Transcription
Optimizing thyroid is more than just about speeding up your metabolism or your weight loss. Thyroid hormone directly controls your cholesterol levels as well as your steroid hormone production. Without adequate thyroid hormone, your cholesterol levels can rise and your cells aren't able to produce normal levels of hormones like testosterone, progesterone, estradile, or cortisol.
If you've tried lowering your cholesterol levels or fixing your hormones, but nothing seems to work, it might be because you're treating the symptoms and not the source. So, in today's video, I'm going to show you one, how thyroid brings cholesterol into the cell and then the mitochondria to begin steroid hormone production. Two, how thyroid hormone increases mitochondrial function and energy production, the foundation of all steroid hormone synthesis. Three, how low thyroid function can cause low testosterone, low progesterone, low adrenal function, and even menstrual and fertility problems. And then four, how to improve your thyroid function so you can dramatically improve your hormonal balance.
Now, before we get started, if you want a way to support your thyroid, your metabolism, and hormone production through a personalized diet, I created a free protetabolic diet calculator and food guide that helps you determine the right calories, macros, and foods for your individual context. You can grab it in the link using the description.
All right, to start out here, the first important thing to discuss is how thyroid hormone actually controls cholesterol metabolism because it will lead us into understanding how thyroid hormone actually controls steroid hormone production. One of thyroid hormones main jobs is to take cholesterol out of the bloodstream and bring it into the cells. And so this is actually one of the ways that thyroid hormone is able to lower your cholesterol levels and why people who are hypothyroid tend to have high levels of cholesterol inside their blood. So we see this from a paper here titled a renewed focus on the association between thyroid hormones and lipid metabolism. But the researchers say lipid levels increase in a graded fashion as thyroid function declines. While patients with TSH values between 5.1 and 10 micro unit uh international units per liter have significantly higher mean total cholesterol uh low density lipoprotein cholesterol levels as compared to youth thyroid subjects. So basically as TSH increase so thyroid stimulating hormone is a marker of low thyroid function as that starts to increase the higher the levels are the typically the lower the thyroid hormone function is the higher the cholesterol levels are. So we see this relationship and we see this in humans. Okay.
So we see this relationship between thyroid and cholesterol. But the question is how does this actually work mechanistically? What's going on that in terms of thyroid adjusting cholesterol levels? And so the researchers actually tell us this. What they tell us is that thyroid is able to increase cholesterol uptake by increasing the LDL receptor at the cell so that the cells can take in more LDL cholesterol from the blood. So the researchers here say they say in parallel with lowering of cholesterol excretion there's a rise in the LDL cholesterol by a factor of about three. The latter being due to a decreased LDL receptor activity accompanied by a suppression of the uptake of LDL by the LDL receptor in the liver and this is in hypothyroidism. They say indeed the LDL receptor mRNA levels decreased by nearly 50% indicating that the LDL receptor is regulated at the N mRNA level. results appear to be reduced catabolism and turnover which would account for the presence of dysipidemia and hypothyroidism. So when you are hypothyroid the LDL receptor levels at the cells in the tissues actually decrease so they're they don't take up quite as much cholesterol. We'll see why that happens in just a second. You know it's weird. It's like why would the thyroid control this but we'll talk about this in just a second here. Okay.
So there's one more piece to look at with this thyroid cholesterol picture versus when we look at the effects of thyroid hormone versus a hypothyroid state. And so in a thy in a normal or a u thyroid state, what you see is that thyroid hormone can actually increase the production or the synthesis of cholesterol at the liver as well as of bile acids. And in a hypothyroid state, you actually see a decreased production of cholesterol at the liver, which is weird, right? You would think that if you have a a decreased level of thyroid hormone, you would and you have a higher level of cholesterol in the blood, why would production actually be decreasing? Again, this is due to clearance. And the other question is why is the thyroid gland actually increasing cholesterol production at the liver directly and also increasing LDL receptor at the cells so the cells can uptake them. And so the researchers just to exemplify this with a quote they say thyroid hormone increases the synthesis of cholesterol bile acid flow resulting in the depletion of hippatic cholesterol and the enhancement of cholesterol uptake from the circul from circulation to the liver. By contrast in hypothyroidism, dimmunition of the thyroid hormone results and slowing of bile acid flow marked dimmunition in the rate of cholesterol secretion into the bile increase of intrahypatic cholesterol despite the decrease in cholesterol biosynthesis and a decrease hypatic uptake of cholesterol from circulation. So hypothyroidism decreased cholesterol production but decreased cholesterol uptake at the cells and the tissues and in normal thyroid function you have an uh adequate uptake of cholesterol from the cells and the tissues as well as a normal production of cholesterol at the liver and we can see these effects here at the graphic. So when you have a lack of T3, your bile acids are lower, you have a decreased depletion of paddic cholesterol. So you have a higher amount of cholesterol in the liver and then the cholesterol uptake from circulation is actually decreased. On the flip side, when you have adequate levels of T3, bile flow into the intestines increase. This is important because chole bile is made out of cholesterol. So when you have adequate bile flow into the intestine, you actually decrease your cholesterol p pool to some extent because it's the bile is taken up in the intestine or moved out in the intestine via its binding with certain fibers. You also see a depletion of apatic cholesterol. This is why hypothyroidism when you don't have a lot adequate thyroid signaling, you can actually have an increase in fatty liver. You have an increase of synthesis of cholesterol when you have adequate thyroid hormone levels, which again I'll talk about why that's important in just a second. and you have an increase in cholesterol uptake from circulation. So essentially the big issue in hypothyroidism that leads to the high amount of circulating cholesterol isn't that production's increased. It's that uptake of cholesterol at the peripheral tissues is drastically decreased. Whereas in normal thyroid function you actually have an increase in cholesterol production but you also have an increase in cholesterol uptake which leads to overall lower levels of cholesterol inside the blood.
Now, as a side note, and I've talked about this in a second video, so I recommend you check this out, but when you have these high cholesterol levels and hypothyroidism, this is associated with a worsening of cardiovascular disease. And hypothyroidism itself is directly associated with a worsening of uh cardiovascular disease because it actually drives vascular dysfunction by adjusting endothelial nitric oxide synthes function and the endothelial cell function as well as increasing lipids. So from that same paper we basically see a graphic here where they describe this. So when you have hypothyroidism or subclinical hypothyroidism you have dysipidemia. So that's the lipids are increased because of the lack of uptake by the cells and tissues and then vascular function is actually impaired leading to hypertension because of a negative impact on endothelial nitric oxide synthes function or vasoddilation. So you get stiff vessels with high lipids. This can drive inflammation. When the lipids aren't being uptaken by the cells and the tissues, they circulate for longer, so they're more likely to oxidize. On top of the fact that hypothyroidism is associated with a higher amount of reactive oxygen species stress, and then this ultimately combines together to lead to aththeroscerosis. So, it's it's hypothyroidism provides both the spark um as well as the wood to set the fire. So, it's a combination of multiple factors.
Next thing that's important to understand with this picture, once cholesterol is taken up into the cell, what is the next thing that should happen with cholesterol and lipids? Well, they should move into the mitochondria to be oxidized. The lipids oxidized and turned into ATP. And then cholesterol actually gets pushed into the mitochondria. As we can see here, you have cholesterol which is taken up from the LDL and HDL receptor at the cell. The cholesterol is cleaved and brought into the cell and then it's moved into the mitochondria. We have this protein called star in the mitochondria and star brings the cholesterol into the mitochondria where it's converted into pregnentoolone which is one of the the basically considered the father of all steroid hormones and then from there the steroid hormones your cortisol your DHEA your testosterone your progesterone your estradile eldoststerone etc are then created from this pregnenolone. So cholesterol goes into mitochondria, pregnentolone comes out and then you get the steroid hormones from pregnenolone depending on the cell the or tissue right. So in testicular fun or testicular cells you would see testosterone potentially estradiol in ovarian cells you see progesterone estradi and then from the adrenal cells you would see DHEA aldoststerone and cortisol right so the star the LDL needs to be taken up by the tissues brought into the mitochondria converted to pregnenolone and then depending on the cell you get these different steroid hormones now the thing that's really important to keep to understand here is that thyroid is is essential for that star function. So thyroid increases the activity of star at inside and at the mitochondria to bring cholesterol into the cell. And this actually this is checked out in cell culture size because it's obviously difficult to go look at this in humans. We have a paper here. This is titled thyroid and male reproduction. And what they talk about is they say um the inner mitochondrial membrane in the inner mitochondrial membrane cholesterol is converted to pregnnolone catalyzed by the cytochrome P450 cleavage enzymes using NADPH as a co-actor. Pregnetone then diffuses out to cytoplasmic endoplasmic endopplasmic reticulum where the remaining steps of testosterone biosynthesis are carried out. The conversion of pregnalone to testosterone occurs via two distinct pathways the delta 4 and delta 5 pathway. They go on to say Janna and Badacharia have shown that T3 stimulates production by goat leic cells in a dose dependent manner. They have later shown that T3 induces denovo synthesis of a 52 kilodol in soluble protein which augments the androgen production latic cells. Similarly T3 increased testosterone production by the rat and mouse latic cell in vitro and its precursor progesterone by a latexic cell um uh derived line by about 300%. T3 treatment for eight hours increase star. So that's that same proteins mRNA and the MLTC1 and mouse latic cell line. So basically thyroid's job is to increase star protein to bring cholesterol into the mitochondria so that we can produce that pregnantone and then from there depending again on the cell or the tissue you will get the different hormones.
So the job of thyroid is to not only take cholesterol from the blood and bring it into the cells and the tissues, but also to take that cholesterol once it's in the cell and the tissue and convert it directly into the steroid hormones which again like they have wide ranging extremely important functions. But there's another thing that's extremely important with thyroid function and that's thyroid function is increasing the uptake of the of cholesterol in the mitochondria. But it's also increases the uh production of new mitochondria, increases the quality of mitochondria, increases the energy metabolism, ATP production in the mitochondria, which that's going to be extremely important because in order for the P450 enzymes to take the cholesterol and convert it into steroid hormones, it you need adequate amounts of ATP and reducing equivalents like NADPH. And then on top of that, you need to make sure that you are in order to produce that ATP, you need to make sure that you're taking fuels like carbohydrates and fats and converting them into that ATP. So thyroid hormone is increasing the number of mitochondria to produce steroid hormone, increasing the uptake of cholesterol into mitochondria to produce steroid hormone, and increasing the utilization of fuel sources to produce steroid hormone. Basically steroid hormone production is largely dependent on thyroid hormone function which is controlling the in the mitochondrial function as well as the uptake and utilization of cholesterol. So this is why if you're dealing with any type of hormonal issue, one of the big things to always look at is thyroid hormone function because thyroid hormone function is very far upstream in terms of some of the dysfunction that can occur. Now, you can have hormonal issues that aren't derived from thyroid issues, but if you're not looking at thyroid and you're trying to address a hormonal issue, it could be problematic because if thyroid is not addressed, then this whole process can be shut down or it could be lowered a bit.
So, we have these mechanistic pathways, right? We're seeing this in different cell culture studies and and and different animal models and stuff like this, but does this actually play out in humans? And so the three major glandular systems that we have in humans that are producing steroid hormones are the testicles, the ovaries and the adrenals. And basically what we can see in all three of these systems is a decrease in their function when thyroid hormone function is impaired. So for example for testicular function we have a p paper here titled impact of thyroid disease on testicular function and they say in adult men hypothyroidism causes hormonal changes partly in the opposite direction compared with thyrotoxyosis SHPG total testosterone and seven beta estradile and gonadotropen serum levels are reduced while prolactin levels are increased. These variations are reversible with thyroid hormone replacement therapy. So basically the steroid hormones like testosterone and estradiol are actually lower when you when you have thyroid dysfunction. So on top of that the part of the brain that releases TSH also releases prolactin and prolactin shuts down the testicular function and gonadotropen signaling directly. So you have multiple mechanisms by which hypothyroidism or low thyroid function can have a negative impact on testicular function. It's from the hypothalammic level and then also directly in mitochondrial level and as well as cholesterol uptake.
Now the next tissue that we're going to look at or the the next gland we'll look at is ovarian function. So we have a paper here titled the effect of hypothyroidism on female reproductive hormones. And what they say here is hypothyroidism causes an increase in the levels of thyroid releasing hormone which in turn stimulates secretion of thyroid stimulating hormone and prolactin and prolactin inhibits the synthesis and secretion of gonadotropins. So the same thing I just described in men also happens in women where when you're hypothyroid the increased TSH production it also increases prolactin production from the pituitary gland and then that suppresses ovarian function. They say they go on to say several studies have also confirmed abnormal menstrual patterns and overt hypothyroidism. The associations of hypothyroidism and infertility PCOS metabolic syndrome aththeroscerosis heart disease and cognitive function are well described in the literature. They say in mammals downregulation of thyroid receptors lowers the f fertility and decreases follical number. Hypothyroidism has been associated with altered ovarian function, menstrual regularities, subfertility and higher miscarriage rates suggesting that thyroid hormones affect female reproductive axis. They lastly go on to say your studies have demonstrated a positive correlation in between TSH and prolactin and hypothyroid women. In several studies, it was shown that T4 administration in hypothyroidism normalizes prolactin and LH levels, increases follicularis and estradile secretion, reverses menstrual abnormalities and increases spontaneous fertility. T3 is considered a biological amplifier of the stimulatory action of gonadotropins on granulosis cell function. So essentially adequate T3 which is the active thyroid hormone is extremely important in allowing the ovaries to produce adequate steroid hormones and to optimize their function as well as when thyroid function is low the rise in prolactin can have a negative impact on ovarian function as well. We don't really want to have a circumstance where we have a high TSH value with a high prolactin or a low T3 state where we don't have the adequate amounts of T3 to produce the necessary hormones that we need from our different organs and our tissues.
The last one here is we have we have is the effect of hypothyroidism or lack of thyroid hormone on adrenal function. And basically what these authors say from this paper it's titled gluccocorticoid functional reserve in full spectrum intensity of primary hypothyroidism. They say at the adrenal level and long-standing hypothyroidism, a significant reduction in cortisol secretion after ACT stimulation has been documented in primary adrenal cell culture. This finding was supported by Tohay at all who suggests that hypothyroidism directly causes adrenal dysfunction and that hypers secretion of corticotropen releasing hormone and arginine basin is due to a reduction in the negative feedback effect of gluccocorticoids. So basically you get a high amount of these hypothalamic and pituitary hormones in states where you're have hypothyroidism particularly from the adrenal axis because the adrenal glands aren't producing adequate amounts of hormone again because thyroid hormone is controlling that cholesterol uptake into the cell and into the mitochondria to produce the steroid hormones and then that stops the negative feedback loop on the hypothalamic pituitary system. They go on to say here in our study adrenal corticotropen hormone levels were mildly elevated in hypothyroid patients that had an inadequate cortical cortisol response to coentropen before live with their oxine therapy. Remarkably adrenal function was completely restored after reaching a u thyroid state. So a normal thyroid state in nine out of 11 patients using the 515 nanomal cortisol cutoff value. These results suggest a direct adrenal level and transitory rather than permanent adrenal dysfunction provoked by low concentrations of hyp of of thyroid hormones.
So the question is if thyroid function is low, what are some things that you can do to correct your thyroid function? So the first thing you can do is actually look at what's going on under the hood. And so there's some labs that I recommend looking at if you are thinking that you're dealing with hypothyroidism. So the first ones are going to be your TSH. Then you have your total T3, total T4, your free T3, your free T4, and your reverse T3. These look at your full thyroid axis. It gives you an idea of how you're metabolizing the different thyroid hormones and do you have a lot of the active thyroid hormone in the form of T3 and free T3 or are you shifting more towards reverse T3 or staying mainly in T4? This is quite important especially when you're looking at your context in terms of what type of diet you're using, whether you're low carb or higher carb or you've been in a caloric deficit or your training volume's been high, etc. The next thing you want to look at is a comp comprehensive metabolic panel so you can see what's going on with your liver function. That's a big one in terms of determining what's going on with thyroid function because as I talked about in other videos, the liver function directly controls the conversion of inactive thyroid hormone T4 into active thyroid hormone T3. A large portion of thyroid hormone is converted there via the de diodinase enzymes.
Now the next things to look at are going to be your mineral status. So these are going to be things like your iron panel and your feritin, your serum copper, your plasma zinc and your plasma selenium. If you have deficiencies, even if they're marginal in any of these minerals, it can have a negative impact on thyroid function because these are directly involved in thyroid hormone signaling, thyroid hormone production, and also the effects of thyroid hormones at the cell in terms of increasing the production of proteins in the mitochondria that are involved in the electron transport chain like cytochrome coxidase. So, you want to make sure that you're not low in any of these minerals because it can impair the function and activity of the thyroid. And I've seen this quite a few times in clients where they're quite low on some of these minerals. Their thyroid functions wonky, their hormonal functions wonky, and the upstream correction was bringing the minerals on board, adjusting the diet and nutrition, and then the hormonal systems came back online instead of needing to directly just replace with hormones from the jump. So, this is really important to look at and I think it's kind of a blind spot that a lot of people don't look at. The other one is iodine. This one's talked about uh quite a bit in relation to thyroid, but it's very difficult to actually test iodine levels because they tend to be more in the tissues. So, the testing would be like a 24-hour urinary test, which would give you a rough idea of where your iodine status is instead of giving you a full picture of what your tissue levels are. And on top of this, highdosese iodine can actually have paradoxically negative effects on the thyroid gland via the wolf takeoff effect. So you want to make sure that you're actually careful with iodine and when you're looking to use that to correct thyroid dysfunction.
Now outside of looking at some of that testing and obviously looking at some of the other hormonal uh systems with the testing can be quite important, but you can also look at what's going on to your diet. If you've been in a heavy caloric deficit, you know, you've been in more than 30% deficit for an extended period of time, there's a good chance that that can have a suppressive effect on thyroid function because again, thyroid's job is to control energy metabolism and it's to increase energy metabolism. So, if your body is registering that it's in a huge energy energy deficit, it's not going to try to increase thyroid hormone signaling in that state because you don't have enough fuel coming in. So, it's going to conserve some of the fuel source. And you see this in the literature with with very low calorie diets and also starvation settings. You see the active thyroid hormone T3 starts to drop. Another thing with this is prolonged fasting can actually have a negative impact on thyroid signaling as well. Uh so you want to avoid very long fast, three-day fasts and you know multi-day fast, things like this. They could be quite negative for thyroid function. even longer uh like alternate day fasting regimens over the long term can have a negative impact on hormonal function because again you're creating both a caloric deficit and you have extended windows where you're not eating. The next one is going to be protein intake. If your protein intake is excessively high, this can have a negative impact on thyroid function because it starts to upregulate the ura cycle and the breakdown of ammonia and the protein can also crowd out some of the other energy macronutrients like carbohydrates and like fats. So you want to make sure you have an adequate protein intake because too low protein intake can impact thyroid function in a negative fashion. But also too high protein intake can have quite a negative effect as well. And again I recommend you check out the pro metabolic diet calculator that I put because it gives you a range of protein. The typical range I'm looking for is between 64 to82 grams per pound.
Now the next one is carbohydrates. Carbohydrates are absolutely essential for thyroid function. Adequate carbohydrate intake is important for appropriate insulin signaling that controls the iodine function. The iodinase enzymes are the enzymes that convert the inactive thyroid hormone T4 to the active thyroid hormone T3. So you want to make sure that you have adequate carbs on board so you have adequate insulin signaling so that the liver gets the message that you have you're in a good state. You have a quite a good amount of fuel coming in so that you can have active thyroid hormone signaling. And this is also why low carbohydrate diets can have a negative impact on thyroid function even if caloric intake is kept at an appropriate level. It's because of that decreased insulin signaling overall.
Now the last one here that's really important to make sure is dialed in is that your microbiome, your gut function is working appropriately. If you have a high amount of endotoxin or toxins coming in from the gut microbiome into your system, this can have a negative impact overall on your thyroid function by basically shifting you your T4, your inactive thyroid hormone towards the anti thyroid hormone anti in quotations here, which would be reverse T3 and also can impair thyroid hormone production, T4 production from the thyroid gland directly. So you don't want to have a high amount of circulating endotoxin coming in from the gut. This can also impact liver metabolism and via impact liver metabolism, lower your active thyroid hormone levels. So, this is another really big one and I've seen quite a few clients who have serious gut issues, things going on that get very high reverse T3 values because of dysfunction inside the gut. So, that's something that's important to actually look at and address. It's actually you can get thyroid function humming along again. There's also other anti-thyroid compounds in certain foods like raw cruciferous vegetables and high soy intake, but most people are avoiding those at least in a coming from a bioenergetic or a paleo or carnivore or keto sphere. You tend to see those things minimized, but that's also something that's important to look at or consider if you're not coming from those spheres. Some foods can have plant compounds that can actually negatively impact thyroid function if you have high amounts of these inside the diet.
All right. So, now that you understand how integral thyroid is to your cholesterol, your mitochondrial, and your hormonal metabolism, one of the major drivers, as I mentioned, for low thyroid function for most people isn't actually thyroid damage or direct thyroid damage. It's the diet they're following that's keeping their thyroid functions depressed, keeping their free T3 levels or active thyroid hormone levels low. And watch this next video to learn how certain diets, like low carb diets, can actually lower your active thyroid hormone levels and how you can reverse.