Autoimmune
Hashimoto's, Lupus, RA, MS, and more
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High-achieving professionals who reversed chronic conditions and reclaimed their vitality through our cellular regeneration protocols.
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Hashimoto's, Lupus, RA, MS, and more
"Hard to believe now but I had 8 years of Hashimoto's. Impossible to thank Mostafa enough to finally have my energy back. My antibodies dropped 80% in the 6 months and are still improving"Read Full Case Study →
Thyroid, adrenal, PCOS, testosterone
Patient OverviewRead Full Case Study →
Female, 25 years old, Italian, typically with late diagnosis (7–10 years delay after symptom onset). Chief complaints included severe dysmenorrhea (8–10/10 pain, disabling), chronic pelvic pain (6–8/10, cyclical worsening premenstrually), deep dyspareunia, GI symptoms (bloating, diarrhea, constipation), fatigue, brain fog, and infertility or subfertility (30–50%).
Patient OverviewRead Full Case Study 2 →
Female, 22–28 years old, often with a high-achieving personality (student, athlete, or professional), who presented with greater than three months of absent menstrual cycles (severity: complete cessation). Additional complaints included low energy (4–5/10), hair thinning, cold intolerance, loss of libido, persistent stress, restrictive eating, or intense exercise patterns.
Diabetes, weight, blood pressure, cholesterol
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"A 45-year-old male software engineer presented with a 5-year history of progressive weight gain, severe post-prandial fatigue, intense mid-meal hunger, brain fog, poor sleep quality (5-6 hours/night), increased abdominal adiposity, and declining exercise tolerance."
Patient OverviewRead Full Case Study 2 →
"A 50-55-year-old male corporate executive presented with severe mixed dyslipidemia, central obesity, chronic fatigue, exertional chest discomfort, erectile dysfunction, and strong family history of premature cardiovascular disease"
IBS, SIBO, leaky gut, Crohn's, ulcerative colitis
Patient OverviewRead Full Case Study →
A 32–38-year-old high-achieving individual from the MENA region presented with a 7-year history of relapsing-remitting irritable bowel syndrome (IBS).
Patient OverviewRead Full Case Study 2 →
A 28–55-year-old, high-achieving individual from the MENA region with a history of chronic dieting presented with several years of progressive, multi-system complaints.
Brain fog, anxiety, depression, cognitive decline
“I went from barely functioning to restarting leadership of my business to running it at full capacity. Yes that transformation in just a short time was incredible for me”.Read Full Case Study →
Asthma, allergies, histamine intolerance
“I literally couldn’t eat without reactions. The result of the program was amazing, I am eating every day without that stress”Read Full Case Study →
Arthritis, fibromyalgia, chronic pain
“I can still remember the call when we saw all my inflammation markers were normal. It was the first time after 5 years. Biggest change is playing sports with the kids again”Read Full Case Study →
Eczema, psoriasis, acne, skin conditions
“I have had this skin problem since childhood basically. I really can’t express how much more confident and happy I am”Read Full Case Study →
A 32–38-year-old high-achieving individual from the MENA region presented with a 7-year history of relapsing-remitting irritable bowel syndrome (IBS).
Chief complaints included abdominal cramping (5–8/10 severity), bloating (6–9/10, pronounced in the afternoon/evening), and alternating constipation–diarrhea with mucus and urgency.
Symptom flares were noted after stress and high-FODMAP foods. Extensive gastrointestinal workups—colonoscopy, celiac serology, and conventional interventions (antispasmodics, fiber, probiotics, PPIs)—proved ineffective.
Notable comorbidities included high anxiety and a prior post-infectious episode. Work absences (1–2 days/month), social withdrawal, and dietary restriction substantially impacted quality of life, comparable to major chronic illnesses.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Contributing factors included genetic predisposition, stress, NSAID use, environmental exposures, high wheat/FODMAP intake, and vitamin D deficiency despite abundant sunlight.
Medically, this case involved:
Contributing factors included genetic predisposition (e.g., TNF-α polymorphisms), stress, environmental triggers (water quality, pesticide residues), high wheat/FODMAP intake, NSAIDs, and vitamin D deficiency—despite abundant regional sun exposure due to indoor, covered lifestyles.
Clinical patterns consistent with IBS-M were observed, with negative impacts peaking during significant cultural events—Ramadan, family gatherings— necessitating dietary and lifestyle adaptation.
Supported by: Ford AC, et al. N Engl J Med. 2017;376:2566-78. PMID: 28657832
Chey WD, et al. JAMA. 2015;313:949–58. PMID: 25734736
Khanna R, et al. J Clin Gastroenterol. 2014;48:505–12. PMID: 24100754
Whorwell PJ, et al. Lancet. 1984;2:1232-4. PMID: 6150275
Use with clinician oversight due to limited longitudinal safety data.
Research indicates 60–70% of multimodal protocol patients achieve ≥50-point IBS-SSS reduction at 4–6 months.
IBS is multifactorial and chronic; complete symptom eradication may not be achievable for all. Realistic expectations and regular reassessment are critical.
Individual results may vary. This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before making any health decisions or implementing protocols.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
A 28–55-year-old, high-achieving individual from the MENA region with a history of chronic dieting presented with several years of progressive, multi-system complaints.
Chief concerns included chronic fatigue (4–6/10, worse after meals), multiple and expanding food sensitivities, bloating/gas (5–8/10, worsens through the day), persistent brain fog, migratory joint aches (3–6/10, no clinical arthritis), skin issues (eczema, rashes, acne), mood disturbances (anxiety, depression, irritability), recurrent infections, and slow wound healing.
Medical history revealed exhaustive but “normal” test results, prior exposure to antibiotics, NSAIDs, alcohol, chronic stress, failed elimination diets, borderline autoimmune markers, and GI infections.
The condition led to work impairment (from cognitive symptoms/fatigue), strict dietary limitation, social isolation, anxiety related to food, reliance on expensive supplements with marginal benefit, and feeling dismissed by conventional medical providers.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Key roots included genetics (HLA-DQ2/DQ8, TNF-α/IL-10 polymorphisms, MTHFR), environmental and microbial triggers (gastroenteritis, NSAIDs, antibiotics, toxins, chronic stress), and dietary factors (Western diet, gluten, alcohol, infections).
The main mechanism is zonulin-mediated opening of intestinal tight junctions, allowing entry of LPS/antigens, which activates immune and inflammatory pathways, drives systemic inflammation and mitochondrial dysfunction, and creates a feedback loop sustaining gut hyperpermeability.
Diet: Strict elimination for 4–6 weeks. Remove gluten, dairy, soy, corn, eggs, nightshades, sugar, alcohol, processed/high FODMAP foods
Sleep: 8–9h nightly, blue light blockers in evening, Mg/glycine at night
Stress management: Meditation 10–20min daily, breathwork, gentle yoga 3–4x/week, time in nature, therapy (CBT/EMDR if indicated)
Movement/environment: Daily walking, gentle yoga/tai chi/swimming, avoid intense exercise. Filter water, use organic produce, avoid plastics, check for mold/EMF exposure.
Expected milestone: Detox symptoms weeks 1–2 (fatigue, headaches, breakouts), improvement in bloating/energy/brain fog by week 4 (20–40%).
Expected milestone: 40–60% improvement, expanded food tolerance, improved mood/skin/joints
Strategy: Intensive BPC-157 + TB-4 8–12 weeks, then BPC-157 3x weekly as needed for maintenance
A simultaneous multi-modal protocol combining intestinal barrier support, immune modulation, microbiome support, homeopathy, stress management, and peptide therapy was associated with measurable symptom reduction and food tolerance expansion.
This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before implementing any protocols.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Female, 25 years old, Italian, typically with late diagnosis (7–10 years delay after symptom onset).
Chief complaints included severe dysmenorrhea (8–10/10 pain, disabling), chronic pelvic pain (6–8/10, cyclical worsening premenstrually), deep dyspareunia, GI symptoms (bloating, diarrhea, constipation), fatigue, brain fog, and infertility or subfertility (30–50%).
Medical history often included misdiagnosis as IBS, PID, or “just bad periods,” multiple ER visits during menses, prior failed treatments (NSAIDs, oral contraceptives, surgery), and positive family history (7x risk if first-degree relative affected).
Current impact: Work/school absences 1–3 days/month, relationship strain, occasional chronic opioid use, anxiety/depression from chronic pain, and financial burden from treatments/surgeries.
Patient details modified for privacy and clinical accuracy.
Key contributors: Genetics (multiple genes), retrograde menstruation, immune clearance failure, toxins (dioxins, phthalates), estrogen excess (diet/xenoestrogens), inflammatory diet (omega-6, gluten, dairy).
Cellular mechanism: Endometrial tissue outside uterus responds to hormone cycling, triggers inflammation/scarring, nerve growth/sensitization, pain cycling and chronicity.
Complete pain relief rare without surgery; aim for 50–70% pain reduction. Excision may be needed; protocol preps body, reduces recurrence risk. Lifelong management vital; disease is chronic. Pregnancy may help symptoms short-term. Menopause resolves most symptoms.
Red Flags: Worsening pain, acute fever, GI obstruction, urinary symptoms, no improvement after 6mo intensive conservative protocol (consider surgery), rapid endometrioma growth, infertility—refer to specialist as appropriate.
Individual results may vary. These protocols are based on published research and clinical observations documented in this case. This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before making any health decisions or implementing protocols. The practitioner does not claim to diagnose, treat, cure, or prevent any disease.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Female, 22–28 years old, often with a high-achieving personality (student, athlete, or professional), who presented with greater than three months of absent menstrual cycles (severity: complete cessation).
Additional complaints included low energy (4–5/10), hair thinning, cold intolerance, loss of libido, persistent stress, restrictive eating, or intense exercise patterns.
Medical history commonly included previously regular cycles until a clear trigger event (move, breakup, occupational or athletic stress), frequent undiagnosed disordered eating behaviors, a high-cortisol/stress lifestyle, and unsuccessful use of oral contraceptives for cycle restoration.
Current impact involved fertility concerns (generating additional stress), body image distress, relationship strain, and performance anxiety in work or athletics.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Key root causes included insufficient energy intake for metabolic demand, psychological stress (perfectionism, anxiety, control behaviors), excess exercise, micronutrient deficiencies (zinc, B vitamins, iron, omega-3), and gut dysfunction affecting nutrient absorption.
Cellular mechanism: Low leptin reduces kisspeptin neuron function → suppressed GnRH → pituitary fails to release LH/FSH → hypoestrogenism → endometrial lining doesn’t build → no menses.
Individual results may vary. These protocols are based on published research and clinical observations documented in this case. This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before making any health decisions or implementing protocols. The practitioner does not claim to diagnose, treat, cure, or prevent any disease.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
A 45-year-old male software engineer presented with a 5-year history of progressive weight gain, severe post-prandial fatigue, intense mid-meal hunger, brain fog, poor sleep quality (5-6 hours/night), increased abdominal adiposity, and declining exercise tolerance.
Height 5'10" (178 cm), weight 228 pounds (103.4 kg), BMI 32.7 (Class I Obesity), waist circumference 44 inches. Chief complaint: "I've been gaining weight steadily despite trying various diets. I'm constantly tired, especially after meals, and my doctor mentioned my blood sugar is creeping into the pre-diabetic range."
Medical history: Pre-diabetes diagnosed 6 months prior (HbA1c 6.2%), hypertension controlled on lisinopril 10mg daily, non-alcoholic fatty liver disease (NAFLD, Grade 2 steatosis on ultrasound), mild acanthosis nigricans. Strong family history: father developed type 2 diabetes at age 52, maternal grandmother with diabetes and cardiovascular disease.
Lifestyle: High refined-carbohydrate/processed-food diet, minimal physical activity (<30 min/week), high work-related stress (60-hour workweeks), 2-3 alcoholic drinks on weekends.
Baseline labs: Fasting glucose 118 mg/dL (elevated), fasting insulin 28.4 µIU/mL (hyperinsulinemia), HOMA-IR 5.8 (severe insulin resistance), HbA1c 6.2%, triglycerides 285 mg/dL, HDL-C 38 mg/dL, LDL-C 153 mg/dL, hsCRP 4.8 mg/L, ALT 68 U/L, AST 52 U/L, vitamin D 18 ng/mL (deficient), magnesium RBC 4.2 mg/dL (low-normal).
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Contributing factors: Sedentary lifestyle, refined carbohydrate/processed food diet, chronic stress, poor sleep, genetic predisposition, visceral adiposity, NAFLD, low-grade chronic inflammation.
Berberine effectively mimics several GLP-1 pathway effects. Future protocols may incorporate research peptides under professional supervision. These are not FDA-approved and require qualified healthcare supervision.
This case demonstrates complete reversal of severe insulin resistance within 24 weeks using an integrated approach. Critical success factors included aggressive AMPK activation via berberine and resistance training, carbohydrate moderation, and high patient adherence (≥90%).
Limitations include limited human RCT evidence for homeopathic remedies and the high cost of supplements (~$150-200/month). For patients with pre-diabetes, this protocol should be considered first-line therapy before pharmaceutical intervention.
Individual results may vary. These protocols are based on published research and clinical observations. This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before implementing protocols. Patient details have been modified to protect privacy while maintaining clinical accuracy. Peptides mentioned are research compounds and should only be considered with qualified healthcare supervision.
A 50-55-year-old male corporate executive presented with severe mixed dyslipidemia, central obesity, chronic fatigue, exertional chest discomfort, erectile dysfunction, and strong family history of premature cardiovascular disease.
Baseline BMI was 30.4 (Class I obesity), weight 218 lbs (99 kg), waist circumference 42 inches. The patient described a long-standing high-saturated fat and refined-carbohydrate diet, heavy restaurant eating, 3-5 alcoholic drinks nightly, minimal structured exercise (<45 min/week), chronic sleep restriction (5-6 hours/night), and 70-hour workweeks with sustained stress.
Conventional evaluation identified severe hypercholesterolemia and hypertriglyceridemia: total cholesterol 312 mg/dL, LDL-C 218 mg/dL, triglycerides 342 mg/dL, HDL-C 34 mg/dL, non-HDL-C 278 mg/dL, ApoB 168 mg/dL, LDL-P 2,180 nmol/L, small dense LDL 68%, and elevated Lp(a) 86 nmol/L. Advanced risk markers were markedly abnormal: hsCRP 6.2 mg/L, homocysteine 18.4 µmol/L, fibrinogen 412 mg/dL, oxidized LDL 87 U/L, MPO 588 pmol/L, Lp-PLA2 278 ng/mL.
Imaging showed carotid IMT 1.2 mm (thickened), coronary artery calcium (CAC) score 158, and NAFLD Grade 2 on ultrasound. Ten-year cardiovascular risk by Framingham and Reynolds scores was 28.4% and 32.1%, respectively. Statin therapy was recommended but declined due to concerns about myopathy and cognitive side effects; the patient expressed preference for an intensive natural protocol.
Patient details have been modified to protect privacy while maintaining clinical accuracy.
Contributing factors included long-term high intake of saturated fat and refined carbohydrates, heavy evening alcohol, chronic stress with HPA-axis activation, metabolic syndrome with insulin resistance (HOMA-IR 4.2), NAFLD, prior smoking history, vitamin D deficiency (22 ng/mL), and very low omega-3 index (3.2%).
Type A, overworked, sedentary profile with hepatic congestion, metabolic syndrome, cardiovascular risk anxiety, fitting Nux vomica plus hepatic and cardiac-oriented remedies (Lycopodium, Crataegus).
This case demonstrates that severe mixed dyslipidemia with subclinical atherosclerosis can be substantially reversed using a rigorously applied integrative protocol. Results rival typical statin-based regimens, with significant LDL-C and TG reductions accompanied by NAFLD improvement and inflammation normalization.
Individual results may vary. These protocols are based on published research and clinical observations. This case study is for educational purposes only and does not constitute medical advice. Consult qualified healthcare providers before implementing protocols. Patient details have been modified to protect privacy while maintaining clinical accuracy.

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