June 2, 2025 • 21 mins
Dive into the fascinating world of innovative therapies for age-related macular degeneration as we explore a potential breakthrough for the millions suffering from this sight-threatening condition. What happens when carefully controlled oxidative stress becomes the catalyst for healing? The answer challenges everything we thought we knew about treating degenerative eye disease.
The spotlight falls on ozone therapy—specifically a method called major autohemotherapy—which shows remarkable promise for the dry form of macular degeneration affecting nearly 10 million Americans. We unpack the science behind this treatment that works through a seemingly paradoxical mechanism: introducing a precisely calculated amount of oxidative stress to activate the body's own powerful antioxidant defenses.
At the heart of this therapy lies an elegant biological pathway. When blood is treated with medical-grade ozone outside the body, it triggers the release of "messenger molecules" that activate the Nrf2 pathway—essentially flipping the master switch for over 200 protective genes. This cascade supercharges the body's production of antioxidant enzymes precisely where they're needed most: in the delicate tissues of the macula with its extraordinarily high oxygen demands.
The clinical results shared are truly striking. While conventional vitamin treatments showed limited effectiveness, patients receiving ozone therapy experienced not just stabilization but actual improvement in vision. Most remarkably, none of the ozone-treated patients lost significant vision over a 12-month period, while 40% in the vitamin control group experienced substantial decline. For a condition with no FDA-approved treatments, these findings represent a beacon of hope worth investigating further.
Could this therapeutic approach that harnesses the body's own healing mechanisms have applications beyond eye health? The research suggests similar principles might apply to other conditions driven by oxidative stress and inflammation. Connect with Dr. Kumar's team at LifeWellMD by calling 561-210-9999 to learn more about evidence-informed approaches that could transform your health journey.
Disclaimer:
The information provided in this podcast is for educational purposes only and is not intended as medical advice. Always consult with a qualified healthcare professional before making changes to your supplement regimen or health routine. Individual needs and reactions vary, so it’s important to make informed decisions with the guidance of your physician.
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If you enjoyed today’s episode, be sure to subscribe, leave us a review, and share it with someone who might benefit. For more insights and updates, visit our website at Lifewellmd.com.
Stay Informed, Stay Healthy:
Remember, informed choices lead to better health. Until next time, be well and take care of yourself.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Welcome back to the Deep Dive.
You know this is where we takethe sources you send our way
Could be articles, researchpapers, notes and we really try
to cut through the noise.
Speaker 2 (00:08):
Yeah, our job is basically to find those key
insights, maybe the surprisingdetails, and help you get up to
speed fast.
Speaker 1 (00:15):
Think of us as expert guides, really digging into the
material you give us to figureout what's most important in
that data.
And today, well, we've got atopic that came from a listener
question.
Actually.
Speaker 2 (00:26):
Yeah.
Speaker 1 (00:26):
All the way from Denver Colorado.
Speaker 2 (00:28):
Oh great, what was the question?
Speaker 1 (00:30):
They were curious about innovative approaches,
potential ones for dryage-related macular degeneration
, ARMD, and they specificallyasked about something called
ozone therapy.
Speaker 2 (00:43):
Ah, ozone therapy.
Yes, that's definitely an areapeople ask about.
It's fascinating and to lookinto this specific question
using the source material we got, we've actually been working
with Dr Kumar and his team overat LifeWellMDcom.
Speaker 1 (00:55):
LifeWellMD right.
They focus on health, wellness,longevity, always looking at
new, evidence-informed options,aren't they?
Speaker 2 (01:03):
Exactly Trying to find ways to potentially help
patients improve theirwell-being, their health span.
So this deep dive fits rightinto that kind of exploration
they do Okay, so what's our mainsource for this exploration?
We're focusing on a specificreview paper.
It's titled Visual ImprovementFollowing Ozona Therapy in Dry
Age-Related Macular Degenerationa review Dry Age-Related
(01:23):
Macular Degeneration a review.
The authors are Borelli andBocci and it was published in
AHD Ophthalmology back in 2013.
2030.
Okay, so our mission todayunpack this specific paper Right
.
Understand what suggests aboutozone therapy for dry ARMD.
Look at the mechanisms theypropose, the clinical findings
they report.
Basically see what insightsthis particular source holds.
Speaker 1 (01:45):
Okay, let's get into it Before we even talk about
potential solutions.
This paper makes it clear thatdry ARMD is a really big deal.
Can you lay out just how commonit is and why it's such a
concern?
Speaker 2 (01:55):
Absolutely.
The source really emphasizesthat ARMD is a growing problem,
particularly, you know, aspopulations age.
Yeah, it estimates that itaffects about 25 percent of
people over 65.
That's one in four and it's amajor cause of significant
vision loss, even blindness.
The paper throws out some bignumbers like 250,000 affected in
(02:16):
the UK, maybe close to 10million in the USA.
Speaker 1 (02:19):
Wow, 10 million in the US alone, that's huge.
Speaker 2 (02:22):
It really is, and you know, armd comes in two main
flavors.
There's the wet form, which isactually less common, and then
there's the dry or atrophic form.
That's the one this review isall about, and it accounts for
almost 90 percent of all cases90 percent, so the vast majority
.
Speaker 1 (02:37):
What does that dry form actually look like
clinically speaking?
According to the source?
Speaker 2 (02:41):
Well, the paper details the classic signs you
get these yellowish depositsunder the retina.
They're called drusen.
Drusen okay, right.
Plus, you see pigment clumping,changes in a really important
layer called the retinal pigmentepithelium, the RPE, and
eventually areas where thetissue just wastes away, known
as geographic ashen free.
Speaker 1 (02:59):
And for the patient, what does that mean?
Speaker 2 (03:06):
Usually it means a slow, gradual loss of that sharp
central vision, often over manyyears.
It might start with like blurryspots or blind spots right in
the middle of what they'relooking at.
Speaker 1 (03:11):
You mentioned the RPE .
The source seems to put a lotof weight on that layer.
What is it and why is it socritical here?
Speaker 2 (03:19):
Oh, the RPE is absolutely crucial.
Think of it like the supportcrew for the photoreceptors, the
cells that actually detectlight.
It sits right between thosephotoreceptors and the blood
vessels underneath in thechoroid.
Speaker 1 (03:30):
Like a middleman.
Speaker 2 (03:31):
Kind of yeah.
It manages waste products,recycles essential molecules for
vision, transports nutrients.
It does a lot.
And the macula, especially thattiny central pit called the
foveola, where our vision issharpest, it has the highest
oxygen demand of any tissue inthe body the highest wow.
Yeah, and it completely dependson that blood supply from the
choroid delivered via the RPE.
(03:51):
So the paper points out if thatarea gets starved of oxygen,
even for a short time, thosecritical vision cells start to
die off.
Speaker 1 (03:59):
So it's like a double hit.
The RPE itself is degenerating,messing up nutrient delivery
and waste cleanup, and the areahas these incredibly high oxygen
needs that aren't being met.
Speaker 2 (04:08):
That's exactly it, and the paper suggests this
breakdown is driven by a nastymix of things bursts of free
radicals, damage from calciumions, maybe glutamate toxicity,
certainly chronic inflammationand just intense oxidative
stress.
They even mention a link tohigh C-reactive protein levels
in the blood, which points rightback to that inflammation.
Speaker 1 (04:28):
Okay Now you mentioned the wet form earlier,
that one does have treatmentslike injections, right?
How does that compare to whatthis source says about dry ARMD?
Speaker 2 (04:37):
Yeah, that's a key difference.
The wet form involves abnormalblood vessel growth and those
injections target that.
But for dry ARMD this paper ispretty blunt.
It says there is currently noeffective therapy available
except for the illusory oraladministration of antioxidant
vitamins.
Speaker 1 (04:53):
Illusory.
That's strong language.
Speaker 2 (04:55):
It is.
They do clarify these vitaminsaren't harmful and they might
maybe slightly slow things downafter years and years of taking
them, but the main point isthere's a huge gap, no proven
treatment to really stop orreverse the dry form.
And they make anotherabsolutely critical point.
Speaker 1 (05:11):
We do.
Speaker 2 (05:12):
The ozone therapy discussed in this review is only
for the dry form.
Explicitly the source warns itcannot be used in wet ARMD
because it might actually speedup the disease process there.
That distinction is vital.
Speaker 1 (05:23):
Okay, vital distinction Dry form only,
according to this source, andthat therapeutic gap really
highlights why exploringinnovative ideas, like the work
Dr Kumar's team does atLifeWellMD, is so important,
which brings us right to themain subject ozone therapy.
Speaker 2 (05:39):
Right.
So the paper introducesozonotherapy, specifically a
method called major autohemotherapy or O3-AHT, as
something that had been lookedat since the mid to late 90s.
It does acknowledge right upfront that there's been
skepticism about it in the widermedical world Understood.
Speaker 1 (05:54):
So, according to this review paper, what's the actual
goal of using O3-AHT for dryair?
Md?
Speaker 2 (06:00):
The authors state the aim isn't necessarily a cure,
but to try and stop or at leastslow down the natural downhill
course of the disease andhopefully improve the patient's
quality of life in the process.
They are careful to note,though, that it might not fully
bring back vision that's alreadybeen lost completely.
It's more about preservingwhat's left and potentially
improving function.
Speaker 1 (06:21):
OK, slowing or stopping progression, improving
quality of life.
So the big question how mightit actually work?
This is where the paper getsinto some pretty complex
biochemistry, isn't it?
Speaker 2 (06:34):
It does, yeah, but it lays out a really interesting
hypothesis.
It starts with what happenswhen you mix that medical grade
oxygenazone gas mixture with thepatient's blood outside the
body.
Okay, the ozone O3, dissolvessuper quickly and immediately
reacts within minutes withthings like antioxidants and
unsaturated fatty acids in theblood plasma and on cell
membranes.
Speaker 1 (06:54):
And that reaction creates something else.
Speaker 2 (06:56):
Exactly it generates what the paper calls key
messengers.
Two main times are highlightedHydrogen peroxide, h2o2.
Yes, the same stuff you mighthave in your medicine cabinet,
but in tiny, controlled amountshere.
And a group of reactivemolecules called aldehydes and
alkanols, like one called4-H-N-E.
Speaker 1 (07:15):
So ozone itself isn't the direct actor, it's these
things it creates.
Speaker 2 (07:19):
That's the idea presented.
They describe ozone actingalmost like a pro-drug.
It kicks off the process, butthe downstream effects come from
these messengers it generates.
Speaker 1 (07:27):
Okay, let's break that down.
What are these messengerssupposed to do according to the
paper?
Let's start with the hydrogenperoxide.
Speaker 2 (07:33):
Okay.
So the hypothesis is that thissmall amount of H2O2 gets into
red blood cells.
Once inside, it activates aprocess called glycolysis, which
bumps up ATP production energyfor the cell.
But, crucially, it alsosignificantly boosts something
called 243-defosphoglycerate or243-DPG 243-DPG.
Speaker 1 (07:51):
Why is that important here?
Speaker 2 (07:53):
Ah, this is key for oxygen delivery.
You see, increased 2003-DPGmakes hemoglobin, the
protein-tearing oxygen in redblood cells, less sticky to
oxygen.
It shifts what's called theoxyhemoglobin dissociation curve
to the right.
Speaker 1 (08:08):
Less sticky, so it lets go of oxygen more easily.
Speaker 2 (08:10):
Exactly, especially in tissues that are struggling
for oxygen, like an ischemicmacula.
So the proposed benefit isbetter oxygen release right
where it's desperately needed.
Speaker 1 (08:19):
Okay, improving oxygen supply, that makes a lot
of sense for a tissue that'sstarved of it.
Now, what about those othermessengers, the alkanols you
said?
Ozone creates oxidative stress,which sounds bad, especially in
a disease linked to oxidativestress.
Speaker 2 (08:32):
It does sound counterintuitive absolutely, but
the paper frames it veryspecifically.
It says these alkanols areproduced in very small,
calculated amounts.
They call it a calculated andwell-tolerated oxidative stress.
Speaker 1 (08:44):
Calculated stress.
Speaker 2 (08:47):
That's actually a pretty good analogy the paper
hints at.
You know, stressing yourmuscles makes them stronger.
The idea here is that thissmall controlled oxidative
signal is meant to activate thebody's own powerful defense
systems.
Speaker 1 (08:59):
Okay, so how does that signal work?
Speaker 2 (09:01):
Well, these alkanols travel through the bloodstream,
often attached to proteins likealbumin.
The paper proposes that whenthey get inside cells, they
interact with a protein calledKEEP1.
Speaker 1 (09:11):
KEEP1.
And what happens then?
Speaker 2 (09:13):
This is where a really critical defense pathway
gets switched on.
Normally, KEEP1 acts like aleash on another molecule called
NRF2, keeping it inactive.
But when these alkanols bindKEEP1, it's like they cut the
leash.
Speaker 1 (09:27):
So NRF2 is set free.
Speaker 2 (09:29):
Exactly.
Nrf2 is then free to travelinto the cell's nucleus, the
command center.
Speaker 1 (09:34):
Right, and what does NRF2 do in the nucleus?
Speaker 2 (09:36):
Once inside, NRF2 binds to specific sections of
DNA called antioxidant responseelements, or AREs.
The paper calls this bindingthe crucial event.
Speaker 1 (09:46):
The crucial event.
Why?
What's the result?
Speaker 2 (09:48):
This binding acts like flipping a master switch it
dramatically stimulates theproduction, the upregulation of
around 200 different genes.
And these aren't just any genes.
They're the genes responsiblefor making the cells own
powerful protective arsenal.
Speaker 1 (10:01):
Like what kind of protection?
Speaker 2 (10:03):
Things like potent antioxidant enzymes, sod,
catalase, glutathione peroxidase, gsh, piaquexis, also phase two
detoxification enzymes and anenzyme called hemeoxygenase 1,
which they describe as beinghighly protective against
cellular stress.
Speaker 1 (10:19):
Wow, so let me see if I've got this.
The hypothesis outlined in thepaper is introduce a tiny
controlled bit of oxidativestress using these ozone
generated alkanols, which thentriggers this NRF2 pathway,
leading the body to ramp upproduction of its own mass of
antioxidant and protectivedefenses, defenses that can then
fight back against the chronicoxidative stress and
(10:40):
inflammation that's actuallycausing the damage in dry ARMD.
Speaker 2 (10:43):
That's precisely the core mechanism they detail.
It's about stimulating your ownbody's defenses to counteract
the disease process, and thesource also mentioned some other
potential pluses, like makingblood flow a bit better, helping
blood vessels relax by boostingnitric oxide and maybe
releasing some growth factorsfrom platelets.
It's presented as amulti-pronged effect.
Speaker 1 (11:04):
That is a fascinating theory, really complex, but
fascinating.
Okay, theory is one thing.
What about results?
The paper talks about actualclinical findings from two
studies they did at theUniversity of Siena.
What did they report seeing inpatients?
Speaker 2 (11:18):
Right the clinical data.
The first study they discussedran from 1996 to 2001, involving
77 patients.
They compared a group gettingthe ozone therapy, o3-aht, for
at least two years against acontrol group.
Now the control group got theirown blood treated just with
oxygen, not ozone.
Speaker 1 (11:36):
Okay, so oxygenated blood versus ozonated blood?
What was the outcome?
Speaker 2 (11:39):
Well, first they noted the oxygen-only group
didn't really show much benefit.
But for the ozone therapy groupthey reported a statistically
significant difference in visualacuity improvement Improvement.
Speaker 1 (11:49):
How much?
Speaker 2 (11:49):
They defined improvement as gaining more than
two lines on the ETDRS eyechart.
That's like being able to readtwo extra lines of smaller
letters and they found 66.6percent.
So two-thirds of the ozonetherapy group reached this level
of improvement.
Speaker 1 (12:04):
Two-thirds Okay Compared to.
Speaker 2 (12:06):
Compared to just 30.4 percent in the oxygen-only
control group.
So a pretty big differencereported there.
They also mentioned that labtests for the treated group
either stayed the same oractually improved.
Speaker 1 (12:17):
Hmm, interesting.
What about the second study?
Speaker 2 (12:20):
The second one was larger 140 patients and ran from
2008 to 2011.
This time they compared theozone therapy group 70 patients
against a control group takingstandard antioxidant
multivitamins, also 70 patients.
Speaker 1 (12:34):
OK, ozone versus vitamins.
How did the vision changescompare over time in this one?
Speaker 2 (12:41):
They used a different vision scale here, Logmar, but
the trend was similar.
The paper reported that theaverage vision in the
ozone-treated eyes actuallyshowed improvement over both 6
months and 12 months.
Speaker 1 (12:49):
Improvement, not just slowing the decline.
Speaker 2 (12:51):
That's what their average data showed.
Yes, In stark contrast, thecontrol group taking the
multivitamins, their averagevision actually got worse.
It deteriorated over that samesix and 12-month period.
Speaker 1 (13:02):
Wow, okay, that's one thing, but what about, like,
preventing significant visionloss?
Did they look at that?
Speaker 2 (13:08):
They did, and this data as presented in the paper
is quite striking.
Did they look at that?
They did, and this data aspresented in the paper is quite
striking.
According to their results,none zero of the eyes treated
with ozone showed a worsening ofvision by more than two lines
on the eye chart at either sixmonths or 12 months.
Speaker 1 (13:21):
None lost that much vision.
Speaker 2 (13:23):
Correct.
Compare that to themultivitamin control group.
At 12 months, 40% of thosepatients had lost more than two
lines of vision and 38% had lostmore than three lines.
Speaker 1 (13:37):
The difference between the groups was highly
statistically significant,according to the pager.
Okay, hold on.
Nobody in the ozone group losttwo lines, but 40% in the
vitamin group did.
That seems really significantbased on their report.
Speaker 2 (13:45):
It really stands out in their findings.
Yes, it aligns well with thatstated goal of trying to stop or
slow the disease progression.
Yes, it aligns well with thatstated goal of trying to stop or
slow the disease progression.
And, interestingly, they alsomeasured markers of oxidative
stress in the blood in thissecond study and they found that
plasma oxidative stressdecreased in the group treated
with ozone, which lends somesupport to that whole mechanism.
(14:06):
We talked about boostingantioxidant defenses.
Speaker 1 (14:09):
Did they mention anything else like how patients
felt they?
Speaker 2 (14:11):
did Beyond the eye charts?
The source says that patientsin the ozone group assessed
using boosting antioxidantdefenses.
Did they mention anything elselike how patients felt they did
Beyond the eye charts?
The source says that patientsin the ozone group assessed
using a standard vision-relatedquality of life questionnaire
also reported subjectiveimprovements, things like
feeling better overall, havingmore energy, better
concentration, even improvedmemory.
Speaker 1 (14:28):
Potential wider benefits maybe Interesting.
So okay, let's talkpracticalities.
How is this O3 auto-hemotherapyactually done?
What does the paper describe?
Speaker 2 (14:37):
Right the procedure as they outline it.
It involves drawing a specificamount of the patient's own
blood, usually somewhere between150 and 225 milliliters,
depending on body weight.
Then they add an anticoagulantlike heparin or citrate to stop
it clotting.
Next, that blood is gentlymixed with a very precise volume
of the oxigenazone gas mixture.
(14:59):
This is done using a certifiedmedical ozone generator, and the
ozone concentration iscarefully measured and
controlled, often using aspectrophotometer.
Speaker 1 (15:08):
Precision seems key there.
Speaker 2 (15:10):
Absolutely crucial.
The paper emphasizes that,After mixing for a few minutes,
the treated blood is then simplyre-infused back into the
patient's vein like a standardIV drip.
Speaker 1 (15:20):
And you said patient's own blood.
Speaker 2 (15:22):
Yes, 100%.
The source stresses it must beautologous, using only the
patient's own blood.
They describe the procedure,when done correctly with these
small, precise, precise ozonedoses and medical-grade
equipment, as absolutely safe.
The safety, they argue, comesfrom the precision and the fact
that it's your own blood goingback in.
Speaker 1 (15:38):
Okay, how often do people need to do this according
to the paper?
Speaker 2 (15:42):
Typically they mention starting with treatments
twice a week for an initialphase, maybe around nine or ten
weeks.
They also note that patientsoften start noticing some
improvement after about four tosix treatments.
After that initial birth Thenmaintenance therapy is needed.
The paper suggests at leastonce every 10 days or so to
maintain the effects.
Speaker 1 (16:00):
Why the need for ongoing maintenance?
Speaker 2 (16:03):
Well, they explain that the biochemical effects
triggered by the treatment seemto have a rather short memory.
As they put it, If you stop thetreatments completely, the
benefits tend to wear off,usually within about six to nine
months.
Speaker 1 (16:17):
So it sounds like it requires a pretty consistent
commitment from the patient.
Speaker 2 (16:20):
It definitely does.
But the paper makes a point ofsaying that patient compliance
tends to be quite high once theystart seeing positive results
because you know they feel it'sworking.
They also make a point ofmentioning the minimal cost
compared to some other potentialtherapies being researched.
Speaker 1 (16:35):
Right, OK, so let's try and wrap this up.
This Borelli and Bochy reviewgives us a detailed look at the
theory, the proposed mechanismand some clinical findings they
reported regarding ozone therapyfor dry ARMD.
From their perspective, what'sthe main takeaway message?
Speaker 2 (16:51):
I think their core conclusion centers on what they
see as ozonotherapy's uniqueability, what they see as
ozonotherapy's unique ability,specifically via this O3-AHT
method, to basically wake up thebody's own built-in defense
systems, systems that fightagainst the kind of damage, the
lack of oxygen, theneurotoxicity that drives dry
ARMD.
So by improving oxygen deliveryand boosting those internal
(17:17):
antioxidant enzymes.
Right, the goal is to try andstop those precious
photoreceptor cells from dyingoff.
Speaker 1 (17:20):
And they had that point about when to start
treatment too, didn't they?
Speaker 2 (17:23):
Yes, that seemed important.
In their observations theynoted that the improvements in
vision were generally morenoticeable and happened faster
in patients who startedtreatment when they still had
some vision left, even if it wasalready declining, compared to
patients who were already nearlyblind.
Which suggests it stronglysuggests, based on their
findings, that startingtreatment earlier, before a
massive cell death has occurred,is likely to be more beneficial
(17:46):
, getting there before thedamage is too extensive.
Speaker 1 (17:49):
So this whole deep dive sparked by that listener
question from Denver reallyexplores the possibility and we
stress possibility based on thissource that innovative
approaches like ozone therapymight offer a potential avenue
for conditions like dry ARMD,supported by research like this
review paper.
Speaker 2 (18:07):
Exactly, and you know that's precisely the kind of
exploration that clinics likeLifeWellMDcom engage in as part
of Dr Kumar's team.
Their focus is on health,wellness and longevity, and they
are constantly looking at thescience, evaluating
evidence-informed approachesmuch like the research we've
just discussed to see how theymight help patients improve
their overall health and,importantly, their health span.
Speaker 1 (18:29):
It's really about staying informed on the
cutting-edge research,understanding the potential
mechanisms, like the NRF2pathway we talked about, and
then seeing what options mightmake sense for an individual,
based on their specific needsand the current state of
evidence.
Speaker 2 (18:42):
Definitely so.
If you, the listener, arecurious about the kind of
research we've covered today, orif you have questions about
innovative approaches for yourown health journey maybe related
to macular degeneration, maybesomething else entirely
connecting with the team atLifeWellMDcom could be a really
worthwhile step.
Speaker 1 (19:00):
Yeah, they can talk through your specific situation,
look at your health goals andhelp you understand how they
might explore possibilities withyou, drawing on the latest
research and their clinicalexpertise.
Speaker 2 (19:10):
We really encourage you, if this resonates, to maybe
take that first step on yourpersonal wellness journey.
You can give them a call.
The number is 561-210-9999.
Speaker 1 (19:21):
561-210-9999.
Speaker 2 (19:24):
It's a chance to connect with professionals who
are dedicated to exploringinnovative, evidence-informed
options to help you optimizeyour health.
Speaker 1 (19:31):
It really is.
It's about having aconversation with a team that
looks seriously at thepossibilities presented by
research and works with you tofigure out what might be
appropriate for your uniquehealth picture.
You know, diving deep intosources like this 2013 review
reminds us that there's alwaysmore going on beneath the
surface, doesn't it?
Insights often missed in justthe headlines or general health
info.
And maybe a final thought toleave you with something
(19:54):
provocative based on this paperJust consider that core idea
that a carefully controlled doseof something we normally think
of as bad, like oxidative stress, could actually be harnessed
therapeutically, that it couldtrigger the body's own powerful
healing and protective systems.
Speaker 2 (20:10):
Yeah, or maybe think even broader, building on the
mechanisms they described.
The review actually mentionspotential relevance to other eye
conditions involvingdegeneration or lack of blood
flow, things like degenerativemyopia, diabetic retinopathy,
even retinitis pigmentosa,stargardt's disease, ischemic
optic neuropathies, maybeglaucoma.
Could similar approachesactivating these defense
(20:31):
pathways be relevant?
There, too, something to ponder.
Speaker 1 (20:35):
Definitely food for thought.
Well, thank you for joining uson this deep dive into the
potential of ozone therapy fordry ARMD, as presented in the
Borelli and Bocci review andexplored with the perspective of
Dr Kumar's team at LifeWellMD.
Speaker 2 (20:49):
Yeah, we really hope this exploration has been
informative and maybe sparkedsome new questions for you.
Speaker 1 (20:54):
And we will see you on the next deep dive.
Welcome back to the Deep Dive.
You know this is where we takethe sources you send our way
Could be articles, researchpapers, notes and we really try
to cut through the noise.
Speaker 2 (00:08):
Yeah, our job is basically to find those key
insights, maybe the surprisingdetails, and help you get up to
speed fast.
Speaker 1 (00:15):
Think of us as expert guides, really digging into the
material you give us to figureout what's most important in
that data.
And today, well, we've got atopic that came from a listener
question.
Actually.
Speaker 2 (00:26):
Yeah.
Speaker 1 (00:26):
All the way from Denver Colorado.
Speaker 2 (00:28):
Oh great, what was the question?
Speaker 1 (00:30):
They were curious about innovative approaches,
potential ones for dryage-related macular degeneration
, ARMD, and they specificallyasked about something called
ozone therapy.
Speaker 2 (00:43):
Ah, ozone therapy.
Yes, that's definitely an areapeople ask about.
It's fascinating and to lookinto this specific question
using the source material we got, we've actually been working
with Dr Kumar and his team overat LifeWellMDcom.
Speaker 1 (00:55):
LifeWellMD right.
They focus on health, wellness,longevity, always looking at
new, evidence-informed options,aren't they?
Speaker 2 (01:03):
Exactly Trying to find ways to potentially help
patients improve theirwell-being, their health span.
So this deep dive fits rightinto that kind of exploration
they do Okay, so what's our mainsource for this exploration?
We're focusing on a specificreview paper.
It's titled Visual ImprovementFollowing Ozona Therapy in Dry
Age-Related Macular Degenerationa review Dry Age-Related
(01:23):
Macular Degeneration a review.
The authors are Borelli andBocci and it was published in
AHD Ophthalmology back in 2013.
2030.
Okay, so our mission todayunpack this specific paper Right
.
Understand what suggests aboutozone therapy for dry ARMD.
Look at the mechanisms theypropose, the clinical findings
they report.
Basically see what insightsthis particular source holds.
Speaker 1 (01:45):
Okay, let's get into it Before we even talk about
potential solutions.
This paper makes it clear thatdry ARMD is a really big deal.
Can you lay out just how commonit is and why it's such a
concern?
Speaker 2 (01:55):
Absolutely.
The source really emphasizesthat ARMD is a growing problem,
particularly, you know, aspopulations age.
Yeah, it estimates that itaffects about 25 percent of
people over 65.
That's one in four and it's amajor cause of significant
vision loss, even blindness.
The paper throws out some bignumbers like 250,000 affected in
(02:16):
the UK, maybe close to 10million in the USA.
Speaker 1 (02:19):
Wow, 10 million in the US alone, that's huge.
Speaker 2 (02:22):
It really is, and you know, armd comes in two main
flavors.
There's the wet form, which isactually less common, and then
there's the dry or atrophic form.
That's the one this review isall about, and it accounts for
almost 90 percent of all cases90 percent, so the vast majority
.
Speaker 1 (02:37):
What does that dry form actually look like
clinically speaking?
According to the source?
Speaker 2 (02:41):
Well, the paper details the classic signs you
get these yellowish depositsunder the retina.
They're called drusen.
Drusen okay, right.
Plus, you see pigment clumping,changes in a really important
layer called the retinal pigmentepithelium, the RPE, and
eventually areas where thetissue just wastes away, known
as geographic ashen free.
Speaker 1 (02:59):
And for the patient, what does that mean?
Speaker 2 (03:06):
Usually it means a slow, gradual loss of that sharp
central vision, often over manyyears.
It might start with like blurryspots or blind spots right in
the middle of what they'relooking at.
Speaker 1 (03:11):
You mentioned the RPE .
The source seems to put a lotof weight on that layer.
What is it and why is it socritical here?
Speaker 2 (03:19):
Oh, the RPE is absolutely crucial.
Think of it like the supportcrew for the photoreceptors, the
cells that actually detectlight.
It sits right between thosephotoreceptors and the blood
vessels underneath in thechoroid.
Speaker 1 (03:30):
Like a middleman.
Speaker 2 (03:31):
Kind of yeah.
It manages waste products,recycles essential molecules for
vision, transports nutrients.
It does a lot.
And the macula, especially thattiny central pit called the
foveola, where our vision issharpest, it has the highest
oxygen demand of any tissue inthe body the highest wow.
Yeah, and it completely dependson that blood supply from the
choroid delivered via the RPE.
(03:51):
So the paper points out if thatarea gets starved of oxygen,
even for a short time, thosecritical vision cells start to
die off.
Speaker 1 (03:59):
So it's like a double hit.
The RPE itself is degenerating,messing up nutrient delivery
and waste cleanup, and the areahas these incredibly high oxygen
needs that aren't being met.
Speaker 2 (04:08):
That's exactly it, and the paper suggests this
breakdown is driven by a nastymix of things bursts of free
radicals, damage from calciumions, maybe glutamate toxicity,
certainly chronic inflammationand just intense oxidative
stress.
They even mention a link tohigh C-reactive protein levels
in the blood, which points rightback to that inflammation.
Speaker 1 (04:28):
Okay Now you mentioned the wet form earlier,
that one does have treatmentslike injections, right?
How does that compare to whatthis source says about dry ARMD?
Speaker 2 (04:37):
Yeah, that's a key difference.
The wet form involves abnormalblood vessel growth and those
injections target that.
But for dry ARMD this paper ispretty blunt.
It says there is currently noeffective therapy available
except for the illusory oraladministration of antioxidant
vitamins.
Speaker 1 (04:53):
Illusory.
That's strong language.
Speaker 2 (04:55):
It is.
They do clarify these vitaminsaren't harmful and they might
maybe slightly slow things downafter years and years of taking
them, but the main point isthere's a huge gap, no proven
treatment to really stop orreverse the dry form.
And they make anotherabsolutely critical point.
Speaker 1 (05:11):
We do.
Speaker 2 (05:12):
The ozone therapy discussed in this review is only
for the dry form.
Explicitly the source warns itcannot be used in wet ARMD
because it might actually speedup the disease process there.
That distinction is vital.
Speaker 1 (05:23):
Okay, vital distinction Dry form only,
according to this source, andthat therapeutic gap really
highlights why exploringinnovative ideas, like the work
Dr Kumar's team does atLifeWellMD, is so important,
which brings us right to themain subject ozone therapy.
Speaker 2 (05:39):
Right.
So the paper introducesozonotherapy, specifically a
method called major autohemotherapy or O3-AHT, as
something that had been lookedat since the mid to late 90s.
It does acknowledge right upfront that there's been
skepticism about it in the widermedical world Understood.
Speaker 1 (05:54):
So, according to this review paper, what's the actual
goal of using O3-AHT for dryair?
Md?
Speaker 2 (06:00):
The authors state the aim isn't necessarily a cure,
but to try and stop or at leastslow down the natural downhill
course of the disease andhopefully improve the patient's
quality of life in the process.
They are careful to note,though, that it might not fully
bring back vision that's alreadybeen lost completely.
It's more about preservingwhat's left and potentially
improving function.
Speaker 1 (06:21):
OK, slowing or stopping progression, improving
quality of life.
So the big question how mightit actually work?
This is where the paper getsinto some pretty complex
biochemistry, isn't it?
Speaker 2 (06:34):
It does, yeah, but it lays out a really interesting
hypothesis.
It starts with what happenswhen you mix that medical grade
oxygenazone gas mixture with thepatient's blood outside the
body.
Okay, the ozone O3, dissolvessuper quickly and immediately
reacts within minutes withthings like antioxidants and
unsaturated fatty acids in theblood plasma and on cell
membranes.
Speaker 1 (06:54):
And that reaction creates something else.
Speaker 2 (06:56):
Exactly it generates what the paper calls key
messengers.
Two main times are highlightedHydrogen peroxide, h2o2.
Yes, the same stuff you mighthave in your medicine cabinet,
but in tiny, controlled amountshere.
And a group of reactivemolecules called aldehydes and
alkanols, like one called4-H-N-E.
Speaker 1 (07:15):
So ozone itself isn't the direct actor, it's these
things it creates.
Speaker 2 (07:19):
That's the idea presented.
They describe ozone actingalmost like a pro-drug.
It kicks off the process, butthe downstream effects come from
these messengers it generates.
Speaker 1 (07:27):
Okay, let's break that down.
What are these messengerssupposed to do according to the
paper?
Let's start with the hydrogenperoxide.
Speaker 2 (07:33):
Okay.
So the hypothesis is that thissmall amount of H2O2 gets into
red blood cells.
Once inside, it activates aprocess called glycolysis, which
bumps up ATP production energyfor the cell.
But, crucially, it alsosignificantly boosts something
called 243-defosphoglycerate or243-DPG 243-DPG.
Speaker 1 (07:51):
Why is that important here?
Speaker 2 (07:53):
Ah, this is key for oxygen delivery.
You see, increased 2003-DPGmakes hemoglobin, the
protein-tearing oxygen in redblood cells, less sticky to
oxygen.
It shifts what's called theoxyhemoglobin dissociation curve
to the right.
Speaker 1 (08:08):
Less sticky, so it lets go of oxygen more easily.
Speaker 2 (08:10):
Exactly, especially in tissues that are struggling
for oxygen, like an ischemicmacula.
So the proposed benefit isbetter oxygen release right
where it's desperately needed.
Speaker 1 (08:19):
Okay, improving oxygen supply, that makes a lot
of sense for a tissue that'sstarved of it.
Now, what about those othermessengers, the alkanols you
said?
Ozone creates oxidative stress,which sounds bad, especially in
a disease linked to oxidativestress.
Speaker 2 (08:32):
It does sound counterintuitive absolutely, but
the paper frames it veryspecifically.
It says these alkanols areproduced in very small,
calculated amounts.
They call it a calculated andwell-tolerated oxidative stress.
Speaker 1 (08:44):
Calculated stress.
Speaker 2 (08:47):
That's actually a pretty good analogy the paper
hints at.
You know, stressing yourmuscles makes them stronger.
The idea here is that thissmall controlled oxidative
signal is meant to activate thebody's own powerful defense
systems.
Speaker 1 (08:59):
Okay, so how does that signal work?
Speaker 2 (09:01):
Well, these alkanols travel through the bloodstream,
often attached to proteins likealbumin.
The paper proposes that whenthey get inside cells, they
interact with a protein calledKEEP1.
Speaker 1 (09:11):
KEEP1.
And what happens then?
Speaker 2 (09:13):
This is where a really critical defense pathway
gets switched on.
Normally, KEEP1 acts like aleash on another molecule called
NRF2, keeping it inactive.
But when these alkanols bindKEEP1, it's like they cut the
leash.
Speaker 1 (09:27):
So NRF2 is set free.
Speaker 2 (09:29):
Exactly.
Nrf2 is then free to travelinto the cell's nucleus, the
command center.
Speaker 1 (09:34):
Right, and what does NRF2 do in the nucleus?
Speaker 2 (09:36):
Once inside, NRF2 binds to specific sections of
DNA called antioxidant responseelements, or AREs.
The paper calls this bindingthe crucial event.
Speaker 1 (09:46):
The crucial event.
Why?
What's the result?
Speaker 2 (09:48):
This binding acts like flipping a master switch it
dramatically stimulates theproduction, the upregulation of
around 200 different genes.
And these aren't just any genes.
They're the genes responsiblefor making the cells own
powerful protective arsenal.
Speaker 1 (10:01):
Like what kind of protection?
Speaker 2 (10:03):
Things like potent antioxidant enzymes, sod,
catalase, glutathione peroxidase, gsh, piaquexis, also phase two
detoxification enzymes and anenzyme called hemeoxygenase 1,
which they describe as beinghighly protective against
cellular stress.
Speaker 1 (10:19):
Wow, so let me see if I've got this.
The hypothesis outlined in thepaper is introduce a tiny
controlled bit of oxidativestress using these ozone
generated alkanols, which thentriggers this NRF2 pathway,
leading the body to ramp upproduction of its own mass of
antioxidant and protectivedefenses, defenses that can then
fight back against the chronicoxidative stress and
(10:40):
inflammation that's actuallycausing the damage in dry ARMD.
Speaker 2 (10:43):
That's precisely the core mechanism they detail.
It's about stimulating your ownbody's defenses to counteract
the disease process, and thesource also mentioned some other
potential pluses, like makingblood flow a bit better, helping
blood vessels relax by boostingnitric oxide and maybe
releasing some growth factorsfrom platelets.
It's presented as amulti-pronged effect.
Speaker 1 (11:04):
That is a fascinating theory, really complex, but
fascinating.
Okay, theory is one thing.
What about results?
The paper talks about actualclinical findings from two
studies they did at theUniversity of Siena.
What did they report seeing inpatients?
Speaker 2 (11:18):
Right the clinical data.
The first study they discussedran from 1996 to 2001, involving
77 patients.
They compared a group gettingthe ozone therapy, o3-aht, for
at least two years against acontrol group.
Now the control group got theirown blood treated just with
oxygen, not ozone.
Speaker 1 (11:36):
Okay, so oxygenated blood versus ozonated blood?
What was the outcome?
Speaker 2 (11:39):
Well, first they noted the oxygen-only group
didn't really show much benefit.
But for the ozone therapy groupthey reported a statistically
significant difference in visualacuity improvement Improvement.
Speaker 1 (11:49):
How much?
Speaker 2 (11:49):
They defined improvement as gaining more than
two lines on the ETDRS eyechart.
That's like being able to readtwo extra lines of smaller
letters and they found 66.6percent.
So two-thirds of the ozonetherapy group reached this level
of improvement.
Speaker 1 (12:04):
Two-thirds Okay Compared to.
Speaker 2 (12:06):
Compared to just 30.4 percent in the oxygen-only
control group.
So a pretty big differencereported there.
They also mentioned that labtests for the treated group
either stayed the same oractually improved.
Speaker 1 (12:17):
Hmm, interesting.
What about the second study?
Speaker 2 (12:20):
The second one was larger 140 patients and ran from
2008 to 2011.
This time they compared theozone therapy group 70 patients
against a control group takingstandard antioxidant
multivitamins, also 70 patients.
Speaker 1 (12:34):
OK, ozone versus vitamins.
How did the vision changescompare over time in this one?
Speaker 2 (12:41):
They used a different vision scale here, Logmar, but
the trend was similar.
The paper reported that theaverage vision in the
ozone-treated eyes actuallyshowed improvement over both 6
months and 12 months.
Speaker 1 (12:49):
Improvement, not just slowing the decline.
Speaker 2 (12:51):
That's what their average data showed.
Yes, In stark contrast, thecontrol group taking the
multivitamins, their averagevision actually got worse.
It deteriorated over that samesix and 12-month period.
Speaker 1 (13:02):
Wow, okay, that's one thing, but what about, like,
preventing significant visionloss?
Did they look at that?
Speaker 2 (13:08):
They did, and this data as presented in the paper
is quite striking.
Did they look at that?
They did, and this data aspresented in the paper is quite
striking.
According to their results,none zero of the eyes treated
with ozone showed a worsening ofvision by more than two lines
on the eye chart at either sixmonths or 12 months.
Speaker 1 (13:21):
None lost that much vision.
Speaker 2 (13:23):
Correct.
Compare that to themultivitamin control group.
At 12 months, 40% of thosepatients had lost more than two
lines of vision and 38% had lostmore than three lines.
Speaker 1 (13:37):
The difference between the groups was highly
statistically significant,according to the pager.
Okay, hold on.
Nobody in the ozone group losttwo lines, but 40% in the
vitamin group did.
That seems really significantbased on their report.
Speaker 2 (13:45):
It really stands out in their findings.
Yes, it aligns well with thatstated goal of trying to stop or
slow the disease progression.
Yes, it aligns well with thatstated goal of trying to stop or
slow the disease progression.
And, interestingly, they alsomeasured markers of oxidative
stress in the blood in thissecond study and they found that
plasma oxidative stressdecreased in the group treated
with ozone, which lends somesupport to that whole mechanism.
(14:06):
We talked about boostingantioxidant defenses.
Speaker 1 (14:09):
Did they mention anything else like how patients
felt they?
Speaker 2 (14:11):
did Beyond the eye charts?
The source says that patientsin the ozone group assessed
using boosting antioxidantdefenses.
Did they mention anything elselike how patients felt they did
Beyond the eye charts?
The source says that patientsin the ozone group assessed
using a standard vision-relatedquality of life questionnaire
also reported subjectiveimprovements, things like
feeling better overall, havingmore energy, better
concentration, even improvedmemory.
Speaker 1 (14:28):
Potential wider benefits maybe Interesting.
So okay, let's talkpracticalities.
How is this O3 auto-hemotherapyactually done?
What does the paper describe?
Speaker 2 (14:37):
Right the procedure as they outline it.
It involves drawing a specificamount of the patient's own
blood, usually somewhere between150 and 225 milliliters,
depending on body weight.
Then they add an anticoagulantlike heparin or citrate to stop
it clotting.
Next, that blood is gentlymixed with a very precise volume
of the oxigenazone gas mixture.
(14:59):
This is done using a certifiedmedical ozone generator, and the
ozone concentration iscarefully measured and
controlled, often using aspectrophotometer.
Speaker 1 (15:08):
Precision seems key there.
Speaker 2 (15:10):
Absolutely crucial.
The paper emphasizes that,After mixing for a few minutes,
the treated blood is then simplyre-infused back into the
patient's vein like a standardIV drip.
Speaker 1 (15:20):
And you said patient's own blood.
Speaker 2 (15:22):
Yes, 100%.
The source stresses it must beautologous, using only the
patient's own blood.
They describe the procedure,when done correctly with these
small, precise, precise ozonedoses and medical-grade
equipment, as absolutely safe.
The safety, they argue, comesfrom the precision and the fact
that it's your own blood goingback in.
Speaker 1 (15:38):
Okay, how often do people need to do this according
to the paper?
Speaker 2 (15:42):
Typically they mention starting with treatments
twice a week for an initialphase, maybe around nine or ten
weeks.
They also note that patientsoften start noticing some
improvement after about four tosix treatments.
After that initial birth Thenmaintenance therapy is needed.
The paper suggests at leastonce every 10 days or so to
maintain the effects.
Speaker 1 (16:00):
Why the need for ongoing maintenance?
Speaker 2 (16:03):
Well, they explain that the biochemical effects
triggered by the treatment seemto have a rather short memory.
As they put it, If you stop thetreatments completely, the
benefits tend to wear off,usually within about six to nine
months.
Speaker 1 (16:17):
So it sounds like it requires a pretty consistent
commitment from the patient.
Speaker 2 (16:20):
It definitely does.
But the paper makes a point ofsaying that patient compliance
tends to be quite high once theystart seeing positive results
because you know they feel it'sworking.
They also make a point ofmentioning the minimal cost
compared to some other potentialtherapies being researched.
Speaker 1 (16:35):
Right, OK, so let's try and wrap this up.
This Borelli and Bochy reviewgives us a detailed look at the
theory, the proposed mechanismand some clinical findings they
reported regarding ozone therapyfor dry ARMD.
From their perspective, what'sthe main takeaway message?
Speaker 2 (16:51):
I think their core conclusion centers on what they
see as ozonotherapy's uniqueability, what they see as
ozonotherapy's unique ability,specifically via this O3-AHT
method, to basically wake up thebody's own built-in defense
systems, systems that fightagainst the kind of damage, the
lack of oxygen, theneurotoxicity that drives dry
ARMD.
So by improving oxygen deliveryand boosting those internal
(17:17):
antioxidant enzymes.
Right, the goal is to try andstop those precious
photoreceptor cells from dyingoff.
Speaker 1 (17:20):
And they had that point about when to start
treatment too, didn't they?
Speaker 2 (17:23):
Yes, that seemed important.
In their observations theynoted that the improvements in
vision were generally morenoticeable and happened faster
in patients who startedtreatment when they still had
some vision left, even if it wasalready declining, compared to
patients who were already nearlyblind.
Which suggests it stronglysuggests, based on their
findings, that startingtreatment earlier, before a
massive cell death has occurred,is likely to be more beneficial
(17:46):
, getting there before thedamage is too extensive.
Speaker 1 (17:49):
So this whole deep dive sparked by that listener
question from Denver reallyexplores the possibility and we
stress possibility based on thissource that innovative
approaches like ozone therapymight offer a potential avenue
for conditions like dry ARMD,supported by research like this
review paper.
Speaker 2 (18:07):
Exactly, and you know that's precisely the kind of
exploration that clinics likeLifeWellMDcom engage in as part
of Dr Kumar's team.
Their focus is on health,wellness and longevity, and they
are constantly looking at thescience, evaluating
evidence-informed approachesmuch like the research we've
just discussed to see how theymight help patients improve
their overall health and,importantly, their health span.
Speaker 1 (18:29):
It's really about staying informed on the
cutting-edge research,understanding the potential
mechanisms, like the NRF2pathway we talked about, and
then seeing what options mightmake sense for an individual,
based on their specific needsand the current state of
evidence.
Speaker 2 (18:42):
Definitely so.
If you, the listener, arecurious about the kind of
research we've covered today, orif you have questions about
innovative approaches for yourown health journey maybe related
to macular degeneration, maybesomething else entirely
connecting with the team atLifeWellMDcom could be a really
worthwhile step.
Speaker 1 (19:00):
Yeah, they can talk through your specific situation,
look at your health goals andhelp you understand how they
might explore possibilities withyou, drawing on the latest
research and their clinicalexpertise.
Speaker 2 (19:10):
We really encourage you, if this resonates, to maybe
take that first step on yourpersonal wellness journey.
You can give them a call.
The number is 561-210-9999.
Speaker 1 (19:21):
561-210-9999.
Speaker 2 (19:24):
It's a chance to connect with professionals who
are dedicated to exploringinnovative, evidence-informed
options to help you optimizeyour health.
Speaker 1 (19:31):
It really is.
It's about having aconversation with a team that
looks seriously at thepossibilities presented by
research and works with you tofigure out what might be
appropriate for your uniquehealth picture.
You know, diving deep intosources like this 2013 review
reminds us that there's alwaysmore going on beneath the
surface, doesn't it?
Insights often missed in justthe headlines or general health
info.
And maybe a final thought toleave you with something
(19:54):
provocative based on this paperJust consider that core idea
that a carefully controlled doseof something we normally think
of as bad, like oxidative stress, could actually be harnessed
therapeutically, that it couldtrigger the body's own powerful
healing and protective systems.
Speaker 2 (20:10):
Yeah, or maybe think even broader, building on the
mechanisms they described.
The review actually mentionspotential relevance to other eye
conditions involvingdegeneration or lack of blood
flow, things like degenerativemyopia, diabetic retinopathy,
even retinitis pigmentosa,stargardt's disease, ischemic
optic neuropathies, maybeglaucoma.
Could similar approachesactivating these defense
(20:31):
pathways be relevant?
There, too, something to ponder.
Speaker 1 (20:35):
Definitely food for thought.
Well, thank you for joining uson this deep dive into the
potential of ozone therapy fordry ARMD, as presented in the
Borelli and Bocci review andexplored with the perspective of
Dr Kumar's team at LifeWellMD.
Speaker 2 (20:49):
Yeah, we really hope this exploration has been
informative and maybe sparkedsome new questions for you.
Speaker 1 (20:54):
And we will see you on the next deep dive.
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