate and I've found that my thinking process is much cleaner and crisper.

Unanswered Questions

Taubes criticizes a number of scientists in his book for over-simplifying the science of physiology in an effort to understand it. In that respect, reducing the argument of "Good Calories, Bad Calories" to carbohydrates-bad, fat-good is probably guilty of the same offense.

Taubes dose throw us a couple of bones, in the form of some of the more buzzword lines of research in nutrition today. One is Advanced Glycation End-products (AGEs); we know that AGEs are tightly correlated to age. From what I've read, thus far the early reports on AGEs are similar to those on cholesterol fifty years prior: lot's of smoke, but no fire. Efforts to link AGEs to ingestion of AGE materials (e.g. burned meat) has thus far failed, IMO.

Fat-soluble vitamins

One aspect of carbohydrate/fat balance that Taubes does not cover is the impact of the fat-soluble micro-nutrients. We, as humans, have given up our abilities to fabricate the majority of vitamins that we need in favour of having big brains. We are very poor at transforming one complex of a vitamin (typically the vegetable source) to the type we need to function.

As our consumption of fats has declined in favour of carbohydrate the quality of fats that we eat has also declined. As such, we are typically deficient in fat soluble vitamins, in particular D3 and K2. Not only we as a society getting far less vitamin D3 from sun exposure, but the animals we eat are also more often than not locked in a barn eating corn, so they also contain less fat soluble vitamin. When you consider that your skin can produce something like 10,000 IU of D3 in an hour compared to a multivitamin at 400 IU, it's not a giant stretch to believe that the majority of Western people are going through life deficient in it. K2 is similar; butter is a good source, but butter has been demonized by our corporate media.

Poly-unsaturated Fats

Palmitic acid is the fatty acid that your liver manufactures from sugars. In fact, the only fat humans evolved to burn for fuel directly is saturated fat. All other fats we trans-saturate first, and then burn. It would seem strange then given the complexity of the human body that we evolved to preferentially make saturated fats over polyunsaturates, unless we prefer saturated fat because it is more stable and hence less prone to oxidation.

The canard that saturated fats, "clog your arteries," is just that, bogus. The medical establishment has never believed this since they knew full well plaques form inside the arterial wall, not on the surface. Why this idea was allowed to percolate through the public, I do not know.

This begs the question, should we eat polyunsaturates at all? They are, after all, highly unstable and very easily oxidized. I ask a question: when was the last time you bought a nut oil, e.g. walnut or sesame, at the supermarket? Was is refrigerated on the shelf? Was is in a brown bottle to prevent light from damaging the polyunsaturated fat? I've seen flax oil sold in such a fashion but no other. Much of the fat we eat is oxidized by the time it reaches our mouths.

Fish oil (omega-3) is clearly doing people a lot of good, even if it sits in a cylinder for months. A lot of people do feel that we get far too much Linoleic acid, an Omega-6 essential pre-cursor, from soy, corn, safflower and other vegetable oils. It does, after all, have a significant hormonal effect.

This has led some to suggest that one should balance omega-3 and omega-6 consumption. I.e. if your omega-3 consumption is 3-4 one gram capsules of fish oil a day, then you shouldn't eat more than ~5-10 grams of vegetable oil. The American Heart Association apparently felt the need to push out an editorial recommending that the diet 5-10 % of calories should be in the form of omega-6 polyunsaturates to counter this meme. The fascinating thing about this editorial is that there are 81 references in 3 pages (which is beyond extreme), yet, there are no references — no studies, no research — that support the advised level of dietary intake. Take a look at the article (it's free access), it's quite amazing.

Rebuttal: Conservation of Energy

One of Taubes' chapters deals with the idea that energy balance in humans can be reduced to the First Law of Thermodynamics:

ΔE = E_in - E_out

I was somewhat confused to see this Surely the nutritional scientists did not not really believe this, right? I mean, any idiot undergraduate students knows that the 1st Law is only useful in a closed system, and humans live on the planet Earth, not in an insulated box. Right?

Enter a rebuttal by G. Bray in the journal Obesity Reviews. Bray is a to be a major obesity researcher and one of the 2nd tier villains in the book. Taubes relates a story of Bray excising a section of a British report on obesity, where Bray removed the material pertaining to the relationship between insulin and obesity. He clearly has editorial support to make his case. Bray is one of the second-tier villains in Taubes' book. Taubes has a footnote (p. 421), which suggests that Bray actively suppressed the carbohydrate-insulin hypothesis.

* According to Novin, when he wrote up his presentation for the conference proceedings Bray removed the last four pages, all of which were on the link between carbohydrates, insulin, hunger, and weight gain. "I couldn't believe he would make that kind of arbitrary decision," Novin said.

Unfortunately, to a physicist this energy balance hypothesis looks like a silly hand-waving exercise, not a serious argument. Frankly I was flabbergasted when I first read this article. This conservation of energy argument is on the same scientific level as the ridiculous "drink cold water to lose weight" idiocy. A human organism is:

1. Not in thermal equilibrium with their environment. Last time I checked I have a body temperature around 38 °C and spend most of my time in 21 °C rooms.
   
2. Capable of significant mass flows (e.g. respiration).
3. Capable of sequestering entropy (e.g. protein synthesis).
   

Is wearing a sweater fattening (by insulating you from your environment)? Here's a quote from the rebuttal,

Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction from overeating.

According Bray's thermodynamics argument, wearing sweaters makes you fat. This illustrates the greatest fallacy of trying to apply the 1st Law to a human: it makes the implication that living organisms consume kilocalories for the purpose of generating heat rather than perform useful work (i.e. breathing, contracting cardio and skeletal muscle, generating nervous action pulses, etc.). In reality heat is the waste product of basal metabolism. The first law does not distinguish between different types of energy. Heat, work are all equal under the First Law of Thermodynamics.

Applying the 1st Law to living organisms is Proof by Tautology. Yes, 1 + 1 = 2, but this tells us absolutely nothing about the underlying mechanics. The 1st Law does not (I repeat N-O-T) tell us whether you store excess energy in the form of fat, or bleed it off into the atmosphere by dilating blood vessels next to the skin, sweating, etc. To do so would require an accounting of entropy.

What would a semi-rigorous description of the thermodynamics of a human organism look like? Look at the title strip on the top of the page. See that equation in the background?

This type of equation would be a bare starting point for energy balance in a complex system like a living organism. Good luck actually accounting for all the terms. Those Σs are sums.

If anyone else has seen any other critical reviews to "Good Calories, Bad Calories," please feel free to post them in comments and I will take a look.

Environmental Aspects

As most people are aware, feedlot meat production produces copious amounts of greenhouse gases, both in terms of the fertilizer required to grow the corn to feed the animals, and the methane produced by rudiment digestion. This provides a bit of a moral quandary, in that feedlot meat is not readily described as sustainable.

First, greenhouse gases are perfectly fungible, so since my personal greenhouse gas emissions are about 1/3 normal, I am still well under any proposed quota. Although this has an aspect of the "beer refrigerator paradox" to it, it's still valid if the numbers work out.

Second, as it happens, I do live in Alberta and I can and do buy pasture-raised meat. Meat that feeds on unfertilized prairie grasses not only has a different composition but a far lower greenhouse potential. The visual difference between feedlot beef and pasture Elk is fairly startling. About 50 - 65 % of what I buy is via individual farmers at the market. In particular, I try to ensure that all the offal (organ meats) that I buy are from pastured, hormone and antibiotic-free animals since they are more likely to concentrate in the organs.

It's true that if everyone tried to by pasture-fed meat, there would not be enough to go around, but at the moment it is sustainable for me.

Misplaced Priorities

So the Securities Exchange Commission is said to be probing Apple over accusations that they may have misled the public over the state of Steve Jobs' health.

Let's play a word association game:

Pancreatic cancer
+
Corporate executive
=
?Healthy?

One can imagine that if Jobs had cancer in the Islets of Langerhans, the portion of the pancreas responsible for insulin regulation, that yes, he might have some diabetic-like health issues associated with that. Doesn't the SEC have something better to do? E.g. meanwhile we learn that Merrill-Lynch maneuvered to deliver $3 billion inbonuses before being bought-out by Bank of America. Merrill-Lynch lost over $20 billion in that quarter, and BoA is demanding that it be bailed out by the US taxpayer now for the same amount. This idea that financial companies need to pay out bonuses to retain "top talent" during a period when the financial sector is undergoing a severe contraction is a canard. Where are they going to go work, the construction industry?

Bitumen-producer Suncor Posts Significant Loss

Via Nathan Vanderklippe at the Globe and Mail, we learn that Suncor, one of the original and bigger oil sands producers, has posted a C$215 million loss for the 4th quarter of 2008.

The price of oil has fallen since then. I don't imagine the other producers will be doing much better, although Suncor does burn the least amount of natural gas and predominately runs an open-pit mine to the best of my knowledge. As I've pointed out previously, the marginal cost-of-production for synthetic crude from bitumen is around $50/bbl. The article is claiming it's more like $36/bbl although that may not include refining. If the oil sands of Alberta shut down due to extended low prices, that's approximately $1.3 million barrels per day taken off the market.

Column-like Films of Silicon for Battery Applications

About a year-ago I relayed the story of Chan's work on using silicon nanowires as a potential anode material for Lithium-ion batteries. Silicon can store some ten-times more charge than Carbon, the current industry standard, but this comes at the expense of a huge volume change. The difference in volume between charged and uncharged is 300 % for Si. Just to give you an idea, the alloy of Lithium and Silicon that's formed is Li₁₄Si₄ from metallic Si. The article from Nature Nano suggested that forming the silicon into high aspect-ratio wires would allow the silicon freedom to expand along the long-axis of the wire and hence be less likely to physically break and no longer have a physical, conductive pathway to the anode.

In general, the lifetime of a battery is determined by how great of a volume change it undergoes when cycling from the charged to uncharged state and vice versa. Volume changes imply stress and the gradual introduction of defects that can trap electrons and reduce electrical conductivity. For LiFePO₄ cathodes, the volume change is around 4-7 %, but this is a crystalline material. Silicon nanowires are amorphous (i.e. poorly ordered) and the introduction of defects on cycling is not necessarily an issue.

The previous work was truly proof of principal, but unlikely for variety of reasons to be a direct path to commercialization. There's some new work out by a local group that expands on the work of Chen. Fleischeur et al. tried their specialty, glancing angle vapour deposition, to form a thin-film of Silicon composed of many, regular pillars. (Disclosure: our research group collaborates with the group that did this research. I personally do not, however.) In glancing angle deposition, the substrate (onto which the film is deposited) is at nearly right angles to the incoming vapour stream. In thin film deposition, one tends to see small clusters form first due to surface tension. As the clusters grow, they amalgamate together and form a (porous) solid thin film. When the substrate is at high angles of incidence, the first clusters to form shadow any smaller trees and grab more than their fair share of the incoming mass stream. Hence glancing-angle deposition typically forms column-like thin films.

The glancing-angle fabrication method has a number of potential advantages over Chan's technique:

1. Chan's thin film process relied on a gold catalyst ($$$), whereas the GLAD process only requires a thin layer of chromium for adhesion on Si substrate and none at all on a stainless steel substrate.
   
2. Glancing-angle deposition can easily control the spacing of pillars by patterning the substrate.
3. The glancing-angle films were "robust" when I asked the author about it. He said hitting the batteries with a hammer had no effect on performance, so presumably the pillars were not breaking.
   
4. Glancing-angle deposition requires a microscopically smooth surface for proper column formation.

Let's look at some results. The question is, how durable are these anodes compared to graphite? The charge curve is really all we are interested in.

Figure 1: Chan et al. charge capacity after 10 total cycles.
Figure 2: Fleischauer et al. charge capacity after cycling up to cycle 70. I don't recall the reason for the discontinuities but I vaguely recall it had something to do with the test electronics.

Both authors show a very large drop in charge capacity after the first recharge. This means there is some sort of irreversible change to the material occuring from film fabrication to charged and uncharged Si. Then there is a progressive loss in capacity. Evidently Chan and company are less confident in their material as they are only showing results up to ten cycles. Average capacity fade for Fleischeur's battery was found to be 0.3 % per cycle. If we extrapolate, that would imply it would take approximately 750 cycles for the charge capacity of the silicon anode to drop below that of a conventional graphite one. Obviously, that's not good enough for commercial applications.

Overall, I think that this is an important step in terms of fabrication and longevity. We are still looking at a minimum of a decade before any such silicon Li-ion batteries hit the shelves; this is progress on that path.

Poster Boy

http://online.wsj.com/article/SB122903010173099377.html

Wow.

Oh yeah, GM and Chrysler are bankrupt, just like 80 % of US banks. Piffle.

GM Sales Fall 45 % YoY; Average 31 % Drop

That's going to leave a mark! USA automobile sales are way way down in October 2008 versus October 2007, as consumer sentiment and credit heads South fast.

About 25 per cent of GM's volume in October 2007 was from leasing, but the auto maker did almost no leasing last month through GMAC, Mr. LaNeve said.

As I mentioned in the comments of this post, when you have to relax your credit requirements to sell cars, you're setting yourself up for trouble in the long-run. I've actually been impressed how well the USA has been holding up under the credit crisis thus far (compared to countries like Iceland, Hungary, Pakistan, etc.) but obviously if the steady drip—drip—drip of job losses continues things will really come to a head. I definitely still stand by my prediction of the US financial sector shrinking in half. The US Treasury bail-outs to date are not solving the trust issue as everyone continues to hoard cash. Tacking on $500 billion a month in federal debt isn't sustainable either.

I'm working towards my doctoral candidacy at the moment so posting will remain sparse until the middle of December.

My Thoughts on the US Election

Since it's becoming fashionable for energy bloggers (such as Geoffrey Styles and Robert Rapier) to comment on the US election, I thought I would lend my 'formidable' intellect to the debate:


I for one am surprised how many US provinces are polling favourably for the NDP.

Furthermore, I would like to pontificate on one of life's greatest mysteries... Why does the eye perceive the combination of red and blue as purple?

Demand Destruction

With oil now hovering around $70/bbl, we've seen a decline of roughly 50 % from the peak this year over only a couple of months. I've stated in the past that I felt the run-up starting in February was largely speculation whereas the push from 2002-2007 was more fundemental. Is this new drop an evidence that 2002-2007 was speculation or is it a fundamental move based on supply and demand? I'm going to argue here that this is, once again, a real move, based largely on demand destruction on-going around the world but in particular inside the United States of America.

Oil consumption in the USA started a downhill roll around December last year. In September, it had a Will-E Coyote moment and rolled off a cliff. It's now in free-fall. Oil demand is highly inelastic in the short-term but their is some phase lag that results in more long-term elasticity. What I mean by that is, it takes awhile for individuals and business to adapt to oil price by drilling for more supply, replacing SUVs with econoboxes, driving slower, etc. But when demand drops fast, the price can drop fast too, because supply is short-term inelastic too.

The latest EIA data estimates US petroleum consumption at 18,865,000 bbl/day. Compared to the same time last year, at 21,024,000 bbl/day, that's a drop of just over 10 % yoy. That's a really big deal. From a GDP-to-oil-consumption relation, it suggests the US is headed into a depression. Even during the 1970s oil shocks the US only experienced drops of 3-4 % a year in consumption.

Figure 1: EIA Weekly Oil Consumption (estimate). The chart shows the story: a gradual downturn and then a sudden drop.

That speculative oil bubble that appeared in February? Gone. Yes, Dorthy, a major recession in the country that consumes a quarter of the world's oil can cause a big drop in price. The USA isn't the whole story, but it is driving this price movement.

Figure 2: IEA consumption estimate for OECD countries.

The story starts with the OECD countries, and extends to the BRIC (Brazil-Russia-India-China) 'growing' economies. Consumption was pretty flat from 2005-2007, and then it started dropping in 2008. Note that Figure 2 only extends to August, and the US demand dropped over a million barrels a day in September!

Note when looking at these IEA plots, they are all 12-month moving averages, so any moves you see in the curves likely started a few months earlier. Also note that EIA (US DoE) and IEA (France) data are not strictly equivalent, since they use different methods to come up with their estimates.

Figure 3: IEA Germany and Japan Oil Consumption.

Oil demand in a number of big economies, e.g. Germany and Japan already fell in response to oil prices last year. They are largely unchanged this year, or indeed up. France is already headed back up, as are a number of smaller countries. In North America, Canada's demand is flat and Mexico is well up.

Figure 4: IEA UK and Italy Oil Consumption.

The big weakness in Eurozone oil consumption is coming from Italy, and the UK. However, their drops are still minor in comparison to the story in the `States. If we look over a longer term view, the IEA consumption data (Figure 5) suggest US demand was flat for 2005-2007, so perhaps this recent drop is just the USA making up for lost ground. Looking at US consumption, and world consumption, the two graphs have very similar shapes.

Figure 5: IEA oil consumption data for USA. Future versions of this graph will show a sharp downturn in September.

The BRIC countries are all less transparent. As a consequence of that, releases of their numbers is even slower than OEDC results we see above that are a couple of months behind. In the same manner that the USA drives OEDC and the other countries are just noise, China drives the BRIC numbers. Unfortunately, we don't have any numbers yet on the Olympic effect in China. Vehicle-kilometers in China was probably way down in August, and that's going to have a short term impact on oil demand. China's skies are once again as smoggy as ever before, so unless they've also changed their stockpiling strategy, this is going to have a short-term impact.

Figure 6: China oil consumption (and projections) beside Vehicle Sales in China. Taken from Malcolm Shealy's (Alacrites Inc.) presentation hosted on IEA website.

So outside of a massive step up in China in August and September (which is unlikely) the only other likely variable to examine is oil supply. Production data (Figure 7) indicates supply is actually up this year. This isn't unexpected. It took a couple of years after oil took off in 2002 for the oil companies to get enough confidence to jump into new projects, but a number of projects started in 2003-2004 are now up and running contributing to supply. While the new oil price may choke off new projects, there's still a number in development to stave off the depletion of existing fields.

Figure 7: World oil plus condensates production, 2005-July 2008 (Data from EIA).

So, in conclusion, I think the supply and demand data show pretty conclusively that supply is up, demand is down, hence the price of oil is dropping like a rock. In fact, we have this event occurring at the same time as a commodity is being popped, so the effect is especially strong. This is a good thing. The world economy and the USA in particular is hurting thanks to the bubblicious real-estate fiasco and low energy prices will help conventional economic activities drag us back out of this big hole. I think the housing bust will be extended — adjustable-rate mortgage resets in the US are only about half-way through the pool of potential defaults — and the world economy is not decoupled from the USA so expect fallout damage to hit exporting countries in manufacturing (China, Japan) and commodities (Canada, Russia, Australia) in waves going forward. The US consumer is going to have to live within his or her means, and hopefully revert back to being a citizen first and consumer second.

Can OPEC squeeze the price by implementing quotas? Yes and no. Production of oil products is up big in 2008. There's slack they can take out of the system. Will they? I don't know. OPEC countries in general have not been diversifying their economies so they will have to do something or face the potential for unrest as revenues come back to earth. Basically it comes down to whether or not Saudi Arabia wants to arrest the fall in price, or if Russia as a non-OPEC producer decides to sacrifice some cash flow or not. If I was the Saudi's, I would be thinking about whether or not OPEC as an organization has outlived its usefulness. A Saudi-Russian oil alliance would probably be more practical, and effective.

Looking into the future, it's likely that demand in the USA will be suppressed for awhile, so as a result, investment in new capacity is going to drop especially in conjunction with higher credit rates. Speculative plays in oil shale, gas-to-liquids, and coal-to-liquids are effectively dead. Remember that in order to develop alternative fossil fuels to oil you need to not just cover the marginal cost of production, but also amortize the capital costs, and the capital costs in non-conventional oil are usually very high. I would also expect new deep water plays (Brazil, Atlantic Canada) to come to a grinding halt, but existing ones should go ahead as the cost of production is not excessive.

The most marginal cost-of-production oil in the world is Alberta bitumen, at around $50/bbl. That's not accounting for capital costs at all, which have been in the range of $150,000 /bbl/day capacity recently. Lower than that, and salaries will have to come down to lower costs. Taking that capacity out of the world's supply would only knock off 1.3 million bbl/day. Alberta's provincial government may be facing the end of yet another oil boom with little to show for it.

Banana Republic Bubble Bail-outs

So, how's that short ban working for you, Mr. Market? I have some further comments to get off my chest with regards to the impetus for this crisis and the attempted bail-out. I see a lot of finger pointing going on but as far as I can tell everyone is doing so from their very own glass house. Let's itemize the combination of failures shall we?

1. Low interest rates have obviously contributed to the blowing of bubbles. However, general failure of the federal government to provide transparent and even regulation of the financial markets is as big a factor. Part of the problem is that government never reacted to and regulated financial 'innovation', in particular the credit default swaps and options that are now causing a chain-reaction melt-down. The other half of the problem is not enforcing existing regulations particularly in regards to accounting tricks that have allowed insolvent zombie banks to appear to be in the black as they file for bankruptcy or are bought-out. Moves to increase leverage limits haven't helped either.
   
2. The financial sector of the US economy has become out-sized relative to the real economy. A symptom of this is the blowing of successive bubbles required to keep such a bloated sector operational. This in turn supported the fraud at the mortgage broker level by creating such a huge demand for bad loans. By historical measures, the financial sector is about twice as big as it should be to fulfill its function of providing credit to business and mortgages to citizens. It is ironic that the financial sector was the biggest proponent of free trade and told manufacturing to suck it up when the race to the bottom was destroying that industry. Now that the underlying base of the US economy has perished and finance is being forced back to reality they are crying for a bail-out. The hypocrisy is deafening; it's your turn to learn about outsourcing.
   
3. An excessive concern with status and sense of entitlement amongst the stereotypical consumer-citizen (with the emphasis on consumer). McMansions, Ford Extinctions, granite counter tops, etc. What was the purpose of all this? How did people get fooled into thinking that they needed such things? I believe people are entitled to food, medical care, etc. but such entitlements need to be reigned in to the point that living off the dole isn't anyone's choice. You're not entitled to a 52" plasma-screen TV you purchased with your HELOC.
   

If these sound like huge, fundamental problems, they are. Around when 'personnel' department became 'human resources' and employees became interchangeable cattle the smart kids stopped going to engineering schools and instead enrolled in law and finance. Unfortunately, financial innovation is a synonym for confidence game. The LCD screen you're looking at? Not finance. The hyperlink? A rare application from the super collider at CERN. In fact I can make a pretty good argument that innovation in the telecommunications industry has stagnated over the last seven years after finance blew it up. I challenge anyone to locate a financial instrument developed in the past 100-years that is necessary to run our modern economy.

The proposed Paulson bail-out was bizarre in that it never even tried to determine which institutions needed to be quarantined. Why the House of Representatives used it as the basis for their counter-proposal I am left without words.

Bank of America, CitiGroup, and JP Morgan Chase have all been busy building the Jenga tower higher (see making the pie higher) in the effort to become too ginormous to fail. Clearly they all expect to be bailed out, which is a pretty amoral way to run a business. "Bail us out or your retirement savings get it!" The appropriate response at this stage is to raise their moral hazard one and audit them, find out that, "Surprize, you're broke!" and nationalize the lot of them temporarily. Cashier the executives, amalgamate the trash from all three and quarantine it, then start breaking them into non-antitrust sized chunks and IPO them off in sequence.

China, Japan, and the sovereign wealth funds are going to get hosed, but they weren't acquiring those assets in order to enrich their own citizens so I'm not going to cry over their spoiled milk. People like to think that these guys are innocent money but I think it's more a matter of the distinction between strategy and tactics. It's likely that this will impair the auction of treasuries at some level but the US needs to tell these currency peggers to get stuffed at some point at time. May as well do it now when you have a good excuse; the US federal government needs to aggressively trim its budget too. 401k's are a tax shelter and hence they really shouldn't have equities/securities in them — they should be a bastion of safety — but they do, so individuals need to be compensated (but not made whole). I think the whole idea of being restricted to picking investments your company's human resources department likes is inane, however.