Spinocerebellar Ataxia Autosomal Recessive Type 8 (SCAR8)

Spinocerebellar ataxia, autosomal recessive type 8 (SCAR8) is a rare, inherited brain disorder. It mainly affects the cerebellum, the part of the brain that controls balance and coordination. People with SCAR8 slowly develop unsteady walking, clumsy hand movements, and slurred speech. Symptoms usually start in late childhood to adulthood, and they get worse over many years. The condition is autosomal recessive, meaning a person gets the disease only if they inherit a non-working copy of the same gene from both parents. NCBI+2PMC+2

SCAR8 is a rare, inherited ataxia caused by harmful changes in the SYNE1 gene. It usually begins in teens or adult life and slowly affects balance, walking, speech, and eye movements. The problem starts in the cerebellum (the body’s balance center). Over time, many people need a cane, walker, or wheelchair, but thinking and lifespan can be near normal in “pure cerebellar” forms. In some families, weakness, stiff muscles (spasticity), or breathing or swallowing problems can appear. There is no cure yet; care focuses on therapy, safety, nutrition, and treating symptoms. PubMed+2NCBI+2

SCAR8 happens because of harmful changes (variants) in a gene called SYNE1. This gene makes a large protein called nesprin-1. Nesprin-1 helps the cell’s nucleus (the control center) stay connected to the cell’s inner skeleton. When SYNE1 is not working, nerve cells in the cerebellum do not function well and slowly degenerate. This damage causes the ataxia symptoms. NCBI+1

Doctors first recognized SCAR8 in families from Quebec, Canada. We now know it occurs in many countries. Some people have a “pure” form with mostly balance and speech problems. Others can also have muscle, joint, or heart problems because SYNE1 is used in many tissues. The age when symptoms begin and the extra features can vary a lot from one person to another. OUP Academic+1

Another names

SCAR8 is known by several names. These include “SYNE1 ataxia,” “autosomal recessive cerebellar ataxia type 1 (ARCA1),” and “autosomal recessive spinocerebellar ataxia type 8 (SCAR8).” In older reports, you may also see “autosomal recessive ataxia, Beauce type.” All of these refer to SYNE1-related recessive ataxia. National Ataxia Foundation+2preventiongenetics.com+2

Types

Doctors often group SYNE1/SCAR8 into simple “types” based on what they see in patients:

1) Pure cerebellar type. The main issues are balance, coordination, and speech. Eye control may be mildly affected. This is the classic presentation first described in Canada. NCBI

2) Cerebellar ataxia with motor-neuron features. Some people also show weakness, muscle wasting, or abnormal reflexes suggesting involvement of upper and/or lower motor neurons. PMC

3) Cerebellar ataxia with extra-neurologic features. A few cases report joint contractures (arthrogryposis), muscle disease, or heart problems, reflecting SYNE1’s wide role in body tissues. PubMed

4) Broad SYNE1 deficiency spectrum. GeneReviews describes a range from cerebellar ataxia to severe congenital forms such as arthrogryposis multiplex congenita. This reminds us the same gene can cause a spectrum of problems. NCBI

Causes

Although SCAR8 is a single-gene disorder, many different ways SYNE1 can be damaged or factors that influence risk exist. Here are 20 plain-language “causes” or contributors, grouped by biology and inheritance:

1. Biallelic SYNE1 loss-of-function variants. Two damaging variants (one from each parent) stop the gene from working. JAMA Network

2. Nonsense variants. A “stop” signal appears too early, making a short, non-working protein. JAMA Network

3. Frameshift variants. Small insertions or deletions shift the reading frame and wreck the protein. JAMA Network

4. Splice-site variants. Errors at intron–exon borders make the cell cut and paste RNA wrongly. JAMA Network

5. Large deletions/duplications. Big pieces of the gene can be missing or repeated, disrupting function. preventiongenetics.com

6. Missense variants in key domains. A single amino-acid change in critical regions weakens nesprin-1. OUP Academic

7. Defective nesprin-1 “LINC” coupling. Nesprin-1 helps link the nucleus to the cell skeleton; failure hurts neuron health. Frontiers

8. Cerebellar Purkinje cell vulnerability. These neurons are sensitive to nuclear-envelope stress, leading to ataxia. (inference from SYNE1 biology and cerebellar signs). Frontiers+1

9. Founder variants in some populations. Certain communities have shared ancestral variants that raise local risk. OUP Academic

10. Consanguinity. Parents who are related may both carry the same rare SYNE1 variant. NCBI

11. Compound heterozygosity. Two different harmful variants (one on each chromosome) can cause disease. e-jmd.org

12. Gene dosage below a critical threshold. Too little functional protein pushes neurons past their coping capacity. (mechanistic inference consistent with loss-of-function). JAMA Network

13. Modifier genes. Differences in other genes may shift age at onset or severity across families. (reported variability across cohorts). OUP Academic

14. Nuclear envelope stress pathways. Disturbed connections around the nucleus can impair signaling and resilience. Frontiers

15. Axonal transport strain. Poor nucleo-cytoskeletal coupling may hinder long neuron processes. (biologic inference aligned with nesprin-1 role). Frontiers

16. Muscle involvement in some variants. Some SYNE1 variants contribute to myopathy, adding weakness/fatigue. PubMed

17. Developmental wiring differences. In severe, early-onset cases, motor pathways may be affected from birth. NCBI

18. Environmental stress does not cause SCAR8 but may worsen function (falls, deconditioning) once disease exists. (general clinical inference; SYNE1 variants remain the root cause). NCBI

19. Age-related neuronal stress. With time, the same defect causes more noticeable imbalance. (matches slow progression). NCBI

20. Diagnostic delay. Not a biological cause, but late recognition can allow preventable complications (falls, malnutrition). (clinical inference consistent with natural history). OUP Academic

Symptoms

1. Unsteady walking (gait ataxia). People sway and have a wide-based walk. Turning and tandem walking are hard. This is the hallmark symptom. NCBI

2. Hand clumsiness (limb ataxia). Fine tasks like buttoning or writing feel slow and shaky. Reaching may overshoot targets. NCBI

3. Slurred, drawn-out speech (dysarthria). Words sound slow and “scanning.” Speaking long sentences is tiring. NCBI

4. Eye movement problems. People can have nystagmus (eye jerks) or trouble with smooth pursuit, which blurs vision when tracking objects. MalaCards

5. Intention tremor. The hand may tremble more as it nears a target, like a cup or a door handle. NCBI

6. Poor balance in the dark. Without visual cues, standing and walking become harder, raising fall risk. NCBI

7. Slow progression. Symptoms usually worsen gradually over years, not suddenly. NCBI

8. Upper/lower motor neuron signs (in some). Some individuals show increased reflexes, weakness, or muscle wasting, suggesting broader nerve involvement. PMC

9. Mild cognitive or emotional changes. Some people have problems with planning, attention, or mood (cerebellar cognitive affective syndrome). PMC

10. Fatigue. Extra energy is needed to keep balance and speak clearly, so people tire easily. (clinical inference aligned with progressive ataxia). OUP Academic

11. Frequent falls. Tripping and falls increase as balance worsens, especially on uneven ground. NCBI

12. Speech fatigue. Talking for long periods becomes effortful; the voice can sound monotone or broken. NCBI

13. Swallowing difficulty (later in some). Coordination of swallow muscles may slow, raising choking risk. (general ataxia feature; severity varies in SYNE1). OUP Academic

14. Double vision or blurred vision during head moves. Eye tracking and gaze holding can be unstable. MalaCards

15. Need for walking aids over time. Many people eventually use a cane, walker, or wheelchair for safety. MalaCards

Diagnostic tests

A) Physical exam (bedside observation)

1. General neurologic exam. The doctor checks walking, stance, coordination, reflexes, strength, and sensation to confirm a cerebellar pattern and look for motor-neuron signs. NCBI+1

2. Gait assessment. Observing stride width, base, turns, and tandem walking shows the degree of ataxia and fall risk. NCBI

3. Speech exam. Listening for slow, scanning speech confirms dysarthria from cerebellar dysfunction. NCBI

4. Eye movement exam. The clinician checks for nystagmus and pursuit/saccade problems that are common in cerebellar disease. MalaCards

5. Postural stability tests. Simple stance tests (feet together, Romberg) show how vision and proprioception support balance. NCBI

B) Manual (bedside) coordination tests

6. Finger-to-nose. The person alternates touching their nose and the examiner’s finger; overshoot (dysmetria) suggests cerebellar dysfunction. NCBI

7. Heel-to-shin. Sliding the heel down the opposite shin checks lower-limb coordination. NCBI

8. Rapid alternating movements. Fast hand flips (diadochokinesia) expose rhythm and timing problems. NCBI

9. Tandem gait (heel-to-toe). Walking in a straight line heel to toe is very sensitive for cerebellar ataxia. NCBI

10. Rebound test / check reflex. The examiner resists and suddenly releases the patient’s arm; poor “checking” suggests cerebellar issues. NCBI

C) Laboratory & pathological tests

11. Targeted genetic testing of SYNE1. Sequencing and copy-number analysis confirm biallelic pathogenic variants and clinch the diagnosis. NCBI+1

12. Ataxia gene panels. When the cause is unclear, multi-gene panels that include SYNE1 can speed diagnosis. PMC

13. Exome or genome sequencing. Comprehensive testing can find rare or novel SYNE1 variants when panels are negative. PMC

14. Family testing (segregation). Testing parents/siblings helps show variants are on different chromosomes and inherited as expected in recessive disease. NCBI

15. Exclusion labs. Blood tests rule out other ataxias that are treatable (vitamin E deficiency, thyroid disease, Wilson disease). These do not cause SCAR8 but are important to exclude. NCBI

D) Electrodiagnostic tests

16. Nerve conduction studies (NCS). These can detect peripheral nerve involvement if weakness or numbness is present. Some SYNE1 cases show motor-neuron features. PMC

17. Electromyography (EMG). EMG looks for denervation or myopathic changes when weakness or muscle wasting is suspected. PubMed

18. Evoked potentials (as needed). Visual or somatosensory tests can support central pathway involvement if symptoms suggest it. (general neurophysiology use in ataxias). NCBI

E) Imaging tests

19. Brain MRI. MRI typically shows cerebellar atrophy, especially of the vermis and hemispheres, matching the symptoms. MRI also helps exclude other causes. American Academy of Neurology

20. Spinal MRI (selected cases). If there are motor-neuron signs or unexplained weakness, spine imaging checks for additional structural problems. (contextual clinical use). PMC

Non-pharmacological treatments (therapies & others)

1. Physiotherapy (gait & balance) – Regular balance, stepping, and coordination drills improve walking confidence and lower fall risk by training the brain to use remaining pathways better (neuroplasticity). Home exercises plus supervised PT sessions work best. Mayo Clinic

2. Strength & core training – Light resistance for legs, hips, and trunk improves posture, step control, and endurance without over-fatigue. It helps joints stay stable when the cerebellum sends “noisy” signals. Mayo Clinic

3. Task-specific coordination practice – Repeating real tasks (sit-to-stand, reaching, turning) teaches safer patterns and compensations. Short, frequent sessions are better than long ones. Mayo Clinic

4. Assistive devices – Canes, trekking poles, or walkers widen your base and reduce falls. Physiotherapists match the device to your speed and environment. Mayo Clinic

5. Home fall-proofing – Remove loose rugs, add night lights and grab bars, use non-slip shoes; this cuts hip fractures and hospital visits. Mayo Clinic

6. Speech therapy – Clear speech drills, pacing, and breath control make words easier to understand; communication apps help when speech is tired. NCBI

7. Swallow therapy & diet texture – Thickened liquids and paced intake lower choking and pneumonia risk; the plan is personalized after a swallow study. NCBI

8. Occupational therapy – Adaptive grips, weighted utensils, and kitchen tips reduce tremor impact during eating and writing, keeping life independent. Mayo Clinic

9. Energy conservation – Plan rests, sit for tasks, and break work into short blocks to fight fatigue while keeping activity daily. Mayo Clinic

10. Vision & oculomotor strategies – Eye‐movement drills and simple gaze tricks can ease reading and tracking. Prism lenses may help some people. PreventionGenetics

11. Breathing exercises (if weak cough) – Airway clearance routines and assisted cough devices reduce infections if bulbar weakness appears. Mayo Clinic

12. Nutrition support – High-calorie, high-protein small meals protect weight; a dietitian balances fiber and fluid to prevent constipation from low activity. Mayo Clinic

13. Mental health care – Counseling and, if needed, medicines can treat anxiety or low mood that commonly follow progressive disability. Mayo Clinic

14. Sleep hygiene – Fixed sleep/wake times and a quiet room fight insomnia that worsens daytime balance. Mayo Clinic

15. Spasticity self-management – Daily gentle stretches and heat packs reduce stiffness before walking or therapy. nhs.uk

16. Community exercise (tai chi, dance-based balance) – Slow, controlled moves build posture reactions and confidence with fewer falls. Mayo Clinic

17. Driving assessment – Early testing and training keep you and others safe; alternative transport planning preserves independence. Mayo Clinic

18. Work/school accommodations – Extra time, rest breaks, and speech-to-text tools keep you productive with less strain. Mayo Clinic

19. Caregiver training – Teaching safe transfers, choking first aid, and device setup lowers emergency visits and stress. Mayo Clinic

20. Clinical-trial readiness – Genetic counseling and research registries help you learn about trials as they open, even though none target SCAR8 yet. NCBI

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Drug treatments

1. Baclofen (oral) – Class: antispastic. Common dosing: 5 mg 3×/day, titrate; multiple FDA baclofen products exist. Purpose: reduce leg stiffness/spasms to steady steps. How it works: activates GABA-B receptors to dampen spinal reflexes. Side effects: sleepiness, dizziness; do not stop suddenly (withdrawal). FDA Access Data+1

2. Tizanidine – Class: α2-agonist antispastic. Dose: start low (e.g., 2 mg) and titrate; short-acting—time to most needed activities. Purpose: ease spasticity without strong weakness. Mechanism: reduces excitatory neurotransmitter release. Side effects: low blood pressure, sleepiness, dry mouth; food/formulation affect levels. FDA Access Data+1

3. Dantrolene – Class: direct-acting muscle relaxant. Dose: often 25–100 mg 3–4×/day if tolerated. Purpose: backup for severe spasticity. Mechanism: lowers calcium release in muscle. Important risk: liver toxicity—use only when needed and monitor. FDA Access Data

4. OnabotulinumtoxinA (Botox) – Class: neuromuscular blocker (injectable). Use: focal spasticity or tremor muscles every ~3 months by trained injectors. Mechanism: blocks acetylcholine release at nerve-muscle junction. Risks: local weakness, rare spread of toxin effects. FDA Access Data

5. Clonazepam – Class: benzodiazepine. Dose: 0.25–0.5 mg at night, titrate. Purpose: dampens action tremor/tone and helps sleep. Mechanism: enhances GABA-A signaling. Risks: sedation, falls, dependence; taper slowly. FDA Access Data

6. Gabapentin – Class: neuromodulator. Dose: commonly 300 mg at night then 300 mg 3×/day as tolerated. Purpose: reduces ataxia-related neuropathic pain/tremor in some. Mechanism: α2δ calcium-channel binding. Risks: dizziness, somnolence; taper to avoid withdrawal seizures in epileptics. FDA Access Data

7. Riluzole – Class: glutamate modulator (approved for ALS). Dose: 50 mg twice daily (tablet/oral suspension). Purpose: experimental symptomatic benefit in cerebellar ataxias has been studied; off-label only. Risks: elevated liver enzymes, nausea; rare lung inflammation. FDA Access Data+2FDA Access Data+2

8. Amantadine – Class: dopaminergic/antiviral; ER and IR forms. Dose: varies by product. Purpose: may brighten fatigue or gait timing in some. Risks: insomnia, ankle swelling, hallucinations in elders. FDA Access Data+1

9. Dalfampridine (4-aminopyridine) – Class: potassium-channel blocker (approved to improve walking in MS). Dose: 10 mg twice daily. Purpose: sometimes tried off-label to sharpen gait cadence; avoid in seizure or severe kidney disease. FDA Access Data+1

10. Carbidopa/Levodopa – Class: dopaminergic combo. Dose: product-specific; small test doses may help parkinsonian features if present. Risks: nausea, low blood pressure, dyskinesia with higher doses. FDA Access Data

11. Trihexyphenidyl – Class: anticholinergic for tremor/dystonia. Dose: divided doses titrated carefully (elderly sensitive). Risks: dry mouth, blurred vision, confusion; use sparingly. FDA Access Data+1

12. Propranolol – Class: non-selective beta-blocker. Use: can reduce action tremor in selected patients; check asthma and BP first. Risks: bradycardia, fatigue, bronchospasm. FDA Access Data+1

13. Primidone – Class: barbiturate-like anticonvulsant used for essential tremor. Dose: start very low at night and titrate. Risks: sedation, ataxia worsening if overdosed. FDA Access Data

14. Sertraline – Class: SSRI antidepressant. Use: treats anxiety/depression that often worsen function in progressive ataxia. Risks: GI upset, sleep change; boxed warning for suicidality in young. FDA Access Data+1

15. Modafinil – Class: wake-promoting agent. Use: for disabling daytime sleepiness or fatigue; watch for headaches and rare rash. FDA Access Data

16. Droxidopa – Class: norepinephrine precursor. Use: for neurogenic orthostatic hypotension if present (lightheadedness on standing). Risks: headache, high BP when lying down. FDA Access Data+1

17. Glycopyrrolate – Class: anticholinergic. Use: burdensome drooling; try low, go slow. Risks: constipation, dry mouth, blurry vision. FDA Access Data+1

18. Metoclopramide – Class: pro-kinetic anti-nausea. Use: reflux or delayed stomach emptying that worsens swallowing; limit duration due to tardive dyskinesia risk. FDA Access Data+1

19. Omeprazole – Class: proton-pump inhibitor. Use: protects esophagus if reflux from poor swallowing is an issue. Risks: long-term use needs review. FDA Access Data+1

20. OnabotulinumtoxinA (for sialorrhea or focal dystonia) – second listing for a different problem domain; dosing and precautions per label. FDA Access Data

Important: None of these medicines is approved specifically for SCAR8. They are used to treat symptoms seen in SCAR8 and should be started, titrated, and monitored by your clinician. GeneReviews notes symptomatic care (spasticity meds, speech/swallow therapy) as the standard of care for SYNE1 deficiency. NCBI

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Dietary molecular supplements

1. Coenzyme Q10 – may support cellular energy; small studies in ataxias suggest benefit for fatigue in some. Typical trial doses range 100–300 mg/day with food. Monitor for GI upset. Mayo Clinic

2. Vitamin E – antioxidant; corrects ataxia only when there is deficiency, so test first. 200–800 IU/day if low. Too much can raise bleeding risk. Mayo Clinic

3. Vitamin B12 – needed for nerve health; replace if low (oral or injection). Replacement can improve paresthesia and gait in deficiency states. Mayo Clinic

4. Thiamine (B1) – treat deficiency from poor intake; can aid fatigue and neuropathy when low. Mayo Clinic

5. Folate – replete if deficient to support nerve and blood cell health. Mayo Clinic

6. Vitamin D – protects bone strength; keeps fracture risk down in frequent fallers. Check and replete to sufficiency. Mayo Clinic

7. Omega-3 fatty acids – general cardiometabolic support; may ease inflammation and help lipids. Use 1–2 g/day of EPA+DHA with meals. Mayo Clinic

8. Creatine – muscle energy buffer; mixed data, but some patients report endurance help in rehab programs. 3–5 g/day trial with hydration. Mayo Clinic

9. Magnesium (constipation/cramp aid) – gentle osmotic effect and may relax muscles. Start low to avoid diarrhea. Mayo Clinic

10. Protein-rich oral supplements – shakes between meals help maintain weight when chewing/swallowing are tiring. Choose high-calorie, high-protein formulas guided by a dietitian. Mayo Clinic

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Immunity booster / regenerative / stem-cell drugs

There are no FDA-approved immune-booster, regenerative, or stem-cell drugs for SCAR8. Stem-cell offerings you may see online for ataxia are not approved and can be risky. If a clinician addresses specific complications, they use approved drugs for other indications (for example, riluzole for ALS, omaveloxolone for Friedreich ataxia, IVIG for immune neuropathies). Any such use in SCAR8 would be off-label and individualized. FDA Access Data+1

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Procedures/surgeries

1. Botulinum toxin injections – office procedure for focal spasticity or sialorrhea to improve comfort and function for ~3 months. FDA Access Data

2. Feeding tube (PEG) – considered if severe aspiration or weight loss persists despite therapy, to provide safe calories and fluids. NCBI

3. Orthopedic procedures – rare; for painful contractures or deformity affecting braces or hygiene. Decision is individualized. Mayo Clinic

4. Laryngoscopy-guided interventions – occasionally for severe voice or airway protection issues after swallow work-up. NCBI

5. Sleep/airway devices – non-invasive ventilation or cough-assist if bulbar or respiratory weakness reduces cough or sleep quality. Mayo Clinic

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Preventions

Fall-proof the home; use the right mobility aid; keep vaccinations current; manage reflux to reduce aspiration; regular dental care to lower pneumonia risk; strength and balance sessions most days; maintain weight with high-calorie snacks; review medicines yearly to prune sedatives; treat mood/sleep issues early; and plan heat safety/hydration during summer, when fatigue and dizziness are worse. Mayo Clinic+1

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When to see a doctor (red flags)

Sudden worse balance or many falls; choking, coughing, or weight loss; new severe stiffness or painful spasms; fainting or big drops in blood pressure on standing; mood crisis or sleep attacks; new muscle weakness; or any medication side effect like yellow eyes/skin, severe sleepiness, or rash. Early contact prevents complications and allows dose changes or new supports. NCBI+2FDA Access Data+2

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What to eat / what to avoid

Eat: soft, moist, high-calorie foods (yogurt, smoothies, eggs, well-sauced rice/pasta), healthy fats, protein with every meal, and fiber + fluids to prevent constipation. Avoid: dry, crumbly foods (dry biscuits, chips) and thin liquids if you cough while drinking—use thickened liquids if advised. Space small meals through the day so fatigue does not cut intake. NCBI

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FAQs

1) Is SCAR8 the same as SCA8?
No. SCAR8 = SYNE1 recessive ataxia. SCA8 is usually a dominant repeat disorder and is different. NCBI+1

2) How is SCAR8 confirmed?
With SYNE1 genetic testing after a neurologic exam and MRI suggest cerebellar ataxia. PreventionGenetics

3) Is there a cure?
Not yet. Care is supportive and symptom-based. NCBI

4) What therapies matter most early on?
Physiotherapy, speech/swallow therapy, and home safety changes make the biggest difference early. NCBI+1

5) Are there approved drugs for SCAR8?
No. Drugs listed here treat symptoms (off-label). NCBI

6) Can diet help?
A high-calorie, high-protein, texture-modified diet maintains weight and reduces choking. NCBI

7) Should family members test?
Genetic counseling helps families decide about carrier testing and planning. NCBI

8) What about stem cells?
No FDA-approved stem-cell therapy exists for SCAR8. Be cautious with commercial offers. NCBI

9) Can symptoms vary by person?
Yes—SYNE1 variants range from pure cerebellar to complex phenotypes with spasticity or muscle issues. PubMed

10) Are there research groups to follow?
Ataxia foundations and registries provide updates and trial news for recessive ataxias, including SYNE1. National Ataxia Foundation

11) Why do I get dizzy when I stand?
Some people develop orthostatic hypotension; droxidopa can help in selected cases. FDA Access Data

12) My hands shake most when reaching—what helps?
Task-based therapy, weighted utensils, and sometimes clonazepam, primidone, or propranolol. FDA Access Data+2FDA Access Data+2

13) Can spasticity be targeted locally?
Yes—botulinum toxin injections to specific muscles. FDA Access Data

14) Do I need regular blood tests?
Yes, if you use medicines like baclofen (if high dose or intrathecal), tizanidine, riluzole, or others that affect liver or blood pressure. FDA Access Data+1

15) Is Friedreich ataxia medicine (omaveloxolone) for SCAR8?
It’s approved only for Friedreich ataxia, not SCAR8. Use in SCAR8 would be experimental/off-label. FDA Access Data

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.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: October 05, 2025.

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