Real Food VII: Lentils

Lentils are a healthy food that comes with a few caveats. They have more protein and less carbohydrate than any other legume besides soybeans and peanuts. In fact, the ratio of protein to digestible carbohydrate is almost 1:1. The carbohydrate in lentils is slow-digesting, giving them a relatively low glycemic load. They also contain a remarkable array of vitamins and minerals, particularly B vitamins. One cup delivers 90% of your RDA of folate, so between lentils and liver there's no need for those sketchy prenatal vitamins.

Lentils must be properly prepared to be digestible and nutritious! I can't emphasize this enough. We did not evolve eating legumes, so we have to take certain steps to be able to digest them adequately. As with all beans and grains, proper soaking is essential to neutralize their naturally occurring toxins and anti-nutrients. Anti-nutrients are substances that interfere with the absorption of nutrients. Soaking activates enzymes in the seeds themselves that degrade these substances. It also cuts down substantially on cooking time and reduces flatulence.

Phytic acid is an anti-nutrient that's abundant in beans, grains and nuts. It can dramatically reduce the absorption of important minerals such as iron, calcium, magnesium and zinc, leading to deficiencies over time. It may be one of the main reasons human stature decreased after the adoption of agriculture, and it probably continues to contribute to short stature and health problems around the world.

Lentils and other seeds also contain trypsin inhibitors. Trypsin is one of the digestive system's main protein-digesting enzymes, and seeds probably inhibit it as a defense against predators. Another class of toxins are the lectins. Certain lectins are able to bind to and damage the digestive tract, and even pass into the circulation and possibly wreak havoc. This is a short list of a few of the toxins found in beans and grains. Fortunately, all of these toxins can be reduced or eliminated by proper soaking. I like to soak all legumes for a full 24 hours, adding warm water halfway through. This increases the activity of the toxin-degrading enzymes.

Here's a method for preparing lentils that I've found to be effective. You will actually save time by doing it this way rather than cooking them without soaking, because they cook so much more quickly:

1. 24 hours before cooking, place dry lentils in a large bowl and cover with 2" of water or more.
2. After 12 hours or so, drain and cover the lentils with very warm water (not hot tap water).
3. Drain and rinse before cooking.
4. To cook, simply cover the soaked lentils with fresh water and boil until tender. I like to add a 2-inch piece of the seaweed kombu to increase mineral content and digestibility.

many thanks to *clarity* for the CC photo

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...

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.

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.