Delve into cardiometabolic care and obesity to understand its implications for your overall health and lifestyle choices.
Abstract: Integrative Obesity Care Across Women’s and Men’s Health — A First-Person Educational Journey in Evidence-Based Practice
I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In this educational post, I guide you through a deeply detailed, clinically grounded, first-person journey that unifies women’s and men’s metabolic health, obesity treatment, insulin resistance, PCOS, binge eating disorder, sarcopenia, cardiometabolic risk, and fertility considerations. I present modern evidence from leading researchers and show how it translates into stepwise, patient-centered protocols. This post also demonstrates how our multidisciplinary model at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas integrates internal medicine oversight by Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), with integrative chiropractic care, functional medicine, personal injury expertise, rehabilitation, nutrition, and behavioral support to achieve safe, durable outcomes. You will see why insulin acts as a master energy regulator, how GLP-1 and GIP therapies recalibrate gut-brain appetite signals, how resistance training protects muscle during weight loss, and how chiropractic care improves movement efficiency, reduces pain, modulates autonomic balance, and underpins sustainable activity. I include narrative case journeys that span women’s PCOS and binge eating, male metabolic syndrome and fertility, perimenopause and menopausal hormone therapy, and advanced sarcopenic obesity with cardiovascular disease—each mapped to precise physiological mechanisms and evidence-based protocols. The goal is simple: provide a clear, comprehensive, and humane roadmap that patients and clinicians can follow together.
Meet Our Integrative Team: How Internal Medicine and Chiropractic Work Together in El Paso
I practice integrative chiropractic and functional medicine with one focus: restore metabolic health using safe, coordinated, evidence-based methods. Our clinic, Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), operates as a multidisciplinary injury and integrative care center in El Paso, Texas. We combine chiropractic, internal medicine, functional medicine, rehabilitation, nutrition, and personal injury care in one coordinated model.
At the center of our medical governance is Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749; Texas MD License #J2933). With more than 40 years of experience as an internist, Dr. Cardenas is our Medical Director and Collaborative Physician. She ensures medical oversight for diagnostics, pharmacotherapy, lab safety, and cardiometabolic risk management, while I lead integrative chiropractic and functional protocols. This multidisciplinary setup is common in integrative or injury care clinics, where an MD provides medical direction alongside a chiropractor—ensuring safety and aligning complex physiology with day-to-day implementation.
Key collaborative areas:
- Internal medicine oversight for diagnostics, labs, imaging, and pharmacotherapy
- Integrative chiropractic care for biomechanical optimization, pain reduction, autonomic regulation, and movement-based metabolic support
- Functional medicine for root-cause analysis: insulin resistance, inflammation, endocrine dysfunction, sleep, stress, microbiome, toxins, and nutrition
- Rehabilitation and therapeutic exercise for musculoskeletal integrity and metabolic conditioning
- Personal injury care for safe return to function, medical-legal documentation, and graded rehabilitation
- Behavioral health support addressing disordered eating, stress management, sleep hygiene, habit formation, and relapse prevention
Our Care Philosophy: Patient-Centered, Data-Driven, and Team-Coordinated
We do not treat obesity as weight alone. We treat obesity as a multi-system metabolic condition with cardiometabolic, endocrine, neurobehavioral, and musculoskeletal dimensions. We build individualized treatment maps that align physiology with function and sustainability. We sequence interventions—starting with low-risk, high-benefit changes, then layering medical, rehabilitative, and behavioral strategies to reinforce metabolic stability.
Core pillars:
- Identify physiologic drivers: insulin resistance, hyperinsulinemia, dyslipidemia, hepatic stress, inflammation, reproductive hormone imbalance, sleep disruption, pain, and autonomic dysregulation
- Establish safety parameters: medical clearance, contraindications, lab monitoring, medication side effects, pregnancy plans, and psychological risks.
- Integrate movement and chiropractic care: reduce pain, improve range of motion, optimize breathing mechanics, and enhance insulin sensitivity through sustainable activity.
- Align nutrition with physiology: prioritize protein adequacy, fiber density, glycemic control, and satiety over rigid caloric restriction.
- Support behavior change: address binge triggers, reward loops, distress tolerance, and habit consistency through structured, empathetic coaching.
- Monitor outcomes: serial labs, body composition, strength, sleep, cravings, menstrual or testosterone status, mood, and functional capacity
Women’s Health Case Journey: PCOS, Insulin Resistance, and Binge Eating — A Coordinated Plan in Action
Meet a 25-year-old woman whose story mirrors many clinical realities. She is married, a fitness director, and presents for an annual exam with long-standing concerns: hyperlipidemia, irregular, infrequent menses, acne, and weight cycling. Her BMI is 37.5. Past attempts include low-fat, low-calorie plans that collapse after two months. She experiences anxiety if her calories exceed 1,200 per day and has intermittent evening binges that began in adolescence. She eats two large meals daily—lunch and dinner—with evening snacking driven by cravings. She exercises vigorously (elliptical, strength training, yoga), sleeps reasonably well, drinks modest alcohol on weekends, and does not smoke.
Laboratory patterns:
- Fasting insulin 36.1 μIU/mL (elevated)
- Fasting glucose 107 mg/dL (elevated)
- HOMA-IR 9.5 (high insulin resistance)
- A1C 6.0% (prediabetes)
- Dyslipidemia pattern: elevated triglycerides, low HDL, elevated LDL
- Elevated liver enzymes
- Physical exam: high waist circumference, apple-shaped adiposity, acanthosis nigricans, skin tags, cystic acne, and upper lip hair
Clinical impressions:
- Class II obesity (BMI ~37.5)
- PCOS indicators: hyperandrogenism (cystic acne, hirsutism), ovulatory dysfunction (irregular menses), meeting two Rotterdam criteria
- Infertility risk due to chronic anovulation
- Insulin resistance with hyperinsulinemia and prediabetes
- Dyslipidemia and hepatic stress
- Restrictive eating tendencies, binge eating behavior, and weight cycling
From an integrative perspective, elevated insulin and glycemic dysregulation impair adipose dynamics and reproductive signaling; restrictive patterns perpetuate binge cycles via stress and reward loops; high-effort fitness fights uphill without correcting insulin resistance. This is why we address root mechanisms and behaviors together.
The Physiology Behind Her Symptoms: Why Insulin Resistance Drives PCOS and Binge Patterns
Insulin as a master regulator:
- Insulin signals cells to absorb glucose; chronically high insulin promotes lipogenesis and suppresses lipolysis. Elevated fasting insulin marks insulin resistance, where skeletal muscle and liver fail to respond effectively, pushing the pancreas to compensate (Shanik et al., 2008).
- In adipose tissue, insulin resistance skews toward visceral adiposity, which secretes pro-inflammatory adipokines (TNF-α, IL-6), worsening systemic insulin resistance and endothelial dysfunction (Ahima, 2006; Shoelson et al., 2006).
- In the liver, insulin resistance drives hepatic gluconeogenesis, raises fasting glucose, and dyslipidemia via elevated VLDL production (Ferrannini et al., 2013; Ter Horst et al., 2017).
PCOS, hyperandrogenism, and insulin:
- In PCOS, insulin acts on ovarian theca cells to augment androgen production, amplifying hyperandrogenism and suppressing ovulation (Dunaif, 1997). Hyperinsulinemia reduces hepatic SHBG, increasing free androgens—driving acne, hirsutism, and anovulation (Azziz et al., 2016; Moran et al., 2019).
- Weight loss of 5–10% can restore ovulation in many patients, particularly when insulin sensitivity improves (Legro et al., 2013; Moran et al., 2011).
Binge eating, stress, and reward axis:
- Restrictive eating elevates stress and cortisol, biasing metabolism toward central adiposity and high-sugar cravings (Adam & Epel, 2007). Dopamine reward pathways, with modulation by ghrelin and neuropeptide Y, increase drive for palatable foods during scarcity or distress (Berthoud, 2011; Stice et al., 2013).
- Hypocaloric rigidity without satiety signals promotes loss-of-control eating, especially with high cognitive restraint and anxiety (Fairburn & Harrison, 2003; Hudson et al., 2007).
Skeletal muscle metabolic dynamics:
- Skeletal muscle is the primary postprandial glucose sink; resistance training increases GLUT4 and insulin sensitivity (Hawley & Lessard, 2008; Richter & Hargreaves, 2013). Short frequent bouts of activity, including walking, improve glycemic variability and reduce postprandial excursions (DiPietro et al., 2013).
Autonomic balance and chiropractic care:
- Pain, mechanical inefficiency, and restricted mobility elevate sympathetic tone, impair sleep, and worsen insulin resistance (Thayer & Lane, 2007). Optimized joint mechanics, posture, and neuromuscular control support parasympathetic engagement, improve breathing mechanics, reduce pain-driven inactivity, and restore consistent quality movement (Pickar, 2002; Bialosky et al., 2009).
Why this matters:
- Addressing insulin resistance, reducing sympathetic drive, supporting satiety and metabolic efficiency, and structuring compassionate behavior change is required for durable success.
Stepwise Treatment Plan: Sequencing for Safety and Sustainability in PCOS and Binge Eating
Treatment goals:
- Initial 10% body weight reduction
- Reduce cardiometabolic markers (insulin, glucose, A1C, lipids, liver enzymes)
- Improve PCOS features and restore ovulation
- Reduce binge frequency and anxiety around eating
- Prevent muscle loss and weight cycling
- Align contraception with treatment and pregnancy planning
- Optimize movement quality and sleep
Interventions:
- Nutrition and meal patterning
- Shift from calorie anxiety to reduced-carbohydrate patterns emphasizing protein adequacy (90–100 g/day) and fiber to satiety via vegetables and low-sugar fruits.
- Eat every 3–4 hours, aiming for 4–5 smaller meals to reduce glycemic volatility.
- Minimize ultra-processed foods, sweets, refined starches, excess grains, and alcohol.
- Rationale: Protein increases satiety via PYY and GLP-1 signals; fiber slows glucose absorption; regular meal timing lowers postprandial spikes and reduces cravings (Hall et al., 2019; Leidy et al., 2015)
- Physical activity and therapeutic exercise
- Continue aerobic and strength routines; add daily 10-minute walks post meals to enhance insulin sensitivity and lower glucose peaks.
- Rationale: Short postprandial movement improves skeletal muscle glucose uptake independent of insulin, reducing glycemic load and stabilizing appetite (DiPietro et al., 2013)
- Integrative chiropractic care
- Assess spinal and pelvic mechanics, rib and diaphragmatic motion, foot and ankle function, and myofascial restrictions.
- Provide manual therapy, joint mobilization, and neuromuscular re-education to reduce pain, improve movement economy, and boost autonomic balance.
- Rationale: Mechanical efficiency reduces energy waste and pain signals, supports vagal tone, improves sleep, and increases exercise adherence—directly impacting metabolic control (Bialosky et al., 2009; Pickar, 2002)
- Pharmacotherapy under internal medicine oversight
- Metformin ER 500 mg daily, titrating to 2,000 mg as tolerated
- Rationale: Lowers hepatic gluconeogenesis, improves insulin sensitivity, may aid ovulatory function in PCOS (Viollet et al., 2012; Lord et al., 2003)
- Safety: GI side effects; rare lactic acidosis; monitor B12 over time (de Jager et al., 2010)
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- Contraception with combined oral contraceptives, given potential fertility restoration
- Rationale: Supports cyclical control, reduces endometrial risk, acne/hirsutism via increased SHBG and lowered free androgens (Azziz et al., 2016)
- Safety: Consider VTE risk factors; coordinate with lifestyle and metabolic care
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- GLP-1/GIP therapy such as tirzepatide, titration to effect
- Rationale: Appetite suppression, improved glycemic control, weight reduction, potential benefits for hepatic steatosis and lipids (Jastreboff et al., 2022; Frias et al., 2021)
- Contraception note: For 4 weeks after initiation and each dose increase, advise barrier contraception due to delayed gastric emptying and possible impaired oral contraceptive absorption
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- If binge episodes persist: Consider lisdexamfetamine for binge eating disorder when indicated and supervised
- Rationale: FDA-approved for binge eating disorder; improves executive control, reduces compulsive episodes (McElroy et al., 2015)
- Behavioral care and support
- Screen using BEDS-7; track binge frequency, triggers, and distress
- Shift focus from restrictive control to satiety-based patterns; coach distress tolerance, stress management, and sleep hygiene
- Rationale: Stabilizing metabolic signals and reducing cognitive overcontrol lowers binge risk; structured support sustains habits (Fairburn & Harrison, 2003)
- Monitoring and follow-up
- Labs every 3–6 months: fasting insulin, glucose, A1C, lipids, liver enzymes; body composition when feasible
- Track menstrual regularity, ovulatory signs, acne/hirsutism, binge frequency, cravings, sleep, mood, functional capacity
- Adjust nutrition, activity, chiropractic work, and medications to maintain progress and safety.
Why this sequence works:
- It respects physiology, aims for stable progress, prevents harm, and prioritizes autonomy and dignity while ensuring medical oversight and integrative movement care.
Transform Your Body!- Video
Six-Month Outcomes: Physiologic Improvements and Behavior Stabilization
With consistent execution and compassionate support:
- Weight reduction ~11%
- Fasting insulin decreased from 36.1 to ~21.4 μIU/mL
- Fasting glucose and HOMA-IR improved
- A1C trending down
- Decreased acne and hirsutism
- Binge episodes reduced from weekly to monthly, increasingly stress-triggered rather than calorie-triggered
- Movement routine sustained and expanded; alcohol reduced
Clinical significance:
- Lower insulin improves lipolysis and reduces lipogenesis; less inflamed adipose tissue enhances metabolic signaling
- Improved menstrual symptoms suggest recovering hypothalamic–pituitary–ovarian axis function
- Reduced binge episodes indicate neurobehavioral recalibration: satiety signals reinforced, reward pathways less activated by stress
Refinements:
- Add a second 10-minute walk daily
- Maintain medication protocols
- Hold lisdexamfetamine as contingency if binge patterns resurge
Two-Year Outcomes: Cardiometabolic Normalization and Fertility Planning
At two years:
- Weight reduction ~24.1%
- Fasting insulin ~8.4 μIU/mL (near optimal)
- HOMA-IR normalized
- A1C ~5.2%
- Lipids improved; liver enzymes normal
- Binge behavior controlled; minimal evening cravings
- Stable physical activity; healthy sleep; minimal alcohol
Contraception planning:
- Explore non-oral methods or barrier methods to assess menstrual regularity ahead of pregnancy planning
- Internal medicine oversight and reproductive counseling: adjust contraceptive planning safely, confirm metabolic stability, maintain structured nutrition, movement, and chiropractic support to guard against relapse
- If lisdexamfetamine was introduced earlier, review risks/benefits in preconception planning and taper appropriately with behavioral reinforcement
Clinical insight:
- PCOS-related cardiometabolic risks significantly decreased
- Ovulatory function likely restored or improving; pregnancy planning can proceed more safely
- Sustained movement efficiency and autonomic balance from chiropractic care and physical training support metabolic resilience
Integrative Chiropractic Care in Obesity and PCOS Treatment: Why It Belongs and How It Works
Chiropractic contributions:
- Pain reduction and joint function
- Manual therapy and mobilization decrease nociceptive input and muscle guarding, making daily movement more comfortable and efficient.
- Breathing and rib mechanics
- Diaphragmatic training improves oxygenation, reduces sympathetic tone, and enhances postprandial glycemic control via better activity tolerance.
- Postural and gait optimization
- Correcting foot/ankle mechanics, pelvic tilt, and spinal alignment decreases energy expenditure for movement and reduces compensatory pain patterns.
- Neuromuscular control and balance
- Proprioceptive and stability drills enhance activity safety, allowing consistent adherence to walking and strength programs
Metabolic impact:
- Lower pain increases NEAT (non-exercise activity thermogenesis), contributing significantly to daily energy expenditure without triggering stress or hunger compensation
- Improved sleep via pain reduction and autonomic balance supports leptin and ghrelin regulation
- Enhanced movement quality supports GLUT4 translocation and insulin sensitivity
Clinical observations:
- I have documented patients whose insulin and A1C improved in parallel with pain reduction, expanded gait capacity, and respiratory mechanics training. As barriers are removed, patients sustain gentle daily activity that converts short-term metabolic changes into long-term resilience. See ongoing updates and case reflections:
Internal Medicine Oversight: Medication Safety, Lab Interpretation, and Ethical Guardrails
With Dr. Maria Guadalupe Cardenas serving as Medical Director and Collaborative Physician:
- Medication selection, titration, and monitoring
- Metformin ER, GLP-1/GIP receptor agonists, binge eating pharmacotherapy
- Contraception planning and pregnancy safety
- Oral contraceptives, barrier methods, timing around pharmacotherapy, guidance during GLP-1 initiation and dose changes
- Cardiometabolic risk management
- Lipid-lowering strategies, liver function surveillance, hypertension monitoring
- Diagnostic fidelity
- Proper PCOS criteria application, differential diagnosis, comorbidity screening
Ethical framework:
- Avoid polypharmacy; monitor for side effects
- Co-create sustainable patterns; avoid rigid diet pressure
- Align therapy with guidelines and current research
- Prioritize informed consent and shared decision-making, especially around contraception and medication adjustments
Functional Medicine Layer: Root Causes, Personalized Nutrition, and Whole-Person Health
Functional medicine priorities:
- Precision nutrition
- Emphasize protein and fiber; modulate carbohydrate quality; ensure micronutrient adequacy (vitamin D, magnesium, omega-3s, B12 monitoring with metformin)
- Gut health and glycemic control
- Fiber variety supports microbiome diversity; improved incretin signaling assists appetite regulation and insulin sensitivity.
- Inflammation and oxidative stress
- Encourage anti-inflammatory dietary patterns; monitor liver health; support sleep as a natural anti-inflammatory process.
- Stress physiology
- Teach stress-reduction practices and build routines that lower cortisol spikes and reward-driven eating
Principles:
- Tailor dietary patterns to preference and tolerance; avoid one-size-fits-all dogma
- Aim for sustainable satiety and stable glycemic control—not perfection or rigid restriction
Binge Eating Disorder: Screening, Neurobiology, and Treatment Rationale
Screening and diagnosis:
- Structured intake targeting frequency, amount, loss of control, distress, compensatory behaviors
- Validated tools like BEDS-7 to quantify risk and monitor change over time
Neurobiology and intervention:
- Chronic restriction and stress sensitize reward pathways; dopamine responses amplify high-calorie food seeking under distress
- GLP-1 therapies reduce binge frequency by enhancing satiety and reducing preoccupation with food
- Lisdexamfetamine, when indicated for moderate-to-severe binge patterns, helps regain executive control over impulses
- Behavioral strategies—structured meals, stress coping, sleep stability—shift the system away from binge triggers
Why integrate:
- Binge episodes erode metabolic stability, confidence, and sustainability. Addressing them prevents weight cycling and consolidates progress.
Men’s Health Case Journey: Metabolic Syndrome, Hormones, Fertility, and Cardiovascular Risk
Meet “George,” a 35-year-old project manager with depression, anxiety, elevated blood pressure, low sperm count, and early metabolic dysfunction. He is ambitious, with a long commute, access to free food and drinks at work, and significant personal stress (home buying, family goals). He and his spouse are trying for a second child. He fears hypertension readings echo his father’s heart failure. He reports occasional erectile dysfunction, attributing it to stress.
Initial clinical picture:
- Waist circumference elevated (visceral adipose tissue risk)
- Blood pressure significantly elevated
- Fasting glucose and insulin increased; HOMA-IR 3.1 (insulin resistant)
- Lipids slightly elevated
- Missing labs: A1C, full thyroid panel, liver panel (ordered immediately)
- Symptoms: poor sleep, frequent hunger, shame about appetite control, stress-eating patterns
Key concept: chemical versus character
- Shame and self-blame cloud progress; appetite dysregulation is biochemical, not moral failure
- Releasing self-blame opens collaborative, curiosity-driven healing
Hormonal cascade of obesity and stress:
- Excess adipose increases aromatase, converting testosterone to estrogen—lowering testosterone, impairing mood, energy, muscle mass, and worsening fat accumulation
- Insulin resistance and chronic stress elevate insulin and cortisol, driving visceral fat storage and cravings
- Ghrelin rises (hunger), leptin resistance blunts satiety, GLP-1 signaling impaired
- Adipokine storm from visceral fat fuels chronic inflammation and cardiovascular risk
- Stress-sleep-cortisol spiral keeps cortisol elevated, disrupting repair and amplifying cravings
Goals:
- Protect heart health and prevent hypertension sequelae
- Prevent progression to type 2 diabetes
- Improve fertility
- Manage stress effectively
- Increase energy to be an active father
Initial plan:
- Complete missing labs: A1C, thyroid panel, liver panel
- Nutrition support with Registered Dietitian Nutritionist
- Start blood pressure medication; home BP log
- Refer for polysomnography (sleep study)—OSA suspected
- Foundational tools: simple meditation and movement goals
- Open dialogue on obesity medications as a tool to recalibrate hormonal imbalances
Four-week follow-up:
- Started BP medication; kept detailed log
- Labs: A1C 5.9% (prediabetes); thyroid/liver normal
- Sleep study scheduled
- Dietitian visit identified large portions, soda intake, stress-eating patterns
- Did not start meditation or structured exercise; slight weight increase—normalized and reframed
Adjustments:
- Increase BP medication dose based on logs
- Consider bupropion-naltrexone after sleep study completed
- Bupropion for mood, energy, focus
- Naltrexone to reduce reward-based cravings for sugar
- Make mindfulness accessible: 3-minute guided meditation in the car after commute, twice weekly
- Integrate movement: NEAT strategies (stairs, periodic walks)
Four-month check-in:
- Sleep apnea confirmed; CPAP initiated—energy and mood improved
- Blood pressure controlled
- Mood improved with bupropion-naltrexone; midday walks started
- Weight down; nutrition improved
- Persistent hunger remained—consider incretin-based therapy
Chiropractic integration:
- Assess and correct biomechanical imbalances from sedentary work and commuting
- Spinal adjustments restore motion, alleviate nerve interference, reduce strain in spine/hips/knees
- Support adaptation to new movement patterns; reduce injury risk and improve function
- Enhance nervous system balance, shifting toward parasympathetic tone—lower stress, better digestion and sleep
Incretin-based therapy:
- Insurance coverage for semaglutide confirmed
- Start semaglutide 0.25 mg weekly
- Taper off naltrexone due to GI overlap; continue bupropion for mood
- Body composition analysis to ensure fat loss over muscle loss; add resistance training to protect muscle
One-year transformation:
- Spouse pregnant; fertility improved
- Blood pressure controlled
- HOMA-IR dropped from 3.1 to 1.64; no longer insulin resistant
- A1C normalized; weight and waist reduced
- Semaglutide effective at 1.7 mg—lowest effective dose found
- Sustainable habits: restorative sleep; daily walks; dietitian check-ins less frequent
Data at a glance:
- Weight down 15%
- Waist circumference reduced
- Blood pressure controlled
- Fasting glucose and insulin normalized
- HOMA-IR normalized
- A1C normalized
- All goals met
Clinical insight:
- Symptoms converge on a common root: metabolic and hormonal dysregulation
- Integrative approach—internal medicine oversight, functional medicine, chiropractic care—transforms outcomes beyond weight alone.
Perimenopause Case Journey: Menopausal Hormone Therapy, Tirzepatide, and Muscle Preservation
Meet “Lynn,” a 42–45-year-old woman, non-smoker, full-time event planner, presenting with overwhelming fatigue, brain fog, poor sleep, mood swings, hot flashes, and recent 20-pound weight gain. Periods irregular and heavy; difficult pregnancy at age 35. Grief over father’s recent death. Third primary care provider in 18 months; prior dismissal of perimenopause concerns. Elevated cholesterol and A1C; slightly elevated liver enzymes; thyroid and kidney normal; waist circumference elevated; BP slightly elevated.
Goals:
- Alleviate perimenopausal symptoms
- Reduce blood pressure
- Prevent further weight gain and reduce visceral fat
- Lower cardiovascular risk
Initial plan:
- Nutrition and lifestyle with RDN
- Physical activity: walking during daughter’s ballet/gymnastics hour
- Emotional support: therapy for grief
- Start menopausal hormone therapy (MHT): transdermal estrogen-progesterone combination
- Why prioritize MHT:
- Addresses underlying hormonal shifts driving brain fog, mood swings, sleep issues, and insulin sensitivity (NAMS, 2022)
- Shared decision-making: Lynn’s primary distress was cognitive/emotional; treating root physiology aligns with her goals
- Safety: within 10 years of menopause and under age 60; transdermal route may lower clot risk
Follow-up at six weeks:
- Subjective improvements: brain fog and fatigue lifted; sleep better; energy and motivation increased
- Behavioral changes: regular walks; considering classes
- Objective: small weight loss; BP improved trend
Introduce tirzepatide:
- Dose: start at 2.5 mg weekly
- Mechanisms:
- GLP-1 agonism: improves glucose-dependent insulin secretion; slows gastric emptying; reduces appetite and food noise
- GIP agonism: enhances insulin secretion; modulates adipose metabolism; augments weight loss beyond GLP-1 alone (Jastreboff et al., 2022)
- Continue MHT, dietitian, therapist, and exercise routine
Critical considerations:
- Monitor muscle mass and body composition
- GLP-1/GIP therapies can reduce lean mass; must protect muscle (EWGSOP2; Cruz-Jentoft et al., 2019)
- Baseline and periodic BIA or DEXA; aim for fat loss while maintaining muscle
- Reinforce protein intake: 1.2–1.5 g/kg ideal body weight, spaced across the day for muscle protein synthesis
- Prioritize resistance training: weight lifting, bands, bodyweight—non-negotiable during incretin therapy
- Manage side effects: nausea, vomiting, diarrhea, constipation, reflux—transient; diet adjustments help
- Red-flag symptoms: severe persistent abdominal pain (pancreatitis, gallstones), intractable vomiting (dehydration, AKI), rigid abdomen—seek urgent care
Three years later:
- Tirzepatide titrated to 15 mg weekly; MHT continues
- Found preferred exercise genres: cardio plus resistance classes; regular walking
- Dietitian tune-ups every 6–9 months; therapy resumed for anxiety related to mother’s illness
- Weight journey: initial drop followed by minor regain—normal homeostatic response; body composition confirms fat loss with muscle preservation
- Without body composition tech: assess sarcopenia via gait, sit-to-stand, handgrip strength, physical exam, and energy reports
Clinical insight:
- Treat hormonal foundation first, then layer pharmacotherapy thoughtfully
- Resistance training and protein distribution are critical to prevent sarcopenia during weight loss
- Patient-centered approach transforms quality-of-life outcomes and opens new goals
Advanced Sarcopenic Obesity Case Journey: Type 2 Diabetes, Cardiovascular Disease, and Insulin Deprescribing
Meet “Amit,” a 57-year-old man of North African ancestry with complex disease:
- Type 2 diabetes on basal and bolus insulin plus metformin
- Myocardial infarction three years prior; Stage 2A peripheral artery disease (PAD) with intermittent claudication
- Obstructive sleep apnea (CPAP), hypertension, hyperlipidemia, MASLD (Stage 2), low testosterone, erectile dysfunction
- Family history: obesity, diabetes, heart attacks
- Diet: three large meals plus frequent snacking; daily fast food lunch; low fruits/vegetables; frequent hunger and poor satiety—profound insulin and leptin resistance
- Activity limited by claudication; alcohol regular
Baseline:
- BMI 38.4; waist 51.25 inches (central adiposity)
- A1C 6.9% (controlled by high insulin doses—masking underlying insulin resistance)
- Lipids: elevated triglycerides; HDL 29 mg/dL (atherogenic)
- Liver enzymes elevated (MASLD)
- Body composition: 56.7% body fat; skeletal muscle 20.7% (4th percentile)—sarcopenia; visceral fat 4.4 liters
- Physical exam: acanthosis nigricans, skin tags, hepatomegaly, 1+ pitting edema
Risk:
- Extremely high for MACE (MI, stroke)
- Concern for PAD progression, liver disease, functional decline
Goals:
- Achieve 10% weight reduction
- Improve body composition: increase muscle mass and function while reducing adiposity and visceral fat
- Reduce cardiometabolic risk factors: lower A1C, triglycerides, BP; raise HDL
- Improve PAD symptoms and stamina
- Enhance energy and quality of life
Plan:
- Nutrition: protein-focused Mediterranean diet
- Protein 90–100 g/day, spaced every 3–4 hours to trigger multiple muscle protein synthesis pulses; animal protein preferred for leucine content
- Reduce ultra-processed foods, sweets, starches, grains, alcohol—combat carbohydrate intolerance in insulin resistance
- Focus on non-starchy vegetables and low-glycemic fruits
- Physical therapy:
- Walk-rest-walk protocol for PAD; build collateral circulation
- Strength training twice weekly, start light weights/resistance bands
- Stationary bike often better tolerated than walking
- Chiropractic care to optimize biomechanics: spinal and extremity adjustments, soft tissue work to reduce pain and improve gait mechanics
- Pharmacotherapy: semaglutide with cardiovascular indication
- SELECT trial: semaglutide 2.4 mg FDA-approved for secondary prevention of cardiovascular events in patients with pre-existing cardiovascular disease and obesity (Lincoff et al., 2023)
- Titrate from 0.25 mg weekly to target dose
- Deprescribe insulin:
- High exogenous insulin promotes lipogenesis and suppresses lipolysis—locks metabolism into fat storage and inflammation
- As semaglutide titrates, taper mealtime insulin (often stop outright in well-controlled) and reduce basal insulin as glucose improves
- Continuous glucose monitoring (CGM) for precise and safe tapering
Six-month follow-up:
- Semaglutide titrated to 2.4 mg; completely tapered off insulin
- Subjective: “Food noise” silenced; portion control now possible; 75% adherence to nutrition plan; spontaneous reduction in alcohol
- Physical therapy maintained; exercise bike 15 minutes/day; strength training with light weights; increased stamina; less claudication pain
Objective:
- Body weight reduction 10.2%
- Improved energy and function
- Removing insulin “brake” allows metabolism to re-engage fat loss; aerobic activity acts as insulin sensitizer, lowering endogenous insulin
Clinical insight:
- Aggressive, integrative approach—targeted nutrition, supervised physical activity, advanced pharmacotherapy correcting root physiology—can reverse severe, long-standing metabolic disease
- Deprescribing insulin under medical oversight reshapes the hormonal landscape, enabling meaningful fat loss and reduced inflammation
Coordinated Care in El Paso: Team Roles and Integrated Services
Team structure:
- Medical direction and safety (Dr. Cardenas)
- Diagnostics: metabolic labs, liver enzymes, lipid profiles, inflammatory markers when indicated
- Pharmacotherapy: selection and titration of GLP-1 (semaglutide), dual agonists (tirzepatide), and adjunct agents (bupropion, naltrexone, topiramate, phentermine)
- Perioperative considerations: naltrexone-opioid interactions, infection risk stratification, comorbidity optimization, hospital requirements
- Internal medicine comorbidities: hypertension, lipid disorders, diabetes, sleep issues, medication reconciliation
- Integrative chiropractic and functional medicine (Dr. Jimenez)
- Musculoskeletal assessment: gait, posture, joint integrity, fascial restrictions, spinal segmental function
- Manual therapy and adjustments: reduce pain, improve mobility, modulate autonomic tone, restore efficient movement patterns
- Functional medicine mapping: nutrition, protein targets, micronutrients, gut health, inflammation control, behavioral coaching
- Body composition guidance: exercise planning for muscle preservation/gain during weight loss; aerobic and resistance progression
- Rehabilitation and allied services
- Physical therapy referrals for osteoarthritis and sarcopenia, ensuring psychological safety and addressing weight bias experiences
- Dietitian referrals to obesity-informed practitioners
- Personal injury care integration for trauma backgrounds, synchronizing metabolic and musculoskeletal plans
- Follow-up and advocacy
- Regular tracking: fasting insulin, HOMA-IR, A1C, visceral adipose tissue, waist circumference, muscle mass percentiles
- Advocacy against blanket BMI barriers; individualized risk assessment for surgical readiness
Why it works:
- Multidisciplinary alignment ensures safety, clarity, and sustained behavior change
- Chiropractic care underpins movement adherence by removing pain and mechanical barriers
Physiological Deep Dive: Insulin Resistance Across Organs and Pathways
Insulin resistance is a multi-organ story:
- Liver:
- Visceral fat releases free fatty acids into portal circulation, increasing hepatic triglyceride synthesis, impairing insulin signaling via serine phosphorylation of IRS proteins, and elevating gluconeogenesis—raising fasting glucose (Samuel & Shulman, 2012)
- Skeletal muscle:
- Lipid intermediates (DAG) activate PKCθ, impairing insulin receptor signaling; reduced mitochondrial function limits glucose oxidation (Hojlund, 2014)
- Adipose tissue:
- Hypertrophic adipocytes secrete pro-inflammatory adipokines and exhibit impaired insulin-mediated lipolysis suppression, causing FFA spillover (Ouchi et al., 2011)
Why we target VAT reduction, muscle preservation, and aerobic/resistance training together:
- These changes yield metabolic improvements beyond weight alone—better glycemic control, reduced inflammation, improved endothelial function, and enhanced insulin sensitivity
GLP-1 and Dual GIP/GLP-1 Agonists: Appetite Biology, Glycemia, and Cardiometabolic Protection
Semaglutide (GLP-1 receptor agonist):
- Enhances glucose-dependent insulin secretion, reduces glucagon, slows gastric emptying, acts centrally to reduce appetite and cravings; produces substantial weight loss and glycemic control (Wilding et al., 2021)
Tirzepatide (dual GLP-1/GIP agonist):
- Adds GIP-mediated effects that may enhance adipose metabolism and amplify weight loss with potent glycemic improvements (Jastreboff et al., 2022)
Cardiometabolic benefits:
- SELECT trial shows semaglutide 2.4 mg reduces cardiovascular events in people with obesity and pre-existing cardiovascular disease (Lincoff et al., 2023)
Clinical reasoning:
- These agents recalibrate gut-brain signals, reduce hedonic eating, and rebalance satiety pathways blunted by obesity-related neurohormonal changes
Pharmacological Adjuncts: Matching Mechanisms to Patient Profiles
Adjunct options:
- Phentermine:
- Sympathomimetic appetite suppressant; useful for daytime appetite spikes or motivational initiation; monitor BP/HR (Hendricks et al., 2011)
- Topiramate:
- GABAergic/glutamatergic modulation; can reduce binge-like patterns; monitor cognitive side effects and paresthesias (Bray et al., 2016)
- Bupropion:
- Dopaminergic/noradrenergic modulation supports reward-based eating control and energy; improves mood, valuable post-menopause (Greenway et al., 2010)
- Naltrexone:
- Opioid receptor antagonist dampens reward signaling around food; combined with bupropion enhances cravings control; discontinue ahead of opioid analgesia (Apovian et al., 2015)
When and why:
- Select, titrate, or switch under medical oversight to balance efficacy, tolerability, comorbidities, and surgical plans
- Avoid overlapping mechanisms with limited incremental benefit and increased adverse effects
Muscle Protein Synthesis, Sarcopenia Reversal, and Body Composition Strategy
Protein dosing:
- Older adults need higher per-meal protein (25–35 g) to overcome anabolic resistance; leucine-rich sources stimulate mTOR and MPS (Gorissen & Witard, 2018)
Resistance training:
- Stimulates satellite cell activation, increases fiber cross-sectional area, improves tendon stiffness—key for knee OA stabilization and functional independence (Morton et al., 2018)
Frequent feeding:
- Distributes amino acid availability; supports satiety; reduces evening cravings; aligns with circadian repair rhythms
Why it matters:
- Muscle preserves basal metabolic rate, improves insulin sensitivity via GLUT4, acts as an endocrine organ (myokines) counteracting inflammation (Pedersen & Febbraio, 2012)
Pain, Autonomic Regulation, and Movement: The Chiropractic Contribution
Osteoarthritis pain:
- Mechanosensitive nociceptors, synovial inflammation, subchondral bone changes; pain cycles drive inactivity and sarcopenia (Felson, 2006)
Chiropractic interventions:
- Optimize mechanical load distribution; reduce nociceptive input; normalize segmental motion; support autonomic balance (Pickar, 2002; Bialosky et al., 2009)
- Parasympathetic engagement improves sleep, appetite regulation, and recovery
Aerobic conditioning:
- Increases endorphins, improves capillary density, enhances endothelial NO production—benefits leg discomfort and overall stamina (Hambrecht et al., 2003)
Why integrate:
- Pain relief and efficient mechanics are prerequisites for sustained exercise adherence
Incremental Exercise Strategy: Micro-Progressions That Stick
Behavior and bioenergetics:
- Micro-commitments sustain motivation and reduce all-or-nothing patterns (Fogg, 2019)
- Small increases stimulate mitochondrial biogenesis via PGC-1α and build tendon resilience and neuromuscular coordination (Handschin & Spiegelman, 2008; Kjaer, 2004)
Practical steps:
- Add 1–2 minutes to bike sessions weekly
- Increase resistance one notch if pain-free
- Walk snacks: short bouts across the day
- Pair movement with routine triggers (after morning coffee, 5-minute mobility)
Identity shift:
- From inactive to capable—self-efficacy increases adherence (Bandura, 1997)
Nutrition Strategy: Protein First, Smart Carbs, Fence the Evenings
Counseling:
- Protein anchors: eggs, Greek yogurt, cottage cheese, seafood, poultry, lean meats; shakes for low appetite or chewing difficulty
- Carbohydrates: fibrous vegetables and low-glycemic fruits; limit refined starches—especially late day—to reduce evening cravings
- Meal timing: every 3–4 hours for sarcopenia risk; structured timing to prevent grazing and manage hunger waves
GLP-1 therapy considerations:
- Appetite suppression requires prioritized protein intake; smoothies and dairy options often practical anchors
Weight Bias and Health Equity: Building Trust, Safety, and Access
For older women with obesity:
- Validate experiences of dismissal; directly confront weight bias
- Empower with coaching scripts for PT and orthopedics; role-play interactions; encourage changing providers if fit is poor
- Advocate against blanket BMI thresholds; present functional gains and individualized risk mitigation
Clinical advocacy:
- We contact surgeons and hospital coordinators to explain barriers and active mitigation (medications, nutrition, sleep, PT), optimizing surgical readiness beyond BMI alone
Surgical Readiness and Osteoarthritis: Dolores’s Path to Mobility, Strength, and Travel
Dolores, 72:
- Severe bilateral knee OA; hospital requires BMI <40 for total knee replacements
- No major weight issues until perimenopause; now central adiposity with gynoid pattern and visceral increase
- On rosuvastatin, trazodone, diclofenac, multivitamin
- Diet: three meals daily, low protein, high vegetables/fruits, evening sweets
- Activity: swimming 20 minutes three times weekly; walking limited by knee pain
- Sleep: improved with trazodone; occasional early waking
- Labs: fairly metabolically healthy; fasting insulin 8.4 μIU/mL; BMI 41.5; body fat 56.8%; skeletal muscle 15.1% (2nd percentile—sarcopenia); VAT 2.3 liters; waist 43.1 inches
Goals:
- 9% weight reduction (~10 pounds) to meet BMI threshold
- Improve mobility, body composition, sarcopenia indices
Plan:
- Nutrition:
- Increase protein to 90–100 g/day, focusing on animal proteins and frequent feeding every 3–4 hours
- Reduce sweets and high-glycemic starches, especially evenings
- For protein aversion: eggs, seafood, cottage cheese, yogurt, cheese, protein smoothies/drinks
- Activity and rehab:
- Continue swimming
- PT for OA and sarcopenia; exercise bike; strength training respecting knee loading
- Medication:
- Consider naltrexone/bupropion for cravings, then switch to bupropion alone before surgery to avoid opioid antagonism
- Consider semaglutide or tirzepatide to sustain appetite control and loss ahead of second knee surgery
One-year outcomes:
- 7% weight reduction
- Fasting insulin normalized
- Body fat decreased to 49.8%
- Muscle mass increased to 10th percentile
- VAT reduced; waist circumference lowered
- One knee replaced without complications; mobility improved
- Transitioned to semaglutide 1.7 mg for sustained appetite control
Chiropractic integration:
- Lumbar-pelvic adjustments improved knee load distribution; facilitated cycling/swimming
- Soft tissue and fascial work around hip flexors, quadriceps, calves reduced stiffness and compensated gait patterns
- Proprioceptive drills enhanced neuromuscular control; improved confidence during PT
- Autonomic regulation (breathing, vagal tone) improved sleep synergy with trazodone; reduced pain amplification
Clinical insight:
- Chiropractic care optimizes biomechanics pre- and post-operatively; supports PT adherence; accelerates return to function
- Advocacy against blanket BMI thresholds helps align surgical decisions with individualized risk and functional goals
Translating Evidence Into Practice: Why Each Step Matters
- Reduced carbohydrate patterns with adequate protein/fiber stabilize insulin and satiety and address PCOS drivers
- Short postprandial walks exploit skeletal muscle glucose uptake to reduce glycemic excursions
- Chiropractic care removes mechanical barriers and autonomic stress, allowing patients to move more and sleep better
- Metformin targets hepatic gluconeogenesis and improves insulin sensitivity; may aid ovulatory function
- GLP-1/GIP therapies reduce appetite, improve glycemic control, and yield significant weight loss with cardiometabolic benefits
- Lisdexamfetamine, when indicated for binge eating, assists early behavior change while nutrition and stress strategies take root
- Internal medicine oversight guarantees medication safety, lab monitoring, and reproductive planning, including contraception timing with GLP-1/GIP therapy
- Functional medicine integrates root-cause analysis, personal preference, and real-life constraints—turning evidence into lived habits
Coordinated Care Timeline: From First Visit to One Year
- Initial assessment:
- Labs: fasting insulin, A1C, liver enzymes; body composition: fat %, muscle %, VAT, waist; functional baseline: pain, mobility, sleep
- First 4–8 weeks:
- Medication initiation or adjustment; nutrition plan; gentle exercise; chiropractic sessions; PT scheduling
- 3–6 months:
- Incremental progress: bike minutes, strength loads; protein targets more consistent; cravings reduced; lab improvements begin
- 9–12 months:
- Consolidation: body fat down, muscle up, VAT reduced, A1C stabilized; surgical readiness if indicated; functional goals realized
Clinical Observations from My Practice
In daily work, I see recurring patterns reinforcing these strategies:
- Patients combining GLP-1 therapy with progressive resistance training retain more muscle, feel stronger, and report fewer plateaus—especially when we troubleshoot evening eating and sleep quality
- Knee OA patients avoid walking due to pain yet tolerate bike and pool work; adding chiropractic manual therapy accelerates comfort with PT and improves adherence
- Patients with dismissive healthcare experiences gain confidence when we explicitly address bias, set realistic goals, and celebrate micro-progress—leading to better long-term outcomes
Explore more of my clinical insights:
Practical Takeaways for Patients and Clinicians
- Focus on satiety and stability, not restriction and anxiety
- Move often in small bouts; post-meal walks are metabolic tools
- Protect and build muscle to defend insulin sensitivity
- Use chiropractic care to reduce pain and optimize movement, enhancing daily activity adherence
- Consider metformin and GLP-1/GIP therapies under medical supervision for insulin resistance and PCOS features
- Screen early and compassionately for binge eating; combine behavioral strategies and pharmacotherapy when appropriate
- Align contraception carefully with medications that affect gastric emptying
- Measure progress beyond the scale: labs, sleep, menstrual regularity, cravings, mood, and function
- Build a team—internal medicine, chiropractic, functional medicine, nutrition, rehabilitation—so you never fight physiology alone
Key Concepts Highlighted for Search Optimization
- Insulin resistance as a master regulator of energy balance
- PCOS physiology, hyperandrogenism, and ovulatory dysfunction
- GLP-1 and GIP dual agonists: appetite biology and glycemic control
- Muscle preservation during weight loss: protein targets and resistance training
- Chiropractic care’s role in autonomic balance, biomechanics, and pain modulation
- Binge eating disorder: screening, neurobiology, and medication integration
- Men’s metabolic syndrome and fertility: aromatase, testosterone, stress, sleep apnea
- Perimenopause and MHT: symptom relief, metabolic effects, timing and safety
- Cardiometabolic risk reduction: viscerally focused strategies and cardiovascular indications for semaglutide
- Health equity and weight bias: ethical care and patient advocacy
References
Adam, T. C., & Epel, E. S. (2007). Stress, eating and the reward system. Physiology & Behavior.
Ahima, R. S. (2006). Metabolic syndrome: common pathophysiology and potential therapeutics. The New England Journal of Medicine.
Apovian, C. M., Aronne, L. J., Bessesen, D. H., McDonnell, M. E., Murad, M. H., Pagotto, U., Ryan, D. H., & Still, C. D. (2015). Pharmacological management of obesity: an Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 100(2), 342–362.
Azziz, R., et al. (2016). Polycystic ovary syndrome: pathophysiology, diagnosis, and treatment. The Journal of Clinical Endocrinology & Metabolism.
Bandura, A. (1997). Self-efficacy: The exercise of control. W. H. Freeman.
Berthoud, H.-R. (2011). Metabolic and hedonic drives in the neural control of feeding. Obesity Reviews.
Bialosky, J. E., et al. (2009). The mechanisms of manual therapy in musculoskeletal pain. Pain.
Bray, G. A., et al. (2016). Pharmacological treatment of obesity: Mechanisms and clinical recommendations. Current Hypertension Reports, 18(4), 19.
Cruz-Jentoft, A. J., et al. (2019). Sarcopenia: Revised European consensus on definition and diagnosis (EWGSOP2). Age and Aging, 48(1), 16–31.
de Jager, J., et al. (2010). Long-term metformin therapy and vitamin B12 deficiency: prevalence and associated factors. Diabetes Care, 33(11), 2330–2333.
DiPietro, L., et al. (2013). Moderate walking can reduce postprandial glycemia in older adults. Diabetes Care, 36(2), 326–333.
Drucker, D. J. (2006). Enhancing incretin action for the treatment of type 2 diabetes. The Lancet.
Dunaif, A. (1997). Insulin resistance and polycystic ovary syndrome: Mechanisms and implications. The New England Journal of Medicine.
Fairburn, C. G., & Harrison, P. J. (2003). Eating disorders. The New England Journal of Medicine.
Ferrannini, E., et al. (2013). Insulin resistance: Pathogenesis and clinical implications. Diabetes.
Frias, J. P., et al. (2021). Efficacy and safety of tirzepatide for type 2 diabetes. JAMA.
Gadde, K. M., et al. (2011). Effect of low-dose, controlled-release, phentermine plus topiramate on weight and associated comorbidities in overweight and obese adults (CONQUER). JAMA.
George, J., et al. (2014). Body mass index and outcomes in total knee arthroplasty: A systematic review and meta-analysis. The Journal of Arthroplasty, 29(9), 1796–1803.
Gorissen, S. H. M., & Witard, O. C. (2018). Characterizing the muscle anabolic potential of dairy and plant-based protein sources in older adults. Nutrition Reviews, 76(9), 616–631.
Greenway, F. L., et al. (2010). Naltrexone/bupropion therapy for obesity: A 56-week randomized, double-blind, placebo-controlled study. The New England Journal of Medicine, 363, 245–256.
Greenway, F. L. (2015). Phentermine and topiramate for weight management. Current Hypertension Reports.
Hambrecht, R., et al. (2003). Effects of exercise on coronary endothelial function. Circulation, 107(25), 3152–3158.
Hall, K. D., et al. (2019). Ultra-processed diets cause excess calorie intake and weight gain. Cell Metabolism, 30(1), 67–77.
Handschin, C., & Spiegelman, B. M. (2008). The role of exercise in mitochondrial biogenesis via PGC-1α signaling. Nature Immunology, 9, 353–356.
Hawley, J. A., & Lessard, S. J. (2008). Exercise training and insulin action: GLUT4 translocation mechanisms. Journal of Applied Physiology.
Hendricks, E. J., et al. (2011). Phentermine for obesity: Efficacy and safety review. Obesity, 19(12), 2359–2367.
Hojlund, K. (2014). Skeletal muscle mitochondrial dysfunction in insulin resistance. Diabetes, 63(9), 3063–3065.
Hudson, J. I., et al. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. American Journal of Psychiatry, 164(12), 1877–1886.
Ibrahim, M. M. (2010). Adipose tissue and the metabolic syndrome. Nature Reviews Molecular Cell Biology, 11(2), 88–99.
Jastreboff, A. M., et al. (2022). Tirzepatide once weekly for the treatment of obesity (SURMOUNT-1). The New England Journal of Medicine, 387(3), 205–216.
Kelly, D. M., et al. (2015). Testosterone, obesity, and metabolic risk in men. Clinical Endocrinology.
Kjaer, M. (2004). Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. The Journal of Physiology, 559(1), 333–336.
Lean, M. E. J., et al. (1995). Waist circumference as a marker of cardiovascular risk. BMJ, 311(6998), 158–161.
Legro, R. S., et al. (2013). Weight loss and ovulation in PCOS. Diabetes Care.
Leidy, H. J., et al. (2015). Higher protein intake leads to improved satiety and weight loss. American Journal of Clinical Nutrition.
Lincoff, A. M., et al. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes (SELECT). The New England Journal of Medicine, 389(24), 2221–2232.
Lovejoy, J. C., et al. (2008). Abdominal fat distribution and menopause. The Journal of Clinical Endocrinology & Metabolism, 93(12), 4606–4614.
Matthews, D. R., et al. (1985). Homeostasis Model Assessment: Insulin resistance and beta-cell function. Diabetologia, 28(7), 412–419.
McElroy, S. L., et al. (2015). Lisdexamfetamine in binge eating disorder. American Journal of Psychiatry.
Moran, L. J., et al. (2019). PCOS and metabolic health: A clinical review. Clinical Endocrinology.
Morton, R. W., et al. (2018). Resistance training and hypertrophy: Systematic review and meta-analysis. Medicine & Science in Sports & Exercise, 50(10), 1939–1948.
Neeland, I. J., et al. (2012). Visceral fat and cardiometabolic risk. Circulation, 125(8), 1101–1109.
NAMS (2022). The 2022 Hormone Therapy Position Statement of The North American Menopause Society. Menopause, 29(7), 767–794.
Ouchi, N., et al. (2011). Adipokines in inflammation and metabolic disease. Nature Reviews Molecular Cell Biology, 12(2), 85–97.
Pedersen, B. K., & Febbraio, M. A. (2012). Muscle-derived myokines and their role in metabolism. The Journal of Physiology, 590(5), 1059–1068.
Pickar, J. G. (2002). Neurophysiologic effects of spinal manipulation. Spine Journal, 2(5), 357–371.
Puhl, R. M., & Heuer, C. A. (2009). Weight bias in healthcare. Obesity, 17(5), 941–964.
Richter, E. A., & Hargreaves, M. (2013). Exercise, GLUT4, and type 2 diabetes. Journal of Applied Physiology.
Samuel, V. T., & Shulman, G. I. (2012). Mechanisms for insulin resistance: DAG/PKCθ and mitochondrial dysfunction. Nature, 485(7399), 58–64.
Shanik, M. H., et al. (2008). Insulin resistance and hyperinsulinemia. Journal of Clinical Endocrinology and Metabolism.
Shoelson, S. E., et al. (2006). Inflammation and insulin resistance. The New England Journal of Medicine.
Stice, E., et al. (2013). Neural vulnerability for obesity: Reward processing mechanisms. Biological Psychiatry, 73(9), 876–886.
Sumithran, P., et al. (2011). Long-term hormonal adaptations to weight loss. The New England Journal of Medicine, 365, 1597–1604.
Ter Horst, K. W., et al. (2017). Hepatic insulin resistance mechanisms. Diabetes, 66(2), 398–406.
Thayer, J. F., & Lane, R. D. (2007). The role of vagal tone in health. Biological Psychology.
Viollet, B., et al. (2012). Cellular and molecular mechanisms of metformin. Trends in Endocrinology & Metabolism.
Wilding, J. P. H., et al. (2021). Semaglutide for obesity. The New England Journal of Medicine, 384, 989–1002.
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Professional Scope of Practice *
The information herein on "A Comprehensive Guide for Obesity & Cardiometabolic Care" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.
Blog Information & Scope Discussions
Welcome to El Paso's Premier Fitness, Injury Care Clinic & Wellness Blog, where Dr. Alex Jimenez, DC, FNP-C, a Multi-State board-certified Family Practice Nurse Practitioner (FNP-BC) and Chiropractor (DC), presents insights on how our multidisciplinary team is dedicated to holistic healing and personalized care. Our practice aligns with evidence-based treatment protocols inspired by integrative medicine principles, similar to those found on this site and our family practice-based chiromed.com site, focusing on restoring health naturally for patients of all ages.
Our areas of multidisciplinary practice include Wellness & Nutrition, Chronic Pain, Personal Injury, Auto Accident Care, Work Injuries, Back Injury, Low Back Pain, Neck Pain, Migraine Headaches, Sports Injuries, Severe Sciatica, Scoliosis, Complex Herniated Discs, Fibromyalgia, Chronic Pain, Complex Injuries, Stress Management, Functional Medicine Treatments, and in-scope care protocols.
Our information scope is multidisciplinary, focusing on musculoskeletal and physical medicine, wellness, contributing etiological viscerosomatic disturbances within clinical presentations, associated somato-visceral reflex clinical dynamics, subluxation complexes, sensitive health issues, and functional medicine articles, topics, and discussions.
We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for musculoskeletal injuries or disorders.
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Dr. Alex Jimenez DC, MSACP, APRN, FNP-BC*, CCST, IFMCP, CFMP, ATN
email: [email protected]
Multidisciplinary Licensing & Board Certifications:
Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Texas DC License #: TX5807, Verified: TX5807
New Mexico DC License #: NM-DC2182, Verified: NM-DC2182
Multi-State Advanced Practice Registered Nurse (APRN*) in Texas & Multi-States
Multistate Compact APRN License by Endorsement (42 States)
Texas APRN License #: 1191402, Verified: 1191402 *
Florida APRN License #: 11043890, Verified: APRN11043890 *
Verify Link: Nursys License Verifier
* Prescriptive Authority Authorized
ANCC FNP-BC: Board Certified Nurse Practitioner*
Compact Status: Multi-State License: Authorized to Practice in 40 States*
Graduate with Honors: ICHS: MSN-FNP (Family Nurse Practitioner Program)
Degree Granted. Master's in Family Practice MSN Diploma (Cum Laude)
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
Digital Business Card
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)
(Licensed Medical Doctor)
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426749
MD License #: J2933
Licenses and Board Certifications:
MD: Medical Doctor
DC: Doctor of Chiropractic
APRNP: Advanced Practice Registered Nurse
FNP-BC: Family Practice Specialization (Multi-State Board Certified)
RN: Registered Nurse (Multi-State Compact License)
CFMP: Certified Functional Medicine Provider
MSN-FNP: Master of Science in Family Practice Medicine
MSACP: Master of Science in Advanced Clinical Practice
IFMCP: Institute of Functional Medicine
CCST: Certified Chiropractic Spinal Trauma
ATN: Advanced Translational Neutrogenomics
Memberships & Associations:
TCA: Texas Chiropractic Association: Member ID: 104311
AANP: American Association of Nurse Practitioners: Member ID: 2198960
ANA: American Nurse Association: Member ID: 06458222 (District TX01)
TNA: Texas Nurse Association: Member ID: 06458222
NPI: 1205907805
| Primary Taxonomy | Selected Taxonomy | State | License Number |
|---|---|---|---|
| No | 111N00000X - Chiropractor | NM | DC2182 |
| Yes | 111N00000X - Chiropractor | TX | DC5807 |
| Yes | 363LF0000X - Nurse Practitioner - Family | TX | 1191402 |
| Yes | 363LF0000X - Nurse Practitioner - Family | FL | 11043890 |
| Yes | 363LF0000X - Nurse Practitioner - Family | CO | C-APN.0105610-C-NP |
| Yes | 363LF0000X - Nurse Practitioner - Family | NY | N25929 |
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
Digital Business Card
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)*
(Licensed Medical Doctor)*
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426749
MD License #: J2933
