Obesity & Weight Management
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Obesity & Weight Management
Obesity is a chronic, relapsing, multifactorial disease characterized by excessive adipose tissue accumulation that impairs health and metabolic function. It develops when energy intake chronically exceeds energy expenditure, but this simple caloric model fails to capture the complex neuroendocrine, genetic, environmental, and inflammatory mechanisms driving weight gain. Key manifestations include central adiposity, metabolic dysfunction, insulin resistance, chronic low-grade inflammation, and increased risk of cardiovascular disease, type 2 diabetes, and certain cancers. Body Mass Index (BMI) >=30 kg/m2 defines obesity, though waist circumference (>102cm men, >88cm women) better predicts metabolic risk.
Recognizing Obesity & Weight Management
Common symptoms and warning signs to look for
Persistent fatigue and low energy despite adequate sleep
Uncontrollable food cravings, especially for sugar and refined carbohydrates
Difficulty feeling full or satisfied after meals (impaired satiety signaling)
Weight gain despite eating what others consider 'normal' portions
Joint pain and stiffness, particularly in weight-bearing joints
Brain fog and difficulty concentrating, especially after meals
Emotional eating patterns and food addiction behaviors
Slow metabolism - difficulty losing weight even with strict dieting
What a Healthy System Looks Like
In a healthy metabolic state, the hypothalamus maintains energy homeostasis through precise neuroendocrine signaling. Leptin, produced by adipose tissue in proportion to fat mass, signals satiety to arcuate nucleus POMC neurons while inhibiting NPY/AgRP hunger neurons. Ghrelin, secreted by the stomach when empty, stimulates appetite but is rapidly suppressed after eating. Insulin facilitates glucose uptake into muscle and adipose tissue while suppressing hepatic gluconeogenesis. The gut microbiome produces short-chain fatty acids (SCFAs) that enhance GLP-1 secretion and improve insulin sensitivity. Adiponectin, secreted by healthy adipose tissue, improves insulin sensitivity and reduces inflammation. Mitochondria efficiently oxidize fatty acids through beta-oxidation, and brown adipose tissue contributes to adaptive thermogenesis. This integrated system maintains body weight within a narrow set-point range through automatic compensatory mechanisms.
How the Condition Develops
Understanding the biological mechanisms
Obesity develops through multiple interconnected mechanisms: (1) Leptin resistance - chronically elevated leptin from expanded adipose mass leads to downregulation of hypothalamic leptin receptors (LEPR) and impaired JAK-STAT signaling, causing the brain to perceive starvation despite abundant energy stores; (2) Insulin resistance - ectopic lipid accumulation in muscle, liver, and pancreatic beta-cells interferes with insulin receptor substrate (IRS-1/2) phosphorylation and PI3K/Akt pathway activation, leading to compensatory hyperinsulinemia; (3) Adipose tissue dysfunction - hypertrophic adipocytes become hypoxic, attracting pro-inflammatory M1 macrophages that secrete TNF-alpha, IL-6, and IL-1beta, creating a chronic inflammatory state; (4) Mitochondrial dysfunction - impaired fatty acid oxidation, reduced oxidative phosphorylation capacity, and increased reactive oxygen species (ROS) production; (5) Gut microbiome alterations - reduced bacterial diversity, decreased Bacteroidetes/Firmicutes ratio, and impaired SCFA production compromise metabolic signaling; (6) Endocrine disruption - environmental obesogens (BPA, phthalates, pesticides) interfere with estrogen, androgen, and thyroid hormone signaling; (7) Hypothalamic inflammation - microglial activation and astrocytosis in the mediobasal hypothalamus disrupt appetite regulation; (8) Impaired browning - reduced beige adipocyte formation and decreased uncoupling protein-1 (UCP-1) expression limit adaptive thermogenesis.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| Body Mass Index (BMI) | 18.5-24.9 kg/m2 | 20-23 kg/m2 | BMI 25-29.9 = overweight; BMI 30-34.9 = Class I obesity; BMI 35-39.9 = Class II obesity; BMI >=40 = Class III (severe) obesity |
| Waist Circumference | <94 cm (men), <80 cm (women) | <90 cm (men), <75 cm (women) | Visceral adiposity marker; elevated levels indicate increased metabolic risk independent of BMI |
| Fasting Insulin | 5-15 μIU/mL | 3-6 μIU/mL | Early marker of insulin resistance; elevated before glucose abnormalities appear |
| HOMA-IR (Insulin Resistance Index) | <2.5 | <1.0 | Calculated from fasting glucose and insulin; >2.5 indicates significant insulin resistance |
| Hemoglobin A1c (HbA1c) | <5.7% | <5.0% | Reflects 3-month glucose average; 5.7-6.4% indicates pre-diabetes |
| Fasting Plasma Glucose | 70-100 mg/dL | 70-85 mg/dL | 100-125 mg/dL indicates impaired fasting glucose (pre-diabetes) |
| hs-CRP (High-sensitivity C-Reactive Protein) | <3.0 mg/L | <1.0 mg/L | Marker of systemic inflammation; elevated in obesity-related chronic inflammation |
| Leptin | 1.0-15.0 ng/mL (varies by body fat) | <10 ng/mL | Elevated levels indicate leptin resistance; disproportionately high relative to BMI suggests hypothalamic resistance |
| Adiponectin | 4.0-30.0 μg/mL | >15 μg/mL | Inverse relationship with obesity; low levels associated with insulin resistance and cardiovascular risk |
| Lipid Panel - Triglycerides | <150 mg/dL | <100 mg/dL | Elevated in insulin resistance and metabolic syndrome; marker of hepatic fat content |
| ALT (Alanine Aminotransferase) | 7-56 U/L | <30 U/L | Marker of hepatic steatosis; elevated in non-alcoholic fatty liver disease (NAFLD) |
| Thyroid Panel - TSH | 0.4-4.0 mIU/L | 1.0-2.0 mIU/L | Hypothyroidism can contribute to weight gain and metabolic slowing |
| Vitamin D (25-OH) | 30-100 ng/mL | 60-80 ng/mL | Deficiency associated with obesity, insulin resistance, and inflammation |
| Cortisol (Morning) | 6.2-19.4 μg/dL (8 AM) | 12-18 μg/dL | Elevated cortisol promotes visceral fat accumulation and insulin resistance |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Predisposition","contribution":"40-70% of obesity risk is heritable; over 100 genetic loci identified (FTO, MC4R, POMC, LEPR genes)","assessment":"Family history, genetic testing for monogenic forms if early-onset severe obesity"}
{"cause":"Leptin Resistance","contribution":"Primary driver of failed satiety signaling; affects 30-50% of obese individuals","assessment":"Fasting leptin levels (should be proportional to fat mass), clinical assessment of persistent hunger despite adequate intake"}
{"cause":"Insulin Resistance and Hyperinsulinemia","contribution":"Promotes fat storage, inhibits lipolysis, drives hunger; present in 60-80% of obese individuals","assessment":"Fasting insulin, HOMA-IR calculation, glucose tolerance testing"}
{"cause":"Chronic Inflammation","contribution":"Adipose tissue inflammation drives metabolic dysfunction; elevated CRP, IL-6, TNF-alpha","assessment":"hs-CRP, inflammatory cytokine panel, assessment of inflammatory symptoms"}
{"cause":"Gut Microbiome Dysbiosis","contribution":"Altered bacterial composition affects energy extraction, inflammation, and metabolic signaling","assessment":"Comprehensive stool analysis, assessment of digestive symptoms, food sensitivities"}
{"cause":"Chronic Stress and HPA Axis Dysfunction","contribution":"Elevated cortisol promotes visceral fat accumulation and insulin resistance","assessment":"Four-point cortisol testing (saliva or urine), DHEA-S, assessment of stress levels and coping mechanisms"}
{"cause":"Sleep Deprivation and Circadian Disruption","contribution":"Reduces leptin, increases ghrelin, impairs glucose tolerance; <6 hours sleep increases obesity risk 55%","assessment":"Sleep diary, actigraphy, sleep study if sleep apnea suspected, assessment of sleep hygiene"}
{"cause":"Environmental Obesogens","contribution":"Endocrine-disrupting chemicals (BPA, phthalates, pesticides) interfere with metabolic signaling","assessment":"Exposure history, heavy metal testing, assessment of environmental toxin burden"}
{"cause":"Processed Food and High Glycemic Diet","contribution":"Ultra-processed foods dysregulate appetite hormones, promote inflammation, drive overconsumption","assessment":"Detailed dietary history, food diary analysis, assessment of processed food intake"}
{"cause":"Sedentary Lifestyle","contribution":"Reduced energy expenditure, impaired insulin sensitivity, loss of muscle mass","assessment":"Physical activity questionnaire, accelerometer data, assessment of daily movement patterns"}
{"cause":"Medications","contribution":"Antipsychotics, antidepressants, anticonvulsants, steroids, insulin, beta-blockers","assessment":"Complete medication history, timing of weight gain relative to medication initiation"}
{"cause":"Emotional and Psychological Factors","contribution":"Emotional eating, food addiction, trauma history, depression, anxiety","assessment":"Psychological evaluation, eating behavior assessment, trauma history, mood screening"}
{"cause":"Social and Environmental Factors","contribution":"Food environment, socioeconomic status, food insecurity, social determinants of health","assessment":"Social history, food access assessment, living situation, support system evaluation"}
Risks of Inaction
What happens if left untreated
{"complication":"Type 2 Diabetes Mellitus","timeline":"5-15 years of progressive obesity","impact":"7-12 fold increased risk; leads to retinopathy, nephropathy, neuropathy, cardiovascular disease; reduces life expectancy 10-15 years"}
{"complication":"Cardiovascular Disease","timeline":"10-20 years","impact":"Increased risk of myocardial infarction, stroke, heart failure; obesity accounts for 20% of cardiovascular deaths; each 5-unit BMI increase increases CVD mortality 30%"}
{"complication":"Non-Alcoholic Steatohepatitis (NASH) and Cirrhosis","timeline":"10-20 years from NAFLD onset","impact":"Progression from simple steatosis to NASH to fibrosis to cirrhosis; 20-30% of NAFLD progresses to NASH; liver failure requiring transplant"}
{"complication":"Obstructive Sleep Apnea and Cardiopulmonary Complications","timeline":"5-15 years","impact":"Pulmonary hypertension, right heart failure, arrhythmias; 3-fold increased risk of motor vehicle accidents; severe cases have cardiovascular mortality risk"}
{"complication":"Osteoarthritis and Disability","timeline":"10-20 years","impact":"Chronic pain, reduced mobility, joint replacement surgery; each pound of weight adds 4 pounds of pressure to knees; leading cause of disability"}
{"complication":"Cancer","timeline":"15-30 years","impact":"Obesity associated with 13 types of cancer; accounts for 40% of endometrial cancers, 25% of kidney cancers; increased mortality from all obesity-related cancers"}
{"complication":"Depression and Reduced Quality of Life","timeline":"Chronic","impact":"55% increased risk of depression; social stigma, discrimination, reduced employment opportunities; significant impact on mental health and relationships"}
{"complication":"Premature Mortality","timeline":"Progressive","impact":"Severe obesity (BMI >40) reduces life expectancy by 6-14 years; comparable to smoking; Class III obesity has mortality risk similar to lifelong smoking"}
{"complication":"Economic Burden","timeline":"Chronic","impact":"Direct medical costs $1,429-2,740 higher annually; total economic impact $147-210 billion annually in US; lost productivity, disability, premature death"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Comprehensive Metabolic Panel with Advanced Lipids","purpose":"Baseline metabolic assessment and cardiovascular risk stratification","whatItShows":"Glucose, insulin, comprehensive lipid panel including particle size (NMR), ApoB, Lp(a)"}
{"test":"Body Composition Analysis","purpose":"Distinguish fat mass from muscle mass; assess visceral vs subcutaneous fat","whatItShows":"DEXA scan, bioelectrical impedance, or BOD POD; visceral adipose tissue volume, lean mass, bone density"}
{"test":"Hormone Panel","purpose":"Identify endocrine contributors to weight gain","whatItShows":"TSH, Free T4, Free T3, cortisol, leptin, adiponectin, fasting insulin, HbA1c"}
{"test":"Inflammatory Markers Panel","purpose":"Assess chronic inflammation driving metabolic dysfunction","whatItShows":"hs-CRP, IL-6, TNF-alpha, ferritin; elevated markers indicate inflammatory phenotype"}
{"test":"Liver Function and NAFLD Assessment","purpose":"Detect hepatic steatosis and assess liver health","whatItShows":"ALT, AST, GGT, alkaline phosphatase, bilirubin; FibroScan or ultrasound for liver fat and stiffness"}
{"test":"Continuous Glucose Monitoring (CGM)","purpose":"Detailed glucose pattern analysis and glycemic variability assessment","whatItShows":"Time in range, postprandial spikes, dawn phenomenon, glycemic variability patterns"}
{"test":"Comprehensive Stool Analysis","purpose":"Assess gut microbiome composition and digestive function","whatItShows":"Bacterial diversity, pathogenic overgrowth, digestive markers, inflammation markers, SCFA production"}
{"test":"Sleep Study (Polysomnography)","purpose":"Diagnose obstructive sleep apnea","whatItShows":"Apnea-hypopnea index (AHI), oxygen saturation, sleep architecture; indicated if snoring, daytime somnolence, or resistant hypertension"}
{"test":"Nutritional and Micronutrient Assessment","purpose":"Identify deficiencies that impair metabolism","whatItShows":"Vitamin D, B12, folate, iron panel (ferritin), magnesium, zinc, omega-3 index"}
{"test":"Genetic Testing (Selected Cases)","purpose":"Identify monogenic forms of obesity or pharmacogenomic factors","whatItShows":"MC4R, POMC, LEP, LEPR mutations; FTO variants; pharmacogenomic markers for medication selection"}
Our Treatment Approach
How we help you overcome Obesity & Weight Management
Phase 1: Assessment, Stabilization & Foundation (Weeks 1-4)
{"phase":"Phase 1: Assessment, Stabilization & Foundation (Weeks 1-4)","focus":"Complete diagnostic workup, establish baseline, begin foundational interventions, build therapeutic alliance","interventions":"Comprehensive diagnostic panel as outlined above. Detailed dietary and lifestyle assessment. Begin food journaling and self-monitoring. Initiate basic nutritional modifications: eliminate sugar-sweetened beverages, reduce refined carbohydrates, increase protein and fiber. Begin walking program (goal: 30 minutes daily). Optimize sleep hygiene (7-9 hours target). Stress management introduction. Address any urgent medical issues (severe hypertension, uncontrolled diabetes). Set realistic expectations and establish non-scale victories.\n"}
Phase 2: Metabolic Reset & Root Cause Correction (Months 2-4)
{"phase":"Phase 2: Metabolic Reset & Root Cause Correction (Months 2-4)","focus":"Reverse insulin resistance, restore leptin sensitivity, address inflammation, personalized nutrition protocol","interventions":"Implement personalized nutrition plan based on metabolic phenotype: low-carbohydrate (20-50g/day) for insulin-resistant individuals, Mediterranean pattern for inflammatory phenotype, or time-restricted eating (16:8) for circadian disruption. Targeted supplementation: berberine 500mg 2-3x daily (AMPK activation), omega-3 fatty acids 2-3g EPA+DHA (anti-inflammatory), vitamin D to optimal levels, magnesium 400mg. Resistance training 2-3x weekly initiated. Address gut health if dysbiosis present. Sleep apnea treatment if diagnosed. Stress reduction techniques implemented. Medication review and adjustment if contributing to weight gain. Consider GLP-1 agonists or metformin if indicated.\n"}
Phase 3: Deep Metabolic Optimization & Body Composition Change (Months 4-8)
{"phase":"Phase 3: Deep Metabolic Optimization & Body Composition Change (Months 4-8)","focus":"Accelerate fat loss while preserving lean mass, optimize hormones, enhance metabolic flexibility","interventions":"Intensified exercise program: combination of resistance training (3-4x weekly) and high-intensity interval training (2x weekly). Advanced nutritional strategies: ketogenic diet for selected patients, extended fasting protocols (24-72 hours supervised), protein pacing (25-30g per meal). Address hormonal imbalances: optimize thyroid function, balance cortisol, address sex hormone deficiencies if present. IV nutrient therapy if indicated. Continue targeted supplementation. Behavioral therapy for emotional eating. Regular body composition monitoring (monthly DEXA). Medication optimization: consider phentermine/topiramate, naltrexone/bupropion, or GLP-1 agonists (semaglutide, tirzepatide) for appropriate candidates.\n"}
Phase 4: Maintenance, Optimization & Long-Term Success (Month 8+)
{"phase":"Phase 4: Maintenance, Optimization & Long-Term Success (Month 8+)","focus":"Sustain weight loss, prevent relapse, optimize health markers, establish lifelong habits","interventions":"Transition to sustainable long-term eating pattern. Continue regular physical activity (minimum 150 minutes weekly plus 2 resistance sessions). Ongoing monitoring: quarterly labs, annual body composition, continuous support. Address weight loss plateaus promptly. Manage loose skin if significant weight loss achieved. Psychological support for body image adjustment. Prevent weight regain through continued accountability. Annual comprehensive metabolic review. Focus on healthspan optimization beyond weight. Support group participation or ongoing coaching. Consider maintenance medication if needed.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Physical activity: minimum 150 minutes moderate or 75 minutes vigorous aerobic exercise weekly, Resistance training: 2-3 sessions weekly to build muscle and improve insulin sensitivity, NEAT (Non-Exercise Activity Thermogenesis): aim for 8,000-10,000 steps daily; take stairs, stand more, Sleep optimization: 7-9 hours nightly; consistent schedule, cool dark room, no screens 1 hour before bed, Stress management: daily mindfulness, meditation, breathing exercises; chronic stress drives weight gain, Morning sunlight exposure: 10-30 minutes within 1 hour of waking; supports circadian rhythm and metabolism, Social support: engage family and friends; consider support groups or accountability partners, Environment design: remove trigger foods from home, make healthy choices convenient, Self-monitoring: regular weighing (weekly), food tracking, activity monitoring, Behavioral strategies: cognitive behavioral techniques for emotional eating, stimulus control
Recovery Timeline
What to expect on your healing journey
Initial Assessment (Week 1): Comprehensive diagnostic workup, body composition analysis, metabolic and hormonal assessment, sleep evaluation. Establish baseline metrics and identify root causes.
Foundation Phase (Weeks 2-4): Implement basic nutritional modifications, begin walking program, optimize sleep hygiene, start stress management. Early wins: elimination of sugar-sweetened beverages, improved sleep quality, increased energy.
Active Weight Loss Phase (Months 2-6): Personalized nutrition protocol based on metabolic phenotype. Target 0.5-1 kg (1-2 lbs) weekly loss. Resistance training initiated. Address hormonal imbalances. Expect 5-10% body weight reduction by month 6.
Optimization Phase (Months 6-12): Intensified exercise program, advanced nutritional strategies if needed. Target 10-15% total weight loss. Significant improvements in metabolic markers: HbA1c, insulin, lipids, inflammatory markers. Resolution or improvement of comorbidities.
Maintenance Phase (Year 1+): Transition to sustainable long-term lifestyle. Continue monitoring and support. Focus on body composition rather than just weight. Prevent regain through ongoing accountability and periodic reassessment.
Note: Individual timelines vary significantly based on starting weight, metabolic health, adherence, number of root causes, and use of adjunctive therapies. Patients with severe obesity (BMI >40) or significant metabolic dysfunction may require 18-24 months to achieve optimal results.
How We Measure Success
Outcomes that matter
5-10% body weight reduction (clinically significant for health improvement)
10-15% body weight reduction (optimal for metabolic disease remission)
Waist circumference reduction: >5 cm indicates visceral fat loss
HOMA-IR normalized (<1.0) or significantly improved (>30% reduction)
Fasting insulin normalized (<6 μIU/mL)
HbA1c <5.7% or individualized target achieved
Triglycerides <150 mg/dL and HDL >40 mg/dL (men) or >50 mg/dL (women)
hs-CRP <1.0 mg/L (resolution of chronic inflammation)
Resolution or improvement of obesity-related comorbidities
Improved sleep quality and resolution of sleep apnea
Increased energy levels and physical function
Preservation or increase of lean muscle mass
Sustained lifestyle habits and prevention of weight regain
Frequently Asked Questions
Common questions from patients
Why can't I lose weight even though I eat very little?
This is extremely common and frustrating. Several mechanisms explain this: (1) Metabolic adaptation - prolonged calorie restriction lowers basal metabolic rate by 15-30%; (2) Leptin resistance - your brain perceives starvation despite adequate fat stores; (3) Insulin resistance - high insulin locks fat in storage and prevents fat burning; (4) Thyroid dysfunction - reduced T3 conversion slows metabolism; (5) Chronic stress - elevated cortisol promotes fat storage. The solution requires addressing these metabolic factors, not just further calorie restriction.
Is obesity really a disease or just a lifestyle choice?
Obesity is recognized as a chronic, relapsing, multifactorial disease by major medical organizations including the American Medical Association, WHO, and NIH. While lifestyle factors contribute, genetic predisposition accounts for 40-70% of risk. Neuroendocrine dysregulation (leptin resistance, insulin resistance), chronic inflammation, gut microbiome alterations, and environmental obesogens create a biological drive toward weight gain that cannot be overcome by willpower alone. Treatment requires medical intervention, not just advice to 'eat less and exercise more.'
What is the best diet for weight loss?
The best diet is one you can sustain long-term that addresses your specific metabolic phenotype. For insulin-resistant individuals, low-carbohydrate or ketogenic diets show superior results. For inflammatory phenotypes, Mediterranean or anti-inflammatory diets work well. For those with circadian disruption, time-restricted eating is beneficial. Common elements of successful diets: adequate protein (25-30% calories), high fiber, elimination of processed foods and sugar-sweetened beverages, and caloric deficit achieved through whole foods rather than restriction.
Are weight loss medications safe and effective?
Modern weight loss medications have evolved significantly. GLP-1 agonists (semaglutide, tirzepatide) achieve 15-22% weight loss on average with favorable safety profiles, though GI side effects are common. They work by reducing appetite, slowing gastric emptying, and improving insulin sensitivity. Phentermine/topiramate achieves 8-10% weight loss. Naltrexone/bupropion achieves 5-8% and helps with food addiction. All require medical supervision and work best combined with lifestyle intervention. They are appropriate for BMI >=30 or >=27 with comorbidities.
How does sleep affect weight?
Sleep is critical for weight management. Sleep deprivation (<6 hours): (1) Increases ghrelin (hunger hormone) by 28%; (2) Decreases leptin (satiety hormone) by 18%; (3) Increases cravings for high-calorie foods by 45%; (4) Impairs glucose tolerance and insulin sensitivity by 30%; (5) Elevates cortisol promoting fat storage; (6) Reduces physical activity and thermogenesis. Studies show sleeping <6 hours increases obesity risk by 55%. Optimizing sleep to 7-9 hours is as important as diet and exercise.
Can obesity be cured or just managed?
Significant weight loss (10-15% or more) can put type 2 diabetes into remission, normalize blood pressure, resolve fatty liver disease, and dramatically improve health outcomes. However, metabolic adaptation and hormonal changes make weight regain common (80-95% regain within 5 years without ongoing support). The goal shifts from 'cure' to 'sustained remission' through: (1) addressing root causes, (2) establishing sustainable habits, (3) ongoing monitoring and support, (4) medication when needed. Many patients maintain significant improvements with comprehensive functional medicine approaches.
Medical References
- 1.Heymsfield SB, Wadden TA. Mechanisms, Pathophysiology, and Management of Obesity. N Engl J Med. 2017;376(3):254-266. PMID: 28099824 - Comprehensive review of obesity pathophysiology and management.
- 2.Garvey WT, Mechanick JI, Brett EM, et al. American Association of Clinical Endocrinologists and American College of Endocrinology Comprehensive Clinical Practice Guidelines for Medical Care of Patients with Obesity. Endocr Pract. 2016;22(Suppl 3):1-203. - Evidence-based clinical guidelines for obesity management.
- 3.Jensen MD, Ryan DH, Apovian CM, et al. 2013 AHA/ACC/TOS Guideline for the Management of Overweight and Obesity in Adults. Circulation. 2014;129(25 Suppl 2):S102-S138. - Cardiovascular-focused obesity guidelines.
- 4.O'Neill S, O'Driscoll L. Metabolic Syndrome: A Closer Look at the Growing Epidemic and Its Associated Pathologies. Obes Rev. 2015;16(1):1-12. PMID: 25407540 - Review of metabolic syndrome and obesity-related pathologies.
- 5.Rosen ED, Spiegelman BM. What We Talk About When We Talk About Fat. Cell. 2014;156(1-2):20-44. PMID: 24439368 - Comprehensive review of adipose tissue biology.
- 6.Myers MG Jr, Leibel RL, Seeley RJ, Schwartz MW. Obesity and Leptin Resistance: Distinguishing Cause from Effect. Trends Endocrinol Metab. 2010;21(11):643-651. PMID: 20846876 - Review of leptin resistance mechanisms.
- 7.Turnbaugh PJ, Ley RE, Mahowald MA, et al. An Obesity-Associated Gut Microbiome with Increased Capacity for Energy Harvest. Nature. 2006;444(7122):1027-1031. PMID: 17183312 - Landmark study on gut microbiome and obesity.
- 8.Wilding JPH, Batterham RL, Calanna S, et al. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. PMID: 33567185 - Seminal trial on GLP-1 agonists for obesity.
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Obesity & Weight Management.