Normal-tension glaucoma challenges the old idea that glaucoma is simply a disease of high eye pressure. In this episode, Dr. Saikumar Gandapodi joins us to unpack what the evidence actually shows about optic nerve damage occurring at statistically normal intraocular pressures, and why blood flow, vascular regulation, and systemic factors matter so much here.

We explore Flammer syndrome, a described pattern of vascular dysregulation that shows up in some patients with normal-tension glaucoma, and separate what is established from what is still emerging. Dr. Gandapodi explains how conventional pressure-lowering care remains the proven foundation, and where careful, evidence-informed integrative support may complement it.

This is a research-driven conversation for an educated audience curious about the future of eye care. No cures are promised. Instead, we look honestly at the science of neuroprotection, ocular perfusion, and whole-person care around a condition that still keeps clinicians humble.

Welcome to the Netra Eye Institute Podcast,

where modern vision science meets the wisdom of integrative ophthalmology.

Today, we are joined by Dr. Saikumar Gandipoti,

founder and director of Netra Eye Institute,

whose work is dedicated to redefining how patients understand and approach chronic

and degenerative eye conditions. His goal is simple:

to help patients, families, and clinicians explore a more comprehensive and

integrative approach to long-term eye health.

This is the Netra Eye Institute Podcast. Let's begin.

Welcome back to the show. Today, we're getting into a condition that quietly

overturns a lot of assumptions about glaucoma,

normal tension glaucoma,

and a related pattern called Flammer Syndrome.

My guest is Dr. Saikumar Gandapodi, board-certified doctor of Oriental

medicine, an Ayurvedic practitioner, and founder and director of the Netra Eye

Institute, a holistic eye care center.

-Dr. Gandapodi, welcome. -Thanks for having me. This is one of my

favorite topics because it forces us to think about the eye as part of the whole

-body. -Let's start simple. Most people think

glaucoma means high eye pressure. What is normal tension glaucoma?

It's glaucoma, meaning progressive optic nerve damage and vision loss, but the

intraocular pressure stays in the statistically normal range.

So the classic villain, high pressure, isn't obviously there. The nerve is still

-being injured. -So if pressure isn't elevated, what's

driving the damage?

The honest answer is it's multifactorial, and we don't have it fully solved.

Pressure still matters even when it's normal, but the field has increasingly

looked at blood flow to the optic nerve and at how well the eye regulates that

-blood flow. -Before we go deeper, tell me about your

center and about Netra Restoration Therapy since it'll come up.

Netra Eye Institute is a holistic eye care center.

Netra Restoration Therapy, or NRT, is our full-spectrum integrative approach.

The idea is to support several biological pathways at once. Ocular blood flow,

mitochondrial function, oxidative stress balance, and neuroprotection as a

complement to standard care.

I wanna be clear on that word, complement.

Absolutely.

NRT is adjunctive. It does not replace an ophthalmologist. It doesn't replace

pressure-lowering drops or surgery, and I make no cure claims.

The proven backbone of glaucoma care is lowering intraocular pressure. Everything

else is supportive and still being studied.

That's a good anchor.

So let's talk about lowering pressure in a disease where pressure is already normal.

Does that even help?

It does, and that's one of the most important established findings.

The collaborative normal tension glaucoma study showed that lowering pressure by

around thirty percent slowed progression in many patients.

So even when pressure looks normal, reducing it further is protective.

That's the evidence-based foundation.

So the nerve in these patients may just be more vulnerable to whatever pressure they

have?

That's part of it. The same pressure that one nerve tolerates fine, another nerve

can't.

And when the nerve is more fragile, other stressors, especially poor perfusion, seem

to matter more.

Let's get into that vascular side.

This is where Flammer Syndrome enters.

What is it?

Flammer Syndrome is a term coined by Professor Josef Flammer to describe a

cluster of features tied to what he called primary vascular dysregulation,

the blood vessels overreacting to stimuli like cold or stress.

People with it often have cold hands and feet,

low blood pressure, a tendency toward migraine, and they feel cold easily.

And the link to the eye?

The hypothesis is that this dysregulation also affects the small vessels feeding the

optic nerve.

Instead of smoothly matching blood flow to need, the vessels are unstable, so the

nerve gets swings between too little and normal flow.

Those unstable episodes may promote oxidative stress and injury over time.

How solid is the connection between Flammer Syndrome and normal tension

glaucoma?

I call it a well-described association, not a proven cause.

Studies, mostly from Flammer's group and related European centers, have found this

vascular profile more often in normal tension glaucoma patients, particularly

younger, slender women.

But an association isn't proof it drives the disease, and Flammer Syndrome itself

isn't a formal diagnosis everyone accepts.

That's a fair distinction.

So what's the actual mechanism people propose for how unstable blood flow

damages the nerve?

The leading idea is reperfusion type stress.

When flow drops and then returns, that instability generates reactive oxygen

species, oxidative stress, right at the vulnerable tissue.

Over years, that can contribute to retinal ganglion cell loss, the nerve cells that

carry vision from the eye to the brain.

And is there direct evidence of reduced ocular blood flow in these patients,

or is it theoretical?

There's real measurement evidence. Techniques like OCT angiography and

Doppler studies have shown reduced perfusion in the optic nerve head and

around it in many glaucoma patients, including normal tension cases.

What's still debated is chicken or egg. Does low flow cause the damage, or does a

damaged nerve simply need less blood?

That's the honest ambiguity.

Are there other systemic clues that point to the vascular story?

Nocturnal blood pressure dips are a big one.

If blood pressure drops too much overnight, sometimes worsened by

aggressive blood pressure medication taken at night, perfusion to the optic nerve

can fall during sleep.

There's reasonable evidence linking large nighttime dips to progression in some

-patients. -So a patient could be doing everything

right for their heart and inadvertently starve their optic nerve at night?

It can happen,

which is why this needs coordination with the primary care doctor.

Nobody should adjust blood pressure medication on their own. But it's a good

example of why glaucoma isn't only an eye problem. It's a circulation problem too.

Let's talk endothelium. You mentioned vascular dysregulation.

Is endothelial dysfunction part of this?

It appears to be. The endothelium is the inner lining of blood vessels that helps

them relax and constrict properly.

In flammatype dysregulation, there's evidence of altered endothelin-1

signaling, a powerful vessel-constricting molecule.

Elevated endothelin has been reported in some normal tension glaucoma patients,

which fits the vasoconstriction picture.

So where does conventional care sit with all this vascular thinking?

Conventional care is excellent, and it's the foundation, but its main proven lever

is pressure.

There are effective drops, laser, and surgery to lower it.

What conventional care doesn't yet have is a well-proven targeted therapy to fix the

blood flow instability itself.

That gap is where research and careful integrative thinking are focused.

Let's go there. What does the evidence support for supporting ocular blood flow?

The most cited example is ginkgo biloba. A small crossover study published in

Ophthalmology suggested ginkgo improved visual field measures in some normal

tension glaucoma patients over a short period. It's intriguing, but it's small

and preliminary,

not a reason to abandon standard care.

What might ginkgo be doing mechanistically?

It's studied as a multi-target agent. It may modestly improve microcirculation,

act as an antioxidant, and support mitochondrial function. That's actually a

nice bridge to how I think about herbal medicine generally,

as complex mixtures hitting several pathways at once rather than a single drug

-on a single target. -Say more about that network idea.

It's central to how you frame these therapies.

A single botanical formula can contain dozens of phytochemicals.

Modern researchers study this as network pharmacology, many compounds nudging many

targets gently instead of one molecule blocking one receptor hard.

For a multifactorial disease like normal tension glaucoma, that framing is

appealing. But I want to be clear, appealing isn't the same as proven in

large human trials.

Let's translate some traditional concepts.

In Chinese medicine,

how would you map this vascular picture?

I'd offer it as a conceptual parallel, not a scientific equivalent.

In traditional Chinese medicine, poor or stagnant circulation is described as blood

stasis

and low functional energy as qi deficiency.

The cold hands, sluggish flow to the nerve, that pattern rhymes with blood

stasis.

But that's an interpretive lens, not proof of a mechanism.

And in Ayurveda?

Again, as a parallel, the vascular tone and cold sensitivity picture resembles a

vata pattern, movement and regulation gone irregular, and the blood tissue, rakta

dhatu, is central to nourishing the eye.

These are frameworks for thinking about the whole person.

I never present them as replacements for measured intraocular pressure or visual

field testing.

Let's talk neuroprotection directly. If the nerve is vulnerable, can we protect

-the cells themselves? -That's the holy grail,

and it's still largely unproven in humans.

The one drug with real trial data is memantine,

and honestly, the large glaucoma trial didn't meet its primary endpoint.

Neurotrophins like BDNF protect ganglion cells in lab and animal models,

but we don't yet have a delivery method proven to save vision in patients.

So neuroprotection is promising biology but thin clinical evidence?

Exactly right.

I'd separate it cleanly.

Strong at the bench, encouraging in animals, not yet established in humans.

Anyone who tells you they can regrow your optic nerve is overselling.

What we can talk about honestly is reducing the stressors, oxidative stress,

unstable perfusion that push vulnerable cells over the edge.

Where does mitochondrial function fit?

You mentioned it in NRT.

Retinal ganglion cells, especially their long fibers, are energy-hungry,

so they lean heavily on mitochondria. There's genuine interest in mitochondrial

support in glaucoma.

Some researchers have looked at nicotinamide, a form of vitamin B3.

Early human data, including a small crossover study, hinted at improved

retinal function, but it's early and needs larger confirmation.

You keep drawing that line between early and established

-Why is that so important to you? -Because vision is irreplaceable,

and patients deserve to know exactly how sturdy the ground is under each

recommendation.

If I blur early signals into settled facts, I've failed them.

-Hope has to be honest to be useful. -Let's talk oxidative stress since it keeps

-recurring in this vascular story. -It's a plausible common pathway.

Unstable blood flow generates reactive oxygen species, and the antioxidant

defenses at the nerve can get overwhelmed.

So dietary antioxidants, colorful vegetables, adequate omega-3s, sensible

lifestyle are reasonable general support.

But I frame that as good health, not as a proven glaucoma treatment.

Is there any role for the gut in this picture,

or is that a stretch?

For normal tension glaucoma specifically, I'd call the gut-eye axis interesting but

speculative.

There's emerging work on inflammation, the microbiome, and neurodegeneration

broadly, but I don't have strong human glaucoma trials to point to.

So I mention it as a research frontier, not a clinical recommendation.

Let's get practical.

A patient is newly diagnosed with normal tension glaucoma.

What should the workup include beyond eye pressure?

First, confirm it's really normal tension with careful pressure measurements over

time and corneal thickness.

Then I'd want a vascular history, cold hands and feet, migraines, low blood

pressure, and a conversation about nighttime blood pressure and any

medications.

And sleep apnea should be screened since it stresses oxygen delivery to the nerve.

Sleep apnea. That's a nice systemic catch.

-How does it connect? -Repeated drops in oxygen overnight are

exactly the kind of intermittent stress the vulnerable nerve doesn't like.

There's an association between sleep apnea and glaucoma, and treating apnea is well

worth it for whole body health regardless.

It's a great example of root cause thinking that stays fully

-evidence-grounded. -So where exactly does NRT come in for such

-a patient? -Alongside their ophthalmologist's

pressure-lowering plan,

never instead of it. We'd look at supporting circulation and perfusion

stability,

reducing oxidative stress, sensible mitochondrial and nutritional support,

stress and cold exposure management for the vascular reactivity and lifestyle.

It's a complementary layer aimed at resilience with realistic expectations.

And you'd still want them getting regular visual field and OCT scans?

Always.

The objective testing is how we know if anything is working or if we need to

escalate.

Integrative care without objective monitoring is just guessing, and I won't

do that with someone's sight.

What about acupuncture, since it's part of your training?

Any evidence in glaucoma?

The evidence in glaucoma is weak and inconsistent.

Some small studies suggest transient changes in ocular blood flow,

but nothing I'd present as established for preserving vision.

I'm comfortable saying that plainly.

If I use it, it's for general circulation and stress support,

not as a proven optic nerve therapy.

Let's zoom out.

What is conventional medicine, in your view, still missing about this condition?

Not missing so much as still lacking tools for a proven way to stabilize ocular

blood flow and directly protect the nerve.

Conventional care nailed the pressure problem.

The vascular and neuroprotective pieces are where the whole field, conventional

and integrative alike, is still searching.

I see them as partners, not rivals.

Where do you think the most exciting research is heading?

Better imaging of ocular blood flow to actually identify who has a

perfusion-driven disease,

cleaner neuroprotection trials, and mitochondrial support like nicotinamide

getting larger, rigorous testing.

If those pan out, we could finally treat the nerve and the circulation, not only

the pressure.

If a listener takes away just a few things from this conversation,

what should they be?

One,

normal pressure doesn't mean safe. Get monitored.

Two,

lowering pressure still helps here. That's proven.

Three,

this can be a circulation story, so systemic health matters.

And four,

integrative support is a complement with evolving evidence, never a substitute for

your ophthalmologist.

Dr. Gandapodi, this has been genuinely clarifying.

Thank you.

My pleasure.

Protect the pressure, respect the blood flow, and treat the whole person honestly.