Hallucinogen Persisting Perception Disorder (HPPD)

Hallucinogen Persisting Perception Disorder (HPPD) is a condition where people continue to see changes in vision long after taking a hallucinogenic drug. In simple terms, it’s like having flashbacks or seeing “visual disturbances” even when you are completely sober. These changes can be mild for some people, but for others they can be very distracting or frightening. To diagnose HPPD, doctors must be sure the symptoms are not caused by another illness, such as epilepsy or a mood disorder, and that they cause real trouble in daily life Wikipedia.

Hallucinogen Persisting Perception Disorder (HPPD) is a condition in which visual disturbances and other sensory anomalies re-emerge long after a person has used a hallucinogenic drug, such as LSD, psilocybin (“magic mushrooms”), or MDMA. These lingering symptoms can range from mild visual “trails” behind moving objects to intense, disruptive hallucinations. Although HPPD can be distressing, many people learn to manage symptoms through therapy, lifestyle adjustments, and—in some cases—medication or other medical interventions.


Types of HPPD

There are two main forms of HPPD, often called Type I and Type II:

  • Type I (Flashbacks): Brief, random episodes where a person re-experiences aspects of a past hallucinogenic trip. These episodes usually last seconds to minutes and often go away on their own Wikipedia.

  • Type II (Persistent HPPD): Ongoing visual disturbances that can last months or years. People with Type II may see trails behind moving objects or small, static-like dots (visual snow) all the time Wikipedia.


Causes of HPPD

  1. LSD (lysergic acid diethylamide): The most common trigger for HPPD involves past LSD use Wikipedia.

  2. Psilocybin (“magic mushrooms”): Psychoactive mushrooms can also lead to persistent visual effects Wikipedia.

  3. Mescaline (peyote cactus): A natural hallucinogen linked to afterimages and halos Wikipedia.

  4. MDMA (ecstasy): Though primarily an entactogen, MDMA has been reported to cause HPPD in some individuals Wikipedia.

  5. 2C-B and related phenethylamines: Synthetic drugs in the phenethylamine family can trigger persistent perception changes Wikipedia.

  6. DMT and other tryptamines: Rapid-acting hallucinogens may leave lasting visual traces PMC.

  7. Ketamine: A dissociative that sometimes leads to flashback-like experiences Wikipedia.

  8. Dextromethorphan (DXM): A cough suppressant at high doses can cause hallucinogen-like symptoms Wikipedia.

  9. Salvia divinorum: An herb with strong short lived visual effects; rare cases of HPPD have been reported Wikipedia.

  10. Synthetic cannabinoids (“spice”): Though not classic hallucinogens, these products can lead to HPPD Wikipedia.

  11. Cannabis (THC): Heavy or high-potency use may worsen existing HPPD or trigger it in sensitive people Wikipedia.

  12. Datura and other anticholinergics: Nightshade plants can provoke long-term visual distortions Wikipedia.

  13. Ibogaine: A psychoactive from African iboga shrub sometimes linked to persistent effects Wikipedia.

  14. SSRI-like drugs: Medicines such as sertraline or fluoxetine may worsen HPPD in people with past hallucinogen use Wikipedia.

  15. Polydrug use: Combining several of the above substances raises the risk Wikipedia.

  16. High dose use: Larger doses of any hallucinogen make lasting effects more likely Wikipedia.

  17. Frequent use: Using hallucinogens many times increases chance of HPPD Verywell Health.

  18. Genetic predisposition: Some people may have a vulnerability in how their brain filters sights Wikipedia.

  19. Anxiety and panic: High anxiety at the time of drug use can cement perceptual changes Wikipedia.

  20. Sleep deprivation: Poor sleep during or after intoxication may impair visual processing systems Wikipedia.


Symptoms of HPPD

  1. Visual snow: A static-like “snow” across the whole visual field Wikipedia.

  2. Afterimages: Seeing an object’s outline even after it’s gone Wikipedia.

  3. Trails: Faint trails following moving objects Wikipedia.

  4. Halos and auras: Rings of light around objects Wikipedia.

  5. Intensity shifts: Colors or brightness suddenly seem too strong Wikipedia.

  6. Palinopsia: Recurrence of visual images Wikipedia.

  7. Micropsia/macropsia: Objects look smaller or larger than they are Wikipedia.

  8. Pareidolia: Seeing meaningful shapes in random patterns Wikipedia.

  9. Floaters: More floaters in the eye or noticing them more often Wikipedia.

  10. Blurred vision: Vision may feel smeared or unclear Wikipedia.

  11. Tunnel vision: A narrowing of the visible area Wikipedia.

  12. Blue field entoptic phenomenon: Seeing tiny bright dots moving Wikipedia.

  13. Distorted motion perception: A sense that stationary objects move Wikipedia.

  14. Intensified hypnagogic imagery: Strong dreams or images at sleep onset Wikipedia.

  15. Anxiety or panic: Fearing the visual changes or worrying about them Verywell Health.


Diagnostic Tests for HPPD

Before diagnosing HPPD, doctors rule out other causes like brain injury, epilepsy, migraine, or substance intoxication.

A. Physical Exam

  1. General neurological exam: Checks balance, coordination, and reflexes PMC.

  2. Visual acuity test: Measures how clearly you see at various distances PMC.

  3. Pupil reaction: Tests how pupils react to light and dark PMC.

  4. Eye movement tracking: Observes if eyes move smoothly when following a target PMC.

B. Manual Tests

  1. Snellen chart: Identifies difficulties recognizing letters at a distance PMC.

  2. Amsler grid: Detects visual snow or distortion in the central field PMC.

  3. Confrontation visual field: Maps out peripheral vision by counting fingers PMC.

  4. Color vision test: Checks for abnormal color perception PMC.

C. Lab & Pathological Tests

  1. Blood toxicology screen: Looks for recent or ongoing drug use PMC.

  2. Thyroid function tests: Rules out thyroid issues that affect vision PMC.

  3. Metabolic panel: Measures electrolytes and organ function for systemic causes PMC.

  4. Vitamin B12 level: Low levels can cause visual and neurological problems PMC.

D. Electrodiagnostic Tests

  1. Electroencephalogram (EEG): Records brain waves to exclude epilepsy Wikipedia.

  2. Visual evoked potentials (VEP): Measures brain response to visual stimuli Wikipedia.

  3. Electroretinography (ERG): Tests retinal cell function PMC.

  4. Brainstem auditory evoked response (BAER): Checks brainstem pathways for other neuro issues PMC.

E. Imaging Tests

  1. Magnetic Resonance Imaging (MRI): Rules out structural brain lesions PMC.

  2. Computed Tomography (CT): Quick scan to exclude bleeding or mass PMC.

  3. Functional MRI (fMRI): Observes brain activity during visual tasks PMC.

  4. Positron Emission Tomography (PET): Measures metabolic changes in visual areas PMC.

Non-Pharmacological Treatments

  1. Cognitive Behavioral Therapy (CBT):

    • Description: Structured therapy focusing on changing unhelpful thought patterns.

    • Purpose: Reduce anxiety and negative beliefs about perceptual symptoms.

    • Mechanism: Teaches coping skills and cognitive reframing to lessen distress.

  2. Mindfulness Meditation:

    • Description: Practice of nonjudgmental awareness of the present moment.

    • Purpose: Decrease anxiety and reactivity to visual disturbances.

    • Mechanism: Strengthens attention control and emotional regulation.

  3. Grounding Techniques:

    • Description: Exercises (e.g., focusing on the five senses) to anchor in reality.

    • Purpose: Interrupt distress during flashbacks.

    • Mechanism: Shifts focus away from internal hallucinations to external stimuli.

  4. Biofeedback:

    • Description: Uses sensors to monitor physiological signals (e.g., heart rate).

    • Purpose: Teach self-regulation of stress responses.

    • Mechanism: Real-time feedback enables conscious control of bodily functions.

  5. Eye Movement Desensitization and Reprocessing (EMDR):

    • Description: Therapy involving guided eye movements while recalling distressing images.

    • Purpose: Reduce the emotional impact of flashbacks.

    • Mechanism: May facilitate adaptive processing of distressing perceptual memories.

  6. Transcranial Magnetic Stimulation (TMS):

    • Description: Noninvasive magnetic pulses applied to specific brain regions.

    • Purpose: Modulate neural circuits related to perception and mood.

    • Mechanism: Alters cortical excitability to reduce hallucinations and anxiety.

  7. Neurofeedback:

    • Description: Real-time EEG feedback to train desirable brainwave patterns.

    • Purpose: Improve neural stability and reduce symptoms.

    • Mechanism: Reinforces brainwave states associated with calm, focused attention.

  8. Relaxation Training:

    • Description: Techniques such as progressive muscle relaxation.

    • Purpose: Lower baseline stress and arousal.

    • Mechanism: Systematically tenses and relaxes muscle groups to promote calm.

  9. Support Groups:

    • Description: Peer-led meetings for sharing experiences and coping strategies.

    • Purpose: Reduce isolation and stigma.

    • Mechanism: Social support fosters resilience and shared learning.

  10. Psychoeducation:

    • Description: Educational sessions about HPPD and symptom management.

    • Purpose: Empower individuals with knowledge and realistic expectations.

    • Mechanism: Increases self-efficacy and adherence to treatment.

  11. Stress Management Training:

    • Description: Techniques like time management and problem-solving skills.

    • Purpose: Reduce triggers such as chronic stress.

    • Mechanism: Enhances resilience to environmental stressors.

  12. Yoga and Tai Chi:

    • Description: Mind-body exercises combining movement, breath, and focus.

    • Purpose: Improve emotional regulation and bodily awareness.

    • Mechanism: Modulate autonomic nervous system toward balance.

  13. Controlled Exposure Techniques:

    • Description: Gradual, supervised exposure to benign triggers.

    • Purpose: Desensitize responses to flashback-provoking stimuli.

    • Mechanism: Habituation reduces the intensity of perceptual reactions.

  14. Art Therapy:

    • Description: Creative expression through drawing, painting, or sculpting.

    • Purpose: Externalize and process internal experiences nonverbally.

    • Mechanism: Engages right-brain imagery, reducing rumination.

  15. Music Therapy:

    • Description: Guided listening and musical creation with a therapist.

    • Purpose: Alleviate anxiety and distract from visual distortions.

    • Mechanism: Modulates limbic system activity through auditory pathways.

  16. Regular Physical Exercise:

    • Description: Aerobic activities like walking, swimming, or cycling.

    • Purpose: Improve mood and neurochemical balance (e.g., endorphins).

    • Mechanism: Enhances neuroplasticity and reduces stress hormones.

  17. Sleep Hygiene Interventions:

    • Description: Establishing consistent sleep–wake patterns and environment.

    • Purpose: Minimize fatigue-related symptom exacerbation.

    • Mechanism: Proper rest supports brain recovery and emotional regulation.

  18. Nutritional Counseling:

    • Description: Guidance on balanced diet to support brain health.

    • Purpose: Address deficiencies that may worsen symptoms.

    • Mechanism: Ensures optimal nutrient supply for neurotransmitter synthesis.

  19. Habit Reversal Training:

    • Description: Techniques to interrupt maladaptive coping behaviors.

    • Purpose: Replace unhelpful reactions (e.g., avoidance) with positive habits.

    • Mechanism: Reinforces adaptive behaviors to improve functioning.

  20. Therapeutic Journaling:

    • Description: Writing about experiences, emotions, and coping efforts.

    • Purpose: Clarify thought patterns and track symptom triggers.

    • Mechanism: Promotes introspection and cognitive restructuring.


Drug Treatments

  1. Clonazepam

    • Class: Benzodiazepine

    • Dosage: 0.25–0.5 mg at bedtime, up to 2 mg daily

    • Time: Start low; adjust over weeks

    • Purpose: Reduce anxiety and visual distortions

    • Mechanism: Enhances GABAergic inhibition in the central nervous system

    • Side Effects: Sedation, dependence risk, cognitive slowing

  2. Lamotrigine

    • Class: Anticonvulsant

    • Dosage: 25 mg/day, titrate to 100–200 mg/day

    • Time: Slow titration over 5–6 weeks

    • Purpose: Alleviate visual snow and perceptual distortions

    • Mechanism: Stabilizes neuronal membranes by inhibiting voltage-gated sodium channels

    • Side Effects: Rash (rare Stevens-Johnson syndrome), dizziness, headache

  3. Sertraline

    • Class: SSRI (Selective Serotonin Reuptake Inhibitor)

    • Dosage: 25–50 mg/day, up to 200 mg/day

    • Time: Daily; benefit often in 4–6 weeks

    • Purpose: Treat co-occurring anxiety and depression

    • Mechanism: Inhibits serotonin reuptake in synaptic cleft

    • Side Effects: Nausea, sexual dysfunction, insomnia

  4. Risperidone

    • Class: Atypical Antipsychotic

    • Dosage: 0.5–1 mg/day, up to 3–4 mg/day

    • Time: Daily

    • Purpose: Reduce distressing hallucinations

    • Mechanism: Dopamine D2 and serotonin 5-HT2A receptor antagonism

    • Side Effects: Weight gain, metabolic changes, extrapyramidal symptoms

  5. Baclofen

    • Class: GABA-B Agonist

    • Dosage: 5 mg three times daily, up to 80 mg/day

    • Time: Titrated slowly

    • Purpose: Dampen visual disturbances and anxiety

    • Mechanism: Increases presynaptic inhibition in spinal cord and brain

    • Side Effects: Drowsiness, dizziness, muscle weakness

  6. Naltrexone

    • Class: Opioid Antagonist

    • Dosage: 25 mg/day, may increase to 50 mg/day

    • Time: Daily

    • Purpose: Theorized to disrupt flashback circuitry

    • Mechanism: Blocks opioid receptors implicated in flashback generation

    • Side Effects: Nausea, headache, hepatotoxicity at high doses

  7. Fluvoxamine

    • Class: SSRI

    • Dosage: 50 mg/day, up to 300 mg/day

    • Time: Daily; effect in 4–8 weeks

    • Purpose: Address anxiety, obsessive rumination on symptoms

    • Mechanism: Selective serotonin reuptake inhibition

    • Side Effects: Sedation, nausea, sexual side effects

  8. Topiramate

    • Class: Anticonvulsant

    • Dosage: 25 mg/day, titrate to 100–200 mg/day

    • Time: Gradual titration

    • Purpose: Decrease visual snow and flashbacks

    • Mechanism: Blocks sodium channels, enhances GABA, antagonizes AMPA receptors

    • Side Effects: Cognitive slowing, paresthesia, weight loss

  9. Valproate (Divalproex Sodium)

    • Class: Anticonvulsant

    • Dosage: 250 mg twice daily, up to 60 mg/kg/day

    • Time: Daily; monitor blood levels

    • Purpose: Stabilize neural activity to reduce symptoms

    • Mechanism: Increases GABA levels, modulates sodium channels

    • Side Effects: Weight gain, tremor, hepatic toxicity

  10. Memantine

    • Class: NMDA Receptor Antagonist

    • Dosage: 5 mg/day, titrate to 20 mg/day

    • Time: Daily

    • Purpose: Block glutamatergic excitotoxicity implicated in flashbacks

    • Mechanism: Noncompetitive NMDA receptor blockade

    • Side Effects: Dizziness, headache, constipation


Dietary Molecular & Herbal Supplements

  1. Omega-3 Fatty Acids (Fish Oil)

    • Dosage: 1,000–2,000 mg/day EPA+DHA

    • Function: Support neuronal membrane health

    • Mechanism: Anti-inflammatory and promotes synaptic plasticity

  2. Magnesium Glycinate

    • Dosage: 200–400 mg/day

    • Function: Reduce neuronal hyperexcitability

    • Mechanism: NMDA receptor antagonism and GABA enhancement

  3. Vitamin B6 (Pyridoxine)

    • Dosage: 50–100 mg/day

    • Function: Coenzyme for GABA and serotonin synthesis

    • Mechanism: Converts glutamate to GABA and tryptophan to serotonin

  4. N-Acetylcysteine (NAC)

    • Dosage: 600–1,200 mg twice daily

    • Function: Antioxidant support and glutamate modulation

    • Mechanism: Precursor to glutathione; modulates glutamatergic transmission

  5. L-Theanine

    • Dosage: 100–200 mg twice daily

    • Function: Promote relaxation without sedation

    • Mechanism: Increases alpha-wave activity and GABA levels

  6. Rhodiola Rosea

    • Dosage: 200–400 mg/day standardized extract

    • Function: Adaptogen to reduce stress response

    • Mechanism: Modulates cortisol and monoamine neurotransmitters

  7. Lion’s Mane Mushroom

    • Dosage: 500–1,000 mg/day extract

    • Function: Neurotrophic support

    • Mechanism: Stimulates nerve growth factor (NGF) production

  8. Ashwagandha

    • Dosage: 300–600 mg/day standardized extract

    • Function: Reduce anxiety and cortisol

    • Mechanism: GABA-mimetic and stress-hormone modulation

  9. Ginkgo Biloba

    • Dosage: 120–240 mg/day extract

    • Function: Improve microcirculation and cognition

    • Mechanism: Antioxidant and platelet-activating factor antagonism

  10. Curcumin (Turmeric Extract)

    • Dosage: 500–1,000 mg/day with black pepper

    • Function: Anti-inflammatory, neuroprotective

    • Mechanism: Inhibits NF-κB and upregulates BDNF

  11. Phosphatidylserine

    • Dosage: 100–300 mg/day

    • Function: Membrane fluidity and cognitive support

    • Mechanism: Restores neuronal membrane function

  12. Valerian Root

    • Dosage: 300–600 mg at bedtime

    • Function: Improve sleep quality to reduce symptom flares

    • Mechanism: Enhances GABAergic transmission

  13. Cannabidiol (CBD) Oil

    • Dosage: 25–50 mg/day, titrate as needed

    • Function: Anxiety reduction and neuroprotection

    • Mechanism: Modulates endocannabinoid receptors and serotonin

  14. Melatonin

    • Dosage: 1–5 mg at bedtime

    • Function: Regulate sleep-wake cycle

    • Mechanism: Binds melatonin receptors to promote sleep

  15. Coenzyme Q10

    • Dosage: 100–200 mg/day

    • Function: Mitochondrial support and antioxidant

    • Mechanism: Electron transport chain cofactor, reduces oxidative stress


Regenerative & Stem-Cell-Targeted Drugs

  1. Granulocyte-Colony Stimulating Factor (G-CSF)

    • Dosage: 5 µg/kg/day subcutaneously for 5 days

    • Function: Mobilize neural progenitor cells

    • Mechanism: Stimulates bone marrow and may support neurogenesis

  2. Erythropoietin (EPO)

    • Dosage: 40,000 IU/week subcutaneous

    • Function: Neuroprotective and anti-inflammatory

    • Mechanism: Activates EPO receptors in neural tissue

  3. Mesenchymal Stem Cell-Derived Exosomes (experimental)

    • Dosage: Under clinical trial protocols

    • Function: Deliver regenerative factors to the brain

    • Mechanism: Exosomal transfer of miRNA and proteins

  4. Nerve Growth Factor (NGF) Analogues

    • Dosage: Experimental dosing per protocol

    • Function: Promote neuronal survival and growth

    • Mechanism: TrkA receptor activation

  5. Brain-Derived Neurotrophic Factor (BDNF) Mimetics

    • Dosage: Under investigation

    • Function: Enhance synaptic plasticity

    • Mechanism: TrkB receptor agonism

  6. Stem Cell Transplantation (in research settings)

    • Dosage & Timing: Per clinical trial design

    • Function: Replace or repair damaged neural circuits

    • Mechanism: Integration of transplanted cells into host tissue


Surgical & Procedural Interventions

  1. Occipital Nerve Stimulation

    • Procedure: Implant electrodes along the occipital nerves

    • Why: Modulate visual cortex excitability to reduce visual snow

  2. Vagus Nerve Stimulation (VNS)

    • Procedure: Implant stimulator on the left vagus nerve

    • Why: Alter limbic and cortical circuits involved in perception

  3. Deep Brain Stimulation (DBS)

    • Procedure: Electrodes placed in thalamic nuclei

    • Why: Target aberrant sensory processing pathways

  4. Transcranial Direct Current Stimulation (tDCS)

    • Procedure: Noninvasive scalp electrodes deliver low-level current

    • Why: Normalize cortical excitability in visual areas

  5. Phototherapy Desensitization

    • Procedure: Controlled exposure to specific light frequencies

    • Why: Habituate visual system to reduce perceptual distortions


Prevention Strategies

  • Avoid Hallucinogens Altogether: The most direct way to prevent HPPD.

  • Use in Controlled Settings: Minimize dosage and frequency under supervision.

  • Screen for Vulnerabilities: Personal or family history of anxiety or psychosis.

  • Stay Hydrated & Well-Nourished: Support healthy neurotransmission.

  • Limit Stimulants (Caffeine, Amphetamines): Reduce neural excitability.

  • Manage Stress Proactively: Chronic stress can lower the threshold for flashbacks.

  • Maintain Regular Sleep Patterns: Prevent fatigue-related exacerbations.

  • Moderate Alcohol Use: Alcohol can worsen visual disturbances.

  • Practice Grounding Daily: Build resilience against hallucinations.

  • Seek Early Intervention: At first sign of persistent symptoms, consult a professional.


When to See a Doctor

  • Symptoms Lasting Beyond One Month: Flashbacks persisting for weeks.

  • Impairment in Daily Life: Work, school, or social activities suffer.

  • Severe Anxiety or Depression: Co-occurring mood disorders.

  • Self-Harm Thoughts: Urgent care needed if symptoms trigger harmful urges.

  • Medication Side Effects: Consultation if prescribed drugs cause intolerable reactions.


Foods to Eat and Avoid

Eat:

  1. Fatty Fish: Salmon, mackerel (rich in omega-3).

  2. Leafy Greens: Spinach, kale (magnesium, B-vitamins).

  3. Nuts & Seeds: Flaxseed, walnuts (antioxidants).

  4. Berries: Blueberries, strawberries (polyphenols).

  5. Whole Grains: Oats, brown rice (steady energy release).

  6. Fermented Foods: Yogurt, kefir (gut-brain axis support).

  7. Legumes: Lentils, chickpeas (steady protein, fiber).

  8. Colorful Vegetables: Bell peppers, carrots (vitamins A, C).

  9. Lean Poultry: Turkey, chicken (tryptophan for serotonin).

  10. Turmeric-Seasoned Dishes: For curcumin’s anti-inflammatory effects.

Avoid:

  • High-Caffeine Beverages: Coffee, energy drinks.

  • Excessive Sugar: Soda, candies.

  • Alcohol: Especially binge drinking.

  • Processed Foods: High in trans fats and additives.

  • Artificial Sweeteners: Aspartame may exacerbate mood swings.

  • Excessive Salt: Can raise blood pressure and stress.

  • High-Histamine Foods: Aged cheese, cured meats.

  • MSG-Rich Snacks: Potential neuroexcitatory effects.

  • Red Meat in Excess: High in saturated fat.

  • Deep-Fried Foods: Inflammatory and heavy to digest.


Frequently Asked Questions

  1. What exactly is HPPD?
    HPPD is when visual disturbances return long after hallucinogen use—like seeing trails or halos around objects.

  2. How common is HPPD?
    Estimates vary, but about 4–5% of hallucinogen users report lasting perceptual changes.

  3. Can HPPD resolve on its own?
    Some people improve over months; others have chronic symptoms needing ongoing management.

  4. Is there a cure for HPPD?
    No definitive cure exists, but many treatments can reduce symptom severity.

  5. Will antidepressants help?
    SSRIs like sertraline can ease anxiety and depression but may not directly reduce visual disturbances.

  6. Are benzodiazepines safe for HPPD?
    Short-term use can relieve symptoms, but long-term use risks dependence.

  7. Can non-drug approaches really work?
    Yes—therapy, mindfulness, and stress reduction often lead to significant improvements.

  8. Should I avoid all drugs if I have HPPD?
    It’s safest to avoid psychoactive substances, including alcohol and caffeine in excess.

  9. When should I seek psychiatric help?
    If symptoms last over a month or impair your quality of life, see a psychiatrist.

  10. Is HPPD considered a psychotic disorder?
    No, it’s classified under “Hallucinogen Persisting Perception Disorder” in DSM-5, distinct from psychosis.

  11. Can diet make a difference?
    Yes—nutrient-rich foods support brain health and may reduce symptom triggers.

  12. Are there support groups for HPPD?
    Yes—online forums and local peer support groups exist for sharing coping strategies.

  13. Can children develop HPPD?
    Symptoms typically appear in adolescence or adulthood after hallucinogen use; pediatric cases are extremely rare.

  14. Is stem cell therapy available?
    It is experimental and not yet approved specifically for HPPD.

  15. How do I talk to family about HPPD?
    Explain that it’s a medical condition with real sensory symptoms—not “just in your head.”

Disclaimer: Each person’s journey is unique, treatment planlife stylefood habithormonal conditionimmune systemchronic 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: August 05, 2025.

 

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