Monday, April 28, 2008

More Liver

It's time to celebrate your liver. It's a hard-working organ and it deserves some credit.

One of the liver's most important overall functions is maintaining nutrient homeostasis. It controls the blood level of a number of macro- and micronutrients, and attempts to keep them all at optimal levels.

Here's a list of some of the liver's functions I'm aware of:
  • Buffers blood glucose by taking it up or releasing it when needed
  • A major storage site for glycogen (a glucose polymer)
  • Clears insulin from the blood
  • Synthesizes triglycerides
  • Secretes and absorbs lipoprotein particles ("cholesterol")
  • Stores important vitamins: B12, folate, A, D, E, K (that's why it's so nutritious to eat!)
  • Stores minerals: copper and iron
  • Detoxifies the blood
  • Produces ketone bodies when glucose is running low
  • Secretes blood proteins
  • Secretes bile
  • Converts thyroid hormones
  • Converts vitamin D (D3 --> 25(OH)D3)
The liver is an all-purpose metabolic powerhouse and storage depot. In the next post, I'll give you a recipe for it...

The Liver: Your Metabolic Gatekeeper

As I've been learning more about the different blood markers of metabolic dysfunction, something suddenly occurred to me. Most of them reflect liver function! Elevated fasting glucose, low HDL cholesterol, high LDL cholesterol, high triglycerides and high fasting insulin all reflect (at least in part) liver function. The liver is the "Grand Central Station" of cholesterol and fatty acid metabolism, to quote Philip A. Wood from How Fat Works. It's also critical for insulin and glucose control, as I'll explain shortly. When we look at our blood lipid profile, fasting glucose, or insulin, what we're seeing is largely a snapshot of our liver function. Does no one talk about this or am I just late to the party here?!

I read a paper today from the lab of C. Ronald Kahn that really drove home the point. They created a liver-specific insulin receptor knockout (LIRKO) mouse, which is a model of severe insulin resistance in the liver. The mouse ends up developing severe whole-body insulin resistance, dramatically elevated post-meal insulin levels (20-fold!), impaired glucose tolerance, and elevated post-meal and fasting glucose. Keep in mind that this all resulted from nothing more than an insulin resistant liver.

LIRKO mice had elevated post-meal blood glucose due to the liver's unresponsiveness to insulin's command to take up sugar. Apparently the liver can dispose of one third of the glucose from a meal, turning it into glycogen and triglycerides. The elevated fasting glucose was caused by insulin not suppressing gluconeogenesis (glucose synthesis) by the liver. In other words, the liver has no way to know that there's already enough glucose in the blood so it keeps on pumping it out. This is highly relevant to diabetics because fasting hyperglycemia comes mostly from increased glucose output by the liver. This can be due to liver insulin resistance or insufficient insulin production by the pancreas.

One of the interesting things about LIRKO mice is their dramatically elevated insulin level. Their pancreases are enlarged and swollen with insulin. It's as if the pancreas is screaming at the body to pick up the slack and take up the post-meal glucose the liver isn't disposing of. The elevated insulin isn't just due to increased output by the pancreas, however. It's also due to decreased disposal by the liver. According to the paper, the liver is responsible for 75% of insulin clearance from the blood in mice. The hyperinsulinemia they observed was both due to increased secretion and decreased clearance. Interestingly, they noted no decline in beta cell (the cells that secrete insulin) function even under such a high load.

Something that's interesting to note about these mice is they have very low blood triglyceride. It makes sense since insulin is what tells the liver to produce it. Could this have something to do with their lack of beta cell dysfunction?

The really strange thing about LIRKO mice is that their blood glucose becomes more normal with age. Strange until you see the reason: their livers are degenerating so they can't keep up glucose production!

LIRKO mice reproduce many of the characteristics of type II diabetes, without degenerating completely into beta cell death. So insulin resistance in the liver appears to reproduce some elements of diabetes and the metabolic syndrome, but the full-blown disorders require other tissues as well. As a side note, this group also has a skeletal muscle-specific insulin receptor knockout which is basically normal. Interesting considering muscle tissue seems to be one of the first tissues to become insulin resistant during diabetes onset.

So if you want to end up like your good pal LIRKO, remember to drink high-fructose corn syrup with every meal! You'll have fatty liver and insulin resistance in no time!

I have a lot more to say about the liver, but I'll continue it in another post.

Sunday, April 27, 2008

Book Review: Blood Sugar 101

I just finished reading "Blood Sugar 101" by Jenny Ruhl. It's a quick read, and very informative. Ruhl is a diabetic who has taken treatment into her own hands, using the scientific literature and her blood glucose monitor to understand blood sugar control and its relationship to health. The book challenges some commonly held ideas about diabetes, such as the notion that diabetics always deteriorate.

She begins by explaining in detail how blood glucose is controlled by the body. The pancreas releases basal amounts of insulin to make glucose available to tissues between meals. It also releases insulin in response to carbohydrate intake (primarily) in two bursts, phase I and phase II. Phase I is a rapid response that causes tissues to absorb most of the glucose from a meal, and is released in proportion to the amount of carbohydrate in preceding meals. Phase II cleans up what's left.

In a person with a healthy pancreas, insulin secretion will keep blood glucose under about 130 mg/dL even under a heavy carbohydrate load. The implications of this are really interesting. Namely, that blood glucose levels will not be very different between a person who eats little carbohydrate, and one who eats a lot, as long as the latter has a burly pancreas and insulin-sensitive tissues.

Most Americans don't have such good control however, hence the usefulness of low-carbohydrate diets. This begs the question of why we lose blood sugar control. Insulin resistance seems like a good candidate, maybe preceded by
leptin resistance. As you may have noticed, I'm starting to think the carbohydrate per se is not the primary insult. It's probably something else about the diet or lifestyle that causes carbohydrate insensitivity. Grain lectins are a good candidate in my opinion, as well as inactivity.

Diabetics can have blood glucose up to 500 mg/dL, that remains elevated long after it would have returned to baseline in a healthy person. Ruhl asserts that elevated blood sugar is toxic, and causes not only diabetic complications but perhaps also cancer and heart disease.

Heart attack incidence is strongly associated with A1C level, which is a rough measure of average blood sugar over the past couple of months. It makes sense, although most of the data she cites is correlative. They might have seen the same relationship if they had compared heart attack risk to fasting insulin level or insulin resistance. It's difficult to nail down blood sugar as the causative agent. More information from animal studies would have been helpful.

Probably the most important thing I took from the book is that the first thing to deteriorate is glucose tolerance, or the ability to pack post-meal glucose into the tissues. It's often a result of insulin resistance, although autoimmune processes seem to be a factor for some people.
Doctors often use fasting glucose to diagnose diabetes and pre-diabetes, but typically you are far gone by the time your fasting glucose is elevated!

I like that she advocates a low-carbohydrate diet for diabetics, and lambasts the ADA for its continued support of high-carbohydrate diets.

Overall, a good book. I recommend it!

Thursday, April 24, 2008

Scientist Discovers that Only Pills can Control Hypertension

I went to a presentation today by a prominent hypertension researcher. His talk began with a slide that had two pictures side-by-side: one of the late fitness advocate Jim Fixx, and the other of Winston Churchill. Fixx was a marathon runner, while Churchill was inactive, overweight and had a famous appetite. Fixx died of a sudden heart attack at 52, while Churchill lived to 90. The presenter went on to state that this is an example of how genes control CVD risk, implying that despite Fixx's exemplary lifestyle, his genes had condemned him to an early death.

I wanted to jump up and yell "I think you're leaving out the alternate hypothesis: running marathons and stuffing yourself with grains isn't healthy!" But instead I suffered quietly through what ended up being an inane yet informative presentation.

His lab looks for gene variations that affect blood pressure (BP). There's a huge amount of money and research going into this. His lab and others have come up with two classes of mutations:
  • Common allele variants that have an insignificant but measurable effect on blood pressure.
  • Rare genetic mutations that have a significant effect on BP. The most common affects 1 in 2,000 people in the US.
Despite truckloads of funding and research, they have yet to uncover any gene or combination of genes that accounts for even a fraction of hypertension in Americans. So what's the next step? Keep looking for genes.

I suspect they will never find anything interesting. The reason? Hypertension is tightly linked to lifestyle. It's a quintessential aspect of the "disease of civilization". It's highly responsive to carbohydrate restriction, as a number of clinical trials have shown. Remember the Kuna? They don't get hypertension when they live a non-industrial, grain-free lifestyle (despite eating more salt than the average American), but as soon as they move to the city their hearts explode. It's been demonstrated in a number of other similar cases as well. Genetics are clearly not responsible.

Don't get me wrong, I do think genetics can modify a person's response to a poor lifestyle. But when the lifestyle is healthy, the vast majority of these differences fade away. I have a more thorough discussion of this point here.

If you give just the right dose of poison to a group of animals, 50% will die and 50% will survive (called the EC50 dose). You might then conclude that genetics had determined who lived and died. You wouldn't be wrong, but you'd be missing the point that what killed them was the poison.

The thing that really bothers me about this thinking is it's disempowering. The presenter suggested that the reason for the difference between Fixx and Churchill was their genes. If genes have us in such a tight grip, why bother trying to live well? The only logical solution is to pop hypertension pills and eat cake all day.

My guess is that if they had lived a more natural lifestyle, Fixx would have made it to 90 and Churchill would have been fit and lean.

Wednesday, April 16, 2008

Olive Oil Buyer's Guide

Olive oil is one of the few good vegetable oils. It is about 10% omega-6 (n-6) fatty acids, compared to 50% for soybean oil, 52% for cottonseed oil and 54% for corn oil. Omega-6 fatty acids made up a smaller proportion of calories before modern times, due to their scarcity in animal fats. Beef suet is 2% n-6, butter is 3% and lard is 10%. Many people believe that excess n-6 fat is a contributing factor to chronic disease, due to its effect on inflammatory prostaglandins. I'm reserving my opinion on n-6 fats until I see more data, but I do think it's worth noting the association of increased vegetable oil consumption with declining health in the US.

Olive oil is also one of the few oils that require no harsh processing to extract. As a matter of fact, all you have to do is squeeze the olives and collect the oil. Other oils that can be extracted with minimal processing are red palm oil (9% n-6), hazelnut oil (10% n-6) and coconut oil (2% n-6). These are also the oils I consider to be healthy. Due to the mild processing these oils undergo, they retain their natural vitamin and antioxidant content.

You've eaten corn, so you know it's not an oily seed. Same with soybeans. So how to they get the oil out of them? They use a combination of heat and petroleum solvents. Then, they chemically bleach and deodorize the oil, and sometimes partially hydrogenate it to make it more shelf-stable. Hungry yet? This is true of all the common colorless oils, and anything labeled "vegetable oil".

Olive oil is great, but don't run out and buy it just yet! There are different grades, and it's important to know the difference between them.
The highest grade is extra-virgin olive oil, and it's the only one I recommend. It's the only grade that's not heated or chemically refined in any way. Virgin olive oil, "light" olive oil (refers to the flavor, not calories), "pure" olive oil, or simply olive oil all involve different degrees of chemical extraction and/or processing. This applies primarily to Europe. Unfortunately, the US is not part of the International Olive Oil Council (IOOC), which regulates oil quality and labeling.

The olive oil market is plagued by corruption. Much of the oil exported from Italy is
cut with cheaper oils such as colza. Most "Italian olive oil" is actually produced in North Africa and bottled in Italy, and may be of inferior quality. The USDA has refused to regulate the market so they get away with it. If you find a deal on olive oil that looks too good to be true, it probably is.

Only buy from reputable sources. Look for the IOOC seal, which guarantees purity, provenance and freshness. IOOC olive oil must contain less than 0.8% acidity. Acidity refers to the percentage of free fatty acids (as opposed to those bound in triglycerides), a measure of damage to the oil.
Fortunately, the US has a private equivalent to the IOOC, the California Olive Oil Council (COOC). The COOC seal ensures provenance, purity and freshness just like the IOOC seal. It has outdone the IOOC in requiring less than 0.5% acidity. COOC-certified oils are more expensive, but you know exactly what you're getting.

Thanks to funadium for the CC photo

Monday, April 14, 2008

Real Food V: Sauerkraut

Sauerkraut is part of a tradition of fermented foods that reaches far into human prehistory. Fermentation is a means of preserving food while also increasing its nutritional value. It increases digestibility and provides us with beneficial bacteria, especially those that produce lactic acid. Raw sauerkraut is a potent digestive aid, probably the reason it's traditionally eaten with heavy food.

Sauerkraut is produced by a process called ‘anaerobic’ fermentation, meaning ‘without oxy
gen’. It’s very simple to achieve in practice. You simply submerge the cabbage in a brine of its own juices and allow the naturally present bacteria to break down the sugars it contains. The process of ‘lacto-fermentation’ converts the sugars to lactic acid, making it tart. The combination of salt, anaerobic conditions, and acidity makes it very difficult for anything to survive besides the beneficial bacteria, so contamination is rare. If it does become contaminated, your nose will tell you as soon as you taste it.

Store-bought sauerkraut is far inferior to homemade. It's soggy and sterile. Ask
a German: unpasteurized kraut is light, crunchy and tart!

My method is inexpensive and requires no special equipment. I've tested it many times and have never been disappointed.

  • Wide-mouth quart canning jars (cheap at your local grocery store)
  • Beer bottles with the labels removed, or small jars that fit inside the canning jars
  • Three tablespoons of sea salt (NOT iodized table salt-- it's fatal to our bacteria)
  • Five pounds of green cabbage
  1. Chop cabbage thinly. Ideally the slices should be 2 mm or so wide, but it doesn’t matter very much. You can use a food processor, mandolin or knife.
  2. Put all the cabbage together in a large bowl and add the salt. If the salt is not very dense (sometimes finely ground sea salt can be fluffy), you can add up to 5 tablespoons total. Mix it around with your hands. Taste some. It should be good and salty.
  3. Let the salted cabbage sit in the bowl for 30 minutes or so. It should be starting to get juicy.
  4. Pack the cabbage tightly into the canning jars. Leave 2-3 inches at the top of the jar. When you push on the cabbage in the jar, you should be able to get the brine to rise above the cabbage. Try to get rid of air bubbles.
  5. Put water into the beer bottles and place them into the canning jars. The weight of the bottles will keep the cabbage under the brine. It’s okay that some of the brine is exposed to the air; the cabbage itself is protected.
  6. Let it sit for 2 weeks at room temperature! As the fermentation proceeds, bubbles will form and this will raise the level of the brine. This is normal. You might get some scum on top of the liquid; just check for this and scrape it off every few days. It won’t affect the final product. If the brine drops to the level of the cabbage, add salt water (1 tsp/cup, non-chlorinated water) to bring it back up.
  7. Taste it! It should be tart and slightly crunchy, with a fresh lactic acid flavor. If fully fermented, it will keep in the fridge for a long time.
Here are some photos from making sauerruben, which is like sauerkraut but made with turnips:

Wednesday, April 9, 2008

Leptin and Lectins: Part III

Thanks to everyone for the great comments, this has been an interesting discussion.

I received a very kind e-mail response from Dr. Lindeberg, in which he told me that his group didn't measure leptin levels in his paleolithic pig study because it would have required special reagents. He also sent me two very interesting papers, both hot off the presses.

The first paper shows that glycosylation (bound sugars) of the leptin receptor is required for normal leptin binding. One of the molecules they use to probe the function of the leptin receptor is our good friend wheat germ agglutinin (WGA), a lectin found in wheat, barley and rye. They used WGA to specifically block leptin binding at the receptor.

This fits in very nicely with the hypothesis that grain lectins cause leptin resistance. If WGA gets into the bloodstream, which it appears to, it has the ability to bind leptin receptors and block leptin binding. It doesn't take much imagination to see how this could cause leptin resistance.

One caveat is that they used a high concentration of WGA in the study; 10 ug/mL was the lowest concentration they used. I can't imagine that concentration is possible in an actual human body. However, the paper doesn't explore the lower limit of WGA's ability to block leptin binding. At the lowest concentration used, it blocked 50% of the leptin from binding. It's possible that much smaller amounts could still have a significant effect.

The second paper Dr. Lindeberg sent me was on the soy isoflavone genistein. Here's the executive summary: it's bad. Unless you are a man who really wants to embrace his feminine side. It gets into all tissues and effectively activates the estrogen receptor in mice. It shrinks the prostate just like administering estrogen. It also passes into pups through the mothers' milk at levels high enough to activate their estrogen receptors. All this from the same amount of genistein you can get by eating a meal of soy.

The bad news doesn't stop there. Fermentation doesn't break it down. Miso, tempeh and natto actually have more genistein than non-fermented soy. Sigh...

Monday, April 7, 2008

Leptin and Lectins: Part II

Why do Americans become overweight and diseased on a high-carbohydrate diet while the carbohydrate-loving Kuna and Kitavans remain exceptionally free of chronic disease? Dr. Lindeberg proposes an answer- grains.

Dr. Lindeberg's hypothesis is that grains cause leptin resistance, which as we saw in the last post, has the potential to precipitate the metabolic syndrome and its various consorts. It's an attractive idea. The Kitavans (who he has studied personally), Kuna, and other cultures in Melanesia, Malaysia, Africa, the Arctic and South America, do not suffer from the diseases of civilization. These are all cultures that consume little or no grain, despite some having starchy diets. The Kitavans have low circulating leptin and remain lean and disease-free despite a high intake of carbohydrate.

Dr. Lindeberg says that grain-based cultures almost universally suffer from varying degrees of our illnesses, although his references to support that statement are unsatisfying. He did provide a reference showing that stroke occurs in affluent grain-based societies (whereas it seems not to in Kitavans), but I would really have liked to see a side-by-side comparison of cultures with similar lifestyles and differing grain intakes.

One thing that's certain is humans have not been eating grains for very long. Before the invention of agriculture in the fertile crescent, grains were a minor and seasonal crop for a small number of groups. Something we have been eating for a long time however is starchy tubers, bulbs and roots. Hunter-gatherers didn't generally go after wild grass seeds (grains) because they weren't a concentrated enough food source in most places. If you collect grass seeds all day, you might end up with a mouthful, after which you have to soak, grind, and cook them before chowing down. Dig up a few camas bulbs however, and you've got yourself a meal in 5 minutes.

The distinction between different sources of starch may lie in a class of molecules called lectins. Lectins were originally defined by their ability to aggregate red blood cells (erythrocytes). They do this by binding to the natural coating of carbohydrate on the cells' surface. A more current definition of a lectin is a molecule that specifically binds carbohydrate. Lectins are found throughout all kingdoms of life, and they serve a variety of useful functions. Many plants use lectins as a defense against hungry animals. Thus, an animal that is not adapted to the lectins in the plant it's eating may suffer damage or death.

Grains and legumes (beans, soy, peas, peanuts) are rich in some particularly nasty lectins. Especially wheat. Some can degrade the intestinal lining. Some have the ability to pass through the intestinal lining and show up in the bloodstream. Once in the bloodstream, they may bind all sorts of carbohydrate-containing proteins in the body, including the insulin receptor. They could theoretically bind the leptin receptor, which also contains carbohydrate (= it's glycosylated), potentially desensitizing it. This remains to be tested, and to my knowledge is pure speculation at this point. What is not so speculative is that once you're leptin-resistant, you become obese and insulin resistant, and at that point you are intolerant to any type of carbohydrate. This may explain the efficacy of carbohydrate restriction in weight loss and improving general health.

Another thing I have to mention about lectins is they can be broken down by certain food processing techniques. Remember all those old-fashioned things our grandparents used to do to grains and beans before eating them, like soaking beans overnight, sourdough-fermenting bread dough and nixtamalizing corn? All those things we've abandoned in favor of modern convenience foods? You guessed it, those reduce lectins dramatically, along with a long list of other toxins like phytic acid and protease inhibitors. Modern yeast-leavened breads, pastries, crackers, corn and soy products are no longer prepared according to these methods, and their lectin levels are typically much higher. One thing to keep in mind is that these processes reduce but generally do not eliminate lectins and other toxins.

The thing I really like about Dr. Lindeberg's idea is it explains a lot of what is happening in the world around us. The Kitavans eat yams, sweet potatoes, taro and tapioca as their staples. Incidentally, the long-lived Okinawans also eat sweet potatoes as a staple. The Kuna eat mostly plantains, yucca and kidney beans. These are three exceptionally healthy populations with a very low intake of grains. What happens when you feed these same people wheat? The Kuna have a well-documented rise in blood pressure, diabetes and cardiovascular disease mortality when they move to an urban, westernized setting. Okinawans became obese and unhealthy when American food was introduced. Wherever white flour and sugar go, the diseases of civilization follow. Weston Price documented this in the dental and skeletal health of 14 different cultures throughout the world.

It also explains what's going on under our very noses. Like I mentioned earlier, modern processed food is rich in lectins because it hasn't been treated by soaking, sprouting or bacterial fermentation. Soy has one of the highest lectin activities of any food, unless it's traditionally fermented into miso, tempeh, tamari or natto. As we've begun relying more and more on industrial food, our health has taken a major turn for the worse. Obesity is soaring in the US and diabetes is close on its heels.

I think it's very likely that grains are one of the major culprits in the diseases of civilization. This could be due to lectins causing leptin resistance. It's a fantastic hypothesis that could explain the health problems we see in modern grain-based societies.

Sunday, April 6, 2008

Leptin and Lectins

I've been puzzled by an interesting question lately. Why is it that certain cultures are able to eat large amounts of carbohydrate and remain healthy, while others suffer from overweight and disease? How do the pre-industrial Kuna and Kitavans maintain their insulin sensitivity while their bodies are being bombarded by an amount of carbohydrate that makes the average American look like a bowling ball?

I read a very interesting post on the Modern Forager yesterday that sent me on a nerd safari through the scientific literature. The paper that inspired the Modern Forager post is a review by Dr. Staffan Lindeberg. In it, he attempts to draw a link between compounds called lectins, found in grains (among other things), and resistance to the hormone leptin. Let's take a step back and go over some background.

One of the most-studied animal models of obesity is called the "Zucker" rat. This rat has a missense mutation in its leptin receptor gene, causing it to be nonfunctional. Leptin is a hormone that signals satiety, or fullness. It's secreted by fat tissue. The more fat tissue an animal has, the more leptin it secretes. Normally, this creates negative feedback that causes it to eat less when fat begins to accumulate, keeping its weight within a narrow range.

Zucker rats secrete leptin just fine, but they lack leptin receptors in their brain. Their blood leptin is high but their brain isn't listening. Thus, the signal to stop eating never gets through and they eat themselves to morbid obesity. Cardiovascular disease and diabetes follow shortly thereafter, unless you remove their
visceral fat surgically.

The reason Zucker rats are so interesting is they faithfully reproduce so many features of the disease of civilization in humans. They become obese, hypometabolic, develop insulin resistance, impaired glucose tolerance, dyslipidemia, diabetes, and cardiovascular disease. Basically, severe metabolic syndrome. So here's a rat that shows that leptin resistance can cause something that looks a whole heck of a lot like the disease of civilization in humans.

For this model to be relevant to us, we'd expect that humans with metabolic syndrome should be leptin-resistant. Well what do you know, administering leptin to obese people doesn't cause satiety like it does in thin people. Furthermore, elevated leptin
predicts the onset of obesity and metabolic syndrome. It also predicts insulin resistance. Yes, you read that right, leptin resistance comes before insulin resistance.

Interestingly enough, the carbohydrate-loving Kitavans don't get elevated leptin like europeans do, and they don't become overweight, develop insulin dysfunction or the metabolic syndrome either. This all suggests that leptin may be the keystone in the whole disease process, but what accounts for the differences in leptin levels between populations?

I'll talk about a possible explanation in my next post.

Thursday, April 3, 2008

Hydration: Attempt Only Under Medical Supervision

I've noticed how the word "hydration" has crept into the popular lexicon in the last decade or so. Before that, we were so primitive, we just "drank water". Now you need a PhD just to put a glass to your lips. I'm not sure I'm qualified!

I've been hearing so many people, including health professionals, tell me to drink 8 glasses of water a day for my entire life. In my middle school health class, I was told by my hydrophilic teacher that I should be urinating every hour and my urine should always be clear. For my whole life, I've thought it was nonsense. Yet the message has reached people. Walk around any college campus and you'll see undergrads faithfully carrying around their endocrine-disrupting plastic-water everywhere they go.

You see, our bodies have this very sophisticated mechanism to ensure water homeostasis. It's called thirst. If we need so much water to be healthy, why aren't we thirsty more often?

I skimmed through a paper today in the Journal of the American Society of Nephrology that reviews the evidence for health benefits from drinking more water than your thirst demands. Their conclusion: there's no evidence to suggest it helps anything. Water is just a nice harmless placebo.

The term "hydration" has helped fuel a whole industry to satisfy our need for hydration technology. Gatorade claims it hydrates better than water. It must be the high-fructose corn syrup and yellow #5... And make sure to bring your "hydration pack" when you go on your 20 minute jog; you might get lost and end up in the Kalahari desert!

I actually think the water craze isn't totally harmless. Drinking large amounts of water with a meal interferes with digestion by diluting digestive enzymes and stomach acid. Drinking a tall beer does the same. Wine is better because it tends to be a smaller volume.

As far as I'm concerned, with minor exceptions, the only thing to drink is water. I'll have an occasional glass of wine, beer or whole raw milk, but 99% of what I drink is good old-fashioned dihydrogen oxide.

The only time I drink a large amount of water without being thirsty is if I'm about to do vigorous exercise or spend time outside in hot weather.

Thanks to Snap for the CC photo.

Wednesday, April 2, 2008

A Shift in Tastes

I noticed it for the first time a few weeks ago. One of my labs was having a cake and ice cream party for someone's birthday and it didn't tempt me in the slightest. Today, I looked at a box of candy on the table at work and it seemed distinctly unappetizing. My taste for sugar has all but disappeared.

When I was a child, I couldn't get enough sugar. My parents would buy reduced sugar cereal and I would add a heaping tablespoon of sugar to each bowl. My favorite part was the sweet slurry at the bottom after the cereal was gone.

By the time I went to college, I knew sugar was unhealthy. It took massive amounts of willpower to keep myself from gorging on donuts and ice cream. Often, my willpower wasn't enough. Since then, I've been gradually refining my diet and the cravings have become more manageable. Sugar binges became rare.

In the past six months, I've made some new lifestyle changes based on my current understanding of nutrition and health. I've reduced my carbohydrate intake, drastically reduced my grain intake, and increased my fat intake. Most of my carb intake comes from vegetables now, with small portions of legumes from time to time as well. I've also added interval training and weight lifting to my exercise routine, which was formerly a 30 minute bike commute every day.

After an adjustment period of 3-4 months, my tastes have changed. I don't crave sugar or starchy foods anymore, and I can't get enough fat. I could eat practically nothing but fatty meat, but I don't for environmental and financial reasons. I do eat a lot of eggs, and an amount of lard, butter, olive oil and coconut oil that would make Dean Ornish weep. I see it as a very good sign that my body has made the shift from a carbohydrate-burning metabolism to a fat-burning one. Since carbohydrate and sugar cravings are related to insulin levels in my opinion, my insulin has probably dropped.

I'm going to get my bloodwork done sometime soon; I'll post it on the blog so you can all see how my self-experimentation is working. Then we can decide whether I'm onto something or full of hot air. I'd like to know my total cholesterol, HDL, LDL, triglycerides, fasting insulin, HbA1c and perhaps glucose tolerance.

Thanks to Andrew Huff for the CC photo.

Tuesday, April 1, 2008

Low-carb Review Article

The other day, I came across this nice review article from the American Journal of Clinical Nutrition. It gives a thorough but accessible overview of the current state of research into carbohydrate-restricted diets, without all the fatophobic mumbo-jumbo. It points out a few "elephants in the room" that the mainstream likes to ignore. First of all, the current approach isn't working:
The persistence of an epidemic of obesity and type 2 diabetes suggests that new nutritional strategies are needed if the epidemic is to be overcome.
Preagricultural diets were low in carbohydrate:
In contrast to current Western diets, the traditional diets of many preagricultural peoples were relatively low in carbohydrate (1, 2). In North America, for example, the traditional diet of many First Nations peoples of Canada before European migration comprised fish, meat, wild plants, and berries. The change in lifestyle of several North American aboriginal populations occurred as recently as the late 1800s, and the numerous ensuing health problems were extensively documented (3-5). Whereas many aspects of lifestyle were altered with modernization, these researchers suspected that the health problems came from the change in nutrition—specifically, the introduction of sugar and flour.
Carbohydrate reduction leads to a normalization of appetite:
It may also be that the mere lowering of serum insulin concentrations, as is seen with LCDs, may lead to a reduction in appetite. In support of this idea, several studies have found that insulin increases food intake, that foods with high insulin responses are less satiating, and that suppression of insulin with octreotide leads to weight loss (27-29).
I can't believe it; all that fat isn't going to clog my arteries??
Several outpatient diet studies have shown reductions in CVD risk factors after an 8–12-wk LCKD, during weight loss, and during weight maintenance (21, 60-62).
The last paragraph is a zinger:
We emphasize that strategies based on carbohydrate restriction have continued to fulfill their promise in relation to weight loss and that, contrary to early concerns, they have a generally beneficial effect on most markers of CVD, even in the absence of weight loss. In combination with the intuitive and established efficacy in relation to glycemic control in diabetics, some form of LCD may be the preferred choice for weight reduction as well as for general health.