Dr. Dan Harper: Can you hear me?
Mike Mutzel: Yeah, you’re good. Dr. Harper, so what we’re going to do – I just made you presenter so that we can make sure that everything is working properly.
Dr. Dan Harper: Okay.
Mike Mutzel: There you go. Perfect. Looking good. If we want to kick it off with the video, how are you going to…
Dr. Dan Harper: I’m just going to put this screen up right now before they can come in on it, and then after the introduction, I’m going to say a few words, and then I will go to the video and kind of talk my way through the short version of it, not the long version of it, and then come back to the presentation.
Mike Mutzel: Perfect.
Cory Adams: Okay, cool.
Mike Mutzel: That sounds good. I’m just going to leave this special. I’m just going to take it back really quick to Dr. Harper, and just leave this special screen going so people can see that. I want to make sure that everyone’s up to speed on that, and then we’ll pass it by to you to do the introduction and get this thing going.
Dr. Dan Harper: Okay. That’s good.
Mike Mutzel: Yeah, we have some new products, too. I mean, I know you inquired in the last week because it was gone, and stuff like that. But this new OmegaPure900, that’s really a…
Cory Adams: Yeah, we haven’t been able to talk about that yet, Dr. Dan.
Dr. Dan Harper: I’ve heard about it in Dr. Perlmutter’s conferences. I saw the stuff is coming out.
Cory Adams: Yeah, that is true.
Mike Mutzel: Nice. Yeah, that will be exciting. We’ll talk a little bit about it at the end, but the short and sweet of it – it’s ultra-concentrated and one of the cleanest omega-3 products in the market. This new IFOS certification; it’s really cool.
Dr. Dan Harper: Your 780 was fabulous.
Mike Mutzel: Yeah. So, this can be 782.0, and it’s only I think a dollar more retail, or wholesale. Right in there. So, that would be really nice.
Thanks so much for joining us everyone. It’s Mike Mutzel, Bettina Newman and Cory Adams here. We just want to make sure that you have access to this special announcement that you have to get off before we end the official webinar. So, you want to write down this code here. I’ll scroll my screen down so you can see it. It’s the date today – SP-WEB-110613. It’s a really new product that we’ll mention tonight, and I’m going to pass it over here to Dr. Harper. Cory Adams, our functional medicine consultant here can do a quick introduction on Dr. Harper. Cory, you’re welcome to take over.
Cory Adams: Thanks. Dr. Harper has been over 30 years as a medical doctor. His current practice is in Solana Beach in Southern California, close to San Diego. He has a very unique background with extensive practice in emergency and trauma, family medicine, and what’s probably most impressive is his extensive background in preventative medicine. He truly is one of the most passionate and hardworking individuals I have ever been associated with, so without further ado, Dr. Dan Harper.
Dr. Dan Harper: I’d like to take a minute to show you a video that has really impressed me. Dr. Jeffrey Bland was presenting this at one time; it’s called “The Inner Life of a Cell.” I usually show this to my patients the first time they come in, so they can understand the physiology that we’re talking about. You’re going to see a white cell coming down the lumen of an artery. We’re going to be talking about arteries in the heart today. These cells are communicating with the capillary or the cells on the outside of this endothelium and communicating with those little things. This is the surface of the white cell. The omega-3s here with the lipid raft, and there are insulin receptors or neurotransmitter receptors, and they activate things; they go down into the cell. We’re seeing the skeletal network of the cell. We’re going to go down inside the cell because the messages that are imparted on the cell membranes from things in the environment will describe either a good response, a not-so-good response, or really ugly – the good, bad, and the ugly. These are some of the networking that will push out and come in the actin fibers. This is a cleaving enzyme; it’s a remodeling of the actin. These are microtubules that are coming from the centromeres to the outside that will transport things to the outside and bring things in; when they’re done, they fall apart. This is my hero. This is the motor protein that is bringing the vesicle of the things that were collected in the endoplasmic reticulum and come to the surface. This, that you see there, is the inside of membrane; it will fuse and it will dump out the hormones, the proteins, or put new receptors on the surface. These are particles; these are the messenger RNAs that will transcribe on the DNA, according to the French, crucial factors that were activated out there. Now, you see ribosomes coming up, and they’re going to be translating various proteins or enzymes that will have an effect inside the cell. This one’s being carried to the mitochondria to help with the Kreb’s Cycle, or it could be gathered up as a hormone or some other enzyme that would be transported in this vesicles later on to carry to the outside, to be released to the cell. Here we have a motor protein coming up carrying this large vesicle, the proteins or the chemicals that have been generated by the cells to bring this to benefit the rest of the body. As it comes out, you saw the endoplasmic reticulum there. Now, this vesicle is merging, and we have new receptors. This could be pitocin receptors that the uterus is ready to go into labor. This could be a receptor for insulin if you just had a meal, so that more glucose could go in. But here, you see the cell receptors, and they’re communicating and receiving things in the environment – different messages. This could be a cyto thing, a cytocrine response. Here’s the white cell is receiving messages from the surface of the lining, and it’s changing; it’s shifting from a monocyte into a macrophage; it’s releasing a metallo matrix proteins sliding in there to go into, in this case, it could be the lumen of the artery. So, this is a response to an environment. This could have been in response to the heart, and what was going on in the environment around there, so that fat or these white cells are going after the small dense lipoproteins that we need to deal with.
Let me get into my slide presentation. Slow down a little bit; take a deep breath.
Mike Mutzel: Yeah, take a breath. Dr. Harper, great job by the way. Sorry, I don’t mean to interrupt to you. You did a fantastic job. I know that’s a lot to memorize. I really commend you for that video interpretation. Thank you so much. That was great.
Dr. Dan Harper: I’m supposed to make some disclaimers, so that you can see this. This is sort of like the insurance agent that his 62nd program and then at the end, you’re going to talk about, “This is Xymogen…” That’s what I have to do here for the disclaimer. I have to disclose that I am a very satisfied Xymogen customer, but I am not an employee. I do not own any stock in the company. I will receive compensation for my time talking to you today. I have used many products from other nutraceuticals companies; many of them are not anymore near as good as Xymogen. I’ll also mention some techniques and other laboratory studies that are not recommended or endorsed by the Xymogen Company, and I do not receive compensation from any of them. And I’m sorry, there are no CMEs for this presentation, but we’ll have to work on that in the future.
I’m trying to talk about the leading cause of death in the United States, and ultimately, the world, which is cardiovascular disease. No. 2 is cancer. We know that all chronic diseases have inflammation as their base, so we need to try to deal with that inflammation, where it’s coming from. We do not need to consider cholesterol the enemy; that’s a myth that’s been going on since the invention of the stat drug. Cholesterol is our friend. It is in 10-30% of our brain. Our brain is 75% fat; I think that’s why they call us fat heads. Anyway, the cholesterol is used to make vitamin D3 in our body. It is used to make our sex hormones, our stress hormones, adrenal hormones. It makes our CoQ10 in our Kreb’s Cycle, so we can make adenosine triphosphate or ATP for the energy or the vitality or our body electric that we need. It is not the enemy. Please never consider the cholesterol to be the enemy. I’m probably preaching the choir; you guys know this. So, I’ll move on.
A 3rd of our cardiovascular disease is autoimmune in nature. This is something that in 1940, they didn’t even know autoimmunity was around, and now then, it is so common, there’s 50 million people in the United States that have autoimmune diseases, and once you get one, you’ll get multiple ones. But every autoimmune disease contribute, has a higher instance of cardiovascular disease, heart attack or stroke, than people who do not have autoimmune disease. So, watch out for autoimmune conditions. It’s under-recognized, but needs to be addressed very quickly. Complications of autoimmune disease are the No. 3 killers, are No. 3 cause of death in the world today. So, we want to try to stop that.
I keep an eye on the PubMed articles and, I want to show you something else that has happened. They’ve been saying the LDL has been in the LAD, but if you read this article, LDL does not cause inflammation. It is the remnant cholesterol, not the LDL or the small dense LDL that is a problem; the remnants, not the LDL itself. LDL carries triglycerides to the mitochondria, the muscle, to make energy. So, we need to recognize that this is not the enemy. We need to rethink things. Here is the gut associated lymphoid tissue; this is where 70% of our immune system comes from. Our immune system is what initiates the inflammation in our body. Here is a dendritic cell, an antigen-presenting cell, and it’s sending up a little bit, sort of like a proboscis or a periscope up. I don’t know what happened here. We’ll try to…
Mike Mutzel: Sometimes, the animations don’t come through in the PowerPoint on the webinar for some reason.
Dr. Dan Harper: Okay. I think we got it here. Anyway, the proboscis coming through here at the end of the end of the presenting cell, he’s sampling what food we took in, what bacteria’s here, what chemicals are there, and he’s going to make a decision. He’s going to bring it back inside here. This is the antigen-presenting cell down here, the dendritic cell, and it brings the little proboscis back and it takes it to the major histocompatibility complex 2 and decides, “Is this friend or foe?” Years and years ago, our grandparents gave to us our DNA with the information of who is friend and who is stranger. And if this is something our immune system’s never seen before, it says, “Help… Stranger, stranger… Help, help…” It reacts with a response to try to deal with that stranger, or if it’s something friendly, it will give a better cytokine or a better response in there. This particular company I love, it’s Research and Development Systems; it’s RNDsystems.com. They will send you incredible charts and little cheap things that explain what a TNF-alpha is, and how it’s used and how it’s produced, and stuff, so that if you’re wanting to look at that particular card, it’s like a little flash card, and they have hundreds of self-little flash cards for all these little cytokines and things where you don’t look like a dummy when you’re trying to talk to your patients when something has come in that’s gotten all these weird alphabets on it. Anyway, this makes a decision, and you can see that if it makes mostly interleukin-6, it’s going to go up and activate the memory cells and plasma cells and will make antibodies. If it makes interleukin-4, it will make a Th2, an antibacterial response. If it makes mostly interleukin-12, it’s going to go in the Th1 cell response – anti-cancer, anti-viral. If it makes interleukin-2, it’s going to mostly do a Treg. This guy sits on top of the teeter-totter. This is T1 go down, and then lifts it up and pushes T2 down, and just sits there going back and forth letting them do their little seesaw thing. But, there are several different forms of autoimmunity, many of them I wasn’t even aware of a year ago. There is a Th9 that if you have an interleukin-4, but transforming growth factor beta, that kicks that dude up into an autoimmune that attacks the lungs – really bad emphysema, certain types of asthma. If you have this transforming growth factor beta with the interleukin-6, it goes to a Th22. We’ve seen this arises eczema – all kinds of autoimmune skin diseases – pemphigus. Here is mostly predominantly transforming growth factor beta, and it goes into a Th17. All these others – whenever you went into a Th1, it produced the interleukin Tn; whenever you went into a Th2, it produces an interleukin Tn in the end; or Th9, interleukin tn; Th22, an interleukin Tn. All the interleukin Tn comes down the immune system, and it has the dendritic cells reregulate things. There is no interleukin Tn on the Th17. It’s going to keep chasing this tail until that little tiger becomes butter in the Sambo story. So, we need to take and recognize we have to stop Th17, and the marker for that is on the Singulex test – it’s called the “Interleukin-17A.” So, when you see that dude, you really need to start working with your autoimmune stuff, and one of my favorite ways to doing that is elevating my D3 and changing the food that is a problem.
This comes from Dr. Sanger’s work, and these are the enterotypes of the human gut microbes. Remember that little proboscis went up and talked to the bacteria in the gut? Well, if he talked to a guy called “bacteroides,” which are your acidophilus and your bifido factor, they gave him good sound council. They said, “Okay. Let’s wait a while. We’ll see how this thing goes. I think he’s friends and we’ll be alright.” So like a national council advisor to the president, and they say, “Let’s just watch it and see.” But if you do the prevotella, the prevotella is going to advise autoimmunity; it’s going to say, “I hear there’s terrorist in Ohio, let’s just noop the heck out of the whole state and we’ll get rid of the terrorist,” not taking account you’re destroying your own self. And so, prevotella is not a really good guy to have.
This is ruminococcus, and he has the opinion that, “Well, it’s time to incur a big stick, and we’ve walked enough. Let’s start using the big stick.” It causes a lot of inflammation, and you have an increased risk of stroke and heart attack. This was confirmed by the Danish studies and some of the other studies in Japan. They call their bacteroides something else, I mean the ruminococcus something else, but Medimetrics tool is giving you prevotella and bacteroides levels. They haven’t gotten ruminococcus; they’re going to start doing that, but if you see a predominant prevotella, you’ve got somebody that’s having some symptoms, you might want to do an autoimmune work up because this bacteria is giving them unwise council to the immune system that’s located in the gut. Also, when you set foods that are made from Monsanto; Monsanto foods have been hybridized. It’s an F2. It’s not GMO I’m talking about. I’m talking about hybridization. The F2 allows the seed to be planted once, but if you plant it again, it won’t grow. We have never had F2 seeds before like this, and so, what used to be good over in Russia in the Baltics from the ancestors when they come over here and they start eating Monsanto F2 hybrid food; it’s a foreign protein, and it is going to be a major problem, that’s why we’re getting so many gluten reactions to everything that Monsanto has touched, but even the soy has been hybridized and they’re beginning to hybridize our rice. And so, we need to be careful with hybridization. I’d like to use a company called “Singulex,” and you can call the national headquarters there and they will have a rep contact you. They draw some really exciting labs that show the amount of inflammation and the risk of cardiovascular disease and how much inflammation is in your system. The dyslipidemia and particularly, with the sdLDL, and they actually calculate the LDL, instead of just a measure thing, and so you can be able to use this and find out what your real remnant cholesterol is and the risk of that going on. They have other metabolic contributors, too – heart disease that I don’t find in a regular chem panel. The nice thing about this is they would accept whatever the insurance pays. I don’t care what kind of insurance it is; if they don’t pay anything, they will accept it. So, my patients are paying no co-pay; nothing out of pocket, and all this goes to work with their deductible. So, it’s an incredible value for my client. They don’t mind having it done. In fact, they like to come in and have me go. You can repeat it every three months; it’s covered by Medicare. There’s no reason that I can see not to have it done. This company – their flagship is the high sensitivity, their ultrasensitive high-definition cardiac troponin-l. In the emergency room, when somebody came in with a heart attack, I know that the cardiac troponin-I is the only thing that is not made by the liver and muscle or influenced by the kidneys, and so that is the only marker I would look at, and if it was over a certain level, I would diagnose someone a heart attack. Well, this is 1000th step level, and it can begin to see changes early on. They found out that if you had above a 30, where a heart attack is diagnosed at a thousand. If you had above a 30, sometime in the next 10 years, you are 8.53 times more likely to have a heart attack or stroke than if you had something less than 10.
The NT-proBNP, we know about congestive heart failure. I use this as a marker of mitochondria function. If this is seen in my patients with chronic fatigue or fibromyalgia, their mitochondria are not working well. It will be in the yellow zone between 130 and 200, not enough to be diagnosed as congestive heart failure. When I improve their mitochondria, it drops down into the green zone, down around 50 or 70, so I use this to follow my fatigue patients and things. Interleukin 6 – it makes the antibodies. Interleukin-17 – the autoimmune antibodies.
Tumor necrosis factor-alpha – major inflammation – and when you’re trying to follow cancer, this is a thing that makes cancer grows really fast because it will kick in Nuclear Factor-KappaBeta, and your lymphoma is out of sight. They used to do vascular endothelial growth factor; it’s on hold for now because there were too many people getting positive. Well, when you exercise and you develop more cells, this thing was going up, but it was freaking amount thinking they’re about ready to have a cancer or heart attack or something. So, they’re going to have to get some values for people who are active or growing.
Cystatin C is another muscle. We know about the Lp-PLA2 and the risk of active plaque formation and vulnerable plaque about to rupture. High-sensitivity C-reactive protein, which is a marker of inflammation whenever your body comes in contact with the phosphocholine and the cell membrane of gram-positive and gram-negatives, candida and certain grains. So, if you have an elevated C-reactive protein, I look first for self-infection then I ask them, “What are you eating?”
Homocysteine – having to do with methylation. Vitamin B12, folic acid – also, those are methylation things.
The dyslipidemia – I focus on the sdLDL. I don’t care that much about the other things. It’s not cholesterol, it’s not LDL the body has made. I want the little guy that’s getting into the enema of the artery that’s causing the plaque, and that’s the sdLDL, and then I look at other things on the page. They try to cluster this way. I also cross-cluster; I want to show that to you just a moment with that.
The Singulex has so much there that if you just look at one thing and try to develop a protocol or you try to treat one symptom, you’re going to miss the whole thing. You need to lump everything into a basket, and start taking quite your history and looking at all your labs and your finding. You try to put them together with the one diagnosis. You don’t want to have 400 different diagnoses. If you want to try to find out the underlying path of physiology, not just treat the symptom with the drug.
So, as I look in PubMed for inflammation and autoimmunity as related to heart disease, I found 24,000 publications, and these are things that on that Singulex test relate to that.
Here’s more information concerning inflammation on heart failure. High-sensitivity C-reactive protein – 1.25 more likely to have congestive failure than somebody who’s in the normal range. The tumor necrosis factor-alpha is 1.83, and the interleukin-6 is 1.61 times more likely to have that, and the same thing applies to instance of stroke and heart attack, and other inflammatory problems.
Metabolic syndrome – there’s 33,000 plus.
Osteopenia, osteoporosis associated with heart disease – 6,000 plus.
Methylation issues – almost 4,000.
So, all these markers are giving us the idea… Here are people who have chronic fatigue, fibromyalgia – 900 articles – with increased risk of heart attack or heart disease and stroke in people who have chronic fatigue, fibromyalgia. We got to get these mitochondria working again. And so, when we look at the cardiovascular risk again, you look at the plaque, you look at the vulnerable myocardium and the vulnerable blood, and begin to see. You can use various labs to look at the – are there some genetic weaknesses or some SNPs that are contributing to this? Do they have active expression of genes, message to RNA that is being produced? Do they have chemoattractants and adhesion molecules and a high number of things that they’re ready to have a heart attack? If you find that high, you need to intervene very quickly. So, there are many different ways of evaluating it, but whatever you do, don’t fall in the trap of looking at the LDL and thinking that’s going to stop the problem because with all of these studies, lowering the LDL to below 70 and even lower did not decrease the risk of a cardiovascular more than 25%. They’re saying something else is going on here – what is it? And they begin to find out it is not the LDL, and so the American Heart Association is going to have some guidelines coming out in the next few months. They’re very confusing; they really don’t know what they’re shooting at because it’s not a like a statin drug that can lower the LDL to a certain level. They don’t know what the problem is, but they do know that this thing called the “remnant cholesterol” is their enemy, and it’s not the LDL or the cholesterol like they’ve been saying.
Here is an artery. Here is the gut. People eat different fries, and they consume this, and it gets absorbed. That fat is chylomicrons. They go through the lymphatics, they drop off some of the triglycerides at the muscles or the fat, have a remnant cholesterol. They go into this superior vena cava to the liver. The liver takes them, translates them into very low-density lipoproteins. These carries the triglycerides to the exercising muscles or to the fats, becomes intermediate density lipoproteins that go to the muscles. They then become LDL, and every stop that they come to, they hit an LDL receptor and they drop triglycerides into the muscle, and it can be used to make ATP in the mitochondria. This will continue until it becomes nothing or, if it’s not a real good particle, it would become sdLDL; that will go to the liver and make a large VLDL, which only delivers its messager to adipose tissue; it does not go to the muscle. These large particles – large VLDL and large IDL – are not able to dock at the muscle LDL receptors. What is left after dumping off the fat is this sdLDL, and this has the ability to slide into through the lumen of the artery and to the intima, and then the white cells are going to send it there just like we saw in “The Inner Life of the Cell,” that monocyte shifting gears, become a macrophage, it could have been chasing one of these sdLDL particles, as well as a microbe into this and starting some warfare. High fructose corn syrup raises the sdLDL higher than any other food. White sugars will raise it, and the flours will raise it. Those are the things in our foods that are causing these LDL to be a problem. Eat eggs, eat lean meat; do not be afraid of cholesterol, but watch out for the processed foods – it’s killing us.
Mike Mutzel: Dr. Harper, really quick. I think that point is so important that you just said. Do you mind just going over the VLDL differences between the large and small? Just one more time so that it really sinks in for everyone.
Dr. Dan Harper: Okay. The body brings in chylomicrons. These huge molecules have cholesterol in the triglycerides, mostly triglycerides. This is the way the fats are absorbed and mycelized, and it goes through the lymphatics. As it pulls out triglycerides at the LPL or your lipoprotein lipase interactions, it becomes smaller and smaller, and the remnant chylomicron goes to the liver. The liver then processes these things either into a very good, very low-density lipoprotein, which is a large molecule mostly; it’s like 80% triglycerides, and this goes around and docks on the LDL receptors of the muscles and other tissues, hopefully mostly muscle, and lets the triglycerides go out and that triglycerides then is used to make ATP in the mitochondria; it burns the fat, especially if you’ve got the L-carnitine to encourage that, those types of things will take place in the muscle. As it gets smaller, it becomes an intermediate-density, a little bit smaller IL, but the really dense ones are these low-density LDL, and it’s a nice size particle, but it’s not so small that it can go into the artery lumen and cause issues, and it will actually once it dumps the triglycerides, it mostly becomes cholesterol and can go into the artery as good cholesterol and can even actually help out the HDL that’s in there. Most of it will go back to the liver and be put together by your hepatic lipase, your acetyl-CoA thinks and it will process a good guy, but when you start eating bad foods, it brings in these sdLDLs. When an sdLDL is coupled in with your VLDL, it’s too large, it would not attach to the skeletal muscles anymore, and it will only go to fat tissue. So, when you’re eating sugar – high fructose corn syrup, white flours, white rice, even a good grain that is ground into a flour that is really strongly processed – it is going to cause this sdLDL to be formed and you end up with really non-functional lipids of all different sizes, and they’re only going to put the triglycerides into the adipose tissues, and it will not go into the muscles. You’ll start wasting your own muscle to produce amino acids to be used in your mitochondria. You will start trying to burn simple carb that you can get that, but your body quickly turns those carbs into fats. 70% of your cholesterol comes from your carbohydrate you ingest, not from your eggs. Eggs will never (unless you get really sick eggs) give you a bad cholesterol. So, we’re wanting to know that our foods, the types of foods we eat, aren’t what was killing us. Dr. Triffon, who is our lipidology specialist down here in Southern California, he’s head of the Scripps Integrative Cardiology. He says that remnant cholesterol can be calculated by taking a non-fasting total cholesterol, and taking away the HDL measured and the LDL that’s measured in anything that is still over 30 is significant. When it gets to above 40 – yikes – because there could only be a few of those big boys, the VLDLs, and a few of the IDLs, and that most of what you’re going to see in a high number is the sdLDL. I’ll show you something in just a minute on the measurements of the ApoB and the LDL where you’re getting the idea of when you got some free load and sdLDLs or some IDLs that shouldn’t be there. Now, look at that. But he’s saying that only the sdLDL can enter the endothelium of the arteries to form intimal plaque, and that’s what we need to be looking at. This sdL are responsible for causing the dysfunctional VLDL and IDL, and it cause it to deposit only in the adiposites and not in your muscle cell mitochondria. Is that okay so far, Mike?
Mike Mutzel: That’s fantastic. I just think it’s so huge because a lot of practitioners, Dr. Harper, as you may know, are still running standardized lipid testing – just standardized free Wald, or estimated or calculated LDLs – and I really like how that illustration showed the different phenotypes or flavors, and different LDL particles, and drives on the point, and you really need – practitioners should really be doing advanced testing. Look at these bad things because the behavior is so different physiologically.
Dr. Dan Harper: Exactly. I do not ever look at the cholesterol and triglycerides that comes in from LabCorp. I just say, “Well, I’m glad your cholesterol’s high. Dr. Perlmutter, in his talk a couple of weeks ago, says that people who have high cholesterols – they live years longer and better health. 50% are more decreased in Parkinson’s, Alzheimer’s, dementia, ALS, multiple sclerosis.” It’s not the fat that’s hurting us; it’s the inflammation. You have to have good cholesterol or you’re going to have consequences in your health. And so, when he sent that home and said, “You should see the New England Journal of Medicine. The article in February 25th 2013, they stopped the 10-year study on the high-carb, low-fat diet versus the Mediterranean diet because 30% increased death rate in the people with the low-fat diet versus the good-fat in the Mediterranean diet. They stopped the study 4.8 years early because it was killing people. And you got to realize, maybe Atkins wasn’t so stupid except he did say he ate a bunch of bad oils, and I don’t want to agree with that, but the Mediterranean diet with good fats gives good life.”
Now, here’s the sdLDL. Up here are the red cells going in the lumen of vessel, and here’s your endothelium. This sdLDL has the ability to slide right through it so small. When he gets there, he likes to get oxidized. You know – if you’re going to go to bar, get a little something and get a little high here. When he does that, he creates a chemoattractant that is going to attract some monocytes, and these monocytes smell it – you know a little white cell that’s going down the artery he saw, he was smelling things out and he stopped, he smelled it, and he got stuck in that piece of molecule and he changed, he went through and became a macrophage, a pacman, and he’s going to gobble up this oxidized sdLDL, and he’s going to make foam cells – and some of these foam cells become necrotic, some of them get larger, and they become all tangled up, they set up inflammation fibrosis – you get some smooth muscle cells coming in there, you’re going to get some new blood vessel forming that are going to have to take place; some of these cells, they begin to rapture, and that attracts more macrophages that are going to have to come in there and devour them, and these particular macrophages, the ABC is actually the ATP binding complex A1 and G1, they’re activated to devour these dead macrophages that have all the foam cells in there, and so you get more swelling in there, like a pus in a boil, and you begin to bulge and then suddenly, this plaque becomes very friable because of the action of this necrosing foam cells, and you get this plaque rapture that blocks this. Well, with all bad stories, there’s a hero. And here’s my hero – HDL3. Now, HDL3 will not work if you do not have peroxidase-1, and this paroxidase-1 is deficient, and people who react very poorly to insecticides, and the reason why they react poorly to pesticides is the HDL can’t stop the inflammation that’s going on, the oxidized stress that the pesticides cause inside the intima of the cells. There are different SNPs that you can use to look at to see do they have a weakness in that, so if things are not healing, this is one of the things you can look at – this particular single nucleotide polymorphism genetic weakness. So, HDL3 stops the oxidative process; it takes and stops the release of chemoattractant; it goes up there and will actually interfere with the monocytes trying to sneak inside, they’ll say, “No, no, no. Everything’s fine. Just go down the way. You don’t have to come inside.” And then it will produce nitric oxide, so that you didn’t have oxygen coming in; you have vasodilation, you have better blood flow. Good things happen whenever you release the endothelial nitric oxide. And then it takes and it begins to help activate this ABCA1 and G3, so that you can become to produce large amounts of the HDL2B, which is the dump truck that carries the cholesterol back to the liver, and you begin reverse cholesterol transport, so you can take the cholesterol out of here and reassemble it as a sex hormone (You know guys like their testosterone; women like their estrogen for some strange reason.), and it begins to help. I also like to use something that’s called endothelial compliance testing that is just as accurate as coronary artery catheterization. First I need to show you the endothelial, or the luminal damage. You can have major, major oxidation foam cells and reactions here in this lumen before you even begin to start getting any narrowing, and that’s why an exercise stress test will not show this. Even at cardiac cath, this center guy is going to look normal, and that’s the reason why over 70% of the MIs had less than 50% stenosis. Many of them had less than 10%. Only 14% had any type of significant stenosis associated with MI. And so looking for stenosis is not the answer. 90% of the women have no stenosis; it’s the friable plaque underneath here. So, you need to be looking for markers of endothelial dysfunction that are going on. Your Lp-PLA2 – you need to be looking at your inflammatory markers; you need to be looking at the chemoattractants and things – your lipid peroxidase and things. Or, you will miss it in women if you’re just going by stenosis. Now, there is a company called “Pathway Genomics” in San Diego that will do several of the single nucleotide polymorphisms or the genetic weaknesses. Since 30% is genes and 70% environment, so I focus on prevention – environmental stuff – but they can show you, the genetic weaknesses tell you who needs to be on a good-fat diet, who needs to be off this freebie carbs, and I think that’s everybody. It will tell you the ones who are going to make a lot of LDL and the ones that won’t make HDL. It’s going to tell you about the ApoB, and it’s going to tell you about the ApoE. It’s going to tell you a whole lot of stuff; there are over a hundred different markers this company identifies that will set your risk. It also has panels concerning how do you process your various drugs; if you take Plavix, is it going to kill you after a few doses; if you take a statin drug, are you going to end up rhabdomyolysis and kidney failure, or congestive failure or Alzheimer’s because you’re using a statin drug. All of these cytochrome P-450 pathways are revealed in these particular testings, but I want to focus on the endothelial lining right now because this is where the action’s at; I use this is a marker for vascular disease. Now, the Singulex Company is coming out with endothelial-1 test, and that is going to be showing when the endothelial cells are under stress and they’re sheer, and there’s an obnoxious thing going on, this is made; this will activate the production of nitric oxide if you have the right things in place. If you don’t have the ability to make nitric oxide because something is wrong with your nitric oxide synthase or there’s too much inflammation, this is a marker of bad things happening; this causes vasoconstriction; this causes weakening of the intima if it’s not dealt with appropriately.
So, I love to use endothelial compliance testing, so that you can look at the reactive hyperemia index of a person. When you have them sitting down in your office, you can rent this machine very reasonably. The patient pays for the probe. Insurance companies cover this test; Medicare covers this. You put one probe on one finger and another probe on a different hand, and then blow up the cough for five minutes, let it go, and the artery should respond very nicely. You have a controlled arm to see where things are; if it does not respond in that fashion, then you got endothelial compliance issues. This particular machine can also – you hold it a little bit longer and it will show you dysautonomia if you’re trying to document that for someone who has disabilities or you’re trying to figure out why somebody’s sympathetic dominance is there all the time and they have no parasympathetic. It could be a result of dysautonomia, and you can document it with this particular machine.
Here is a good response. Look at how much it opens up. If it does not go up to 1.67 times larger than this, you got an issue. If it stays flat like that, guess who’s going to have poor outcomes very, very soon. And so, to improve the endothelial compliance, I use omega-3s, methylation support because you need a methyl group to convert arginine to nitric oxide. You can support it with arginine. This is why the NO Max ER when it was given to South Carolina and Baler’s students athletes, they have a 325% increase in their endurance, in their tracking, basketball, football. You wonder where those guys came from nowhere to national prominence – I think it has to do a lot with this NO Max ER because it allows for more blood circulation, they can keep getting oxygen and they can get glucose to their mitochondria, their muscles, and they can start continue to make ATP and not hit the wall. You can use DioVasc; this has been fabulous; the diosmin that’s in there will take and stabilize the endothelial lining of both arteries and things – works very well on varicose veins, hemorrhoids, spider angiomas. I have a lady who had mycoplasma; she developed these little angiomas all over these blood vessels (look like cherry angiomas all over); I put them on this and they disappeared.
Magnesium for vasodilatation. Antioxidants add in the mitochondrial support for the endothelial cells to continue to function.
Now, Mayo did a study where they looked at people baseline. They did the Framingham Risk Score where they looked at high blood pressure, diabetes, smoking, obesity, and high lipids – those are their five factors that they say that’s going to kill you and something’s wrong here. More of them, the more I hear the high sinner. They did an EndoPAT test to see endothelial brachial compliance. Those people who had no risk factors in the normal endothelial compliance test, their risk of hospitalization within the next seven years was only about 10%. The people that have poor endothelial compliance test – look at that – three times the number of hospital admissions. Here are people who had high-risk factors. Here’s the one that had a normal endothelial compliance with high-risk factors – he only doubled. But here, these guys are five times higher. They had poor risk factors and poor endothelial compliance, and the only people who died during this seven-year study were those who have endothelial dysfunction. The risk factors did not predict the risk of dying the way that this endothelial compliance did. So, here are the markers – high sensitivity C-reactive protein increased the risk for cardiovascular death, it’s 1.73 fold; NT-proBNP, which is marker of (I call it) mitochondrial dysfunction, they call it congestive heart failure risk – 5.67 fold increase; and here’s Cardiac Troponin-I, the flagship of Singulex, 8.53 more likelihood chance of them dying within the next 10 years if these things are not addressed and changed. So, this is what one of those tests look like, and here is a lady, who several months before, her cardiac troponin-I was normal, but her CPAP did not work for two nights, and look, she’s beginning to have cardiac strain. I have people coming in the thousands in their cardiac troponin, I put them on a CPAP for sleep apnea, and it returns to normal with a matter of months. I also warn people that the FDA requires this company to put a little red box – “Oh, it’s dangerous. Stop,” – with the B12 of over, I think, is 1,200 or so – no, it’s 946. They say that’s dangerous, but B12 is a good thing; if you have too much, you‘ll just pee it out, but it is a brain stabilizer, neuro stabilizer, It helps make energy, it helps detox, so I would say it should be two gold stars and that’s why I drew that in there. Here was her risk – during this period of time, she wasn’t sleeping; she was raiding the refrigerator and eating a bunch of junk food, and went from 25 to 48.
So, I have to put this disclaimer here saying that the supplements I’ll mention here they do not cure, they do not anything except make money for Xymogen, the practitioners who are ordering them, but I find them to help my patients so I use them.
Here’s a study of a lady. She’s been complaining of joint pains, digestive issues (that we talked about the gut and inflammation), focus issues, and when you have a leaky gut, you also have a leaky brain and fatigue. Her BMI was slightly elevated. She didn’t know she had fibromyalgia until I poked on her 18 points. You could see her Heberden’s nodules. She had white mucous all of her tongue, and on question, there were other symptoms of candida. Her NT-proBNP was elevated; I believe it was from the mycotoxins of the candida suppressing the mitochondria. She had evidence of autoimmunity so I drew an ANA, and it was elevated – goes along with the connective tissue stuff. TNF-alpha was elevated; she had some evidence that there were some things going on inside the lumen. Elevated cholesterol and ApoB. Now then, the LDL and ApoB – this ratio I want you to look at – if you have a good ratio – apoB is the limousine driver that takes LDL around to the different receptors on the mitochondria fat, and this apoB should have 40% more LDL than he has numbers, so this is a good ratio; if you see less LDL in there, the LDL is being pushed out by a large number of sdLDL or something else that shouldn’t be in there. This ApoB 100 pulls around your VLDL, your IDL, and the LDL – it’s the chauffer of those guys, and he should about 40% more than he has numbers or whatever you want to look at it to be a correct value; if it’s not that ratio, something’s going on. In her, I diagnosed some autoimmune disorder and I consider fibromyalgia a type of autoimmunity, and osteoarthritis a type of autoimmunity. She had candida and hyperlipidemia. We treated her with Candicidal 3x a day; we gave her the EPA/DHA; put her in some vitamin D3 because D3 levels above 80 in the blood will stop autoimmunity; I put her on some good probiotics; I used another company’s SKRM to control some of the inflammation in the joints; I did some oxidative therapy; and a friend, Sean Berger, taught me the minor autoheme, which really knocks down antinuclear antibodies within a matter of two to three months to negative; I used some cytokine homeopathics from Guna, and some homeopathics knowing that the candida, when you got a 1M, it’s deep, deep, deep embedded in the DNA effects and a mycotoxin inhibitor do that for three weeks – and she became totally pain-free and the next ANA four weeks later, was negative. Here are her labs with those values that were showed earlier. The first set is the last one and these are the most recent ones. I have to tell you that between here and here close the cortisol going up from 8.42 to 22. Her dog had to have a hip surgery, and her poor little dog grow things in her body crazy. The calcium came out because of the inflammation – the cortisol – because of the stress. Everything started shooting up and she started snacking carb, comfort food, and had the problems. Like I say, I believe the candida released mycotoxins, shut down her mitochondria that were getting much better. This has become normal in the most recent test. The autoimmunity was there with the Th17, some type of inflammation, lumen may be some plaque forming, there are gold stars again, and the dyslipidemia from the stress.
Another lady came in – fatigue, shortness of breath. Remember if you don’t deal with the fatigue, there is an increased risk of myocardial advance. She had an S4 gallop. She had a III/VI murmur of mitral regurgitation. ECHO did confirm she was in diastolic congestive failure, which goes along with fibromyalgia and chronic fatigue and mitochondrial dysfunction. She had a liver that was tender and a centimeter below the right costal margin, which I thought was more than right side of the congestive failure. She had poor capillary filling, and I was concerned that she have some Raynaud's or something that has impacted her as her capillaries work, but there was no cyanosis or edema, no ascites, but her parathyroid hormone was elevated but she had a normal calcium, so I wasn’t worried about parathyroid adenoma, though I have discovered five adenomas I did not suspect and I would never find them without this test. Her ferritin level was high, and I know that ferritin is released from the cells when there is a fear of virus infections and things. Insulin level was elevated, and the NT-proBNP. She was in obvious congestive failure. So, I put these things in my mind and I looked at these things. The liver enzymes were elevated, and so I was wondering – is this infection or just fatty liver from insulin resistance? When I drew the titers, I did a hepatitis C panel, E and B, EB (Epstein Barr) and C and B, and she came back positive for both Epstein Barr and hep C. I obtained history about blood transfusion 10 years earlier prior to hysterectomy, and in the early 2000 Gen-Probe went to the American Red Cross and asked, “Can we have some of your blood that you’ve tested for your IgG titers to hep C?” They said, “Sure.” They took 200 units – 30% of them were positive to the DNA PCR to hep C, and it was negative to the IgG titers they were using, so we changed things. Anyone who has a transfusion 10 years or more, you might want to suspect hepatitis C if they have elevated enzymes. What we did – we put her on the OmegaPure; alpha-lipoic acid because that really cleans up the liver, stops a lot of neuropathy and helps with the mitochondria function; CoQ10 for the heart function and mitochondria; Cardiogenics; Mitochondria Support; treat her with a form of energy that we use, a microcurrent frequency specific that really work for the viruses, the liver fibrosis and inflammation, and done a marvelous job ahead two patients that were on the list for transplants that got the machine and they have cancelled the need for transplant and the liver enzymes are normal with this. She got enrolled in the Gideon GS7977, a hepatitis C antiviral trial, which unlike the interferon ribavirin studies, there was a 10% fatality rate with those guys and only 10% long-term results. These guys – they’re five of them out there now – are getting anywhere from 75 to 95% cure rates. I mean cure allegedly – they don’t have any remission or relapse on.
Another patient – this is probably my most dreaded person I have to work with. He does not take his supplements. He will not exercise. He does not do anything I ask him, but because the test was free, this dude came in a lab about to be drawn. We see some vascular endothelial growth factor elevation, and he was having a lot of gum issues. He was beginning an exercise program because he thought he might be a little overweight. Homocysteine was up so we got the 5-methyltetrahydrofolate reductase alleles and his C677T allele is messed up that leads to high homocysteine. His lipids were elevated up, and his sdLDL was up because he believed that eating gluten-free you can have the white gluten-free flour, and it didn’t work. He also was having insulin resistance and hemoglobin A1C that was up to 5.9. I looked at those things and here he is. His mother has diabetes; his sister has diabetes; both of them are insulin-dependent. The sister has undergone a renal/pancreatic transplant. All of his aunts, his grandmothers, have died of diabetes, and he just thought it was an ex-chromosome thing. Wise don’t get this, and so he ignored it until this came down. So, when he was handed the diagnosis of metabolic syndrome, our early metabolic syndrome with insulin resistance with an increased risk of cardiovascular advance, he got off his gluten-free diet, he started his OmegaPure, he got his NiaVasc, he got his methylated folic acid, decreased his carbs and ate a Mediterranean diet, had a 20-pound weight loss, and I sure am feeling better right now; this was me. So, I was not motivated to do anything until I saw that. That’s what I’m saying – use your labs to verify what you suspect; use your labs to motivate people; and use the follow-up labs to show them that what they’re doing is working.
So, they want me to go through here and show you some of the supplements here that might be useful for you. I use the ALAmax; this is the best thing for peripheral neuropathy that I have, taking twice a day; also, it’s the only thing that neutralizes mycotoxin exposures. Dr. Sherry Rogers, in “Detoxify or Die,” talks about how the World Health Organization uses ALA to put into feeds since they don’t have anything that’s not contaminated with mold, and keeping the animals and people from dying in Africa. And so, the CoQ10 we know about. The 5-methyltetrahydrofolate – we know the importance of it. I sometimes like to use the Methyl Protect because it’s got other things. If you have somebody who’s missing the COMT or the CBS enzymes in the methylation pathway, sometimes just the 5-methyltetrahydrofolate can push them into an anxiety profile, so if that happens, put them on Methyl Protect and look at the SAMe, TMG that Xymogen makes, and begin to use possibly some taurine and l'theanine to calm down their inability to take that methyl group off of the norepinephrine with the COMT enzyme. If somebody will not take their NiaVasc because of flushing, use a Berbemycin. Berbemycin lowers both blood glucose and lipids. Dr. Whitaker’s been using berberine and niacinamide for over a decade to control metabolic syndrome or in both cholesterol and blood glucose. Berbemycin – it also kills off parasites and a lot of dysbiotic bacteria, which causes the inflammation which leads to dyslipidemia, too. So, those are some of the little perils, and they’re coming with this new OmegaPure 900, which is one of the purest there is out there. I love their capsule; it doesn’t cause people to have a lot of belchy stuff, and it doesn’t have any shwack like some of the competitors that have some good stuff, but leave that awful taste. This is an incredibly pure product.
So, I think I need to stop here and see if there are any questions.
Mike Mutzel: Yeah. Good call. There are quite a few questions here, and that’s a great presentation, Dr. Harper. Thanks so much. Give me a second and I will get these questions fired up here. I’m just trying to gather these guys. Now, if you do have a live question, you can go ahead and raise your hands so to speak and I can unmute you. First couple of questions that came in on the SNPs that you talked to about halfway to the talk – do you look like at the genetics? I know you mentioned Pathway Genomics and different genetics or SNPs related to HDL phenotypes.
Dr. Dan Harper: Yes. I use these with my patients who have a family history of heart disease and I want to find out why, then I can use things that would be able to augment that or help improve the problems that are going on. So, if they have a weakness, I use a supplement or a lifestyle modification to protect them – like people who do not detoxify petrochemicals really well, I do not want them working as a diesel mechanic, so I will put them in another environment that is healthy enough. Talking with the VA hospital right not in the military concerning people who have a double whammy homozygous COMT deficiency because these are the people that get the Gulf War syndrome, but they have the severe PTSD that does not respond. Their amygdala put out too much norepinephrine and they cannot get it back under control again. These people should be your clerks; they should not be in the military zones. They should be doing other things, but they shouldn’t be out there where they’re going to end up being PTSD because once it happens, it’s bad news. So, looking at these SNPs, you can help your patient to know what would be best for them, and it’s an individual thing; you do not have protocols, you have to look at their combination of things, and then put together a program that you would recommend for them.
Mike Mutzel: Awesome. So how does Singulex’s technology compare with NMR, Berkeley and SpectraCell, and all these different companies?
Dr. Dan Harper: Well, Berkeley is beginning to change. They’re going back into the cheaper form. They’re not doing that GEL electrophoresis that will give you all the particle sizes. Berkeley would have given you the sdLDL and whenever they did not see that on the GEL electrophoresis, they call that the death band because they know their raised horses are going to die in the next year if they don’t correct that. So, it’s very important to recognize that Berkeley gives you a good thing. The Cleveland HeartLab is going to tell you a lot about the oxidative things that are going on in the vessel particularly in the venous aspect of it and deep pain thrombosis and all, and that’s happening. The SpectraCell is going to tell you – it really is kind of hard to interpret – but it looks at percentages of different minerals and vitamins and things. I kind of look at it and say, “Okay. I will probably order a NutrEval that gives me actual levels of amino acids or vitamins or whatnot rather than a dapple of ‘this is happening in the white cells that I inoculated and there’s enough to keep it going’ – I don’t know how to interpret that, but each lab has strong points. To me, the best bang for the buck considering it doesn’t cost the patient anything is the Singulex, and it gives me more information about what I’m dealing with. I just have to order the SNPs one time because they don’t change, and then my Singulex, and we pretty will have a program that we can follow up to see how they’re complying or how their body is responding to what is being recommended for them.
Mike Mutzel: Nice. That’s great. The Singulex – that kind of grips people into four different – you have the four different columns – we have the cardiomyopathy or cardiopathology and different things. Do you like to go off that? Is that kind of like your treasury approach?
Dr. Dan Harper: Yup. They put those into the cardio metabolic or their cardio dyslipidemic or the inflammatory or the cardiac. If you saw, I did a thinking process and I had little circles with all the different think clusters from each of the four in there. So that you take and put them, “This one is high in this category and this was high in this one,” “Why were they high,” “Oh, this one is an inflammatory thing,” “This one’s high; this one’s high,” “Why is that,” “Oops, this is a mitochondrial dysfunction,” “This one’s high; this one’s high; this one’s high,” “This one’s low,” “Oh, this is probably contributing to this person’s osteopenia and I need to really address that with different things.” I use my D3 levels. Anyone below a 40 does not have functional macrophages. They cannot pacman and eat up stuff. If they’re really dealing with the inflammation act, they get it to 60; and if they’re dealing with autoimmunity, it has to be between 80 and 120. I had one person with lupus, I had to push it to 200; it did not mess up their calcium, but we were able to get them off of their Plaquenil and their Prednisone and their Enbrel by simply pushing up the D’s and doing a few minor autohemes, and getting them off of their gluten and lectins in their diet.
Mike Mutzel: Fantastic. Along diet and GIL and stuff, where does this stool testing come in? Is that more if you have an autoimmune type, inflammatory process that’s going in? Describe your patient where you would… What’s your order of testing I guess?
Dr. Dan Harper: Okay. When my patient comes in, the first thing I say is, “Life and death begins in the gut.” I think like a naturopath. And so, they understand right away that I’m going to ask them about, “How’s your poop? When you pass gas, do people leave the room or you have to find an exhaust fan before somebody says that something died in here?” Are they bloating? Do they have reflux? Are they passing food out undigested? So, I have questions in that regard and sometimes, I just mention, “Life and death begins in the gut,” and they say, “I knew it. I’m in the right place. I have leaky gut.” If they’re a medical person, you have to say, “Increase intestinal permeability,” because they don’t believe in leaky gut. So, you use the right terminology, but in my opinion, most people would benefit from a good stool analysis where they use Doctor’s Data, the Metametrix. Metametrix is good for me if I’m looking for the autoimmune coming from the gut because they do break out the prevotella, and none of the others do for me. So, I’m trying to get them to do an enterotype because I really believe it’s going to be important for our ability to go forward with the GAL tissues and the immune response is systemically knowing the different types of bacteria and parasites and critters that are there activating those dendritic cells to cause – are we Th1, Th2, Threg? Are we going to go Th9, Th22 or Th17? And all is determined in the gut.
Mike Mutzel: That’s huge. So, that’s step number one on most patients as what you’re saying?
Dr. Dan Harper: Right. While they’re collecting their stool and getting ready to send it off, I give them a little container and a little trap to put over the toilet to where they can catch it and they don’t have to play go fishing. Sometimes, I give my clothes pin to go over their nose and they laugh about that, and then I get them ready for the Singulex test. I spend two hours on the initial evaluation, and then in about four weeks, they come back and sit down and go over their stool test, their lab test, and see how they’re doing with the program that was suggested, make a few little tweaks in what’s going on, and then about three months later, we draw another Singulex and see how they’re responding.
Mike Mutzel: Wow. That’s awesome. Fantastic. So, question for you. Interestingly, last week, we had Dr. Susan Blum, and she’s written a book on autoimmune disease and everything else. She was leaning more towards the culture-based stool testing. Just out of curiosity, are you a PCR-based or a stool testing? What’s your preference?
Dr. Dan Harper: Yes. There are indications for both. I like to see what the predominant organism is. Sometimes, when you’re trying to culture things, it’s very difficult because they compete with various medias for the different things and will kill each other off. There’s a biological warfare going on. These bacteria make toxins that kill them, so the others can’t grow and consume the… That’s why I like the DNA PCR. If it’s there, even if it’s dead, it’s registering. And so sometimes, I will do the culture; sometimes, I will do the DNA PCR depending on my mood for the day.
Mike Mutzel: Oh, okay. Right. Well now, they’re owned by the same company anyway, so it’s still Genova, right?
Dr. Dan Harper: Well, there are many other companies out there so that’s why you have to pick and choose, but the Metametrix and the Genova are combined, and they both did excellent work.
Mike Mutzel: Alright. Well, thank you so much, Dr. Harper. We learned a lot tonight. We’re going to make the replay available to folks. How do you feel about people looking at your slides? Would you allow them to see the video? There are quite a few comments and questions requesting your slide.
Dr. Dan Harper: Go with the slides. They’re available to look at the slides anytime. If you want me to send you the CD so you have that or if you have that presentation, please let them review the slides anytime they want to. They can Google in “Inner Life of the Cell” video. There’s 8 minutes and 13 seconds that narrated that wanted people to look at biology from an animated standpoint. So, he tells all these different things and they label everything. I was just giving you a very fast version. I did the poor man’s version of Jeffrey Bland’s presentation, though I don’t have his many such a plethora of polished symbolic words that he has. I was just trying to tell you that what happens on the cell membrane and its environment has a tremendous effect upon what’s transcribed by the DNA and brought into the world as a result of that cells interactions.
Mike Mutzel: No, you did a great job. I didn’t mean to interrupt with you early. I thought it was fantastic. I just want you to know that. It was great.
Dr. Dan Harper: Thank you.
Mike Mutzel: Alright guys, thank you so much. By the way, we do have these great specials here on some of the products that Dr. Harper did mention. Here’s the special code. They’re only available for 24 hours and as Dr. Harper did allude to that Xymogen does have a new, really one of the cleanest fish oil omega-3 fatty acid product on the market; it’s an enteric coated 900 mg of EPA/DHA per dose, very small capsule, and this is a five-star, IFOS-certified fish oil, which is the International Fish Oil Standards Committee. It’s a voluntary extra step that Xymogen is taking to ensure that their fish oil is one of the cleanest in the business looking at the dioxin levels and levels of oxidation and PCBs and so forth. So, super clean, great price playing on that, and then you can take advantage of this special that’s going to end at the end of the year. So, look forward to seeing you guys next week. We have Dr. Todd LePine that’s going to expend on some of those microbial GI health aspect on that, and then on the 20th we have some talks on leptins. Hope you all have a great night and talk to you soon. Thank you.