Hi, everyone. Welcome back to round 13 of our Crowdcast series. Just happy to, to be here this Saturday morning and got a lot of really interesting questions. And so we're going to just dive into some of those. Just as a reminder, This does not constitute medical advice. I'm not a medical doctor. I am a scientist. So answering these questions, you know, my team and I are doing sort of deep dives in some cases into the scientific literature just to kind of talk about what the empirical data shows or suggests thus far. So keep that in mind. Any, any— these are not recommendations. Any, any type of dietary lifestyle change, you should always run that by your, your general practitioner.

Um, another thing is that, uh, sometimes the most upvoted questions don't get, uh, the mo— don't become most upvoted until, um, you know, a couple of days before we start this Crowdcast. And so what typically what I do is I go through the list of questions and I will, I will do a combination of both the top upvoted questions, questions that I repeatedly get that I think are of interest to everyone, and also questions that are things that I don't typically talk about. I try to address, you know, a few of those things that are really new topics. So I also make note of questions that are kind of really big questions that require you know, a long deep dive. So, um, those are, those are things that we do circle back to eventually. So just keep that in mind.

So we'll go ahead and get started, and, uh, we'll start with one of the, probably one of the newer questions that I, I don't think I've really addressed before previously. So this question was from Callum, and he asks, is there any evidence that CBD oral or oil has benefits. It appears as though doing a little bit of a literature search that most of the data for topical CBD is— it's pretty scant, and I would say weak. Pretty much all the data that I'm going to mention, with the exception of one, a few studies, is oral. So let's start with randomized controlled trials from meta-analyses and review articles, starting with anxiety.

Now, there were a few studies that looked at CBD oil on anxiety, and about half of the studies show no effect, and half of the studies show some sort of effect with the CBD oil. And these studies are really small sample size ranging from 10 to 60 people, so I don't think there's a really clear answer on oil CBD oil in terms of anxiety. But there are some other studies looking at the effects of oral CBD on anxiety. So some studies show that using a dose of 600 milligrams could show. significantly reduced anxiety, also reduced cognitive impairment and discomfort. There's a couple of studies showing that. Other studies showing a slightly smaller dose of 400 milligrams a day could reduce subjective anxiety in people that have social anxiety disorder, and also in healthy volunteers as well.

And another study showed that a dose of 300 milligrams also reduced subjective anxiety And so what we're seeing here is that there seems to be a continuum with dose ranging from 300 milligrams to 600 milligrams. Although another study saw that actually if you start to go down less than 300 milligrams, you might not— there was no effect. And then the same goes for really, really high doses, interestingly. Some studies are showing that if you go up to like 900 milligrams of CBD, that there seems to be no effect. And in fact, some cases show that a higher dose could actually cause more anxiety in some individuals. So it really seems to be a sweet spot in terms of dosing.

Too low of a dose and even too high of a dose, there doesn't seem to be much of an effect, at least according to the limited studies that have been done so far, but doses around 300 to 600 milligrams appear to possibly reduce anxiety in some individuals, although some studies you have, you know, you really want to find placebo control because when it's an open-label study, a person is receiving a treatment and they're very subject to placebo effect. So I would say that The evidence on CBD oral for anxiety, still, I think larger studies need to confirm whether or not there is an effect on anxiety. There does seem to be in, you know, the few limited studies that have been done, an effect, but they're not always high-quality studies.

There's also some studies looking at memory extinction and consolidation, but there's only actually— I should say there's only been one study that looked at that, and it found that a single dose CBD, and actually was quite low of a dose, seemed to enhance consolidation and extinction of learning in healthy volunteers. But it's just one study, very preliminary. Sleep is something a lot of people ask about with respect to CBD. So just of note that THC does also affect— so THC is the active, the psychoactive component found in cannabis— that does also affect sleep. But the studies that I'm talking about today are only CBD. So there's been a few studies looking at a pretty low to moderate dose of CBD oral, so 160 milligrams a day.

It's been shown to increase total sleep time and decrease the frequency of arousal, so how many times you wake up during the middle of the night. Although within that same study, Volunteers also had much less dream recall, which could imply a change in REM sleep architecture. So, so really more, more data needed there. And interestingly, very, very low doses of CBD, about 15 milligrams a day, have been shown in one study to have the opposite effect. It's actually— it was actually associated with increased wakefulness. So I, again, you know, just real limited research in this area.

I think that possibly looking at, you know, a sweet spot of dose again with the CBD, it seems like the CBD, there is a sweet spot, whereas too low and too high of a dose, you know, they can have paradoxical effects or no effect, and there seems to be a sweet spot, and that sweet spot really needs to be established in larger randomized controlled trials. So Janet is asking in the chat if there's any studies involving children taking CBD supplements. Yes, a lot of the literature with children has to do with children that have different types of epilepsy, and so there has been some beneficial effects with CBD oral and certain types of epilepsy that have been measured. So I'm going to move on to the next question from Roy.

And Roy asks, when you discover you have vitamin D deficiency, and you want to quickly raise your vitamin D levels, can you take a very high single oral dose of vitamin D3, for example, 300,000 IUs, followed by daily maintenance low doses? Or should you limit your dose to 10,000 IUs a day to reach the same dose after 30 days? Again, this is not medical advice. I'm just going to give some surrounding information regarding this question. So the National Institute of Health has set the upper tolerable intake, safety intake of vitamin D at 4,000 IUs a day. However, taking between 7,000 and 10,000— or sorry, 7,000 and 14,000 IUs a day of vitamin D3 for 1 year has shown to be safe in patients that were vitamin D deficient at baseline. Yeah.

Higher doses can be more bioavailable, so there have been multiple studies showing this, but weekly and daily doses are also more— have been shown to be more effective at raising what are called 25-hydroxy vitamin D, which is the major precursor for the steroid hormone, vitamin D steroid hormone, that's measured in blood. So it's been much better than a monthly dose. And that's been shown, like some studies have done monthly doses of vitamin D and have had negative effects— not negative effects, but have had no effect on a certain outcome that's trying to be measured. And whereas similar studies have done looking at the same outcome have found that daily and weekly doses have been effective.

So I don't think it's— so far the data seems to suggest that monthly super high doses only once a month are not really as effective at raising serum vitamin D3 levels. But to specifically address the question of a really, really high dose like 300,000 IUs, it's important to know that there have been case reports Uh-huh. Where doses ranging from 100,000 IUs to 600,000 IUs have been reported. So doing a single dose like that can cause dangerously high levels of calcium in the blood and possibly even death. And that's obviously very rare and most people don't— you know, most physicians are not administering super, super high doses like that. Taking 10,000 IUs a day can, you know, can basically increase vitamin D levels pretty quickly, at least according to studies.

And so they— so some studies have found that vitamin D levels can double from, for example, 20 nanograms per milliliter to 40 nanograms per milliliter within the first week, and then they can double again within the next month. So that's been shown in studies where people were given 10,000 IUs a day. So I think, you know, basically the, the best thing is to get a vitamin D blood test at baseline and then start a supplementation routine and then measure again after a month. A month is about a good time frame to, to, you know, adequately raise vitamin D levels. And, um, generally speaking, most people can raise their vitamin D levels for each 1,000 IUs of vitamin D taken, that can raise blood levels between 5 and 10 nanograms per milliliter depending on the person's genetics.

There's a lot of— there's a lot of genes involved in vitamin D metabolism. Magnesium is also very important for, for, for converting both vitamin D3 into 25-hydroxy vitamin D and 25-hydroxyvitamin D into the active steroid hormone. And there's been studies showing that people that have insufficient magnesium intake, which by the way, almost half the country, half of people in the United States have an inadequate magnesium intake. Um, they— they basically ha— don't— don't make as much of the active vitamin D steroid hormone because magnesium is a cofactor that's required to basically make the active steroid hormone. So that's another really important factor with respect to vitamin D metabolism. There's a related question on vitamin D from Emily.

And Emily asks, is there an amount of sunshine you would recommend to get vitamin D, perhaps a time suggestion according to the amount of UV rays present? Is there an optimal time or is it better to put sunscreen on and take a supplement? So again, this is not a recommendation, but vitamin D production in the skin, there are many, many different factors that complicate this. And these factors basically— one of the major factors is, as Emily mentioned, you do need UVB radiation from the sun to hit the atmosphere. order to make vitamin D3 in the skin. And the time of year and the latitude at which you live regulates how much UVB radiation actually reaches the atmosphere.

In many parts of regions that are more northern, more of a northern latitude, for example, the Northeast in the United States, you know, many, many places in like the UK, Finland, you know, these Northern European countries, um, during, during fall, winter, you know, autumn, winter months, the UVB radiation is not even reaching the atmosphere. And so, um, it's, it's difficult to make vitamin D3 from sun exposure in those circumstances. Uh, now, people with fair skin can make a lot more vitamin D3 from the sun than people with more melanin pigment in their skin.

So, people with darker skin pigmentation, whether we're talking about people that originated from Africa or from South India or Southern Asia or any of the Aboriginal places in Australia, New Zealand, people with darker skin color have a natural sunscreen. Melanin is a natural sunscreen, and so it filters out UVB radiation. And so people that migrate from more equatorial regions like, you know, Africa and South Asia and South India and things like that where they're closer to the equator where this— the UVB radiation is reaching this— the atmosphere majority of the year, when they migrate to other places like Chicago, New York, Minnesota, Sweden, the UK, there becomes an issue of, you know, dark skin in combination with low UVB rays, you know, during certain periods of the year that can cause severe vitamin D deficiency in those populations.

And it's not enough to just say, go out and get sun. There's been studies, for example, in Chicago that have compared vitamin D levels and sun exposure in African Americans versus Caucasian populations. And it was found that African Americans, they were severely more deficient in vitamin D and that they required 6 to 10 times more sun exposure than, you know, fair-skinned Caucasians to make the same amount of vitamin D. And so you can imagine, you know, having to stay out in the sun 6 to 10 times longer. That's quite an effect. Uh-huh. So, um, the other thing that also regulates production of vitamin D3 in the skin is age. So as we age, we become less able to make vitamin D3 from— from the sun.

And like, for example, a 70-year-old— 70-year-old makes about a quarter of the amount of vitamin D that they used to make when they were— their former 20-year-old self. So age is another big factor as well as BMI. Because vitamin D3 is a fat-soluble vitamin, when you make vitamin D3 in the skin, it gets released into the bloodstream and it's stored in fat. So basically, you know, once it's time to release it in the bloodstream, it's less— it's about 50% less bioavailable. So that's another thing to keep in mind is BMI. I think with all that said, You know, you may read some guidelines that, you know, 15 to 20 minutes of sun exposure is enough to make vitamin D3. And I think that's a very general statement that is not applicable to pretty much the larger population.

It's applicable to a very, very, very, you know, limited population of people with, you know, age and skin color and region of where they live. I mean, all those factors are important. So I think that that is something to keep in mind. And it's a real big pet peeve of mine when I hear people say all you need to do is go out in the sun. You know, it's just way more complicated than that. We live in a modern world where people have migrated from, from, from places where their, you know, ancestors lived and where their genes were optimized. to live and move to other regions, and things happen, as I just mentioned, with the vitamin D3 deficiency in darker-skinned populations that are living in more northern latitudes.

So Nikki is asking in the chat, so vitamin D levels would rise if you lose weight as you metabolize, as you, as you, as you basically lose body fat? Yes, in theory, the, the less body fat you have, the more bioavailable vitamin D is to be released into the bloodstream. Again, that's been shown. That's been shown in studies before, and it's also something that most people don't don't discuss when they're talking about lifestyle factors that regulate vitamin D levels or that are important important for regulating vitamin D levels. BMI is also is also one that's usually kind of left out. So, Paige, the next question is from Paige, and this is sort of a big question, and there's a related question that I will tag on after we start to get into this.

But Paige asks, can you speak on the continuum of longevity versus growth factors like IGF-1, particularly in relation to exercise? When do these growth factors become detrimental? For longevity or healthspan. And there's a related question that has to do with these growth factors like IGF-1 with respect to high-protein diets as well. So for those of you that are not familiar, IGF-1, insulin growth factor-like 1, is a— it's a hormone that is— it plays a lot of important roles in normal human biology during growth and development. It's essential to grow. You know, people with genetic deficiencies in IGF-1 have stunted growth and are— have, you know, certain types of dwarfism. It also plays really important roles during adulthood. So IGF-1 is required to repair damage to muscle tissue.

It's produced locally in muscle tissue. upon exercise, and we'll talk about that in a minute. IGF-1 also crosses the blood-brain barrier, and it plays a very important role in neurogenesis, so in growing new neurons. It plays an important role in allowing already existing neurons to survive. So, it really plays an important role in brain function, particularly with respect to If you think about, you know, neurodegenerative diseases where you've got diseases of losing, you know, losing brain mass, I mean, you lose brain mass with age in general. So having a growth factor in your brain that's important for growing new neurons and allowing your neurons to survive is good. IGF-1 also has bad roles.

It is a very powerful growth factor and that means that in addition to allowing cells like neurons to survive, which you want, and also facilitating the growth of new neurons. It also can allow cells that are damaged to survive and facilitate the growth of potentially of tumors and cancer. And that's because, you know, when a cell has accumulated damage and it's enough damage that the body says, okay, I cannot repair this damage. I need to kill this cell. And if I don't kill this cell, the damage could result in potentially mutations, chromosomal breaks that could lead to cancer. And so you get activation of these death signals that become over— they're overridden by IGF-1 being around.

So the death signals aren't strong enough because IGF-1 is a stronger signal and says, no, no, Hey, you don't have to die. You can keep growing. And so that becomes a big problem with cancer promotion. IGF-1 doesn't initiate cancer. Initiation is something like a carcinogen, something— or even normal byproducts of normal metabolism like reactive oxygen species or byproducts of normal immune function, things that are produced when your immune system's activated, things like— hydrogen peroxide, hypochlorite, which is bleach. Those things, you know, damage, damage cells. That also can, can lead to potential mutations that could be oncogenic or cancer-forming. IGF-1 doesn't do that.

It just allows that damage that's already occurred to basically keep— basically allow the cell to keep surviving. The other, the other role IGF-1 plays against I would say, as a mark against longevity is that it activates the— I'm sorry, it inactivates the FOXO3 pathway. FOXO3 is what is called transcription factor. It's a gene, a master gene regulator of hundreds of genes, many of which are involved in autophagy, in stem cell production, in antioxidant production, anti-inflammatory genes. So, these are all genes that are involved in promoting longevity. And a lot of times these genes that get activated via FOXO3 are activated through types of stressors that are good like fasting or exercise or plant polyphenols can activate them as well. So those can become inhibited by too much IGF-1.

The major Lifestyle factors that regulate IGF-1 are essential amino acids that are found in dietary protein, and essential amino acids are particularly higher in in quantity in in animal protein products compared to plant. Exercise also increases IGF-1, but it does so locally in muscle tissue, and the effects that I'm talking about with Cancer promotion. Those those are things that are happening when IGF-1 is in the circulation, not not specifically in muscle tissue. You actually want IGF-1 in muscle tissue. It plays an important role in preventing muscle atrophy and repairing muscle damage, and also plays an important role in in growing new muscle. So IGF you actually want IGF-1 in in muscle tissue.

The other thing is that exercise it's itself has been shown to help basically relocalize IGF-1 that's in the circulation and go to the brain and go to the muscle tissue. So that's a really important factor when we're gonna basically talk about the role of particularly animal protein in raising IGF-1 levels and how that is associated with increased cancer mortality in in meat eaters. So there's a related question that was submitted by Justin that basically talks about, you know, that high protein diets are associated with higher IGF-1 and that impacts cancer and, you know, basically mortality. And if people are worried about just increasing muscle mass and, you know, basically maintaining muscle mass, shouldn't they just exercise rather than taking a bunch of animal protein?

So that's basically the gist of the question. And I think to kind of answer that is it's a very, very nuanced topic. And indeed, exercise is incredibly important for longevity and healthspan. And in fact, in general, high-protein diets are important for and optimal for muscle mass, but they're not necessary for muscle mass gains. If a person is doing resistance training, you know, you can really— you know, there's been some studies showing that you can get these muscle mass gains without the higher level of dietary protein intake. But again, that's still a little more nuanced, particularly when it comes to older populations.

But you know, there's been there's been a lot of studies looking at all cause mortality and cancer mortality in in meat eaters versus plant people that are getting their protein from plant sources. And you know, a few of these studies have even looked at different age populations. And so it was found that, for example, people that were age 50 to 65, if they had a higher protein intake from animal sources. They had a threefold increased cancer mortality and, um, you know, a fourfold— no, a fourfold increased cancer mortality and, and like a threefold all-cause mortality. Uh, and that was not found if the protein sources were coming from plants. Um, in that same study, if the individuals were older than 65, the opposite effect was found.

In other words, people older than 65 that had a higher protein intake from meat actually had a lower all-cause mortality and a lower cancer mortality paradoxically than, than individuals, um, you know, that were younger. And, um, you know, frailty, frailty obviously really increases as age— as you get from 65 onwards, and muscle mass is really important for lowering the frailty index. And while resistance training in many older people is recommended, you're not going to take someone that's been sedentary their entire life, particularly if they're already over 65, and get them on a resistance training program very easy. It's— that's going to be a very big challenge.

And so because there have been studies that have found that in elderly men that have not been exercising, that they lose way more muscle mass if they eat less protein compared to men that eat more protein. So I think that there's really a strong— there seems to be at least strong evidence that definitely people over the age of 65 should be increasing their protein intake. And certainly if they could add in resistance training, that would be even better. But what about these younger individuals? Further studies have been done that were even larger studies, even by the same authors of the study I just mentioned, where there is an increased cancer mortality and increased all-cause mortality with meat eating.

And a lot more confounding factors have been measured, have been taken into account, which is very, very important anytime you're doing an observational study because it can't establish causation. And there's so many potential other factors that could be responsible for the results that are being observed that are not actually the factor that's of interest. And so I've talked about this study many, many times that basically, you know, large, large populations of people, over 170,000 people, looking at protein intake from animal sources versus vegetable sources. Again, there was a higher all-cause mortality and a higher cancer mortality if you just compare those 2 populations.

But then when you do further analysis and say, okay, within that meat-eating population, let's look at people without any unhealthy lifestyle factors, which were deemed as being obese, sedentary, smoking, or excess alcohol consumption. If those individuals didn't have any of those factors, they had the exact same mortality rate as plant eaters in terms of cancer mortality and all-cause mortality. So I think the bottom line here is that observational studies are incredibly nuanced and oftentimes have to be looked at in the broader scope of things, including randomized controlled trials, which can look at biomarkers of, you know, maybe cancer risk and heart disease risk, for example. And there have been those as well.

There was a study pretty recently that analyzed 24 different randomized controlled trials showing that eating red meat every day did not influence biomarkers of cardiovascular disease risk. And I don't remember exactly the duration of each of these studies, but again, looking at the whole scope of data including observational studies, including randomized controlled trials, including animal studies that support mechanism is really important because observational studies again are really just one little dot in the whole plot, you know. And without the confounding factors oftentimes can basically lead you to a conclusion that's inaccurate.

As the case, as I just mentioned with the meat eaters, if you looked at all the unhealthy lifestyle factors, they basically, and if they didn't have any of those, they had the same mortality as the plant eaters. So really important, I think, to consider all that. And another thing is also— that's also really important is that animal studies where, for example, rodents are fed a high-protein diet, the IGF-1 does get elevated, but that does not cause cancer. Mice that are implanted when they've been transplanted with human tumor cells, so they've already got cancer, And then they're fed a high protein diet, it it's like fuel for the cancer, right?

I mean, the the cancer just you know grows you know uncontrollably, which is to be expected because you know the high protein diet increases IGF one. But it's important to distinguish those two factors: the the mice without the cancer weren't getting the cancer from the high protein diet, but the mice with the cancer that you know exacerbated the growth of it accelerated the growth of it. And we're gonna talk a little bit more about IGF-1 in a minute when we get into some of the fasting questions. But I'm gonna move on to another question which was— which had to do with something very interesting that I was not very familiar with called the inflammatory index. And the question was, how much should we trust the NIH's inflammatory index? It looks pretty thorough.

If we should trust it, should we use this to heavily influence what we eat in general? So basically, let's start with what the inflammatory index is. It was actually a tool designed by Dr. Susan Steck at the Arnold School of Health at the University of Southern Carolina. So it's not actually the NIH's inflammatory index. And it was designed to determine if a person's diet was either pro-inflammatory or anti-inflammatory. So it's, you know, and the way that it was determined to, you know, trying to determine that is by summarizing the findings of about 1,943 different studies where biomarkers of inflammation Such as IL-1 beta, IL-4, IL-6, IL-10, TNF-alpha, high-sensitivity C-reactive protein.

All these biomarkers of inflammation were measured in response to giving people certain different types of, you know, dietary food sources. And so I think it's a very interesting tool that has a lot of potential, but there's also some pros and cons. About this inflammatory index. It's very— it's got a very simple— it's simplified in terms of how it came to this index. So hopefully there'll be more accurate tools in the future. One of the cons is that it's basically a poor predictor of cancer risk. But— and another problem is that the way it determined its index was a little flawed. So for example, It looked at the inflammatory index of a food, for example, that has 90% of the studies showing a 10% increase in inflammation.

So, you have 90% of studies showing there's a 10% increase in inflammation to a certain food. That will have the same index as if there were 90% of studies showing a 50% increase in inflammation to food. So it's really looking at the summary of the studies rather than actually the effect or the change in inflammation of the food. So I think, I think that really needs to be modified with respect to the inflammatory index. But, you know, on the pro side, this is a nice start where we have a tool that does, you know, much like the glycemic index, tries to measure the glucose response to various foods. This is trying to measure the inflammatory response to certain foods. So I think it's a start. It's far from being perfect.

There— I do think there needs to be some tweaks in it, but it's nice that, that, that's being looked at in general. Okay, so I'm going to move on to the next question, which is going to go into a lot of detail. And this question was from Scott, and Scott asks, About autoimmune treatments when, when standard of care treatments fail. Again, um, really, this is not medical advice. I am not a physician. I cannot recommend any treatments for anyone with any autoimmune disease. Um, so, so the, the scientific literature that I'm going to cite right now needs to be shared with any physician for a person that wants to, uh, you know, trying sort of experimental lifestyle changes.

With that said, there's really— this is a really interesting area to me because there's been really strong evidence in 2 big areas with respect to autoimmune disease, and those areas are microbiome composition and fasting. So starting with microbiome composition, the gut microbiome is a very important regulator of immune cell types, uh, particularly immune cells that are involved in autoimmunity. So different species of bacteria in the gut will produce different types of compounds, which, um, a lot of these compounds— many of them, a majority of them— are short-chain fatty acids. And these short-chain fatty acids like butyrate, propionate, acetate.

These things can act as— they get released into the bloodstream and they act as signaling molecules to immune cells that basically determine what kind of immune cell will be formed. And a big— one of the big things these short-chain— one of the big types of immune cells that these short-chain fatty acids have been shown to regulate are what are called T regulatory cells or Tregs for short. And T regulatory cells basically are a really important immune cell that tell your immune cells whether or not your own tissue is yourself or something foreign. And when there's defects in these T regulatory cells, there can be dysfunction in immune cells, and immune cells can start to recognize your own cells, your own tissue as something that is foreign.

And so the immune cells start to attack attack its own tissue, and this can, depending on the tissue type, can sort of manifest itself as an autoimmune disease. There have been many different— so that's the sort of the mechanism with the microbiome, one of the major mechanisms, not the only one. But there have been several human and animal studies that have found that gut microbiome does play a very important role in both autoimmunity. It can be both good and bad. And so, in fact, actually using antibiotics to sort of wipe out bacteria, which antibiotics are a very blunt tool that can wipe out both beneficial or commensal bacteria but also pathogenic bacteria, which are the bad bacteria.

There's been studies in animals showing that just treating animals with various you know, types of autoimmune diseases, treating them with antibiotics can basically have a positive effect on the autoimmunity. And there's been, you know, pinpoints to certain strains of bacteria that basically in the gut can lead to the production of autoantibodies. And basically when you clear out that bacteria in the gut, the autoantibody production sort of wanes away. There's also been some studies— and I'm— by the way, I'm not saying that antibiotic treatment is a way to treat autoimmune disease. I'm just giving a proof of principle of how the gut microbiome plays a role in autoimmune disease. Antibiotic treatment has a lot of terrible long-term effects as well, right?

I mean, it's great for, you know, killing off potentially pathogenic you know, bacteria that can lead to, you know, sepsis and death and things like that. But I just sort of like want people to understand that there, there have been both animal and also human studies. So there's been some human trials, phase 3 trials, where antibiotics like minocycline have been given to people with multiple sclerosis, which is an autoimmune disease. And they're basically— it can prevent the progression of the disease by almost 30%. Wow. When this, you know, minocycline antibiotic is given prophylactically. However, as the study duration goes on, they're basically— that effect goes away and, you know, you start to sort of have a negative effect of having so much antibiotic treatment.

So the sort of bottom line here is that the gut microbiome does play a very important role in autoimmune diseases. There— there are other ways of changing the gut microbiome. For one, actually, a pilot clinical trial found that intermittent fasting for 15 days— so people— people that were actually intermittent fasting, but on the days of their fasting in this pilot study, people could eat with like up to 500 calories It's sort of like a fasting-mimicking diet almost in a way. They basically did this for 15 days. So, they were fasting for a total of 7 days and then not fasting for a total of 7 days. And there was an increase in bacterial richness in the gut microbiome in certain types of bacteria that have been shown to promote the production of T regulatory cells.

And basically, there's— this was including lactobacilli bacteria, which are commonly used in probiotics as well. Those have been shown to play a role in promoting T regulatory cell numbers through the production of short-chain fatty acids. It also enriched other bacterial species like Prevotella, which is another one that's also been shown to play a role in T regulatory cell production in the gut. Interestingly, it was also shown that fasting induced sort of its own, you know, like ketone body metabolism was happening that was regulating the micro that basically was facilitating microbiome growth as well. So I thought that was a really interesting study because fasting itself.

Has been shown to also affect autoimmunity through other mechanisms aside from the gut microbiome, which that study I just cited really focused on. But there have been other studies, a lot, a lot of studies have been done by Dr. Valter Longo and colleagues that have found either fasting, a fasting-mimicking diet, or even a ketogenic diet has been shown in animal studies and a very, very small pilot clinical study in patients with multiple sclerosis, again, an autoimmune disorder, where individuals basically after just, just 1 week of the fasting mimicking diet or, or 6 months on the ketogenic diet, so much longer period to be on the ketogenic diet versus the week of the fasting mimicking diet, they had an improvement in clinical measures.

For a variety of clinical measures for multiple sclerosis. And then animal studies sort of confirmed that the, you know, there was a lot of effects on T regulatory cells and a variety of different effects on autoimmune regulation from the fasting mimicking diet or also fasting. So other studies have found that fasting itself can basically lead to, to preferentially lead to the death of dysfunctional cells. And this seems to happen quite a bit in the immune system. So as a fast becomes more prolonged, autophagy starts to happen. And autophagy is basically clearing out damaged stuff within a cell. Yeah. But as the stressor becomes stronger, if the entire cell is actually damaged enough, the cell will die via apoptosis.

And this has been shown to occur in— definitely occur in animal studies where basically if you take a mouse and fast it for 48 hours, about 28% of the immune cells in the mouse will die off. And this activates stem cells in the blood system and the hematopoietic system where the stem cells increase by 6-fold. And this causes stem cells then to make brand new immune cells, young brand new healthy immune cells. And interestingly, Valter has shown that they make functional immune cells. So you can clear out a nonfunctional immune cell that perhaps would be— was playing a role in autoimmunity and replace it with a healthy functional immune cell that, you know, that basically is not having that autoimmune sort of defect.

But it's really, you know, those animal studies were shown to be dependent on IGF-1 levels just plummeting, going way down. And it's important to realize the translation of animal studies like that to humans There's a lot of factors to consider. So, for example, a mouse or rodent will lose 20% of their of their body weight after a 48-hour fast, whereas a human will only lose one to two percent. So it's a big difference, and it's also been shown that within that two-day period, rodents can lower their IGF-1 by 50%. Whereas it takes a human 5 days on a water on a you know of basically not eating anything to to lower their IGF-1 levels by 50%. So big differences there, and with respect to translating animal to mouse studies.

But again, there has been some pilot studies looking at fasting and the effects on autoimmune disease, like the multiple sclerosis one I just mentioned. There's also been some pilot studies. Looking at a 48-hour water fast in humans, and there was a trend towards the hematopoietic stem cell activation, like I just mentioned with the animal studies. So I think that, you know, without giving any sort of recommendation, I think that, you know, it would, you know, people with autoimmune diseases, we may find physicians start to become more familiar with this research. Feel free to share that research, please, with, with, with your physician.

And perhaps as the research becomes stronger— a lot of it's still in the preliminary phase— perhaps as it becomes more established, we'll start to find things like a fasting-mimicking diet, low-calorie diet, or even just, you know, general fasting Perhaps even ketogenic diets will start to be used in a clinical setting. That's the hope. There's a related question that I see people asking in the chat. So let me just skip down to that question real quick. And that has to do with, since we're talking about fasting and I was talking about autophagy a little bit, I know there's been, there's been quite a few questions, one from Xavier and another from Jay, I believe, asking about a few things. One, fasting duration required to activate autophagy in humans as well as biomarkers.

And also what are called these caloric restriction mimetics, or sometimes they're referred to as fasting mimetics, like resveratrol or spermidine during a fast to promote autophagy. So, so let's start off, you know, autophagy. I just, I mentioned what autophagy is. It's basically, you know, the clearing out of damaged organelles like mitochondria or other, other organelles inside of a cell, even damaged, even bits of, uh, you know, pieces of DNA floating around, or, you know, piece protein aggregates, things like that. You know, it's just clearing around all that, clearing out all that stuff that could be basically causing dysfunction. Um, and there are, there are several things that can activate autophagy.

Exercise is one, a variety of plant polyphenols that are found in coffee and tea, um, and also that are some that are found in in fruits like the skins of blueberries and grapes, resveratrol, for example. Fasting is definitely a major activator of autophagy. There is very limited evidence looking at autophagy in humans. There's one study that I like to refer to from Dr. Guido Kroemer, who I've interviewed on the podcast a few years ago. He is one of the world's experts on autophagy, and he published a preliminary clinical study where they were measuring biomarkers of fasting, which I'll talk about in a minute, that in humans to determine how— what was the soonest time point at which, you know, the biomarkers could be measured. And that time point was found to be 24 hours in a human.

Doing a water fast. That doesn't mean that autophagy isn't occurring when you're overnight fasted for 14, 16, 18 hours. Your biomarkers are only as good as the sensitivity of them. And in order to really be able to empirically measure when autophagy starts in humans, you have to have a very, very sensitive biomarker. And that just hasn't been established. I mean, we, we don't even have that, you know, those types of sensitivity biomarkers for inflammation. I mean, C-reactive protein, high sensitivity C-reactive protein. You know, my, my high sensitivity C-reactive protein comes out as 0.1. Does that mean I have no inflammation going on in my body? No, it just means that, that according to that biomarker, you know, that biomarker is very low for me. And, and it's only so sensitive.

So, so I don't— I tend to think that, that autophagy, there's a continuum of it. And, you know, enough of it, if you have— if you're having, you know, if you measure, you know, you need a certain amount or quantity of cells for autophagy to be occurring in those cells in order to detect it. So what if it's occurring in 50% of those cells at 12 hours, but you can't detect that because it's not enough cells for your measurement to detect, right? Doesn't mean that autophagy doesn't happen after a 12-hour fast. It just means that you're not detecting it. So one of the major signals for autophagy to happen is a decrease in what's called protein acetylation. And, and that biomarker that I'm referring to that was measured was protein acetylation on lysine residues in proteins.

And so, so basically, that, that was what was used to detect autophagy. And, and it, you know, it is a biomarker. There are other biomarkers that are used, the conversion of you know, ATG1, ATG2, there's— or sorry, LC3-1, LC3-2 conversion is another biomarker, but those are not really readily used in a clinical setting. So those— there's still a lot of development there in terms of the biomarker sensitivity. The reason that protein acetylation is important to realize is because That happens— acetylation, you know, is something that, you know, happens when you eat food. You make acetyl-CoA and, you know, some of that is, you know, acetyl-CoA gets used or converted and metabolized into basically acetyl groups that are used in acetylating proteins.

As well as other things, so that for that decrease to occur, there needs to be a caloric deficit. There needs to be a decrease in food intake. There are other things that can decrease protein acetylation as well. One of those things is spermidine, and another one is resveratrol. And so that sort of was the question from from a couple of individuals. We've talked quite a bit about resveratrol. Resveratrol indirectly decreases protein acetylation. Because it activates sirtuins, a group of enzymes that are histone deacetylases. So essentially, these enzymes are removing acetyl groups from proteins. So, so that's basically mimicking what happens when you are not eating food, your protein acetylation is going down. Well, another way to do that is to activate sirtuins.

Sirtuins then remove, remove these these acetyl groups from, from proteins as well. So resveratrol has been shown to activate autophagy in animal studies as well as in, in culture studies as well. Spermidine directly lowers protein acetylation. And let's talk a little bit about spermidine. So spermidine is something— it's a, it's a polyamine. It's, it's found in very high concentrations in natto. Which is the fermented soybeans that are commonly consumed in Asian countries, particularly in Japan. It basically inhibits protein acetylation and it inhibits basically the direct transfer of acetyl groups to proteins.

So, whereas sirtuins are taking the acetyl groups that have already been put on off, Spermidine stop— prevents that whole process from even happening so the seal groups don't even ever get put on. Um, it's— spermidine has been shown in animal studies or in lower organism studies of yeast and flies and also nematode worms to extend lifespan. It's extended lifespan in an autophagy-dependent manner. Um, so basically, you know, it's been shown to increase the lifespan of these lower organisms by increasing autophagy Okay. Spermidine has been shown to basically when you give dietary spermidine to mouse strains that are short-lived, so accelerated aging mouse strains, it can prolong their lifespan.

There's been some studies looking at the brain concentration of spermidine in flies and that correlates with memory capacity. There's also been some studies in mice that have the aged older animals that giving those older animals dietary spermidine can improve their heart function. It actually has been shown to enhance autophagy and specifically mitophagy, which is the clearing out of damaged mitochondria within a cell. It's been shown to do that within the hearts of mice that were given spermidine. And, you know, so mitochondria are extremely important for heart function. The heart is, is basically primarily using what's called beta oxidation as the energy source, meaning it's using fatty acids, which require— beta oxidation occurs within the mitochondria. So it's not using glucose.

And, and glucose can be used outside of the mitochondria in a process called glycolysis. That doesn't happen in the heart. The heart is using using mitochondria solely as a source of energy. So, that's been shown in animal studies in mice. And again, spermidine and resveratrol have both been shown to basically induce autophagy in basically animal rodent studies and cell cultures. So, I think That's sort of in detail, a detailed response to some of these fasting mimetics or caloric restriction mimetics as they're often referred to. Also the autophagy, when does autophagy start and the fasting duration. Again, aerobic exercise, and Hillary's mentioning— or sorry, Andrew Bennett is mentioning in the chat about aerobic exercise.

Being doing aerobic exercise fasted can induce autophagy more easily than in a fed state. There's been many studies looking at a variety of adaptations that occur specifically in mitochondria in response to exercise either in a fed or fasted state, and doing exercise in a fasted state does lead to better and more robust adaptations in general. But most of the studies that were done looking at a fed state were really high— were simple sugars mostly. So, you know, more of like a refined type of carbohydrate like toast with jam on it and things like that. Jay's asking in the chat, are there any human studies with spermidine and autophagy? Not that I'm aware of yet. Again, we really have blunt, blunt, you know, tools with respect to measuring autophagy in humans.

And I really haven't even seen very many studies looking at that. So, you know, until we sort of improve those tools of measurement, it's hard to look at autophagy in humans and whether X, Y, or Z affects autophagy. Without the actual tools to detect it. And there was also a related question with the autophagy and fasting that had to do with fasting-mimicking diet promoting autophagy. As well as basically, you know, doing doing the the water only fast and you know again I think that if we if we look at you know even IGF one levels that that go down you know it takes five days of a water fast to lower that by fifty percent you know the the The 24-hour fast that I referred to where after 24 hours autophagy was detectable in humans, that was, you know, after 24 hours of full fasting.

So it's not clear. It is my, you know, opinion that having some calories would basically slow that process, but, you know, it may still occur. It just may not occur as quickly. And you know, for some people, some people fasting is not an option, and a fasting mimicking diet is an option. And so it's you know it's it's nice to have more than one option, particularly for some people that can't do full fasting. But this is all still very preliminary work that is that needs much more you know larger studies to confirm. In order for this to really start to be translated into a clinical setting. You know, so I think that as more data comes out, we'll start to have more of that translated into a clinical setting.

But until that happens, it's still difficult to translate this to a clinical setting. And certainly, getting the information out to physicians also is another challenge. Which, which hopefully that, you know, I think Found My Fitness is one of the, you know, platforms trying to reach physicians in addition to everyone. So hopefully that helps getting the information out there with the podcasts and the variety of episodes that we put out there. And by the way, I guess also there have been some studies looking at autophagy in long-term caloric people that, that are, that have been practicing caloric restriction long-term. So for about 6 years, and there are increased markers of autophagy found in, in those individuals.

And so, so that is, that is, I would say, evidence that even a low caloric restriction diet, which is what a fasting mimicking diet is, a fasting mimicking diet is even more than what a caloric restricted restriction diet would be. But basically, you know, autophagy biomarkers have been measured in humans that have been practicing caloric restriction for 6 years or longer. With respect to exercise, there's quite a few questions in the chat about exercise increasing autophagy and, you know, what type of exercise is needed. You know, There's just really limited evidence in this field. A lot of studies were done by the late Beth Levine.

She had done a variety of studies in animals looking at autophagy, but I have yet to see really studies that have been done in humans looking at different types of exercise, you know, and how that can promote autophagy. So again, it's one of those things where we're sort of getting ahead of ourselves by making a statement like, well, autophagy does increase— sorry, exercise does increase autophagy. But we just don't really know how much exercise, how much autophagy is happening. What types of exercise? Are there some that are better than others? You know, that's the thing is, is that exercise is a metabolic— it's a type of metabolic stress like fasting. You know, exercise, you are, you are basically putting yourself in You know, your your your blood glucose levels are going down.

You're you're you're sometimes shifting into ketosis, so exercise can sort of kick you into ketosis. Something that I've, you know, measured in myself. I wear a continuous glucose monitor, and you know, exercise, you know, is very consistently. I mean, that's the one thing that it does. It you know takes your blood glucose levels and plummets them, and and that is something that. You know, this has been another question that I've seen submitted on several occasions. Are there sort of indirect markers of autophagy that we can use, you know, that are proxies of, you know, potentially some autophagy is occurring? And, you know, I think, I think, you know, blood glucose levels going down and ketone going into ketosis.

Could potentially be, be one of those markers because protein acetylation, a decrease in protein acetylation requires a decrease in glucose intake, in food intake in general, also in fatty acids. So I'm not sure that a ketogenic diet is going to induce autophagy because fatty acids can be used to make acetyl-CoA. And while that is being done, when you are in a fasted state, you're immobilizing fatty acids that are stored in adipose tissue, and those are going to be used as energy sources. If you're giving yourself more and more and more of that, you know, that's just more potential acetyl-CoA and more than acetyl groups that can be used to acetylate proteins.

So I'm not sure you could make the direct comparison of fasting versus a ketogenic diet, for example, where you're still taking in fat, you're still taking in food. Because again, one of the strong signals that's needed to activate autophagy is a decrease in protein acetylation. And so that does happen when you are exercising because you are using your— you're using up energy. And so there's less acetyl-CoA and less acetyl groups going around. So I think it's— it is possible to possibly use, you know, glucose measurements. And Nikki's asking about ketosis. Do you have to measure— can you measure— does your blood glucose go below a certain level? Is that— can you use that as a proxy for being in ketosis, or do you have to directly measure ketone levels?

And I would say that, you know, as you start to get down to 70 nanograms per deciliter, you know, you're basically, you're basically probably going into ketosis. So you might be able to use that as an indirect marker, I would, I would say. I mean, if you want to really be empirical, the best thing to do would be to measure ketone bodies. And if you were certainly doing a ketogenic diet, you would you would want to do that, directly measure that for sure. I typically, when I'm doing like my continuous glucose monitor and I sort of think I'm being, you know, shifting into ketosis, that happens when I start to go below 70. All right. I'm going to address some rapid-fire questions.

And for that, from this, this round, as well as a few from last month, since those got— those had gotten cut off last time. So Jen asks, can you share some of your high-intensity interval training workouts on the bike? I have an indoor cycle bike, and I feel like the workouts are just high intensity the entire time. Do you do Tabata style or just normal cycle class rhythm? So I have a Peloton. And I'll say, I have no affiliation with them at all whatsoever. But I find it, I really like it. Sure, there's some drawbacks. I, you know, I've heard people complaining about if you're comparing yourself to the class, you know, all the bikes are sort of calibrated differently. And, you know, potentially some other drawbacks.

But I really like the, the class, you know, being able to take the class and have that instructor there. For many, many different reasons. One is I definitely tend to work harder. I push myself harder. And I think that I'm not alone in that. You know, there's been, there's been studies showing that that happens when you're, when you have that, that group setting or that instructor setting as well. I really switch up my, my, my, my high-intensity workouts. I, you know, depending on how much time I have, I love that I can just get on the bike for 20 minutes, you know, and be very efficient. With a workout when things are really crazy, when I'm very, very busy.

I can get on there for 20 minutes and just have an amazing workout, you know, where I am, I'm just sweating up a storm and I am just pushing it. I do Tabatas. I switch it up. I do, I do a variety of different, you know, interval classes, high-intensity interval classes. You know, sometimes I do the 1-minute where there's like a 1-minute, you know, HIIT and then you follow by 1-minute recovery. Sometimes I do where it's 20-second HIIT, then a 40-second recovery. recovery, followed by a 30-second HIIT, 30-second recovery, 40-second HIIT, 30-second recovery, 50-second HIIT, 10-second recovery, and 60-second HIIT, and then a 60-second recovery. You know, so I, I just switch up my, my, my different types of, um, HIIT workouts that I do.

But, um, I use the Peloton, and the fact that they have so many classes to choose from and so many different types of HIIT, um, different instructors and stuff, I just, I just love it. I think I think it's really, really great. And I honestly am trying to get like everyone in my family, extended family, to try to, to try to get one. You know, they're a little pricey, but they're, you know, there's payment programs and stuff too. I think, you know, now more than ever too, it's really great because you can just have it in your home or in your office and just get on there and do it really quick. And it's, you know, there are times when I'm trying to make my PR. And then there are times where I'm checking it off a list where I'm just like, I gotta do this. I gotta do it today.

I gotta get my my brain drive neurotrophic factor on. You know, I gotta I gotta get that in. And and the Peloton makes it super easy because that that activation energy that you have to go over. You know, some people, you know, they have to if they have a you know a gym membership. You know, just getting themselves to go to the gym is is some of the hardest part, right? The motivation to do that. But when you have that bike right there, you know, you just. just in your house, um, it's so much easier to get over that activation energy. So I really just think it's— I just really think it's great and, um, can't speak the praises enough. Um, again, I have no affiliation with them at all.

Another rapid-fire question, uh, from Callum: Can you cover all the popular supplements known to prevent exercise-induced mitochondrial adaptations? And whether taking things like vitamin C and vitamin E on recovery days can still can inhibit these adaptations. So some of the popular supplements and over-the-counter things that people do take that have been shown to inhibit some exercise-induced adaptations are. Anti-inflammatories like NSAIDs. Part of, you know, part of the benefit of exercise is that exercise itself induces inflammation.

This, this happens, you know, within an hour after exercise, and that inflammation itself acts as a signaling mechanism to, to activate a variety of genetic pathways that are involved in in blunting inflammation, a variety of anti-inflammatory pathways that are much, much stronger than the little bit of inflammation that was generated from the exercise. And so you have a net anti-inflammatory effect. So NSAIDs can blunt that signal, and thus you're not getting some of the benefit there. Some high-dose supplemental antioxidants, particularly vitamin E, alpha-tocopherol, the alpha-tocopherol form of vitamin E in doses that are orders of magnitude really higher than the RDA. So we're talking, you know, the RDA is like 24, 25 IUs a day.

And studies have shown that 400 IUs a day can blunt some of the adaptations that occur with exercise. And again, exercise itself, much, much like the inflammation that's generated, exercise itself also creates a very Uh, transient burst of reactive oxygen species because you are— your metabolism, you're, you're working hard, your mitochondria are working hard, and so more reactive oxygen species are being produced as a consequence of that or as a result of that. And those reactive oxygen species are acting as signal— signaling molecules that activate a whole host of genetic pathways that basically are, you know, involved in Um, you know, antioxidant benefits and anti— you know, activating these antioxidant pathways.

Again, the antioxidant pathways are much, much stronger than the little bit of reactive oxygen species that's generated from the exercise, so there's an overall net antioxidant effect. But when you blunt that oxidation, or when you blunt those reactive oxygen species from being ever, you know, being able to signal out, then you basically don't get that adaptation. Vitamin C, really, there's only been— the studies that have found a negative effect on exercise-induced adaptations with vitamin C have been in combination with vitamin E. And they're generally pretty high doses, like 1,000 milligrams a day, again, in combination with vitamin E. So, I'd really like to see the vitamin C sort of teased apart from the vitamin E sort of uncoupled from that.

It's possible, you know, that taking, taking some of these supplements on recovery days, you know, like vitamin C half-life is pretty short for sure. So that, you know, probably wouldn't have an effect on inhibiting the adaptations. And taking vitamin E within RDA ranges have not been shown to inhibit or blunt these adaptations either. Other things, metformin has been shown to blunt exercise-induced adaptations in healthy individuals and also in individuals with type 2 diabetes. And resveratrol, there's been some mixed evidence of resveratrol blunting some exercise-induced adaptations with other studies showing the opposite effect, it enhanced. So it sort of seems to be dose-dependent and time-dependent as well.

So it's very possible that resveratrol may, you know, at lower doses and certainly on recovery days may not have an effect, particularly because there's been some really mixed evidence in that field. A related question, another rapid-fire from Brenda. She's talking about the genetic reports stating that some SNPs of supplemental vitamin E can be harmful. And her question is, is this all forms of vitamin E? There's many different forms. The studies referred to in the genetic report were alpha-tocopherol form, high dose, again around 400 IUs a day, and the reason for that is because taking large doses of alpha-tocopherol can blunt the activation of a variety of glutathione related genes that are enzymes that are, you know, using glutathione.

So glutathione transferase, glutathione synthase, and glutathione, these, these, you know, the glutathione pathways in the body are much, much stronger antioxidants and have more beneficial effects than supplemental vitamin E. And so people that do have SNPs in their glutathione that decrease the— decrease, um, you know, their glutathione-related enzymes. Those individuals have been shown to actually benefit from, uh, alpha-tocopherol supplementation, but individuals without those SNPs, um, which is the majority of the population, uh, have been shown to not benefit from that. Um, another rapid-fire question from Ron.

Ron's saying that he went to the International Fish Oil Standards website and to check for a good omega-3 supplement, found that Life Extension Super Omega-3 got a 5 stars but had caramel color in it for lowering oxidation levels. Um, should I be concerned about caramel color? Uh, I have not found any studies showing that caramel color is genotoxic or carcinogenic to humans at all. Question is, is there an effect on gut microbiome? There's really no studies that have addressed this and that I've seen so far. So it's not something that I'm typically currently, you know, concerned with. But, you know, so again, only future studies would tell. But so far, it seems by and large the literature says doesn't seem to show that caramel color is has a toxic effect. Effect in humans.

Another rapid-fire question was from Mia. Mia is saying that some doctors are saying firefighters should not use the sauna after a fire because the exposure to chemicals and toxins can be absorbed deeper into the body. Can you elaborate? Actually, things that are on, on subcutaneously on the skin, heat can actually make you absorb them Uh-huh. Better. They can, they can actually increase the absorption through the skin. So, um, that— there, there's definitely, uh, some science behind why a physician would recommend that. Uh, washing off, you know, if a firefighter just, you know, basically did, you know, was in a fire, um, they should absolutely wash off, uh, the— their skin, you know, in a shower. preferably with soap and stuff before, before getting in the sauna.

It's one of the reasons why I am very aware of things that are on my skin, any creams or things like that, because, you know, compounds can be absorbed better into the skin. Another quick question from Hannah. Hannah was talking about DHA from algae oil for toddlers. Is there a fish oil supplement that's better? Um, so the DHA found in algae oil is much, much lower than a DHA that you're going to find from a fish oil supplement. Um, I, I like the Pure Encapsulations, um, fish oil gummy, which is, uh, it's got 250 milligrams per gummy, and the gummy has xylitol, no sugar in it. It's very, very, very soft, um, and it's, it's what I, I give my, my son, and he really loves it. Some rapid-fire questions from last Crowdcast. Kevin, he says, what do you use for your super green smoothie now?

You mentioned changing it a while back. So I use kale, avocado, blueberries, and currant. Recently, I've been adding some egg white protein powder and collagen powder and water. I use a continuous glucose monitor. My, my blood glucose levels, I mean, the The blueberries don't even get me above 105, and then I— if I do exercise, then I immediately go— you know, immediately go down, you know, into the low 70s. So it's really not having a real big effect on my glycemic response. And the protein powder also seems to really keep my satiation down. And I think the protein powder is also having an effect on the glycemic response. There's been some studies showing that food order itself— protein, having protein a little bit before, before carbohydrates can lower the glycemic response.

Alex is asking, what are the best hygiene, care, beauty products you recommend, what you use? Are there things we should pay attention to, things like, you know, facial products and cleaning products? So I personally like to use a product called Cell Bone. Um, for my— all my face wash and cream and serums and stuff. I don't have any affiliation with any of these products that I'm mentioning, but that's what I like to use. I use Hello brand with xylitol for my toothpaste. For my deodorants, I like to use Salt Sticks or La Vanilla because they don't have any aluminum in the deodorant. And so I, I like, I prefer to use the, the deodorants without aluminum, which means no antiperspirant deodorants.

And the reason the Salt Stick is in, is good in combination with like, uh, uh, something that, a deodorant that doesn't have aluminum, uh, is because the Salt Stick really helps prevent the, the stink. Um, since, since there's no aluminum, the Salt Stick seems to really kind of fill that purpose. Fill that gap. I try to use or avoid— I try to avoid shampoos that use laurel sulfates or parabens, and I generally use 7th generation cleaning products for cleaning. That's pretty much it for this Crowdcast. I drank way too much water, and so I'm going to have to get off. I really appreciate all the questions. And I appreciate all the support. Thank you so much for all the support. I hope you guys are really enjoying these Q&As. And I look forward to, to the next one next month.

We'll be sending out the— an email reminding people to sign up. And also this Q&A again will be available on your dashboard. You can find that at foundmyfitness.com/dashboard for a replay of the video. Awesome. You can also on your dashboard download the private podcast feed if you haven't done so already. If you've already downloaded that private podcast feed, you will get a notification when this Crowdcast will be uploaded on the feed, and we will have a timeline that we post on that, that feed as well with links to some studies. And again, I'll talk to you guys soon and look forward to the next Crowdcast. Have a great rest of your weekend. Bye. Bye.