Yes, I'm finally diving headfirst into blog-land. Welcome to the blog section of Whole Health Source.
This blog will be a collection of my thoughts on health, food, the environment, science, wholesome living and whatever else captures my interest.
Maybe this will help me stop clogging up other blogs' comment pages.
C 2008
Friday 29 August 2014
Thursday 28 August 2014
Genetics and Disease
There is a lot of confusion surrounding the role of genetics in health. It seems like every day the media have a new story about gene X or Y 'causing' obesity, diabetes or heart disease. There are some diseases that are strongly and clearly linked to a gene, such as the disease I study: spinocerebellar ataxia type 7. I do not believe that genetics are the cause of more than a slim minority of health problems however. Part of this is a semantic issue. How do you define the word 'cause'? It's a difficult question, but I'll give you an example of my reasoning and then we'll come back to it.
A classic and thoroughly studied example of genetic factors in disease can be found in the Pima indians of Arizona. Currently, this population eats a version of the American diet, high in refined and processed foods. It also has the highest prevalence of type II diabetes of any population on earth (much higher than the US average), and a very high rate of obesity. One viewpoint is that these people are genetically susceptible to obesity and diabetes, and thus their genes are the cause of their health problems.
However, if you walk across the national border to Mexico, you'll find another group of Pima indians. This population is genetically very similar to the Arizona Pima except they have low rates of obesity and diabetes. They eat a healthier, whole-foods, agriculture-based diet. Furthermore, 200 years ago, the Arizona Pima were healthy as well. So what's the cause of disease here? Strictly speaking, it's both genetics and lifestyle. Both of these factors are necessary for the health problems of the Arizona Pima. However, I think it's more helpful to think of lifestyle as the cause of disease, since that's the factor that changed.
The Pima are a useful analogy for the world in general. They are an extreme example of what has happened to many if not all modern societies. Thus, when we talk about the 'obesity gene' or the 'heart disease gene', it's misleading. It's only the 'obesity gene' in the context of a lifestyle to which we are not genetically adapted.
I do not believe that over half of paleolithic humans were overweight, or that 20% had serious blood glucose imbalances. In fact, studies of remaining populations living naturally and traditionally have shown that they are typically much healthier than industrialized humans. Yet here we are in the US, carrying the very same genes as our ancestors, sick as dogs. That's not all though: we're actually getting sicker. Obesity, diabetes, allergies and many other problems are on the rise, despite the fact that our genes haven't changed.
I conclude that genetics are only rarely the cause of disease, and that the vast majority of health problems in the US are lifestyle-related. Studies into the genetic factors that predispose us to common health problems are interesting, but they're a distraction from the real problems and the real solutions that are staring us in the face. These solutions are to promote a healthy diet, exercise, and effective stress management.
Reclaiming Food
We, as individuals, are gradually losing control of our food.
For the majority of human existence, we have been in more or less full control of food preparation. We roasted our own meat, churned our own butter, and stewed our own vegetables. Gradually, mostly over the course of the last hundred years, we have ceded this control to others.
People in industrialized nations now rely on processed food and restaurants for the majority of our diet. Our food has been outsourced, and it's killing us.
The problem is that the incentives of individuals are different from the incentives of restaurants and corporations. The individual cares about the enjoyment and healthfulness of food. The corporation and restaurant care about money. It's not a conspiracy against our health, it's just a difference of motivation.
This explains why processed food is so unhealthy. Is a food manufacturer going to use butter or dirt-cheap hydrogenated soybean oil in that cookie if you can't tell the difference?
The only reason we accept this state of affairs is we're completely disconnected from the preparation of these foods. For example, let me tell you how hydrogenated soybean oil is made. First, the oil is separated from the rest of the bean using heat and extraction with organic solvents like hexane. Then, the oil is mixed with nickel (a catalyst) and exposed to hydrogen gas at high temperatures. This causes a chemical reaction (hydrogenation) that results in trans fat, which is solid at room temperature like saturated fats. The oil is now a grayish, rancid-smelling mush. They filter out the nickel and use chemicals and heat to deodorize and bleach it, creating the final product that is ubiquitous in processed snack foods. Delicious!
If you were able to watch this whole process with your own two eyes, would you still eat hydrogenated oil? If you had to make it yourself, would you? How about if I told you eating it is associated with a dramatic increase in the risk of cardiovascular disease, insulin resistance and probably many other diseases?
It's time to re-connect ourselves with real food. It's time to reclaim food preparation.
Join me as I explore traditional methods of food preparation, one of our most valuable conduits to health and well-being.
For the majority of human existence, we have been in more or less full control of food preparation. We roasted our own meat, churned our own butter, and stewed our own vegetables. Gradually, mostly over the course of the last hundred years, we have ceded this control to others.
People in industrialized nations now rely on processed food and restaurants for the majority of our diet. Our food has been outsourced, and it's killing us.
The problem is that the incentives of individuals are different from the incentives of restaurants and corporations. The individual cares about the enjoyment and healthfulness of food. The corporation and restaurant care about money. It's not a conspiracy against our health, it's just a difference of motivation.
This explains why processed food is so unhealthy. Is a food manufacturer going to use butter or dirt-cheap hydrogenated soybean oil in that cookie if you can't tell the difference?
The only reason we accept this state of affairs is we're completely disconnected from the preparation of these foods. For example, let me tell you how hydrogenated soybean oil is made. First, the oil is separated from the rest of the bean using heat and extraction with organic solvents like hexane. Then, the oil is mixed with nickel (a catalyst) and exposed to hydrogen gas at high temperatures. This causes a chemical reaction (hydrogenation) that results in trans fat, which is solid at room temperature like saturated fats. The oil is now a grayish, rancid-smelling mush. They filter out the nickel and use chemicals and heat to deodorize and bleach it, creating the final product that is ubiquitous in processed snack foods. Delicious!
If you were able to watch this whole process with your own two eyes, would you still eat hydrogenated oil? If you had to make it yourself, would you? How about if I told you eating it is associated with a dramatic increase in the risk of cardiovascular disease, insulin resistance and probably many other diseases?
It's time to re-connect ourselves with real food. It's time to reclaim food preparation.
Join me as I explore traditional methods of food preparation, one of our most valuable conduits to health and well-being.
Real Food I: Soup Stock
Making soup stock is a common practice in cultures throughout the world. It's a way of maximizing the value, nutrition and flavor of foods that are not always abundant. It's particularly relevant in the 21st century, when it's important to make the most of animal products that have a large environmental footprint.
The simplest way to make stock is to keep a "stock bag" in the freezer. Keep two plastic freezer bags (or whatever container you prefer) in the freezer, ready to accept food scraps whenever you have them. One is for vegetable scraps such as carrot peels, onion skins (not the brown part!), radish tops, etc. The other is for animal scraps such as bones, fish heads/tails, gristle, etc.
These are examples of vegetable scraps that are appropriate for stock:
Vegetable peels
Carrot ends
Onion scraps
Wilted greens
Asparagus stems
These are examples of animal products that are good for stock:
Bones
Gristle
Fish heads/tails
Chicken feet
Parmesan rinds (thanks Debs!)
These should not be used for stock:
Brown onion skins
Anything covered in dirt
Anything rotten or unpleasant-smelling
Celery greens, carrot greens and other bitter greens
Vegetable stock is the easiest. Take a generous amount of vegetable scraps out of your stock bag and put them in a pot full of water. Boil for one hour, then strain.
In my opinion, the best stock is made with animal bones. It's rich in minerals and gelatin, and has a full, meaty flavor. Break the bones to expose the marrow, put them in a pot full of water or a crockpot, add 2 tablespoons vinegar, and simmer for 1-20 hours. Add vegetable scraps for the last hour, then strain. Large bones from beef or lamb require long cooking to draw out their full flavor, while thinner chicken bones and fish parts require less. The vinegar helps draw the minerals out of the bones into solution.
Fish heads also make a delicious, nutritious stock. They're full of minerals (including iodine), omega-3 fats and vitamin A from the eyes. You can often get them dirt-cheap at the fish counter. Boil them for one hour with vegetable scraps and two tablespoons of vinegar, strain, pick off the meat and add it to your soup.
The simplest way to make stock is to keep a "stock bag" in the freezer. Keep two plastic freezer bags (or whatever container you prefer) in the freezer, ready to accept food scraps whenever you have them. One is for vegetable scraps such as carrot peels, onion skins (not the brown part!), radish tops, etc. The other is for animal scraps such as bones, fish heads/tails, gristle, etc.
These are examples of vegetable scraps that are appropriate for stock:
Vegetable peels
Carrot ends
Onion scraps
Wilted greens
Asparagus stems
These are examples of animal products that are good for stock:
Bones
Gristle
Fish heads/tails
Chicken feet
Parmesan rinds (thanks Debs!)
These should not be used for stock:
Brown onion skins
Anything covered in dirt
Anything rotten or unpleasant-smelling
Celery greens, carrot greens and other bitter greens
Vegetable stock is the easiest. Take a generous amount of vegetable scraps out of your stock bag and put them in a pot full of water. Boil for one hour, then strain.
In my opinion, the best stock is made with animal bones. It's rich in minerals and gelatin, and has a full, meaty flavor. Break the bones to expose the marrow, put them in a pot full of water or a crockpot, add 2 tablespoons vinegar, and simmer for 1-20 hours. Add vegetable scraps for the last hour, then strain. Large bones from beef or lamb require long cooking to draw out their full flavor, while thinner chicken bones and fish parts require less. The vinegar helps draw the minerals out of the bones into solution.
Fish heads also make a delicious, nutritious stock. They're full of minerals (including iodine), omega-3 fats and vitamin A from the eyes. You can often get them dirt-cheap at the fish counter. Boil them for one hour with vegetable scraps and two tablespoons of vinegar, strain, pick off the meat and add it to your soup.
Superstimuli
During the 1940s and 50s, an Austrian psychologist named Konrad Lorenz studied the behavioral patterns of geese.
One of the things he observed was the egg-retrieving behavior of the greylag goose. When an egg rolls out of a goose's nest, it gently uses its bill to roll it back in. However, when Lorenz took an egg from the nest and placed it next to a larger round white object, the goose preferentially rolled the larger object back into its nest while ignoring the real egg. He called this larger object a superstimulus. It was an abnormally strong stimulus that was able to hijack the bird's normal behavioral pattern in a maladaptive way.
Our brains are wired to respond to the stimuli with which they evolved. For example, our natural taste preferences tell us that fruit is good. But what happens when we concentrate that sugar tenfold? We get a superstimulus. Our brains are not designed to process that amount of stimulation constructively, and it often leads to a loss of control over the will, or addiction.
It's a very similar process to drug addiction. Addictive drugs are able to plug directly into the brain's pleasure centers, stimulating them beyond their usual bounds. Food superstimuli do this less directly, by working through the body's taste reward pathways. In fact, sweet liquids are so addictive, rats prefer them to intravenous cocaine. You can't take just one hit of crack, and you can't have just one Hershey's kiss.
Our bodies are finely honed to seek out healthy food, but only in the context of what we knew when our tastes developed during evolution. If all that's available is grass-fed meat, pastured eggs, vegetables, fruit, and nuts, your appetite will naturally guide you to a healthy diet.
If you surround yourself with superstimuli such as sugars, refined grains and MSG, your body will not guide you to a healthy diet. It will take you straight into a nutritional rut because it's not adapted to dealing with unnatural foods.
Your brain is pretty simple in some ways. It has these very basic hard-wired associations, like "sweet is good" and "free glutamate is good". If your brain likes a little bit of sweet, then it really likes a lot of sweet. If it likes a little bit of glutamate from meat, then it really likes a flood of glutamate from MSG. Just like the graylag goose that prefers the big white ball over her own egg, your brain drives you to ignore normal stimuli in favor of more potent superstimuli.
This explains the partially true saying "Everything that tastes good is bad for you". Why would your body deliberately encourage you to damage your health? In our hunter-gatherer state, it didn't. In this age of processed food, our technology has outstripped our ability to adapt.
One of the things he observed was the egg-retrieving behavior of the greylag goose. When an egg rolls out of a goose's nest, it gently uses its bill to roll it back in. However, when Lorenz took an egg from the nest and placed it next to a larger round white object, the goose preferentially rolled the larger object back into its nest while ignoring the real egg. He called this larger object a superstimulus. It was an abnormally strong stimulus that was able to hijack the bird's normal behavioral pattern in a maladaptive way.
Our brains are wired to respond to the stimuli with which they evolved. For example, our natural taste preferences tell us that fruit is good. But what happens when we concentrate that sugar tenfold? We get a superstimulus. Our brains are not designed to process that amount of stimulation constructively, and it often leads to a loss of control over the will, or addiction.
It's a very similar process to drug addiction. Addictive drugs are able to plug directly into the brain's pleasure centers, stimulating them beyond their usual bounds. Food superstimuli do this less directly, by working through the body's taste reward pathways. In fact, sweet liquids are so addictive, rats prefer them to intravenous cocaine. You can't take just one hit of crack, and you can't have just one Hershey's kiss.
Our bodies are finely honed to seek out healthy food, but only in the context of what we knew when our tastes developed during evolution. If all that's available is grass-fed meat, pastured eggs, vegetables, fruit, and nuts, your appetite will naturally guide you to a healthy diet.
If you surround yourself with superstimuli such as sugars, refined grains and MSG, your body will not guide you to a healthy diet. It will take you straight into a nutritional rut because it's not adapted to dealing with unnatural foods.
Your brain is pretty simple in some ways. It has these very basic hard-wired associations, like "sweet is good" and "free glutamate is good". If your brain likes a little bit of sweet, then it really likes a lot of sweet. If it likes a little bit of glutamate from meat, then it really likes a flood of glutamate from MSG. Just like the graylag goose that prefers the big white ball over her own egg, your brain drives you to ignore normal stimuli in favor of more potent superstimuli.
This explains the partially true saying "Everything that tastes good is bad for you". Why would your body deliberately encourage you to damage your health? In our hunter-gatherer state, it didn't. In this age of processed food, our technology has outstripped our ability to adapt.
Wednesday 27 August 2014
Real Food II: Vinaigrette
Store-bought salad dressing is a crime against humanity.
'Ranch', '1000 Island' and other industrial monstrosities are a good way to put yourself underground in a hurry. From bottom-rung oils to artificial preservatives, they contain some of the most frightening ingredients you're likely to see in a grocery store.
Homemade salad dressing is one of the simplest, tastiest and healthiest recipes I know. If made properly, it's creamy, light and flavorful. I consider it my civic duty to spread the word about homemade salad dressing, also known as vinaigrette.
For a medium-sized salad, put two tablespoons of vinegar into your empty salad bowl. Add a pinch of salt and a tablespoon of dijon mustard. Add three tablespoons of olive oil and stir until it's creamy and homogenous. That's it! Add your salad, toss and enjoy. The tossing is essential.
I always use extra-virgin olive oil. My favorite vinegar is unpasteurized, unfiltered apple cider vinegar. You may add garlic, tarragon, mint, basil, green onions or miso to your dressing for extra flavor.
'Ranch', '1000 Island' and other industrial monstrosities are a good way to put yourself underground in a hurry. From bottom-rung oils to artificial preservatives, they contain some of the most frightening ingredients you're likely to see in a grocery store.
Homemade salad dressing is one of the simplest, tastiest and healthiest recipes I know. If made properly, it's creamy, light and flavorful. I consider it my civic duty to spread the word about homemade salad dressing, also known as vinaigrette.
For a medium-sized salad, put two tablespoons of vinegar into your empty salad bowl. Add a pinch of salt and a tablespoon of dijon mustard. Add three tablespoons of olive oil and stir until it's creamy and homogenous. That's it! Add your salad, toss and enjoy. The tossing is essential.
I always use extra-virgin olive oil. My favorite vinegar is unpasteurized, unfiltered apple cider vinegar. You may add garlic, tarragon, mint, basil, green onions or miso to your dressing for extra flavor.
The French Paradox
According to the World Health Organization, 82 out of every 100,000 French men between ages 35 and 74 died as a result of cardiovascular disease (CVD) in the year 2000. In that same year, 216 out of 100,000 men between the same ages in the U.S. succumbed to the same disease.
According to the Food and Agriculture Organization of the UN, during roughly the same time period, the average French person ate slightly more total fat and almost three times more animal fat than the average American. Animal fats came from dairy, lard, red meats, fish and poultry, and contributed to a much higher overall saturated fat intake in the French. This has been called the "French paradox", the paradox being that saturated fat is supposed to cause CVD.
Researchers have been scrambling to identify the factor that is protecting French hearts from the toxic onslaught of saturated fat. What could possibly be preventing the buttery sludge coursing through their arteries from killing them on the spot? One hypothesis is that wine is protective. Although the modern French don't actually drink much more alcohol than Americans on average, wine contains a number of molecules that are potentially protective.
One of these that has gotten a lot of attention is resveratrol, an activator of SIRT1, a deacetylase enzyme that is involved in stress resistance and lifespan regulation. But lo and behold, it turns out that there isn't enough of it in wine to be helpful. Now researchers are turning their attention to a class of molecules called procyanidins, but I suspect that this will turn up negative as well. The protective molecule is probably ethanol, but no one wants to hear that because it doesn't resolve the paradox.
As a person with a French background who has spent quite a bit of time in France, the notion of a French paradox is insulting. It implies that the French are eating an unhealthy diet, but are somehow miraculously protected by a compound they're ingesting by accident. Any French person will tell you there is no paradox. When you make a commitment to seek out the freshest, most delicious ingredients available and cook them yourself, your diet will be healthier than if you count the grams of this and that on your TV dinner.
There's more. Americans consume almost twice the amount of sugar as the average French person. I find this surprising, given the large amount of sugar I've seen on French tables, but I think it speaks to the huge amount of sugar we consume in the US. Much of it probably comes from the high-fructose corn syrup in soda. I'll save my rant about that for another time.
Another thing that stands out about French food habits is the absence of snacking. Mealtimes in France tend to be well-defined, and grazing is looked down upon. I think this is probably essential for maintaining adequate insulin sensitivity in the face of (delicious) refined carbohydrates like baguette.
And finally, the French enjoy their food more than the average nation. I wouldn't underestimate the value of this for health and overall well-being.
So what was the paradox again? I can't remember. Maybe a more parsimonious explanation of the data is that saturated fat isn't so bad after all, and enjoying wholesome food and limiting sugar is the true prescription for health.
Thanks to Gaetan Lee for the creative commons photo.
Two Tons of Steel
While I was waiting for the bus one morning, I decided I'd count cars to see how many were single-occupancy vs. two or more. I came up with a ratio of roughly 20 single-occupancy vehicles for every multiple-occupancy vehicle. The multiple-occupancy vehicles were most often work trucks, containing plumbers or construction workers going to a job.
People have to get to work. Maybe they don't have public transit where they are, or maybe they just don't feel like sitting next to smelly commuters, but for whatever reason, here in the U.S. they drive their cars.
The average American weighs about 180 lbs. Due to our love affair with SUVs, the average American car weighs over 2 tons and climbing. That means every time a person drives a single-occupancy vehicle to work, they aren't just expending the energy it takes to move 180 lbs 15 miles. They're also lugging around a hulking two-ton chunk of steel and plastic. The passenger of the average single-occupancy vehicle is only about 1/24 (4%) of the mass that's being moved to and from work. That's ridiculous!
Of course, we make up for the big weight of our cars with big engines so they can go vroom. That adds up to a lot of gasoline burned, for no clear benefit. In other words, most of us could easily be driving vehicles that perform the exact same function but burn 1/3 the gasoline. I'm not talking about space-age technology here; these vehicles are already on the market.
Why do we commute so inefficiently when better options surround us? I think there are several reasons. First of all, gasoline is dirt cheap. We have no incentive to be efficient beyond our own consciences. Even with the recent price jumps, gasoline doesn't cost much more than it ever has, if you adjust for inflation. In Europe, where high taxes mean gasoline can cost four times as much as in the US, vehicles are lighter and more efficient.
Secondly, we've always been a very car-centric society. Cars appeal to our desire for independence, power and control. A large, powerful car is a status symbol in the US. We've inherited these attitudes from previous generations and we're just beginning to question them. Are there healthier and less wasteful ways of getting to work?
There are, and many of them are very simple. The first and simplest is a carpool. If we put two average Americans in our two-ton car, all of a sudden the people are 1/12 the weight of the vehicle. With four people, the number jumps to 1/6. We've just made our vehicle almost four times as fuel efficient, per passenger! 1,000 lbs per person is still a lot of weight to be lugging around though, so let's look at some other options.
If you are on the market for a new car, fuel-efficient models abound. The new hybrid cars by Toyota and Honda are twice as efficient as their non-hybrid brethren, and not much more expensive. Some people truly need SUVs for their business, but I have good news for them too: there are now hybrid SUVs as well. That's right ladies and gentlemen, they're the most efficient gas guzzlers on the market.
Public transportation is another great option where it's available. Buses are big and heavy but they can accommodate many people.
Now let's get into the really efficient vehicles. Motorcycles and scooters weigh from 250-500 pounds, meaning that a passenger would be from 1/2 to 1/4 the total weight of the vehicle. Now we're beginning to make some sense. Certain scooters can go over 100 miles per gallon of gasoline.
An even better option is to use vehicles that don't burn gasoline at all. A bicycle weighs about 20-30 pounds, making the passenger about 9/10 of the total vehicle weight. That weight ratio might change as the average American loses some weight however. Even if you factor in the extra food you eat when you cycle regularly, it's still terribly efficient. Best of all, bikes allow us to get exercise and feel the sun for a while.
The title for the most fuel-efficient and low-tech vehicle around goes to feet. When using a pair of these, the passenger is 100% of the weight of the vehicle. You can walk until you wear them out and you still won't have burned a single molecule of gasoline. Now that's efficient.
Thanks to lairdscott for the CC photo.Convenience Store Survival Training
I was on the road yesterday driving to a county court to defend myself (unsuccessfully) against a speeding ticket. I reluctantly stopped into a convenience store on my way back, to see if there was anything I would eat for lunch.I actually did find two things that were palatable and not too unhealthy: canned sardines and toasted cashews. The total was $2.50, affordable even for a grad student.
The sardines were canned in "tomato sauce", which I realized later contained soybean oil. Oops. Well I suppose when you get your food at a convenience store, you have to expect such things.
The main thing that bothered me was the trash. I posted a mugshot (above) of the can, fork and plastic bag that I either trashed or recycled as a result of the meal. The total volume of trash was probably almost as much as the total volume of food.
I think if you stick to nuts, canned fish and fresh fruit, it's possible to survive a convenience store stop. And Baby Ruths. Those are healthy, right?
Improving Fuel Economy
OK, you know driving isn't good for the environment, but you're going to do it anyway. Here's how to substantially increase your fuel economy without buying a new car:
1- Drive deliberately; accelerate gradually. A car uses a lot of fuel when it's accelerating rapidly.
2- Drive 55 mph on the highway. This makes a huge difference. It maximizes fuel efficiency by reducing wind resistance, which exponentially increases with speed. This reduces gas consumption by more than 20% relative to a speed of 75 mph. 60 mph is almost as good, if 55 is to slow.
3- Draft a truck. Large trucks with flat, square backs leave a massive low-pressure zone behind them, which you can exploit to save gas. At 20 feet behind a standard 18-wheeler, you will use about 27% less fuel. If that's too close, you still save 20% at 50 feet, and 11% at 100 feet. Be careful because trucks have a blind spot behind them, and some truckers do not appreciate drafting.
4- Keep your car well-maintained. Clogged filters, faulty oxygen sensors and flat tires all hurt fuel efficiency.
5- Lose the cargo. The more weight you have in your car, the more fuel is required to get it up a hill or accelerate it.
6- Turn off accessories. AC is the biggest power drain, but the fan used to circulate air also draws power.
1- Drive deliberately; accelerate gradually. A car uses a lot of fuel when it's accelerating rapidly.
2- Drive 55 mph on the highway. This makes a huge difference. It maximizes fuel efficiency by reducing wind resistance, which exponentially increases with speed. This reduces gas consumption by more than 20% relative to a speed of 75 mph. 60 mph is almost as good, if 55 is to slow.
3- Draft a truck. Large trucks with flat, square backs leave a massive low-pressure zone behind them, which you can exploit to save gas. At 20 feet behind a standard 18-wheeler, you will use about 27% less fuel. If that's too close, you still save 20% at 50 feet, and 11% at 100 feet. Be careful because trucks have a blind spot behind them, and some truckers do not appreciate drafting.
4- Keep your car well-maintained. Clogged filters, faulty oxygen sensors and flat tires all hurt fuel efficiency.
5- Lose the cargo. The more weight you have in your car, the more fuel is required to get it up a hill or accelerate it.
6- Turn off accessories. AC is the biggest power drain, but the fan used to circulate air also draws power.
Tuesday 26 August 2014
Real Food III: Yogurt
Fermented milk is regarded by many cultures as a delicious health food. It has cropped up all over the world in different forms: kefir from Caucasia, laban from the Middle East, dahi from India, creme fraiche from Western Europe, piima from Finland, mursik from Kenya, and yogurt from your grandmother's house. But these same people would scarcely recognize the colored, sweetened gel that passes for yogurt in grocery stores today.Most if not all dairy-eating cultures ferment their milk. Why is this? There are three main reasons. First of all, unpasteurized milk spontaneously ferments at room temperature, usually becoming delicious "clabbered milk"- whereas pasteurized milk becomes putrid under the same conditions. So fermented milk is difficult to avoid. The second, related reason, is that fermentation prolongs the life of milk in the absence of refrigeration. Fully fermented milk is stable for weeks at room temperature.
The third reason is that these cultures know cultured milk is delicious and nutritious. Fermentation with specially selected cultures of lactic acid-producing bacteria and sometimes yeast work to break milk down into a form that is more easily assimilated. They partly (or fully) digest the lactose, which can be a problem for some people, turning it into tangy lactic acid. They also partially digest casein, a protein in milk that is difficult for some to digest. And finally, the lower pH of fermented milk makes its minerals more bioavailable.
Traditionally, milk was fermented in its unpasteurized state, but raw milk is hard to find in many industrialized countries. Raw milk has its complement of enzymes intact, such as lactase and lipase, which aid in its digestion. It also contains lactose-digesting bacteria that make milk easier for some to digest, and contribute to intestinal health. These are all eliminated by pasteurization. Fortunately, fermentation restores some of the benefits of raw milk. It reintroduces lactic-acid bacteria, along with their digestive enzymes. With that in mind, here's a simple yogurt recipe:
Ingredients/equipment:
1/2 gallon whole, raw or pasteurized, cow or goat milk (add extra cream if you wish)
Starter culture (commercial starter or 2 tbsp of your favorite live-culture yogurt)
Thermometer
Glass jars with lids
Cooler or yogurt maker
Recipe:
1. Heat the milk to 110-115 F (43 C). If the temperature exceeds 115 F, let it cool.
2. Add the starter culture. If the starter is yogurt, whisk it into the milk.
3. Pour the milk into glass jars and keep it at about 110 F for 4-10 hours. 4 hours will yield a mild yogurt, 10 will be tangy. If you don't have a yogurt maker, this is the tricky part. You can use a cooler filled with 100 F water to maintain the temperature and spike it with hot water after a few hours, or you can ferment it in your oven with the pilot light on if the temperature is in the right range.
If you want a thicker yogurt, bring the milk to 180 F (82 C) and let it cool to 110 F before adding the starter. Add fruit, honey or other flavors before fermenting. Enjoy!
As a final note, I'll mention that milk simply does not agree with some people. If you've tried raw milk and homemade yogurt, and they cause intestinal discomfort or allergies, let them go.
Say Hello to the Kuna
For those of you who haven't been reading the comments, we've been having a spirited discussion about the diet and health of hunter-gatherers here. I brought up the Kuna indians in Panama, who are immune to hypertension, live a good long time, do not gain excess weight, and seem to have less cardiovascular disease and cancer than their city-dwelling cousins.
I was hungry for more information about the Kuna lifestyle, so over the last few days, I've dug up every paper I could find on them. The first paper describing their lack of hypertension was published in 1944 and I don't have access to the full text. In 1997, a series of studies began, headed by Dr. Norman Hollenberg at Harvard. He confirmed the blood pressure findings, and collected data on their diet, lifestyle and kidney function. Here's a summary:
The Kuna are half hunter-gatherers, half agricultural. They cultivate plantains, corn, cocoa, yucca, kidney beans, and several types of fruit. They trade for sugar, salt, some processed cocoa and miscellaneous other foods. They drink 40+ oz of hot cacao/cocoa per day, some locally produced and some imported. A little-known secret: the Kuna eat an average of 3 oz of donut a week. They also fish and hunt regularly.
In the first recent study, published in 1997, the Kuna diet is described as 29% lower in fat than the average US diet (56 g/day), 23% lower in protein (12.2 g), 60% higher in cholesterol, and higher in sodium and fiber. The study doesn't specifically mention this, but the reader is left to infer that 65% of their calories come from carbohydrate. This would be from plantains, corn, yucca, sugar and beans. The fat in their diet comes almost exclusively from coconut, cocoa and fish: mostly saturated and omega-3 fats.
In the next study, the picture is slightly different. Their staple stew, tule masi, is described as being 38% fat by calories (from coconut and fish), exceeding the American average. In the final study in 2006, Hollenberg's group used a more precise method of accounting for diet composition than was used in previous attempts. The paper doesn't report macronutrients as a percentage of calories however.
I was able to find some clues about their diet composition. First of all, they report the meat consumption of the Kuna at approximately 60 oz per week, mostly from fish. That's 8.6 oz per day, identical to the American average.
By putting together the pieces from the later studies, a new picture emerges: a diet high in fish and moderate in protein, moderate in unprocessed fat (especially saturated and omega-3), and moderately high in mostly unprocessed carbohydrate.
Here's my interpretation. The Kuna are healthier than their city-dwelling cousins for a number of reasons. They have a very favorable omega3:6 ratio due to seafood, wild game and relatively saturated vegetable fats. Their carbohydrate foods are mostly unprocessed and mostly from non-grain sources. They also live an outdoor life full of sunshine (vitamin D) and exercise. The chocolate may also contribute to their health, as it contains high levels of potentially protective polyphenols. They're healthier than industrialized people because they live more naturally.
Another lesson to be learned from the Kuna and other exceptionally healthy indigenous peoples is that the human body can tolerate a large amount of carbohydrate under the right conditions.
Thoughts on Obesity, Part I
From the US Centers for Disease Control website:
According to certain nutrition experts, we know exactly what causes overweight. It's a character flaw known as overeating. Calories in, calories out. And the cure is to eat less. The problem is, this treatment has a poor record of efficacy.
Restricting calories is also fraught with problems. Each person's metabolism has a preference for a specific body composition within the context of a particular lifestyle. If total calories are restricted without changing diet composition, the body reacts vigorously to maintain homeostasis. Energy expenditure is reduced; muscle and organ mass diminish. The psychological effects are particularly bad, as anyone can tell you who has been on a low-calorie diet. In 1944, Ancel Keys undertook a calorie restriction trial in conscientious objector "volunteers" in Minnesota. They remained on a 1,570-calorie diet that was low in fat and protein and high in carbohydrate, for 24 weeks. Hardly a draconian calorie count. Here's a quote from the study:
There are some diet trends that have associated with rising obesity in the US. Per capita calorie consumption has increased. This increase is due to a higher consumption of carbohydrate. Total protein and fat consumption have been almost identical for the past 30 years. This period also saw increases in the consumption of unsaturated vegetable oils, hydrogenated vegetable oils and high-fructose corn syrup. It's hard to say from this association which of these factors (if any) has caused us to gain weight in the last 30 years, but it certainly isn't total fat or protein. Fortunately, we have other clues.
Since the mid-seventies, the prevalence of overweight and obesity has increased sharply for both adults and children. Data from two NHANES surveys show that among adults aged 20–74 years the prevalence of obesity increased from 15.0% (in the 1976–1980 survey) to 32.9% (in the 2003–2004 survey).In hunter-gatherer and some semi-agricultural societies, obesity is rare. In most, it's nonexistent. Wild animals typically do not accumulate enough fat to interfere with vigorous exercise, and when they do, it's because they're about to hibernate or migrate. Wild animals also tend to have similar amounts of body fat between individuals (at a given age and sex), unlike industrialized humans. This makes me think that obesity is an unnatural effect of our current lifestyle. Whatever the cause, it's getting progressively more common.
According to certain nutrition experts, we know exactly what causes overweight. It's a character flaw known as overeating. Calories in, calories out. And the cure is to eat less. The problem is, this treatment has a poor record of efficacy.
Restricting calories is also fraught with problems. Each person's metabolism has a preference for a specific body composition within the context of a particular lifestyle. If total calories are restricted without changing diet composition, the body reacts vigorously to maintain homeostasis. Energy expenditure is reduced; muscle and organ mass diminish. The psychological effects are particularly bad, as anyone can tell you who has been on a low-calorie diet. In 1944, Ancel Keys undertook a calorie restriction trial in conscientious objector "volunteers" in Minnesota. They remained on a 1,570-calorie diet that was low in fat and protein and high in carbohydrate, for 24 weeks. Hardly a draconian calorie count. Here's a quote from the study:
As starvation progressed, fewer and fewer things could stimulate the men to overt action. They described their increasing weakness, loss of ambition, narrowing of interests, depression, irritability, and loss of libido as a pattern characteristic of "growing old".Some of the men ended up suffering from neurosis and borderline psychosis before the end of the study, one culminating in self-mutilation. This is what we're being prescribed for weight loss?
There are some diet trends that have associated with rising obesity in the US. Per capita calorie consumption has increased. This increase is due to a higher consumption of carbohydrate. Total protein and fat consumption have been almost identical for the past 30 years. This period also saw increases in the consumption of unsaturated vegetable oils, hydrogenated vegetable oils and high-fructose corn syrup. It's hard to say from this association which of these factors (if any) has caused us to gain weight in the last 30 years, but it certainly isn't total fat or protein. Fortunately, we have other clues.
Real Food IV: Lard
Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.
If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.
Ingredients and Equipment:
- Lard
- Cheesecloth
- Baking dish
- Jars
2. Cut off any pieces of meat clinging to the fat.
3. Cut fat into small (~1-inch) cubes.
4. Place them into a non-reactive baking dish and then into the oven.
5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.
6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.
7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.
8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.
Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.
Monday 25 August 2014
Okinawa and Lard
The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, sweet potatoes, exercise, and the fact that some of them may have been mildly calorie restricted for part of their lives.
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but a moderate amount certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but a moderate amount certainly won't stop you...
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat in many people.
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:
Carbohydrate reduction leads to a normalization of appetite:
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.They claim that 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.But of course, many of them were very high in carbohydrate, and these cultures seemed in fine health as well.
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.
Sunday 24 August 2014
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.
Leptin
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 may come 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?
Real Food V: Sauerkraut
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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 oxygen’. 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.
Materials
- 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
- 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.
- 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.
- Let the salted cabbage sit in the bowl for 30 minutes or so. It should be starting to get juicy.
- 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.
- 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.
- 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.
- 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.
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
Saturday 23 August 2014
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!
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.
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.
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:
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)
Real Food VI: Liver
Liver was a highly regarded food among many hunter-gatherer and traditional agricultural societies. It's not surprising once you realize it's quite literally the most nutritious food in the world. It's because the liver is a storage depot, into which important nutrients are deposited in case of later need. A modest 4-oz serving of calf's liver contains 690% of your RDA of B12, 610% of preformed vitamin A, 215% of folate, 129% of B2, 24.5 g protein, and the list goes on. The nutrients found in liver are particularly important for development, but are also helpful for continued health in adulthood. Preformed vitamin A is one of the nutrients Weston Price suggested was responsible for the glowing health of the cultures he studied in his book Nutrition and Physical Degeneration. It's an essential nutrient, but it's different from most vitamins (except D) because it acts like a hormone, entering cells and altering gene transcription. Thus, it has its hand in many important bodily processes.
"Vitamin A" from plant sources such as carrots is actually a group of vitamin A precursors called carotenes, which the body inefficiently converts to actual vitamin A. The efficiency of conversion varies around 10%, depending on the carotene and how much fat is ingested along with it. Nutrition labels in the US do not reflect this. When a nutrition label on a plant-based product says "30% vitamin A", you can assume you will get about 3% of your RDA from it. This doesn't apply to eggs, dairy and liver, which contain preformed vitamin A.
I'm not sure how this happened, but somewhere along the line we decided in the US that muscle is the only proper animal tissue to eat. We are missing out on the most nutritious parts of the animal, and our health is suffering.
I recommend purchasing organic calf's liver, 100% grass-fed if possible. Chicken livers are also nutritious but ruminant livers are the most concentrated in vitamins by far.
Here is a recipe for a liver pate. I recognize that many people don't like the taste of liver, which is why I chose this recipe because it is very mild.
Ingredients
- 1/2 to 1 lb calf's liver, chopped into 1-in strips
- 3 eggs
- 1/2 stick butter
- 1/2 onion
- 1-2 carrots (optional)
- Sage and/or rosemary (optional)
- Salt to taste
- Saute the onions and carrots in 1 tbsp butter until they're soft.
- Add liver and herbs and cook until the liver is just done.
- Crack the eggs right into the pan and stir them until they're cooked.
- Turn off the heat, add the remaining butter.
- Blend until smooth.
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