In part I, I discussed nutrition facts about rice. These pages are intended to be standalone, so there’ll be some overlap here. Corn and rice are both grains, but their nutrient & anti-nutrient loads are quite different, as is their standard forms of preparation.

Overview

Several varieties of corn

The food known as “corn” in the US and Canada is known as maize elsewhere. It gets the name “corn” from its kernels; the word ‘corn’ actually means grain, as in grain of sand. Corned beef, for example, has had grains of salt added to cure it. In English-speaking countries, “corn” or “sweet corn” is often used in culinary contexts while “maize” is used in scientific or agricultural contexts.

Corn is often considered a vegetable in American cuisine, but it’s actually a grain, like wheat, rice, rye, and barley. It’s the most heavily produced grain in the world, ahead of rice (#2) and wheat (#3), with barley a distant fourth. Originally cultivated in Mesoamerica, it spread rapidly throughout the Americas and eventually worldwide. About 40% of the worldwide supply of corn is grown in the US.

Unlike wheat and rice, the corn grain is typically eaten whole. Immature grains are soft but unpalatable, and so cooked usually by boiling. Corn on the cob and packaged corn kernels are these immature grains. In traditional preparations, the kernels are soaked in alkali water, a process known as nixtamalization. Cornmeal, polenta, and various fermented corn drinks & foods are made from unripe ears; dry, ripe kernels are used for popcorn. As corn ages, more of the sugar in the kernels turns into starch. Hence, “sweet corn” is especially unripe, picked while there is still a lot of sugar available.

Nutrients

Corn’s a good source of starch. What, starch isn’t a nutrient? Damn. Nevermind!

Anti-Nutrients

OK, actually I’m just trying to make a point here. There are nutrients in corn – protein, B vitamins, and many minerals in the hull of the kernel. But it’s not a nutrient-dense food. The presence of anti-nutrients means many of the nutrients in corn aren’t bioavailable; what use is it to eat a lot of vitamins or minerals if they wind up passing straight through your digestive system?

Let’s start with protein. Corn isn’t a complete protein source, however; it provides low levels of several amino acids, which is why it’s often combined with other foods (such as beans) in traditional diets. You couldn’t thrive with corn as your only protein source.

The fats in oil, like in almost all vegetables, are polyunsaturated. These aren’t the good fats. If you’ve spent some time in the paleo community, you’ve surely come across the admonition to watch your omega-6 to omega-3 ratio, and to keep it under 2 (or as close to 1 as you can). Stephan and Richard (head on over and search for ‘omega ratio’) have both commented often on the omega 6:3 ratio; the research they’ve dug up suggests that a low ratio is great, but avoiding both is even better. Either way, vegetable fats are double-plus ungood.

Except for Bs, corn isn’t a good source of vitamins. NutritionData provides a good summary, but one thing to note: the “vitamin A” in plant foods isn’t the same as what one gets from animal foods. Veggies contain beta-carotenes, which need to be converted into retinol. That conversion isn’t always 100%, and often minimal in people with many health problems. Conversion requires bile salts in the upper intestines, which means Vit A needs to be eaten with fats (like butter!), and requires thyroxine. Those with hypothyroidism (like me! I’m not going to get shit for retinol from beta-carotenes) and diabetes lack the hormones and enzymes needed to make the conversion.

Also, animal foods contain a whole complex of vitamins. The research that “isolated” vitamins identified only single molecules. Generally, foods high in that specific molecule tend to be high in other compounds, as well. For example, animal foods high in retinol are also high in retinal, retinoic acid, retinyl esters, and other retinoids. “Animal Vitamin A” is far more than retinol itself.

Like most grains, corn in high in minerals. Those minerals are in the kernel hull, however, and that hull comes with compounds that block uptake of those minerals by animal digestion systems. Grains don’t want to be eaten – they reproduce by spreading pollen, not by letting animals eat their seeds. Blockers like phytate and trypsin inhibitors in corn hulls reduce the bioavailability of those minerals, and as with many other grains cooking reduces but does not completely destroy these antinutrients.

Summary

As with many foods not approved in a paleo diet, corn is a poor source of nutrients. If you’re starving, it’s got enough calories to keep you alive – but it lacks the protein, vitamins, and minerals to optimize health and allow humans to thrive. The “technical” amount of nutrients in corn (as suggested by the nutrition data on packaged corn products or given at a site like NutritionData) is misleading due to the anti-nutrients, and some of the anti-nutrients in corn are effectively like negative vitamins, in that they block uptake of the real thing hence increasing the demand for the real thing!

The calories in corn also crowd out other, better foods. A diet containing corn will be far less nutritious than an isocaloric diet containing animal foods. For the same nutrient supply, a diet containing corn will be a lot more calories, and that means weight gain. I won’t go into the evil of carbs, glycation, and insulin spikes here, although that’s another reason to avoid starchy foods.

In further installments, I’d like to cover wheat, other random grains, recipes & preparation, and provide a general overview of grains as a food source.

Is there anything else in a low-carb diet that can contribute to dehydration?

Glycogen Loss

From a comment by Peter on his blog: “there is a marked release of water from the liver as glycogen is lost, but this drops straight in to the circulation. It seems to be the excretion of this excess water through the kidneys, to maintain fluid balance, which takes potassium out with it.”

Glycogen is a storage form of glucose; it is how glucose is stored in the liver and in muscle cells. The glycogen stored in muscles can’t be extracted to be used by the body in general; it’s locked in there for the muscle alone. If you want to burn off that glycogen, you need to do exercise, and ensure you’re not stuffing any more glucose in there — which means keeping your blood sugar and insulin levels low. Liver glycogen is the result of some carb digestion; both alcohol and excess carbs will be stored as glycogen in the liver. But… this glucose storage isn’t really a big deal. As long as you’re not overloading the liver with either alcohol or carbs, the glycogen stores aren’t a health hazard.

When you burn off that glycogen, the water that glycogen binds to is released into the blood stream, as mentioned in the comment linked above.

This isn’t dehydration; this is the loss of excess water when one first switches to a low-carb diet. If you take a cheat day (I recommend one every two weeks), you’ll build up some glycogen stores that you’ll need to burn off, too. Dehydration is when there is a low volume of water in the blood; the loss of this glycogen-related water is just restoration of your normal plasma levels. Dehydration is having too little water in the blood, and that’s generally caused by something stripping water out.

Essential Fatty Acids (EFA)

From a page on Chris Masterjohn’s cholesterol-and-health site: “Arachidonic acid is necessary for growth, proper hydration, healthy skin and hair, gut health, and fertility.” Chris points out (in another page) that he’s concluded that only Arachidonic Acid (AA) and DHA are the only true essential fatty acids. EFAs are important in cell growth, and hence important to growing children, pregnant women, bodybuilders, and people recovering from injury, and needed in lesser amounts for general repair.

EFA concentration is highest in liver and giblets, especially of grass-fed beef and organically-raised pigs and fowl. This is one important reason to cook your own foods using organic, grass-fed meats; protein is protein, but the important vitamins contained in animal fat will vary significantly based upon the diet of the animal. I aim for grass-fed and organic meats not because I care about the lifestyle of the cow, but because I care about the quality of my food. Getting a good balance of fatty acids will help ensure your body’s hydration-level mechanisms are all running smoothly.

Poly-Unsaturated Fatty Acids

From that same page on Chris Masterjohn’s site: “When total PUFA intake or EPA intake is very high, however, the EPA may interfere with arachidonic acid metabolism and contribute to deficiency symtoms such as growth retardation, dehydration, flaky and scaly skin, hair loss, gastrointestinal syndromes, or infertility.”

The importance of the omega-3:omega-6 ratio is something that has reached the mainstream media. However, a number of researchers in the paleo community have argued that if you’re not consuming a lot of omega-6 fatty acids, then you don’t need so much omega-3. If you avoid PUFAs from vegetable oils, you don’t need to obsess about getting omega-3 eggs or eating the right other vegetable oils. Just stop eating fried food, fake queso and “cheese” sauces, and soybean oil-based salad dressings; and don’t cook with industrial vegetable oils. Butter and coconut oil are fine for pan-frying and sauteeing, and olive oil & vinegar are good choices for topping your salad (if you don’t create your own salad dressings).

Excess PUFAs have the effects listed above — including dehydration and flaky skin. Instead of worrying about getting enough omega-3 fatty acids, avoid the omega-6 acids. (Arachidonic Acid is an omega-6, by the way, but if you’re eating liver once a week, it won’t be a major component of your diet, as it is for people who eat a lot of fast food or use heavy amounts of industrial vegetable oils.)

Lectins

Lectins might induce diarrhea, by pulling water into the intestines; hence dehydration. Food poisoning can also lead to diarrhea and dehydration, so … yeah, avoid that, too. It’s the same basic mechanism, and why you’re encouraged to drink a lot of water if you have diarrhea — obviously you’re losing a lot of water, and you need to replace it.

I wish I had some good sources for the lectin-diarrhea link; I’m hunting up some links so that I can make a post specifically about lectins.

This is one concern that recommends a paleo diet instead of just a low-carb diet: beans, often eaten in great quantities by people trying to go low-carb, have a lot of lectins. Many cases of “food poisoning” are actually cases of eating under-cooked beans. Avoid beans, and definitely skip the grains, as both contain lectins and can lead to diarrhea.

And one last quote, which I need to move some place better:

“roughage — which includes beans — help people stay ‘regular’ by causing more cell tears, which enables more mucus to escape from cells, essentially greasing the GI tract” — PloS Biology in 2006

Conclusions

Saying “dehydration isn’t caused by not drinking enough water” misses the point. Dehydration is caused by losing too much water and not replacing it. If you’re participating in an activity that causes water loss, then yes you should replace that water. Drink when you’re outside on a hot day, for example after a long hike or bike ride, or mowing the grass. But if you’re not actively doing one of these dehydrating activities, then you shouldn’t be losing that much water.

Dehydration is an imbalance in the blood, and is caused by digestive problems, the lack of vitamins, or overactive kidneys (such as from caffeine!). If you’re losing water from one of these sources, then you need to drink more water. Don’t drink water just because some dood on TV said so; drink when you’re thirsty, or if you think you’re losing excess water from one of the ailments listed above, drink some extra — but if you’re not thirsty, don’t bother.

Why would our body require us to drink water when we’re not thirsty? Sometimes I do get very thirsty, and I obey that signal and drink as much water as I can. If I’m not thirsty, I don’t worry about it. When I switch from high-carb to low-carb, I’ll try to drink water whenever I get cravings for food; drinking something helps distract me from the hunger. Otherwise… just when I’m thirsty.

My skin is much softer when I’m taking levothyroxine (the generic form of Synthroid, due to my hypothyroidism) and also Vitamin K2, and I usually use skin dryness as a measure of dehydration. My skin has been much softer these past two years, and the major differences are going paleo and taking K2, A, and D. Caffeine and alcohol are drying me out, so I’m trying to cut out the tea and cut down on drinking. I think I’m doing pretty good, and I’m glad for the changes!

1. synthetic T4
2. natural thyroid extract (Armour Thyroid)
3. low-dose naltrexone
4. nothing

Doctors will ask for a TSH test if you think you have hypothyroidism, or if for some other reason they suspect that you might be hypothyroid. TSH stands for “thyroid stimulating hormone”; it’s put out by the pituitary gland in response to the production of TRH by the hypothalamus. Patients with hypothyroidism and low free T3 and T4 levels will have high TSH levels, but I haven’t found any research directly linking T3 or T4 to TRH production. It seems to make sense, but there’s no knowledge there; just theory. For the most part the theory works. But not always.

And that’s really why I’m writing this post. Some people with hypothyroidism report that some symptoms improve when they start taking synthetic T4 (basically bypassing production from the thyroid), but that other symptoms persist. These people report much improved symptoms when they switch to a natural thyroid hormone replacement (ie Armour Thyroid), which contains not a synthetic T4 but a natural T4, as well as T3, and a bit of T2 and T1. T4 is the storage form of the thyroid hormone; T3 is the active form used by cells. (The number indicates the number of atoms of iodine in the molecule.)

Some people have trouble with T4-to-T3 conversion; some have adrenal fatigue; there’s a whole range of problems. Most doctors give you a TSH test, look at the number, then prescribe Synthroid and tell you any remaining symptoms are just because you’re a lazy fuck and should stop whining. Yeah, I haven’t been happy with my doctors, and many other hypothyroid patients haven’t either. Anyway, the most common cause of hypothyroidism is what’s called Hashimoto’s Thyroiditis; it’s an autoimmune disease, in which your own immune system attacks your thyroid, preventing the production of thyroid hormone. Research on molecular mimicry by Dr Loren Cordain suggests that this process is started when foreign proteins cross from the digestive system into the bloodstream; prevention is to not have a leaky gut, perhaps caused by grains, one reason why us paleo people avoid eating them. And one damn good reason why you should never feed grain to your kids.

The third treatment option is what’s called low dose naltrexone. I won’t write much on it here other than to say that the theory behind it’s effectiveness is to tell the immune system to calm the f down, which then allows the thyroid to do its own thing.

The fourth option isn’t really an option. That is, I don’t suggest it. I did feel great when I went off of my meds for a couple months, but I also changed my diet and started some serious exercise, too. If the molecular mimicry theory is correct, then once you’ve got Hashimoto’s, you’ve got memory B cells that know what the antigen looks like. What happens in molecular mimicry is that a protein gets from your gut into your bloodstream; the immune system recognizes the protein as foreign and produces antibodies. Hashimoto’s is when that foreign protein is a molecular mimic of thyroid gland cells. (People with different genetics or different proteins will get other autoimmune diseases, such as rheumatoid arthritis or multiple sclerosis.) To the immune system, the foreign protein and the thyroid look like the same protein; the immune system then attacks the thyroid. Reducing the presentation of foreign proteins to the immune system might help reduce symptoms, but it seems that there is no cure for Hashimoto’s; you’ve basically vaccinated yourself against your thyroid gland, and there’s no way to remove those memory B cells.

Eating iodine-rich foods or supplements might help; some recent talk in the blogosphere suggests that 8-50 milligram range iodine supplement is needed; Lugol’s and Iodoral were two suggestions in the comments over at Richard’s site.

My current T4 refills are up in another month. I plan on switching to Armour. Meanwhile, I take iodine, but crappy microgram amounts; I’ll try and find Lugol’s and do that for a month.

The mainstream (Oz, Michaels) contention is that “just 100 calories a day” of extra food (or less exercise) is what causes obesity. Thermodynamics is often brought in: calories in = calories out! It’s all sciency so therefore it’s true! “Weight is an energy equation,” Michaels says.

But it’s not an independent equation. Oz kinda hints at this: exercise isn’t awesome because it burns calories, but because it builds muscle, and muscle is what burns calories. Yet cardio doesn’t build muscle (in most people it probably breaks it down). Biggest Loser is all about cardio, too. You don’t get buff and pump up your basic metabolic rate (BMR) by sitting on the exercise bike for an hour a day; you’re just burning off whatever fuel your body can find.

AND IF YOU’RE EATING CARBS, your body can’t burn fat. Carbs up-regulates insulin and down-regulates glucagon. Burning fat is very hard if your hormones aren’t cooperating. Exercise burns through any circulating blood sugar, muscles need more energy, and the body responds by releasing stress hormones, which then scavenge lean tissue for some protein to convert into energy. (And some researchers theorize that those stress hormones then lead to heart disease.) Riding a bike and running burn off your muscles and give you heart disease. A great way to burn off body fat? Not at all.

Strength (resistance) training is a great way to build muscles. The smart way. Whether you’re at a gym, doing body-weight exercises (like pushups and pullups), or something like Crossfit, you’re putting on muscles. 24 hours a day, those muscles need food. About 20% of your total BMR is muscles, so being more muscular won’t dramatically increase your daily energy expenditure, but indeed it does only take about 100 calories a day to shift to weight loss; a few pounds of muscle can do that. Maximize muscle gain by working out after a long fast; the absence of insulin and the presence of growth hormone will help you bulk up faster and more efficiently.

So more muscle tissue increases BMR, which means the negative side of the weight equation gets bigger, which means weight loss. The positive side of the equation is calories in. And this is really what Taubes was getting at in the interview: what you eat isn’t just calories; it also produces hormonal responses.

Trading one meal for another calorically equivalent food isn’t neutral. The presence of cofactors and/or anti-nutrients will change what gets absorbed, so just because you put it in your mouth doesn’t mean you’ll get those calories. The elephant in this room is the insulin response from consuming carbs. Eat carbs and you’re body won’t want to burn fat for the next four hours. Eat a meal (or snack) every 3-4 hours and you won’t burn fat til you sleep.

Well, not strictly true. Triglycerides are constantly going in and out of adipose tissue. Insulin suppresses the burning of body fat, but it doesn’t drop it to zero. It’s just much much harder. This is why the Biggest Loser contestants are able to drop so much weight — that, and at 400 pounds, an hour of exercise burns an obscene amount of calories. Reduce carbs a bit, starve yourself, and burn five thousand or more calories a day, and you’ll drop weight.

Alternately, you could drop to <20g of carbs a day, fast a couple times a week, and skip the exercise — and lose weight anyway. Avoid the antinutrients (like phytate and lectins), get a full complement of vitamins (eg A, D3, and K2 together), and you’ll be healthier in addition to weighing less.

Would you listen to this guy's diet advice?

A phrase I like to mock the mainstream with is “everyone knows.” If you watch TV, whether news or dramas or sitcoms, you’ll see people bash bacon, eggs, and meat as unhealthy food choices. Everyone knows that they’re bad for you. Countless scientists say so. Study after study states, quite clearly, that continuing to eat saturated fat is a quick and tasty ticket to heart disease.

It’s hard to overcome that bias. Whatever forum I’m in — online, friends, coworkers, dates, etc — a common refrain is “how can thousands of scientists be wrong?” Then the obvious conclusion: you paleo-diet people are crazy nutjobs. And I’m often stuck trying to dig my way out of a hole and explain what’s going on.

Not every scientist does their own novel research. As is the case with climate science, in which nearly every researcher relied on the East Anglia temperature data, health/diet/nutrition researchers rely on existing literature and reviews to base their opinions. Starting over from scratch is a waste of time. So you start with what’s already been published.

The risk in such an approach is that the published, peer-reviewed literature might be suspect, such as the East Anglia data that relied on a cherry-picked dozen samples, out of hundred available. As long as you throw out data that disagrees with your theory, it’s easy to prove a theory. Scientists are responsible not just for reading existing literature, but critically evaluating it.

For example, that Japanese emmigrant study, often cited as evidence that the American diet (assumed to be a meat & butter diet) is to blame for heart disease. Yet the study itself was unable to correlate coronary mortality with diet, and adhering to traditional Japanese culture was sufficiently “healthy” that it overcame the American diet: acting Japanese and eating American was healthier than the reverse. The following year (1976!) a study showed that the original data did not implicate the American diet as a cause for heart disease.

This is a weird example, in part because I do blame the American diet. Just not the meat and dairy part, which has been in decline for decades. The USDA started telling us to eat more of its products (grains), we obliged, and Americans started coming down with more cancer, heart disease, and diabetes. Deaths decreased, so obviously the program was working, right? Yet incidence of disease increased.

-

Again I come back to: who should you believe? Don’t believe me. Go read the sources. Go read both sides of the debate. One side is saying “thousands of scientists can’t be wrong” and the other side is saying “thousands of scientists didn’t do the same research; one guy did the research and dozens cited him and then thousands more assumed everything previous was done correctly.” Which is the more convincing argument?

One of my favorite exchanges is that between Taubes and Fumento. Taubes writes an article in the NYT (What if it’s all been a big fat lie). Michael Fumento responds. Taubes replies. Fumento tries to get in the last word. If you haven’t read this exchange, please do. Go ahead, I’ll wait. I even re-read it myself.

The reason why it’s so awesome is because it’s plain to see who is on the side of reason, and who is shrilly trying to claim some kind of authority.

And that’s what each of us should do with the issues that are important to us. Do you care about your health? Then you owe it to yourself not just to find out what each side is saying, but to find the debates between the two. Both sides will have zealous evangelists and ignorant nutjobs. Both sides will have ardent supporters that think they’re on the right side. But one of them has to be wrong; it’s possible that both sides are mistaken and the truth lies somewhere else!

But if the best argument the mainstream can come up with is “there are thousands of us, and we have badges!” then I declare them all to be a bunch of poopyheads. I care about my health, and I want to see the best arguments both sides can come up with. I’m in the minority here (and hence a crazy nutjob), but the logic and evidence convinced me.

Do your parents have cancer, heart disease, and diabetes (like mine) and do you want to avoid it yourself? Do you care about exercising efficiently and in a way that will keep you on your feet for decades, and avoid stress and strain injuries that sideline many middle-aged athletes? Do you care about global warming? Economics? Politics? Freedom? Snowboarding?

Cuz if you care about snowboarding (and are a crazy nutjob) then you’d know about TonyC’s snowfall comparisons!

“it is still important to limit the amount of cholesterol you eat” – Harvard School of Public Health

“a diet high in cholesterol can contribute to elevated blood cholesterol levels” – Mayo Clinic

“The jury is still out on whether there is a direct link between dietary cholesterol, which is found in the foods we eat, and blood cholesterol, which is manufactured by the body” – about.com

Association

Early studies found that high blood cholesterol levels are associated with heart disease. But association is not causation. Does high cholesterol cause heart disease? Does heart disease cause high cholesterol levels? Or are they both caused by some separate, third factor?

The message got out: high cholesterol levels are associated with heart disease. But the caveats, caution, and confusion did not. Many people relied on reporters to interpret the dense scientific jargon of research papers and distill it to something that you could rely on when shopping at the grocery. The media filled with the simple message to avoid eggs, red meat, and other cholesterol-rich food. My family switched from butter to margarine, as did many Americans in the middle of the 20th century.

Studies

In the scientific community, after the initial association was identified, scientists set off to find out what causes what. And that’s when the simple model broke down. Cholesterol turned into Good Cholesterol (HDL) and Bad Cholesterol (LDL), and then that broke down too. Now there’s light, fluffy LDL and small, dense LDL and … bah! Life was just easier when we could avoid eggs and everything would be OK.

Strangely, Ancel Keys (who kickstarted the whole hatefest on saturated fat) authored a study claiming no link between diet and serum cholesterol. The oft-cited Framingham study also produced such a study, although it was never published. A 1976 study in Michigan found no link between food (not just dietary cholesterol) and serum cholesterol. Ravnskov links to a whole bunch more studies.

One thing to note is that these studies found no correlation with the ranges of their study population. Maybe everyone in each group already ate so much cholesterol that more didn’t matter? Maybe the range of nutrients in the diet wasn’t enough to effect a change in cholesterol? Yet the cholesterol values did vary widely; something was causing spikes in cholesterol, but it wasn’t anything that the researchers measured. It could be genetics (such as hypercholesterolemia), an untracked element of the food, etc. One Finnish study found that reducing saturated fat and cholesterol intake led to higher serum cholesterol, and studies on indigenous hunter-gather populations such as the Masai indicated that ultra-high-fat-and-cholesterol diets themselves didn’t lead to CVD.

Homeostasis

The body is replete with homeostatic systems, that is, systems that try to maintain a constant level of some hormone or enzyme or other protein or chemical in your body. Cholesterol is one such homeostatic system. The liver produces cholesterol as part of a complex balancing system. Cholesterol is a precursor to dozens of hormones, including Vitamin D and the sex hormones testosterone and estrogen; it’s used to build cell walls; and insulates nerve fibers. It also plays a role in inflammation, such as repairing damaged tissue after trauma or disease. It’s a critical molecule, and your body will manufacture about 3000 mg of cholesterol each day — that’s the equivalent of over a dozen eggs.

Why would a bit of extra cholesterol in the diet lead to catastrophic disease? Our bodies are built to use cholesterol, not to expel it like a waste or toxin.

The Myth

Yet somehow the myth was born. Perhaps from a confusion between dietary cholesterol and serum cholesterol, maybe a mistake made by news reporters. The myth persists, if not in research than at least in the public consciousness.

Although carefully controlled, short-term trials have found that eating cholesterol raises serum cholesterol values, that raise is just a blip. No correlation has been found in long-term studies. Your body regulates cholesterol levels in response to disease and trauma in addition to the daily needs of living. The cholesterol in your diet won’t kill you.

I think it’s useful to be prepared. I want to say “I’m taking it because I read a couple studies that showed it did X.” I don’t want to say I’m taking a supplement just because I read about it on a blog, although that was really what happened.

The difference between “reading something on the internet” and “reading a study” is just the vagueness of communication. If you read a study on the internet, then you are getting peer-reviewed info. If that study was linked from a blog, then you’re getting peer-reviewed science from an “unreliable blog,” as I think the MSM would prefer to call it.

I don’t think there’s anything unreliable about Peter, Richard, or Stephan. Quite the contrary. Their posts, the discussion in the comments, and then the studies (that I could read without paying anything, at least) convinced me that K2 was a good thing. I believe in getting my beliefs from evidence. I think believing something because you read a convincing argument is, well, foolish. It’s not the argument itself that should be convincing, but rather the evidence. So go read Richard and Stephan, and read the papers. You owe it to yourself to get the info directly from research whenever you can; us bloggers are here just to point you towards the papers and provide some context and interpretation.

These bloggers did mention that supplementing wouldn’t be necessary if one eats a decent amount of organ meat, fish roe, shellfish, fermented foods like sauerkraut miso and natto, and/or pastured dairy products. I eat a good bit of raw, pastured cheese, but not a lot of organ meat; maybe just once  a month. And except for some roe sprinkled on sushi, I eat very little roe and shellfish. K2 is a pretty expensive supplement; about 50c a day. (I’m not breaking the bank here, but still, that’s an expensive pill. I’m glad I’m not paying $3 a day for a statin.)

So, what’s K2 do?

* prevents heart attacks

* prevents arterial calcification

* reduces the chance for osteoporosis-related fractures

* activates clotting factors (as a substitute or conversion into K1)

Since my dad and my mom both have had heart attacks, and my dad’s father died in his early 40s from heart disease, I’m very concerned about my own heart health. If there’s anything genetic to it (tho I think it is primarily dietary), I want to do what I can to keep my heart healthy.

I’ll continue supplemental probably until I’m eating organ meats weekly, and these other great sources (eg sauerkraut and fish roe) more often.

I googled “protein poisoning” and the first thing that pops up is an ezinearticle post that’s filled with such rabid tripe that I felt the need to respond. I was really thinking I’d be posting here once a day, saving my ideas to make sure each post had the biggest impact (ie no thin, content-free posts), but google flat-out failed in this case. That ezine article is lies, half-truths, and misinformation.

There are hundreds of thousands of identified proteins in the body, so any and all forms of disease will be associated with some over-abundance of one of those proteins. Does that mean that they are “protein poisoning?” No — the phrase is a tactic to scare people away from eating meat. “Protein poisoning” is a real thing, and it isn’t the cause of cancer, or schizophrenia, or arthritis, or any of the other things mentioned on that page.

Brain Food

My interest I’ve been wondering how humans can sleep (or fast longer than 7 hours, really) without breaking down muscle tissue. I’ve been poking around and what I came up with is this:

The human brain burns about 10g an hour doing its thing. At less than 6g an hour, you’ll go into a coma, and this is why diabetics are so worried about insulin shock: too much insulin means too little glucose which means brain pain. The brains of people that are adapted to low-carb diets need less glucose than those on high-carb diets, and from what I’ve read I’m guessing that ketogenics have lower limits here (maybe 6-7g an hour normally and a minimum requirement of 3-5g/hr). The brain of us low-carbers burn ketones for some of its energy, but not 100% — it still needs glucose.

That glucose can be provided by eating carbs (which produces blood sugar directly) or by the liver, which will cough up its glycogen stores to produce glucose. But the liver only stores 75-100g of glycogen; again, those adapted to a low-carb diet will have a smaller store of glycogen. And 100g is the maximal amount; high-carb dieters that carbo-load before a race have been estimated at storing more, but 75g is more common. That means you and I have about seven hours of glucose available when we go to bed.

What happens when the glycogen runs out? One option is to eat late at night, and let the slow uptake of nutrients during digestion provide some extra carbs, but this seems strange to me — and still leaves the issue of dealing with extended fasting periods. If my brain only needs 6g/hr, I’d need 90g to cover a 15-hour fast, and a 36-hour fast would need over 200g. My liver won’t be providing that.

Gluconeogenesis

When blood glucose and liver glycogen stores are both depleted, the liver resorts to gluconeogenesis. This is the de novo production of glucose from lactate, pyruvate, or glycerol. Glycerol is a byproduct of ketone production — glycerol is the backbone of triglycerides, and once the fatty acids are stripped off and turned into their own energy source, the remaining gylcerol can be converted to glucose. Lactate, likewise, is the byproduct of energy production, but this time of glucose metabolism. Except for sleepwalkers, who exercises in their sleep? That means overnight gluconeogenesis comes from pyruvate, from the breakdown of proteins. And that means breaking down muscles.

Combine this with intense workout sessions (as is common in the primal community) and the primal practitioner needs 200g or more of protein every day. I ran into some quotes that suggested that 300g is the upper limit that a person can eat each day lest they run into protein poisoning — specifically, the liver’s inability to remove excess ammonia (a byproduct of the breakdown of amino acids in gluconeogenesis).

Rabbit Starvation is a similar thing, but the two are hard to tease apart. It appears that consuming fat helps in overcoming this protein barrier, perhaps by preventing protein from being absorbed from the digestive tract, or by assisting in clearing excess nitrogen. Or, maybe, because those that eat fat find it much harder to eat 300g of protein a day.

The Debate

While putting this post together I’ve been comparing Don’s Primal Wisdom posts on potatoes to a post by the Rambling docs that disagrees with Don. The debate comes down to, how much glucose does the body need each day? What if you’re doing high-intensity activity?

The docs make a few points about how far a person can run on aerobic metabolism, but that’s really beside the point. Does high-intensity activity burn through glycogen stores rapidly or not?

Protein Poisoning

The brain alone will burn 240g of glucose a day. The glycerol in triglycerides will provide some of that glucose demand, but I’m not sure how much. If you’re eating zero carbs, that means 240g of protein a day — assuming you’re ok with wasting your muscles away to nothing. Assuming 1g/kg/day of protein to maintain nitrogen balance, and that’s over 300g of protein daily just to avoid coma and wasting. If the protein-to-glucose conversion ratio is 1:0.7, this pushes the daily need over 400g.

To quote Cordain, “The mean maximal protein intake for the average weight U.S. male (189.4 lbs ) is then 270 g/day (range 233-322 g/day), and for an average weight female (162.8 lbs ), 246 g/day (range 208-288 g/day).”

What happens if you consume that much protein? We’re talking over two pounds of lean meat, which will be nearly three pounds if you eat fatty cuts. I find it hard to consume more than about a pound and a half of meat each day, and even that is pretty rare; I’d guess my average daily consumption is about 120g of protein.

Near as I can tell, too much protein means you get sick: diarrhea, vomiting, nausea, weakness, dizziness, encephalopathy, and death. Absent disease (like kidney damage) that interferes with normal ammonia clearing, it would take 7-10 days for serious complications to set in, although the milder effects would occur within a day of starting a 300g+ protein diet. This is primarily the result of the buildup of ammonia in the body, which taxes the kidneys, possibly even with heightened water consumption.

Glycogen demands?

so… what? I’m at a loss here. I need more info. It seems to me that the only way to maintain lean mass (or grow it) while keeping my brain fed is to consume some carbs. Otherwise, I’m going to be breaking down lean mass in order to produce the glucose that my brain demands.

I did see someone postulate that someone adapted to ketosis only needs 4g/hr to feed their brain; this means about 200g per day to feed my brain and keep body mass intact, and it also means that 75g of liver glycogen will last nearly 20 hours.

There’s unanswered questions here. However they come out, it seems that intense exercise demands carbs; intensity without carbs means the loss of lean tissue, which might be built up on off days — but that means one can’t do intense exercise daily. Hence carbs enable daily intense exercise.

And more on that later!

If you can shed some insight to any of my questions, I’d appreciate it.

But I won’t talk about them per se. Instead, my point today is to say that when you eat carbs matters more than how much you eat. Carbs (whether sugars or starches) quickly convert to blood sugar. Excess blood sugar causes your pancreas to produce insulin, which then shuttles that sugar off into adipocytes (fat cells). But there’s a trick here between the conversion and insulin production; I said excess blood sugar.

When you’re fasting, you burn off the glycogen stored in muscles and your liver. The brain has a constant demand for glucose and if you’re not eating, it has to get it from somewhere. The major source is liver glycogen (muscle glycogen can not move out of muscle cells; it can only be used locally), and if your glycogen stores are depleted, your body wants to restore them. Consuming carbs when fasted, therefore, won’t increase body fat as much as it would right after a meal.

So here’s my point: The same calories consumed at different times can have different effects. Don’t eat dessert right after dinner. If you’ve got bad cravings for sweet things, consume them after fasting (whether that means at breakfast or after an all-day fast).

Of course, avoiding trouble carbs like fructose, alcohol, and grains is better than consuming them — but if you’re working on improving your diet, and need to take steps, the first thing I recommend is changing when you eat those carbs. You’ll start getting your insulin under control, and that makes it easier and easier to remove carbs altogether.