Adapted from episode 89 of The Perfect Stool podcast and edited for readability with biochemist and natural health researcher Barrie Tan, PhD.
Lindsey:
So, I heard you speaking on the Chris Kresser podcast, and I immediately went out and got some tocotrienols to try. And so I was really excited when you were able to come on the podcast. Why don’t we just start with talking about what tocotrienols are and how they differ from tocopherols, which are the typical form of vitamin E contained in most multivitamin formulas.
Barrie Tan, PhD:
Yes. Vitamin A has two groups of compounds called tocopherols and tocotrienols. The tocopherols are more known, and you can see them on your cereal box, and tocotrienols are less known. The plant makes these two compounds, when the protection in the plant is more serious, then the plant likes to make tocorienols. So you intuitively know that it’s probably more potent, and otherwise, if it’s normal ones that use tocopherol. So, in the US diet, most of our vitamin E are tocopherols with a few exceptions than the tocotrienols, so the last 30 years of my life has been spent looking for the active form of vitamin E.
Lindsey:
Okay, so the tocotrienols are the active form, whereas, the tocopherols are inactive? Is that-
Barrie Tan, PhD:
Not inactive – less active, the tocopherols and the tocotrienols are active enough that about this book, you can see from the title of the book, “Tocotrienols: Vitamin E Beyond Tocopherols.” Tocopherol is the only E people know and tocotrienols people know less. You see, I was one of the authors so it’s more an academic book, so I don’t tell people much about it. This is a more consumer book, I wrote it as a labor of love and people can download on your website free of charge: “The Truth about Vitamin E,” is the book and they can download it from here.
So I started my career as a University of Massachusetts professor in 1982. And then I started to study vegetable oil. So intuitively, if vegetable oil is where you find vitamin E, the plant makes vitamin E to protect the oil from going rancid. So that is like that. So I know we are all to some extent very self-centered, somehow the plant makes things for us. The plant never makes things for humans. We ought to be grateful that they make things that are helpful to human health like that. They make it to protect themselves and for their own survival. Plants typically don’t make a lot of fat, but when they do have a lot of fat like corn oil, soy oil – actually corn and soy is not a huge huge amount of fat, but when they take the meal out and feed the animal or make tofu, left behind would be the vegetable oil and then the vitamin E goes there to protect it. When you think of a human being we typically have anywhere from a 20%, which would be exceedingly lean, to 40% is on the obese side. If you average a person of 30% fat, so in general, a human person has more fat than the plant ever would have. From there you can tell if we carry on average of 30% fat, then this fat needs to be protected. So that’s where I study Vitamin E to find out how it can protect us from oxidative damage.
Lindsey:
Okay. So, I understand that the tocotrienols that you work with are sourced from the annatto plant, so tell me how you came across this source of tocotrienols.
Barrie Tan, PhD:
Yeah, I discovered the three major sources of tocotrienols from plants which I had said earlier are difficult to find compared to tocopherols. The first one I found was in palm – palm oil. And people have questioned about taking palm oil, saturated fat and all that, but palm oil has a fair bit of tocotrienols. And then rice bran – the brown part of the rice bran, also has tocotrienols. It’s kind of like an open secret. When you eat Japanese tempura, they deep fry it with rice bran oil and rice bran oil is stable because of the tocotrienols in it, otherwise the oil will go rancid even faster; however, rice and palm contain about 25 to 50% tocopherols. Now, I’ll come back to that later.
So I was looking for a source that is very rich in tocotrienols, then the year was 1994. There was a professor at Harvard. Her name was Joanna Seddon and she discovered that on the back of the retina of the eye, they’re laden with zeaxanthin lenses to filter out the blue light. If you fast forward to today, everybody knows that if you take lutein and zeaxanthin, it’s good to prevent macular degeneration, but this was back in 1994. It wasn’t long ago. So now I know that in South America, in Peru, there would be a huge, giant marigold plant. I went there to look for marigold petals to extract lutein from the petal that it will be good for the eye. But then, by this time I was already studying tocotrienols. Then fate has it literally 20 feet away from me, I saw the annatto plant. You will have heard of the annatto plant because we use the color for coloring cheeses, Dorito chips and macaroni and cheese. If you touch it like I pretend to do here, it will stain (the plant). I intuitively knew something was unusual. By the way, the color is also a carotene, like lutein and zeaxanthin. Except it’s very unusual. If you look at this fruit, it doesn’t have a fleshy part, like fruit has. If you think of any fruit you eat, it has the fleshy part, but this just has the seed and then this stamen. Because I was a carotenoid chemist, I thought of something. If you think of a carrot, you have to cook the carrot to get the beta carotene out. You’ve got to cook a tomato for a long time in oil to get it out if you do Italian sauce. I knew that carotenes are so unstable; they are protected inside the cell of the cytoplasm. And even in lobster and crustaceans you have to cook them and then they deprotonate. And suddenly the yucky green or blue color becomes an orange or red color. Like you come to New England to eat a lobster.
Now when I explain it, it sounds so trivial like that, but it’s in my DNA, I kind of know this thing. But when you touch this guy here, it is not bound to anything. Notice that? You just stained your finger. So, I intuitively thought, “It must be a powerful antioxidant to protect the carotene from oxidative damage.” It was only a figment of my guess. I thought that it would be a polyphenol, which will happen a lot in nature. Surprisingly, it wasn’t. And more surprisingly, it is a vitamin E molecule. And most surprisingly, it is a vitamin E molecule that only contains tocotrienol and not tocopherols. So that would be my third attempt. Palm and rice contain 25 to 50% tocopherols. Annatto tocotrienols are completely free of tocopherols. By this time, I had already been studying tocotrienols for some 2025 years. I immediately called my professor friend. At the time he was at University of Wisconsin, Madison, and asked him, “What do you think?” I remember he told me, “Barry, if tocotrienols were to mitigate human chronic conditions, this tocotrienol better be, otherwise, you and I are completely a lost cause for our desire to bring this to bear.” So the last 25 years, I’ve been committed to do a chronic condition with this sort of vitamin E. And happily, they work on many chronic conditions that we study.
Lindsey:
Interesting, and we will talk about that. But I did just want to mention I lived in Costa Rica for a year and a half. And I learned how to make a few dishes there and one of them, Arroz con Pollo, uses annatto as a spice and they come in tubs in the grocery store. They’re just bright red, orange sort of tubs that you can take a chunk out of and it was like a refrigerated margarine, about that consistency.
Barrie Tan, PhD:
Wow.
Lindsey:
Not like the pebbly stuff that you find here in the spice aisles. And of course it tastes terrible if you eat it straight but it adds a subtle flavor and of course an obvious color to the whole dish when you add like a teaspoon or two. I bought a couple of tubs years ago and I still keep it in the fridge and of course it doesn’t seem to go bad at all which is because of obviously the protection that it has.
Barrie Tan, PhD:
Yes and if you could sometime, you have my email, send me that you said the Spanish word. I will try to look for dishes. I know they’re not classically American dishes. South Americans use it for a lot of their food. I was able to track, even the Inca Indians use it for their food in Peru and other places. Here it’s a very sterilized use, like we put it in cheese, but besides that it’s not used in any food dimension that I’m aware of. And curiously, I thought of this one time. It is not known to the Asian context. I’m Asian. With the exception of Filipino, and then I was able to track it because the Spanish that went to South America also were in the Philippines for 400 years. Sometimes when I tell my American colleagues, it’s hard for them to put their heads together. The Spaniards were in the Philippines for 400 years, as long as they were in South America. So not surprisingly, many of my Filipino friends, they have Hispanic names, and they look like me. They’ve been there for a long time. A lot of Filipino foods also use annato. Isn’t that interesting? So they brought the flavor and the seeds and they grow it in the Philippines. So a lot of Filipino empanadas – and that’s a Spanish word, but if you ask any Filipino, they know empanadas. And then they make this little reddish looking and then they put this annatto in. But otherwise the other part of Asia or Southeast Asia it’s an unknown spice; they don’t use it at all.
Lindsey:
Yeah, well, I’ve got two recipes, I think, that call for it: the Arroz con Pollo which is chicken and rice, and then one another is a chicken dish. I will send you both those recipes and I’ll post them in the show notes. So I’m wondering, are tocopherols harmful to take as a supplement?
Barrie Tan, PhD:
Not harmful unless you take them in high amounts. If you remember, the late 90s into the 2000s, all the published work on Vitamin E was negative, even women who take it, Harvard Women’s Health Study, and some of the women have higher incidence of breast cancer and men who took it had prostate cancer. I think that the reason is because of all the eight Vitamin Es (four tocopherols and four tocotrienols), alpha tocopherol is the only one that has a transport protein. That means that when they cross the cell membrane, they have a right of passage. They have a protein that takes them in. Only alpha tocopherol has it, the other ones just go in by diffusion. Diffusion simply is an engineering phrase: “low concentration, high concentration.” You will move from the high concentration to the low concentration. Just like if you put sugar in a glass of water, and the sugar first sinks to the bottom. Over time, you see some wiggly thing, it will move from the high concentration as the sugar dissolves into the low concentration. That is a process of diffusion. And that’s how Vitamin E would work with the exception of alpha tocopherol. Because they have a transport protein that helps. So in those studies, when they use alpha tocopherol, they use 400 ones and 1000 milligrams. So a lot of this vitamin E goes in, it had no place to go. And I think that they are not good for you. However, if we were to eat a normal diet containing 10 to 15 milligrams (15 milligrams is 100% of the recommended daily allowance), that would be fine. However supplemented, people will have 10-20, even 30 times higher concentration of alpha tocopherols. That’s a problem. But we did not find that to be a problem with tocotrienols.
Lindsey:
And so what conditions has the research shown that tocotrienols can benefit?
Barrie Tan, PhD:
Okay, how about I tell you some of the conditions we’ve studied, and then we can fractionate them? We did a lot of studies in the last 20 years on chronic conditions. And I think that for the audience to appreciate this, right, we’re not talking about a drug. We’re talking about supplements. and this is almost my entire lifetime studying this. So this is, if I weren’t here, I doubt a very large company would put this kind of money and time and effort and energy to do it. So we did probably about 15 to 20 clinical trials. And the kinds of studies we were involved in, chronic conditions we initially studied were dyslipidemia: high cholesterol, high triglycerides; insulin resistance; people who are prediabetic (but not yet diabetic) and finally we studied a group of people who are diabetic. And now we have committed to have a huge amount of resources to study fatty liver disease.
Now if the audience is having any of these conditions, you would understand. For the audience members that do not have these conditions, you’re blessed, but just to give you some numbers. People who are prediabetic are about 90 million Americans. People who are diabetic, 35. And about another 100 million people who have fatty liver disease. Of course, some of these things overlap. So therefore, huge numbers of the American population has this kind of problem. Most recently, we are studying people beyond overweight. They are obese – men and women in Texas. So in the studies that we are doing, people with prediabetes and dyslipidemia, our study calls for anywhere from 100 to 250 mg. Say you round it up 100 to 200 mg. For people who are diabetic, the studies were about 250 to 350 mg. For fatty liver disease, (remember, the liver is a larger solid organ), we actually did three studies on this, Lindsey. We did a three-month study, a six-month study and a 12-month study. We already were convinced 600 mg was needed for this. We didn’t change the amount, we just did the time, because I wasn’t sure that after three months, if we were to be successful, that it would continue to be so in six months. So therefore, it’s not a dose-dependent study, but instead a time-dependent study. So we stayed with the same dose. We studied different things at three months. We studied stress enzymes and the stress enzymes come down and drop.
And the second study, we studied steatosis, which is fat in the liver. We used our ultrasound to map it like you use ultrasound to look for a baby in a mother. We were able to see the fat egress from it in a six-month study. In the 12 month study, we decided to go for gold. We decided that I have to go beyond getting consumers to be interested, or a primary physician to be interested. I have to convince the specialist to be interested, which means that these are liver specialists. So we decided to do CAT scans. And we saw that the fibrosis score is reduced the steatosis also is reduced. When the fat stays in the liver for too long, it forms a scar. So the doctors call it fibrosis. And that’s kind of like considered not reversible. So now we can clearly confirm that fat is reduced. Inflammation is reduced, liver enzyme is reduced, steatosis and fibrosis.
But there is something I will keep last to tell because I’m initially very skittish to talk about this. We noticed this in the three months. I was not very convinced. So in the six months, we saw it again. And my science director, says, Barry did you notice this?” I saw this, but I’m hesitant to make a comment on this. How about we do a 12-month study? And we repeated it. The shorthand is, the people who have fatty liver are already generally overweight; they lost weight. And in our clinical trials, we did not have that as a primary outcome. See, when you design a trial, you have to make a hypothesis. What are you looking for? We did not look for weight loss, but then they lost about 10 to 15 pounds consistently in three months, six months and 12 months. So I asked, “How are we going to report this? Factually it is true.” Can you imagine that? Most people will do the opposite. They just say weight loss and then they go sell a heck of a lot of product. I’m doing the opposite. You know why I was worried Lindsey? When when you say the word weight loss, people expect a weight loss in two to four weeks. Well, I never had data at one month. My shortest data was three months, even so you saw weight loss at three, six and 12 months and just say that. If people say, “Would I see weight loss in one month?” No, we don’t have data on that, but you can say that we saw the weight loss. So now we can consistently see sustainable weight loss on the largest organ in the body that at three, six and 12 months. I think tocotrienol is not intrinsically a weight loss product. Instead, it helps people’s metabolism out of kilter to come back to balance and the inflammation drops, the stress to the liver drops, and as a consequence of that, their weight also comes back to normality.
Lindsey:
Interesting. So does it matter whether the fatty liver is non alcoholic or could it be alcoholic fatty liver too that this would impact?
Barrie Tan, PhD:
This is a brilliant question. We only studies non alcoholic fatty liver. But the reason this disease was called non alcoholic fatty liver disease – It was discovered by the Mayo Clinic in 1984. Not so long ago. I don’t know if you know this story. This is a cute story. Well, it wasn’t cute when it happened. There was this guy. He went to see the doctor. And the doctor looked at the numbers came back and said (I just made up his name), “Mr. Jones. Do you drink alcohol?” Mr. Jones says, “No, I don’t drink alcohol.” So the doctor went back to the lab and came back again. And now a little bit more accusatory tone. He spoke with Mr. Jones and said, “Are you sure you don’t drink alcohol?” See, with that kind of intonation, Mr. Jones is upset. He says, “I told you I don’t drink alcohol!” So that was the reason because Mr. Jones’ liver looked like a cirrhotic liver from somebody who drinks alcohol. It wasn’t. So all this to say that when we take in a lot of carbohydrates and fat, we can make the liver almost look like someone who drinks alcohol. So a short way to answer your question is we believe that people who have a cirrhotic liver caused by alcohol also would benefit from tocotrienols because their liver looks the same, which is why awkwardly this disease is NAFLD. After NAFLD, they become NASH – non alcoholic steatohepatitis. So the liver looks like a person with hepatitis A, B and C. Hep A, B and C are different because they are caused by a virus. And by the way, this tocotrienol worked positively for people with hep C virus, totally different mechanism.
And that was done, sorry I to have to tell so many stories, but when we designed this study, Lindsey, the investigator and I decided that if you have people with Hep C, you have to recruit people. He said we have to exclude people with Hep C, if they have alcoholic liver, we have to exclude them, otherwise, we have all the “monkey on my back.” I cannot interpret my data. That’s how you randomize a study. He was fine with that. When he was recruiting the 100 older patients, about 12 to 15 of them had hepatitis C. So he had to exclude them. But what he didn’t tell me was curious. He separately gave them a tocotrienol. It was not in the study, it was excluded. He didn’t tell me. A few years later, I found an answer “Barrie, did you see this? Our tocotrienol is used on people with Hep C. It actually worked to reduce the viral titre in the people.” Then it tracked back to the author, and the author is the same one that did the NAFLD. So he excluded it. It also helped people with that. So we did not continue that study because Hepatitis C is a different direction; it is caused by a virus but it probably, I think, any damage to the liver, whatever the reason might be, at minimum, tocotrienols would help the liver.
In animal studies. we also studied hepatoma, animals with liver cancer. It also has support to reduce the severity of the cancer in the liver. So you can generalize the phrase that tocotrienol is hepatotonic, a liver tonic. But well, of course, if you say it like thatm it’s too general and people don’t know what it’s for. So I have to tell people about the clinical studies. The best we have done so far is this huge group of people with fatty liver due to dietary mismanagement and that works on them.
Lindsey:
Was the dosage for those people 600 mg a day?
Barrie Tan, PhD:
Yeah, for the fatty liver 600 mg. For the type two diabetes anywhere from three to 400 mg in those studies. And for the prediabetic and people with dyslipidemia, it’s about 125 to 250 milligrams. So those are the range I know. We didn’t discuss this. We have about six or so clinical trials in Denmark, of people with cancer and the cancer we studied, two of them are specifically for women. Ovarian cancer, breast cancer, lung and colon cancer. And my colleague in Florida is studying pancreatic cancer. And in that case, we are studying stage four cancer. So as you know, stage four, there are no options available, it is the end stage. So we use the highest dose, which is 900 mg, people take 300 mg for breakfast, lunch and dinner. And in that series of trials, we have the ovarian cancer result back. The audience should remember, this is stage four cancer, which means that there are no more options available. So they were taking Avastin, which means that this is anti-angiogenic. It prevents the tumor from sucking food from the nearby artery. Angiogenesis is the growth of arteries, anti-angiogenesis is you cut the artery off, essentially, you starve the tumor to death. They take chemo for that. And in another group that does the same, they take chemo because it’s the standard of care, plus tocotrienols. That’s it, no other differences. Inoperable, not radiatable like that. And they have in the registry in Denmark already, after six months, then in the group that had Avastin, they are not around anymore. In the group that took the tocotrienols as well, 60% of them survived. In Denmark, this is a woman’s disease, so the nurses are predominantly women, and they really want the study to continue. The principal investigators said, “If we continue to study, what do we compare it with?” The group that they compared with were no longer there. Anyway, for good reason they persisted and they were able to, and I’m glad they did. They persisted the study for four times longer into 24 months, two years. And even after two years, 25% are living. So that’s a remarkable thing I consider.
We are still hopeful that the tocotrienol would work on cancer, but I don’t think I’ll have a prayer to ask the FDA for any claim. Maybe under the Compassionate Care Act of United States passed by Congress. When there are no options available, then the FDA may allow its usage. I don’t know if we have the wherewithal and financial muscle power at FDA, but we’re willing and have the will to complete the study. And then let people read the study. So hopefully, in another year or two, if you still remember me, you can call me, “Dr. Tan, have you completed the study, I’d like to find out more on that.” At the end of the day, I am as fascinated and as touched by this as an audience listening to this would be. I believe that it is this powerful because it is uniquely tocotrienols and it’s the most potent Vitamin E I have ever put my hands on.
In the end, and as I told you in the story earlier, I didn’t even go to South America to look for this. I was looking for something else. And I consider this spiritual to me. If you look at me, I’m Asian, I’m supposed to go to Asia and look for this thing. And then I cannot speak a word of Spanish. And then everything is an oddity, but then this meant to me when I get to this part of the Amazonia, other people could have discovered it, but they didn’t. They weren’t curious enough to look. I was curious enough to look. And I’m not supposed to be there. I’m supposed to be in all these other wonderful places in Asia. But that was not where I found it. I showed you the picture. I was in Peru. And I cannot speak – I’m sure you speak a lot more Spanish than I do. I do speak it, yes. That’s amazing.
Lindsey:
So you mentioned dyslipidemia, and I’m curious, do tocotrienols have any impact on Apolipoprotein A?
Barrie Tan, PhD:
We only did a study early on. It did drop the Lp(a) a little bit, but it’s not dramatic. On the whole cardiovascular emphasis, I should bear out so that you will know where it works better than others. It consistently dropped triglycerides. That’s a good thing. I’m going to give you a teaching moment here. Before people become diabetic when they’re prediabetic, their triglycerides are high, but the sugar is normal high, but still normal. The person who discovered metabolic syndrome, he call it syndrome X before, and that was a professor Gerald Reaven, you can Google, he gave talks. He is a retired Stanford endocrinologist and passed away now. I remember one time, I caught him when he finished his talk on the run to catch his flight. So he was a little bit irritated that I stopped him as he was walking out. I said, “Just tell me how to put my hand around this metabolic syndrome thing.” He said one sentence, and then he left like that. He said, “Dr. Tan, 10 hypertriglyceridemia always precedes hyperglycemia.” I never forgot it. So, in other words, before people have high sugar, they have high triglycerides. So therefore, if the triglycerides dropped, that’s a very good sign, and then the LDL drops. Most of the LDL that dropped are the dense LDL, not the buoyant LDL, but in LP(a), we didn’t study that in serious depth. We also studied oxidized LDL, because oxidized LDL is atherogenic. And then tocotrienols is a very powerful antioxidant. So not surprisingly, the LDL stays LDL and does not get oxidized. So we were thrilled to see that as well. So pretty much that is the group. Oh, the HDL did increase, not by a lot. It’s very difficult to increased HDL except when you exercise and the HDL increased typically about 5% better than the other direction. When people take a lot of carbohydrates, the HDL drops. And when you exercise the HDL increases, we noticed that tocotrienols, the HDL increases, not dramatic, by 5%, consistently, we see this.
Lindsey:
Okay, so I know that soluble vitamins do build up in the body. So I’m wondering if you can reach harmful or excessive levels of tocotrienols?
Barrie Tan, PhD:
To the best of our knowledge? No, because of the 15 to 20 clinical trials we study, the short one is about two to three months. And the long one is about a year, we didn’t see that. Like this fat delivery study, we asked the physician please to report any unbecoming side effects. They reported and they did not see any liver enzymes go up, no kidney function was compromised, nothing like that, that they saw. We didn’t see that at all. By the way, right now, the study in Texas is of men and women who are obese. So we were able to get an IRB, Institutional Review Board to approve. We found this in animals all the time. There when you take tocotrienol because they’re lipid soluble, they are deposited into fatty tissues like vitamin D or K. So we knew that in the animal. So this is a first study, where we have biopsies of the adipose tissue. And then so we will be able to measure how much storage of the tocotrienol is in the adipose tissue in this obesity study. So the obesity study will also be complete by the end of next year.
Lindsey:
Okay, and is it important to divide up the dosage that you take each day? Or can you take it all at once?
Barrie Tan, PhD:
It’s important if you can take tocotrienol up to about 300 milligram and after that, if you need to take more than that, you divide it, which is the classic example in the Kansas study. They take 900 mg at 300 mg soft gel for breakfast, lunch and dinner to get the 900 mg. And indeed, in the fatty liver study they take two 300 mg with lunch and dinner. And notice I always say with a meal, they’re lipid soluble so you shouldn’t take it with on an empty stomach like that. And then for studies that only require 100 to 200mg, they can take all of it at one time. Do not take more than 300 mg.
Lindsey:
Okay, so I use some of the typical functional medicine lab tests with my clients like the Genova NutrEval or the Metabolomix. And they only show tocopherol levels on those tests. So can you infer anything about tocotrienol status from tocopherol levels?
Barrie Tan, PhD:
No, you cannot. On tocopherols, they readily do that. And I know that had made the tocopherol story last as long as it did, because of the alpha tocopherol transport protein. Frequently when people take bloodwork because they’re looking for lipid profile for cholesterol in a fasting stage. And then it’s about 12 hours overnight fast. Then they look for vitamin E. If you asked for a blood work for vitamin E, besides alpha tocopheral like tocotrienol, in 12 hours, you’re not going to see any tocotrienol, even if they take it with the dinner about 10-12 hours last night before. On that one, it also has a story too. We did that 20 years ago and we found out that there were no tocotrienols in the fasting blood 12 hours after and, the research professor said, “See, the tocotrienol is not absorbed, it’s useless.” It nearly got thrown away, the baby with the bathwater. So then I said, “Wait a minute, you cannot say that, because the blood is only a snapshot on that day. Not that in the blood is no good based on a snapshot.”
So I have to go back to animal study. And in the animal study, this is it. In the cholesterol thing, because of the alpha tocopherol, let’s say if you think of it 2, 3, 4- 10 hours like that, the alpha tocopherol will go up like this. But with the tocotrienol let’s say this is five hours. It goes up for five hours, and then it quickly goes down six, eight hours. So if you have an overnight fast, it’s almost zero. First we showed this an animal and we showed this in humans. For me, it is as painful as it is heartwarming, we actually did the study just to show the pharmacokinetic at five hours, and then it dropped back like that. So why did it drop? It doesn’t have a transport protein, and when it dropped back, it was not picked up. It has already delivered to the organ. But the alpha tocopherols kept being in the blood. So therefore, as a clinician, if you say that it is in the blood, therefore it is absorbed, believe that but only to a certain extent.
Many things are not shown in the blood. It’s already been deposited into the organ, or if it’s deposited in the organ, it is not going to spool and continue to be in the blood. We found that we have consistently found that in all the different organs like I expressed in the liver, and when in animals, you can excise all the tissue, we see them all over in the brain, in the eye and in the other organs. Each person with 130 to 160 pound weight, has 38 trillion cells about 5000 times the population of the Earth. Each one of them is like a cell, say like a bean shape and has a cell wall. And most of the fat in the body is in the cell membrane. And the tocotrienol goes to the cell membrane and the fattier the organ is the more tocotrienol would be there. So you would expect that the tocotrienol would be found in your brain, in your liver, in your lung and in all fatty tissues, of course in your adipose tissue. Of course in people who said well, “How do you know that?” We know this because they work to kill the cancer in those tissues, but we cannot poke and get a biopsy because humans are not animals. In the fatty liver study, we were not allow to do biopsies. It’s a luxury we cannot have, however; if the person has cirrhosis, has liver cancer or Hep C, well that’s different, so they’ll do a biopsy.
The closest and the first ever we have this is with the obesity study. And for that we are only allowed to have biopsies of the adipose tissue where the love handle is. It is minimally invasive, but otherwise we are not allowed to do that. So therefore, in that case, it is legitimate to study it from the animal. We did have one study, it is a cadaver study and it was from that that we found out the liver thing. A lot of these are story findings. This professor at Ohio State got a US government grant to study tocotrienols in the brain. He was going to get a $5 million grant, but NIH told him, you have to show us before we give you the 5 million bucks to do your study that the tocotrienol is in all the different tissues and he said he was drawing a blank. How am I going to show him that the tocotrienol is in all the tissues? The reason NIH asked that was because they did not see it in the blood. That was the reason. so he had a problem. He didn’t know how to deliver to the government. And then the university was so creative. He said, “We have end stage liver failure patients and if they are on a liver transplant list and waiting, they may wait in vain and they may not get the transplant and then they die.” So if they give consent to take the tocotrienols and if and when they die, and they allowed their organs for human research, then you are good. So he did, he gave it to give it to the 20 or so patients, half of them passed away. That’s when he showed that the tocotrienols were found in the brain, in the eye, in the heart, in the lung, everywhere. So he’s got his money. A side note was half of the patients improved. Remember, he was doing this to show what he needed to get the grant for the brain study.
It was because of that that we decided to do a study on fatty liver. The study was, just show me that the tocotrienols go to different organs. He did! He got his money. But he published a study in the Journal of Nutrition, then he did, and we did. And so now, because he was asked by the US government to show that is found in different organs, now we’re able to find that, indeed, it even helped people with fatty liver. So sometime, findings are not a straight path. But it did lead to a good path. So that’s a blessing. So it did not come from me, Lindsey, so I cannot make the claim. I’m thankful that that professor did it. So we took the the cue from that and decided to engage in clinical studies.
Lindsey:
That’s awesome. So we’re kind of running out of time, but I want to get to GG or geranylgeraniol? So I know you’ve done research on that, and that it might have some relationship to gut health. So can you tell me about that?
Barrie Tan, PhD:
GG is an endogenous nutrient, which means your body makes it. I know that the body makes GG for at least three reasons, probably more. The body makes GG to make the first two easier. Behind me, that’s a molecule of GG here, and the other molecule is Coenzyme Q10. So GG is used in the human body for the synthesis of CoQ10. So everything you know about CoQ10, which I don’t have time to explain, you need GG, otherwise, you cannot make CoQ10 in the body. So second, GG is required in the body for making MK4. Everybody in our industry knows the gut fermentation makes MK7 so you can read everything about MK7, and other menaquinones using vitamin K. But I wanted to change the audience and your understanding. In the colon our body makes MK7 and other MKs. That is to make the good bugs go up and the bad bugs go down so that your gut is in a good place. But when people push the idea of making menaquinones remember, when menaquinone 7 is made in the gut, they are not absorbed. Absorption of nutrients is in the small intestine. So when you make it in the colon, it’s in the process of making poop. It’s excretory material through the rectum. So only water is absorbed back and forth like that. I’m saying that GG helps the good bugs to grow because they’re feeding material for the bugs to grow into. So they are growing more like a prebiotic.
By the way, another time, if you send me an email, we can send you the study: tocotrienols work in people with Crohn’s disease and inflammatory bowel syndrome. Maybe you should have me for another interview where I just talk about the colon. This one is more a general health. But for the GG PPs, the GG goes in the body and makes MK4. And the last part is, about 30 to 40% of our body weight is skeletal muscle. Skeletal muscle cannot be synthesized without GG. We need GG for making skeletal muscle. Not surprisingly, as we age we have sarcopenia and loss of muscle mass. And in the very specific instance, and I’m sure your audience will know this, many people take statin drugs to lower cholesterol. The same pathway to lower cholesterol, just right below it is GG. So therefore when you inhibit cholesterol, it’s obligatory, you will inhibit GG and the inhibition of GG is the reason why when people take statins they have low CoQ10. Now, did I connect the dots? Because you inhibit cholesterol synthesis, GG drops, and when GG drops, CoQ10 drops. So CoQ10 did not drop just because they took statins. CoQ10 drops when people take statins, it’s because there isn’t enough GG that statins inhibit and therefore CoQ10 drops. So in other words, if your patient takes statins, if you measure CoQ10 and the CoQ10 drops, it is very likely that the GG has dropped because GG is required for the synthesis of CoQ10.
And of course also MK4 and MK4’s story is very simple. It will affect the bone health process, the porosity, it would also litter the calcium in places you don’t want it to be like calcified arteries, kidney stones and gallstones. So that’s a very short story about the GG piece, it’s a very powerful biochemical. And I’m only talking about it today because humbly, on the same plant that I extract tocotrienols from, after I removed the tocotrienols and color, I still had some some chemical there. It looks yellowish like corn oil when extracted and studied it. And would you believe it? It is GG. So I’m blessed, you know? So this particular plant is an ancient plant in South America. It yielded the secret of tocotrienol, which I explained to you and now further yielded the GG, which the plant makes for making all kinds of things. For the human, it makes the three things I mentioned to you.
Lindsey:
Would GG then be something that’s helpful for people who have already calcified arteries?
Barrie Tan, PhD:
Yes, we are hoping to do a study now. Currently, our two studies we are doing: the main one we are doing is people who are on statins, who are under a cardiologist’s care and have myopathy. And if they take a GG, it it would mitigate the myopahty on those on statins. And so it’s a muscle type question at this point. And then we’re hoping to do some exercise sign on the muscle thing. And someday we also will get to the sarcopenia on the elderly population, we hope to get into those areas. And we hope also to study MK4; we believe the calcification is the MK4 piece. When the body does not have enough MK4, the calcium is not shuttled to the bone. You need MK4 for the shuttle to the bone and not leave it in the artery nor the gallbladder nor the kidney. So we are now working to see how we can conduct a study to do that. It is so exciting. I’m supposed to retire after the tocotrienols. And then I fumble on this GG. And GG is very exciting.
I know that the time is up, I want to tell you one thing. Please allow me, it will only take less than a minute. GG is found in the plant. It is the last common step that the plant and the animal share. The plant and animal are vastly different. They need green chlorophyll to photosynthesize. We need heme red to make oxygen, one needs carbon dioxide the other one needs oxygen. Like do you know that tonight when you go home and then you eat your food, your vegetables, you see green, you think GG. Without GG there’s no chlorophyll. And then when you see your color, your beta carotene, your lycopene, your astaxanthin, your lutein, everything, all this beautiful color, you have to think GG. Without GG, there will be no cartenoids. So now I feel very spiritual that I had this finding. GG is the last common step between these two. In the plant, it is essential. The plant cannot survive without GG. In the human, I just told you the three things that are essential. So I’m just thinking, wow, this GG is really cool. It is really an endogenous nutrient. And even if you take the statin thing away, when we grow old, why do we have low energy, and then we don’t make enough CoQ10. But nobody told me we don’t make enough CoQ10 because we don’t make enough GG SBH. Oh that’s an important thing. And we have a calcified artery because we don’t make enough GG and it’s unable to make MK4. And then don’t quickly jump onto MK7. They are several menaquinones, but the only menaquinone that is made in the human body is MK4 using GG, not the other menaquinones. The other menaquinones are made in the gut however, but they’re not absorbed.
Lindsey:
So would you be an advocate of the MK4 form of vitamin K, as opposed to the MK7?
Barrie Tan, PhD:
That is correct. I am a pro that; not for pushing any people to buy my GG. I’m saying that in true honesty. If our body makes MK4 to the exclusion of all the other MKs, don’t you think we should take notice? You can Google, do that. If not, you send me an email, I will send you all things. I hope the Japanese scientists and the scientists in the world who figured this out, I hope that they are nominated for the Nobel Prize. This is actually a classic vitamin thing. They deserve a Nobel Prize. I don’t deserve. I’m lucky that they told me this. And then I’m bearing these things out to people. If you Google menaquinone 4, it’s the only menaquinone made in 25 to 30 organs. You will never find an organ in the human body that makes MK7 or 9 or 11 or 13. Those menaquinones are made by the bacteria in the colon. Now in the colon however, you want them to be made, so the good bugs go up and the bad bugs are controled. That you want. So I don’t want to confuse that. That’s a good place, but when they make them, they’re not reabsorbed therere, only water is absorbed so that you either have diarrhea or constipation, you know, at that stage. But MK4 depends on vitamin K1 being absorbed and then the tail is cut off. The ring, which is on your dark green vegetables, go in and look for 25 to 30 organs, look for GG endogenous, stitch it on and when they do, that’s your MK4. I’m giving you it as simple as I possibly can. And then if you Google it, you’ll find a Japanese scientist studying this.
Lindsey:
Okay, well now I know I should be recommending the vitamin D/K MK4 supplements not the MK7.
Barrie Tan, PhD:
Yes. And then if you want to know of a company to do that, Designs for Health, they are a very good company. I think their product is called Tri-K. So they have three: vitamin D/GG, they have GG in it, and then vitamin MK4, I forgot. So if you just go to Designs for Health Tri-K.
Lindsey:
Yeah, I have a dispensary. I’ll put a link to it and people can go in there and I’ll put in my discount code (HDH15OFF) for the dispensary in the show notes.
Barrie Tan, PhD:
Wow, thank you Lindsey! Bless you and bless your all your listeners! Hopefully in another year from now when more of my clinical studies come out, you can have another interview of me particularly more specific on the colon health thing. And also on the other general overall health of the people. By then I will have more clinical trials completed.
Lindsey:
I’d love to. So briefly, can you just tell me about the supplements that you have that has the tocotrienols and the GG?
Barrie Tan, PhD:
Okay, you mean who sells them? Designs for Health as I mentioned, AC Grace, Allergy Research Group and then there are many people sell them on the internet. If you go to my website, American River Nutrition, and you say buying tocotrienols; usually people say you can buy from me. We don’t sell the finished product, so we’ll list all the companies that use ours. If you want to be sure that they come from us and not from other people, if it’s referring to GG, it’s called GG Gold, and if it’s annatto tocotrienols, it will be Delta Gold, because the main component is delta tocotrienol. We call it Delta Gold. We also make a product which is CoQ10 and GG. We call it DuoQuinol, it’s a play on the word. And then some companies out there sell it. So make sure that at the back of the bottle it will say DuoQuinol, GG Gold or Delta Gold, you will know it is from us. And we make this product in the United States of America, right here in Massachusetts.
Lindsey:
So the supplements sold through Designs for Health are sourced through your stuff.
Barrie Tan, PhD:
Yes, they are. They validated us to the nth degree and then we worked with them and we are pleased that they did a thorough job. They came, they looked, they did definitely, and then we’re also FDA approved, GRAS, kosher, halal and the whole works.
Lindsey:
Awesome. And then listeners can find you at BarrieTan.com?
Barrie Tan, PhD:
And if you want the book, BarrieTan.com/book, otherwise, if you lost that track, just simply type American River Nutrition, it will lead you there.
Lindsey:
And I’ll have these links in the show notes so they should be able to find them quite easily. Well, thank you so much. This was awesome. I love your stories and I’ll definitely have you back on and we’d love to hear more about Crohn’s and colitis and the outcomes of your studies.
Barrie Tan, PhD:
Thank you so much.
If you’re struggling with dysbiosis, diarrhea, constipation, leaky gut, candida, IBS, IBD, or other gut health or all over body problems, you’re welcome to set up a free, 30-minute breakthrough session with me (Lindsey). We’ll talk about what you’ve been going through and I’ll tell you about my 3- and 5- appointment health coaching programs in which I recommend lab tests, educate you on what the results mean and the protocols used by doctors to fix the problems revealed. Or if you’re ready to jump in right away or can just afford one appointment at a time, you can set up an 1-hour consultation with me.
