Reducing Oxidative Stress in Mitochondria: Key Strategies and Insights

foreign for people to to join in um to start with the tonight's webinar

foreign thank you for joining us um for tonight's pants webinar thank you

for everyone who's joining us live and to everyone who's listening to this presentation later on my name is Alma

Ahmad I will be your host for this evening so before we start tonight's webinar I just wanted to go through some

housekeeping the webinar will be recorded it will be available from the band's website it will last for about an

hour and we will have 10 to 15 minutes at the end for some questions and answers so if you do have any questions

as we go along please type them in the chat box and I will run through them at the end at the end of the presentation

so I'll presenter this evening is Jillian Crowder Dylan is a naturopath and nutritional therapist she's been a

senior senior member of the Academy of nutritional medicine since 2010 and she's the director of research Jillian

specializes in complex multi-system disorders and finds mitochondrial dysfunction underlines much of days

chronic diseases so this is part two of a three-part webinar um in part one Jillian talked about

about providing targeted micronutrients for mitochondrial support and function if

you missed part one the recording is available from the band website and their science and education section so

tonight is part two and um in this webinar Janine will talk to us about reducing oxidative stress in

mitochondria so it is my pleasure to welcome Jillian to tonight and um please dealing with alfredo dude

please welcome thank you very much thank you Elma for giving me this opportunity and and to

bend um very very grateful it's a topic I'm so passionate about so this is um a bit

different to last week's well I say last week's um the previous one because it's about

reducing um stress primarily oxidative in the

mitochondria and the first section will be about um an overview of free radicals reactive

oxygen species and um reactive nitrogen species which is sometimes combined in one term one

acronym r-o-n-s the second section will be about agents to remove to reduce excess oxidative

stress the third will be about supporting antioxidant enzymes and the final section will be about exogenous

antioxidants that have a good evidence base so first of all to just um

mention these two terms free radicals versus reactive oxygen species free radical is any molecular species

that has an unpaired electron as here the red one and that is thus highly unstable and

reactive and it can either contribute or accept an electron and therefore behave either

as an oxidant or a reductant and reactive oxygen species are a subset of free radicals they contain oxygen

and several of the most common reactive oxygen species are found inside mitochondria which is um

that the mitochondria are actually the greatest producers of um reactive oxygen species in the body and

we'll be going through which these are in a further slide so as mentioned the mitochondria are the

key source of oxidative stress in most cells and we have along the electron transport chain in particular where

oxygen is being metabolized um we have superoxide anions and hydrogen

peroxide and the hydroxyl radical which is actually the most damaging of all and these are produced primarily by

the electron transport chain complexes one and three and are hopefully scavenged by

endogenous antioxidants and we'll be going through which these are again in a further slide in Greater

detail so um interestingly mitochondrial

reactive oxygen species are required for normal physiology but only at a low level in a tightly controlled quantity

um it wasn't known until relatively recently in biology how very important they are for

cellular signaling um they do signal to the nucleus and Signal back to each

other as well they have a sort of Quorum sensing very light bacteria from which they originated they are responsible for

maintaining homeostasis and promoting adaptation to stress and um low levels of reactive oxygen

species activate stress responses that can be beneficial to the organism and even extend lifespan

so this image here from a scientific article shows that they can be responsible for differentiation for

example um the production of fresh tissue from stem cells for immunity particularly our

um innate immunity is driven to a large extent by the mitochondria metabolic

adaptation for example in hypoxia if the organism is undergoing starvation putting

specific mechanisms in place to to preserve life as well as possible even if that does mean autophagy which means

cell um death but it's um the recycling of the portions of the cell and the

mitochondria that can still be used and otherwise discarding the debris so um another term for actually doing

that with mitochondria in other words recycling them discarding their dysfunctional pieces is mitophagy

so the Ross are all very involved in that process and um essential for life now

interestingly um Dr Robert navio who I mentioned last time who was the

um sort of key driver of the cell danger response that's become um you know very well researched I mean

millions of NIH dollars have been put into researching it related to um me CFS and um autism as well

um he wrote a really rather stunning article that reflects what of course other researchers have determined before

him but taking it really to a further level which is could free radicals actually be

oxidative shielding rather than oxidative stress and I'll just read one paragraph out of that

in this review I report evidence that the mainstream field of oxidative damage biology has been running fast in the

wrong direction for more than 50 years reactive oxygen species and chronic oxidative changes in membrane lipids and

proteins found in many chronic diseases are not the result of accidental damage instead these changes are the result of

a highly evolved stereotyped and protein-catalyzed oxidative shielding response that all eukaryotes adopt when

placed in a chemically or microbially hostile environment and so this reflects what we did briefly

touch on last time which is the ability of the mitochondria to actually sense danger in the cell and in the overall

environment and to push out or stop using the oxygen that they would normally metabolize and

instead it's utilized in the cytosol to fight battles um like

infections whether viruses or bacteria or to attempt to push out contaminants and heavy metals and so on

so this is when they have switched protectively in order to do that though there are many many other processes

involved but one of them is instead of utilizing the oxygen inside the mitochondria

using it as a very very um actually dangerous radical when it's not being metabolized very very

carefully along all the steps of the electron transport chain it's capable of preventing viruses and bacteria from

multiplying and um many other processes that are helpful including changing the pH of the cytosol

so this is what he's talking about here partially and um absolutely fascinating article do have a

look at that if you can but of course he was putting a point on it but completely realizes that free radicals do have

these two um at least um sort of sides of the coin which are

that they are a mix of both an Adaptive physiological stress

involving redox reactions that's reductive and oxidative reactions but if too high if the load is too high or this

continues for too long unnecessarily then you're going to get pathological oxidative damage and this article

describes that so um there are different roles of free

radicals I'll just go through what they are redox cell signaling which we've just described or mesis which is where

they activate stress responses that are beneficial to the organism protective which again is this

cell danger response that we've just described when it's acute and destructive when the load is too

high and um the they overwhelm the reactive oxygen species overwhelm antioxidant

defense mechanisms and play a key role in neurodegenerative processes and then they can get stuck

um which is a rather sort of um but you know informal word for the CDR

the cell danger response um reacting to either a very high stress of whatever

kind it can be infectious heavy metals even physiological if that then becomes uh sorry I meant psychological and then

that can become physiological trauma for example and then it the the cell danger response can become jammed

due to the hyper vigilance of the mitochondria um and the cells overall understanding

that possibly um this this could continue could recur and um navio calls this uh difficult

term and Acro adaptive metocellular dysfunction but um I prefer to just say that the cells are

jammed or stuck and um interestingly this does help to see what may be going on with patients who just don't recover

as fast as you would expect even when the um you know clear stressors appear to

have been removed so um this

image here kind of summarizes what we're talking about you've got a low level of Ros I'm

just using that term to mean all the free radicals including the nitrogen species as well a low level

um is essential for homeostasis a medium level moderate for adaptation to stress but too much then it can induce

um damage including death it's just useful for us though to remember as therapists that you can

provide excess antioxidants it's important to remember um that you need to balance it's the

modulation between Pro and antioxidants that is actually the essence of of of cellular processes

so going on to the next section um what can cause

um oxidative stress that we can actually have an influence on that we can remove well electromagnetic frequency is a

major cause of oxidative stress including in the mitochondria it can lead to the depolarization of the very

delicate membranes that actually have a voltage between them and um once they're fully depolarized the

mitochondria die so um the huge electromagnetic stresses that we are

surrounded by um do need um particular attention and some

patients are more sensitive to these than others we did mention that briefly last time so I won't go into how to do

that um another is heavy metals which can induce

reactive oxygen species production within the mitochondria and here we have one article evidencing how severely

arsenic can do this by inhibiting complex one which leads to excessive generation of these and

also Mercury and aluminum of course too none of this is a surprise in fact cadmium I mean you're doing

um tests of heavy metals all the time with your patients but it's just useful to remember that this can also cause

that huge down regulation of the mitochondria and then other stressors that can cause

the same are um of course what we've been struggling with the last three years at

the sarskoff II and other viruses can create havoc in the mitochondria Riot via the production of these um

oxidative species as well and um I'll just read this sentence at the

bottom from this article that's referenced we demonstrate that sarskoff 2 induces mitochondrial damage of

mitochondrial membrane depolarization mitochondrial permeability transition Port opening

that's the opening of the pores of the membrane of the mitochondria and basically letting the innards out and of

course eventually it's going to cease to function properly and increased Ros release and this is part of what's

happening in in some cases of long covert that we're all seeing and other viruses can do that too

cardiotropic viruses particularly cause mitochondrial dysfunction and there's an entire Cascade that's beautifully

explained in this article here the viruses that are particularly able to do that are Coxsackie coronaviruses parvo

and a few others and then borrelia the causative agent of Lyme disease upregulates mitochondrial

free radicals and depletes their antioxidant enzymes explained in this article along with

many many others and this I think is particularly fascinating the frightening this is the

flagellum of the Spiral sheet of Lyme disease that's these again the bacteria that causes it it needs to move fast and

in a spiral direction through tissues it'll bore straight from the bloodstream into the

um tissues quickly and for that it needs a lot of energy it's stealing your ATP it's not able to produce ATP of its own

accord and so um this steel of ATP from your mitochondria means a a lot of inflammation

lack of oxygen oxygen within them to drive their own energy and um a lot of oxidative stress as a result

mycotoxins too you know this of course that mold can dig deep into the mitochondria and cause oxidative stress

interestingly they all have their own different actions and this article does describe that very nicely

and um iron overload can cause mitochondrial issues that leads to reactive oxygen species we did

touch on this last time but it is a very very big cause of mitochondrial dysregulation especially in the wake of

covid um for various reasons that uh I touched on but it would take a lot longer to

sort of go into that in detail but um I've linked to several articles here and um indeed an entire protocol that

describes why that happens pesticides too I don't need to say a lot about that because I'm sure you know how

very very harmful pesticides can be organophosphates for example induce neurotoxicity in the mitochondria and

that's partly due to the oxidative stress that they drive so

to the greatest extent you can remove your patients from these stressors attempt to identify them if you can

there is Resveratrol mentioned here as being effective against organophosphate damage I love this

um article which describes how the mitochondrial membrane potential can actually be restored by glutathione and

trans Resveratrol which is simply the extract of Resveratrol ideally from Japanese knotweed

and fluoroquinolones along with other antibiotics can cause um

mitochondrial stress ciprofloxacin particularly there's a black box warning on that by the

European medicines agency that doctors don't always seem to pay attention to just two days of that can

cause huge damage to patients and this um that I've linked to at the bottom of the slide actually explains why from the

European medicines agency so that's due to what it can do to the mitochondria

hyperglycemia interestingly also a Big Driver of mitochondrial stress and um that's due to oxidation

at least um I would say largely I think uh you know we could we could

spend the rest of our lives seeing patients on the um sort of metabolic syndrome and uh or

who've already got full-fledged diabetes there's so much we could do related to the mitochondria and um that aspect of

Health um and um interestingly

superoxide is produced in the electron transport chain when patients are hypoglycemic and just note here that the

CoQ10 that you're hoping will go to the third complex of the electron transport chain and continue triggering the

um transport of electrons through to the end where ATP synthase is produced for our key mitochondrial energy that is um

um sort of triggered by hyperglycemia to produce superoxide instead which is a highly

um damaging radical and that has to be anti-oxidized by manganese

um superoxide dismutase and so that in a way wastes your antioxidant capacity

within your mitochondria and this is a reason why it's not always a good idea to dose too high with CoQ10 because it

just gets way laid here if the patient is struggling and has to sort of backtrack and be

antioxidized so sometimes I mean there have been studies done where a hundred milligrams of CoQ10 of surf patients

very well but suddenly 300 seem to have the opposite effect it's worth considering

so all these things avoid if possible and what is what is it possible to do

um in terms of supporting the antioxidant enzymes within the mitochondria well you've got three

categories of them here um of of antioxidants you've got the

enzymes themselves you've got external sources of antioxidants and then you've got water called here the small

um molecular weight molecules like Alpha tocopherol and

glutathione and lipoic acid that's alpha lipoic acid and so on that you can't directly give as a as a food but you can

of course give nutraceuticals so um the specific mitochondrial antioxidant

enzymes are sod particularly sog2 which is here you can see um

glutathione peroxidase glutathione reductase and several others that are that were a bit less familiar with like

thyroidoxin reductase and perioxiridoxin and we'll only concentrate on those that you can actually directly do something

about clinically which is quite a lot because there's sorry the slides are hopping a bit

because there is a master antioxidant regulator called Nrf2 with a long name here that I won't read but

um there is a lot you can do to support Nrf2 and by supporting that you're supporting

all of the antioxidant enzymes within the mitochondria as well as many within the

cell as well so I'll just turn to the next page where I've given you a list of them and this

is only a subset of them just have some water so um

a lovely article here the master regulator of antioxidative responses but what we want to know is what what can we

do about it how can we support a patient's antioxidant capacity

um without it it is quite hard to get antioxidants

directly into the cell this is the problem and into the mitochondria it's um more effective if you can to see what

the Nrf2 is doing and then support it if it's very low and you've got a whole mass of different

um nutritional and nutraceutical supports that you can give here I won't read all of them but um I will

just mentioned that each one of them has good scientific backings so do ask me if you'd like further

um you know sort of scientific substantiation for any of them I think uh particularly on the next page

we have two that are um uh you know strong candidates for being

really effective which are self-european probably comes as no surprise um the extract of cruciferous

um vegetables particularly broccoli and oleonic acid which um is uh the uh sort of effective extract of olive oil

that's a study that establishes how useful it is and um

this is a lovely um study that shows how many Nrf2 activators there are in various juices

and other beverages and this is just one page out of three lists that there are in this particular

article um talking about the study that was performed and what particular

aspect of um Health that was it was being examined on and blue Bridges beetroot juice apple juice I think this

one here actinidia chinensis sounds so opaque but actually that's kiwis garlic juice noni fruit juice and so on

so it isn't actually that hard to access Nrf2 activators and it could be very encouraging to

um let the patient know who's really suffering from oxidative stress um what kinds of but as I'm sure you do

you know what kinds of nutrition they could take to improve their status um so how can you support superoxide

dismutase um it's called when it's sod1

copper zinc superoxide just mutase so obviously there because it has such a high copper Affinity bioavailable copper

will be really helpful as well as zinc and sod2 is manganese superoxide dismutase and that's localized within

the um mitochondrial Matrix and inner membrane and that requires manganese so um particularly in patients who are

suffering from cryptopyaluria and who are literally losing all of some of their manganese

anyway um and as well as perhaps um B6 and zinc

um it's uh likely that they're going to be suffering from oxidative stress particularly due to the lack of ability

to fire up their superoxide dismutase which means basically that they cannot get their oxygen running well across

their electron transport chain to produce ATP ATP synthes the fifth complex and natural sources of sod are

listed here as well interestingly as several forms of lactobacillus which can upregulate

that enzyme and then food sources of zinc and copper to support sod1 are listed here as

mentioned last time it is important to build the ceruloplasmin carrier for bioavailable copper before

that can really hope to get into the mitochondria um

a few more notes about that below so catalase is also available in various food sources and is a very crucial

[Music] um antioxidant enzyme so I've listed some

here quite hard to find catalase is a bit tougher to trigger directly with nutritional sources but interestingly

mitochondrial catalase which is here surrounded by this red circle they found that when they upregulated

that in animal models it's hard to do this in human models they got an 18 extension of lifespan

attenuated cardiac aging sarcopenia even and reduce the incidence of cancer

so it is very protective and interestingly the follicles the follicles of our hair apparently get

filled with um hydrogen peroxide and this is the cause of gray hair and um up regulating your

catalase can counter that so glutathione of course is a vital antioxidant I'm not sure if the previous

page was also about glutathioneous it was and um that's actually our key intracellular antioxidant crucial for

mitochondria II you can measure the levels of oxidized glutathione versus free glutathione to find out whether

it's being excessively used if you have a higher oxidized glutathione than free glutathione then that's a sign that

you've got huge oxidative stress that is requiring glutathione good that you have it but this level here shouldn't really

ever be above that of the free glutathione and ratios are put together by some Labs so that you can see where

you are and how you're improving this is a lovely article written by Ben Brown who you'll all know

and Diana minich and this gives many dietary tips on how to increase glutathione

both nutraceutically and from nutrition and Recent research this is direct from that article suggests that when

glutathione is administered in liposomal or sublingual forms it may be more bioavailable

and um of course it's expensive and there are some questions as to whether it's rebuilt efficiently in the

cells because it does need to be um you know the precursors need to be um dis

um combobulated and then reassembled in the cells but at least you're getting the

right ratios when you're taking reassembled glutathione and um you can support it from food sources

picture of many of them down there and this again is from Ben Brown's and Deanna minich's article giving the exact

um recommended dosage of these different um sources of it so what exogenous antioxidants have a

good evidence base um because as mentioned it's quite hard to

get them into the mitochondria so um alpha lipoic acid is one where we have some very good um scientific

studies also on human beings not just um rodents Etc acetyl-l-carnitine ginseng a specially

red ginseng CoQ10 Resveratrol and vitamin C of course melatonin though we have problems

prescribing that in the UK so I won't be going into that lactoferrin and foods containing

glutathione that we've already looked at and interestingly also hydrogen-rich water

so um the first I'll talk about is alpha lipoic acid that is an excellent

mitochondrial antioxidant and this study here describes how it acts and the fact that

you can of course obtain it from food many common animal and plant foods are used as food supplements and have been

for many decades it's um it's a a cofactor for several enzymes in

the antioxidant defense system and can regenerate other essential antioxidant molecules

so um the following

slide shows just a snippet out of the many studies

that have been done on alpha lipoic acid quite an interesting [Music]

um Source here examine.com that gives the different studies that have been done on

various supplements and alpha lipoic acid is is well populated there with outcomes and um

some of them are well powered it can reduce for example idiopathic pain

it significantly reduced the numerical rating scale in this randomized placebo-controlled study that was well

powered with 210 study subjects and this was due partly at least to the

antioxidant action of alpha lipoic acid which is described in the study and this here is alpha lipoic acid

combined with acetyl-l-carnitine and this had a positive action on

vascular function and blood pressure via the reduction of reactive oxygen species and um described how

brachial artery diameter for example increased and um

it appears it tended to decrease systolic blood pressure for the whole group and many of these markers were

actually significant statistically significant so um that was eight weeks per treatment

so very impressive really are lipoic acid is a better one to use um for various reasons it's more

bioavailable carnitine orotate

in this controlled trial had a significant effect on non-alcoholic fatty liver disease and

this was the corona trial and um subjects who were suffering from type 2 diabetes

and it was found on along many markers that that had a beneficial effect on their glucose metabolism

particularly in relation to hepatic steatosis in this in this case so um

it showed that carnitine orotate complex inhibited weight gain and fat volume gain without food intake as well as

improving insulin sensitivity and of course it's insulin resistance that prevents the cells from taking up

glucose and therefore stymies the uptake of the precursors for the mitochondria in the first place so

insulin resistance is is a very very sort of primary marker that you do need to look at with

what you suspect to the insulin sorry mitochondrial dysfunction natural sources of alpheniperic acid and

L-Carnitine are listed here some of them we went through last time and this again

shows as a reminder how vital carnitine is for ferric ferreting um the broken down long chain fatty

acids into the mitochondria and um helping to give them the prime fuel that they

really most prefer to use which is fatty acids ginseng targets mitochondrial reactive

oxygen species too with numerous ginsenazites and this article describes how after only four weeks the number of

mitochondrial DNA copies actually increased in the red ginseng group compared to the placebo group and um

that was impressive there are several Pathways along which it worked here outlined and they are explained in

Greater detail in a later um both text and image in the study and um

it also works along numerous different Pathways as well so that again was a randomized clinical

study in human beings CoQ10 II um almost the very best studied nutrient for the mitochondria it

improved heart failure patients symptoms and one likely pathway for this was altering

redox signaling favorably and stabilizing the um membrane

permeability transition poor which is this weakening of the voltage

membrane between the two the two membranes of the mitochondria that have to contain a certain voltage in order to

actually be able to function and so a lovely study here which was called Q Symbio

and this is actually one that um Dr Sinatra wrote about in um his book

at least an earlier version of it he's unfortunately just passed away I think last year

very very brilliant um cardiologist who elucidated a lot about the mitochondria that is is so important to our current

understanding it was also found CoQ10 to significantly increase the various enzymes that we've

already discussed as long as as well as reducing melon dioaldehyde which is a um

an indicator of fatty acid degradation in the mitochondrial and cellular membranes and so these were all

very impressive um markers here that improved this was again a randomized controlled

trial in human beings flavonoids also have numerous antioxidant Properties or I should

better say um mitochondrial oxidation modulation

properties because they're able to act both as pro-oxidants and antioxidants and are able to understand what's needed

in the particular situation ideally anyway and so these are six different um flavonoids that are described in huge

detail in this lovely article here cited at the bottom and um

flavon's isoflevens the anthocyanins you'll know from their red purple and blue colors in flowers seeds and fruits

and they induce enzymes that can remove reactive oxygen species or modulate the enzymes as required in mitochondria and

the connection with colors is something that Diana minich has been looking into in huge detail as you'll know the

phytonutrient spectrum of the institute for functional medicine and we need to look into that a bit more in order to

understand exactly how the colors of these different um

nutrients here are actually acting on our mitochondria and the antioxidant action of them I won't go into that more

now and I can't say that I understand that fully myself but the colors definitely do have you know are

reflected in the spectrum of light and what's happening to cellular function

this is a little more detail on that taken from partly anyway the ifm work on the phytonutrient Spectrum

phytonutrients the cell signaling agents and eating a rainbow as um bant has so beautifully described in their Wellness

Solutions will give you lots of mitochondrial oxidation modulators so these ones here

are all described in various different references at the bottom there and there's so much more to say about those

um loading mitochondria with ascorbic acid can quench mitochondrial reactive oxygen species so this is backing for

vitamin C and actually this interesting article here describes how Vitamin C can enter

mitochondria via a specific glucose transporter blood one and confirm mitochondrial protection

against oxidative injury and um as you'll know

cells preferentially take up glucose if they're presented with glucose and vitamin C at the same time

because of the fight or flight reaction they think you know this means we need the glucose we've got to flee or take

some in a really radical action physiologically so um that's why taking

sugar in any form will reduce your immunity because the cells are not able to take up vitamin C so this is a very

interesting article describing a parallel mechanism existing for the mitochondrial transporter vitamin C so

even if your cells are being a bit depleted somehow and I don't know if it's fully elucidated yet

vitamin C is if you're giving it to your body is able to a larger extent to get into the mitochondria and do its

anti-oxidative work Alpha tocopherol2 this is not so much within the mitochondria themselves but

it does protect mitochondrial membranes that's the tocopherol fraction of vitamin E

um so it plays a major role in the lipid soluble um as as a lipid-soluble antioxidant and

protects the membranes from excessive oxidative damage this article describes that very nicely

lactoferrin interestingly can also reduce hydrogen peroxide and um

apolactopherin especially is able to scavenge excess iron so that can be very helpful and that is described

particularly in this section of the diagram and um

apple means without I believe that APO lactoferrin is slightly different in lactofherein and has a greater ability

to scavenge iron um hydrogen-rich water the last antioxidant we'll talk about today this

is able to increase biological antioxidant potential um a blind

double-blind controlled trial here showed in a four-week trial how it was able to

um for example increase the biological yes this Bap biological antioxidant

potential and um reduce apoptosis of peripheral blood nuclear cells and this is likely due to

the suppressive effect of hydrogen water on the production of eight hydroxy D oxyguanazine which is a marker that you

measure or we measure in oat tests it's right there at the end and indicates mitochondrial damage

so um how hydrogen water acts um is is fascinating and you can either actually Buy tablets that will be absorbed in in

the water that the patient drinks over the course of the day or before some sort of you know exhausting Sports

activity and it can boost your mitochondria or you can actually buy a little water generators which will add

hydrogen to the water um of course as mentioned last time around deuterium appears to have an even

stronger effect when I say deuterium I mean deuterium depleted water appears to really have its place in supporting the

mitochondria too but that I haven't covered here I don't think there are that many

um human trials on that yet but um let's watch this space and see because actually this week the um deuterium

depletion Summit is running all week and there's fascinating information there on that so the next

time around will be about regenerating healthy intact mitochondria partially through the action of

mitophagy and autophagy if that's the first step that you'd ideally take in other words removing before adding

and um these are the wonderful sources among many that are available for reading about the mitochondria and thank

you very much indeed yep I'm back here hello Julian thank you so much for

um that is a fascinating topic and very interesting presentation thank you very much once again

um thank you yes I want to let everyone know a couple of people asked about the availability of the slides in the

presentation so just to let you know that it will all be available from the band websites

um in in a couple of days um I also wanted to tell everyone that as I mentioned this is part two of the

three-part Series so the next the The Last presentation will be on the 22nd of May but you will be notified

um before it happens so um just looking for the questions

um lots of Praises very interesting thank you for a very informative presentation so

if you don't if you do have any um questions I'm just waiting to see if anybody does said um could I just

mention one thing which is that I listed Resveratrol amongst the um sort of dietary antioxidants that can

be obtained either from food or um from a nutraceutical but um I didn't go into it in detail and I didn't show

the studies because actually that's particularly important as a PGC one alpha activator which helps with

mitobiogenesis in other words the generation of new mitochondria and I'll be talking about that more next time so

you know antioxidant capacity is just one of its many functions thank you

um again thank you for the great presentation it's hydrogen water available naturally

oh gosh that's a fascinating question I I haven't looked into that myself um I know that there's cocoon water for

example which is especially oxygenated water um again that's not necessarily natural

but um you can sort of go to Hungary and lie in baths where uh your your cells are being sort of permeated with this

extra oxygen but I haven't heard of naturally High hydrogen in water that's not um

sort of actually generated in this specific way that I mentioned but I'm sure because

Waters do differ by their composition by the pH by the Purity all around the world and from various Springs glaciers

for example so um I'll look into that and um whoever asked that question maybe maybe

you can tell us next time um do Nrf2 activators have to be delivered in Juice form

no they don't have to be no the um I mean the broccoli for example as we mentioned with the sulfurophane you can

take that as broccoli you you know just lightly cooked steamed um or even raw and the organic uh acid

that I mentioned that's from olive oil that may be one of the reasons why the Mediterranean diet is so very helpful

and we've had many talks that went uh about the importance or the use of using that

um overall health so uh not at all no it's just I found it fascinating to be honest that there was this uh long long

list suddenly of all these different juices that uh you could obtain NRF to activate us from but

um it's a possibly a bit more bioavailable I noticed garlic juice there I can't say I've sort of

made garlic juice for myself that's just been pure garlic and drunk that but um obviously it will have its benefits and

perhaps it's more readily available to get into the cells than if it's a food that you have to you know break down

through the digestive system and maybe you don't have the digestive ability that that would

pull the max out of it I think that's for the brave ones yeah I would be tempted and what is your approach in

case of GST T1 and GST M1 double deletion and it's a technical question so

um yes there's there's genetic deletions um I think it depends on whether they're homozygous in other words whether both

chromosomes or um affected or whether it's just heterozygous just one and also whether

it's expressed or not so I'm uh somebody who uses um genetic testing a bit less in my

patients than maybe others do um through feeling that you can do so much with epigenetics but it doesn't

mean that you know the genetics aren't important of course and um so I I do I just feel it's sad if patients get

absolutely terrified by being told that they have a you know homozygous gstm1 which I believe is the liver primarily

unable to metabolize you know to to um process glutathione well but um I I I can't say that uh you can't

overcome that and um also you can't ever know whether it's really being expressed in a homozygous will give you some

degree of utilization and if you've got the other gsts as well yeah thank you um question right um about vitamin C and

sulforaphane so is it um correct that if you're taking sulforaphane that you shouldn't also

take antioxidants such as Vitamin C at the same time because sulforaphane is a pro-oxidant that stimulates Nrf2 so if

you're taking antioxidant like vitamin c does it counteract it I think if you're taking high doses

medicinally for example um either infusions or

um for a particular condition I'm thinking of of cancer therapy then yes it is

important to separate the pro-oxidants and the antioxidants but otherwise I wouldn't uh over emphasize that with

patients because they can become either you know highly um attentive to that to the exclusion of

almost anything else we do know of patients who find it very hard to eat after a while because they've been given

so many rules um just just but yes it is a good idea to not overload the body with

antioxidants at the same time as giving a pro-oxidant I'm thinking of artisanate for example

um the German clinics are very good at mentioning how important it is to not give with artisanate for example if

that's being either given as an IV or as an oral nutrient and not um uh combine that with an an antioxidant yeah thank

you and just linking that with another question about vitamin C is there a difference between food source vitamin C

um and ascorbic acids as an antioxidant yes um food sourced vitamin C has um four um atoms of tyrosinase for every

molecule of it and tyrosinase contains bioavailable copper and that is something I've mentioned both last time

and this time it does very much have its place um in good mitochondrial function

um it's essential actually for complex four without complex four working properly you're not going to get your

ATP synthase producing your mitochondrial ATP so um having food State vitamin C is

actually a lovely way to get some of that bioavailable copper but it's not just that it's also the routine and the

other bioflavonoids in full um Natural State vitamin C that you're getting whereas ascorbic acid is rather

just the shell of the vitamin C so um I was delighted actually to see that article that I showed you earlier about

how in its oxidized form ascorbic acid can really support the mitochondria which backs up many of our therapists

who are suggesting that you can do an awful lot with ascorbic acid alone but um I would always argue for a certain

proportion of natural food State vitamin C as well for its other properties

brilliant well thank you that concludes our questions there um several messages of saying great presentation thank you

for um really nice fascinating presentation so

I would just like to join everyone to say thank you for taking um defining time for to present to bands

webinar to band members and I very much look forward to welcoming you again um in May

and thank you to everyone who's listening to this presentation whether it's live or recorded and I hope you all

have a lovely evening thank you very much thank you very much thank you everybody for being there for taking the

time to listen and thank you again very very much and for giving us the opportunity giving me the opportunity to

talk about my greatest passion thank you very much thank you see you soon bye thank you bye