I was diagnosed with hypothyroidism ten years ago, after my sister was diagnosed and I went in to get my TSH checked. I’ve been on synthetic T4 (levothyroxine, aka Synthroid) for most of that time, except for a small period that I was off meds altogether. Chances are, your doctor will only tell you about one option, but I think treatment can be grouped into four choices:

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.

A few of the paleo bloggers have mentioned Dr Mehmet Oz’s new year’s guidelines. Oz is also in the Larry King interview with Gary Taubes (part 1, part 2). The interview is interesting because it brings in not just Oz but also Jillian Michaels.

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.

A 1975 study on Japanese expats in Hawaii and California showed the US-based ethnic Japanese had a much greater rate of heart disease than their counterparts back in the mother country. “Researchers pinpointed the likely cause to be diet-related – fish consumption specifically.” (link) So what kind of crazy nutjob would claim that eating more meat, cheese, butter, and bacon would be healthy?

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!

When talking to friends (and worse, acquaintances) about the paleo diet, often the first sticking point is my suggestion that eating meat and eggs is healthy. The message that cholesterol is dangerous is common in the public consciousness, specifically the idea that eating cholesterol-heavy foods leads to heart disease. In this post, I review the connection between dietary cholesterol (ie how much is in the foods you eat) and serum cholesterol, and the relationship to heart disease.

“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.

After reading about K2 on a number of blogs, including Richard’s and Stephan’s, I started taking a K2 supplement (Carlson’s 5mcg, 1x per day). A couple months later when I stopped by my doc, she asked why I was taking it (and a bunch of the other supplements I was taking), but by that time I had forgotten.

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.

Protein poisoning is a condition that happens when one consumes too much protein and not enough fat to balance it. A pure-protein diet will produce it, but a mixed diet will not. Even in a mixed diet, however, there appears to be an upper limit to the amount of protein that a human can eat before their body gives up.

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.

The conventional view of dieting and weightloss is calories in = calories out. People (especially geeks like me) love to cite the first law of thermodynamics: energy can neither be created or destroyed. Hey, that’s great — but humans aren’t closed systems or bomb calorimeters. The digestive system is complex, and the thousands of compounds that reach our bloodstream are then managed by an equally complex array of hormones, vitamins, anti-oxidants, immune cells, carriers, receptors, and more. The idea that the complexity of the human body can be neatly summed up into the simple phrase “calories in = calories out” is silly. As appealing as it is to dress up the phrase with an appeal to scientificalityness, it misses the important role that hormones (et al) have.

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.