Episode 89
This podcast covers the following four topics:
✈️ Wellness Journey – Adversity
📘 Study #1 – Does increasing fat intake increase LDL
📘 Study #2 – Artificial sugars impair the gut microbiome
💊 Supplement Discussion – Ashwagandha
Lifestyle Medicine with Dr. Harris
Episode Transcript:
Dr. Richard Harris: [00:00:00] Hello, and welcome to Strive for Great Health Podcast. And today we’re going to be talking about wellness journey, two studies and our supplement discussion. That’s right. It is our November Wellness Review. Our wellness journey is going to start off talking about adversity and some adversity that we’ve had recently.
The first study is talking about something that’s really prevalent these days, insulin resistance, and actually looking at the lipid abnormalities that come with insulin resistance and how you can fix that. The second study is a really technical study, but we’re not going to get that technical. It’s looking on the impact of artificial sugar and the microbiome.
And then we’re still talking about Alpha Male X, our hormone supplement. And we’re going to be talking about one of my favorite supplements today, ashwagandha. Are you ready to boost your health EQ and IQ? Cue the music.
Join me, Dr. Richard Harris, as we strive to unlock the secrets of the human body strive for wellness strive for great health. Follow the show on iTunes, Spotify, Google, and Android.
Real quick before we get started, the Strive for Great Health Podcast is a lifestyle wellness and mindset podcast, but we can’t put everything about health, wellness, and mindset into the podcast. There’s just not enough time, it’s such a complex subject. That’s why we created our lifestyle medicine and health mindset wellness courses.
Now you may be asking, are these courses right for me? If you’re someone who wants to increase their health span, longevity, how long we live without chronic disease. If you’re someone who’s been told you have risk factors. If you’re someone that’s been told, there are some things that you need to watch out for. Some things you need to change otherwise you’re heading down a road that leads to disease, or if you’re someone who has a chronic ailment and you’re wanting a more holistic approach to fix your self, to heal yourself, then the wellness courses are for you. If you’re not willing to invest in your health. If you’re not someone who is willing to do things in a sustainable manner, if you’re someone who’s looking for a quick fix, then the courses are not for you.
The courses are designed to teach you everything that I have learned reading hundreds of studies, hours of clinical practice, years of devotion to this lifestyle medicine and the health mindset, so you can live a life full of joy and purpose. If that sounds good to you, head to theghwellness.com and click courses at the top. Now to this week’s episode.
Welcome the Strive For Great Health Podcast with your host, Dr. Richard Harris, and welcome back to one of our wellness reviews. This is our four segment episode where we cover four different things, four segments for different things. The first is our wellness journey. We’re going to be talking about adversity.
We got two studies on deck that I found really interesting, and of course you can get access to all the studies in our strive for great health podcast group. There will be a link to a Google Drive. So you have access to everything I have access to. And then finally, we’re talking about supplements and we are still talking about Alpha Male X.
We’re talking about my favorite part of Alpha Male X, and that is ashwagandha. Let’s dive right into our wellness journey adversity. Man, I’m telling you it has been a rough [00:04:00] two months. Short story of it is we moved into a new place on move in day AC wasn’t working. AC was broken, I think it was 10 times in six weeks.
It needed a new unit. It needed new wiring. There was a lightning strike about a week before we moved in, the landlord was informed of this, didn’t do anything. So we moved into a place without AC in Texas. It was 95 degrees in there on move in. And we spent six weeks fighting to try to get out of the lease.
Eventually we got out of the lease and it costs us a lot of money to do so. But it was rough. We were living out of hotels. We were living out of friend’s houses. We’re living out of suitcases in the city that we actually live in. And I’ve been through similar things on my own. I’d never been through that where I had a family, my wife and the dog, and he had just recovered from chemotherapy.
He’s cancer free now, but it was rough on everyone. And I asked myself throughout that process, instead of saying why me and feeling down and feeling out. I said, what is this teaching me, God, what are you trying to have me learn? And there was a couple of things that we learned through the process. Number one, old saying, but it’s so true.
The grass isn’t always greener .Little backstory. We moved because we wanted to get more space. But moving into this place, we got more space, but then it came with a whole bunch of problems, including a landlord that was highly suspect. We should have taken more inventory of what we had and we realized the place that we left, we love. We love the community. We love being able to walk to Discovery Green. We love being across the street from the Astro’s stadium. We love that our dog loved walking around the area. And we should have taken more inventory on what we had instead of what we wanted. And I think sometimes we always look towards acquiring new things or look at deficiencies instead of looking at what is going great in our life.
And what do we have that brings us joy and brings us blessings because if we had, we wouldn’t have moved. The other thing is what we’ve talked about on this podcast. The difference between joy and happiness. I was not happy moving into that place, but I was still joyful. I really tried to find the time to strengthen my gratitude practice and focus on the things in my life that were still going right.
We were still making business moves, acquiring assets. We still were able to spend time together. No one was hurt or injured or anything like that. There was so much to still be joyful for. Even though my happiness, my emotions were not the best at that point in time, there was a lot of frustration, a lot of anger.
I still tried to find things to be joyful, and it really helped me to find the joy in life. ,No matter the situation. Third thing is ask God, I didn’t spend enough time talking to God about the move, about what was right for us and where he wanted us to be. We came back to the place that we left. We moved into a bigger apartment and talking to my wife, I said that, you know, I don’t know why, but I really feel like for whatever reason, God is calling us to be at 500 Crawford where we live.
And she said, you know what, I feel the exact same way. And if we had asked God what he wanted us to do, instead of doing what we wanted, it would have saved us some pain some time and some heart ache. The fourth thing is being clear on what you want and the trade-offs. Again, we looked at what we didn’t have. We didn’t look at what we had and we didn’t spend enough time thinking about, okay, if we move out of this area, what’s the trade off.
Even moving inside the city, it changes the routes of going to the gym. Changes going to the grocery store, changes how we get to and from work. Changes our access to a lot of the old places that we used [00:08:00] to hang out. There’s a lot that changes and it may seem small, but even subtle shifts in your routine can have dramatic impact.
And we talk about that in our wellness courses. And so we didn’t spend enough time thinking about what will happen with these subtle trade-offs and how will it affect us. And the fifth thing that I learned is, we need to have more communication between me and my wife about really what it is we want out of the roof that’s over our heads. We both had different wants and needs sets in that regard. And we didn’t spend enough time talking about that and coming to a consensus on something that we can both be comfortable with going forward. So that was a major source of adversity in our lives and something that we had to overcome, but we moved through it.
We were joyful. We praised God and it taught us some valuable lessons. And like we always say, there is no such thing as failure. We didn’t fail in this situation. We just learned some things, some things that we’re going to apply next time we move. And it really helped us get clear on our value set. And what’s important to us.
Let’s move into study number one. The title of this study is effects of a low carbohydrate diet on insulin resistant dyslipoproteinemia, a randomized controlled feeding trial. All right. I probably just had a bunch of jibberish to a lot of you. What does that actually mean? Well, we’re looking at something that’s very popular these days, which are low carbohydrate nutrition plans and then insulin resistant dyslipoproteinemia.
What is it? We’ve talked about insulin resistance. We have two episodes on it, the why we get sick episode with Dr. Ben Bikman. I highly suggest you check that out. And then we have our own episode. Well, this is abnormalities in the lipid profile, your HDL, your LDL, your cholesterol, your triglycerides caused by insulin resistance, which is the number one or number two cause of abnormalities in a lipid profile in a cholesterol profile.
And what they looked at was they wanted to do a feeding trial, meaning they orchestrated a certain nutrition plan and then they had different groups and they wanted to see the effect on the marker of insulin resistance as it correlates to our lipid panel. And before we go into this, if you haven’t listened to our truth about cholesterol podcast, stop and listen to that podcast first, because there’s going to be some terms that you may not understand or be familiar with, but if you’ve listened to that podcast, we’re going to go over a lot of stuff that we talked about in that podcast. Now, in the introduction, the authors talk about replacing saturated fat by processed carbohydrates does not reduce cardiovascular disease risk, and we’ve actually seen this and they can actually have adverse effects like increasing triglycerides, lowering HDL, and increasing insulin resistance.
We’ve talked about this on the podcast before. The low fat movement caused way more harm. Rates of obesity and diabetes have skyrocketed since that. We’ve replaced good whole fats with processed carbohydrates, and that’s a big problem. Now, low carbohydrate plans are becoming more popular keto, low carb plans becoming more popular, but there is concern that you can increase LDL with these plans and increase cardiovascular disease risk. Now we’ve talked about this before, LDL is a surrogate. The problem is that LDL does not capture cardiovascular disease risk from insulin resistant, dislipoproteinemia.
If you have insulin resistance and it’s causing your lipids to be abnormal. The LDL by itself is not a good marker. In fact, what I do and what a lot of practitioners do when we’re evaluating cardiovascular disease risk is we check multiple biomarkers. I need to know what your triglycerides are doing.
I need to know your particle [00:12:00] counts. I need to know your homocysteine. I need to know your CRP, your markers of inflammation. There are multiple things that I get together, I aggregate, and then that gives me an overall cardiovascular disease risk from a perspective of inflammation and insulin resistance. Two of the biggest factors in cardiovascular disease.
This study wanted to compare low, moderate, and high carbohydrate intake with varying amounts of saturated fat on something called LPIR. We talked about LPIR before LPIR is a metabolic marker that captures the effect of insulin resistance and insulin sensitivity on lipoproteins your LDL, your HDL, your triglycerides, all of that.
And the good news about LPIR. It’s very well associated with type two diabetes, premature heart disease, it’s a very robust marker for looking at someone’s actual cardiovascular risk specifically when it comes to lipoproteins in the setting of insulin sensitivity or insulin resistance. This is something I recommend that everyone gets checked.
We talked about that in the cholesterol podcast, that NMR lipoprofile, it gives you an LPIR. In this study and the methods, what they did was they had a run-in phase where energy intake was restricted to promote a 10 to 14% weight loss over nine to 10 weeks. And this is really interesting because it’s actually mimicking a real world scenario where if someone has cardiovascular disease risk factors, obesity, you’d want to put them on a calorie restricted plan to help them lose unwanted body fat.
And then they were saying, okay, in the setting of calorie restriction where people lost weight, and then we’re going to put them on the test plans, which is mimicking a real-world scenario to see what happens with their LDL. And then once they achieve this, they were randomly assigned to low, moderate, or high carbohydrate groups.
The test phase was 20 weeks and energy intake was adjusted to maintain the weight that they had lost within two kilograms either way. Now an interesting effect that they notice was total energy expenditure was higher by about 200 kilocalories in the low versus high carbohydrate plan. And this correlates with previous research.
One of the reasons why we like low carbohydrate plans for fat loss is because previous evidence shows that for every about 10% reduction in carbohydrates you intake, you burn about 50 more calories per day. So it enhances your metabolism just by decreasing your carbohydrate intake. They also measured lipoprotein a, lipoprotein, a levels are very robust and correlating with risk of cardiovascular disease and they measured the requisite six variables for LPIR and they did this pre weight loss at the start of the trial.
And at the end phase. And the participants were 18 to 65 years old with a BMI greater than 25. And they excluded those with known cardiovascular disease or diabetes. We’ll talk about that in the discussion portion, the run-in diet, it was hypo caloric, but they had 45% carbs, 35% fat, 25% protein. The other reason you want to do this run-in phase was you wanted to make sure that when you started the intervention that everyone was on the same page as far as nutritional intake. So that way you’d know that your result at the end of the study were more valid. That it wasn’t what people were doing before the study. So you standardize them before the study and then you put them on the test interventions.
The test interventions had 20% protein intake that was standardized and they varied carbs and fat. The low carb was 20% carbs, 60% fat. The moderate was 40 40, and the high [00:16:00] carb was 60% carbs, 20% fat and saturated fat was standardized at 35% of total fat for each diet, but the amount of energy varied based upon the composition. Saturated fat accounted for 21% of total energy in the low carb, 14% in moderate, 7% in high carb. And they even showed you what percentage of each. So mono unsaturated fat was 25%, 16 and eight poly and saturated was 11, nine and five. And that’s low carb, moderate high-carb .Dietary fiber was more in the high carb.
You’d expect that with more complex carbohydrate, so it was 25, 30, 35, which is still pretty good fiber intake. That’s more fiber than most people get. Added sugar relative to the total carbohydrates was controlled at 15% and they even measured the glycemic loads of the food. Glycemic load was 28 grams, 80 grams and 135 grams per 2000 calories.
Glycemic load, I can’t remember if this is something we’ve talked about on the podcast or not, but glycemic load is a way to describe the quality and quantity of carbohydrate in food. There is an equation to calculate glycaemic load. It is the glycemic index times the amount of carbohydrate per serving divided by a thousand.
Most often, this is reported per a hundred grams and this study 500 grams was the amount they reported. They reported 2000 calories. There’s four calories per gram in carbohydrates, that’s 500 grams. To convert it over to the way it’s normally reported. You’d have to divide by five. So the glycemic load was 5.6, 16, and 27.
Why did I do that? Because in general, it’s thought that a high-glycemic load is above 20, 11 to 19 is moderate and less than 10 is low. So if you break it down by the conventional thought on glycaemic load, it aligns quite nicely with the low, medium and high carbohydrate groups. Glycaemic index is the ability of a food to raise blood sugars when compared to straight glucose.
So for example, a glycemic index of 50 means the food has a 50% of the response to the same amount of carbohydrate in glucose. If it’s 116, it means it has 116% response to the same amount of carbohydrate in glucose, but just straight glucose. In the outcomes, they measured everything for LPIR, including the particle counts, HDL-P, LDL-P.
They measured the subfractions, small HDL, small LDL, large HDL, large lDL. We’ve talked about the differences between those in the cholesterol podcast. They also measured HS-CRP, which is a marker of inflammation, and they also did IL-6 to measure for inflammation. One of the things they looked at was pretty cool.
Was they looked at high molecular weight adiponectin. We may have mentioned adiponectin on the podcast before, high molecular weight adiponectin is the most biologically active form. They also measured total adiponectin just to be more well-rounded. Adiponectin is a hormone and it has a lot of different effects in the body.
It increases beta-oxidation, which is fat burning. Improves glucose uptake and muscles and actually fat tissue. Now what adiponectin does is it actually regulates the healthy expansion of fat tissue. We’ve talked about this before, even people who are lean marathon runners have like 40,000 calories of fat stored on their body.
We need fat stores and adiponectin make sure that we’re storing fat in a healthy way that we’re burning fat in a healthy way. It improves insulin sensitivity. It suppresses liver glucose production. So you’re not adding [00:20:00] more glucose into the body. One of the things your body’s really, really good at is making sugar really, really good at making sugar.
And this makes sure that we don’t make more sugar when we don’t need it. It also activates AMP kinase, which is the major energy sensor in the cells and by doing so it improves whole body energy expenditure. Adiponectin works with leptin and the brain to signal satiety and hunger.
So it’s part of that leptin, ghrelin axis. Adiponectin levels are usually lower in obesity and in people who have CVD risk factors and the levels get high in associated auto-immune diseases. Things you can do to improve adiponectin levels, exercise, fasting, increased fat intake, low carbohydrate tumeric, ginger, capsaicin. Capsaicin is what makes chili peppers and things like that hot. Outcomes, now, what was really cool was the study had a 90% retention rate. That’s a very high retention rate, 148 people finished the study, meaning that even the low carb plan was able to be done by the majority of people. The weight loss and the running phase was about 10 and a half percent from the start to the end, then it was about 0.55 kilograms.
At the beginning, the pre the LPIR had strong correlations with the six variables related to insulin resistance. Now, the changes in the subgroups, it correlated with the carbohydrate intake. And the low carb group, they decreased their LPIR by about 5.3. That’s significant, the moderate group had about no change in the LPIR, increased by 3.6 in the high carb group.
Usually LPIR is on a scale of zero to a hundred. So a change of five is pretty significant there. The biggest change was in large and very large triglyceride part of. Which were lower in the low carb group. You want your particles to be large. We talked about that in the cholesterol podcast, large HDL was higher for the low carb group.
These are good things. Other components did not change that much between the groups, including particle sizes and small LDL concentration. The LPA decreased in the low carb group by 14.7, there was no change in the other groups that is significant because LPA is a really big risk factor, correlates very well with cardiovascular disease changes in triglycerides and HDL favored the low carb group compared to the high carb group, but it wasn’t significant. LDL increased in all groups without any change in either group. And then the adiponectin was significantly higher, the high molecular weight in the low carb group, 42.9 versus about 27 and the other groups. And the measures of inflammation didn’t change. Blood pressure didn’t change per group.
All groups saw lower inflammation and slightly lower blood pressure from the pre to the end, from start to end, they did. Remember pre was before the run-in start was when that started the test interventions, and the end was the end of the study. In the discussion observational studies linking high saturated fat intake with LDL and cardiovascular disease mortality have a caveat. They also have relatively high carbohydrate intake. So people were eating high carb, high saturated, fat. And usually when that happens, that means you’re eating a lot of processed food. A lot of red herrings there. This study found the carbohydrate restriction had benefits on LPIR without adverse effects on LDL, LDL-P, inflammation or blood pressure.
We also saw an increase adiponectin. All of these things are [00:24:00] beneficial, LPA decreased, which is a major risk factor for atherosclerosis ,heart disease, deposition of plaque in arteries, strokes. And it’s pretty funny, this next part, because this goes against the scientific statement by the national lipid association, the national lipid association says lifestyle therapy, including diet and physical exercise has no significant effect on LPA concentrations.
So I went over to the NLAs website. Didn’t clearly see their sponsors, gave him a call, said, Hey, who are your sponsors? They said, oh, you need to go here to our industry council. We’re sponsored by them. We get dues and other things. I said, okay, who pays for your CME and your grants? Wouldn’t tell me, looked at their industry council, all big pharma.
I tried to ask more questions, got the run around. This group who is sponsored by big pharma is telling people that lifestyle interventions don’t matter when that’s not what the data says, chase the money people. It’s comical. It’s sad, but it’s so comical because this is what’s happening where, oh, you know what you eat and exercise has no control over your cholesterol levels.
OK, thanks big pharma. But of course, statins and lipitor and all that stuff. That’s the way to go for everybody. Anyway, these results in this trial are consistent with other trials showing improvement in triglycerides, blood glucose, blood pressure, liver fat and body weight with low-carb plans. A lot of good evidence starting to come out on this. Low carb plans can sometimes increase LDL and people who are genetically predisposed.
This is why we recommend that whenever you start these, you get your lipid panel checked, and if it’s off, get an NMR to look further. And that way you can see if it’s really something dangerous or not. Also what can happen is with rapid weight loss, you can see an increase in LDL because the body is chewing through the fat cells and all those things that were in the fat cells are now in the blood.
And it can take some time for that to go down as that weight loss, the rate plateaus out. Even at higher LDL concentration. Insulin sensitivity and low inflammation levels is associated with relatively low cardiovascular disease risk. And this is something that’s very important. This is why you cannot just check one biomarker.
If you just check the LDL and say, oh, you’re at high risk for that. That is not true. You have to look at these other things. And one of the quick and dirty ways that you can check this is your HDL to total cholesterol ratio. Or you can take a look at your HDL and triglycerides. If your triglycerides are low and your HDL is high, that’s a sign of insulin sensitivity.
Typically we see that you have low inflammation levels and that is a relatively low cardiovascular disease risk. That’s not my opinion. That’s clinical data. One study showed that insulin resistance leading to abnormal blood lipids, dyslipoproteinemia, compared to LDL alone was a stronger biomarker risk for early onset CVD in women.
That’s important because what we just said, if you just look at the LDL, you’re missing things. Another modeling study concluded that insulin resistance contribute to a greater portion of cardiovascular disease risk than LDL in 20 to 30 year olds. And this is so important because insulin resistance is not being diagnosed accurately. It’s not being told the impact by most physicians to their patients. It’s something that if your hemoglobin A1C, your fasting glucose is off your doctor’s probably going to tell you not anything about it until you’re diabetic. And then you’re going to wonder how all of a sudden you became [00:28:00] diabetic when you’ve been insulin resistant for awhile.
The strengths of the study, they did not have extreme calorie restriction. They had a high retention rate, they had a large sample size for a feeding study. They had a long duration, which was enough and actually exceeded the time necessary for steady state LDL. Meaning with these changes in nutrition, it can take some time three months, maybe even up to six months for your LDL to normalize.
Most of the time, it’s within three months. And this was a 20 week study, plenty of time. And then they control for protein and body weight. And they also did a clinically relevant study because they mimicked weight loss at the beginning, which is a first-line therapy for CVD risk reduction. The limitations, the population was middle aged, people typically had low LDL overall. So you can’t generalize these results to older people, more high risk or people doing keto. Cause it wasn’t a ketogenic type feeding study.
Study number two, and this study is technical. So we’re gonna kind of breeze through this so I can give you the high level important information.
Study two is called inhibitory effects of artificial sweeteners on bacterial quorum sensing. Overview. What did this study look at? It looked at one of our least favorite things, artificial sweeteners, and it looked at its effect on the ability of bacteria to talk to each other. In the introduction, bacterial communities talk to each other through a sophisticated mechanism called quorum sensing.
It’s how bacteria cells talk to each other over distance. Quorum sensing enables bacteria to interact and adjust their gene expression based upon population density. Most gram negative, there’s two types of bacteria, gram-negative, gram-positive use a system called AHL and we’re going to refer to it as AHL going forward because the actual technical term is N Acyl Homoserine Lactone. Yeah science!
Right? We have all of these big fancy words. Thank goodness for abbreviations. Now what happens is these bacterial cells will release this and it diffuses out into the local environment and the concentration will increase as the population of the bacteria increase. So the signal increases as population density increases.
And once there’s a certain level, what happens is they bind to receptors in the bacterial cells and they activate a group of receptors called LuxR receptors, and this changes gene expression to initiate behaviors, beneficial to the entire bacterial community. This is pretty cool stuff. So what happens is once they reach a certain level, the bacteria will accumulate enough of these products from the other bacteria, the other same bacteria in the group.
And then they’ll start to do things to move as a community. That’s why it’s called quorum sensing. And this will create things like biofilms, enzymes, and then on the bad bacteria, they can create toxins through this, but it also affects motility,. The bacteria in our system don’t just sit there, they move, they have ways to move.
And a lot of that requires gene expression and changes in proteins. The gram-positive bacteria use other peptides, other proteins. There’s also a universal signal auto inducer family, meaning there’s another signaling system that is universal throughout the bacteria. A particular type of AHL molecule called 3-OxoC12:2 HSL.
We’re going to say HSL is associated with normobiosis and bowel health. Normobiosis means normal bacterial community. It’s the opposite of dysbiosis. Go check out our dysbiosis podcast. If you haven’t listened to it. But what we know is inflammatory bowel disorders have lower levels of this HSL molecule and it corresponds to a reduction in Firmicutes species, which are beneficial to [00:32:00] us and an increase in lactobacilli compared to controls.
Even lactobacillus different species can be beneficial, but in the right ratio, if we have too many lactobacilli and not enough Firmicutes, that leads to problems. This molecule itself, the HSL is linked to normobiosis. It’s also linked to an anti-inflammatory effect. Rat studies show deleterious effects of artificial sweeteners on metabolic health.
Human studies are conflicting, but some show alterations in gut microbiome that could enhance metabolic disease. This study was done to look at AHL communication due to sweetners. What they did was they use an E. coli bacteria specifically tagged to look for changes in these molecules. Basically what would happen is they use fluorescense.
If the AHL was there, it would cause light to literally show up and they could quantify based upon how much light, how much AHL was there. Low levels of light mean that there’s just residual background of HSL or AHL. And then that would increase based upon increasing levels.
They also wanted it to look and see if the sweeteners were inhibiting growth directly, and then they looked at motility and changes in other quorum sensing molecules. In the results, what they did was they hypothesized that athletes may have the highest consumption of artificial sugars due to sports supplements, they are everywhere.
That’s why I use NutraBio they’re all natural products because they don’t have artificial sugars. And they looked at several products containing at least one artificial sugar. And these products significantly decreased light signals in the bacteria relative to the controls, meaning there was decreased levels of these AHL molecules, meaning that it was impaired quorum sensing.
Then they use pure sweeteners, aspartame, saccharin, sucralose, ACE-K, advantame neotame and they wanted to look at these. Well only aspartame, sucralose, and saccharin had that inhibitory effect on the quorum sensing and all of those sports drinks had at least one of those. The growth plates showed that the sweeteners were not killing the bacteria.
So it wasn’t that mechanism. And they wanted to go and look for the mechanism. And what the mechanism actually was is that the sweeteners decreased the solubility of the HSL receptor LasR. What this means is that this sweeteners bound to the receptor and pulled it out of circulation. It’s like when you’re at a dance and you’re looking for a dance partner, you’re not going to go up to someone who’s already dancing with someone, that person is removed from the available dance partners.
The artificial sugars we’re removing dance partners. And that way the receptor could not bind to the HSL. Next, they looked at motility, the ability of the bacteria to move and the three sweeteners inhibited motility activities. That’s very important because that means that the bacteria can’t move based upon concentration gradients or moving towards nutrients or away from things bad for them a whole host of the issues that can happen with impaired motility. In the discussion, this study found that aspartame, sucralose, and saccharin inhibited quorum, sensing by disrupting that AHL network. They also found disruptions in other quorum sensing circuits by saccharin and sucralose.
The authors also talked about how inflammatory bowel disease is associated with lower HSL levels, decrease in Firmicutes and Bacteroidetes species, which are important for the production of vitamins important for our digestion suppressing pathogens. In fact, the Firmicutes make butyrate, we’ve talked about butyrate, one of our favorite molecules here.
Anti-inflammatory good [00:36:00] for the gut. One of the Firmicutes species prausnitzii works by inhibiting NF-KB the master switch for inflammation and stimulating interleukin eight. Overall is an anti-inflammatory mechanism. And we’ve talked about this before, how our gut bacteria can either fight inflammation or cause inflammation.
The sad thing is the amount of products containing artificial sugars have quadrupled over the years, they’re everywhere. And the authors suggest that increasing artificial sugar intake could dampen the beneficial effects of the gut microbiome. This is something that we’re studying a lot. Something that every single time I look at the research, more and more bad news is coming out about artificial sugars.
That’s why we stay away from them. We use Stevia, we use Monkfruit. We use erythritol. That’s pretty much about it. And then if we want to sweeten something up, we use honey real local, honey, doesn’t take that much cause it’s super sweet. And then we use cinnamon too, or nutmeg.
In the supplement discussion. We’re talking about ashwagandha today because ashwagandha is part of our Alpha Male X supplement. Our hormone supplement for men. It works very well. I take it, it helped me out a lot when my testosterone levels dropped because I was working nights The active ingredient in ashwagandha, the plant comes from many different components.
There’s alkaloids, there’s saponins, there’s lactones. All of these are what we think caused the beneficial effect. Now, what does it do? When you see ashwagandha, people will say adaptogen. What adaptogens do is they help our body with resilience. They help us physiologically deal with mental and physical stress.
And this has been shown in people that ashwagandha supplementation reduces stress and anxiety it is part of a lot of products that are for mental health. You’ll see adaptogens in these products. My favorite is a product called emotional wellness, it’s what I carry in my e-store. It does this probably through binding to GABA receptors.
GABA is our major rest and relaxation brain chemical Something that’s really cool is it prevents stress increase dopamine receptor increase. Remember, we’ve talked about on the podcast that when you get stressed, you’ll stress eat, especially processed foods because processed foods give you a dopamine surge, and that helps cut the stress.
Well, if you’re taking ashwagandha, you won’t get that dopamine receptor increase and you won’t go after motivational behaviors that are bad for you. Like stress eating. It also preventsa stress cause release of cortisol, something we’ve talked about so many times before on the podcast. This is one of the reasons why I love ashwagandha, because it helps in so many different ways with dealing with stress.
And then on top of that there’s data that shows that it enhances serotonin transmission. The ability of serotonin one of our happy neurochemicals or happy brain chemicals to do its job. Ashwagandha also helps normalize thyroid function in people who have underperforming thyroids. You’ll see it in a lot of the high-end thyroid supplements or people who have thyroid issues will take it. There’s data showing it lowers TSH levels increases T3 and T4, meaning that if your thyroid is low, it is helping to balance your thyroid hormones.
There’s data showing that it increases lean muscle mass. It increases the testosterone to cortisol ratio. That’s very important because testosterone and cortisol share the same precursor. If you are chronically stressed, you’re going to make more cortisol. Your testosterone levels are going to drop.
Ashwagandha is anti-inflammatory and helps regulate blood sugars. There’s some in vitro data, meaning cell study data, showing that it increases uptake of glucose into fat cells and muscle cells and it may prevent the ability to [00:40:00] digest glucose in the intestines. So you just poop it out more. It functions as an antioxidant and animal studies, it’s been shown to reduce blood pressure by causing relaxation of the arteries.
It has some immunomodulatory effects. Now, if it’s pro or anti it’s seems to vary. So the data is conflicting there. We just know that it does modulate the immune system, but sometimes it boosts, sometimes it helps tone down. Animal and human studies with ashwagandha show improve memory, it may help restore the normal connections between our nerve cells.
It may increase the ends of the nerve cells, the axons, their density, and increase peripheral myelin connections, myelin sheath. Myelin is a substance made of fats that coats the axons, the ends of our neurons. And it is why signals can transmit so fast from your nervous system. It’s why, if I think about bending my thumb, I can do it almost instantaneously.
Multiple sclerosis is a disease where the myelin sheaths start to get attacked by the body. And that’s why you have all these nervous system issues with multiple sclerosis and also in laboratory data it inhibits cancer cells. Is it safe? Orally, very well tolerated. There’ve been reports of diarrhea or stomach upset, nausea, vomiting.
Rarely extremely rare, in fact, there’s only five reports and it’s liver injury, and that’s usually been in the higher doses above a thousand milligram daily. Doses up to a thousand have been very well tolerated. I usually split it up into two doses. So 500 milligrams in one, 500 milligrams in another. I usually have people start taking it at night because of its relaxing effect.
It can make you feel tired. And I start with 250, usually.. Most products contain between 1.5% and 5% withanolides. That’s the active ingredient. A lot of the high-end products you’ll typically see within that range. Some products claim to have like 32%. I don’t believe it at all, but if it’s in that 1.5 to 5%, that’s typically the range that you’ll see.
All right. Well, this has been our November wellness review. I hope you guys found it educational and informative per usual. Thank you guys for listening. I really appreciate you taking time out of your day to invest in your health. It means a lot to me, and it means a lot to my family. So thank you. And God bless.
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