I've noted another recent trend on the blogosphere appears to be myths re: thyroid; meaning to say the paleo religious nutters have been whining lately that eating a low carb diet EXPLODES your thyroid, apparently.
There's this,
...and then this (FYI carbsane low carb foods are uber high in selenium, check out my feb post, my selenium intake is like 200% RDV)
...and I've observed countless murmurs in comments of various blog posts, that the solution to a thyroid problem (real or suspected or totally made up) is to dive into a bowl of oatmeal.
Here's the truth, and you might not like it, but here it is:
A decrease in thyroid function is inseparable from losing body fat. It is a result of (among many other things) a reduction in insulin, and leptin, and increased cortisol, which is also a logical function of body fat loss, which is a result of energy imbalance in the fat tissue.
Low carb gets the blame because this is the only diet which can result in almost effortless chronic use of contents of adipocytes, without necessitating starvation levels of calories to achieve it, when the real culprit is a chronic energy imbalance at the level of the fat tissue.
Here's an example. We all obviously know what the cause of coldness/hypothyroid symptoms and infertility is in a woman who is eating 900 calories (of a high % carbs). What we don't know, because it's not as obvious, is that the same thing occurs in a woman eating 1400 calories of fat with trivial protein and very few carbs.
The "same thing" is :
1) marked decrease in blood insulin,
2) marked decrease in blood leptin due to #1,
3)a greater efflux of fatty acids from the fat tissue, and a greater concentration of ketones (btw this occurs on any weight loss diet) without as great of a rate of uptake, also a result of #1
4) increased cortisol/HPA axis (related to 1 & 2, as well as an independent effect of negative energy balance).
^^^Together all of these conserve energy, and exert a suppressive effect on HPthyroid axis. They are all forever linked with dieting and losing body fat.
They can only be reversed by reversing the trend to lose body fat (or, by independently altering the endocrine system with exogenous leptin replacement or T3, good luck getting a doctor to help!)
"Reversing the trend" = becoming fat again = eating sufficient food to raise insulin and cause positive energy balance in the fat tissue, suppress fatty acids, raise blood leptin, suppress cortisol, etc.
In other words, the endocrine system and metabolism shift toward conservation at a much higher calorie intake, because low carb diets allow for similar endocrine effects promoting of body fat atrophy at much higher calorie intakes. The problem isn't low carb, the problem is losing body fat will always induce a metabolic conservation state, low carb gets the blame because it is easy to lose body fat on it.
So we arrive at a situation where the carb eating starvation calorie dieter blames her calorie levels for the flip off she is getting from her endocrine system, meanwhile the moderately low calorie eater of a low carb diet, who has the luxury of eating a lot more food, irrationally blames the low carb diet.
Stupid, yes I know.
Ironic, yes I also know, considering most dieters do everything they can to eat more, including eating fake foods like jello and soup, or eating and then exercising.
IF our low carb dieter pigged out on 3000 calories of fatty steak I assure you her basal temp would increase like crazy and she would feel rather well, with a similar endocrine shift which is induced by much lower calorie intakes of a carbohydrate diet. Caveat is that it's so so much easier to get fat on a carb diet, for that same reason. You kinda have to march with cross on back to the gym and experience chronic hunger and low calorie intakes, to get the endocrine situation in the same ballpark as a generous eating of a low carb diet.
For evidence of how easy it is to lose wt on low carb, see the previous entry on my blog. I am super thin, used to be hugely fat, and eating this much WITHOUT exercising, AND losing body fat. Yes, for serious.
The neat thing about the leptin study was they measured so many things that I learned a lot about how my body functions; they measured both my RQ and RMR. My RMR was measured at a ridiculous 1000-1100 calories (yes sthat bad!) yet I am losing body fat eating over 1800 calories of a mildly ketogenic diet without exercise. At baseline, I am no doubt functionally lower thyroid... and still I resist growing fat tissue eating this much caloric energy. So, in spite of the fact my body is super thrifty with energy, I am losing body fat eating almost 2000 calories a day.
But how! HOW!?
Magic?
...I R a witch?
...SPELLS?!! It's spells, rite?
...Satan?
Nope! cast aside your superstitions, SCIENCE to the rescue! This is physiology. Low carb diets alter the endocrine and nervous system, resulting in a state of heightened lipolysis and fat oxidation.
In addition to measuring my RMR (which was documented to be ridiculous), they also mesured my RQ.
RQ, respiratory quotient, helps descern which types of energy you are using (glucose, fat), and mainly it helps predict whether or not body fat is being oxidized at rest. A higher RQ = oxidizing glucose, a low RQ = oxidizing fat.
It is shown weight reduced people on higher carb diets have an elevated RQ compared to non-dieted people, and this is because the decrease in leptin as well as smaller adipocytes do not release FFA normally, supersensitivity to suppression from insulin, and also low insulin/leptin decrease catecholamines and the sympathetic nervous system which also inhibit fat oxidation. Combined, these = weight reduced people do not oxidize fat at rest, leading to subjective feelings of fatigue and resistance to further weight loss.
Ketosis can circumvent this defect by depleting glucose and forcing the body to use body fat at rest, similar to a non-dieted person, a person with a normal metabolism. A key finding in obesity resistance is the ability to enter a powerful "fasted state" after an overnight fast, marked by endocrine changes (low insulin, low leptin, high ghrelin) and low RQ (suggestive of an unimpaired ability to use body fat for energy in a fasted state). Obese individuals and people actively gaining weight are negative for all these signs - when they wake up in the mornin' insulin is high, leptin is high, ghrelin is low, and the RQ is maintained higher during sleep. Well, in wt stable obese people the RQ will drop normally, but in people actively fattening it won't (inhibited body fat oxidation = gaining weight).
These are all signs and symptoms of not oxidizing body fat normally when one should be oxidizing body fat very well, and most of them are directly a result of glucose intolerance/excessive insulin.
High fasting RQ predicts weight regain in dieted subjects.
High postprandial RQ also correlates with obesity (read as: fat people cannot oxidize body fat after high carb meals, file under D for Duh)
NWCR members: tendency for higher RQs compared to matched undieted controls.
Indeed, the testing showed my RQ was quite low. I don't remember the exact number (threw out all my papers whyyyy!) but it was the low .7s, I remember that much... much lower than even normal controls.
My RQ was this low, in spite of massive weight loss, because I eat very few carbs forcing my body into a no choice proposition of oxidizing body fat at rest.
I usually find, with trivial restriction, I wake up from an overnight fast thinner. For example, yesterday I ate 1600 calories, upon waking I could palpate my hip bones and ribs.
The metabolic tests I was subjected to quite nicely inform me that I am using damn near exclusively body fat when I am sleeping.
Basically, those of us on low carb diets, we can easily access body fat for energy at the same time as storage processes are not activated. They bias the entire endocrine system away from body fat storage, toward body fat use.
The result is I waste food calories as heat + energy in spite of the fact my body is like a dilapidated POS in terms of metabolism, after losing an entire human being of fat tissue and being super duper thin afterward.
It's sort of like type I diabetes, except not as ketoacidosis-y or hyperglycemia-y (I do have the trivial basal insulin for normal metabolic regulation, I am not diseased).
Just like the type I diabetic cannot store *any* food no matter *how* much he eats, and is rapidly breaking down fat to the point where the ketone accumulates to pathology (ketoacidosis), a functional physiological thing happens on the sort of diet I choose to eat.
Sure, if you eat a truck load, it (fat gain) will happen as all food requires insulin and in constitutionally obese people it is entirely possible to (re)gain body fat on ad lib low carb... but there is a grand canyon of leeway as compared to the self abuse required of maintaining low body fat, or god forbid losing body fat on a high carb diet. On a carb diet, 1800 calories every day would = me growing fat, no doubt about it. You can't argue with a RMR of 1100 calories. Sorry. Can't argue with fat tissue that is supersensitive to insulin. I require either leptin replacement OR I require ketosis, otherwise = progressive body fat gain, question is how fast (or slow) and that is usually a function of how many carbs + calories.
Anyway, back to the thyroid.
Should I choose to alter my diet to contain, say, 150-200 carbs instead of 40, insulin would increase, would direct energy to storage, and so would my leptin increase, and this would occur because my fat tissue was growing, as a result of the glucose mediated insulin. The insulin would increase the sympathetic nervous system, and leptin and insulin would both suppress HPA/cortisol, and all of these changes would = tons of thyroid activity.
Leptin: Exerts hypothalamus level effects to make TRH (similar to how it effects GnRH). Low leptin = functional hypothyroidism via lack of the thyroid making hormone.
Insulin (and leptin): Increases the sympathetic nervous system, which increases the conversion of T4 to T3
Cortisol (from higher CRH due to lower blood glucose, low leptin, low insulin): converts T4 into rT3, which blocks thyroid hormone.
If I eat a ton of calories of high carbs I too like cheeseslave and carbsane can *brag* that I was uber duper warm... and indeed I am waaay warmer if I am getting fat. Except, all of this super awesome insulin and thyroid power would result in my clothes eventually not fitting, and the scale would climb, along with this increased thyroid function. Plus I would feel a lot crappier emotionally, but generally most normal people don't get that effect.
Oh, we'll see how cheeseslave's weight situation is doing in a few wks of "ditching low carb". 1 weeks pay says she is right back to her prior body fat level in about 3 seconds.
(It is my understanding she used a low carb diet to deplete her body fat, and she is for some reason surprised at the result of being colder and having a lower temp, eating low calorie and low carb? LOL, oh the internet, you are so full of silly people.)
Hot new info: higher metabolic rates and thyroid is positively associated, and a direct result of the endocrine changes also resulting in body fat growth. Growing fatter amps up thyroid, assuming you are euthyroid in the first place. Big myth on the diet blogosphere that low thyroid causes obesity; nope, obese people are hypermetabolic, it's that whole "bathing in insulin+leptin" thing, that crazy responsive sympathetic nervous system thing.
And also, to restate this ... if cheeseslave and others complaining of low thyroid, were to eat 2500 calories of low carb food, you would also be super duper warm. Carbs totally aren't required. You just need food, enough food calories to shift endocrine system thus metabolism to a fed state. I assure you, 3000 calories of steak + brie cheese + pecans will = SUPER WARM AND ENERGETIC and all of these effects you are irrationally attributing to carbs will magically happen on a diet that contains enough food calories. You just need more of them if you choose to eat low carb. Last time I checked, weren't obesity resistant foods a good thing?
If you are eating moderately low cal of a VLC diet and have lost body fat, why are you surprised that you are cold and your basal body temp is low? I mean, seriously? I just can't get over this.
One last point on the whole "more thyroid = better" idea.
It's generally observed that hypermetabolic states in all animals lead to shorter lifespans.
Research suggests that genes which control lifespan are intimately tied to insulin signalling.
Generally, animals with very rapid metabolisms have shorter lifespans, wheresa animals that have quite low metabolisms live very long. This is true whether they are this way naturally or if scientists starve them, or restrict protein (calorie restriction and protein restriction both acheive a similar state of suppression of insulin & IGF which prolong the lifespan).
The increase in thyroid hormone which occurs by juicing your metabolism with insulin may be the very thing prematurely aging you, leading to diseases of civilization. Sure, this is highly hypothetical, but stands to reason.
Calorie/protein restriction (and thus a low insulin state) will lead to a depression of the sympathetic nervous system. Lower BP, lower heart rate, and yes, lower thyroid hormone conversion (which also amps up the BP and heart rate). This is shown in studies of all lifeforms to improve health, offer resistance to disease of aging, and prolong life span.
I've recently witnessed a few unfathomable morons on the internet, such as Matt Stone, arguing that hypermetabolic states protect against disease. Apparently these silly people are confusing cause with effect. Illnesses which result in higher stress responses (CORTISOL) will lead to physiological hypothyroidism, by altering T4 conversion to rT3. This is euthyroid sick syndrome.
Just because sickness causes low thyroid does not mean high thyroid protects against sickness. This is grossly irrational, but then again, it's a Matt Stone theory, what would you expect? Higher thyroid would merely be a marker for not being sick. However, the state of very high thyroid would also be a marker for excessive insulin signalling, the very thing that is known to control lifespan and disease resilience in worms, mammals and even closely related primates.
SUMMARY!
1) Low carb diets do not hurt the thyroid at all. Low carb diets are superior to induce an endocrine / metabolic milieu permissive of body fat atrophy. When body fat in negative balance occurs, as well as the endocrine status of it, this will lead to physiological lower thyroid activity. It takes very low calorie levels of normal carb diets to equal similar changes in insulin/leptin/body fat growth which are easily acheived with higher calorie intakes of low carb. It is the endocrine changes and body fat growth changes that temporarily decrease theyroid activity. It is entirely reversible upon piling up buttery steaks and avocados.
2) It is generally a good thing that one can eat more food before tipping over into "uh oh fat tissue growing!" so I have no idea why anyone is bitching. Isn't this everything that dieters try to accomplish with their chronic exercising and their fake foods with zero calories?
3) Evidence suggests lower insulin, lower thyroid and lower metabolic rate = anti-aging and prehaps promotes longevity. Far from proven but it does suggest this madness to amp up thyroid maximally may be very misguided, like replacing sat fat with trans fat, a horrible misunderstanding leading to very misguided counterintuitive recommendations.
