Lipemia Retinalis

Lipemia retinalis is a look that eye doctors see at the back of the eye when the fat in the blood (especially triglycerides carried in “chylomicrons”) is extremely high—the retinal blood vessels turn creamy-white (and in the worst stage the whole fundus looks salmon-pink). It usually gets better fast once triglycerides are brought down. NCBIPMC

Lipemia retinalis is an eye finding that shows up when the fat (triglyceride) level in your blood becomes extremely high. The small blood vessels in the back of the eye (the retina) look creamy-white or the whole eye background looks salmon-pink. This color change happens because the blood is crowded with chylomicrons (fat particles) that scatter light. The eye itself isn’t the problem—this sign is a warning that the bloodstream is dangerously loaded with triglycerides, usually at >2,000 mg/dL. When triglycerides are lowered, the retinal color typically goes back to normal. NCBIEyeWiki

Your retina is the light-sensing tissue at the back of the eye. It has tiny arteries and veins. In normal blood, light passes through these vessels easily and they look red. When triglycerides in the blood skyrocket, the blood becomes loaded with chylomicrons (fat-rich particles). These big particles scatter light like milk does, so the vessels stop looking red and start looking milky or creamy. If triglycerides go even higher, the effect spreads from the far edges of the retina to the center, and eventually the whole back of the eye can look salmon-pink. This look is called lipemia retinalis. It’s a sign of dangerous hypertriglyceridemia, not a stand-alone eye disease. Most people don’t notice vision problems from the color change itself, but the underlying high triglycerides carry serious body-wide risks (especially pancreatitis). Getting triglycerides down usually makes the eye look normal again. NCBIBioMed Central

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Types

1) Types by appearance (grading)

Doctors often describe three stages that roughly match how high the triglyceride level is:

• Stage I (early): Creamy, thin-looking vessels out in the periphery of the retina.

• Stage II (moderate): The creamy color reaches the posterior pole (the center area).

• Stage III (marked): The entire fundus looks salmon-colored; arteries and veins both look pale and are hard to tell apart by color.

These stages commonly appear when triglycerides are very high: peripheral changes around 2,500–3,499 mg/dL, posterior changes around 3,500–5,000 mg/dL, and salmon-colored fundus above 5,000 mg/dL. NCBI

2) Types by cause

• Primary (genetic) chylomicronemia: lifelong tendency to extreme triglycerides due to gene changes that cripple lipoprotein lipase (LPL) function or its helpers (e.g., LPL, GPIHBP1, APOA5, APOC2, LMF1).

• Secondary hypertriglyceridemia: a non-genetic trigger (like uncontrolled diabetes, alcohol, pregnancy, thyroid or kidney problems, or certain medicines) pushes triglycerides very high, sometimes on top of a mild genetic tendency. Lipid JournalOxford Academic

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Causes

Lipemia retinalis happens when triglycerides get extremely high. The items below are reasons that can push triglycerides into that range.

1. LPL gene defects (Familial chylomicronemia syndrome): Broken LPL enzyme means fat particles can’t be cleared, so triglycerides stay sky-high from infancy. Lipid Journal

2. APOC2 gene defects: Missing ApoC-II cofactor → LPL can’t work, so chylomicrons pile up. Lipid Journal

3. APOA5 gene variants: ApoA-V helps regulate triglycerides; when faulty, levels soar. Lipid Journal

4. GPIHBP1 gene defects: The “parking dock” that brings LPL to capillaries doesn’t work, blocking fat breakdown. Lipid Journal

5. LMF1 gene defects: LMF1 is needed to mature LPL; without it, LPL stays ineffective. Lipid Journal

6. Familial hypertriglyceridemia / combined disorders: Milder inherited patterns that can spike into very high levels when combined with other risks. American Heart Association Journals

7. Uncontrolled diabetes (especially insulin deficiency): Without insulin, the liver makes more triglycerides and fat breakdown is impaired. Medscape

8. Alcohol overuse: Alcohol boosts liver triglyceride production and raises VLDL. PMC

9. Obesity / metabolic syndrome: Insulin resistance and high calorie intake drive TG up. PMC

10. High-carb or very high-fat diet (excess calories): Extra sugars and fats are converted to triglycerides. PMC

11. Pregnancy (especially 3rd trimester): Hormones raise triglycerides; rarely they reach extreme levels. PMC

12. Hypothyroidism: Low thyroid slows lipid metabolism, raising triglycerides. PMC

13. Kidney disease / nephrotic syndrome: Protein loss and metabolic changes increase TG. PMC

14. Systemic inflammation (e.g., lupus), severe illness (e.g., sepsis): Hormones/cytokines push up TG. PMC

15. Retinoids (e.g., isotretinoin): Reduce VLDL clearance and boost ApoC-III, so TG climb. NCBI

16. Estrogens (including some oral contraceptives): Can raise TG via liver effects. Oxford Academic

17. Protease inhibitors (HIV meds): Can increase triglycerides substantially. Cleveland Clinic

18. Atypical antipsychotics (e.g., olanzapine, clozapine): Often worsen TG and weight. Cleveland Clinic

19. Nonselective beta-blockers and thiazide diuretics: Can raise TG in some patients. Oxford Academic

20. Corticosteroids, tamoxifen, bile-acid resins, propofol (prolonged): Several commonly used drugs that can push TG higher (effect sizes vary). kjim.orgOxford Academic

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Symptoms

The eye signs are dramatic, but most people don’t feel eye symptoms from lipemia retinalis itself. Symptoms, when present, usually come from the underlying high triglycerides or its complications.

1. Often no eye symptoms at all. Vision can be normal even when vessels look milky. NJRetina

2. Mild blurred or hazy vision (some notice “film” or loss of crispness when TG are extremely high). BioMed Central

3. Reduced contrast or color dulling (rare, related to light scatter). BioMed Central

4. Temporary visual fluctuation that improves as TG fall (reported in cases). The Journal of Medical Optometry (JoMO)

5. No eye pain from lipemia retinalis itself (important reassurance). NCBI

6. Skin bumps (eruptive xanthomas): Small yellow-red papules on trunk/extensors—classic in chylomicronemia. NCBI

7. Abdominal pain (warning sign for pancreatitis when TG are very high). BioMed Central

8. Nausea/vomiting (also points toward pancreatitis). BioMed Central

9. Poor appetite/feeding in infants with genetic forms. Annex Publishers

10. Fatigue and malaise (non-specific, common in metabolic imbalance). Oxford Academic

11. Polydipsia/polyuria if uncontrolled diabetes is the driver. Medscape

12. Hepatosplenomegaly (enlarged liver/spleen) in familial chylomicronemia. NCBI

13. Tingling or peripheral neuropathy-like complaints (reported with severe dyslipidemia). The Journal of Medical Optometry (JoMO)

14. Chest discomfort or breathlessness on exertion (not from LR, but from co-existing cardiovascular risk). American Heart Association Journals

15. Anxiety when told the fundus looks “salmon-pink.” (Understandable—education helps; the look usually reverses after TG control.) NCBI

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Diagnostic tests

Goal: confirm the look, prove triglycerides are very high, find the cause, and screen for complications. Many findings reverse when TG improve.

A) Physical examination

1. General inspection for xanthomas and xanthelasma: Small yellowish skin bumps or eyelid plaques hint at severe hypertriglyceridemia. NCBI

2. Abdominal exam for pancreatitis pain: Epigastric tenderness with nausea suggests acute pancreatitis from very high TG. Oxford Academic

3. Blood pressure and cardiovascular exam: High TG often travel with other CV risks; listen for bruits, check pulses. American Heart Association Journals

4. External eye exam: Look for corneal arcus and eyelid xanthelasma; proceed to dilated fundus exam. NJRetina

B) Manual/bedside ophthalmic tests

5. Visual acuity (distance/near): Usually normal in LR; documents any unexpected blur. NJRetina

6. Color vision and contrast checks: May show subtle changes when scatter is extreme. BioMed Central

7. Pupil exam and light reflexes: Rules out other retinal/optic nerve problems if vision seems off. (Good clinical practice.)

8. Dilated ophthalmoscopy (direct/indirect): The key test—shows creamy vessels starting peripherally, progressing centrally; helps stage the LR. NCBI

C) Laboratory / pathological tests

9. Fasting lipid panel with triglycerides: Confirms very high TG (often >2,500 mg/dL in classic LR). Note: calculated LDL is unreliable when TG are very high. PMC

10. Serum appearance (“lactescent” plasma): Blood sample looks milky from chylomicrons when TG soar. NCBI

11. Apolipoproteins (e.g., ApoB, ApoC-II) and lipoprotein profile: Helps distinguish chylomicronemia patterns from mixed dyslipidemia. American Heart Association Journals

12. Genetic testing panel (LPL, GPIHBP1, APOA5, APOC2, LMF1) for suspected familial chylomicronemia, especially in children/young adults. Lipid Journal

13. Glucose and HbA1c: Looks for diabetes driving the TG spike. Medscape

14. TSH (thyroid), kidney and liver panels: Screens secondary causes (hypothyroidism, nephrotic syndrome, renal or hepatic disease). PMC

15. Pancreatitis labs (amylase, lipase): Ordered if abdominal pain or vomiting is present. Oxford Academic

D) Electrodiagnostic tests

16. Full-field electroretinography (ERG): Can show reduced a- and b-wave amplitudes in both rod and cone responses during LR; typically normalizes after TG control. NCBI

17. Visual evoked potential (VEP) (select cases): Usually normal; done if the clinical picture raises concern beyond LR (helps exclude optic pathway issues).

E) Imaging tests

18. Color fundus photography: Documents the creamy vessels and tracks reversal after TG fall—helpful for patient education and monitoring. The Journal of Medical Optometry (JoMO)

19. Optical coherence tomography (OCT): May show hyper-reflective, engorged vessels and small inner-retinal dots that fade over months as TG normalize—changes can lag behind the visible color change. The Journal of Medical Optometry (JoMO)

20. Fluorescein angiography / OCT-angiography (selected): Often unremarkable in pure LR; used when clinicians need to rule out vascular occlusions or ischemia. NJRetina

Non-pharmacological treatments

The goal is to get triglycerides down fast (below ~500 mg/dL) to avoid pancreatitis. These steps are cornerstone care and remain essential even if drugs are used. NCBI

1. Very-low-fat diet: typically <10–15% of calories from fat or ≤20 g/day in FCS; this reduces chylomicron production and lowers triglycerides. Lipid JournalPMCLearnYourLipids

2. Cut refined sugars/simple carbs: sugary drinks, sweets, and refined starches rapidly raise triglycerides; choose high-fiber carbs instead. LearnYourLipids

3. Avoid alcohol completely: alcohol boosts liver triglyceride production and can trigger pancreatitis in severe cases. Medscape

4. Use MCT oil for calories: medium-chain triglycerides are absorbed directly and don’t need chylomicrons, helping meet energy needs while keeping TGs down. LearnYourLipids

5. Weight reduction (if overweight): even 5–10% loss improves triglycerides and insulin resistance. American Heart Association Journals

6. Regular aerobic activity (e.g., 150–300 min/week): improves insulin sensitivity and lowers TG. (Lifestyle consensus in dyslipidemia care.) Oxford Academic

7. Tight diabetes control: normalize glucose to shrink TGs and chylomicrons; insulinization if needed in hospital. NCBI

8. Treat hypothyroidism (with your clinician): correcting thyroid hormone reduces TGs. NCBI

9. Stop or switch offending medicines (doctor-supervised): steroids, estrogens, certain antipsychotics, retinoids, etc. NCBI

10. Pregnancy-specific plan: strict low-fat diet; essential omega-3 intake to protect the fetus; consider hospitalization if TGs soar. PMC

11. Family screening & genetic counseling for suspected FCS. NCBI

12. Hydration and low-fat meal spacing: smaller, frequent meals lessen post-meal chylomicron spikes.

13. Pancreatitis safety plan: if severe upper-abdominal pain/vomiting occurs, go to the ER—you may need IV fluids and acute TG-lowering. ScienceDirect

14. Smoking cessation: supports vascular health as you treat the metabolic issue.

15. Regular lipid monitoring: track TG response and adjust your plan.

16. Dietitian-led meal planning: ensures micronutrients and essential fats are adequate on a very-low-fat diet. Lipid Journal

17. Limit saturated fat & trans fat: prefer lean proteins and plant-based options. (Core guidance in dyslipidemia management.) Oxford Academic

18. Increase dietary fiber (vegetables, legumes, oats): fiber improves TGs and satiety.

19. Sleep/stress management: supports glycemic control and weight loss.

20. Eye follow-up: fundus photos to confirm resolution as TGs fall. NCBI

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Drug treatments

Medicines treat the systemic triglycerides; there is no “eye drop” for lipemia retinalis. Doses below are typical adult doses—your clinician will individualize.

1. Fenofibrate (PPAR-α agonist)
   Dose: often 145 mg once daily (formulation-dependent).
   Purpose: first-line to lower very high TG; helps prevent pancreatitis.
   How it works: boosts lipoprotein lipase activity and fatty-acid breakdown, shrinking TG-rich particles.
   Side effects: stomach upset, liver enzyme rise, gallstones; combine cautiously with statins. NCBI

2. Gemfibrozil (fibrate)
   Dose: 600 mg twice daily, 30 min before meals.
   Purpose/mechanism: like fenofibrate; lowers TG 30–50%.
   Notes/side effects: avoid with statins (higher myopathy risk); GI upset, liver enzyme rise. NCBI

3. Prescription omega-3 fatty acids
   Dose: 4 g/day (e.g., icosapent ethyl 2 g twice daily).
   Purpose: lowers TG substantially; EPA-only products lower TG without raising LDL; EPA+DHA combos lower TG but may raise LDL.
   Mechanism: reduce hepatic VLDL production and increase TG clearance.
   Side effects: fishy aftertaste, GI upset; rare bleeding risk. American Heart Association Journals

4. Atorvastatin or another statin
   Dose: 10–80 mg once daily.
   Purpose: main benefit is cardiovascular risk reduction; can lower TG ~20–30%.
   Mechanism: decreases hepatic cholesterol synthesis, secondarily lowering VLDL/TG.
   Side effects: muscle aches, rare liver enzyme rise. NCBI

5. Niacin (extended-release)
   Dose: typically 500 mg nightly, gradually titrating (often 1,000–2,000 mg if tolerated).
   Purpose: lowers TG 15–35% and raises HDL.
   Mechanism: reduces VLDL synthesis.
   Side effects: flushing/itching, glucose elevation, liver toxicity—use only with clinician oversight. NCBI

6. Intravenous insulin (hospital, acute use)
   Dose: protocol-based IV infusion (commonly ~0.05–0.1 U/kg/h) with dextrose to prevent hypoglycemia.
   Purpose: rapid TG reduction during severe hypertriglyceridemia/HTG-pancreatitis or uncontrolled diabetes.
   Mechanism: activates lipoprotein lipase, clearing chylomicrons.
   Side effects: hypoglycemia, low potassium—requires monitoring. gastrores.orgLippincott Journals

7. Olezarsen (Tryngolza)—apoC-III antisense oligonucleotide
   Dose: 80 mg subcutaneously once monthly.
   Purpose: FDA-approved (Dec 2024) adjunct to diet to reduce TG in familial chylomicronemia syndrome (FCS).
   Mechanism: suppresses apoC-III, removing a brake on TG clearance.
   Side effects: injection-site reactions; low platelets can occur—requires lab monitoring. ReutersIonisMedscape Reference

8. Volanesorsen (Waylivra)—apoC-III antisense oligonucleotide
   Dose (as studied/approved in EU/Canada): commonly 300 mg weekly initially; protocols vary.
   Purpose: for FCS where available; lowers TG markedly.
   Mechanism/notes: apoC-III suppression; thrombocytopenia risk—requires platelet monitoring; availability differs by country. New England Journal of MedicineEuropean Medicines Agency (EMA)+1

9. Evinacumab (Evkeeza)—ANGPTL3 monoclonal antibody (specialist/off-label for TG)
   Dose (studies): 10–20 mg/kg IV every 4 weeks; TG reduction observed in non-FCS severe HTG.
   Purpose: considered in highly selected, refractory cases by specialists.
   Mechanism: blocks ANGPTL3, releasing the “brakes” on lipases that clear TG.
   Side effects: infusion reactions; specialist therapy only. NaturePMC

10. Hospital-based therapeutic plasma exchange (TPE) (a procedure rather than a “drug,” but used acutely)
    Use: in severe HTG-induced pancreatitis or organ failure, to rapidly lower TG when standard care isn’t enough; evidence for outcome benefit is mixed, so it’s individualized.
    Mechanism: physically removes TG-rich plasma and replaces it.
    Risks: line complications, bleeding, electrolyte shifts. JAMA NetworkSpringerOpen

Not routinely recommended: Heparin used to be combined with insulin, but it can deplete lipoprotein lipase after a brief bump; its routine use has become controversial. PMCgastrores.org

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Dietary & supportive supplements

Evidence varies; these are adjuncts—not replacements—for diet/medicine.

1. Fish-oil supplements (EPA/DHA): 2–4 g/day lowers TG; DHA may raise LDL—prescription EPA is preferred when available. American Heart Association Journals

2. MCT oil: 1–3 tbsp/day helps calories without chylomicron load; increase slowly to avoid GI upset. LearnYourLipids

3. Psyllium fiber: ~5–10 g/day; slows carbohydrate absorption and can aid TG control.

4. Plant sterols/stanols: ~2 g/day; mainly lower LDL, small TG help.

5. Berberine: 500 mg twice daily; may modestly lower TG and improve glucose (evidence moderate).

6. Curcumin: 500–1000 mg/day; anti-inflammatory support; TG data modest.

7. Green tea extract (EGCG): 250–300 mg/day; small TG effects; mind liver safety with high doses.

8. Garlic (aged extract): 600–1200 mg/day; minor lipid effects; watch interactions.

9. Coenzyme Q10: 100–200 mg/day; doesn’t lower TG but can ease statin muscle symptoms.

10. Alpha-lipoic acid: 300–600 mg/day; may help insulin sensitivity.

11. Chromium (picolinate): 200–1000 µg/day; glucose support; lipid effects inconsistent.

12. Magnesium: 200–400 mg/day; helps insulin sensitivity and cramps/constipation on low-fat diets.

13. Myo-inositol: 2 g twice daily; helpful in PCOS to improve TG/insulin resistance.

14. L-carnitine: 1–2 g/day; fatty-acid transport; TG data mixed.

15. Taurine: 1–3 g/day; small TG effects in some studies.

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Regenerative / stem-cell” drugs

For lipemia retinalis, there is no role for stem-cell therapy or immune-boosting drugs. What’s new and exciting are gene-targeted lipid medicines that remove biological “brakes” on TG clearance:

• Olezarsen (Tryngolza)—approved in the U.S. for FCS; 80 mg SC monthly. ReutersIonis

• Volanesorsen (Waylivra)—available in parts of the EU/Canada for FCS; weekly dosing with strict platelet monitoring. European Medicines Agency (EMA)

• Evinacumab (ANGPTL3 mAb)—helps many with severe HTG except classic FCS; specialist/off-label use. tctmd.com

These are not eye treatments; they target triglycerides system-wide.

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Procedures/surgeries

1. Therapeutic plasma exchange (TPE / plasmapheresis): rapidly removes TG-rich plasma in HTG-induced pancreatitis or life-threatening settings; outcome benefit evidence is mixed but it lowers TG quickly. JAMA NetworkSpringerOpen

2. Lipoprotein apheresis: a specialized, repeated treatment to filter atherogenic lipoproteins; sometimes considered in refractory severe HTG in expert centers. (Specialist therapy.) UpToDate

3. Exchange transfusion (neonates/infants): used in exceptional pediatric crises to reduce TG when other measures fail. NCBI

4. Bariatric/metabolic surgery (for morbid obesity with refractory HTG): weight-loss surgery can dramatically reduce triglycerides and pancreatitis risk in selected patients. ScienceDirectPubMed

5. (Historical) ileal bypass: improved lipid parameters but is rarely used today and reserved for extreme, refractory cases. NCBI

There is no eye surgery for lipemia retinalis itself; the retinal color normalizes when triglycerides fall. NCBI

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Prevention tips (simple & practical)

1. Keep dietary fat very low if you have FCS or severe HTG. Lipid Journal

2. Avoid alcohol altogether. Medscape

3. Limit refined carbs; choose high-fiber carbs. LearnYourLipids

4. Maintain healthy weight; even 5–10% loss helps. American Heart Association Journals

5. Exercise most days (aerobic focus). Oxford Academic

6. Control diabetes and monitor glucose regularly. NCBI

7. Treat thyroid disease if present. NCBI

8. Review medications that can raise TG and switch if possible (doctor-guided). NCBI

9. Plan for pregnancy with a specialist if you have severe HTG. PMC

10. Check fasting lipids as recommended and keep records.

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When to see a doctor

• Right away / ER: severe upper-abdominal pain, vomiting, fever, or back/chest pain—these can be acute pancreatitis from high TG. Medscape

• Urgent clinic visit (days): if an eye doctor tells you “lipemia retinalis,” if your lab shows TG >1,000 mg/dL, or if you’re pregnant and TG are climbing fast. NCBI

• Routine follow-up: diabetes, thyroid, kidney, or liver conditions; medication changes that affect TG.

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What to eat

Eat/Use more of:

1. Very-lean proteins: skinless poultry, egg whites, legumes, tofu.

2. High-fiber carbs: vegetables, lentils, chickpeas, oats, barley.

3. Whole fruit (watch portions if diabetes).

4. Non-fat dairy (or fortified alternatives).

5. MCT oil (doctor/dietitian-guided) to meet calories. LearnYourLipids

Avoid/Limit strongly:

1. Visible fats and fried foods (chylomicron surge).
2. Refined sugars/sweet drinks (rapid TG rise). LearnYourLipids
3. Alcohol (even “social” amounts). Medscape
4. High-fat desserts & baked goods (hidden fats/sugars).
5. Fatty meats/full-fat dairy (saturated fat boosts TG production).

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FAQs

1) Is lipemia retinalis dangerous to my eyesight?
Usually no. It’s mainly an eye sign of extremely high triglycerides. Vision generally returns to normal as triglycerides fall. The real danger is pancreatitis and cardiovascular risk. NCBI

2) What triglyceride level causes it?
Classically appears when TG are >2,000 mg/dL; the fundus looks salmon-colored at >5,000 mg/dL. NCBI

3) How fast does it resolve?
Sometimes within days to a week once TG drop significantly. NCBI

4) Can children get it?
Yes—especially with familial chylomicronemia; pediatric lipid specialists should guide care. NCBI

5) Does diabetes cause it?
Uncontrolled diabetes is a common secondary cause; fixing glucose control helps TGs fall. NCBI

6) Is there a medicine that directly treats the eye?
No. Treat the triglycerides, not the retina.

7) Which medicines work fastest in a crisis?
In hospital, IV insulin (and sometimes apheresis) can rapidly reduce TGs; choices depend on the clinical scenario. gastrores.orgJAMA Network

8) Are fish-oil capsules enough?
High-dose prescription omega-3s (especially pure EPA) can significantly lower TGs; over-the-counter capsules vary in strength and purity. American Heart Association Journals

9) Do statins help?
Yes, mainly for heart risk; they also lower TGs modestly. NCBI

10) What about niacin?
It lowers TGs but has side effects (flushing, liver issues). Use only if your clinician recommends it. NCBI

11) Is there a “genetic” shot for this?
For FCS, olezarsen (Tryngolza)—a monthly injection—was FDA-approved in Dec 2024 to reduce TGs (with diet). Other agents like volanesorsen are available in parts of the EU/Canada. Reuters

12) Can I drink alcohol again once TG are lower?
If you’ve had severe HTG or pancreatitis, most specialists advise no alcohol. Medscape

13) Will exercise alone fix it?
Exercise helps, but dietary fat restriction and, often, medicines are needed for very high TG. Lipid Journal

14) Are there eye complications?
Rarely, vascular occlusions or ischemia have been reported; again, lowering TGs protects you. NCBI

15) What’s the single most important step?
Adopt a very-low-fat diet and get medical help quickly to bring TG down; the eye finding will usually fade as the blood clears. Lipid Journal

 

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

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Last Updated: August 11, 2025.

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