Jacqui Fahey (00:05): Welcome to Common Ground, a podcast series discussing new research and interesting projects in the field of complementary medicine. Hello, my name is Jacqui Fahey, Head of education at vital.ly.
Today on Common Ground, I'll be speaking with Michael Osiecki. Michael is the managing director of Bio Concepts, who has been diversifying the business through technology for the past year. Prior to this, Michael received his doctorate for research in the field of biological engineering, specialising in isolation and expansion of stem cells in bioreactor systems. Other research experience includes mesenchymal stromal cell differentiation, tissue regeneration, wound healing, hematopoietic stem cell niche, redox signaling and behaviour of antioxidants such as ascorbic acid.
In combination with Michael’s experience as a chemical engineer in raw material manufacturing and extraction through to GMP product manufacturing, this has given Michael experience in the complementary medicine industry from basic research to the clinic and beyond.
Welcome to Common Ground, Michael.
Michael Osiecki (01:16): Thank you, Jacqui. Nice to talking to you.
Jacqui Fahey (01:18): Yeah, thanks Michael. So, Michael, what led you into the field of complementary medicine? If you could share that with our audience today?
Michael Osiecki (01:25): I don't think I had much of a choice given by our family background.
Jacqui Fahey (01:30): Yes. Yeah, true.
Michael Osiecki (01:33): Very, very true. I've always, I was always sort of drawn to it, I guess. But you know, I went from my academic background and I kind of tried to avoid it a little bit and tried to study a little bit broader, I guess, because pretty much every single conversation I had with my dad was always evolving around nutritional medicine anyway, so I was always kind of interested. I think, you know, my dad always said, science is a language that you need to learn young. And so, you know, I was always in that sort of scientific realm, I was always attracted to building and making of things and understanding that more engineering sort of side. I always enjoyed mathematics and that sort of thing.
So that's why I went to the engineering ground, because I always thought, well, part of the big thing is how to make these things, how to make chemicals. I really went into that biological engineering side, so using a lot of chemical engineering processes, a lot of chemical kinetics, you know, biochemistry and applying that in engineering sense as well. And using modeling and things like that for biological systems, be it cellular growth and in its effect with, you know, nutrients and macro nutrients and toxic metabolite like lactate in the bioreactor system. Or even just like, literally I was doing stuff in my undergrad, like silicon chip in a cell, basically designing, you know, modeling a cell. So I was always really fascinated by that sort of work.
Michael Osiecki (03:11): And then that just fits so naturally into that nutritional world because, you know, it's not a drug system of targeting a specific receptor or enzyme or a metabolite. It's multiple pathways being affected that much more complex system biology I was always attracted to, and you know, so I was, I think I was, I, I tried to avoid it and I think it expanded my pathways a little bit more by going down a different area. So when I finished my PhD, academia was definitely not a place I wanted to be in to, a usual sob story of a PhD student. So I was very, very keen to move out and work in the business. And I was sort of, yeah, in product development and education for a number of years before taking on the lead job, finally making dad retire.
Jacqui Fahey (04:16): Yes. Thank you for sharing that, Michael. We're wanting to understand a bit about Bio Concepts approach to education. What are the key elements from a health literacy perspective? For effective education to practitioners and students?
Michael Osiecki (04:33): I think we always wanted to make sure or teach people how to think and how to think, not what to think. And I always sort of, you know, when, you know, when we're doing like NPD or whatever, it's like going, or, you know, something changes in the literature. It's not us defending our product against the tide of literature. No. We have to, you know, change the product due to literature. So it's always, yeah, it's always about how you, how to think about it. Because I think, you know, I was, you know, everybody's brainwashed in a certain way of thinking. I've been brainwashed as a sort of engineer type style thinking. You know, most practitioners are kind of trained in this medical model. Although you do a lot of biochemistry and herbal aspects of it and understanding that sort of systems, it's still very much dose, outcome, what's clinical trial? but not really understanding what's going on. I've been doing a little talk on dementia and Alzheimer’s at the moment, and that's like a long story of just a really poor understanding of, well, what has beta amyloid and tau in terms of Parkinson's disease, what do they do normally in biology? And then you look at it and go, we don't really actually understand that. It's like, it's very low research, all we know is they bad. Yes, that's, but not really understand. So that's what I really focus on, is trying to give people like that deeper understanding of what's going on. And also, like, one of my KPIs when I talk to an educational thing is I want to learn something.
Michael Osiecki (06:24): So if I don’t learn anything new with what we produce, then how do I expect people reading it to learn something new? I would've liked to make sure that we're always trying to find something new and unique and always try to think outside the box, trying to think of how we provide education. And I think what I'd try to do now is offer different sort of way, you know, people learn differently and try to evolve that, you know, with we've launched ‘engage’ and trying to involve that in later in the year and in future years of trying to offer different formats to allow people to learn differently in different ways is very important. But it always comes down to like, I really want to give people that background to make their own decisions.
When we talk about nutritional and herbal medicine, it is so complex. But also biology is beautifully simplistic as well. Like it, you get this complex system, but it, you start breaking it down, break it down, get into the root causes, start, you know, breaking things down, you sort of realise just how simple biology can be and then you can break it out, because you know, you got dose responses and hormesis, you know, if things doing opposite reactions, you know, where people have a negative response to certain nutrients and it could be down to the dosage or, you know, dose or the concentration of other you know, cytokines or nutrients in their system as well.
And I think it's really important that we sort of bring that understanding, everything and everything that we do to, you know, because unfortunately in our industry, we see patients, you know, we’re the last stop of these really complex disease patients. And so you deal with these really complex conditions with multi, you know, mortal mortalities going on in that patient there. And you can't just simply say, do this. And so, you know, I, I think I, so I try to get people sort of think a little bit more like, okay, so this is the disease state, these are the markers, but why is that? why these markers? think why does this thing work? How does it work? And then, you know, that's why, you know, giving this can, you know, will work with these types of patients, but probably might work with these types of patients.
Michael Osiecki (09:14): And it's just trying to break it down a little bit further so you can make that better decision because you know, it's about individualised medicine, not statistical medicine. That's the unfortunate thing we see, you know, with the burden of evidence in terms of efficacy of products like ourselves and drugs, you know, it's all, you know, populational, statistical sort of things. But it's always really interesting looking at confidence interval and the like, and really seeing, well, there's a good portion of the population that this thing worked for, maybe the average, the average population does, but it's clearly something that's working on this group and understanding why does that group work better than, you know, even a negative effect in some groups. So it's, yeah, it's always just about going deep and trying to get that better understanding. And, you know, my goal every time I present is to give someone that aha moment. Just that, you know, just that little thing that excites them going, ’I never heard it that way’, ‘I've been wondering why’ and that sort of thing. And you know, at least that happens to be once a week if I have a chance to sit down and read, which I still try and make time to do. So yeah, it's always very it's, yeah, it's always just about providing something different is what I'm really always about.
Jacqui Fahey (10:32): So flowing on from that, like how does Bio Concepts translate research into products? What's that process?
Michael Osiecki (10:40): I probably could say, there's probably sort of three sort of factors that there's probably, you know, we talked about clinical trials, so what's the clinical trial evidence of the population? What's the mechanisms involved? Is there, you know, particular mechanisms that we can rely on? And then also, I guess clinical knowledge, be it through, you know, the internal team's experience to going out, but really understanding, you know, what's you know, the clinicians use and do, you know...and then it is sort of like pulling that out and go, Well, why, you know, there's lots of clinical evidence for a certain ingredient. I mean, I was always really disappointed bringing out like a psyllium product a little while ago and just never resonated with the market. I go, why the clinical evidence for psyllium is just amazing, so many really top-quality trials on all sorts of different things. But then we sort of realised that, you know, a lot of those different things were probably factors of what clinicians don't think about, fibrin, you know, metabolic syndrome, cardiovascular disease, you know, mental health. We often see, we think of fibre in the treatment of IBS, IBD, you know, gut conditions. So something like PHGG is far more aligned to that in a much more easier, sort of sound. So it's that little bit of commercial knowledge, even though in the research, the evidence for, you know, psyllium is fantastic, that it never resonated in the marketplace because, so there's that sort of aspect.
I think the other sort of thing as well is then, you know, we live in a regulatory landscape, so we've just had a change, you know, the new evidence guidelines just kicked in at the start of the financial year. So that's what I going to say is, what's the clinical evidence? And also, I should also not forget the traditional evidence in terms of herbal medicine. It's kind of actually hilarious in a regulatory sense. You can get away with far more heavier claims or high-level claims in traditional evidence that we can with scientific evidence. So you could have like, you know, I think pretty good clinical trials of, you know, and longitudinal clinical trials on cCQ10 and cardiovascular disease. But, you know, some of those claims are quite limiting, whereas traditional claims are actually quite good. And that sort of thing. So understanding what's the dosages required to actually make those claims in the product. So I guess it's all about understanding the research and it's very, very important to see not only just p values being, you know, being statistically significant, but also is the result clinically significant? There's a big difference between those two.
Jacqui Fahey (13:45): Yeah, absolutely. With regards to nurturing independent critical thinking for practitioners and students, what do you think assists that?
Michael Osiecki (13:59): Always asking questions, I think, and yeah, and making sure you put some time aside to read primary research or learning how to read primary research better. I don't read any opinion leader, you know, key influencer, big person in the fields stuff at all. I might go skim through it and see what they're talking about, but I just go straight, don't read what they say, I read the paper that they're linking to or whatever. Straight to the sources, what I do. And that's sort of what I sort of try and focus on in like, you know, actually been a bit lax in my Facebook being so busy. I haven't done a post of quite a while. Sorry about that. But, you know, that's what I sort of try to do is just get you one good paper or maybe group of papers covering a topic and to support a little bit of a preamble I give, just, you know, just so you're right, because even and you have to be really careful of noticing this. The other day we were looking at inositol’s like myo-inositol and D-chiro inostil and D-chiro for whatever reason has just come back come back into popularity for PCOS. And I'm just like we, that was done, you know, big studies were done in 2010, a little bit earlier, that really investigated this and found that myo-inositol was vastly superior in all sorts of aspects. So why we're going back to D-chiro inositol? and there's a few studies here and there. You know there was like a comparison study through myo-inositol recent one. And you know, I said, Oh, you know, it was a, you know, D-chiro was better in some certain aspects, but I then I looked at the p values for, and the clinical significance of it in the actual text, I bought the paper and, you know, the p values weren't significant. The result wasn't clinically significant. Like it in all objective measures myo-inositol was superior in terms of PCOS and then over really, you know, dug around it than, you know, found, you know, that sort of argument around, you know, D-chiro inositol is probably problematic when we look at, you know, urinary metabolites or urinary inositol, we see a way more D-chiro inositol than myo-inositol in our urine, which indicates that the body wants to get rid of it. Talking to the fertility space you know, the you know, part of the supposed mechanism of action to sort of lead towards PCOS is the fact that myo-inositol is being converted into D-chiro inositol, which actually is an aromatase inhibitor forcing things down the androgen path, which is probably, you know, incredibly problematic in women.
Then in men on the other hand, you know, in inhibiting, the pathways down to oestrogen and the likes. So it's, you know, it's not just really abstracts, I just say people lie, people's words lie. The data that they present, unless they've doctored it, and there's plenty of cases to that, but you know, the data that they present is important. I always look at like error bars. Do error bars overlap? Are the error bars ginormous that I going, my gosh, you're pushing, you, you know, the statistical difference of this. And then I have to go a little bit deeper and look at that, but don't really recommend most people do that. But, you know, I always like look going is does the error bars overlap? Are they ginormous? Because soon as I see, or is there error? you know, any standard deviation, you know, error in the data at all?
Michael Osiecki (17:54): If there isn't, I just ignore it completely. It's totally meaningless data being presented in the data. So it, it's about, yeah, I think it's a bit of, I'm speaking from a very privileged position, I'm coming from a very, you know, you know, scientific background, so I've had lots of time to develop the skills that's a bit hard for somebody to have done, you know, a practical clinical degree that has spent less time doing that. But always sort of look at the data and, you know, because often they sort of say, look is it clinically significant and is it statistically significant? And it's much better to look at confidence intervals than it is to look at feedback. So confidence intervals often sort of say, you know, let's just say a hazard ratio, you know, is reduced by 0.8, the confidence interval, like 0.9 to, you know, 0.2, there's a big confidence interval there.
Very significant. And you can see that there's a, you know, some outliers that are really affected, but also because of, you know, if that, you know, it, you know, awfully if breaks that line at one. So like generally, you know, a reduction of a hazard ratio, you know, sort of is like, you know, a 20% reduction is a 0.8 hazard, you know, hazard ratio sort of thing. And above that increases, but say, you know, it's has a hazard reduction ratio of 0.6, the upper limit may maybe 1.04 and the lower limits, you know, 0.2 you go and which will be the p value is non-significant. But you look at that confidence interval and look at where that population group actually lies and go, well actually hang on a second. There's a tiny little bit of a portion of the population that clearly it's, you know, not working for, but there's a huge portion of that that population that actually has some benefit and looking at those confidence intervals are very important. And, you know, a lot of statisticians sort of complained about the power of the focus on P values. Being a p left value less than point 0.05 or, you know, better being, you know, below 0.01 or 1% chance you know, that that result is, you know, a random sort of thing. It's actually sort of something measurable or more, more precise that the, you know, null hypothesis, you're surprised that the null hypothesis is incorrect. So yeah, it's really trying to, go back to the primary research and look at the data. It's the most, the most important thing you could do. And then sort of ask and then, you know, and that's the sort of in absence of clinical trials and then even just sort of going back and understanding the method because, so often I see very, especially in nutritional field where the decision of intervention is very poorly decided.
Some people might us seen the vital D study where they give 2000 IU of vitamin D and calcium and omega 3, big trial. Problem is, is like a go well, dosage is a bit problematic. And the problem with nutritional research anyway, placebo group, so the placebo group has it naturally in the diet, which assumed to have at least 700 IU of vitamin D. So going, well, you supplement, you know, you're doing this trial where there's only 1300 IU difference between treatment and non-treatment. So, you know, going a little bit deeper in understanding what's going on there and sort of saying, well, that's maybe part of the reason why some of the events go wrong. Also, you know, the intervention just makes no sense in terms of mechanism because, you know, as we know, you need magnesium as well with vitamin D now.
Michael Osiecki (21:56): Calcium, K2 combinations and things like that. Although I am, increasingly like to reduce calcium supplementation actually. Cause I think we get enough in the diet and excess calcium is problematic without the K2 or vitamin D on top of it. So, I mean, we do, that's why I always have the K2 in our calcium products. But I don’t know, I know people like using it. There's sort of some evidence for it, but I'm, you know, once again, it's like that, you know, I always sort of asking the questions of myself and trying to think of how to do things differently and question that.
Jacqui Fahey (22:39): Yeah. You make a great point, an important point rather, going to the primary research, any pointers for practitioners that can get overwhelmed by the research and the biochemistry, sort of any sort of tips for practitioners listening.
Michael Osiecki (22:58): YouTube is great, watching videos to start off with. I mean, that's always really had, it's great, you know, YouTube chat just to get the real, you know, you know, good old Wikipedia, just get a real simple description of just non disease state or whatever. Just to start things off when you, you know, when you just don't know where to go. Like just listening to some basic, you know, first, second year science studies, you know? MIT puts all sorts of lectures up available free. Just, you know, just knowing that basic pathway first is you know, just knowing, you know, when you're reading along, have no idea what that, you know cytokine does or do, or you know, what that, you know, pathway actually, it's just starting at the very, very basic level is sometimes always a good place to start. And, you know, 10-minute video, YouTube.
It is, it is always a little good start. I even do just, you know, to refresh myself or, you know, it's been a little while since I look in that area, just sort of, it, you know, it's kind of you know just to hear that, those basics. I think as I sort of said earlier when you break, you know, when you look at like, you know, the complexity of the disease states, like cancer, you know, is a disease of both hypo and hyper methylation. And you go, what an earth is going on there? And I, you know, this was like a great little, I was like sort of reading and it's always really good to like just read random different non, things that you wouldn't normally read or very sort of like true biochemistry sort of papers.
And there was like this one talking about how, you know, oxidative stress and free radicals causes the DNA repairase to become permanently attached. And a DNA methyl transferase to become permanently attached to the DNA. And so, and it sits there, DNA methyl transferase just sits there going across the DNA methylating, assisting cytokines and whatnot. And it's like, well that's interesting. And then you sort of realise, oh, this is because the first step of DNA repair is to methylate the promoter region of the DNA to stop the transcript from happening. Because the last thing you, the cell wants to happen is it's got a strand break in this gene. And you know, where does damage to the DNA? It's going to happen, in genes that have been expressed because that's where the DNA's open.
It needs to allow transcription factors to bind to allow the gene expression. So that's where the damage is going to occur, not the ones wrapped all up and methylated.
And so what happens is, you know, the DNA methyltransferase, due to, you know, free radicals and other inflammatory situations, gets stuck to the DNA and just sits there methylating across the DNA. So it's all these genes that the cell normally wants to produce, all these genes that, you know, stops the cell cycle. So what, you know, the cell starts saying, oh gee, my DNA's getting methylated, I need to do something about this. So a lot of this stem cell and cell cycle genes and d methylation genes, you know, it starts producing. So it starts expressing those things, which obviously leads to DNA, methylation, cystone D methylation to all these, you know what we call oncogenes.
Michael Osiecki (26:45): But these oncogenes are stem cell genes and cell cycle genes, in their normal function. So what happens is these genes get opened up, try to solve this problem of the d methyl transferase, are stuck at the DNA, I can't get rid of it. I need to de methylate my DNA, so go back to my normal function. And so that's why you see it this pattern of, why you get the silencing of all these cell cycle control genes, which normally should be expressed. Well, DNA's been, you know, methylated there and these expressions of these stem cell oncogene is because the cells trying to solve the problem, but in solving the problem, it then leads towards, you know, cell cycle and activation and the cell loses control and that inflammatory environment and becomes a cancer itself, you know, if the immune system doesn't wipe it out first, so, you know, it's something very simple, explains something, you know, why these, you know, why is the gene expression completely switched over and flipped in a cancer cell?
Jacqui Fahey (27:55): Is that on a YouTube video as a visual?
Michael Osiecki (28:00): Haha. No. That was, I was reading, Forgot where I had that, that was a little while ago, actually a year back. And I was like, and I sort of, you know, I was just going to say, you know, I always try and find that aha moment. Yes. I've always wondered this. And I'll just reading something simple like that just sort of went, oh, that's it. I always wondered that.
Jacqui Fahey (28:20): With your mentioning YouTube, are there any particular channels you like or talks?
Michael Osiecki (28:30): I should look on my YouTube. Not really. I just sort of search and a lot of the universities actually now have stuff up.
Jacqui Fahey (28:39): Okay.
Michael Osiecki (28:42): There's the rest of what's it called? There's a, what do they call? I think it's like minute science and things like that as well. Think it's like minute science.
Michael Osiecki (29:02): Trying to remember, the science show, the sci show. Also it's like, you know, just sort of a few. But yeah, often you see some university lectures and you know, of course content or whatever that, those little pathways and things like that that are just, you know, very, very, it helps to down step it a bit and yeah.
Jacqui Fahey (29:33): Fantastic. Thank you for mentioning those. If I can ask you with regards to COVID- 19, that's having quite the impact on people's health from overproduction of histamine, cardiac issues to cognitive impairment. What nutrients and herbs are playing, and will play an important part of an individualised prescription for those experiencing long COVID-19?
Michael Osiecki (29:52): Yeah. Really, actually, this is actually one paper that managed to do before I had my heitus with Facebook back in April. And also what to get it, I like, I'm, I'm a mechanistic person, so I need to understand what's going on. And then I could make my knowledge a lot better. I mean, starting off with how lovely is this virus binding to ACE-2? you know, like just to tax your entire blood system, which, you know, at every organ, you know, every single organ has this. So like you're just going, you know that for a start it's affecting every single organ. It's going cause, you know, cellular damage to organs. But it's also affecting your vasculature which is then, you know, affecting blood flow, you know, in your brain and lead to, you know, ischaemia or, you know, organ ischaemia as well.
But in Cell about April what's it called? It's called, it was probably the first paper that they just did like this huge multiomic study of long COVID patients, basically found multiple early factors that, you know, post-acute COVID 19 sequalae. So, you know, it's the terminology. Now sequelae, and it's kind of interesting now because you know, this is probably the first paper that talked about it. And now I'm seeing all these other people sort of talking, you know, much more specific about it. But I was just like that, you know, it was like a great, this is like a keystone paper that literally covered it and it's literally sort of, there was four risk factors in terms of that long term effect. And I also sort of, I guess talk about that sort of organ damage a bit later.
So, because it talked about adrenal fatigue, so full on, you know, cortisol deficiency that's independent from, you know, if, you know, if a patient actually goes to the hospital, obviously treated with, you know steroids and cortisol anyway. And it's, if it's happening three months after hallmark of long COVID, so you've got adrenal damage and adrenal insufficiency. We also know that viral load is very important. So a - COVID viral load or enough for infection, and I'm sure many people now aware of the whole Epstein barr virus reactivation as we talked about. But many other viruses and infections are, you know, are leading towards, you know, the fact that these people will all likely have long COVID effect, you know, rather than having one infection, you have two. There are some interesting autoimmune effects targeting your nuclear bodies and interferon alpha two.
So basically, that hyperinflammation, especially in week two of these patients leads towards this autoimmune effect. And then basically we see a dial of and dysregulation of your reactive cytotoxic CD8 cells and CD4 T cells. Which that's your, that's a gastrointestinal complication. So because you're not getting your proper, these gut problems, losing gut immunity access and that gut overgrowth from these, those gut issues. So then, you know, give an example of how I think go. This gives me a lot of details. Okay. These are the risk factors of people getting long COVID and this is what we sort of, you know, we describe someone with long COVID, what are the sort of things we see? we see that brain fog.
When I think about adrenal fatigue I think about mitochondrial dysfunction in the adrenals or pituitary issue I guess as well. So I know that, okay, CoQ10, lipoic acid, acetyl l-carnitine, those sort of mitochondrial nutrients are extremely important across the body. And when we're talking about, you know, we were talking about ACE-2 infecting everything, in epithelial dysfunction, i.e., in your vasculature, you know, cellular repair, you need a lot of energy. And that's why mitochondrial nutrients are so very important for that long term sort of impact of having such an effect that is you know, multi-organ faceted. Then that whole, you know, then it's just the boring old immunity stuff.
You know, the quercetin to get, you know, probably into liposomal form seems to be more effective. Just to get it up. And, you know, I always question like, you know, I need to have a reason, you know, why something needs to be in liposome. Why does it need to be highly absorbed? I was always a bit negative towards quercetin liposomal for a while because going along the mechanism of action, it's happening through the gut fermentation and making all these active metabolites. So in terms of sort of its anti-inflammatory effect and all the other little bits and pieces, you know, maybe it's the, you know, and metabolic syndrome and, and the like, anti-inflammatory that, you know, that's really just regular quercetin and acting in the gut, fermented by the gut and it's metabolites.
Michael Osiecki (35:27): But when we talk about like, antiviral effect of quercetin actually inhibiting, you know, viral replication, it needs to be in the bloodstream. So something like, like liposomal or sort of where it sort of kicks in. So I, so it's nothing really revolutionary I could recommend, but then it's just understanding well, what appears to be, It seems like COVID does affect where your weakness is at. You know, whatever ailment you had. It, it's, you know, if you had heart problems, it makes you heart problems worse. If your diabetes, it makes you type two, it makes your glucose control worse. So it's just understanding what are the problems that you or your patient has previously had in the past. And it's going, you know, you have to be more targeted in that sort of general thing.
But the only addition I would say is the mitochondrial nutrients and, I did a little talk a while ago in Indonesia, you know, I was asked to do a talk on cortisol. I was like, Oh gee, great, that's exciting, okay, I'll see what I can do. And I thought the adaptogenic herbs are very useful and it's definitely going to give you that boost and control. When I was looking deep down in the biology of it all, it's really that mitochondrial aspect that, you know, promoting cellular repair, helping autophagy happen. And you know, then you know that, even like that auto-immune side is well with that long term inflammatory side, it's very important. So I guess probably my emphasis is understanding, well, what's the organ being affected? I know that in 20, 30 years’ time we are going see a lot more people with renal problems because of the cardiovascular issues leads towards renal damage.
In itself it targets the kidneys and, you know, renal, you know, it will affect the kidneys and that may drop a couple of points off depending on your lifestyle and genetic outcomes. And then cardiovascular or diabetic issue, you know, that could accelerate your renal decline. And, and going into different, you know, higher stage of renal failure. So looking after your kidneys is very important and very underappreciated organ. I did a lot in the haemochromatic world and all speak an engineer. So I love blood. You know, blood is so important and the transport of blood, you know, fluid flow. So you know, things around that, cause a lot of that mental brain fog is both that mitochondrial side but also blood flow. Because obviously vascular issue and you know, there's that big overlap between, and I wouldn't be surprised as well given the functionality of, you know, amyloid being, you know, an immune molecule, we'll probably see a lot of people get around more plaques in the brain. Not like that's a cause it's a marker of the fighting Alzheimer, but at the end state of it. But I wouldn’t be surprised that if you're predisposed and don't have once again, good blood flow clearance and also good liver function as well that's going be problematic for helping you clear out because, clearing out, making sure you have good blood flow in the brain be it, you know, making sure that you don't have hypertension or hypotension you know, magnesium, taurine, all that sort of thing. Hibiscus, it's fantastic break for the control efforts. You know, getting that, the, the blood flow going and exercise obviously.
Jacqui Fahey (39:34): Yes. The lifestyle factors.
Micahel Osiecki (39:36): Lifestyle, yes. And that sort of thing is sort of the way I see it. But I think really the cornerstone in my mind, given, like when I sort of read autoimmunity, adrenal fatigue and immune dysregulation my mind goes to mitochondria and really doing that, and honestly, I've been trying to convince myself around ubiquinol stories and I just can't prove myself to, because I haven't seen any evidence at all that it's superior. Clinical relevance and p values are not statistically, not statistically different. I love to use it, I think it's pretty cool, you know, activated B vitamins, all that sort of thing. But, you know, every single trial I've looked at, I’m just like going, all comparison studies and absorption studies and the like that there's actually no, you know, clinical significance whatsoever and statistical significance in its effect.
So that was like going, well, that's disappointing. And, you know, like cardiovascular, there was some arguments, you know, around elderly populations but I’m going, there's plenty of long term, you know, 10 year, you know, 5- 10 year cardiovascular studies and you know, 70 year olds. And then even like, you know, you know, five-year study plus another 12 year follow up study on, you know, elderly population, with ubiquinone, you know, it works, you know, 10- 15% reduction in cardiovascular mortality.
So, you know you know same with some of the B3s, I love B3, I’ve been using them for a long time. You know, that's very important in mitochondrial function. All of them have different degrees of usefulness. I mean if you're putting like your full medical hat on, you'd probably have to say niacin is the best one in terms of clinical trial evidence but then mechanistically, there's, you know, some issues around that.
All of them, you know have to be broken down into methyl amides in the end to get out that B3 cycle. Anyway, that's how it excretes out. So it actually, a lot of the studies that compare a lot of the other ones, it's kind actually seeing how each one except niacin, but like niconamide, mononucleotide, riboside, all three of them equally increase NAD levels. So there's actually no difference between those three, niacin is inferior, but then niacin got that, you know, we don't like the niacin flush but actually that's the beneficial effect. So we're talking about the cardiovascular issues, you know, the low cholesterol and you know, provoke vasodilation, that’s the niacin flush. You need that big, niacin flush to get the boost.
Jacqui Fahey (42:45): Yes. Yeah. And have you heard with those nutrients you've just mentioned much anecdotal evidence, clinical feedback?
Michael Osiecki (42:56): Yeah, I've kind of got a bit bored of COVID. Sorry, I stopped listening a little while.
Jacqui Fahey (43:03): Fair enough. Yes.
Michael Osiecki (43:05): I was in India three weeks ago and I had COVID three weeks before I left. So sort of I was like, I'm glad I got it in a perfect window that I have good immunity when I go to India. Because I was getting really nervous going to India with something. And I know personally those mitochondrial, soon as I got it, so knew that I had it. I just started taking, you know, the mitochondrial nutrients on top of that immunity side. Cause I just knew that, I just knew after reading all these sort of studies that yeah, clearly all the other complications is based off based off that mitochondrial dysfunction. So if I could defend, you know, those antioxidants, you know, protect those mitochondria and keep them going, probably, you know, will help. But that's, you know, what's getting very greater evidence. mean there's more and more sort of studies around the sort of place, you know, it was kind of you know, interesting in India where they government promoted vitamin C, zinc and magnesium for their population. That sort of thing. I mean by you know, some close, actually I've been talking to some, you know clinicians in India were just saying IV vitamin C and even, and it be type supplemental oral, supplemental vitamin C and zinc was cornerstone of what they were doing and were getting very successful. I know that one clinic probably was doing about a hundred patients, you know, a day. So that's not very big in Indian standard, just so you know.
But didn't, no mortality with his protocols of using you know, pretty bulk standard, you know you know, just vitamin C, zinc, magnesium, bit of selenium, some B vitamins and the like which I thought was quite impressive those with those cases.
Jacqui Fahey (45:37): Yes, I'd heard that the AYUSH government of India is promoting homoeopathics as well as hot water yoga, quite a mixed nutritional, herbal and lifestyle approach. I mean you did, as you said, you are dealing with a large population there, so their approach was quite integrative.
Michael Osiecki (46:01): Well it just, it just had to be. There'd be people, people were selling their homes to get treatment.
Jacqui Fahey (46:11): Oh gosh, oh dear.
Michael Osiecki (46:14): Yeah, to get, you know, some of those antiviral treatments, which are, you know some of them are, I wouldn't like to take long term. That's the problem, I mean, that's probably any sort of antiviral treatment in terms of a drug based, they're highly mutagenic thing, sort of something you can't sort of take.
Jacqui Fahey (46:42): Yeah, that's right.
Michael Osiecki (46:44): Long term at the end of the day. So yeah, it’s definitely how to see a pandemic live in the wonderful world of instant communication. It's been a lovely learning experience for me as well. Scientific literacy and trying to explain things, you know, much more deeper sort. I just sort of, you know, sort of realised I'd be quite privileged and, you know, working in a lab and understanding how to do different, you know, assays and how different methodologies are done. And, you know, I've never really studied, you know, virology, you know, undergrad, never really studied the level, but, you know, understanding that know how the general population understands and that, you know, leads to when it's something you don't understand leads to panic and confusion. And that's why education is so important because it gives you a better understanding to, you know, tackle these problems and solve them in a, you know, in a stepwise logical matter.
Michael Osiecki (47:49): Otherwise just Yeah. You know, making decisions in a panic with little knowledge is fraught with danger. I mean, sometimes you have to do that you know you know, you know, lovely case studies on, you know, people dealing with you brain trauma and just, you know, winging it, you know, having some basic knowledge winging and, and working it through and then later reading about it and going about, that’s a very good protocol. So, but that's somebody that had the good knowledge base. So yes. It's so very important around just expanding your knowledge. And keeping on going.
Jacqui Fahey (48:26): That's right. Exactly. And appreciate your posts. I'm not often on Facebook, but I've seen your Facebook posts where you've down stepped some really interesting papers. When will we see some further chat from you on Facebook?
Michael Osiecki (48:41): Well as I said to you before we started podcast, I’m soon heading to Malaysia. It's so, I was sort of earmarking that period to keep myself occupied. So I try to do some stuff there around the place because I, you know, I was doing some reading on, you know neurogenetic diseases at the moment and a bit on renal space as well. So maybe I'll do some posts on that. But I don’t know, it’s, you know, you just see that this exponential expansion, it's very hard to keep up. Yeah, definitely. You know, when you ask that previous question, it's like, it's just hard. And it's just, I think it's just one thing that's going to decide to read one or two papers a week that's different to what you normally would read.
Jacqui Fahey (49:40): Read. Right. Yep.
Michael Osiecki (49:42): And just, you know, go a little bit broader. You know, that's something that sounds slightly interesting, slightly related, maybe one or two words, you know, that you know you are familiar with and do all the time. But something that you'd never really heard of and just understand that little bit and go, Okay, that's something new and different. Yeah. And you never know what you find.
Jacqui Fahey (50:05): Yeah. No, that's a good approach. Well Michael, thank you so much for sharing your insights with us today on Common Ground.
Michael Osiecki (50:12): Thanks, Jacqui. It's been a pleasure. Thank you.
Jacqui Fahey (50:14): Thanks for tuning in today. A transcript of this interview shall be available on our website, vital.ly. Feel free to leave us a review. We'd love to hear from you. Thank you.