Q&A #46: Thyroid Health in Women—Screening, Autoimmunity, & Nutrition

Hi everyone, welcome to Crowdcast 46, our 46th Q&A. Pretty cool. Um, for those of you that are new, typically I see a lot of people posting questions in the chat section, so please remember to post your questions in the Ask a Question section. And I go through those questions and I choose questions based on top voted, based on, you know, interest from the community, also interested for myself. The questions I choose are a combination of deep dives, so things that like require background research, going diving into literature, trying to figure out, you know, contradicting results, for example. But I also go and choose rapid-fire questions, which are basically answers that I can give in a few sentences or even just a sentence.

So I typically do rapid-fire at the end of the Q&A, but I see today that a lot of people— there's a lot of like quick rapid-fire questions in the chat that people had submitted in the chat section. So I might just start with a little bit of a rapid-fire And then end with a little bit of a rapid fire. And today we're we're going to go through. There's quite a few leftover questions that we haven't got that we didn't get to from the last Q&A. So I am going to be going through quite a few of those. If we don't get to your question, just know that we have team members going and reaching out to people and trying to help you know give some guidance like some. References or maybe a couple of sentences or they ask, you know, they ask me for a couple of sentences.

So we email you guys and also you can always resubmit. So today I'm going to be answering a question that I saw was resubmitted probably 3 times. So it worked. And so keep that in mind as well. And always you can go back to these Q&As and you can watch the video. So we send out a summary With time points and a YouTube video. You can watch it. You can also listen to it on the Alaquat, the private podcast feed for FoundMyFitness members. The Aliquot we release usually once a week. And so you can also just listen to that as well. Make sure you've downloaded the private podcast feed. You can find that on your dashboard at foundmyfitness.com/dashboard. And you can also just listen to it On your dashboard as well. So kind of many options there for you guys.

So I'm going to just get started with a couple of questions that are in the chat here. Carmen asks about validity behind, you know, some of these blood tests like the Everly blood test looking for allergies, for example. We actually covered this in depth in a previous podcast episode. So what I recommend you do is Go into your dashboard, again, foundmyfitness.com/dashboard, and you'll see a PDF of many of the previous Crowdcasts that we have done. We do continually update it. And you can just search that PDF for allergy, allergy test, and you'll see the times that we've covered it. So I really suggest doing that.

There was another question submitted by— there was another question about immune function and, you know, intermittent fasting temporarily depressing immune function, and maybe that's why people can feel really good when they're fasting because their inflammation is down. I think that's a good hypothesis. You know, fasting does temporarily temporarily depress the immune function a bit. As you get into a more prolonged fast, you start to actually rejuvenate your immune system. So you actually have a lot of immune cells die off. And typically, it's thought, at least based on animal evidence and very preliminary human evidence, that the cells that die off are the more damaged immune cells, the more prone to autoimmunity type of immune cells.

And then they're replenished with healthy new, you know, immune cells. So I think that's a good observation. There was another question submitted by a name that I can't really pronounce, but they were interested in whether or not an 8-16, like a 16-8-hour intermittent fasting schedule could disrupt fertility for a normal BMI individual. So this is something that Dr. Mark Mattson and I covered in our podcast together. I don't remember the episode number, but you can, again, you can go to the episode page on foundmyfitness.com. There's an episodes page, and then, or you can just search in the search bar, Mark Mattson, and pull up that podcast. And then if you go to the episodes page, there's a timeline tab you can click on. And you'll see where we cover the fertility issue.

And he basically sort of says that fertility can be an issue when you're doing fasting and you basically are also very active. So you're doing a lot of endurance exercise. And the way it affects fertility isn't necessarily negative. So it kind of puts a stop on ovulation. And that, at least in animal studies, it's been shown that that will actually shift the whole fertility window to later in life. And so— and I'm not saying that is something women should practice, but it's not that it's totally detrimental to fertility. If someone is trying to currently get pregnant, it could, you know— Yeah. Possibly dampen the fertility temporarily, but again, what it does is kind of like stops ovulation.

And once the fasting stops and you know caloric intake goes back up, or you know caloric intake also as a as a you know response to exercise, right? So if you're doing a lot of exercise, basically when you go back to normal, ovulation picks back up, but it picks back up as if. You know, where it left off. So it's kind of a way of delaying or prolonging the fertility window. At least that's what's been shown in animal studies. So that's sort of a difficult study to do in humans. I don't know that it's really ever going to be done, but it is something that I find that's interesting and something to keep in mind. So I'm going to start off one of the deep dive with one of the deep dive questions that was left over from last Q&A. It was submitted by Amy. Amy says, hi, Rhonda.

I'm a 48-year-old female recently diagnosed with osteopenia. And basically, over the past year, she's been focusing on weight training, increasing protein intake, getting optimal doses of omega-3, vitamin D, vitamin K2, hydrolyzed collagen. But the data on whether supplemental calcium is beneficial is confusing. And so the question is, is supplemental calcium beneficial for women with osteopenia? And I would say, after looking and reading through quite a few studies, the scientific literature on calcium supplementation for women with osteopenia shows mixed results. So some studies suggesting benefits and others showing little to no effect on bone mineral density or fracture risk.

So I would say the scientific literature generally supports the idea that calcium in combination with vitamin D supplementation could be beneficial for bone health, particularly in reducing the risk of fractures and improving bone mineral density in older adults and postmenopausal women. However, the magnitude of the benefits and the optimal dosage really is— there's a wide range and there seems to be a lot of individual variation. and individual, you know, variation, and also results between studies. So, for example, a 2007 meta-analysis published in The Lancet found that calcium supplementation combined with vitamin D significantly reduced the risk of fractures and improved bone mineral density in people over the age of 50.

In 2012, there was a Cochrane review that concluded combined calcium and vitamin D supplementation reduced the risk of hip fractures and other nonvertebral fractures in older adults. This review also found that supplements appear to be more effective in individuals that are institutionalized, so in some sort of maybe elderly care facility, and because those individuals are often at a higher risk for vitamin D deficiency and also fractures. There was a 2018 review that was published in the Journal of Bone and Mineral Research that suggested that calcium intake from diet alone, even below, a little bit below the recommended levels, might be sufficient for fracture prevention when combined with adequate vitamin D. And this review did not actually support the use of supplemental calcium when co-administered with vitamin D for preventing fractures.

So in other words, This review found that vitamin D, if a person was taking supplemental vitamin D, they were able to basically get adequate levels of calcium from their diet. And that was enough to prevent bone fractures. And basically, additional supplementation with calcium didn't do anything better on top of what people that were supplementing with vitamin D alone were getting from You know, extracting calcium from their diet. And this is a really important point because, you know, I think in our community, most of us by now know the importance of measuring our vitamin D levels, making sure that we're probably supplementing because we do live in a, you know, a very different environment than our ancestors did when we were outside quite often and not inside at a computer. In an office.

So it's important to keep in mind that if— while there's a lot of people in the United States and even globally that are not getting enough vitamin D, if you are supplementing and you are getting— you have your levels between 40, 60, 70, 80 nanograms per milliliter, then you are basically absorbing up to 60% more Dietary calcium. And that's very significant because, again, even this review showed that even if you were below the recommended daily intake or recommended daily allowance for calcium, that, you know, it was still enough because probably— I would hypothesize because the supplemental vitamin D was making more use of basically making that calcium from the diet more bioavailable. So that I just wanted to kind of hit home on that important point.

There was another study in 2015 that reported that while calcium supplements with or without vitamin D really didn't have a significant effect on the risk of total fractures or hip fractures in community-dwelling older adults, there was a benefit with calcium supplementation plus vitamin D supplementation on reduced hip fracture, again, in the institutionalized older adults, so people that are in a facility, care facility. So I would say that generally speaking, if you look at the literature with combined calcium and vitamin D, again, it's still mixed results, but it seems like the really important factor there is vitamin D status.

And, you know, calcium, it's a good idea to calculate calcium intake from food, just get a general idea like where you fall within that RDA range to see if somewhere between 1,000 and 1,200 milligrams a day of calcium, if you're close to that, then it might be enough just to have your vitamin D and not really have to take the calcium. If you look at Just calcium supplementation, the evidence of just calcium supplementation without vitamin D, it's really less clear, to be honest. So there was a 2018 review that basically concluded evidence did not support the use of calcium supplements without vitamin D for preventing fractures. It also suggested that calcium intake from diet alone, even below the recommended levels, could be sufficient.

There was a 2007 study that showed calcium supplementation, even at a low dose, did have a mod— so there's a difference between preventing fractures and then bone mineral density, right? So the calcium supplementation alone, even at a low dose, did have a modest effect on bone mineral density in postmenopausal women with osteopenia. So it's a very select population of women. women, right? So postmenopausal with osteopenia. But there was no— they didn't actually assess the impact of calcium on fracture risk in that study. So they only looked at bone mineral density.

There was a meta-analysis published in 2006 in the American Journal of Clinical Nutrition that found calcium supplementation with vitamin D supplementation did reduce the risk of fractures and improve bone mineral density in postmenopausal women. So I would say, in summary, the scientific literature presents sort of mixed data, again, with respect to the efficacy of calcium supplementation for women with osteopenia. Some studies have found a modest improvement on bone mineral density. Others suggest that calcium supplementation alone really may not be sufficient.

So I think, you know, keeping in mind that vitamin D really is probably the most important here because We do derive calcium primarily from our diet, and that vitamin D status is essential in maximizing the bioavailability of calcium from our diet. And again, the RDA range is about 1,000 to 1,200 or 1,200 milligrams for adults, and that's combined dietary and supplemental. So, I know I think I mentioned to you guys— A couple of months ago that I was taking a very, very low dose of calcium. It turned out to be about 200 milligrams.

And I've since kind of like not— I kind of just take that supplement weekly now, mostly because when I calculated how much calcium I'm getting from my diet, even though it's a little below the RDA after cutting out a lot of my dairy, I still feel Because my vitamin D status is so good that I'm within that range. So taking a little bit of supplemental calcium weekly is good. And I do think the main things are resistance training, really important, getting the vitamin D as well. And I think those 2 things are extremely important. I think sauna may even help, but that has yet to be shown. Sybil is asking in the chat about pregnant women or breastfeeding, if they should take a lot more calcium.

I generally stick to what is in a prenatal vitamin and then trying to derive calcium from foods like, you know, like some sardines are really high in calcium. Like, you can eat a sardine with a bone in it and it's like so high in calcium. And you don't have to eat that every day. But like just even having that like, you know, once or twice a week, that's like— that's a lot of calcium. And there's a lot of other foods that you can eat that are high in calcium that I would focus on. And I would probably include dairy in that as well, for sure, during pregnancy. So the next question was submitted by Christian. And Christian wants to know what I think of the product called NAD3. It's a nutraceutical. That some influencers recommend.

So NAD3, it's basically combined freeze-dried a certain plant, Wasabi japonica. It's a freeze-dried rhizome. It's a type of isothiocyanate, actually. It also has a little bit of copper niacin chelate in it. And it has theacrine in it, which is an alkaloid that is in wild tea plants, and it's kind of structurally similar to caffeine. So my opinion is there is a significant shortage of clinical evidence that NAD3 is meaningful in any way. So there's literally 2 clinical studies using NAD3. that I could find. And one study showed no difference with NAD3 versus any of the groups. So that's out. And the other trial was extremely small. It was 12 males and 16 females. And it was funded by the company selling NAD3. I would say, I mean, there's— you just need more trials.

You need larger trials to make any statements about NAD3. And so to me, it is unclear that it has any benefit at all. And it's unclear if it has a negative— I mean, some negative effects. Like, we don't— there's just like no research in humans out there, essentially. So that's pretty much my opinion. So Dre is asking in the chat about calcium for people that are on Prednisone and have osteoporosis. Again, I think that would be something to discuss with your primary care physician because I don't really know how that steroid interacts with calcium and other, you know, supplements. But that would definitely be a good question for your primary care physician.

Really trying to, if it does interact, you know, or if it's somehow suppresses bioavailability of calcium or the use of it or something like that. Yeah, you would ask your physician if it would be beneficial to take a little extra calcium. The other thing is vitamin K2. I think, you know, it's— I wouldn't say the data is crystal clear on vitamin K2. Like there was a negative— there was a— I call it negative. In other words, there was a randomized controlled trial that came out showing that vitamin K2 supplementation had no effect on bone mineral density, I think it was, or fracture risk, one of the two. And I just want to highlight that while, you know, when you have a big study that shows no effect, it doesn't mean that the supplement or whatever you're looking at has no effect.

It just means the conditions, the doses, the— all the different, you know, you didn't have the right concoction of things to show anything. So, it was just kind of like, well, it was like, no, we didn't find anything. When it comes to vitamin K2, you know, the power of it, I think, really is combined with vitamin D, particularly vitamin D. And, you know, that study didn't— I don't, you know, know that that study— I don't remember it looking at vitamin D status. You know, you need to absorb calcium. You need to have a good vitamin D status. And we know that, you know, approximately 70% of the United States population has levels below 30 nanograms per milliliter. I mean, that's a lot of people. So, my guess would be that, you know, most people are not vitamin D sufficient.

And so, you know, whether or not vitamin K2 is going to have any effect is kind of— It's not clear. I would presume that the vitamin K2 in combination with vitamin D would be more— something more synergistic or additive because they're working together, right? So vitamin D is helping absorb the dietary calcium and vitamin K2 is activating all these proteins that transport calcium out of the vascular system and bring it to the bones. bring it to muscle tissue. So the next question was submitted by David, and David submitted this question quite a few times. So I'm happy to finally be addressing it. David says, how robust is the current evidence for sauna in decreasing the risk of Alzheimer's disease?

And he says, a couple of respected neurologists, Dean and Ayesha Shirazi, I never heard of these people, were a bit dismissive of the idea for limited evidence and confounding factors. I've been devoting a lot of time to sauna, and I hope it's not wasted. So the observational data on sauna use and Alzheimer's disease risk include— so there was a prospective cohort study. It was a population-based sample of about 2,315 middle-aged— they were men in eastern Finland who used the sauna 4 to 7 times per week. They had a 65% reduced risk of developing Alzheimer's disease compared to men who used the sauna only 1 time a week.

So the data was adjusted for baseline age, for alcohol consumption, for body mass index, systolic blood pressure, smoking status, type 2 diabetes, a previous heart attack, resting heart rate, the low-density lipoprotein cholesterol, and other heart disease risk factors, meaning that that 65% reduction in Alzheimer's disease was found after all those factors were considered. So, obviously, prospective observational data, you can never actually, you know, you can never actually say causation is established, like sauna use will absolutely decrease Alzheimer's disease risk. But when you correct for a lot of other factors, and then you have interventional studies and mechanisms, then you kind of put together a bigger picture. There was another prospective cohort study.

This was a study involving almost 14,000 men and women between the ages of of 30 and 69 that were free from dementia diagnosis. That study found that frequent sauna bathing— so this was about 9 to 12 times per month. So I would say a little bit less than the 4 to 7 times a week, right? So that was pretty robust and pretty frequent sauna use, right? 9 to 12 times a month was related to about a 20% reduced risk of dementia compared to people either not sauna bathing at all or sauna bathing less than 4 times a month. So that's like once, basically once a week. And again, this was after adjustment for all these different lifestyle factors I mentioned, metabolic risk factors, socioeconomic status, things like that.

So we have these 2 pretty large population studies showing sauna use is associated with a pretty dramatic reduction in Alzheimer's disease and dementia, especially when it's more frequent. But we also know from the last podcast with Dr. Axel Montagne that Alzheimer's disease and dementia are really, really intimately linked with vascular health. And we know that sauna mimics moderate-intensity aerobic exercise. Many of the same physiological responses occur. It's been head-to-head comparisons of that. Okay, it's really not a question. about sauna mimicking moderate-intensity aerobic exercise. We also know that aerobic exercise also protects against dementia and Alzheimer's disease.

And, you know, maintaining an adequate blood supply, healthy vascular factors, it's really crucial for vascular dementia, but also Alzheimer's disease. So long-term sauna use has been shown to induce protective responses against the processes that drive cardiovascular disease. And some of these protective responses include Lowering resting systolic and diastolic blood pressure. That's been shown in intervention studies, but also we've got observational data. It increases left ventricular ejection fraction. It reduces left ventricular ejection time. It enhances arterial compliance. It improves flow-mediated dilation. All of these things are measures of endothelial function and vascular health. So sauna improves vascular health. So does moderate-intensity aerobic exercise.

There was one study that found— this is out of Jari Laukonen's group in Eastern Finland— found that sauna use 2 to 3 times per week had a 24% lower risk of developing hypertension. And that risk reduction was increased to 46% lower risk for people that use the sauna 4 to 7 times per week compared to only once per week. So again, you know, a lot of data suggesting that sauna use improves blood pressure. There's also been intervention trials with hot tubs as well. So 20 minutes in a 104-degree Fahrenheit hot tub can lower blood pressure as well compared to baseline. So we've got, you know, intervention trials and we got observational data pointing to the same thing, both with sauna use and with hot baths. Well, I should say hot tubs. So I think that's pretty strong evidence.

And we know that blood pressure is very intimately linked to dementia risk as well. There was also a randomized controlled trial with about 149 patients who had advanced congestive heart failure. 2 weeks of what's called Weyon therapy, so this is an infrared far-infrared sauna, about 140-degree Fahrenheit sauna. And it improved a variety of biomarkers. So cardiovascular biomarkers, it improved. I mean, just, I don't want to go through all the medical terminology, but many different ones that improved. This was a randomized controlled trial, by the way, where people were getting a sham treatment and compared it. Basically, people were getting like standard medical care.

And the people that got the infrared sauna had much more improvements in all these different cardiovascular-related biomarkers. Another trial involving 30 congestive heart failure patients with a variety of premature ventricular contractions found that 2 weeks of infrared dry sauna significantly reduced those— the number of premature ventricular contractions. Within a 24-hour period. Lastly, there was a randomized controlled trial with 24 people who had ischemic heart disease and chronic total coronary artery occlusion that were unresponsive to non-surgical procedures. And they basically did 15 sessions of the far-infrared sauna over a 3-week period, and it improved their vascular endothelial function And it improved— so that improved their flow-mediated dilation of the brachial artery.

So these are intervention trials in people with heart conditions, and sauna use is improving their vascular health. I don't think it's really arguable at this point that sauna improves vascular health. I think it's pretty conclusive that it does. So knowing that mechanism, along with the observational data on the effect of, you know, sauna use and Alzheimer's disease is pretty strong in my opinion. But there's more. We have heat shock proteins. So heat shock proteins, as you guys know, I mean, I'll save you going into too much of it, but like they play a critical role in protein folding and misfolding. There's growing evidence that heat shock proteins are involved in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease. and Parkinson's disease.

There's animal studies that have shown that if you overexpress heat shock proteins, they can protect— they can have protective effects on the brain and help prevent and also ameliorate Alzheimer's disease and Parkinson's disease. Certain heat shock proteins, especially heat shock protein 70 and heat shock protein 90, have been shown to directly interact with amyloid beta. This is the protein that causes plaques outside of neurons where the synapses form in the brain and also interacts with tau proteins, which tangle inside of neurons, and they disrupt mitochondrial function. So HSP70 is basically helping, you know, get rid of those proteins and making them not aggregate, essentially.

So I would say a lot of animal evidence suggesting that heat shock proteins are very beneficial in the context of neurodegenerative disease. We also know that There's data showing that in humans that sit in a hot 163-degree Fahrenheit sauna for 30 minutes, it elevates their heat shock protein 70%, 50% over baseline levels. Hot baths have also been shown to elevate heat shock proteins as well. So it's a conserved mechanism. It's a stress— heat shock proteins are increased with many types of stress, but heat stress is a big one. thermal stress. And so I think that's another, you know, sort of just mechanism by which you could imagine sauna, hot tot tubs helping reduce the risk of Alzheimer's disease. Inflammation is another one.

Inflammation is thought to play a really big role in neurodegenerative diseases. And when I say inflammation, I mean chronic inflammation, not acute inflammation from, you know, sickness. And, you know, there's studies showing, many studies showing that sauna use, you know, is inversely associated with C-reactive protein, a biomarker of inflammation. So basically, the more frequent people use the sauna, the lower their C-reactive protein levels are. There's also intervention studies showing that sauna use can, while it does something very similar as exercise, it causes an acute inflammatory response as measured by IL-6, that cytokine. But that induces an even more potent anti-inflammatory response.

IL-10, which is an anti-inflammatory cytokine, has been shown to be elevated after sauna use. And this anti-inflammatory cytokine, you know, basically has a net effect of anti-inflammatory. So similar thing, exercise does a similar thing. There's also brain-derived neurotrophic factor, similar to aerobic exercise. You know, heat stress has been shown to increase brain-derived neurotrophic factor, which helps stave off neurodegenerative disease. So, you know, hot water baths have been shown to do this. So head-out immersion, it was a hot, very hot bath, it was 108°F water for 20 minutes, elevated brain-derived neurotrophic factor. Exercise does the same thing. In fact, exercise combined with heat even does... even elevates brain-derived neurotrophic factor more than exercise alone.

So I think there's a lot of supportive evidence that we're not just looking at confounding factors here or healthy user bias with respect to sauna use and reduced dementia risk. Bar is asking in the chat where to find the sauna protocols for the individuals I was mentioning with with, you know, heart problems. So you can search, go into Google Scholar and search Waon therapy, W-A-O-N therapy. That's the terminology for the far infrared sauna. They have the protocols there. And there's a variety of different— there's quite a few studies. that have been mentioned. Also, I gave a presentation at the Arkansas Little Rock Heart Health Hospital that is on our YouTube channel. It's— there's also an episode page on it, and I have slides on there with references as well.

If you want to look at those slides, you can also find them there. Alan's asking in the chat if there's any benefits of sauna over and above exercising an hour per day at 60% max heart rate. On an indoor rower. So I'll say, I don't know what the specific protocol you're talking about, but there have been 2 studies, one observational study showing that people that are, you know, physically active over a wide range of physical types of being physically active from moderate to vigorous, being vigorously physically active. They have a better cardiorespiratory fitness and VO2 max if they also use the sauna compared to the people that are physically active without using the sauna.

So that suggests that using the sauna, there's a benefit to using the sauna even for people that are very physically active. There was an intervention study done by Jari Laukonen's group published last year where they took people and they I think they had them do, I think it was a stationary cycle, but they had them do, you know, basically made them physically active for a variety of, you know, a few weeks. And they split the groups in 2. One was doing the exercise alone and the other was doing exercise plus sauna. And people that were doing exercise plus sauna had improved, you know, cardiorespiratory fitness. They had improved biomarkers of like lipids and also other— I think also insulin sensitivity and stuff like that was also improved.

So I do think that there is a benefit to people that are already very physically active to actually additionally do the sauna. Also, there's a lot of research coming out that heat stress helps with the times when you are not physically active. So, for example, on recovery days, Going in the sauna helps preserve muscle mass, and that's also really interesting as well. Ernest is talking about with the Waon therapy protocols, there's a lot there. There's a slow cool down, and he's wondering if that's necessary. I think it is because the way they cool down the individuals, it takes a long time to cool them down. So the so the so the protocol is they're basically trying to actually keep them hotter. For a longer period of time, even after they're outside of the infrared sauna.

And so they wrap them in a warm blanket, actually, and they're actually trying to keep their core body temperature and keep them hot for a while. It's kind of almost like a way of extending the heat stress, but in a perhaps not so uncomfortable sort of way, and perhaps even maybe safer for some of these people with specific heart problems. So yeah, it's a very— I agree, it's a very interesting protocol. Okay. So the next deep dive question has to do with thyroid health. So Pri asks, hi, Rhonda, can you do a deep dive into thyroid health, particularly for women? This is something I haven't covered too much in depth before. So I was kind of happy to go into this one. Let's begin with a general overview of the thyroid gland. So the thyroid gland It's like butterfly-shaped.

It's an endocrine organ. It's basically situated in the front of the neck. It's responsible for producing thyroid hormones that are released into the bloodstream. Iodine is a crucial element required for thyroid hormone synthesis. The regulation of thyroid hormones originates in the hypothalamus, which releases a hormone called thyrotropin-releasing hormone, or TRH. So TRH is a peptide hormone. It stimulates the pituitary cells to release thyroid stimulating hormone. This is probably one that most of you are familiar with, TSH. So TSH or thyroid stimulating hormone then circulates in the blood and binds to receptors on thyroid cells. When levels of what's called thyroxine or T4, And T3, so T4 and T3 levels rise, they basically— there's like an inhibitory feedback.

So they will then inhibit the TRH and the TSH release through this negative feedback loop that will then basically reduce T3 and T4 secretion and also reduces iodine uptake. There's a lot of factors. So cold stress, emotional stress, and exercise can all increase TRH release, while glucocorticoids, somatostatin, and dopamine can inhibit TSH production. TSH levels follow— this is important— they follow a circadian rhythm. So they peak between 9:00 PM and 5:00 AM, and then they dip between 4:00 PM and 7:00 PM. Most of the T4 and T3 in circulation are bound to transport proteins, and so they're not free.

Thyroid hormones play a really important role in normal development, various human tissues, and they also regulate metabolism, you know, basically in many, many cells and organs throughout Yeah. The body throughout life. So thyroid functioning is extremely important for metabolism. They also are important for elevating basal metabolic rate, for inducing lipolysis, also for lipid synthesis. So they do both, basically the breakdown of fatty acids, but also the synthesis of them depending on the metabolic status. So in a fasted state, for example, they would help to increase lipolysis. They stimulate carbohydrate metabolism. They promote protein anabolism or catabolism in high doses.

They also enhance the effects of catecholamines, and they work alongside growth hormone to stimulate bone growth in children. They also are crucial for brain maturation during prenatal period, and also they can impact mood. So hyperthyroidism, which leads to hyperexcitability, it can lead to irritability. It also— we're going to go a little more in depth about hyper versus hypothyroidism. But hyperthyroid— I'm sorry, hypothyroidism, the opposite, so lower activity, may cause memory impairment, slowed speech, sleepiness. So thyroid also can affect fertility, ovulation, menstruation. So there's a lot— this is sort of a general background. There's a lot of things that thyroid hormones regulate, and so they're very important for a lot of different processes in the body.

So let's talk for a moment about screening and then sex differences. So when screening for thyroid abnormalities, there's a lot of initial tests that are done. Some of you are probably familiar with it. done them before, but they typically include measuring the TSH, the free T4. So remember I mentioned a lot of times the T4 and T3 are bound to transport proteins. So the tests measure the free T4 and the free T3 levels. And then these tests will help to determine if the dysfunction originates from the thyroid gland itself, which would be a primary, or from the pituitary gland. gland, which would be kind of a secondary effect, or from the hypothalamus, which would be considered a tertiary effect.

And then there's a variety of further examination methods that include sonography and other methods as well. In developed countries, the prevalence of undiagnosed thyroid disease is kind of decreasing because of widespread thyroid function testing. So it's Most of the time, people with thyroid abnormalities are being treated for it because most people are really testing and screening for it these days. So sex differences, thyroid disorders are definitely more common in women than in men, with autoimmunity actually playing a significant role. So women have a much higher Risk of autoimmune type of diseases. Hyperthyroidism occurs 4 to 7 times more frequently in women than in men, regardless of the cause. Then the risk of primary hypothyroidism is up to 10 times higher in women than men.

So sex hormones and also like a skewed inactivation of what's called the X chromosome, so Women have 2 X chromosomes, are thought to contribute to both of these, the hyper and hypothyroidism. Throughout their lives, women experience major endocrinological changes, right? So puberty, menopause, pregnancy, these are all events in a woman's life that really changes endocrine— there's a lot of endocrine changes going on. And that also impacts the immune system. So these changes affect the hormonal environment. They affect interactions between the immune system, so the innate immune system, the adaptive immune system, pro- and anti-inflammatory cytokines, and basically just making women more susceptible to autoimmune diseases in general.

During pregnancy, immunosuppression often leads to a pretty robust decrease in thyroid antibody titers. So postpartum, women's thyroid hormone levels quickly return to pre-pregnancy levels and an immunologic rebound occurs, and that can actually cause an increase in thyroid antibodies. So women who are basically have a normal thyroid but have test positive for these thyroid antibodies before pregnancy can actually have anywhere between a 30% to 50% chance of developing what's called postpartum thyroiditis within 1 year after delivery. There's numerous genes on the X chromosome that are involved in immune function. And so oftentimes women will have multiple copies of these. genes, but one of them will be inactive on one of the chromosomes.

But some women don't have that inactive— those genes aren't inactive on that X chromosome. And so they have an overabundance or an overactive amount of these genes related to immune function, and it really sort of increases the risk of developing an autoimmune-related type of thyroid dysfunction. So let's talk about— let's dive a little bit into the hyperthyroid or this overactive kind of thyroid. In the case where it's like a primary cause, so it's like at the level of the thyroid, free T4 levels are abnormally increased while TSH levels are decreased. Symptoms of hyperthyroidism include heat intolerance, weight loss, increased appetite, sweating, weakness, fatigue, tachycardia, palpitations, Abnormal heart rhythms, muscle tremors, restlessness, anxiety, emotional instability, insomnia.

I mean, like a lot of potential symptoms here that can overlap with many other diseases as well. So it's just another reason why it's kind of good to get either an annual or once every couple of years, you get a thyroid test. I'm talking particularly to women here. So it's really good to do that. The prevalence of hyperthyroidism is not like super, super high, but it ranges from 0.2% to 1.3% in people that have normal iodine levels, so they're iodine sufficient. It's most common in women aged between 20 and 50, and the causes include Graves' disease, which is the most probably common cause. And then there's toxic nodular goiter, which is much, much less common. It's about 16%. And then other causes as well. But Graves' disease is— it's a multi-system autoimmune disorder.

It involves genetic and environmental factors like iodine, smoking, alcohol, stress, infections. The toxic nodular goiter is— it's basically characterized by production and release of thyroid hormones by thyrocytes, and it's independent of TSH or TSH receptor antibodies. Both of these types of hyperthyroidism are usually treated with anti-thyroid drugs, and they usually— which usually reduce the production or the synthesis of thyroid hormones. So hypothyroid. Usually free T4 levels are abnormally decreased while TSH levels are increased. And symptoms of hypothyroidism include fatigue, bradycardia, cold intolerance, weight gain, poor appetite, hair loss, cold and dry skin, constipation, myopathy, stiffness, cramps, depression, Impaired concentration and memory.

Again, wide range of symptoms that you wouldn't be able to necessarily pinpoint to thyroid dysfunction because they overlap with a lot of other diseases. And so one more reason why it's just good to screen your thyroid levels and that's kind of the way to keep on top of things. The prevalence of hypothyroidism is about 4.6% in the US. There was a study in the US that was a screening study that found the prevalence of about 0.4% for overt hypothyroidism and then 9% for what's called subclinical hypothyroidism. So overt would be like, you know, it's pretty strong, very clearly hypothyroidism. But I would say the subclinical one is pretty common in women. that are 75 years or older. The subclinical hypothyroidism really begins to kind of kick in a lot more commonly in women of that age range.

Lots of causes, potential causes, disturbed iodine metabolism like iodine deficiency, also iodine excess. The mechanism for iodine excess isn't really well understood, but some data suggests it basically could induce autoimmunity. There's another cause of chronic autoimmune thyroiditis, which is known as Hashimoto's thyroiditis, which involves a failure of T cells, T cell-mediated inflammatory response, so cytokine release, and basically lymphoid cells, which are like the T cells, B cells, infiltrate the thyroid. There's lots of different ways to diagnose Hashimoto disease. But the condition is present in about 10% of women that actually are considered to have normal thyroid functioning.

In pregnancy, about 2% to 7% of women could basically get these higher TSH levels in the first trimester and then get the postpartum thyroiditis basically leading to— Hypothyroidism. Hypothyroidism. So basically, again, I was talking about some of these women that are thought to have a normal functioning thyroid, but they have these what are called thyroid antibodies. They're called TPOAb antibodies or TPO antibodies. Women with normal thyroid hormones, but that have those antibodies and then get pregnant have a very high risk of getting the postpartum thyroiditis and then eventually potentially that thyroiditis leading to hypothyroidism. So that is something for women to keep in mind. It's also another reason why women commonly have thyroid issues.

There's been a variety of environmental factors, chemicals, herbicides, pesticides that have been reported to cause thyroid hypofunction. And again, treatment typically involves— there's a variety of common drugs and synthetic versions of thyroxine, for example, which is T4. But there's really not a consensus on whether or not subclinical hypothyroidism requires treatment. There's a variety of dietary and lifestyle factors that may affect thyroid function. So iodine, which is found in seaweed, fish, seafood, eggs, iodized salt, of course, is really essential for proper thyroid function. Mm-hmm. The RDA for adults is about 150 micrograms per day, while the tolerable upper intake is about 1,100 micrograms.

Now, keep in mind, again, both severe iodine deficiency and excess iodine both can contribute to hypothyroidism and hyperthyroidism. So being within that sweet spot. Would be ideal. And looking at what your multivitamin— most multivitamins will have iodine in them. Looking at that combination between— and then looking at your daily food intake and sort of calculating what your estimated iodine intake would be would give you an idea if you're getting enough. Now, again, most people Yeah. In developed countries are eating a lot of processed foods, packaged foods. They eat out in restaurants, and these restaurants are using iodized salt. So typically, people are getting a lot of iodine.

It's not like the most common micronutrient deficiency, but it is a good idea to kind of have an idea of how much iodine you are getting, especially if you don't— if If you're like me, I use pink Himalayan salt, try to limit my eating out and also limit packaged foods and stuff like that. So most of my iodine is coming from food sources and then my multivitamin as well. Selenium. It's a trace mineral found in a variety of foods. Brazil nuts are high in selenium. Organ meat's high in selenium. Muscle meat's also high in it. It is also really important for thyroid function. The RDA for non-pregnant adults is about 55 micrograms with a maximum daily intake of 400 micrograms of selenium from both food and supplements combined.

Selenium directly affects thyroid hormone metabolism and also redox processes. So it's important for glutathione synthesis basically and use, which is a major antioxidant in the body. Insufficient selenium intake is associated with an elevated risk of thyroid disease. While selenium supplementation could reduce the risk of the thyroid peroxidase antibody titers I was talking about, the TPO antibody titers, it's long-term. Like, you don't want to— long-term selenium, high-dose selenium supplementation It's not really known in terms of the safety, right? So it's not like long-term, it's not really known if it's really safe.

But it would be worth, like women that are considering getting pregnant, it would be worth, I would say, getting your thyroid panel done, the typical standard panel, and then getting the TPO antibodies, so the thyroid peroxidase antibody titers measured. And because a woman could have normal thyroid biomarkers but high antibody titers, and we know that puts a woman at a greater risk after pregnancy, postpartum, for that thyroiditis and then again eventually developing hypothyroidism. And so if a woman does see that they fall within that group, optimizing selenium intake before pregnancy may also be an option, and then remeasuring those antibody levels as well, and then making sure sufficient selenium and everything is taken in throughout pregnancy.

And this is another reason why I really think that eating a wide variety, varied diet during pregnancy is extremely important. Even if you're following a more restricted diet, when you're not pregnant, like a low-carb would be considered restrictive, right? Vegetarians considered restrictive because you want to make sure you're getting— the best way to ensure you're getting a good amount of these micronutrients from food is by eating a wide range of healthy meats. So I mentioned organ meats high in selenium. That's a great source of— Yeah. It's good to add in that organ meat. I was doing that during pregnancy.

I was eating— you can buy that mixed meat with the— it's like muscle meat mixed with liver and kidney and I think heart, and it tastes a little better because it's got the muscle meat mixed in. It's ground meat and you can make meatballs with it or chili or whatever, like hamburgers. You can make whatever you want. But it's just really good to eat the the vegetables, the different colors. I just wouldn't go— the restrictive diets, it's not— the time to not do it would be pregnancy. Zinc also plays an important role in thyroid hormone synthesis and function. So the recommended daily allowance is between 8 to 11 milligrams for non-pregnant adults. And I think Zinc supplementation is beneficial in specific populations. Making sure you're not going too high.

I typically, I think my zinc is like 25. You want to make sure you don't go too high over— sorry, I was thinking of vitamin E, not 25. But you don't want to go too high over the RDA on a daily basis. Now, the time to do it is when you're on the onset of a a cold or like a respiratory illness or something like that, like getting it early on, that's beneficial to take higher doses, like even up to 80 milligrams a day for a period of a week. There was a study investigating the effects of zinc and selenium co-supplementation on thyroid function in overweight or obese women with hypothyroidism, and they found improvements in free serum T4 and TSH levels. There's other minerals and vitamins as well that really— there's no— like ashwagandha and all this stuff.

There's really no evidence to support that they have an impact on thyroid disorders. Avoiding gluten and dairy may only have positive impacts in people that have sensitivities to those substances, likely by basically— there's a certain drug, Levothyroxine, I think. The absorption of that can be improved by avoiding gluten and dairy in people that have sensitivities, maybe through an inflammatory response or something like that as well. And then overconsumption of certain cruciferous vegetables, like eating cabbage every day, probably, you know, would Yeah. Would not be beneficial because there are certain isothiocyanates in certain cruciferous vegetables like cabbage. They are not present in broccoli.

There are certain ones that are in cabbage, for example, that can really compete for iodine uptake. And then smoking, body mass index can also influence thyroid function. So a higher BMI can lead to thyroid dysfunction as well. Again, I mentioned, you know, sex. So females are much, much higher risk. And then moderate alcohol intake, interestingly, may be associated with a reduced risk of hypothyroidism. So that was interesting. That's my deep dive. I went really all in on that because I hadn't covered it before. And I know a lot of women are very, very interested in Okay. In the thyroid function. Sybil is asking in the chat about testing for thyroid function. So the panel that I like to do, so I typically do the WellnessFX thyroid test. They have a thyroid test that you can do.

And I actually am due for— and in fact, as I was preparing this thyroid document, I decided I was going to do another test because it had been a couple of years. So like doing it again, like every couple of years. Some people may need to do it every year. It depends on your lifestyle and genetic risk and all that, but it's a good idea. They have a really good panel. But again, additionally measuring— particularly important for women that are planning on getting pregnant, measuring the TPO antibodies in addition to that because women with a normal thyroid function, in other words, The whole biomarker panel that you measure for thyroid function will all look normal, but you could have elevated levels of this specific thyroid thyroxidine peroxidase, I think it was called, antibody that would put a person at about a 50— a woman at a 50% greater risk of developing postpartum thyroiditis and then potentially then that developing into hypothyroidism.

So, Blake's asking about, do you think that if you eat out of a health food store like Whole Foods, do they still put a lot of sugar and salt in their food? I trust them more than other places. Yes and no. I think you're definitely better off eating like a salad out of Whole Foods that you can like put your own— you can make the stuff. But if you're talking about you go to the counter and you get their pre-made, there's a lot of salt and Yeah. I mean, they usually have the ingredients on there and you can look, but like you can just taste the salt too. I mean, it's like, it's pretty obvious to me when I'm eating out because I'm not used to like— I don't put any salt on my eggs in the morning when I make my scrambled eggs in my olive oil.

And so when I eat out and there's like salt, it's like, whoa, like it's just too much. So basically yes and no. I do think it's probably better than other places, but also, you know, anytime someone is preparing your food for you that you don't know personally and tell them what to put in it, then you're at risk of sneaky stuff getting in there, you know? You are asking how best to reduce the thyroid antibodies. So I did just mention In the diet and lifestyle section that there's been limited studies suggesting that supplementation with selenium and— was it zinc?— can help to lower the thyroid antibodies. The next question was submitted by quite a few people, and it has to do with the recent erythritol study, which I'm sure many of you have heard about. Heard of.

People are asking just to kind of COVID it or what are my thoughts on it. You know, is it— am I worried about consuming erythritol? So I'll just generally— I'm not going to spend too much time on this, but generally speaking, what this study found was an association between blood levels of erythritol and the risk of major adverse cardiovascular events in people with a high prevalence of cardiovascular disease. Okay? So these were not healthy people. These were people with problems, metabolic syndrome, cardiovascular problems. There was in vitro, so this is in Petri dish cells and culture, and in vivo animal experience, this is mice, showing that at certain levels, blood levels, Of erythritol, platelet reactivity and aggregation and thrombosis formation was enhanced.

Now, also shown in this study was they took a very small cohort of actually healthy people and they gave them 30 grams of erythritol. And this led to basically high blood plasma levels of erythritol to a level that they found in their animal studies and in vitro studies that actually it was even surpassed that level was associated with that platelet aggregation and thrombosis potential that I mentioned. So there were 3 kind of parts to this study. One was the Correlative data, right? They took these unhealthy people that had cardiovascular problems, metabolic problems, and they measured their plasma erythritol and said, oh, people with higher levels were having more heart attacks and this and that, right?

Second part of the study, took animals, gave them erythritol, looked at their platelets, did this in culture, found that erythritol at a certain level Basically cause platelets to make this thrombosis, right? I mean, that could lead to a stroke, you know, so it's very bad. And then the third part of the study was they go, okay, let's get healthy volunteers and see if we give them 30 grams of erythritol. By the way, that is a level that many Americans these days do take in. And they said, let's see if that increases their plasma levels and what levels does it increase it to and for how long. And so that's what they did, gave them 30 grams. It did increase their levels to even a higher degree what they found caused thrombosis in the animal studies.

And they found it was like, I think it was like 3 days or something that the plasma levels were elevated. So it was a long time. Now you can imagine if someone's consuming that on a daily basis, then their plasma levels are going to be completely elevated all the time. Okay. So that was kind of the summary gist of what the main points of the study were. Okay. How the media covered it, though, was a little bit different. I mean, they were basically putting all those things together and saying that, you know, taking in erythritol was going to give you a heart attack, and that is not what the data showed. So let's talk about the limitations and potential confounding factors and other things.

So the cohort of people had a high prevalence of cardiovascular disease and metabolic-related risk factors. And the study only measured their plasma levels. The problem with that is that we actually make erythritol endogenously in our bodies. So erythritol is an intermediate metabolite that can be formed from, you guessed it, glucose in what's called the pentose phosphate pathway. So erythritol can— so basically, When you take in a lot of glucose, if you have— you're taking in tons of glucose, then, you know, you basically can start, you know, in addition to glucose being used in its meta— you know, the normal metabolic pathway for energy that is used, some of it is shunted into this other pathway called the pentose phosphate pathway. Erythritol is a metabolite of that.

And it then is then used to make fatty acids. So it's used for fatty acid synthesis. which is stored as fat. It's part of the reason why taking in a lot of glucose can also lead to higher fat, right? Fat's fat. You get fatter when you're eating too much glucose. So measuring blood erythritol levels, you know, and in fact, it was only in individuals that had the highest level, blood level of erythritol that had an increased risk of adverse cardiovascular events. And this group of people actually is the group of people with the most diabetes. Again, I just mentioned the whole glucose problem, right? So people with type 2 diabetes have glucose dysregulation. They have high blood glucose levels. The glucose is being shunted into pentose phosphate.

It's all sort of— so what, at the end of the day, that's— that first part of that study where it was looking at the, you know, erythritol in plasma and correlating it to adverse cardiovascular events, it could, you know, most likely could be that you're biomarking, you know, the erythritol, which is sort of a metabolite that is, you know, biomarking dysregulation of, you know, glucose metabolism, which is the case in people with type 2 diabetes, right? It's also very important because this pathway that produces erythritol, the pentose phosphate pathway, can be increased by oxidative stress, inflammatory processes, adipose, so like higher body fat, diabetes, high glucose-fructose intake. All these things can basically influence endogenous production of erythritol.

So there's a lot of problems with saying that consuming erythritol is necessarily going to give you an adverse cardiovascular event, right? Because of all those problems I just mentioned. I would say the strength of the study, though, is that they did take a group of healthy people, give them 30 grams of erythritol, measure those levels in their blood, and they sort of correlated that and said, look, these levels are even higher than what we saw could induce thrombosis types of events in animals and also in, you know, plate— in petri dishes with platelets. And I do think that needs to be investigated more.

And that aspect, getting healthy people, you know, giving them erythritol and then maybe starting to measure, you know, platelet aggregation in those people over a time course for how long? So I would say that, you know, the end of the day, my conclusion from that study is that, one, people that are metabolically unhealthy have higher levels of erythritol. And I think that's biomarking the metabolic status of a person. And they're metabolically unhealthy, and that could be due to glucose dysregulation. It could be due to the inflammatory oxidative stress, that whole environment, right? And that those people are at a higher risk for cardiovascular disease, which we already knew.

Second part of this study that I feel was probably the most enlightening to me that I didn't— this is new data that I didn't know about, was that at certain levels of erythritol, it can cause platelets to aggregate and cause this sort of thrombosis type of phenotype. That was surprising and new data that I do find disturbing. And for that reason, I think that we need to— scientists, research needs to be investigating it in a careful and, you know, calculated manner. And because I am a little concerned about that potential, I have decided to definitely limit my erythritol intake. Now, it wasn't like I was going out and buying erythritol. The thing about erythritol is it's one of those little sneaky things that hitchhikes in on other things.

So I was using monk fruit for, you know, if I were to bake something or put, you know, a sweetening touch on my coffee, I was using monk fruit. And if you look at pretty much all the monk fruit out there on the market, it's got erythritol in it. And in fact, most of the time erythritol is the ingredient before the monk fruit. So I've switched back to stevia for my coffee and for baking. And until I find a brand— so the big brand out there, is it Lakanto, I think it's called? It's like, to me, it's almost like a erythritol brand. I mean, even though they market themselves as monk fruit, everything of theirs has erythritol to a very high level. Right. And like I said, in most instances, more than the monk fruit. So I do— I am limiting my intake of it because I like to be cautious.

And I do think that there is a cause for— I think there's a reason to be cautious. I think that we don't know really what it's doing, what exogenous taking in of erythritol is doing. It's in like drinks. It's in— it's just, if you start to look at everything that you like, keto this, keto that, you know, all this stuff has erythritol and that adds up. And if it's— if, you know, that study, the one strength of it, in my opinion, was they took healthy people and they showed their levels were pretty high for like 3 days after one 30-gram ingestion. So when you start to like add up all the grams you're getting, from all these, you know, this and that, keto that, whatever, then it probably starts to add up and it's like, okay, well, what does that mean? Like, what is— we don't really know.

Is it causing platelet aggregation? It very well could. So that's my thought on it. Allulose, I guess, is another option as well. Now sells monk fruit as powder without erythritol. Oh, thank you so much, Liz. I'm going to look into that. That's great because I was definitely very discouraged because I couldn't really find that. So Mark is saying, why not xylitol then? Any parallel with erythritol? I mean, we don't really know. I haven't seen any studies showing that with xylitol. But it does sort of highlight the importance that we don't really know What's going on with allulose? What's going on with stevia? What's we like? Has anyone done platelet aggregation for any of that? Like if you haven't measured it, then we don't know, right?

So like most of the times with these artificial sweeteners or non sorry I should say non nutritive sweeteners in in the case of xylitol, erythritol, stevia, monk fruit most of the time what's being looked at is like effects on glucose blood glucose levels. Microbiome, for example. Xylitol is one that I do get in chewing gum and I brush my teeth with it and it's very, very good for teeth. It's very, very good for teeth. And I don't know that that amount— I'm not like— if you're not eating food with xylitol, I am much less concerned with the small amounts that like are mostly getting on your teeth. I also make a mouthwash with xylitol and I rinse my mouth with it as well. But it's a good point.

We are taking somewhat of a risk and it kind of makes me just go, maybe we should just go back to eating honey. There's part of me that thinks— we put out a Science Digest a couple of months ago. I think it was like a systematic review of a variety of studies looking at honey. And the honey was improving metabolic parameters. It was crazy. It was doing the opposite of what you would think for a sugar. So I've really— I do kind of struggle and part— I think so Ed and Twili has mentioned about xylitol disrupting microbiome. We went through this in a previous Crowdcast. I mean, there were some animal studies and the levels were just— Unachievable by what you would be getting by chewing xylitol, but even cooking with it. I mean, it was so high what they were giving to these animals.

So it's really just a matter of there hasn't been enough research looking into the effects. And I think that now that it's pretty consensus that too much refined sugars is bad for health in many different ways. And because there's been a big movement towards non-nutritive sweeteners, a lot of people that are health conscientious are using stevia and monk fruit and allulose, right? I think there's going to be a bigger push and pressure to actually do some more research on these non-nutritive sweeteners. Like, we need more research in this area. And so one of the reasons why I don't make very strong statements about them, maybe you've heard other influencers doing so, is because I feel like we don't know what the hell is going on, to be honest.

I feel like there's so little research out there to make any definitive conclusions that you just can't. You can't extrapolate all these animal studies. You can't say based on this very small sample size where they did this high, high dose that it really has any relevance. You know what I mean? Like, there's just not enough. There's tons of research looking at the effects of refined sugars and sugar-sweetened beverages, but I think there's a sort of paucity in research on non-nutritive sweeteners. And for that reason, I haven't— I've gone a little bit in depth on it, but like, I just feel like I can't give a solid— I can't come to a solid conclusion that we know really what's going on with them because of the lack of research. So that was my soapbox.

I'm going to get on to some of these rapid-ish fire questions followed by the rapid fire questions. So there was a question submitted last month and several people commented on this and it was by Mimi and Mimi says, I went all in on my EPA/DHA supplements and my omega-3 index was 15.8%. That high number skewed my omega-6 to omega-3 ratio into the lower range and also skewed my arachidonic acid/EPA ratio into the lower range. Can someone go overboard on it? Is higher always better? So I have discussed this issue of the omega-6 to omega-3 ratio and the arachidonic acid or the AA to EPA ratio being sort of quote unquote off with Dr. Bill Harris, who is the founder of OmegaQuant, the co-creator of the Omega-3 Index. And Bill mentioned a couple of things.

First, he mentioned that, and I agree with him on this, the omega-6 to omega-3 ratio really tells you nothing about— the amounts of omega-3 and omega-6 fatty acids. So you can get that same ratio with infinite sets of actual levels. It tells you nothing about which omega-3 and omega-6 fatty acids are in that ratio. So you could have tons of ALA and hardly any EPA and DHA, right? So it doesn't tell you anything about what types of omega-3 and omega-6 are in that ratio. So, and that just assumes that basically all the fatty acids you know, are equal in their importance and significance and they all have the same relationship to risk. It's just not true. And then third, both ratios assume that the omega-6 component is bad and the omega-3 component is good.

We know that the omega-3 component is good, but we don't know that, you know, having the omega-6 component is bad. You need omega-6. You do need it, you know, and the best way to get it is actually from whole food sources like linoleic acid, getting it from nuts, for example. As for the arachidonic to EPA ratio, the AA to EPA ratio, Bill's concern is that it ignores DHA. So it's kind of unclear, like, does it even mean anything? Like, I don't really know. He's not concerned at all about it. He thinks that, you know, basically having a— we don't know that having an omega-3 index of 16% is better than 12%, but we don't know that it's not.

So, you know, I personally think that— I think we're leaning towards more and more research is suggesting that omega-3, even at high doses, can be basically a therapeutic— have a therapeutic effect. Now, there is a concern of some people getting AFib. And— but as we've talked about many, many times, like, this needs to be investigated further. And most of the studies is in people with already preexisting cardiovascular problems. And also, the whole problem with AFib is that it increases stroke risk, but the omega-3 decreases stroke risk. So even within that population, omega-3 is, you know, decreasing stroke risk, even if some people are getting higher, like they're getting a higher risk of AFib, they still have a lower risk of stroke.

So then the question becomes, well, is it even clinically relevant because the omega-3 is lowering the stroke risk? At the end of the day, that's the problem with AFib. So, you know, I don't know that it— my personal opinion, for me, I take extremely high doses of omega-3. I do not have AFib. I don't have any sort of palpitations and never have. And I'm personally not concerned about it. But it doesn't mean that no one should be concerned about it. I do think we need to study it more. And it is something, of course, probably to discuss with a primary care physician as well. But as you guys will see, we're going to be having a really interesting podcast coming out later this— we're going to be recording it later this month on omega-3 being potentially anabolic in skeletal muscle.

So I have a researcher who is arguing that it is based on his clinical research and the clinical research of others. It's really pretty exciting, but it also requires significantly high doses of omega-3, which comes down again to identifying the right doses for certain populations of people may be something as well, right? So a lot of interest and things to explore there. Rebecca is asking if sauna can play a role in fat loss or maybe at least preserve muscle mass while in a calorie deficit. It's funny that you mentioned that because the omega-3 research that I just talked about, some of the work suggests that omega-3 may have a role in sensitizing skeletal muscle to amino acid intake, and that this is particularly relevant in a scenario where people are not taking in as much protein, for example, and also in a sense which would be more of a caloric deficit, and also in a scenario where, like, elderly people who have, you know, that are not as sensitive to the amino acids as well.

Sauna does play a bigger role in preserving muscle mass while, I think, while in a caloric deficit, probably. I know that the data has at least shown that it helps when— during immobilization. So I haven't seen any evidence of, you know, people doing a hot bath or a hot sauna in people that are in a caloric deficit. But because a lot of the, you know, it's— I think it's possible that it will help preserve muscle mass in a calorie deficit. Definitely resistance training is the way to go there. Resistance training will absolutely— help because it is stimulating skeletal muscle protein synthesis. So that would be the main thing to focus on in a calorie deficit would be resistance training. Hi, Rhonda.

I'm very scared since we used to consume Hu dark chocolate regularly, my toddler as well, and knowing the brand is high in lead and cadmium, how concerned should I be for my 3-year-old who eats quite a bit of this almost every week? I wouldn't be so concerned about the past, but limiting that type of chocolate, I would limit the high-lead chocolate. I would look for the brands that are lower in lead. You can look on ConsumerLab. A brand that I use for my son is called ChocZero, C-H-O-C Zero, and it's actually— it was tested as one of the lowest in cadmium and also in lead. It didn't have a ton of polyphenols in the chocolate, but I don't know that the toddlers really need those anyways. So it's kind of a— and it doesn't have sugar, it has monk fruit without erythritol, so that's nice.

I think it's sort of a win-win for kids in general because they're not getting all the sugar and they're not getting the lead and cadmium. And so I think that for that reason, it's a good one. Sam from Hong Kong was asking about sauna, cold shower post-strength training. Basically wants to know if it's Not a good idea to post-workout strength training workout to do a sauna followed by immediate cold shower. So I'm going to give you guys like I've I've obviously talked a lot about this in the past about like there was like a seminal study showing that cold water immersion immediately after strength training had blunted some hypertrophy adaptations in skeletal muscle. I interestingly went back. There was a new study that came out that showed actually it did not blunt.

Hypertrophy after doing— after strength training. And so I went back to that original study and I was like, what is going on? And I looked at the control group and I found the control group was doing passive— basically what's called passive— it was passive recovery is what they called it, but they were basically exercising. They were doing cycling on a stationary cycle at a very mild It was very mild. It wasn't, you know, even moderate intensity, but they were getting their blood flow going. And as we know from, you know, studies that Brad, Dr. Brad Schoenfeld had cited in our recent podcast together, and also this new guest coming on, he's been— he published a study with Stu Phillips that basically, you know, moderate aerobic exercise, the blood flow when combined with resistance training actually enhances hypertrophy because of the blood flow going to the muscle.

So I'm wondering if that original study was actually— because the cold water immersion group still had hypertrophy. They still had hypertrophy after the strength training. They just didn't have as much as the quote-unquote control group. But as I just mentioned, the control group may have actually had enhanced hypertrophy because they were cycling right after the strength training. They weren't just sitting. They weren't just passively doing nothing. So I question that now. I question that now. I don't know for sure, although I can think of mechanisms by which cold water immersion would blunt hypertrophy by cutting off the circulation, right? So I don't know that it's so key though to like not even do it on the day that you're doing your resistance training.

Do I think a cold shower is the same as sitting in, you know, an ice bath? I don't. So, you know, getting in the sauna, you know, obviously does not blunt hypertrophy after the resistance training. You know, whether or not you want to get— I don't know that a quick cold shower after the sauna is really going to massively blunt adaptations. But again, so like like I said, because of this recent study and because the new study that came out showing that doesn't blunt it, I think there's there's a little bit of what's going on here. To be safe, you know, you could just avoid the cold shower within an hour or so after after doing any type of strength training. Endurance training is different. In fact, it's been shown that cold water immersion in combination with or done before after.

endurance exercise actually improves performance. There's performance enhancements. Ariel asked about advanced glycation end products. They're called AGEs. They're implicated in a variety of different diseases. They're formed by the Maillard reaction, so when you grill foods and stuff. But, you know, they're also in highly processed foods. So, like, the question was, you know, should I avoid grilling my roasted veggies? AGEs are basically— they're really high in uncooked animal foods, and grilling them can accelerate the AGE formation. It's a really big problem also with good old refined sugar because that's why people with type 2 diabetes have such a big problem with advanced glycation end products, because they can't regulate their blood sugar levels. Their blood sugar gets really high.

So advanced glycation end products, they're called glycotoxins. They're a diverse group of basically oxidant compounds. You know, they damage proteins, they damage lipids, and they have all sorts of— they can cause chronic diseases and stuff, particularly in people with diabetes. They're created through a non-enzymatic reaction by reducing sugars and free amino groups on proteins, lipids, and nucleic acids, so in DNA. So that's why the sugar is a big problem. It can react with proteins, lipids, and DNA in circulation or even inside of cells. In addition, These advanced glycation end products, in addition to them forming within the body, they can also exist in foods. And they're not— again, they're naturally present in uncooked animal dry foods, very high in animal dry foods.

And when you cook them, it's sort of the formation of these advanced glycation end products happens. Grilling, broiling, roasting, searing really propagate and accelerate AGE formation. Not really a big issue at all in vegetables. Hi, Rhonda. What is your favorite yogurt brand? So my favorite yogurt that I do is Bio-K Plus, and I mix a little bit of that in with this creamy yogurt called Benoit, B-E-N-O-I-T, and it's the plain one, plain yogurt. And so I mix the Bio-K Plus, which is like super high in probiotics and stuff. It's very, very sour. And I mix those together and that's kind of my fave. During the last Q&A, you mentioned how sprouted bread is much lower in gliadins, but every brand of sprouted bread I've seen has gluten added back in.

Is there a brand that is 100% sprouted wheat flour without added gluten? I don't know that I've seen one either. So sprouted bread is not gluten-free, but the amount that's sort of added back in is like below what you would find in basically regular bread. So I do think brands like Ezekiel still have a lower total gliadid burden in general. Okay. Joanna is asking about reintroducing foods. She cut out gluten 10 years ago and dairy and improved her IBS and joint pain. And she's got no inflammation according to her colonoscopy, and she kind of wants to experiment back with adding dairy back in. What's your opinion? You know, she also has MS, so which could mean dairy might negatively impact— could negatively impact someone with MS. But I do think that El Ruteri yogurt would be the exception.

And the Bio-K Yogurt Plus would be— I would go with maybe some goat milk kefir and adding a little bit of the Bio-K Plus yogurt in with that, or make your own L. reuteri yogurt. I mean, there's lots of protocols online where you can make your own as well. So that would sort of be the exception with respect to the dairy, in my opinion. But of course, not medical advice, and certainly you could talk to your physician and see what they think as well. Hey Rhonda, are you worried about heavy metal exposure from seafood? Is it safer to take fish oil rather than eat fish? Also, anything you do to ensure proper detoxing of the liver in the form of supplements and regular checkups?

So I usually eat fish that's low in heavy metals, so that would— that's the wild Alaskan salmon is one of the lowest, and then I also do some I'll snack on sardines once in a while as well. I don't really, you know, I don't really do take any supplements to like detox my liver. Although if I think like if consuming alcohol, some liposomal glutathione and N-acetylcysteine would be a good one to do like before or after drinking, and also probiotics as well, because alcohol does affect the microbiome and also the liver as well. And the glutathione helps kind of detoxify the alcohol, so it kind of is easier, easier on the liver. So it's kind of good to just have those supplements. Like, I have them in my, in my refrigerator for that, for that purpose.

Magnesium— I know you speak a lot about using magnesium, it's very important, but what about the bad effects? Andrew Huberman says magnesium glycinate can be bad for people with AFib or heart issues. Also, taurine is said to be toxic for the heart. So I don't know if Andrew actually said this or not, or if it was like a misunderstanding, but I've seen no evidence of magnesium glycinate being bad for people at all with AFib or heart issues or anything. So it's actually a very nicely bioavailable form and non-irritating form of magnesium for many people. So I'm unaware of where that is coming from or if it was a misunderstanding. Taurine actually is really good for the heart. In fact, maybe that's also a misunderstanding because it's like quite the opposite.

In fact, my mentor Bruce Ames just— not just, but like within the past like 3 years, wrote a review paper suggesting taurine might be what he calls a longevity vitamin. It is very beneficial for mitochondria. It sort of acts as a buffer for mitochondria. Mitochondria are constantly kicking out proteins and— proteins, protons, which basically are acidic, and taurine helps buffer that. And so it makes mitochondria work better, and mitochondria are the primary, the only source of energy, like in the heart. So the heart muscle predominantly oxidizes fatty acids for energy, and that happens only and solely through the mitochondria. And so you really want your mitochondria to be their best. So I actually think taurine is an interesting potential longevity vitamin.

Do you have any recommendation for daily sunscreen or casual— for casual sun exposure? I know mineral types are safest, but too heavy— some are too heavy for normal use year-round. Do you use something daily throughout the year? I like CeraVe's hydrating mineral sunscreen. Which is— it is a little bit lighter and it's like it doesn't have that like white, you know, look on the face. ConsumerLab has a really good list of sunscreens that are low in benzene. Apparently benzene's like contaminated in a lot of sunscreens like Neutrogena and stuff. So one more thing to worry about. And also it has a list of like, you know, the sunscreens that are mineral-based But don't have like the other sort of chemical sunscreens that are would basically have the effect you're talking about.

The chemical sunscreens don't make your face all white, but they have the effect of like there's a chemical reaction upon UVB UV radiation exposure that changes some of them makes basically causes you know those compounds to be metabolized into metabolites that potentially be carcinogenic. So I think that it's good to look at that list by ConsumerLab. I like taking a short cold shower after sauna. Could that possibly negate the effects of sauna? I don't think so. They both increase heat shock proteins. They both increase norepinephrine. They're both, you know, I think the only concern is, like, doing them back-to-back, like, without waiting, giving yourself a little bit of a rest period.

because you're going from vasodilation to vasoconstriction, it could cause like low blood pressure or sort of faint feeling. So I think it's kind of good to get out of the sauna, wait like 5 minutes, and then get in the cold shower. Your genetic report is a powerful tool. We appreciate it so much. It's been 3 years since you've updated it. Any plans on a new revision? Yeah. So we've been working on updating different— there's been a lot of development going on with, like, programming and stuff. So, like, updating different companies we support, as well as, like, tech-related issues people are having before we update the report. But we do plan on updating the report.

But we need to get all those things sorted out, which, by the way, takes way longer, is way more complicated than you could possibly imagine. And then lastly, Mako says, in your podcast with Dr. Satchin Panda, I learned that circadian rhythm is set in part by when you first eat during the day. Is drinking water enough? Coffee? If not, how much food is necessary? I'd like to get my circadian rhythm going early, but also extend my overnight fasting window. So there's a circadian rhythm that's basically in the central nervous system that is regulated by light exposure. And so that clock is reset with, you know, going outside, getting bright light exposure first thing in the morning, very important.

And a good thing to do for having good sleep at night, because when you reset that clock earlier, the earlier you do it, the easier it is going to be to fall asleep at a normal, reasonable hour, because that clock has been set early. And so it's on a clock, and by the time you get to the end of the clock, it's time to go to bed. But there's peripheral clocks, and I think this is what Mako was referring to, in other organs like the liver, like our gut, for example. That their circadian rhythm is not set by light exposure, it's set by food intake.

And so those clocks, when you set those clocks, when you reset those clocks by taking in calories, then that's sort of the— again, the most important thing with that is the timing window, because we know metabolism is more optimal earlier if you eat your food earlier within that window. So if you end up Yeah. You know, it's not that you have to start your metabolic clock early. It's that knowing that when you take in your first calorie, that is starting the clock. And therefore, you know, you don't want to eat a bunch of calories when it's all the way at the end of the clock, right? Like 12, 13 hours later, right? You want to try to do it maybe 10, maximum 10, 11 hours, right, later. In other words, you want to be done eating by then. So I think that's the main point.

Also consider people that are extending their overnight fasting window. You know, the biggest concern is, you know, so we're constantly in a state of, you know, protein anabolism and catabolism. So protein synthesis in our skeletal muscle and breakdown in our skeletal muscle. And, you know, we need protein intake. We need essential amino acids to come in in order to stimulate the muscle protein synthesis, right? And so as you've been sleeping all night and fasting, you're not getting any essential amino acids. And so everybody is in a little bit— when you wake up in the morning, you're a little bit more on the catabolic side than after you just had a meal of essential amino acids. So careful not to go too long because You know, that, again, you're talking about muscle protein breakdown.

Or alternatively, if you are extending your fasting window, do some resistance training while fasted in that window. That way, you're at least signaling muscle protein synthesis through mechanical stimulation, right? So that you're at least getting a little bit of that as well. All right. This is the end. I went a little bit over today, but thank you guys so much for submitting wonderful questions. Thank you for attending these live. I feel, I feel very privileged to be here. I learn a lot from them. I enjoy them. And thank you for your support. We'll be releasing the summary to this next week along with the aliquot episode that you can listen to again on your private podcast. Player. You can find that at foundmyfitness.com/dashboard. I hope you guys all have a great month.

I look forward to our Q&A next month. You guys know the rigmarole. Go to the Crowdcast, sign up for the next one, and submit your question in the Ask a Question section. That's where we— that's where I choose the questions from each pool for each Q&A. And then the chat, of course, is where I take the questions live. And I'll talk to you guys soon. We got some awesome podcasts coming up. I'm so excited. And talk to you guys next month. Bye.