Good afternoon. My name is Dr. Cameron Jones and welcome to this week's edition of The Mould Show. I'm sorry I'm a little bit late. The last couple of days I've been participating in a legal matter with an overseas client with regard to mould exposure. In any case, my schedule for preparation of these weekly shows has been somewhat delayed. Today, we're going to be talking about mitochondria and mould. What you need to do... What you need to know, I should say, and to some extent what you need to do if you want to protect yourself from mould and also understand some of the reasons why your body might be showing an immune inflammation or an oxidative stress reaction.
My decision to focus today on mitochondria is really due to the fact that in the last couple of days on the 21st till the 24th of February, some really fascinating papers have been released into the peer reviewed literature, and I want to base this week show all around some of this emerging research because a lot of you also are probably aware that mitochondria comes up in the lay literature and all over online and it is being increasingly linked with a range of toxins in a way and talking about how the cell and the cells in your body cope with these exogenous threats to our safety.
So what I'm going to be covering today is, in part one of this is pretty much a helicopter view of what are mitochondria, what does this term mitochondrial dysfunction actually mean, is there a connection between the mitochondria and people's experience or exposure history to mould and water damage, and a very interesting publication that also came out this week that I have the full paper and it's talking about the impact that some well-known mycotoxins, one called ochratoxin A, which is commonly found in water damaged buildings, what its impact is on the reproductive capacity of a rodent model and therefore what the potential impact is at the cellular level. We'll also be doing our regular show sequence or something that we're doing certainly in 2020 where I'm going to be cherry picking from some of the microbiology and mycology news that impacts on our understanding of this very important domain of science and I'll cover that at the end. So stick around till then.
In any case, I want to move quickly into, as I said, a helicopter overview of what are mitochondria. Well, in our cells, there are these things called organelles which are very small objects and these organelles or objects are one of the components that contribute to the cell being able to carry out its natural function. In many cases, the natural aim of a cell is obviously to continue living and reproduce, and one of the types of organelles found in eukaryotic microorganisms and also eukaryotes like ourselves are these things called mitochondria and they are the powerhouse of the cell in the fact that they produce the ATP which powers the cell cycle and essentially they enable the cell to respire. So they're intimately linked with respiration and the use of oxygen.
So up on the slide in front of you, we have a schematic of one of the organelles with the individual components of the organelle, and then the micrograph on the left hand side shows these organelles, the mitochondria in red. In any case, as I said in part one, this is just going to be an overview to introduce you to this fascinating topic of mitochondria and how they're linked with a mould. This first paper I want to highlight is also free on Pub Med. So you can go to the URL that I've linked to the bottom of this slide and you can download it yourself. Essentially, this publication is talking about something fundamental called mitochondrial dysfunction because this is increasingly being talked about with regard to why people are particularly susceptible to mould in their environment and why this leads to a cascade of events at the cellular level, which is then experienced as an adverse health response.
So in our bodies and in our cells, every one of our cells there are mitochondria, these organelles, and they are responsible, as I said, for maintaining cellular energy, and there's this concept of homeostasis, which is the normal functioning of our body and of our cells. So the aim of the human body is to maintain a level of equilibrium or homeostasis, and when anything from outside the cell impacts on the inside of the cell, this can impact on one or more of the organelles systems at the cell level. When the fusion and fission process, which is the mechanism of DNA replication to allow the cell to grow and exchange and function, when this impacts on mitochondria, it's termed a dysfunction. So mitochondrial dysfunction is a catchall term, meaning that the mitochondria just don't do what they're supposed to do and they don't respire as efficiently or effectively as they were designed to do.
There's this other connected concept called oxidative damage as well, and mitochondria also produce something called reactive oxygen species and it's their antioxidant system. So consider this as their own ability to, for example, use vitamin C as an antioxidant. So unfortunately when a cell is dealing with an exogenous toxin like a mould toxin or some other toxin, there is this propensity for the cell to be disrupted and for a build-up of reactive oxygen at the cellular level to cause an inflammatory response as well as oxidative damage, and think of oxidative damage very much like hydrogen peroxide bleaching something or causing an oxidation reaction and we'll get into this in the next couple of weeks as we delve more deeply into mitochondrial dysfunction and the role of mitochondria in our bodies.
In any case, there've been a range of different diseases or adverse health problems which are linked to mitochondrial dysfunction and they include type II diabetes, hardening of the arteries, neurodegenerative conditions like Parkinson's and Alzheimer's disease and of course cardiomyopathy problems and cardiac impacts and impacts on at kidneys as well. In any case, this publication which is free on Pub Med goes into some detail about this concept of mitochondrial dysfunction. I've just provided some highlights from this particular publication. I urge you to go to Pub Med and download this paper yourself and read it.
In any case, another wonderful publication has come out this week as well and this has been focusing on something called mitochondrial antibodies. To give you again a very high level overview of this concept of what a antibody is, in our immune response system, a cell will mount a challenge to an introduce toxin based upon this antigen antibody lock and key hypothesis. Think of triggers for the immune system like the number of mould spores in the air and this paper that came out on February 21 in the literature by Ellen Lieberman and Luke Curtis, they're talking about when airborne mould levels above 100 to 1,000 spores per cubic meter are sufficient to cause a wide range of human health problems.
Now, when an antibody to mitochondria challenge eventuates, this means that there is an immune response to the organelle. Now this is not good because in the same way that an antibody would be raised to a foreign invader, like a bacterium attempting to cause an infection, if an antibody response is raised to one of your own organelles, essentially you are getting self-harm at the cellular level. This paper is going into some good biochemical detail about what the enzyme is or the protein that the antibody is being raised to and it's something called pyruvate carboxylase, and this is known as a major site of antigenicity for something called these mitochondrial antibodies. This particular paper has examined the connection or the correlation between the anti-mitochondrial antibodies and individuals who have known exposures to mould mycotoxins and other toxins in their local environment.
What the scientists did was that the participants in this study received blood tests that mapped out their autoimmune, metabolic, hormonal and nutritional parameters as well as testing for their anti-mitochondrial antibodies. The conclusion that they reached was that high levels of anti-mitochondrial antibodies were all associated with patient exposure to mould and moisture and that the correlation appears to be significant. So the exposure to the water damage and the mould is obviously able to cause adverse health via direct infection via an allergy response to the particulate due to a toxic response to the mycotoxin and that this works at the level of the organelles or inside your cells by damaging your mitochondria and that then leads to this oxidative stress and also an inflammation reaction.
I now want to move onto some other research that also came out and this came out at the tail end of 2019 in November and this is a fascinating paper looking at the impact of a well-known mycotoxin called ochratoxin A, which is a fungal mycotoxin and how this impacts on the reproductive cycle. Yes, this study is done in mice, but the important takeaways from this study are, and what the scientists again we're looking at is how does this mycotoxin, the ochratoxin impact on the reproductive cycle of these mice. So they looked at something called oocytes, which are the immature egg cells and these are the cells that are small enough to haven't even descended through the fallopian tube yet to become an ovum, so they're the very small eggs for want of a better word.
So, when female mice were treated with ochratoxin A over a period of seven days, they determined that it weakened the quality of the oocyte or the immature egg cell and it impaired its ability to mature. Or another way to put it is that messed around with its ability to grow as expected, similar to the problems that we see with the mitochondria and these enzymes being raised or the antibodies against the mitochondria. What they discovered was that when female mice were treated with ochratoxin, they displayed something called an ovarian dysfunction and this led to measurable decreases in the number of offspring that these mice were able to deliver.
So the conclusions to the paper were that ochratoxin A causes oxidative stress leading to oocyte death. The takeaway conclusion from the paper was that ochratoxin definitely impairs and reduces fertility by a combination of oxidative stress and external modifications to the DNA. I will be talking further about this concept of oxidative stress, immune dysregulation, and mitochondria in coming weeks.
Now, as usual, I want to cover the breaking news for this week. Okay, and the first paper that I want to highlight is again a very interesting study that has just come out on something called Curcumin. Now Curcumin is a health food, which is certainly sold as a supplement, and Curcumin has a potent antibacterial, antiviral, and antifungal ability and there's a whole range of publications in the peer reviewed literature demonstrating these really important properties of this particular spice. Now this publication, again, I've put the URL up at the bottom and it'll be in the show notes.
The scientists were looking and did a very interesting experiment, they got two commercially available Curcumin formulations, one from a company under the trade name of Vitamin Shoppe and one under the trade name of GNC. I've put up some diagrams of their bottles. What the scientists did is that they got a group of test subjects, in this case, rats. What they did is they wanted to test how Curcumin would impact on the gene expression of something very important in a particular antioxidant at the genetic level. So some of the groups of rats were fed the Curcumin from the two high street vitamin store options and some of the rats were hooked up to an IV and some of the rats also received a pure formulation of Curcumin from Sigma, which is a well-known chemical supply house that supplies scientists and medical researchers worldwide with reagents of different purity.
So the Sigma product can be considered the most pure and the high street formulation found in the health food supplements is probably not as pure as the Sigma formulation. But what these scientists were looking at, because Curcumin acts and is limited by its what's called bio-availability. So what their conclusion from this study was is that even very low bio-availability percentages of the whole food, natural vitamin was still capable of switching on these antioxidant genes and so therefore it means that there does not seem to be a dose dependent regulation of the concentration of Curcumin to be able to activate or switch on these antioxidant genes.
For anyone who is interested in proactive health and whether or not you can take supplements to improve your own wellbeing, studies like this on Curcumin in rats is certainly demonstrating that there is some strong efficacy, at least in switching on positive antioxidant gene activity and expressing these genes with the supplements that you can purchase yourself.
The next paper again has a wonderful, wonderful title, Stress and Psychiatric Disorders, the role of mitochondria. Again, this links me back to the foundational topic of today and for the next couple of weeks about mitochondria. What these authors are showing in this paper which I have a copy of this, it is going into its final form later in May, 2020 and I'm going to be talking a lot about this paper, is that these authors are positioning with strong language that stress causes mitochondrial changes and that in a sense mitochondria are the organelles or the sites which provide a response to adversity at the biological level and they refer to this as a biological embedding of adversity.
In any case, I think that this is just a fascinating publication and it is one more example of the relationship between how we feel and our mood and our potential anxiety response and how this is all linked at obviously the cellular level and how external triggers can modulate our neurocognitive and also our emotional wellbeing.
The final news item that I want to talk about again comes from a fascinating paper that was looking at a respiratory response to mould exposure. This is an excellent study which studied individuals in Finland and they were particularly looking at people who had something called asthma-COPD overlap syndrome. So that is an asthma response with an underlying respiratory obstructive disorder. So they were able to find 520 participants who were diagnosed with asthma-COPD overlap symptom and they were also able to find 932 individuals with none of these symptoms and for which they were the control.
What they did is that they were looking at common exposure indicators to water damage and mould and these include, have you had water damage, do you see damp stains, is there paint peeling at the property is there visible mould is there mould odour? These two groups of people were polled about their experience of mould and water damage at the home and also at their workplace. The very, very important news is that the risk of asthma-COPD was significantly linked to mould odour in the workplace and that the risk of asthma-COPD was not related to mould exposure at home. Why this is important is that so often the academic literature is focusing on the home environment as the trigger for people's mould exposure and this study is showing that in fact the workplace could be a very underestimated triggering location for those who have mould problems.
In any case, that is the news that I'm bringing you this week. I think that there were just a handful of the articles which impact on our understanding of mould and water damage exposure. I'm not covering the COVID-19 crisis this week because I think that that is playing out in the academic and news medium and so therefore I'm back to focusing pretty much exclusively on mould. In any case, I wish you well. I hope you have a great week. Next week, we will be continuing on with our investigation of the tremendously important field of mitochondrial research, mitochondrial dysfunction. We'll be moving on to glutathione as well. In any case, my name has been Dr. Cameron Jones. I'm an environmental microbiologists. Have a great week and I'll see you next week. Bye for now.
Wang, L., Li, W., Cheng, D. et al. Pharmacokinetics and pharmacodynamics of three oral formulations of curcumin in rats. J Pharmacokinet Pharmacodyn (2020). https://doi.org/10.1007/s10928-020-09675-3
Stress and Psychiatric Disorders: The Role of Mitochondria
Teresa E. Daniels, Elizabeth M. Olsen, Audrey R. Tyrka
Annual Review of Clinical Psychology 2020 16:1. https://doi.org/10.1146/annurev-clinpsy-082719-104030 (to appear: May 2020)
Jaakkola, M.S., Lajunen, T.K. & Jaakkola, J.J.K. Indoor mold odor in the workplace increases the risk of Asthma-COPD Overlap Syndrome: a population-based incident case–control study. Clin Transl Allergy 10, 3 (2020). https://doi.org/10.1186/s13601-019-0307-2
Ochratoxin A exposure causes meiotic failure and oocyte deterioration in mice. Theriogenology. 2019 Nov 10. pii: S0093-691X(19)30505-9. doi: 10.1016/j.theriogenology.2019.11.005.
Mitochondrial Dynamic Dysfunction as a Main Triggering Factor for Inflammation Associated Chronic Non-Communicable Diseases. J Inflamm Res. 2020 Feb 14;13:97-107. doi: 10.2147/JIR.S232009.
Mold Exposure and Mitochondrial Antibodies. Altern Ther Health Med. 2020 Feb 21. pii: AT5799. https://www.ncbi.nlm.nih.gov/pubmed/32088666
Opening Horizons (Kielokaz ID 361) by KieLoKaz. https://freemusicarchive.org/music/KieLoKaz/Free_Ganymed/Opening_Horizons_Kielokaz_ID_361