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Sea Moss and Susac Syndrome: Safety Notes
Sea Moss for Susac Syndrome: Anti-ESAM/Endothelial Autoimmunity, BRAO, SNHL & Brain Microangiopathy Support
Susac syndrome is a rare autoimmune attack on the tiniest blood vessels of your brain, retina, and inner ear. Here is an honest, mechanism-by-mechanism look at where whole-food minerals and marine compounds may offer supportive value for vascular and endothelial health – and the urgent limits that make specialist care non-negotiable.
Try Wildcrafted Sea Moss GelIf you or someone you love has been diagnosed with Susac syndrome, you have likely already lived through one of the scariest stretches of your life. A sudden blind spot in one eye. A strange, muffled wall of low-frequency hearing loss. Headaches and confusion that no one could explain at first. Susac syndrome is rare, frightening, and frequently misdiagnosed – and it deserves a real, mechanistic conversation rather than vague wellness promises.
Susac syndrome, also called retinocochleocerebral vasculopathy, is an autoimmune endotheliopathy: an immune-driven attack on the endothelial cells that line the smallest blood vessels of three organs at once – the brain, the retina, and the cochlea. Wildcrafted sea moss delivers a broad spectrum of the trace minerals your body needs, plus the marine polysaccharide fucoidan, and several of those components touch the vascular and endothelial pathways at the center of this disease. This page walks through what the science actually shows, names every limit honestly, and flags the one risk – permanent vision loss from branch retinal artery occlusion – that nobody with Susac syndrome can afford to ignore.
Before anything else: Susac syndrome is a neuro-ophthalmologic emergency that requires coordinated care from a neurologist, ophthalmologist, and rheumatologist. Sea moss is a supplemental whole food for general vascular and endothelial wellness – never a substitute for immunosuppressive treatment or for the urgent care that prevents irreversible vision and hearing loss. Read the warnings below carefully.
1. What Is Susac Syndrome (Retinocochleocerebral Vasculopathy)
Susac syndrome is defined by a clinical triad: encephalopathy (brain dysfunction), branch retinal artery occlusions (BRAO), and sensorineural hearing loss (SNHL). The unifying lesion is a microangiopathy – an injury to the smallest arterioles and capillaries – driven not by atherosclerosis or clotting disease but by autoimmune inflammation of the endothelium, the single-cell lining of every blood vessel.
It is rare, with prevalence estimated around one in a million, and it overwhelmingly affects women between roughly 20 and 40 years of age. Because the three organs are rarely all affected at the same moment, the disease is notoriously hard to recognize early. A patient may present with hearing loss alone, or a single visual field defect, months before the full picture emerges. The damage is vascular in nature: when an end-arteriole supplying a patch of retina, a segment of the cochlea, or a strip of brain tissue becomes occluded, the tissue downstream is starved of oxygen and can be permanently injured.
Understanding Susac syndrome as an endothelial disease is the key to understanding why nutrition that supports endothelial and vascular health is even part of the conversation. The endothelium is not passive plumbing. It is a metabolically active organ that regulates inflammation, clotting, barrier integrity, and blood flow – and it is precisely this layer that the immune system targets in Susac syndrome.
2. IgG Anti-Endothelial Cell Antibodies: Anti-ESAM, Anti-CLDN5, Anti-CD166
One of the most important discoveries in Susac syndrome biology is the presence of IgG anti-endothelial cell antibodies (AECAs). These autoantibodies bind directly to proteins on the surface of the cells lining the microvasculature, marking those cells for immune attack. The antigens identified include anti-ESAM (endothelial cell-selective adhesion molecule), anti-CLDN5 (claudin-5, a core tight-junction protein), and anti-CD166 (ALCAM, activated leukocyte cell adhesion molecule).
These targets are not random. ESAM and CD166 govern how white blood cells stick to and cross the vessel wall, while claudin-5 is the master sealing protein of the blood-brain and blood-retinal barriers. When antibodies attack these molecules, the result is a double hit: endothelial cells are damaged and the barrier itself begins to leak. The antibodies activate complement and recruit inflammatory cells, setting off the cascade that occludes the tiny end-arterioles.
Why this matters for nutrition: No food removes autoantibodies. What whole-food nutrition can plausibly support is the resilience of the endothelial cells under attack – their antioxidant defenses, their tight-junction proteins, and the resolution of inflammation around them. Sea moss is studied here not as an antibody-clearing therapy, which it is not, but as a source of minerals and marine compounds relevant to endothelial cell biology. The antibodies themselves are the domain of immunosuppressive medicine.
3. CD4+ Th1/Th17 Perivascular T-Cell Infiltration and Endothelial Apoptosis
Alongside the antibodies, Susac syndrome features cellular immunity gone wrong. Biopsies and pathology studies reveal CD4+ T-helper cells of the Th1 and Th17 subtypes accumulating in a perivascular pattern – clustering around the small vessels. Th1 cells release interferon-gamma and Th17 cells release IL-17, two cytokines that drive endothelial activation, recruit more inflammatory cells, and push endothelial cells toward apoptosis (programmed cell death).
When endothelial cells die in the wall of a tiny end-arteriole, the vessel can swell, narrow, and ultimately occlude. That is the mechanical event behind a branch retinal artery occlusion or a cochlear microinfarct. The Th17 axis in particular has become a major focus because it links Susac syndrome to a broader family of autoimmune vasculopathies in which IL-17 amplifies vascular inflammation.
Where supportive nutrition fits: Several components in sea moss – fucoidan, selenium, omega-3 precursors, and zinc – have been studied in laboratory and animal models for their ability to modulate inflammatory T-cell signaling and to support regulatory T-cell (Treg) balance, the calming counterweight to Th1/Th17 activity. This is mechanistic, preclinical interest, not a clinical claim. It explains why a nutrient-dense, anti-inflammatory dietary foundation is a reasonable companion to medical care, never a replacement for the medications that actually suppress the T-cell attack.
4. Complement C4d Deposition on Endomysial Capillaries and End-Arterioles
When autoantibodies bind endothelial cells, they activate the complement system – a cascade of blood proteins that punches holes in targeted cells and flags them for destruction. In Susac syndrome, pathologists have documented C4d, a stable breakdown fragment of complement component C4, deposited along the endomysial capillaries (in muscle biopsies) and the end-arterioles of affected tissue. C4d is a durable footprint that proves the classical complement pathway has been firing against the vessel wall.
Complement-mediated injury is a central driver of the endothelial damage and the microvascular occlusion. It also generates a storm of reactive oxygen species, compounding the oxidative stress that injured endothelial cells already face. This is why complement and oxidative defense are tightly linked in the Susac story.
The fucoidan connection: Sulfated polysaccharides such as fucoidan have been studied in laboratory settings for their capacity to interact with and modulate complement activation. In preclinical work, certain fucoidans can temper excessive complement firing along vascular surfaces. This is genuinely interesting given the C4d signature of Susac syndrome, but it is preclinical, and dietary fucoidan is not a complement-targeting drug. Sea moss provides fucoidan as part of a whole food, not as a purified therapeutic.
5. VEGF-A Upregulation and Blood-Brain/Blood-Retinal/Blood-Labyrinth Barrier Breakdown
Inflamed, oxygen-starved endothelium upregulates VEGF-A (vascular endothelial growth factor A). In a healthy setting VEGF-A is protective, but in the context of Susac syndrome its excess loosens the junctions between endothelial cells and drives breakdown of all three specialized barriers at once: the blood-brain barrier (BBB), the blood-retinal barrier (BRB), and the blood-labyrinth barrier (BLB) of the inner ear.
When these barriers leak, fluid, immune cells, and inflammatory proteins flood into tissues that are meant to be sealed off. In the retina this contributes to the leakage seen on fluorescein angiography; in the brain it underlies the contrast-enhancing lesions on MRI; in the cochlea it disrupts the delicate ionic environment that hearing depends on. VEGF-A excess and tight-junction loss are two sides of the same barrier-breakdown coin.
Nutrients and barrier integrity: The tight junctions that hold these barriers together are built from proteins like claudin-5 and ZO-1, and their assembly depends on adequate zinc and on a low-oxidative-stress environment maintained by selenium-dependent enzymes and omega-3 fatty acids. Supporting the raw materials of barrier integrity is a logical nutritional foundation. It does not stop the autoimmune VEGF-A surge – only medical treatment does that – but it supports the cellular machinery the body uses to keep its barriers intact.
6. NF-kB/IL-6/TNF-alpha Vascular Endothelial Inflammatory Activation
At the molecular heart of endothelial inflammation sits NF-kB, a master transcription factor. When endothelial cells are stressed by antibodies, complement, and inflammatory cytokines, NF-kB switches on and drives production of IL-6, TNF-alpha, and a fleet of adhesion molecules. This is the engine that converts a quiet vessel lining into an inflamed, sticky, leukocyte-recruiting surface.
IL-6 and TNF-alpha amplify the whole process, recruiting more immune cells and sustaining the perivascular inflammation described earlier. The adhesion molecules NF-kB induces – VCAM-1 and ICAM-1 – act as molecular Velcro, grabbing circulating white blood cells and pulling them into the vessel wall. Breaking this self-reinforcing loop is a major goal of medical therapy, and it is the pathway where anti-inflammatory nutrition has the most mechanistic relevance.
Fucoidan and NF-kB: Fucoidan, the sulfated polysaccharide concentrated in red and brown seaweeds, is one of the more studied marine compounds for NF-kB modulation. In laboratory and animal models, fucoidan dampens NF-kB activation and reduces downstream IL-6, TNF-alpha, and VCAM-1/ICAM-1 expression on endothelial cells. This makes it mechanistically interesting for any condition driven by endothelial inflammation. As always, this is preclinical signal, and dietary fucoidan supports rather than replaces the medications that control autoimmune inflammation.
7. Branch Retinal Artery Occlusions (BRAO): Visual Field Defects and Snowflake Retinopathy
The retinal hallmark of Susac syndrome is the branch retinal artery occlusion. When an end-arteriole feeding a wedge of retina is occluded by the endothelial inflammatory process, that patch of retina loses its blood supply and the corresponding part of the visual field goes dark. Patients describe sudden, often painless blind spots or curtains across their vision.
On examination, ophthalmologists may see Gass plaques – yellow-white deposits in the mid-portion of retinal arterioles, away from branch points – which are highly suggestive of Susac syndrome. Fluorescein angiography reveals the characteristic leakage and the so-called snowflake pattern of vessel-wall staining. Each occlusion can cause a permanent visual field defect, which is why early detection and aggressive treatment matter so profoundly.
This is the most urgent warning on this page. A branch retinal artery occlusion can cause permanent, irreversible vision loss. If you have any sudden change in vision – a new blind spot, a dark curtain, blurred or missing field – treat it as an emergency and seek an ophthalmologist and neurologist immediately. No supplement, including sea moss, can open an occluded retinal artery or restore lost vision. Time is sight.
8. Sensorineural Hearing Loss (Low-Mid Frequency): Cochlear End-Arteriole Involvement
The cochlea is exquisitely vascular, and its apex – the region tuned to low and mid frequencies – is supplied by tiny end-arterioles that are especially vulnerable to microvascular occlusion. That is why the sensorineural hearing loss of Susac syndrome characteristically begins in the low-to-mid frequencies, often with tinnitus and vertigo. Patients may describe a sudden muffling, a sense that voices have lost their fullness, or roaring in the ears.
The mechanism mirrors what happens in the eye and brain: endothelial inflammation and complement-mediated injury occlude the cochlear end-arterioles, starving the hair cells of the inner ear. Because hair cells do not regenerate in humans, cochlear microinfarcts can leave permanent hearing deficits. Prompt immunosuppressive treatment offers the best chance of preserving hearing, and in severe cases cochlear implantation may be considered.
Hearing is also time-sensitive. Sudden hearing loss in Susac syndrome is a medical urgency. If you notice new hearing loss, tinnitus, or vertigo, contact your care team without delay. Sea moss supports general wellness; it cannot reopen an occluded cochlear vessel or restore lost hair cells. Audiologic monitoring and prompt medical treatment are what protect hearing.
9. Corpus Callosum "Snowball" Lesions: CNS Microinfarcts and Encephalopathy
The brain signature of Susac syndrome is found on MRI: small, round, central lesions in the corpus callosum – the great band of fibers connecting the two hemispheres – described as snowballs because of their appearance. These central callosal lesions, along with deep gray-matter and white-matter microinfarcts, are highly characteristic and help distinguish Susac syndrome from multiple sclerosis, with which it is often confused.
Each lesion represents a microinfarct: a patch of brain tissue starved by an occluded end-arteriole. Clinically this produces encephalopathy – headaches that can be migraine-like, confusion, memory difficulty, personality change, and in severe cases psychiatric symptoms. The encephalopathy can fluctuate and, like the eye and ear involvement, reflects the same underlying microvascular endothelial attack.
Where vascular nutrition is relevant: Brain microvascular health depends on the same endothelial integrity, antioxidant defense, and barrier proteins discussed throughout this page. A nutrient-dense diet that supplies magnesium, omega-3 precursors, zinc, and selenium supports the general vascular and neuronal environment. But MRI-confirmed brain microinfarcts are managed with immunosuppression and neurologic care. This is foundational support, not treatment, and the distinction is everything.
10. How Sea Moss Fucoidan Modulates NF-kB, Complement C4d, and Endothelial VCAM-1/ICAM-1
Pulling the threads together, fucoidan is the single most relevant marine compound in sea moss for the biology of Susac syndrome, because it touches three of the central pathways at once. In preclinical models it dampens NF-kB activation, interacts with and can temper complement firing, and reduces the endothelial adhesion molecules VCAM-1 and ICAM-1 that recruit white blood cells into the vessel wall.
Each of these is a node in the Susac cascade: NF-kB is the inflammatory engine, complement C4d is the autoimmune footprint, and VCAM-1/ICAM-1 are the molecular grappling hooks of leukocyte invasion. A compound that engages all three is, mechanistically, of obvious interest in an endothelial autoimmune disease.
Keep the honesty front and center: All of this is laboratory and animal-model evidence using often-purified or concentrated fucoidan. Sea moss delivers fucoidan as one component of a whole food, at food-level amounts, and the human clinical evidence in Susac syndrome specifically does not exist – it is far too rare a disease for that. Fucoidan is a supportive dietary compound for vascular and endothelial wellness, not a drug, and not a treatment for Susac syndrome.
11. Selenium and Endothelial GPx1/GPx4 Against Complement-Mediated Oxidative Stress
When complement and inflammatory cells attack endothelium, they unleash a flood of reactive oxygen species. The endothelial cell's primary defense against this oxidative onslaught runs through the selenium-dependent enzymes glutathione peroxidase 1 (GPx1) and glutathione peroxidase 4 (GPx4). GPx1 neutralizes hydrogen peroxide; GPx4 specifically protects cell membranes from lipid peroxidation and from ferroptosis, a form of iron-dependent cell death. Neither enzyme can function without selenium at its active site.
If selenium status is low, this frontline defense weakens precisely when inflamed endothelium needs it most. Maintaining healthy selenium status supports the antioxidant capacity that keeps endothelial cells alive under inflammatory and complement-mediated stress.
Why the source matters: Sea moss provides selenium in the organic selenomethionine form – the form found in food, which the body recognizes and incorporates readily. The goal is not megadosing; selenium has a relatively narrow safe range and excess is harmful. The aim is steady, healthy baseline status so the endothelial GPx enzymes have the cofactor they need. For someone supporting vascular health through Susac syndrome, a whole-food selenium source within sensible limits is a mechanistically reasonable foundation, ideally with your provider aware of your total intake.
12. Omega-3 DHA/EPA: Vascular PGI2/TXA2 Balance, Resolvin D1 Anti-Inflammatory Endothelial Resolution
The endothelium maintains a delicate balance between prostacyclin (PGI2), which keeps vessels open and blood flowing smoothly, and thromboxane A2 (TXA2), which promotes platelet aggregation and vessel constriction. In inflamed, injured endothelium this balance tips toward the pro-occlusive side, contributing to the microvascular occlusions of Susac syndrome. Omega-3 fatty acids, EPA and DHA, favorably shift this balance toward the PGI2 side, supporting smoother microvascular flow.
Even more compelling are the specialized pro-resolving mediators that the body makes from DHA, including resolvin D1. Resolvins do not just suppress inflammation; they actively orchestrate its resolution – clearing inflammatory cells, calming endothelial activation, and helping tissue return to baseline. In a disease defined by unresolving endothelial inflammation, the resolution pathway is conceptually important.
An honest caveat on the source: Sea moss contributes alpha-linolenic acid (ALA), a plant omega-3 precursor, but the body's conversion of ALA into the directly active EPA and DHA is limited, often only a few percent. If the goal is meaningful EPA and DHA for vascular and resolution support, a high-quality marine omega-3 (fish or algae oil) is a more efficient source. Sea moss is a supportive whole food in this picture, and pairing it with a dedicated omega-3 may make more sense for the PGI2/TXA2 and resolvin pathways.
13. Zinc: ZO-1/Claudin-5 Vascular Tight Junction Integrity, Treg Support, and Metalloenzyme Defense – Standard Treatments and What Sea Moss Cannot Do
Zinc is the quiet workhorse of vascular barrier integrity. The tight junctions that seal the blood-brain, blood-retinal, and blood-labyrinth barriers are built from proteins including ZO-1 and claudin-5 – the very claudin-5 targeted by autoantibodies in Susac syndrome. Adequate zinc supports the assembly and stability of these junctional proteins. Zinc also supports regulatory T-cell (Treg) balance, the calming counterweight to the Th1/Th17 attack, and it is the catalytic core of antioxidant metalloenzymes such as copper-zinc superoxide dismutase (SOD1) that defend endothelial cells from oxidative injury.
So zinc touches three Susac-relevant fronts: barrier integrity, immune balance, and oxidative defense. Sea moss provides zinc within its broad mineral profile, making it part of a logical nutritional foundation for vascular and endothelial resilience.
Standard treatments: what actually controls Susac syndrome
Susac syndrome is managed aggressively and medically. First-line treatment usually involves high-dose corticosteroids to rapidly quell inflammation, often combined with intravenous immunoglobulin (IVIG). For more severe or refractory disease, neurologists and rheumatologists add steroid-sparing immunosuppressants such as mycophenolate mofetil, azathioprine, or cyclophosphamide, and increasingly the B-cell-depleting antibody rituximab. Antiplatelet therapy and close ophthalmologic and audiologic monitoring round out the picture. The aim is to halt the endothelial attack before more microinfarcts occur.
What sea moss cannot do: Sea moss cannot clear anti-endothelial autoantibodies, cannot stop complement C4d deposition in a clinically meaningful way, cannot reopen an occluded retinal or cochlear artery, cannot reverse a corpus callosum microinfarct, and cannot replace corticosteroids, IVIG, immunosuppressants, or rituximab. It is a whole-food source of minerals and fucoidan that may support general vascular and endothelial wellness as a companion to – never a substitute for – the specialist treatment that controls this disease. Anyone with Susac syndrome must remain under the care of a neurologist, ophthalmologist, and rheumatologist.
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Shop Wildcrafted Sea Moss GelHow Sea Moss Components Map to Susac Syndrome Biology
| Component | Relevant mechanism in Susac syndrome | Honest limit |
|---|---|---|
| Fucoidan | Modulates NF-kB, tempers complement, lowers endothelial VCAM-1/ICAM-1 in preclinical models | Preclinical only; not a complement or antibody drug |
| Selenium (selenomethionine) | Cofactor for endothelial GPx1/GPx4 against complement-driven oxidative stress and ferroptosis | Narrow safe range; baseline support, not megadose |
| Omega-3 (ALA precursor) | Supports PGI2/TXA2 balance; DHA-derived resolvin D1 aids inflammation resolution | Low ALA conversion; marine omega-3 is more efficient |
| Zinc | ZO-1/claudin-5 tight-junction integrity, Treg balance, SOD1 metalloenzyme defense | Foundational support, not a barrier-restoring therapy |
| Iodine | Thyroid and metabolic support within the broad mineral profile | Manage carefully if thyroid disease is present |
| Magnesium | Vascular tone, endothelial function, mitochondrial energy | General support, not disease-modifying |
A Simple Daily Approach
If you and your specialist team decide sea moss is a reasonable addition to your routine, consistency matters far more than quantity.
- Daily gel: One to two tablespoons of wildcrafted sea moss gel per day, blended into a smoothie, stirred into warm (not boiling) water, or taken straight.
- Pair with omega-3: Because sea moss is a weak omega-3 source, consider a quality marine omega-3 for the PGI2/TXA2 and resolvin pathways, with your provider's input.
- Morning consistency: Mineral status and any endothelial-support benefits build over weeks of steady daily use, not from occasional servings.
- Keep your team informed: Tell your neurologist, ophthalmologist, and rheumatologist what you are taking, especially given iodine, selenium, and fucoidan considerations alongside immunosuppressive medication.
Frequently Asked Questions
Can sea moss help with Susac syndrome?
Sea moss is a whole food that supplies the trace minerals your body needs plus the marine compound fucoidan, several of which relate to endothelial and vascular health that is disrupted in Susac syndrome. It may offer supportive nutritional value for general vascular wellness. However, it cannot clear the anti-endothelial autoantibodies, stop the complement-driven injury, reopen an occluded retinal or cochlear vessel, or reverse a brain microinfarct. Susac syndrome requires urgent, ongoing care from a neurologist, ophthalmologist, and rheumatologist, and sea moss is at most a companion to that care, never a treatment.
How does fucoidan affect complement C4d and endothelial inflammation in Susac syndrome?
Fucoidan is a sulfated marine polysaccharide that, in laboratory and animal models, can dampen NF-kB activation, interact with and temper complement firing along vascular surfaces, and reduce the endothelial adhesion molecules VCAM-1 and ICAM-1 that recruit white blood cells. These are central pathways in Susac syndrome, where complement C4d deposition and NF-kB-driven endothelial inflammation occlude tiny vessels. This is preclinical, mechanistic interest using often-concentrated fucoidan. Sea moss provides fucoidan as part of a whole food at food-level amounts, and it is not a complement-targeting drug or a substitute for immunosuppressive treatment.
What role does selenium play in protecting endothelial cells from autoimmune damage?
Selenium is the essential cofactor for glutathione peroxidase enzymes GPx1 and GPx4, the endothelial cell's frontline defense against the reactive oxygen species generated by complement and inflammatory attack. GPx4 specifically protects cell membranes from lipid peroxidation and ferroptosis. Low selenium status weakens this defense exactly when inflamed endothelium needs it most. Sea moss provides selenium in the food-form selenomethionine, supporting healthy baseline antioxidant capacity. Selenium has a narrow safe range, so the goal is steady baseline status rather than megadosing, ideally with your provider aware of your total intake.
Does omega-3 help restore vascular PGI2/TXA2 balance in Susac syndrome vasculopathy?
Omega-3 fatty acids EPA and DHA favorably shift the endothelial balance between prostacyclin (PGI2), which keeps vessels open, and thromboxane A2 (TXA2), which promotes constriction and platelet aggregation, supporting smoother microvascular flow. DHA also gives rise to resolvin D1, a pro-resolving mediator that helps actively resolve endothelial inflammation. Sea moss contributes the plant precursor ALA, but conversion to EPA and DHA is limited, so a dedicated marine omega-3 is a more efficient source for these pathways. This is supportive vascular nutrition, not a treatment for the autoimmune process itself.
Is sea moss safe alongside corticosteroids, IVIG, or rituximab for Susac syndrome?
For many people sea moss is a well-tolerated whole food, but several cautions apply with Susac syndrome treatment. Sea moss contains iodine, which matters if you have any thyroid condition. Its fucoidan has mild antiplatelet activity, which is relevant if you take antiplatelet or anticoagulant therapy, common in Susac care. And because you may be on corticosteroids, IVIG, immunosuppressants, or rituximab, you should always clear sea moss with your treating physicians first and bring the actual product to your appointment so they can review the iodine, selenium, and fucoidan content against your regimen. Sea moss is supplemental support, not a substitute for any of these treatments.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Susac syndrome is a serious, rare autoimmune endotheliopathy that can cause permanent vision and hearing loss and brain injury, and it requires urgent and ongoing management by a neurologist, ophthalmologist, and rheumatologist. Any sudden change in vision or hearing should be treated as a medical emergency. Consult your qualified healthcare provider before making any changes to your routine.
Branch retinal artery occlusions can cause permanent vision loss without emergency treatment. Any sudden vision change, new blind spot, hearing loss, or vertigo is a medical emergency. See an ophthalmologist, neurologist, and rheumatologist urgently. No supplement can reopen an occluded vessel.
Key Supportive Nutrients
- Fucoidan – modulates NF-kB, complement, VCAM-1/ICAM-1
- Selenium – endothelial GPx1/GPx4 antioxidant defense
- Omega-3 – PGI2/TXA2 balance, resolvin D1 resolution
- Zinc – ZO-1/claudin-5 tight-junction integrity
- Iodine – thyroid and metabolic support
- Magnesium – vascular tone and endothelial function
On This Page
- What Is Susac Syndrome
- Anti-ESAM/CLDN5/CD166 Antibodies
- Th1/Th17 Perivascular Infiltration
- Complement C4d Deposition
- VEGF-A and Barrier Breakdown
- NF-kB/IL-6/TNF-alpha Activation
- Branch Retinal Artery Occlusions
- Sensorineural Hearing Loss
- Corpus Callosum Snowball Lesions
- Fucoidan and Endothelial Pathways
- Selenium and Endothelial GPx
- Omega-3 DHA/EPA Resolution
- Zinc, Standard Treatments, Limits
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